Printable list of all cardiology SAQs

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Question 14 - 2000, Paper 1

Discuss the pharmacology and place in the management of severe chronic heart failure of:

(a) enapapril 
(b) spironolactone 
(c) digoxin

College Answer

A big question for ten minutes. Candidates were expected to only·cover the surface. Some kinetics and dynamics and' the role in CCF would be expected,eg:

(a) Enalapril 
Phannacology: prodrug of angiotension II converting enzyme inhibitor enalaprilat. Long half·life,J 1 hours. Well absorbed orally. No IV preparation available. Offset of action due to renal excretion. 
Indications·hypertension, CCF, EF<JS% 
Ag II is now known to have numerous autocrine and paracrine effects. ACE inhibition produces far-reaching effects including-peripheral vasodilation, increased C.O.• myocardial­ remodeling etc. 
Side effects include hypotension, renal failure in the setting of renovascular disease, hypotensive reaction to albumin infusion, hyperkalaemia, and cough. 
Its role in severe chronic heart failure is well established in improving symptoms and exercise capacity, and improving survival due to myocardial and cerebral events.

(b) Spironolactone 
Pharmacology: competitive aldosterone inhibitor. Orally well absorbed. No IV preparation. 
Metabolised in the liver 
Produces K-sparing diuresis via aldosterone blockade. Aldosterone most likely has other roles in blood vessels promoting fibroblast proliferation and dehydration. Side effects include hyperkalaemia, dehydration and gynaeoomastia. Has been shown to produce increased survival in severe CCF (NHYA IV) when added to 
standard regimen of ACEI and loop diuretic. Recent placebo controlled trial stopped early because of marked benefit. Hyperkalaemia was not a problem.

(c) Digoxin 
Non-sympathetic inotrope. Blocks Na-K ATPase and indirectly increases intracellular Ca. 
Well absorbed orally. Renally excreted. Produces:   

-     increased contractility 
-    increased myocardial automaticity 
-    decreased A V conduction. 
Plasma concentration increased by amiodarone, verapramil. 
Side effects include nausea, vomiting, visual disturbance AV  bradycardias, tachycardias 
(flutter with block, VT, VF...). 
Overdose or toxicity may be treated with K. Mg, and antibodies. 
Its role in CCF is well established in patients with AF to control heart rate, improve mortality, exercise tolerance and symptoms. In patients with sinus rhythm and severe CCF unresponsive to other therapy, digoxin may produce improvement in symptoms but not mortality and hospital admission rate.

Discussion

I will agree with the court of examiners. There is too much ground to cover for a few minutes.  Again, perhaps it is better to tabulate this answer.

 

Enalapril

Spironolactone

Digoxin

Class

ACE-inhibitor

mineralocorticoid receptor antagonist

Cardiac glycoside

Pharmacokinetics

Orally available
Renally excreted
Minimal metabolism

Orally available
Hepatic metabolism

Orally available
Renally excreted
Minimal metabolism

Mechanism of action

Antihypertensive; modulates the activity of the renin-angiotensin-aldosterone system by inhibiting  the conversion of antiotensinogen into angiotensin by ACE (angiotensin-converting enzyme)

Diuretic; inhibits the effects of aldosterone in the cortical collecting duct, disabling the ENaC ion channel and thus increasing the excretion of sodium and water

AV nodal blocker and weak positive inotrope.

Inhibits the Na+/K+ ATPase, thereby lowering the intracellular membrane potential and decreasing the excitability of excitable tissues.
Also increases the  availability of intracellular calcium, and thus acts as a positive inotrope).

Advantages in  severe chronic heart failure

Decreased afterload
Improved cardiac remodeling and thus decreased morbidity and mortality

Decreased preload
Improved cardiac remodeling and thus decreased morbidity and mortality

Increased contractility
Rate control in arrhythmia

Precautions

May cause disregulation of renal blood flow. May contribute to renal failure

May cause type 4 renal tubular acidosis, hyponatremia, hyperkalemia.

Gynacomastia in 10%

Requires monitoring in renal failure
Risk of toxicity

The European statement I have referenced below is particularly helpful for this question.

In particular, section 7.2 (entitled "Treatments recommended in potentially all patients with systolic heart failure") lists the pharmacotherapy for heart failure, and provides evidence for it.

Enalapril must have been particularly exciting because of the CONSENSUS study (1988) which demonstrated an improvement in both mortality and NYHA grade. A smiliar high accolade is afforded to spironolactone by the RALES trial - fewer of those people died. Digoxin, on the other hand, does not seem to decrease mortality, but does seem to decrease the symptoms of people even while they are in sinus rhythm.

References

McMurray, John JV, et al. "ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2012 The Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association (HFA) of the ESC." European heart journal 33.14 (2012): 1787-1847.

CONSENSUS Trial Study Group. "Effects of enalapril on mortality in severe congestive heart failure. Results of the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS)." N Engl j Med 316 (1987): 1429-1435.

Pitt, Bertram, et al. "The effect of spironolactone on morbidity and mortality in patients with severe heart failure." New England Journal of Medicine 341.10 (1999): 709-717.

Hood Jr, William B., et al. "Digitalis for treatment of congestive heart failure in patients in sinus rhythm: a systematic review and meta-analysis." Journal of cardiac failure 10.2 (2004): 155-164.

 

Question 12 - 2000, Paper 2

What is the role of cardioselective betablockers in the management of severe heart failure in
ICU?

College Answer

Cardioselective betablockers  (eg. atenolol, metoprolol  & practolol) have less effect on the beta·2 receptors (less vasoconstriction and less bronchoconstriction). No specific benefits of any subgroup of beta·blockers bas been confumed inthe management of severe heart failure.

The candidates should be able to discuss the complex  role of betablockers in heart failure. The role of betablockers in heart failure management is complex enough outside of the !CU. This has been clarified further in the last few years by publication of articles confirming the benefit of addition of betablockers to the conventional  heart failure regimen (ACE inhibitor + diuretics)  in the outpatient setting  (with   decreased   symptoms,   slowing   progression,   improving   LV   function   and   even improving survival). These benefits have been demonstrated  initially with carvedilol (non-selective betablocker) and more recently with metoprolol (cardioselective betablocker). Titration of the medication needs to be slow and judicious. It is unknown whether similar benefits can be obtained in the ICU setting, especially given the beneficial effects of short term administration of inotropic agents in dilated cardiomypoathy.

Betablockers may have some  benefit in the setting  of tachycardia (mcreased  resting  sympathetic tone),  but  many  patients   may  experience  worsening  of  symptoms.  Success  of   treatment  ofarrhythmias  with   betablockade depends  upon   the   magnitude  of   the   coincident  decrease ·in contractility (other  agents  may be preferred  eg. amiodarone). Prevention of sudden  death (malignant ventricular  arrhythmias) may be achieved.

Treatment   of   myocardial  ischaemia  with   betablockers  may   have   beneficial  effects  (oxygen
requirements, improved relaxation, decreased arrhythmias).
Betablockade may  be  beneficial  in the  setting  of  hypertrophic cardiomyopathy  (with  diastolic dysftmction), by decreasing myocardial oxygen  consumption, decreasing ischaemia and  improving
relaxation (lusitropy).

Discussion

How about another table?

 

Advantages of cardioselective betablockers

Disadvantages of cardioselective beta blockers

Mortality

Improve mortality in heart failure patients

Mortality improvement is no different to non-selective beta blockers

Contractility

Decreased contractility; 
Decreased myocardial oxygen consumption and enhanced subendocardial blood flow

Decreased responsiveness to preload

Heart rate

Decreased heart rate = decreased cardiac workload

Fixed stroke volume x decreased heart rate = poor cardiac output

Afterload

No influence on afterload; maintained good diastolic coronary filling

No decrease in afterload = no decrease in cardiac work against afterload

Myocardial oxygen consumption and cardiac workload

Decreased myocardial oxygen consumption  due to decreased heart rate and contractility

Decreased exercise tolerance

Side effects

Fewer beta-2 effects, thus no disadvantage in peripheral vascular disease and asthma

Nightmares, depression, lethargy

References

Al-Gobari, Muaamar, et al. "Beta-blockers for the prevention of sudden cardiac death in heart failure patients: a meta-analysis of randomized controlled trials."BMC cardiovascular disorders 13.1 (2013): 52.

Tuunanen, Helena, and Juhani Knuuti. "Metabolic remodelling in human heart failure." Cardiovascular research 90.2 (2011): 251-257.

 

Question 13 - 2001, Paper 2

A 70 year old man with an implanted cardioverter/defibrillator is admitted to ICU following elective surgery.   How does the device affect your management?   What problems may be associated with the device?

College Answer

The cardioverter/defibrillator is usually inserted for ventricular arrhythmias resistant to antiarrhythmics or where antiarrhythmics are contraindicated. The patients usually have severe LV dysfunction and this has its own implications. Batteries usually last for 5-7 years and AV pacing facility is included.

In routine elective surgery its presence should not effect the patient’s management greatly but it may have been switched off because of the interference from diathermy. Cardiac surgery may have displaced a lead or fractured a lead, there is a risk of lead or box infection if bacteraemia occurs and threshold may be changed by medications. It is important to check with the responsible technician and cardiologist for programming and idiosyncrasies of the unit and maintain ECG monitoring with external defibrillator available.

Problems that arise from the device include –

•    Battery depletion

•    Lead fracture or displacement

•    Infection

•    Multiple shocks due to algorithm error, sensing failure, oversensing of physiological signals and lead failure

•    EMF interference from shaver, TV remote, MRI are also possible.

Discussion

Conditions which pose as indications for the insertion of an AICD are more threatening than the AICD itself, in my opinion.

Thus, the device itself affects ICU mangement only insofar as

  • it may malfunction, and either fail to pace or fail to shock
  • it may function too well (i.e. shock too often)
  • it may make imaging and procedures more difficult or impossible (eg. MRI).
  • it may act as a nidus for infection.

There is a beautiful and freely available article by Pinski et al which lists not only the common AICD-related problems, but also the solutions to them. In brief, the following problems may be encountered:

Total device failure: there is no pacing or AICD activity. The device appears dead for all intents and purposes. There are several possible causes for this:

  • Its battery may run out if it has not been checked recently.
  • The surgery may have damaged it, rendering it inoperable.
  • The anaesthetist had it turned off, in order to allow safe diathermy, and failed to turn it back on again.
  • The patient was externally defibrillated, and a 200J shock has completely fried the AICD circuitry.

Pacing failure: the device seems to be working (pacing spikes are seen on ECG) but there is no capture. This usually means something has happened to its interface with the myocardium.

  • The leads have become dislodged, eg. in moving the patient, or in the process of CVC insertion (classically, the PA catheter is to blame)
  • The whole device has been dislodged in some way, also pulling out the leads. Classically, this is associated with a demented patient who fiddles with their device.
  • The myocardium underlying the pacing lead has infarcted.
  • The lead has become infected

Failure to defibrillate VT or VF: the patient is clearly dying but the AICD for some reason refuses to rescue them. Why might that be? It is usually some sort of programing error. For instance:

  • Inappropriately high rate cutoff: the VT is not fast enough
  • Failure to satisfy multiple detection criteria (too many criteria)
  • Completed cycle, exhaustion of therapies (the AICD has run out of ideas)
  • Cross-inhibition by separate pacemaker

Overenthusiastic defibrillation: the device is shocking the patient relentlessly.

  • There is a genuine VT storm,
  • There is electrical interference, eg. from diathermy
  • The AICD is suffering a software error and is misinterpreting normal cardiac function or diaphragmatic myopotentials, delivering "spurious" shocks.

Inappropriately normal function: the device missed the family conference, and does not realise the patient is being palliated. In these situations the AICD should be disabled. Ethical issues arise if the patient has an underlying complete heart block or something similar (in which you might want to merely disable the defib function).

Logistic consequences of having an implantable device: i.e. problems with having some implanted object, with or without intrinsic electrical activity.

  • it may act as a nidus for infection
  • it interferes with line placement
  • it makes MRI impossible
  • it creates CT artifact, obscuring chest pathology

Obscure problems not unique to AICDs but common to PPMs as well:

  • Defib pad positioning for external defibrillation (if the AICD has failed) should be at least 8cm from the device, as per ARC guidelines. External defibrillation may cause device malfunction (Gould, 1981) - though, arguably, if you're using it on an AICD-equipped patient then the device has already malfunctioned.
  • Automated external defibrillators, when trying to interpret the rhythm of an arrested patient, may interpret the pacing spikes of a PPM or AICD as QRS complexes (Monsieurs, 1995). The consequences of this would be somebody potentially missing out on a lifesaving shock.
  • Demented patients can dislodge or malposition their own pacemaker leads ("Twiddler's syndrome"- Nicholson et al, 2003). 
  •  The device may explode in the crematorium, and though this is one of the  "problems may be associated with the device"  to mention this would probably generate no marks in this SAQ as it seems to refer to a living elective post-op patient. It is, however, a serious problem. "In the wall of the cremator was a finger-sized hole half an inch deep", report Gale et al (2002)

References

A bit of general information about the AICDs: DiMarco, John P. "Implantable cardioverter–defibrillators." New England Journal of Medicine 349.19 (2003): 1836-1847.

A more specific look at the problems they can cause: Pinski, Sergio L. "Emergencies related to implantable cardioverter-defibrillators."Critical care medicine 28.10 (2000): N174-N180.

GOULD, LAWRENCE, et al. "Pacemaker failure following external defibrillation." Pacing and Clinical Electrophysiology4.5 (1981): 575-577.

Gale, Christopher P., and Graham P. Mulley. "Pacemaker explosions in crematoria: problems and possible solutions." Journal of the Royal Society of Medicine 95.7 (2002): 353-355.

Monsieurs, Koenraad G., et al. "Semi-automatic external defibrillation and implanted cardiac pacemakers: understanding the interactions during resuscitation." Resuscitation 30.2 (1995): 127-131.

Nicholson, William J., Kathryn A. Tuohy, and Peter Tilkemeier. "Twiddler's syndrome." New England Journal of Medicine348.17 (2003): 1726-1727.

Question 4 - 2002, Paper 1

Outline your peri-operative management of a patient with ischaemic heart disease having an elective right hemicolectomy.

College Answer

Recent  evidence  based  guidelines   published  by  ACC/AHA.     Management   in  concert  with cardiologists and surgeons.  Ideal management often limited by resources.

Pre-operative assessment to determine patient risk.  Based predominantly on exercise tolerance (eg. MET [metabolic] equivalents), history (or not) of recent myocardial infarction, and stability of symptoms.   Standard preoperative  investigations  would include creatinine, urea and electrolytes, full  blood  examination,  ECG  and  CXR.    More  detailed  cardiovascular  investigations  may  be required (eg. exercise test, echocardiography and angiography).  Coronary arterial revascularisation (angiography/stenting/surgery)   may  be  indicated  before  elective  surgery  (balance  with  risk  of delaying  surgery  if  for  malignancy).     Left  ventricular  function  should  be  optimised. Cardiopulmonary  exercise  testing  may  enhance  risk stratification.    Peri-operative  beta-blockade would probably  have already been commenced  but is reasonable  unless contraindicated  (started days before surgery and targeting resting heart rate 50-60).

Intra-operative management (this operation = intermediate cardiac risk) may be aided by invasive monitoring (eg. intra-arterial, pulmonary arterial lines and/or trans-oesophageal echocardiography). ST monitoring is reasonable, as are intravenous nitrates.   Prevention of hypertension/tachycardia and hypotension are expected.  Epidural analgesia dependent on anaesthetic preference.

Post-operative  phase continues intra-operative  stability, and optimises pain relief.   Monitoring of ECG and CKMB/troponin  to determine extent of ischaemic risk (determined by 24 to 48 hours). Early reinstitution of beta-blockade (intravenous if necessary) and heparin/LMW heparin.   Severe cardiac failure may require inotropic support and/or longer period of invasive monitoring and observation (eg. 48 hours).

Discussion

This 2002 question refers to the "recently published" ACC/AHA guidelines. 
The 2014 reiteration of these guidelines is now available.

I will not make any attempt to summarise this 50page document.

Ok, maybe a little summary.

  • Preoperative assessment
    • Standard preoperative investigations including ECG, CXR, and bloods
    • Risk stratification, based on
      • Exercise tolerance (METs)
      • History of recent ischaemia
      • Stability of cardiac symptoms
    • High risk patients: cardiology referral for angiography and correction of coronary disease
    • Preoperative TTE and optimisation of LV function
  • Preoperative management
    • Control of hypertension
    • Control of arrhythmias
  • Intraoperative management
    • Precautionary invasive monitoring, eg. arterial line / PA catheter
    • Maintenance of normotension
    • Epidural anaesthesia
  • Postoperative management
    • Monitoring in ICU/HDU, and possibly delayed extubation
    • postoperative support with vasopressors and inotropes

The college, in this 2002 model answer, recommended the use of perioperative beta-blockers to reduce the mortality and risk of MI in these patients. Unfortunately, they recommended this on the basis of some work by Don Polderman, which was discredted after he was fired from his academic position for widespread fraud. Later systematic reviews (eg. Wijeysundera et al, 2014), after performing pre- and post-fraud analysis, determined that beta-blockers actual"y increased perioperative mortality after Polderman's work was excluded from the data set. "Perioperative beta blockade started within 1 day or less before noncardiac surgery prevents nonfatal MI but increases risks of stroke, death, hypotension, and bradycardia" they somberly concluded. As such, the current guidelines do not recommend preoperative beta blockade.

References

Fleisher, Lee A., et al. "2014 ACC/AHA guideline on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines." Journal of the American College of cardiology 64.22 (2014): 2373-2405.

Wijeysundera, Duminda N., et al. "Perioperative beta blockade in noncardiac surgery: a systematic review for the 2014 ACC/AHA guideline on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery: a report of the American College of Cardiology/American Heart Association Task Force on practice guidelines." Circulation 130.24 (2014): 2246-2264.

Question 14 - 2002, Paper 1

Outline the diagnostic features, complications and treatment of patients with Wolf- Parkinson-White syndrome.

College Answer

Diagnosis: history of arrhythmias (palpitations, dizzy, lightheaded), sudden death. ECG in sinus rhythm demonstrates short PR interval and delta waves. Electrophysiological evidence of AV conduction through AV bypass tract (bundle of Kent).

Complications:  recurrent  arrhythmias  (narrow  QRS  complex  orthodromic  AV  re-entrant tachycardia, wide QRS antidromic AV re-entrant tachycardia, atrial fibrillation (broad complex and may be very fast [> 200/min]), ventricular fibrillation), sudden death.

Treatment: (1) acute treatment of arrhythmias: a) Narrow SVT (as per SVT). b) Wide QRS SVT (procainamide; avoid adenosine, verapamil, digoxin and beta-blockers; treat as if VT). c) Atrial fibrilation:  (Appropriate  agents  include  procainamide,  amiodarone  and flecainide.  Avoid  agents which might slow AV conduction but not decrease conduction through bypass tract: i.e. adenosine, verapamil, digoxin and beta-blockers). (2) investigation via electrophysiologic evaluation: usually curative   ablation   of  accessory   pathway,   or  no  treatment   if  asymptomatic,   or  occasionally prophylactic medications.

Discussion

I would never be able to remember such things if they were not organised into headings and point form.

The below "model answer" is derived almost completely from UpToDate.

  • Diagnosis
    • ECG features of WPS are:
      • The PR interval is short (less than 0.12 seconds)
      • There is a delta wave (a slurred upstroke of the QRS complex)
      • Wide QRS (because the delta wave widens it)
      • ST Segment and T wave discordant changes: T waves point in the opposite direction to the QRS.
      • Pseudo-Q waves: negatively deflected delta waves in the inferior / anterior leads
      • prominent R wave in V1-3 (mimicking posterior infarction).
    • Ideally, this sort of ECG should come with a history of syncopal episodes.
    • Characteristic electrophysiology findings of an  accessory pathway (Bundle of Kent) are desirable but non essential.
  • Complications
    • SVT, which comes in two flavours. if the complexes are narrow, its orthodromic. If they are wide and with delta-waves, its antidromic. Does that really matter? Probably not.
    • AF  is disturbingly common in WPW- 10 to 30% of patients will have it at some point. Having AVRT predisposes one to AF in this situation because the reentry circuit via the accessory pathway can cause the atria to contract quite randomly (after all, the accessory pathway is not a serious part of the conducting system, and it doesn’t link into any sort of conduction pathways- its just going to excite any old patch of atrium). The ECG will throw you off. The conduction rate is roughly 1:1.5; the QRS rate is about 180 to 200. It is hard to tell that its irregularly irregular. The QRS complexes will be a mixture of pre-excited delta-waving ones, and normal-looking narrow ones. If the accessory pathway has a short refractory period, it will conduct more often and therefore there will be more broad complexes than narrow ones. The shorter the refractory period of the accessory pathway, the broader the QRS. And the broader the QRS, the greater the chance of this thing degenerating into ventricular fibrillation.
    • Atrial flutter can also conduct via the bundle of Kent. There will be 1:1 conduction. Ventricular rate will approach 300. Because this is an antidromic way of conducting impulses, the QRS complexes will be broad and there will be delta waves. Unlike AF, the rate runs with a metronome-like regularity. The patient will likely look dead.
    • Ventricular fibrillation is a common cause of sudden cardiac death among the WPWs. So, in AF with WPW conduction, the rate of ventricular contraction is increased, and the regularity is decreased. This fractionates the wavefront of ventricular depolarization. Soon enough, there are numerous wavefronts all moving around the ventricle. This is ventricular fibrillation. If you block the AV node, occasionally the accessory pathway will launch the ventricles into this. It’s a known, and extremely uncommon, complication of adenosine use in WPW.
    • Syncope and sudden cardiac death are the natural histories of these arrhythmias in WPW, because they are frequently too fast to be perfusing rhythms. The surviving sufferer is typically saved by their youth, as they may be better able to tolerate hummingbird-like heart rate for sustained periods.
  • Management of acute arrhythmias
    • vagal manoeuvres
    • AVOID ASV node blocking drugs such as adenosine, digoxin, beta blockers and calcium channel blockers
    • Procainamide, ibutilide or (maybe) amiodarone are the only antiarrhytmics useful in WPW
    • DC synchronised cardioversion
  • Long-term management
    • Catheter ablation of accessory pathway
    • Flecainide or propafenone
    • amiodarone also OK - but the side effect profile in long term use is not very nice for younger patients

WPW also crops up in Question 3.1 from the first paper of 2009.

References

Narula, Onkar S. "Wolff-Parkinson-White Syndrome A Review." Circulation 47.4 (1973): 872-887.

and, somewhat more recently...

Scheinman, Melvin M. "History of Wolff‐Parkinson‐White Syndrome." Pacing and clinical electrophysiology 28.2 (2005): 152-156.

Keating, L., F. P. Morris, and W. J. Brady. "Electrocardiographic features of Wolff-Parkinson-White syndrome." Emergency medicine journal 20.5 (2003): 491-493.

 

 

Question 3 - 2003, Paper 1

Compare and contrast the role of Troponin and CKMB in the management of myocardial ischaemia in the critically ill.

College Answer

CKMB is creatine kinase dimer of M and B chains and exists as 4.   It is found in a high ratio predominantly  in  myocardial  cytosol,  but  is  also  present  in  skeletal  muscle  (especially  in myopathies or after injury).  Levels of CK MB rise within 4 to 12 hours of myocardial infarction (high sensitivity and specificity), peak at 18 to 24 hours and return to baseline by 36 to 40 hours. Diagnosis of MI may be enhanced by measuring MB isoforms (higher sensitivity) or use of MBfraction of total CK (problem if significant skeletal muscle damage [eg. surgery, cardioversion], hypothyroidism or renal failure [CKMB elevated in approximately 30 to 70 percent of dialysis patients]).   Not increased in myocarditis.   CKMB level is indicative of infarct size, and is independent prognostic marker.  Rapid return of level to normal allows potential for diagnosis of reinfarction.

Cardiac troponins are cardiac regulatory proteins and exist as “T” and “I” forms.  Early release is from cytosol, and subsequent release from damaged structural components.   Many results from early studies hindered by variability in assays.  More recent (second generation) assays are highly specific for cardiac troponins (both forms).  Levels rise within 4 to 12 hours after myocardial infarction (high specificity but less sensitivity if rely on 6 hour specimen), peak at 18 to 24 hours, but levels stay elevated for up to 10 days (allows late diagnosis of MI, but not reinfarction). cTpI preferred  in  renal  failure  (false  positive  elevations  of  cTnT:  in  one  study  82  percent  of asymptomatic dialysis patients had elevated cTnT levels when the cutoff value was 0.01 µ g/L!). Elevations may occur in pulmonary embolism or myocarditis, but potentially better than CKMB for situations where skeletal muscle damage is present (eg. DCR, trauma, post-op).  Level of troponin also associated with prognosis (? clinical relevance of subtle elevations).

Elevation of cardiac enzymes (if not a false positive) without ECG changes is now considered to represent a non-ST elevation myocardial infarction.

Discussion

This question had found a more detailed incarnation in a later paper - 2010 paper 2, question 27.

An answer to this question lends well to a table format.

Biomarker

Troponin

CKMB

Origin

Highly specific  injured myocardium

Myocardium as well as skeletal muscle;
MB isoform is more specific

Pharmacokinetics

Rise within 4-6hrs;
Peak within 18-24 hrs
Slow to clear (7-14 days)

Rise within 4-12 hrs;
Peak within 18-24 hrs
Rapidly cleared (2-3 days)

Use in critical care

More sensitive than CK for cardiac ischaemia

Rapid rise allows earlier identification of ischaemia

Correlate well with risk stratification

Strongly associated with  30-day mortality

Less sensitive for cardiac ischaemia than TnT

Rapid clearance allows the detection of reinfarction

Causes of elevation unrelated to coronary ischaemia

Pulmonary embolism
Tachyarrhythmia
Post-defibrillation
Post-CPR
Post-cardiotomy
Cardiac trauma
Myocarditis

Pulmonary embolism
Tachyarrhythmia
Post-defibrillation
Post-CPR
Post-cardiotomy
Cardiac trauma

Non-cardiac causes of elevation

Sepsis
Renal failure

Sepsis 
Renal failure
Rhabdomyolysis
Trauma
Major surgery
Burns (esp electrical)

 

References

McLean, Anthony S., and Stephen J. Huang. "Cardiac biomarkers in the intensive care unit." Ann Intensive Care 2.8 (2012): 1-11.

Question 2a - 2004, Paper 1

A 76-year-old woman with severe ischaemic heart disease being treated with aspirin, clopidogrel and metoprolol presents with severe abdominal and back pain, 6 hours after  being discharged home from a routine cardiac angiogram via the femoral route.

a)        How would you investigate the cause?

College Answer

a)        How would you investigate the cause?

The differential could be large and could include pancreatitis, retroperitoneal haematoma, aortic dissection, cholecystitis, infarcted gut, G-I perforation, diverticular disease, pericarditis, myocardial infarction/ischaemia, pneumothorax. Investigation includes, a proper history (character, type, severity, position of pain, associated features etc), full clinical examination (signs of all the above possibilities) and relevant investigations .   Amylase, Hb (has it fallen?), wbc, U&Es, LFTs, ChestXR, ECG and troponin, U/S abdomen, echocardiogram, CT scan abdomen depending on the most likely cause. A good answer would also include what would be expected from the investigations ordered.

A large retroperitoneal  haematoma is diagnosed. After resuscitation, the bleeding is stopped by angiographic embolisation of a branch of the left internal iliac artery.
She  is  still  in  the  intensive care  unit  2  days  later  when  she  becomes suddenly dyspnoeic, hypoxaemic and hypotensive with a BP of 80 systolic.

Discussion

This woman sounds like a retroperitoneal haematoma from the very beginning, but one must go though the motions

a)        How would you investigate the cause?

A thorough history and detailed physical examination would be a good start.

Differentials:

  • Aortic dissection
  • Retroperitoneal hematoma
  • Ischaemic gut
  • perforated viscus
  • cholecystitis
  • pancreatitis
  • splenic infarct

One would assess the abdomen particularly, looking for masses.

One would auscultate the abdomen, listening for a bruit of aortic dissection

One would also look for features of shock, metabolic acidosis, and peritonism, suggestive of ischaemic gut (due to emboli dislodged from the aorta)

A CXR, ABG, ECG, a full panel of bloods including FBC, LFT, amylase/lipase and inflammatory makers.

An abdominal ultrasound looking for vascular tree damage, and a CT of the abdomen with IV contrast to image the intraabdominal organs and their supplying vessels.

References

Question 2 - 2004, Paper 2

Outline your approach to the management of rapid atrial fibrillation in the critically ill patient.

College Answer

Management of atrial fibrillation requires consideration of urgency of treatment, reversal of potentially reversible causes, rate control, rhythm control and risks of thromboembolism. In the acute setting either rate control or reversion to sinus rhythm may provide haemodynamic benefits. Reversion to sinus rhythm is reasonable if atrial thrombi not expected (AF or more than 48 hrs duration or unknown duration). The use of trans-oesophageal echocardiography in excluding atrial thrombi is still uncertain (as not all thrombi identified). If reversion would add risks of thromboembolism then rate control and anticoagulation is preferred. In the presence of haemodynamic instability synchronised cardioversion (before or after administration of drugs/electrolytes) should be considered. If reversion is desired, correction of electrolytes (K and Mg) and specific drugs may be successful (eg. one of amiodarone [especially if impaired LV function], flecainide, procainamide, ibutilide or propafenone). If rate control only is desired then calcium channel blockers, beta-blockers or digoxin can be considered. Many critically ill patients are resistant to rate control with digoxin. Beta- blockers, calcium channel blockers and digoxin can be harmful if the rapid AF is due to Wolff-Parkinson-White syndrome.
Specific reversible causes may include drugs (eg. beta-agonists), mechanical stimuli (eg. guidewire, or catheters) and systemic disorders (eg. thyrotoxicosis, sepsis). Published guidelines (ILCOR, AHA) are available.

Discussion

The question calls for a systematic approach.

Such an approach can be reviewed in the ILCOR guidelines, from which the local ARC guidelines are derived.

A fresh recently published article presents a lovely table of causes of AF in the ICU (Table 1) as well as a lucid and detailed discussion of the therapeutic options. My answer was largely modelled on these suggestions.

  • Assess  the patient by history physical examination; establish the duration of AF and the likely cause for its onset (if possible)
  • Stratify into hemodynamically stable or compromised category on the basis of changes in vital signs and tissue perfusion before and after the episode

Hemodynamically stable patient:

  • Rate control with beta blockers, calcium channel blockers, digoxin or amiodarone
  • Reverse any potentially reversible factors
  • Consider DC or chemical cardoversion if AF is of recent onset
  • Commence anticoagulation if AF is of uncertain onset, or longer than 48 hrs duration. The options are:
    • Warfarin: relative risk reduction for stroke 62%; absolute risk reduction 2.8% per year
    • Aspirin: relative risk reduction for stroke 22%; absolute risk reduction 1.5% per year
    • Warfarin plus aspirin: no additional benefit over warfarin alone
    • Dabigatran: 35% reduction in stroke compared to warfarin
  • Consider TOE to rule out intracardiac thrombi
  • Reverse any potentially reversible factors

Hemodynamically compromised patient

  • Basic  life support as needed
  • Synchronised DC cardioversion
  • Hemodynamic and respiratory support as needed, including emchanical ventilation and inotropes/vasopressors
  • Reverse any potentially reversible factors

Investigation of causes, reversal of reversible factors, and preventative strategies

  • Investigate causes and institiute preventive corrections
    • Screen for sepsis
    • Correct electrolyte abnormalities
    • Correct hypothermia
    • Correct mechanical stimulus to the atria, eg. central lines
    • Corect atrial distension, eg. fluid overload
    • Address issues of pain and anxiety
    • Investigate for cardiac ischaemia
    • Investigate for endocrine abnormalities, eg. thyroid function and phaemochromocytoma

References

Morrison, Laurie J., et al. "Part 8: advanced life support 2010 international consensus on cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendations." Circulation 122.16 suppl 2 (2010): S345-S421.

Arrigo, Mattia, Dominique Bettex, and Alain Rudiger. "Management of Atrial Fibrillation in Critically Ill Patients." Critical Care Research and Practice 2014 (2014).

 

Question 6 - 2005, Paper 1

Critically evaluate the role of cardioversion in Intensive Care practice.

College Answer

Cardioversion is the delivery of energy that is synchronised with the QRS complex in an attempt to revert an abnormal rhythm.  Defibrillation is the non-synchronised (ie. random) delivery of energy and is used in unstable rhythms (eg. pulseless VT or VF).

The potential benefits (correction of the underlying rhythm) need to be balanced against the potential risks, especially in the critically ill, and should not be undertaken lightly.

Success rates vary with the characteristics of the underlying rhythm (highest in SVT and atrial flutter, and lower in AF [inversely related to left atrial size, duration of AF, and precipitating cause still being present {eg. hyperadrenegic state secondary to sepsis}]), and the energy delivered (often deliver 150 to 200J biphasic, lower with atrial flutter). Potential risks include:

•    Failure    of    cardioversion    (insufficient    energy    delivered,    technical     factors, misdiagnosis of rhythm [eg. sinus tachycardia!])

•    Requirement for some degree of sedation and analgesia; potential for awareness

•    Hypotension

•    Myocardial damage (ST changes and myocardial dysfunction usually short term; minimal elevation in troponins)

•    Arrhythmias (eg. SVT, non-sustained VT, rarely more malignant [more likely if digoxin toxic and hypokalaemic])

•    Conduction  abnormalities  (bradycardia,  and  heart  block  common;  occasionally needing temporary pacing)

•    Embolisation (especially if AF present > 48 hrs and not anticoagulated; strategy may include TOE)

•    Damage to permanent pacemaker (if not careful with electrode placement)

•    Others include pulmonary oedema, skin burns and risk of sparking/fire.

Discussion

This is a weird question. Sometimes, one cannot help but cardiovert somebody. For instance, the most recent guidelines from the ARC recommend that synchronised cardioversion be first-line therapy for any hemodynamically unstable tachyarrhythmia. One may as well ask the candidates to critically evaluate micturition; to be sure alternatives exist but it is really the well-established standard.

Anyway, this question could be interpreted slightly differently.

Taking into account the inevitability of cardioversion in certain situations, one could critically evaluate the risks and benefits of it with a focus on the semi-elective patient, in whom pharmacological cardioversion is an option.

Rationale for the use of direct current to convert cardiac rhythm

Cardioversion is the use of a short ( 200msec) discharge of direct current which is synchronised with the QRS complexes, so as to convert an abnormal rhythm to sinus rhythm. It has not always been direct current (Claude Beck's 1947 model defibrillator used AC straight from the wall outlet, and generally only Soviet defibrillators were biphasic DC until the 1960s). Ultimately, direct current was found to be safer: a larger amount of energy could be delivered in a short period of time. The mechanism remains incompletely understood. Various groups have suggested various explanations. Direct current travels around the cells as well as through them;  the effect is to change the transmembrane electrical potentials. One might expect all the cells to depolarise because all of the voltage-gated ion channels suddenly open, but the effect does not seem uniform: some cells depolarise and others hyperpolarise. In any case, this disrupts the normal propagation of action potentials. In this manner, DC current depolarises a sufficiently large amount of cardiac tissue, putting it into a refractory period and preventing the propagation of a reentrant current (which then dies away).

Advantages of DC cardioversion over chemical cardioversion

  • Electrical cardioversion is immediately effective (when it is effective)
  • It may be life-saving in a haemodynamically unstable arrhythmia
  • Automated devices ensure synchronisation so that  R-on-T phenomena should not occur
  • There are relatively few long-term side effects associated with it (i.e. unlike long-term amiodarone it won't give you pulmonary fibrosis) 

Disadvantages of electrical cardioversion in comparison to antiarrhythmic drugs

  • It is not a long-term strategy: if the underlying pathology has not been fixed, reversion to sinus rhythm will not be sustained.
  • There is the risk of arterial thromboembolism, although this is probably much the same risk as with pharmacological cardioversion, or with spontaneous reversion to sinus rhythm for that matter
  • It requires a sedated patient.
  • It will result in a raised troponin, which may obscure the presence of genuine myocardial infarction.
  • It requires the accurate diagnosis of rhythm

Accepted applications of electrical cardioversion

  • Atrial flutter (good chance of success)
  • Supraventricular tachycardia (good chance of success)
  • VT
  • Atrial fibrillation (poor chance of success, especially if the AF has been going on for a very long time).

Potential complications of electrical cardioversion

  • Ventricular fibrillation may develop due to lack of synchronization.
  • Sudden restoration of sinus rhythm can dislodge intracardiac thrombi.
  • Transient left bundle branch block may develop. In fact any sort of conduction block may develop, including complete heart block.
  • Transient left ventricular systolic dysfunction may develop. In fact you could cause myocardial damage.
  • There may be skin burns due to incorrect use of the equipment.
  • If the patient has a pacemaker, you may damage it with the direct current. 
  • If the patient has digoxin toxicity, one may induce VF in such a patient.

References

Mayr, Andreas, et al. "Effectiveness of direct-current cardioversion for treatment of supraventricular tachyarrhythmias, in particular atrial fibrillation, in surgical intensive care patients*." Critical care medicine 31.2 (2003): 401-405.

Trappe, Hans-Joachim, Bodo Brandts, and Peter Weismueller. "Arrhythmias in the intensive care patient." Current opinion in critical care 9.5 (2003): 345-355.

Question 30 - 2005, Paper 1

This is the ECG of a 73 year old man who was noticed to have a slow pulse rate. He has a past  history  of  ischemic  heart  disease  and  is  being  treated  with  digoxin  and  beta- adrenergic blockers.

What is the rhythm?  What is the conduction abnormality?  Please justify your responses.

College Answer

The rhythm is Atrial Flutter with a high degree (but apparently consistent) AV block, and a ventricular rate of approximately 40/minute. There is an obvious saw-tooth pattern of atrial depolarisations (at  a  rate  of  approximately 250/min)  seen  in  many  leads.  Association between the flutter and the ventricular depolarisations is based on the finding of a constant PR interval (with a fixed relationship between the P wave and the QRS complex), which excludes AF, and complete heart block.

The conduction abnormality is a tri-fascicular block as it includes:

•    Second degree (Mobitz II) AV block (as evidenced by constant relationship between P waves and the QRS)

•    Right bundle branch block (QRS > 0.12, RSR in V1, S in lead 1)

•    Left anterior hemiblock implied by left axis deviation (slightly positive in 1, negative with small R waves in II and III)

Discussion

The accuracy and completeness of the college answer makes it difficult to discuss this question.

Certainly, I cannot improve on their response.

One can read further about these ECG abnormalities within the body of this site:

Or one could review the topic properly at LITFL.

References

Question 15 - 2005, Paper 2

A blood gas result and an Electrocardiogram are obtained  from a 26 year old man who presents with recurrent respiratory failure.

Barometric pressure = 760 mmHg

FiO2

1.0

pH

7.46

7.35-7.45

pCO2

54

35-45 mmHg

pO2

50

mmHg

HCO3

37

20-30 mmol/L

Please explain these results.  Outline how you would clarify the cardiac status  in this patient. Justify your choices.

College Answer

This man is profoundly hypoxic with a PaO2 of only 50 mmHg on 100% oxygen (AaDO2=596 mmHg; PaO2/FiO2 ratio 50).

He is alkalemic, with an elevated bicarbonate (metabolic alkalosis) and an elevated PaCO2 (higher than predicted = respiratory acidosis)

Electrocardiographic features of 1st degree heart block and RVH: Right axis, R wave in V1>5mm, R/S in V1>1 and R/S in V6 >2.5.

Further information that may help clarify the cardiac status include:

Clinical examination (RV heave, loud P2, raised JVP, giant v waves, pulsatile liver, ascites, peripheral oedema).

CXR may show lung disease, and show evidence of pulmonary arterial hypertension (prominent pulmonary arteries with peripheral pruning).

Echocardiogram (TTE vs TOE)- will show RV hypertrophy, may reveal PA pressures if there is some TR (which is usual in pulmonary hypertension). Exclude Ostium primum ASD, Eisenmengers complex.

Pulmonary artery catheter will reveal PA pressures and cardiac output. V/Q is a poor test to investigate chronic RV hypertrophy.

Discussion

The ECG features of RVH are explored in this excellent article from LITFL. Thank you, Ed Burns!

In summary, the changes are as follows:

  • Right axis deviation
  • Dominant R wave in V1
  • Dominant S wave in V5-V6
  • Normal QRS duration (i.e. not a right bundle branch block)

Right ventricular strain patterns is also well covered there:

  • ST depression / T wave inversion in the anterior leads, V1 - V2
  • ST depression / T wave inversion in the inferior and right-facing limb leads ( II, III and aVF)

Now, as to what the college means by "clarify the cardiac status" - this is uncertain.

I guess that must mean "investigate the cardiac causes of these ECG changes and blood gas abnormalities".

That would have been a better way to word this question.

Thus, we have RVH on the ECG and a metabolic alkalosis, respiratory acidosis and profound hypoxia on the ABG.

One immediately begins thinking about some sort of pulmonary arterial hypertension, pulmonic valve stenosis, massive PE, or a cyanotic heart defect with a right-to-left shunt.

How would one discriminate among these differentials?

By taking a thorough history, performing a complete examination, and requesting appropriate investigations.

  • History:
    • Features of pulmonary hypertension, incl. SOB, cyanosis, exercise in tolerance
    • History of foetal alcohol exposure or a family history of congenital heart defects
    • History of exposure to volatile toxins, disease-causing dust (eg. asbestos) or heavy smoking
    • History of thromboembolic disease, prothrombotic diathesis
  • Examination:
    • Features of pulmonary hypertension: split P2, opening snap of pulmonic valve, flow murmur though pulmonic valve, prominent a waves
    • Features of RVH: right parasternal heave, prominent a waves, tricuspid regurgitation murmur, cannon v waves
    • Features of RV failure: pulsatile liver, engorged pulsatile veins
    • Congential syndromic features which might lead one to investigate for congenital heart disease
  • Investigations
    • CXR to interrogate the mediastinal contour and to look for features of poulmonary hypertension
    • TTE to observe the characteristic echocardiographc features of the above
    • CTPA and bilateral lower limb dopplers to exclude thromboemolic cause for hypertension
    • Right heart study to measure the oxygen saturation in each chamber, looking for a ventricular septal defect - as well as measuring the pressures.

References

Myers, Gordon B., Howard A. Klein, and Bert E. Stofer. "The electrocardiographic diagnosis of right ventricular hypertrophy." American heart journal 35.1 (1948): 1-40. - this goes back to well before the lazyness of transthoracic echo.

CHEST has an old 1993 article about pulmonary hypertension, which has some relevance to this very day;
Rubin, L. J. "Primary pulmonary hypertension." CHEST Journal 104.1 (1993): 236-250.

If one wishes to avoid the right heart study, one may wish to examine these European guidelines:
Grünig, Ekkehard, et al. "Non-invasive diagnosis of pulmonary hypertension: ESC/ERS Guidelines with Updated Commentary of the Cologne Consensus Conference 2011." International journal of cardiology 154 (2011): S3-S12.

Question 27 - 2006, Paper 1

Clinical examination of a 35 year old man who is short of breath reveals a pansystolic murmur.  Outline  the salient  clinical features and  investigations  which will help you distinguish  between  mitral  regurgitation, tricuspid regurgitation and  a  ventricular septal defect in this setting.

College Answer

This question lends itself to answering with table. An example of the sort of information that could
be provided is included in the following example table:

MR

TR

VSD

Symptoms

Paroxysmal
Nocturnal Dyspnoea, orthopnea, palpitations, Chest Pain

Pedal oedema,
Chest Pain, Short
Of Breath

Chest Pain, Short
Of Breath

Pulse

Commonly AF

May be AF

Usually Sinus
Rhythm

JVP

May be raised

V waves

Prominent a waves
because of pulmonary hypertension

Precordium

Systolic Thrill +/-
Parasternal lift +/-

Systolic Thrill +/-
Parasternal lift +/-

Systolic Thrill +/-
Parasternal lift +/-

Murmur

Apical to axilla

Left Sternal Border,
increases with inspiration

Left Sternal
Border, occasionally concomitant Atrial Regurgitation

Other systemic
signs

Basal crepitations

Pulsatile liver

Other congenital
abnormalities +/-

Chest X-Ray

Straight Left heart
border, pulmonary oedema

Enlarged Right
Atrium

Nil specific

Echocardiogram

Classic features

Classic features

Classic features

Pulmonary Artery
Catheter

Pulmonary
hypertension

Pulmonary
hypertension, V waves on Central Venous Pressure

Step up in O2
saturation at
ventricular level

Discussion

To answer this, I have referred again to my own tabulated summary of heart murmurs.

One can do little to improve on the table presented in the college answer.

The MR and TR are easy to tell apart. TR gets louder on inspiration, and causes a pulsatile liver.

MR gets louder on expiration, and causes pulmonary oedema.

The VSD is a little more tricky, and apart from occasionally causing pulmonary hypertension its murmur is difficult to distinguish from the others.

Both VSD and MR will be loudest on expiration, but VSD will be most audible at the left sternal border, whereas the MR is best heard near the apex.

References

Clinical Examination of the Critically Ill Patient, 3rd edition by L.I.G. Worthley - which can be ordered from our college here.

 

Clinical Examination: whatever edition, by Talley and O'Connor. Can be acquired anywhere.

 

Question 29 - 2006, Paper 1

A 76 year old woman  with severe ischaemic heart disease being treated with aspirin, clopidogrel  and  metoprolol  presents with  severe  abdominal and  back  pain,  6 hours after being discharged home from a routine cardiac angiogram via the femoral route. List the differential diagnosis.   Outline how you would investigate the cause of the abdominal pain.

College Answer

The  differential   diagnosis   could  be  large  and  should  include  pancreatitis,  retroperitoneal
haematoma, aortic dissection, cholecystitis, infarcted gut, Gastro-Intestinal perforation, diverticular disease, pericarditis, myocardial infarction/ischaemia, pneumothorax, etc.
Investigation  includes, in addition to a proper history (character, type, severity, position of pain, associated features etc), and a full clinical examination (signs of all the above possibilities) a number of relevant investigations. Consider: Amylase, Haemoglobin (has it fallen?), white blood cells,  Urea  &Electrolytes,  lactate,  Liver  Function  Tests,  Chest  X-Ray,  ECG  and  troponin, ultrasound abdomen, echocardiogram, CT scan abdomen depending on the most likely cause. A good answer would also include what would be expected from the investigations ordered.

Discussion

This question closely resembles Question 2 from the first paper of 2004.

In short, a thorough history and detailed physical examination would be a good start.

Differentials:

  • Aortic dissection
  • Retroperitoneal hematoma
  • Ischaemic gut
  • perforated viscus
  • cholecystitis
  • pancreatitis
  • splenic infarct

One would assess the abdomen particularly, looking for masses.

One would auscultate the abdomen, listening for a bruit of aortic dissection

One would also look for features of shock, metabolic acidosis, and peritonism, suggestive of ischaemic gut (due to emboli dislodged from the aorta)

A CXR, ABG, ECG, a full panel of bloods including FBC, LFT, amylase/lipase and inflammatory makers.

An abdominal ultrasound looking for vascular tree damage, and a CT of the abdomen with IV contrast to image the intraabdominal organs and their supplying vessel

References

Question 8 - 2006, Paper 2

Critically evaluate the interpretation of plasma troponin measurement in critically ill patients.

College Answer

Key features

•    Troponin I, T and C form a 3 unit complex with tropomyosin in cardiac actin filament, CTnI and cTnT used as cardiac specific markers, small amount in cytoplasm but a large actin pool, slowly released, and slowly degraded with small elevation in renal failure


•    Greater sensitivity to cardiac damage than CK-MB which can also be found in skeletal muscle (increased in myopathies), gut, uterus, and IgG complexes CK-MB, rises 4-6 h after onset symptoms for myocardial infarction, useful prognostic marker in acute coronary syndromes (higher level = worse prognosis)


•    Elevated level also seen with PE, sepsis, myocarditis, pericarditis, cardiac trauma, drug- induced myocardial injury, cardioversion

Discussion

This question is almost identical to Question 10 from the second paper of 2011.

To simplify revision and wreck some SEO, the answer for Question 10 is reproduced below.

Rationale for the use of troponin in the critically ill:

  • Troponin is an enzyme involved in the excitation-contraction coupling of the myocardium.
  • Troponin T serves to attach the troponin complex to actin and tropomyosin.
  • Myocardiac damage (for example infarction) causes the release of troponin.
  • There is a cytosolic pool (which is released early in the infarct) and a structural pool (which is slowly released over days as the damaged myocardium decomposes).

Advantages of using troponin in critically ill patients

  • Its a sensitive and specific marker of myocardial ischaemia.
  • It is more sensitive and specific than AST, CK and CK-MB (which are also found is skeletal muscle)
  • It is an independent predictor of 30-day mortality in STEMI 
  • It is associated with a poorer outcome in the critically ill patients.
  • Troponin levels can be used to monitor for myocardial ischaemia in critically ill patients when history and examination are unreliable.

Advantages of using troponin in acute coronary syndromes

  • Troponin forms a part of the ECS and AHA universal definition of acute coronary syndrome (it consists of a troponin rise as well as a demonstration of ischaemic symptoms,  echocardiographic evidence, or ECG changes.)
  • The troponin levels are not diagnostic, but are a risk stratification tool to be used together with echocardiography, ECG, history and examination.
  • Troponin levels can be used for the late diagnosis of MI and to monitor for reinfarction
  •  The use of troponin as a part of a risk stratification strategy is important in selecting patients for anticoagulation and anti-platelet therapy, so as to prevent the exposure of patients to unnecessary bleeding risk.

Disadvantages for the use of troponin in critical illness

  • A reliance on biomarkers may become unhealthy if it takes focus off clinical examination and history.
  • It is not quantitatively validated outside the setting of ACS / AMI, but only qualitatively: i.e. a "positive" troponin is associated with worse outcomes in noncardiac critical illness, but we don't know whether a higher troponin is associated with a proportionally higher mortality.
  • As with all biomarkers, inappropriately low threshold levels or testing out of appropriate clinical context could give rise to unnecessary treatments (eg. loading doses of antiplatelet drugs) or investigations (eg. angiography, with needless contrast exposure)
  • Troponin levels can be raised for a variety of non-cardiac reasons.In their 2006 article, Korff et aloffer an excellent table of things which cause troponin elevation, together with the mechanism of troponin release or assay confusion. Their Table 1 is reinterpreted here. 
    • Myocarditis 
    • Renal failure - its cleared renally
    • Sepsis
    • Atrial fibrillation
    • Post-cardioversion 
    • Cardiac trauma 
    • Pulmonary embolism 
    • Acute stroke
    • Intracranial haemorrhage
    • Severe burns
    • Rhabdomyolysis (particularly during recovery)
    • Skeletal muscle damage in glycogen storage disease
    • Defective assay (cross-reactivity with skeletal troponin isoforms)

References

This article has a nice graph of cardiac biomarker concentrations over time after an infarct:
Wu et al; National Academy of Clinical Biochemistry Standards of Laboratory Practice: Recommendations for the Use of Cardiac Markers in Coronary Artery Diseases. Clinical Chemistry 45:7 1104 –1121 (1999)

There is a CICM fellowship question regarding the critical appraisal of troponin in the ICU population.

The ECS and AHA statement referred to in the college answer is this article published in Circulation in 2007:

(Kristian Thygesen et al; Universal Definition of Myocardial Infarction. Circulation 2007, 116:2634-2653

This article from Current Opinion in Critical care (2004) discusses the various causes of raised troponin among ICU patients:


Ammann et al,Troponin as a risk factor for mortality in critically ill patients without acute coronary syndromes. Journal of the American College of Cardiology Volume 41, Issue 11, 4 June 2003, Pages 2004–2009

The fact that troponin rise among the critically ill population is associated with a poorer prognosis is supported by this study:


Gunnewiek et al. Cardiac troponin elevations among critically ill patients. Current Opinion in Critical Care: October 2004 - Volume 10 - Issue 5 - pp 342-346

Liu, Michael, et al. "Prognostic Value of Initial Elevation in Cardiac Troponin I Level in Critically Ill Patients Without Acute Coronary Syndrome." Critical care nurse 35.2 (2015): e1-e10.

Ahmed, Amna N., et al. "Prognostic significance of elevated troponin in non-cardiac hospitalized patients: A systematic review and meta-analysis." Annals of medicine 46.8 (2014): 653-663.

Ammann, P., et al. "Elevation of troponin I in sepsis and septic shock." Intensive care medicine 27.6 (2001): 965-969.

Landesberg, Giora, et al. "Troponin elevation in severe sepsis and septic shock: the role of left ventricular diastolic dysfunction and right ventricular dilatation." Critical care medicine 42.4 (2014): 790-800.

Smith, Andria, et al. "Elevated cardiac troponins in sepsis: what do they signify?." West Virginia Medical Journal 105.4 (2009): 29-33.

Tiruvoipati, Ravindranath, Nasreen Sultana, and David Lewis. "Cardiac troponin I does not independently predict mortality in critically ill patients with severe sepsis." Emergency Medicine Australasia 24.2 (2012): 151-158.

Suarez, Keith, et al. "TROPONIN TESTING IN PATIENTS HOSPITALIZED FOR SEPSIS IS ASSOCIATED WITH INCREASED CARDIOVASCULAR TESTING AND LENGTH OF STAY." Journal of the American College of Cardiology 67.13 (2016): 451.

Sheyin, Olusegun, et al. "The prognostic significance of troponin elevation in patients with sepsis: a meta-analysis." Heart & Lung: The Journal of Acute and Critical Care 44.1 (2015): 75-81.

Hunter, J. D., and M. Doddi. "Sepsis and the heart." British journal of anaesthesia 104.1 (2009): 3-11.

Vieillard-Baron, Antoine, et al. "Actual incidence of global left ventricular hypokinesia in adult septic shock." Critical care medicine 36.6 (2008): 1701-1706.

Donzé, Jacques D., et al. "Impact of sepsis on risk of postoperative arterial and venous thromboses: large prospective cohort study." BMJ 349 (2014): g5334.

Korff, Susanne, Hugo A. Katus, and Evangelos Giannitsis. "Differential diagnosis of elevated troponins." Heart 92.7 (2006): 987-993.

Wens, Stephan CA, et al. "Elevated Plasma Cardiac Troponin T Levels due to Skeletal Muscle Damage in Pompe Disease." Circulation: Genomic and Precision Medicine (2016): CIRCGENETICS-115.

Sribhen, Kosit, Rewat Phankingthongkum, and Nilrat Wannasilp. "Skeletal muscle disease as noncardiac cause of cardiac troponin T elevation." Journal of the American College of Cardiology 59.14 (2012): 1334-1335.

Question 15 - 2006, Paper 2

You are phoned for advice by a doctor in a small and remote regional hospital emergency department who has just seen a 66 year old man.   He presents with central chest discomfort and dyspnoea which has been present for 60 minutes. The following ECG has arrived by fax.

a)          Please report the abnormalities on this ECG.

b)          Outline the management advice which you will give to the regional doctor.

College Answer

ECG abnormalities
There is a right bundle branch block

Q waves in leads II, III and aVF - indicative of old inferior myocardial infarction.
>2mm ST segment elevation in leads V2 and V3 . There is also ST elevation leads V4 & V5. This is STEMI (ST elevated myocardial infarction) in a man with ECG evidence of previous myocardial infarction.

Management issues
1) This man should already have had aspirin, GTN, oxygen and morphine –this needs to be checked with the referring doctor.

2) Since he is <12 hrs from presentation and is in a remote hospital, then interhospital transfer to receive Percutaneous Coronary Intervention (PCI) should be considered, but would be impossible within the required 90 minutes from symptom onset. Therefore he needs urgent thrombolysis.

3) Can the hospital administer thrombolysis? What have they got, do they know how to administer it. Do they recognise the urgency of administration?
4) After administration he will need anti-thrombotic treatment (heparin infusion)  and needs urgent transfer to a centre able to perform PCI and/or surgery (particularly if he has evidence of cardiac failure). How he will be transferred and who will escort him must be considered. The receiving cardiologists need to be informed

Discussion

The management issue list in the answer is presented in a manner which most closely resembles a colloquial discussion of this matter over some beers.
Do they recognise the urgency of adminstration, we ponder.

Let us divide this into a structured model answer, based on the 2016 NHFACSANZ recommendations.

  • Immediate management:
    • A: keep nil-by-mouth, given the possibility of impending need for intubation
    • B: maintain normoxia (no need for supplemental oxygen unless he becomes hypoxic)
    • C: Continue ECG monitoring and insert 2 x widebore cannulae. 
    • D: Analgesia with morphine 
    • E: Check electrolytes (even if only by ABG); maintain K+ around 4.5 and Mg++ around 1.0 mmol/L.
    • F: Check renal function to predict risk from contrast; commence pre-hydration with 1-2ml/kg/hr if there is known renal dysfunction
  • Supportive pharmacotherapy:
    • Nitrates - sublingual and then infusion if pain is still poorly controlled
    • Dual anti-platelet therapy (aspirin + clopidogrel/prasugrel/ticagrelor): strictly speaking, one could limit oneself to aspirin alone if the risk stratification put this guy into a low risk category, but already the combination of ST elevation and ongoing chest pain places him into a high risk category which merits DAPT according to the NHF guidelines.
    • Heparin infusion (same reason, risk category for rebound ischaemia is high)
  • Definitive management
    • Thrombolysis (contraindications to thrombolysis are discussed in the chapter on pulmonary embolism)
    • Urgent transfer to cardiac cath lab in nearest hospital capable of percutaneous intervention
    • Hand-over to medical retrieval team and receiving cardiologist

In general, it seems in Australia about 26% of ACS patients fall into this category (i.e. they need transfer to definitive management). The hospital is described as "small and remote", which presumably means that the time to PCI would be more than 30 minutes. The NHF recommend immediate thrombolysis followed by transfer to the nearest cath lab within 24 hours. The logistics of the transfer itself would be unique to the geography of the scenario, and would depend on what facilities for retrieval and PCI are available to this regional doctor. There would be obvious implications if he were surrounded by farmland, in the middle of the outback, aboard an oil platform, or in the Antarctic.  

References

Chew, Derek P., et al. "Acute coronary syndrome care across Australia and New Zealand: the SNAPSHOT ACS study." Medical Journal of Australia 199.3 (2013): 185-191.

Sørensen, Jacob Thorsted, et al. "Urban and rural implementation of pre-hospital diagnosis and direct referral for primary percutaneous coronary intervention in patients with acute ST-elevation myocardial infarction." European heart journal 32.4 (2011): 430-436.

Chew, Derek P., et al. "National Heart Foundation of Australia & Cardiac Society of Australia and New Zealand: Australian clinical guidelines for the management of acute coronary syndromes 2016." Heart, Lung and Circulation 25.9 (2016): 895-951.

Hofmann, Robin, et al. "Oxygen therapy in suspected acute myocardial infarction." New England Journal of Medicine377.13 (2017): 1240-1249.

Question 24 - 2007, Paper 2

Compare and contrast transthoracic and transoesophageal echocardiography in the evaluation of cardiac disease in the critically ill patient. (You may tabulate your answer)

College Answer

TTE

TOE

Time lag to diagnosis

Instantaneous

A certain degree of delay

Need for sedation

None

May need sedation

Invasive

No

Minimally invasive

Morbidity

None

Minimal

Mortality

None

Minimal

Image quality

Good/excellent in non-
vent, reduced in ventilated patients

Excellent in all patients

Infection control

Stricter infectious control
procedures

Cost

More expensive probes

Native and prosthetic
valve endocarditis

TOE is superior

Aortic dissection

TOE is superior

Aortic trauma

TOE is superior

LA appendage clot

TOE is superior

Pericardial effusion

Good

Good

Localised tamponade (post
surgery)

Occasionally useful

Very useful

Discussion

The recommendations for the use of TTE or TOE have been updated in 2003. The update statement, though the "summary" of a much larger statement, is in fact an unwieldy document many pages long. A much better summary of echosonography in the ICU is presented in a review article from 2008.  Thre massive 2007 Appropriateness Criteria for Transthoracic and Transesophageal Echocardiography statement was used to construct the suggested non-college answer below.

A Comparison of TOE and TTE in the Assessment of Cardiac Disease
Category TTE TOE
Equipment
  • Small scale devices available
  • Bedside apparatus ranges from cheap hand-held probes (sub-$10K ) to professional equipment (ranging $70K- $150K)
  • Probes are easily replaceable when they break, as their cost is small
  • There is no cheap bedside option
  • Bedside apparatus is portable but still large and expensive  (ranging $70K- $150K)
  • Expensive probes need to be carefully protected from such threats as patient's teeth
Time lag to diagnosis
  • Instant diagnosis
  • Slight delay
Need for sedation
  • Usually unnecessay
  • Frequently necessary
Invasiveness
  • Non-invasive
  • Minimally invasive
Absolute contraindications
  • None
  • Severe left-sided rib fractures could be viewed as a relative contraindication
     
  • Oral or oesophageal surgery, anastomosis
  • Oesophageal stricture or diverticulum
  • Severe coagulopathy could be viewed as a relative contraindication
Factors affecting image quality
  • Body habitus
  • Mechanical ventilation
  • Patient position
  • Exposure of chest wall (eg. severe burn, or open chest in cardiothoracic theatre)
  • Most of the time image quality is good; most important factor affecting it is the experience of the operator
Infection control
  • Probe needs to be disinfected with surface-acting disinfectant agents (similar to any other patient contact instrument); it is usually not exposed to patient body fluids.
  • It cannot be subjected to autoclaving.
  • Disposable sleeves are available.
     
  • The probe must be disinfected thoroughly in a manner similar to the disinfection of endoscopy probes, as it is exposed to patient body fluids.
  • Protective sleeves are inappropriate.
  • Most probe designs factor in the need to be subjected to automated cleaning, and tolerate high temperatures.
  • The usual probe turnaround time is 20 minutes under ideal circumstances
Mortality and morbidity
  • Essentially, a benign and consequence-free procedure.
  • The greatest risks are misinterpretation of data (leading to inappropriate management) and inaccurate findings (due to operator inexperience).
  • No formal consent process is usually required (verbal / implied consent is sufficient)
  • Each procedure has a small but non-zero risk of major complications, including oesophageal perforation, endotracheal tube dislodgement, and death.
  • The nasogastric tube is often in the way, and ends up being removed. It then needs to be reinserted, with attendent complications.
  • In the non-intubated patient, the use of sedation carries its own risks.
Focused assessment of the cardiac arrest patient
  • The subcostal view does not interfere with CPR, but is a sub-optimal view.
  • Information derived from peri-arrest TTE is frequently useful and tends to change the management
  • Some prognostic interest: patients with absent LV wall movement are highly unlikely to succeed at ROSC (only ~2.4% will go on to ROSC).
  • Also does not interfere with CPR, but offers much better quality of images.
  • Likely to be the only option in perioperative cardiac arrest
  • Same as TTE, changes management in arrest and can offer some prognostic information.
Assessment of ventricular function
  • TTE is a better modality for assessment of LV and RV function as it includes the true cardiac apex
  • Multiple window directions enhance the ability to assess flow with Doppler
  • The cardiac apex is poorly seen with TOE.
  • There are fewer windows, and Doppler assessment of flow is incomplete
Assessment of aortic dissection
  • Descending and thoracic aorta is either impossible or difficult to image.
  • TOE is the US modiality of choice for aortic dissection
Assessment of valve function
  • Valve function can be assessed to a high degree of accuracy provided image quality is satisfactory.
  • Small vegetations cannot be excluded
  • Valve function can be assessed to a high degree of accuracy
  • Valve images are of sufficiently high quality to appreciate small vegetations
  • This is the modality of choice for infective endocarditis
Assessment of septal defects
  • Grossly, large defects and intracardiac shunts can be appreciated, but their quantitative assessment usually cannot be carried out
  • Intracardiac shunts and septal defects are well imaged. This is the modality of choice for such pathology.
Identification of intracardiac thrombi
  • Large LA and LV thrombi can be identified; small thrombi cannot be excluded.
  • All sorts of intracardiac thrombi can be identified; particularly the left atrial appendage is well visualised. This is the modality of choice for pre-cardioversion assessment of embolic risk.

References

Cheitlin, Melvin D., et al. "ACC/AHA/ASE 2003 guideline update for the clinical application of echocardiography." A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/ASE Committee to Update the 1997 Guidelines for the Clinical Application of Echocardiography). American College of Cardiology Foundation and American Heart Association (2003).

Roscoe, Andrew, and Tim Strang. "Echocardiography in intensive care."Continuing Education in Anaesthesia, Critical Care & Pain 8.2 (2008): 46-49.

Douglas, Pamela S., et al. "ACCF/ASE/ACEP/ASNC/SCAI/SCCT/SCMR 2007 Appropriateness Criteria for Transthoracic and Transesophageal Echocardiography⁎: A Report of the American College of Cardiology Foundation Quality Strategic Directions Committee Appropriateness Criteria Working Group, American Society of Echocardiography, American College of Emergency Physicians, American Society of Nuclear Cardiology, Society for Cardiovascular Angiography and Interventions, Society of Cardiovascular Computed Tomography, and the Society for ...." Journal of the American College of Cardiology 50.2 (2007): 187-204.

Question 26.3 - 2008, Paper 1

Examine the ECG shown below.

1.      Describe the ECG as shown.
2.      Which coronary artery territory may be involved in the pathophysiology of this case?

College Answer

1    Sinus rhythm of 92 bpm. ST elevation of >2mm in II, III AVF and V5,6 with reciprocal changes in V1 and AVR. Consistent with myocardial infarction .
2    Right coronary artery territory or LCx if dominant left system.

Discussion

The localisation of coronary artery territories on the ECG is discussed elsewhere.

To simplify revision, here they are:

localisation of coronary artery territories

References

Zimetbaum, Peter J., and Mark E. Josephson. "Use of the electrocardiogram in acute myocardial infarction." New England Journal of Medicine 348.10 (2003): 933-940.

Question 13.1 - 2008, Paper 1

You are asked to assess a 78 year old non-smoker admitted  with progressive exertional breathlessness. On examination,  he has a respiratory rate of 28/min. BP 100/70 mm Hg. The JVP is elevated 8 cm above the sternal angle. The apical impulse is thrusting in nature and localized to the 6th left intercostal space, lateral to the mid-axillary line. On auscultation, there is an ejection systolic murmur, which is heard over the left second intercostal space and conducted to the root of the neck. There were bibasal crackles on auscultation of the lungs.

a) What is the likely diagnosis of his cardiovascular condition?

b) List 4 clinical signs which may indicate that the nature of his condition is severe.

College Answer

a)     What is the likely diagnosis of his cardiovascular condition?

Aortic stenosis

Mention of HOCM or subaortic stenosis ? 2.5 mark
Mention of any other valvular lesion should not score any marks for this question.

b) List 4 clinical signs which may indicate that the nature of his condition is severe.

  • Plateau pulse
  • Aortic thrill
  • S4
  • Paradoxical splitting of second heart sound
  • Length and the harshness of the murmur
  • LV failure – a late sign

Discussion

Talley and O'Connor have a fine list of signs, which one mgiht expect to see in severe aortic stenosis.

  • Delayed carotid upstroke
  • Diminished carotid pulse on palpation
  • Apical impulse sustained (pressure loaded)
  • Absent or decreased A2
  • S4 gallop
  • Late peaking murmur
  • Long murmur
  • Murmur radiates to the neck

References

Clinical Examination of the Critically Ill Patient, 3rd edition by L.I.G. Worthley - which can be ordered from our college here.

Clinical Examination: whatever edition, by Talley and O'Connor. Can be acquired any damn where.

Question 26.2 - 2008, Paper 1

This is the ECG of a 74 year old man who had an out of hospital cardiac arrest.


Describe the ECG.

College Answer

1    Irregular rhythm right bundle branch block left posterior fascicular ( or right axis
deviation) block
2    Rhythm possibly junctional

Discussion

For a deeper discussion of RBBB and the fascicle blocks, I refer the gentle reader to LITFL

References

Question 7.1 - 2008, Paper 2

List the classic cardiac auscultatory signs of atrial septal defect, ventricular septal defect and patent ductus arteriosus. What typical findings on a right heart catheterization will also support your diagnosis?   (You may tabulate your answer)

College Answer

ASD

VSD

PDA

Fixed split of second heart
sound

Harsh pansystolic murmur
confined to the left sternal edge

A continuous murmur
heard over the pulmonary area

Mid diastolic flow murmur
over tricuspid area if significant shunt

Mid diastolic flow murmur
over mitral area if significant shunt

Mid diastolic flow murmur
over mitral area if significant shunt

Step up in oxygen
saturation at atrial level

Step up in oxygen
saturation at ventricular level

Step up in oxygen
saturation at pulmonary artery level

Discussion

There really is no way to answer this question without having either memorised or having become freakishly familiar with the details of cardiological examination.

A summary for these physical examination findings exists elsewhere.

The "step up" findings in right heart catheterisation are self-explanatory once you think about it. They are all the features of "acyanotic" heart defects.

The atrial septal defect contributes oxygenated blood to the right atrium, and the "step-up" occurs there. The VSD contributes oxygenated blood to the ventricle with similar consequences. The PDA carries oxygenated blood from the aorta to the pulmonary artery, and again this change occurs.

Dexter et al first explored this in healthy patients in 1947; a good review article addresses his workand outlines what precisely an abnormal "step up" looks like (turns out it is about 5-7% difference in oxygen content - less than 1 % of such people would be free from septal defects).

References

Freed, MICHAEL D., OLLI S. Miettinen, and ALEXANDER S. Nadas. "Oximetric detection of intracardiac left-to-right shunts." British heart journal 42.6 (1979): 690.

Question 15.3 - 2008, Paper 2

Examine  the ECG provided below

a)  Describe the abnormalities on the ECG

b)  List 2 potential causes

College Answer

a)  Describe the abnormalities on the ECG
Tachycardia
Intraventricular conduction defect probably RBBB Widespread ST elevation

b)  List 2 potential causes
Acute myocardial infarction (extensive)
Maybe myopericarditis

Discussion

There is little to discuss. There are many potential causes for ST elevation, but fewer for ST elevation with bundle branch block. I can think of only the following:

  • Myocardial infarction
  • Cardiac contusion
  • Acute myocarditis
  • LV aneurysm
  • Hyperkalemia
  • Pulmonary embolism
  • Early repolarization (with elevated J point)
  • Left bundle branch block
  • Hypothermia with J point elevation (can be mistaken for ST elevation)
  • Brugada syndrome (characteristic ST changes can be mistaken for STEMI)

References

The above ECG was borrowed gratefully from the STEMI collection at LITFL. Unfortunately there is no tachycardia, but the spirit of the question is preserved I hope.

There is an excellent paper to help you generate differentials about ST segment changes: Wang, Kyuhyun, Richard W. Asinger, and Henry JL Marriott. "ST-segment elevation in conditions other than acute myocardial infarction." New England Journal of Medicine 349.22 (2003): 2128-2135.

 

 

Question 29.1 - 2008, Paper 2

Besides history and clinical examination, what investigations may help distinguish between cardiac and non-cardiac causes of pulmonary oedema in the critically ill patient?

College Answer

1) Measurement of PCWP and CI
2) Serum BNP
3) Echocardiography
4) PICCO

Discussion

Echocardiography is a straightforward answer, as is BNP.

PCWP and cardiac index are indirectly related to this answer- one can cave a patient with a noncardiogenic pulmonary oedama as well as a poor cardiac index; the inference that the oedema has occurred because of the poor cardiac index would be incorrect.

The PICCO is even more obscure. Yes, it gives to you the extravascular lung water, but this only tells you that there is water in the lungs (which you already knew).

However, some authors have asserted that thermodilution measurements of pulmonary permeability can differentiate pulmonary oedema from ARDS.

Causes of Acute Pulmonary Oedema
Cardiogenic Non-cardiogenic

Excessive LV afterload

  • Severe hypertension
  • Aortic stenosis
  • HOCM (LVOTO)

Excessive LV preload

  • Fluid overload
  • Rapid fluid bolus

Excessive left atrial afterload

  • Mitral stenosis
  • Mitral thrombosis
  • Mitral prolapse
  • Atrial myxoma

Poor contractility

  • Cardiomyopathy
  • Drug effect (eg. beta blockers)
  • Metabolic disease (eg. hypothyroidism)
  • Infectious causes (eg. myocarditis)

Ineffective contractility

  • Mitral regurgitation
  • Takotsubo cariomyopathy

Increased capillary permeability

  • ARDS; systemic inflammatory state
  • Reperfusion (eg. following relief of an embolic occlusion)
  • Reperfusion of transplant lung
  • Near drowning (surfactant loss)

Neurogenic pulmonary oedema

  • Intracranial haemorrhage
  • Seizures
  • Electroconvulsive therapy

Drug-induced pulmonary oedema

  • Opiate induced (eg. heroin overdose)
  • Salicylate overdose

Raised pulmonary arterial pressure

  • High altitude pulmonary oedema
  • Massive PE
  • Pulmonary veno-occlusive disease
  • Post pneumonectomy
  • Air embolism

Negative pressure pulmonary oedema

  • Airway obstruction
  • Re-expansion pulmonary oedema, eg. following the drainage of a particularly large pleural effusion
Investigations to Help Discriminate Between Cardiac and Non-Cardiac Causes of Acute Pulmonary Oedema
Investigation Cardiogenic pulmonary oedema Non-cardiogenic pulmonary oedema
History
  • Chest pain
  • Paroxysmal nocturnal dyspnea or orthopnea
  • Worsening exercise tolerance
  • Pneumonia, sepsis, aspiration, high altitude, drug overdose, recent lung transplant, recent pleural effusion drainage, all the obvious stuff.
Examination
  • S3 gallop: suggests an elevated end-diastolic LV pressure; a highly specific finding with low sensitivity.
  • Mitral stenosis or regurgitation murmur
  • Raised JVP
  • Cool extremities
  • Low JVP
  • Warm vasodilated extremities
  • Vigorous strong pulses
ECG findings
  • Ischaemia
  • Heart block
  • Arrhythmia
  • Right ventricular strain, eg. as in PE
Troponin
  • Can confirm cardiac ischaemia
  • May be elevated in renal failure, sepsis, SAH, etc...
Brain natriuretic peptide (BNP)
  • More than 100pg/ml suggests that CCF is contributing to the APO
  • Less than 100pg/ml in ED or 200pg/ml in ICU suggests that the oedema is non-cardiogenic (eg. it may be ARDS)
Chest Xray
  • Cardiac causes of APO usually have more perihilar infltrates. Classical "bat wing" appearance is rare in non-cardic pulmonary oedema
  • Cardiomegaly is a clue
  • One may be able to see engorged pulmonary veins.
  • Non-cardiac APO tends to feature peripheral lung infiltrates. However, all sorts of ARDS look the same on Xray.
  • In massive PE the oedema will be irregular (i.e. limited to areas which are still perfused) whereas the rest of the lung will be oligaemic.
Echocardiography
  • Gold standard for diagnosis of cardiac structural and functional disease, but does not rule out non-cardiac causes. It is possible to have both poor baseline LV function and acute pulmonary oedema of a totally non-cardiogenic cause. 
  • Massive PE and similar things can be found on TTE.
  • A normal TTE all ut excludes cardiac causes of APO.
Swan-Ganz catheter
  • PAWP is valuely related to LA filling pressure, and a PAWP over 18mmHg suggests either cardiogenic APO or volume overload.
  • A normal or increased cardiac output, combined with a normal PAWP, all but excludes cardiogenic causes of APO 

References

Karmpaliotis, Dimitri, et al. "Diagnostic and prognostic utility of brain natriuretic Peptide in subjects admitted to the ICU with hypoxic respiratory failure due to noncardiogenic and cardiogenic pulmonary edema." CHEST Journal 131.4 (2007): 964-971.

Monnet, Xavier, et al. "Assessing pulmonary permeability by transpulmonary thermodilution allows differentiation of hydrostatic pulmonary edema from ALI/ARDS." Intensive care medicine 33.3 (2007): 448-453.

Ware, Lorraine B., and Michael A. Matthay. "Acute pulmonary edema." New England Journal of Medicine 353.26 (2005): 2788-2796.

 

Gluecker, Thomas, et al. "Clinical and radiologic features of pulmonary edema." Radiographics 19.6 (1999): 1507-1531.

 

Karmpaliotis, Dimitri, et al. "Diagnostic and prognostic utility of brain natriuretic Peptide in subjects admitted to the ICU with hypoxic respiratory failure due to noncardiogenic and cardiogenic pulmonary edema." CHEST Journal 131.4 (2007): 964-971.

 

Maisel, Alan S., et al. "Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure." New England Journal of Medicine 347.3 (2002): 161-167.

.

Question 29.2 - 2008, Paper 2

A 70 year old man is admitted with shortness of breath and respiratory failure to the intensive care unit. A systolic murmur is audible  on examination. A chest X- ray reveals upper lobe diversion of pulmonary veins.  A transthoracic echo reveals the following. (abnormal values marked with an asterix)

OBSERVATIONS:

TRICUSPID VALVE:                         Normal
PULMONIC VALVE:                        Normal
RIGHT VENTRICLE:                         Normal size and function
RIGHT ATRIUM/IVC:                       Normal
MITRAL VALVE:                              Normal

*LEFT  VENTRICULAR EVALUATION 
Normal LV size. Moderate to severe impairment of systolic function.  EF 25%. No regional wall motion abnormalities. Moderate LV hypertrophy.

*LEFT  ATRIUM:  Mildly enlarged.

*AORTIC VALVE:  Thickened and calcified, with reduced opening. No aortic regurgitation.

Aortic valve area

0.68cm2

(2-4)

Left ventricular outflow tract:    

Maximum velocity

0.55 m/s;

(0.8 – 1.2)

Velocity time integral (VTI)

8.58 cm;

Aortic valv 

Maximum velocity

2.93 m/s;

(<2.0)

Velocity time integral (VTI)

43 cm;

Max pressure gradient
Mean pressure gradient

34 mm Hg
18 mm Hg

(<16)
(<10)

Dimensionless severity index (DSI)              0.19

Based on the above information, what is the likely underlying diagnosis responsible for this patient’s symptoms? Comment on the severity of the underlying diagnosis and provide reasons for your answer.

College Answer

Severe aortic stenosis (2.0) with impaired LV systolic function. Reasons: Valve area less than 0.7 cm2 (1.5) and DSI less than 0.2.

Pressure gradients may be low in the presence of LV dysfunction

Discussion

This question closely resembles the Question 8.3 from the second paper of 2010.

References

Question 3.1 - 2009, paper 1

a.   List 3 abnormalities on this ECG

b.  Name 2 drugs which are contraindicated in this disorder

c.   Name 2 complications of this disorder

College Answer

a.   List 3 abnormalities on this ECG

°    Short PR

°    Delta wave

°    Wide QRS

°    J wave (candidates mentioning this also received credit)

°    Tall R wave in V1

b.  Name 2 drugs which are contraindicated in this disorder

°    Verapamil

°    Digoxin

c.   Name 2 complications of this disorder

°    VF arrest

°    Syncope

°    AF/tachyarrhythmias

Discussion

This is WPW. The short PR, long QRS and delta waves all suggest that an accessory conduction pathway is present. The J wave is a bit of a red herring here, and is certainly not part of the syndrome; its presence can be a normal variant, which is what I think is happening here (unless this patient was cooled).

ECG features of WPS are:

  • The PR interval is short (less than 0.12 seconds)
  • There is a delta wave (a slurred upstroke of the QRS complex)
  • Wide QRS (because the delta wave widens it)
  • ST Segment and T wave discordant changes: T waves point in the opposite direction to the QRS.
  • Pseudo-Q waves: negatively deflected delta waves in the inferior / anterior leads
  • prominent R wave in V1-3 (mimicking posterior infarction).
  • Ideally, this sort of ECG should come with a history of syncopal episodes.
  • Characteristic electrophysiology findings of an  accessory pathway (Bundle of Kent) are desirable but non essential.

Complications of WPW include:

  • SVT, which comes in two flavours. if the complexes are narrow, its orthodromic. If they are wide and with delta-waves, its antidromic. Does that really matter? Probably not.
  • AF  is disturbingly common in WPW- 10 to 30% of patients will have it at some point. Having AVRT predisposes one to AF in this situation because the reentry circuit via the accessory pathway can cause the atria to contract quite randomly (after all, the accessory pathway is not a serious part of the conducting system, and it doesn’t link into any sort of conduction pathways- its just going to excite any old patch of atrium). The ECG will throw you off. The conduction rate is roughly 1:1.5; the QRS rate is about 180 to 200. It is hard to tell that its irregularly irregular. The QRS complexes will be a mixture of pre-excited delta-waving ones, and normal-looking narrow ones. If the accessory pathway has a short refractory period, it will conduct more often and therefore there will be more broad complexes than narrow ones. The shorter the refractory period of the accessory pathway, the broader the QRS. And the broader the QRS, the greater the chance of this thing degenerating into ventricular fibrillation.
  • Atrial flutter can also conduct via the bundle of Kent. There will be 1:1 conduction. Ventricular rate will approach 300. Because this is an antidromic way of conducting impulses, the QRS complexes will be broad and there will be delta waves. Unlike AF, the rate runs with a metronome-like regularity. The patient will likely look dead.
  • Ventricular fibrillation is a common cause of sudden cardiac death among the WPWs. So, in AF with WPW conduction, the rate of ventricular contraction is increased, and the regularity is decreased. This fractionates the wavefront of ventricular depolarization. Soon enough, there are numerous wavefronts all moving around the ventricle. This is ventricular fibrillation. If you block the AV node, occasionally the accessory pathway will launch the ventricles into this. It’s a known, and extremely uncommon, complication of adenosine use in WPW.
  • Syncope and sudden cardiac death are the natural histories of these arrhythmias in WPW, because they are frequently too fast to be perfusing rhythms. The surviving sufferer is typically saved by their youth, as they may be better able to tolerate hummingbird-like heart rate for sustained periods.

What can we say about the safety of AV nodal blockers in WPW?

  • Theoretically, AV nodal blockers should be safe in WPW-associated SVT, be it antidromic or orthodromic. If one thinks for a minute about the epidemiology of SVT, one will come to the conclusion that a large proportion of SVT is in fact caused by WPW or some other sort of preexcitaton syndrome, which is usually not known at the time of their first presentation. Many of these people get adenosine, which then reveals their delta waves to the horrified emergency personnel. Most of them do not die of VF. On the basis of this, we may conclude that it is probably reasonably safe.
  • Practically, antidromic SVT in WPW may be difficult to discriminate from AF or VT. Broad complexes and 300+ heart rates could be anything in WPW. Sure, it could be supraventricular, and respond to adenosine. Or it could be AF, and turn into VF. Or it could be VT, which will not benefit from an AV nodal blocker, in which case you have wasted precious time.

On this basis, the authorities tend to recommend the use of Class I or Class III agents instead of AV nodal blockers. The model answer to Question 3.1 from the first paper of 2009 lists procainamide and amiodarone as first-line agents, whereas digoxin and verapamil are contraindicated. Digoxin decreases the refractory period of the accessory pathway and verapimil tends to accelerate the ventricular response to AF by a similar mechanism. Since 2009, public opinion has also drifted away from amiodarone. As an acute infusion it is basically a beta-blocker with some AV nodal specificity. It is therefore the wrong drug for acute management of WPW SVT; or rather, it will probably be safe in the narrow-complex-obviously-orthodromic population, with the aforementioned caveats. In the long term, it becomes more useful, as its Class III and Class I effects begin to develop, slowing conduction down the accessory pathway.

References

Wellens, Hein JJ, and Dirk Durrer. "Effect of digitalis on atrioventricular conduction and circus-movement tachycardias in patients with Wolff-Parkinson-White syndrome." Professor Hein JJ Wellens. Springer Netherlands, 2000. 63-68.

Gulamhusein, S. A. J. A. D., et al. "Acceleration of the ventricular response during atrial fibrillation in the Wolff-Parkinson-White syndrome after verapamil."Circulation 65.2 (1982): 348-354.

Munger, T. M., et al. "A population study of the natural history of Wolff-Parkinson-White syndrome in Olmsted County, Minnesota, 1953-1989."Circulation 87.3 (1993): 866-873.

Question 3.2 - 2009, paper 1

You are provided with a report of an echocardiogram of a patient in the ICU.

INDICATIONS/REASON FOR ECHOCARDIOGRAM:

  • Hypotension soon after admission to ICU following prosthetic aortic valve replacement for aortic stenosis . BP 70/30 mm Hg (mean 43 mm Hg). Study performed on adrenalin 10 mcg/min.

LEFT VENTRICULAR EVALUATION

  • Small LV cavity size.
  • Normal systolic function (EF 60%).
  • No regional wall motion abnormalities. E′ = 4 cm/s.
  • Moderate to severe concentric LV hypertrophy.
  • Flow acceleration noted in LVOT on colour Doppler.

LEFT ATRIUM

  • Mildly enlarged. LA area 26 cm2

RIGHT VENTRICLE

  • Normal size and systolic function

RIGHT ATRIUM/IVC Normal.

AORTIC ROOT Normal

MITRAL VALVE

  • Structurally normal mitral valve;
  • Systolic anterior motion of the valve leaflets.  
  • Moderate mitral regurgitation.
  • E-wave 0.8 m/s; A-wave 0.5 m/s; Deceleration time 196 ms

AORTIC VALVE

  • Prosthetic aortic valve is well seated. Trivial paravalvular regurgitation.

LVOT:

  • Max vel 5.0 m/s; Mean vel 3.5 m/s;
  • Max pressure gradient 100 mm Hg;
  • Mean pressure gradient 49 mm Hg

AV:      Max vel 5.1 m/s; Mean vel 3.7 m/s;

  • Max pressure gradient 104 mm Hg; Mean pressure gradient 55 mm Hg

TRICUSPID VALVE

  • Normal tricuspid valve. E-wave 0.3 m/s; Mild regurgitation; TR vel 2.0 m/s

PULMONIC VALVE

  • Normal pulmonic valve

a)  What is the cause of this patient’s  hypotension?   Justify your answer.

b)  List 4 principles of management of this patient’s  hypotension based on the report. (Abnormal values are shown in bold)

College Answer

1.  What is the cause of this patient’s hypotension? Justify your answer

°     Left ventricular outflow tract obstruction.

°     Gradient across LVOT and not across valve

°     SAM

2.  List 4 principles of management of this patient’s hypotension based on the report.

°     Stop adrenalin

°     Volume load

°     Beta blockers to slow the heart rate and reduce contractility

°     Vasoconstrictor without inotropic effect (eg phenylephrine)

Discussion

Success in answering this question relies on the candidate having sufficient familiarity with TTE reports to be able to rapidly skim through the data, identifying only the abnormal findings.

Armed with a detailed understanding of normal TTE measurements, one can immediately pick up on the systolic anterior motion of the mitral valve leaflets. This feature is present in a few other conditions, but combined with the reported LV hypertrophy one begins to think about dynamic LV outflow tract obstruction. This is confirmed by the LVOT peak pressure gradient of over 100mmHg (whereas anything over 30mmHg is defined as LVOT obstruction).

Now, the cause of the hypotension becmes clear (the patient is on 10mcg/min of adrenaline).

Thus, stopping adrenaline is the first step to recovery of normal cardiac output.

Adequate preload and a nice slow heart rate with decreased contractility is the key. Even with the beta-blockers decreasing contractility, the hypertrophied LV will be able to generate a satisfactory stroke volume - provided it does not block its own outflow tract. The idea is to also increase the duration of diastole for as long as possible. Lastly, a high afterload will likely be required - not only to decrease the LVOT-AV gradient, but to increase the diastolic pressure. A higher than average diastolic pressure will be required to perfuse the subendocardium in a hugely hypertrophied left ventricle. The agents to use in this setting would be phenylephrine, vaasopressin or metaraminol - as they have absolutely no beta-1 inotropic effect.

In summary, the management of HOCM in cardiogenic shock consists of

  • Ceasing positive inotropes
  • Starting some negative inotropes
  • Ensuring a slow rate
  • Maintaining a sinus rhythm
  • Increasing preload
  • Inreasing afterload and diastolic pressure

References

Walker, Christopher M., et al. "Systolic anterior motion of the mitral valve."Journal of thoracic imaging 27.4 (2012): W87.

Williams, L. K., M. P. Frenneaux, and R. P. Steeds. "Echocardiography in hypertrophic cardiomyopathy diagnosis, prognosis, and role in management."European Journal of Echocardiography 10.8 (2009): iii9-iii14.

Fraser, J., et al. "Dynamic left ventricular outflow tract obstruction in critically ill patients." Critical Care and Resuscitation 4.3 (2002): 170.

Sahoo, Rajendra K., et al. "Perioperative anesthetic management of patients with hypertrophic cardiomyopathy for noncardiac surgery: A case series."Annals of cardiac anaesthesia 13.3 (2010).

Question 24.2 - 2009, paper 1

List 4 clinical signs on cardiovascular examination which will support the diagnosis of pulmonary hypertension

College Answer

°     Prominent ‘a’ wave

°     Parasternal lift

°     Palpable P2

°     Loud P2

°     Features of tricuspid regurgitation

Discussion

The signs of pulmonary hypertension are mainly indirect.

  • The split loud P2 is the only direct sign - it is the sound of elevated PA pressur slamming the pulmonic valve shut at the end of systole.
  • If the P2 is palpable, the PA pressure is truly uncontrollably high

The rest are all features of right heart failure.

  • Parasternal heave is a sign of RV hypertrophy
  • a prominent "a" wave is the wave of right atrial contraction, reflected from either a stenotic tricuspid valve or a stiff non-compliant right ventricle. This also suggests that the RV is hypertrophied.
  • Features of tricuspid regurgitation suggest that the RV is also dilated, and possibly decompensating.

References

UpToDate: Clinical features and diagnosis of pulmonary hypertension in adults

SLEEPER, JULIAN C., EDWARD S. ORGAIN, and HENRY D. MCINTOSH. "Primary Pulmonary Hypertension Review of Clinical Features and Pathologic Physiology with a Report of Pulmonary Hemodynamics Derived from Repeated Catheterization." Circulation 26.6 (1962): 1358-1369.

(this is a nice old-school article witrh a discussion of several cases of severe pulmonary hypertension, and its various clinical features)

 

Question 24.6 - 2009, paper 1

List 3 causes of a mid-diastolic  murmur over the apex

College Answer

°     Mitral stenosis

°     Severe aortic regurgitation – Autin Flint murmur

°     Severe mitral regurgitation

°     Significant left to right shunt – VSD, PDA

°     Atrial myxoma

°     Carey-Coombs murmur

Discussion

This is a repeat question.

For some reason the college love their mid-diastolic apical murmurs.

Like the identical Question 3.2 from 2010(1), but unlike the very similar Question 26.3 from 2011(2), this specifically asks for MID-diastolic murmurs.

References

Clinical Examination of the Critically Ill Patient, 3rd edition by L.I.G. Worthley - which can be ordered from our college here.

Clinical Examination: whatever edition, by Talley and O'Connor. Can be acquired any damn where

Question 10.2 - 2009, Paper 2

This is the preoperative ECG of a patient.  There has been no recent chest pain or enzyme rise. What are the prominent features of this ECG? (Photo supplied on the next page)

What is the most likely diagnosis based on the ECG?

College Answer

SR at 75/min, normal axis, LVH, Qwaves in Vl-V3, ST elevation antleads (Vl-V4), inv T I, flattened T waves V4-V6)


LV aneurysm, old ant MI +1- new silent MI???

Discussion

My hat is off to the college for providing the exam ECG for future generations of trainees.

The definition of LV aneurysm is persisting ST elevation after an MI. We know that the patient has no current MI (the college tells us so). And we know that a previous MI took place (just look at those Q waves). The ECG changes are characteristic.

 

References

Rosenberg, Benjamin, and William J. Messinger. "The electrocardiogram in ventricular aneurysm.American heart journal 37.2 (1949): 267-277.

Nordenfelt, O. L. O. F. "The electrocardiogram in chronic aneurysm of the heart." Acta med. scandinav 102 (1939): 101.

 

 

Question 12.1 - 2009, Paper 2

List 3 causes of an irregularly irregular pulse.

College Answer

1. AF
2. Multiple VEs
3. Atrial flutter with varying block

Discussion

There is nothing to discuss. This is easy marks. Multifocal atrial tachycardia is another reasonable alternative.

 

References

Question 17 - 2009, Paper 2

Outline the advantages and limitations of the various therapeutic options available for the treatment of right ventricular dysfunction.

College Answer

Therapy

Advantages

Disadvantages

Volume

Effective, as RV needs a
higher filling pressure. A PA catheter may be useful in guiding volume therapy.

Determination of preload
is problematic, RA pressure may be high in chronic right heart failure and may not be a predictor of volume response. Functional parameters of volume responsiveness not useful in right heart failure

Inotropes and vasopressors

-May be of benefit in RV
infarction where they may increase coronary perfusion pressure
- Some suggestion that levosimendan may improve RV afterload in ARDS

No large scale published
data on any specific inotrope or pressor in isolated RV failure

Afterload manipulation
- Control of hypoxia and hypercapnia and acidosis

reduce PA pressures

Optimal target levels unclear.

Prostaglandins

Reduce pulmonary
pressures

May cause systemic
hypotension, flushing

NO

Improves VQ matching,
improves oxygenation

Met Hb, platelet
dysfunction, requires special delivery systems, not shown to improve mortality

Bosentan

Reduce pulmonary
pressures

No large scale data

Phosphodiesterase
inhibitors - sildefanil

Reduce pulmonary
pressures

No large scale data

Pacing to improve A-V
synchrony

Improves preload

Mechanical ventilation

May improve oxygenation
and CO2 transfer and may reduce pulmonary hypertension

Deleterious effects of
IPPV

Discussion

This paper was issued to candidates late in 2009. A pity, because an excellent article on this topic came out in Critical Care in 2010.

I will summarise the suggestions made therein.

Volume management: a weak recommendation to closely monitor the effects of fluid challenge (seeing as conventional methods of assessing fluid responsiveness are quite useless in RV failure)

Afterload management: a weak recommendation to use noradrenaline and vasopressin, because they will only affect pulmonary arteries in very high doses.

Contractility enhancement: milrinone earns a strong promotion, but dobutamine and levosimendan only merit a lukewarm recommendation for lack of good quality evidence.

Afterload reduction: the authors strongly suggest that inhaled pulmonary vasodilators are used, rather than the IV forms. Inhaled NO and prostaglandin are strongly promoted, but oral sildenafil only gets a weak recommendation.

Bosentan and pacing are not mentioned. Mechanical ventilation is promoted as a means of avoiding atelectasis and hypoxic vasoconstriction.

 

References

Price, Laura C., et al. "Pulmonary vascular and right ventricular dysfunction in adult critical care: current and emerging options for management: a systematic literature review." Crit Care 14.5 (2010): R169.

Question 3.2 - 2010, Paper 1

List 4 causes of a mid diastolic murmur over the apex.

College Answer

Mitral stenosis
Aortic regurgitation
Left to right shunts – VSD or a PDA 
Severe MR
Acute rheumatic fever

Discussion

Unlike the very similar question 26.3 from the second 2011 paper, this specifically asks for MID-diastolic murmurs.

Interestingly, this college answer is quite differently worded.

Instead of naming the eponymous Carey Coombs murmur of mitral incompetence in acute rheumatic fever, they just call it "acute rheumatic fever".

In any case, its essentially the same question. Candidates will do well to make themselves intimately familiar with murmurs, where they arise, and at which stage of the cardiac cycle one can expect to hear them.

References

Clinical Examination of the Critically Ill Patient, 3rd edition by L.I.G. Worthley - which can be ordered from our college here.

Clinical Examination: whatever edition, by Talley and O'Connor. Can be acquired any damn where

Question 5.4 - 2010, Paper 2

List the classic clinical  findings  on praecordial  examination  in a patient with 
Tetralogy of Fallot.

College Answer

List the classic clinical  findings  on praecordial  examination  in a patient with 
Tetralogy of Fallot.

•     ESM or PSM
•     Right ventricular heave
•     A loud single second sound

Discussion

Tetralogy of Fallot has a constellation of physical examination findings which the savvy candidate will have to memorise, unless they are constantly dealing with ToF patients.

Basically, the pathology is a sort of pulmonic stenosis, a VSD and RV hypertrophy.

The right ventricular heave is to be expected with RVH.

The ejection systolic murmur in the parasternal region may be either aortic or pulmonic in origin, but most typically is due to RVOT obstruction by the hypertrophied walls. It has a harsh crescendo-decrescendo quality, and tends to diminish as the contractility increases (because as the RV works harder, more blood is shunted to the left venticle across the VSD, and less blood travels via the RVOT thus generating less noise).

The loud second heart sound will be single because the stenosed pulmonic valve does not produce enough noise as it closes.

References

A little history about the Blalock-Taussig shunt...

UpToDate has a good summary: Pathophysiology, clinical features, and diagnosis of tetralogy of Fallot; of course you have to pay for it.

There is an old article which details the diagnostic features in ToF. As it pre-dates TTE, the focus is on physical examination.
MCCORD, MALCOM C., J. A. C. K. VAN ELK, and S. GILBERT BLOUNT. "Tetralogy of Fallot Clinical and Hemodynamic Spectrum of Combined Pulmonary Stenosis and Ventricular Septal Defect." Circulation 16.5 (1957): 736-749.

It would be rude not to reference Arthur Fallot himself. 
Fallot, Dr Arthur. Contribution à l'anatomie pathologique de la maladie bleue (cyanose cardiaque), par le Dr. A. Fallot,... Barlatier-Feissat, 1888.

Question 27 - 2010, Paper 2

What are the advantages and disadvantages of the various biomarkers that can be used to diagnose patients with acute myocardial infarction?

College Answer

Biomarker

Advantages

Disadvantages

TnT, TnI

Onset 2-3 hours, peak 24-36 hours,
elevated for 7-10 days
Virtually cardiac specific
Cut off 99th percentile of normal population
New assays quite sensitive
Negative test predicts low 30 day cardiac risk
Stratify short and long term risk in STEMI
Stratify short and long term risk in non
STEMI 
Detect reinfarction
AUC correlates to extent of MI

Elevated in non MI cases eg PE, myocarditis ie detects cardiac injury not cause

Assay variability (TnI) for reference range Washout and peak altered by reperfusion May need second test if first value taken too early

Modest correlation of size of MI with peak level
Some TnT present in skeletal muscle although genes different. 1st gen assays less specific (TnT)

Incomplete understanding of elevation after cardiac surgery and non cardiac surgery Baseline  higher in chronic renal failure

CK

Widely used and available

Non specific as present in skeletal muscle and brain

CK MB

Level and ratio improves specificity cf CK

Less specific and sensitive than troponin

Myoglobin

Theoretically rapid detection 

Lacks specificity and no earlier detection than Tn

AST

Historically used with CK and LDH 

Non specific

LDH

Late onset and offset 
LD1 and 2 in muscle

Present in many tissues. Requires isoenzymes

CRP

Marker of inflammation

Non specific

ESR

Additive prognostic benefit esp women

Novel biomarkers

Copeptin, if levels low can rule out MI in addition to negative Troponin

Heart-type Fatty Acid Binding Protein (H-FABP) is an early marker of ischaemia.


B-type Natriuretic Peptide (BNP) gives prognostic information post MI 

Other biomarkers of myocyte injury include  glycogen phosphorylase BB (GP-BB), myeloperoxidase, pregnancy associated plasma protein A (PAPP-A)

Raised Copeptin is not specific to cardiac disease.


Studies using H-FABP alone for diagnosis have been disappointing 

Not shown to be superior to Troponin

Discussion

The paper was written for 2010.

Since then, none of these exciting "novel biomarkers" have become commonplace.

Furthermore, the older biomarkers which are non-specific (such as AST and CK) have not fallen off the list, even though we have known since the 1950s that they are essentially useless.

In the event that the above "model" answer table is too easy to memorise, I direct the reader to a lucid interpretation of the current state by Anthony McLean et al (2012). Alternatively, this 2006 article in Circulation covers cardiovascular biomarkers in excessive pedantic detail.

References

McLean, Anthony S., and Stephen J. Huang. "Cardiac biomarkers in the intensive care unit." Ann Intensive Care 2.8 (2012): 1-11.

 

Question 5.3 - 2010, Paper 2

On palpation of the arterial pulse, a double peak was noted with each cardiac cycle.  List 4 conditions/situations  which can produce this phenomenon.

College Answer

On palpation of the arterial pulse, a double peak was noted with each cardiac cycle.  List 4 conditions/situations  which can produce this phenomenon.

•    AS + AR
•    Severe AR
•     HOCM
•     IABP

Discussion

This is a phenomenon known as pulsus bisferiens. The typical cause for it is the combination of aortic stenosis and regurgitation. The four differentials listed above are the classical ones which one may find in any textbook (or in Wikipedia for that matter). The below-referenced article is from 1957, before balloon pumps, but it covers the topic well. The article from 1899 is even cooler, but perhaps less relevant in modern critical care.

References

Talley and O'Connor, any edition

Fleming, Peter R. "The mechanism of the pulsus bisferiens." British heart journal 19.4 (1957): 519.

Broadbent, Walter. "Pulsus bisferiens." British medical journal 1.1985 (1899): 75.

 

Question 25.3 - 2011, Paper 1

A patient who underwent cardiac catheterization yesterday has this appearance of her foot.

a) What is the appearance due to?

b) Give two causes of a metabolic acidosis in this patient related to this event

College Answer

a) What is the appearance due to?
•    Cholesterol emboli or atheromatous emboli
•    (accept ischaemia secondary to damaged / occluded femoral artery)

b) Give two causes of a metabolic acidosis in this patient related to this event
•    acute renal failure
•    mesenteric ischaemia
•    limb ischaemia

Discussion

The damaged foot image has been harvested without permission from dermaamin.com; that is in fact a foot of somebody who has just had a shower of cholesterol emboli from an atheroma.

The possible causes of metabolic acidosis in this situation are well summed up by the college. It could be raised lactate due to limb ischaemia (or bowel ischaemia). Or, it could be due to renal failure.,

The renal injury could be developing as a result of myonecrosis and rhabdomyolysis. The angiography only happened yesterday, and so one would think that it is too early for contrast-induced nephropathy. Historically, the renal failure in these circumstances tends to be "pre-renal", and is blamed on showers of atheromatous debris into the renal vessels.

References

Drost, H. E. N. K., et al. "Cholesterol embolism as a complication of left heart catheterisation. Report of seven cases." British heart journal 52.3 (1984): 339-342.

 

Question 26.1 - 2011, Paper 1

A 70 year old man was admitted to the emergency department with shortness of breath and hypotension. He was discharged a week ago from hospital after having undergone an uneventful coronary artery bypass grafting procedure.

a)  What is the major abnormality on the ECG and what is the likely diagnosis?

b)  What investigation is required to confirm your diagnosis?

College Answer

a)  What is the major abnormality on the ECG and what is the likely diagnosis?

Electrical alternans, Pericardial tamponade

b)  What investigation is required to confirm your diagnosis?

Echocardiography.

Discussion

This pattern recognition question is easy marks and requires little thought.

I picked a relatively subtle ECG to put up here; the Google image search bristles with gratuitously obvious examples of electrical alternans.

I expect the College would want their candidates to be able to recognise it when it is not totally obvious.

References

The ECG above comes from the LITFL library of ECG clincal cases

In addition, there is an influential paper on this: Usher, Bruce W., and Richard L. Popp. "Electrical alternans: Mechanism in pericardial effusion." American heart journal 83.4 (1972): 459-463.

 

Question 26.3 - 2011, Paper 1

A 60 year old diabetic man was admitted following a syncopal episode to the emergency  department.  His GCS is 8. You have been called  to assess  him with a view to taking him to ICU.

a)     Comment on the ECG

b)    List 5 further investigations you will perform

College Answer

a)     Comment on the ECG

Normal ECG with sinus rhythm

b)    List 5 further investigations you will perform

BSL, troponin, CT head, Head and neck vascular studies, Holter monitoring, Echo, EEG.

Discussion

The question really asks the candidate to generate some differentials for an undifferentiated loss of consciousness, with a normal ECG. Creepily, the patient still has a GCS of 8, which suggests that not all is well intracranially.

References

The European Sociaty of Cardiology has a Taskforce on Syncope; and they have produced a guideline statement.

Brignole, Michele, et al. "Guidelines on management (diagnosis and treatment) of syncope–Update 2004 The task force on Syncope, European Society of Cardiology." European Heart Journal 25.22 (2004): 2054-2072.

Table 1 from the above statement seems like a comprehensive list of differentials.

 

Question 6.1 - 2011, Paper 2

This is the ECG of a 74-year-old gentleman who had an out of hospital cardiac arrest. 

RBBB + LPFB

1. What are the abnormalities on the ECG?

2. What would your management plan be if the patient makes a good functional neurological recovery? 

College Answer

1. Right bundle branch block and left posterior fascicular ( or right axis deviation) block

2. Permanent Pacemaker + Coronary angiography to exclude coronary vascular disease

Discussion

This is another "what ECG is this?" question, made harder to discuss because the college has removed the ECG from its paper.

... its a bi-fascicular block:

  • RBBB 
    • Wide QRS
    • RSR pattern in V1
    • Wide slurred S waves in I and V6
  • LPFB
    • Right axis deviation (QRS in III is taller than II; lead I and aVL are negative
    • No better explanation for the right axis deviation

This image was stolen from ecgmedicaltraining.com

As all bifascicular blocks, this one out to be managed with a permanent implanted device.

References

ACC 2008 guidelines are the direct source for all pacemaker-related recommendations.

 

ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices): developed in collaboration with the American Association for Thoracic Surgery and Society of Thoracic Surgeons.

 

Question 6.2 - 2011, Paper 2

This is an ECG of a 77-year-old woman.
 

1. Describe the ECG. 

2. Give two possible reasons for the ST changes. 

College Answer

1 Regular rhythm rate 75. atrial pacing spike, t wave flattening with reverse tick

2 Ischaemia or digoxin

Discussion

Try as I might, I could not find an ECG with both atrial pacing apikes and digoxin toxicity.

I believe digoxin toxicity is probably the main issue here, so the ECG above is from the LITFL opus which discusses its characterisitc ECG effects.

Particularly memorable is their reference to Salvador Dali's moustache as resembling the "reverse tick" appearance of the digitalised ST segment.

References

Question 6.3 - 2011, Paper 2


1 Describe the ECG shown. 

2 Give two interventions that may assist in clarification as to the aetiology of this rhythm? 

College Answer

1 Narrow complex tachycardia rate 170-200 bpm. ST depression inferiorly. Meets voltage criteria for Left ventricular hypertrophy with strain. Could be atrial flutter or atrial fibrillation or SVT

2 Either carotid sinus massage (after auscultation of carotids to exclude bruit) or other vagal manoeuvre or administration of push dose of adenosine if no asthma.

Discussion

This SVT question addresses the candidate's knowledge of the most recent resuscitation guidelines for the management of hemodynamically unstable narrow-complex tachycardia.Unable to locate an ECG with the specific features which the college wanted, I was limited in what I could post up there, and ultimately I settled on an SVT without any features of ischaemia and only the barest hint of LVH.

References

One may turn to the ARC guidelines for management of supraventricular tachycardias (guideline 11.9), which suggests (Class A evidence) that in a stable patient, vagal manoeuvres ought to be tried and then adenosine may be used unless contraindications exist. An unstable patient may also have a trial of adenosine while a defibrillator is being acquired, or while the chest is being shaved etc.....

As their reference for this set of guidelines, the ARC quote the ACC's statement.

 

Question 6.4 - 2011, Paper 2



1. Describe the ECG shown. 

2. Which coronary artery territory may be involved in the pathophysiology of this case?

College Answer

1 Sinus rhythm of 92 bpm. ST elevation of >2mm in II, III AVF and V5,6 with reciprocal changes in V1 and AVR. Consistent with myocardial infarction or pericarditis

2 Right coronary artery territory or LCx if dominant left system

Discussion

This is another "what ECG is this?" question, made harder to discuss because the college has removed the ECG from its paper.

Thankfully, I was able to find an example of an infarct with prciely these characteristics, as well an erudite discussion of its finer points.

This bounty is available for all to see at EMS12Lead.

References

No published evidence is possible or necessary.

However, EMS12Lead has pointed me to an article which may be of interest, if for no other reason then at least because it is by Sgarbossa et al (yes, that Sgarbossa).

Sgarbossa et al., Electrocardiographic diagnosis of acute myocardial infarction: Current concepts for the clinician. Am Heart J. 2001;141:507-17

 

Question 10 - 2011, Paper 2

Critically evaluate the use of plasma troponin in the critically ill patient.

College Answer

Greater specificity to cardiac damage than CK-MB / AST which can also be found in skeletal muscle

• Useful marker in acute coronary syndromes, where a higher level is indicative of a greater mortality and morbidity

• There has been recent discussion regarding the use of troponin and the diagnosis of myocardial infarction, and the definition has been standardised by the ECS / AHA. Myocardial infarction is defined as demonstration of myocardial ischaemia plus the addition of a significant plasma troponin rise (Circulation 2007)

• Numerous studies that show plasma troponin can be raised in other cardiac conditions, e.g. pericarditis, atrial fibrillation cardioversion, and non cardiac conditions e.g. renal failure, PE, sepsis.

• Plasma troponin levels should be used as a risk stratification tool in conjunction with other tests e.g. ecg and echo, depending on the presenting medical condition

• This has significance in critically ill patients in the non ACS-AMI setting. Medications used for a troponin rise in the setting of ACS / AMI, e.g. anti-coagulants and anti-platelet therapy are not benign, and can have detrimental effects in critically ill patients who have troponin rises due to non ACS / AMI

• Monitoring for ischaemia in the ICU patient

Discussion

Though the college answer is different, this question closely resembles Question 8  from the second paper of 2006. One is tempted to point out that these questions do not ask specifically about troponin use in the acute coronary syndromes.

In general, the college seems to have wanted to observe several key points in the answer:

  • Awareness regarding the origins and physiological role of troponin in the myocyte
  • Knowledge that it is specific to the myocardium
  • Understanding of its high specificity and sensitivity for cardiac damage
  • Relationship between high levels and poorer prognosis in acute coronary sydnrome
  • Awareness that troponins can rise in other conditions.

Rationale for the use of troponin in the critically ill:

  • Troponin is an enzyme involved in the excitation-contraction coupling of the myocardium.
  • Troponin T serves to attach the troponin complex to actin and tropomyosin.
  • Myocardiac damage (for example infarction) causes the release of troponin.
  • There is a cytosolic pool (which is released early in the infarct) and a structural pool (which is slowly released over days as the damaged myocardium decomposes).

Advantages of using troponin in critically ill patients

  • Its a sensitive and specific marker of myocardial ischaemia.
  • It is more sensitive and specific than AST, CK and CK-MB (which are also found is skeletal muscle)
  • It is an independent predictor of 30-day mortality in STEMI 
  • It is associated with a poorer outcome in the critically ill patients.
  • Troponin levels can be used to monitor for myocardial ischaemia in critically ill patients when history and examination are unreliable.

Advantages of using troponin in acute coronary syndromes

  • Troponin forms a part of the ECS and AHA universal definition of acute coronary syndrome (it consists of a troponin rise as well as a demonstration of ischaemic symptoms,  echocardiographic evidence, or ECG changes.)
  • The troponin levels are not diagnostic, but are a risk stratification tool to be used together with echocardiography, ECG, history and examination.
  • Troponin levels can be used for the late diagnosis of MI and to monitor for reinfarction
  •  The use of troponin as a part of a risk stratification strategy is important in selecting patients for anticoagulation and anti-platelet therapy, so as to prevent the exposure of patients to unnecessary bleeding risk.

Disadvantages for the use of troponin in critical illness

  • A reliance on biomarkers may become unhealthy if it takes focus off clinical examination and history.
  • It is not quantitatively validated outside the setting of ACS / AMI, but only qualitatively: i.e. a "positive" troponin is associated with worse outcomes in noncardiac critical illness, but we don't know whether a higher troponin is associated with a proportionally higher mortality.
  • As with all biomarkers, inappropriately low threshold levels or testing out of appropriate clinical context could give rise to unnecessary treatments (eg. loading doses of antiplatelet drugs) or investigations (eg. angiography, with needless contrast exposure)
  • Troponin levels can be raised for a variety of non-cardiac reasons.In their 2006 article, Korff et al offer an excellent table of things which cause troponin elevation, together with the mechanism of troponin release or assay confusion. Their Table 1 is reinterpreted here. 
    • Myocarditis 
    • Renal failure - its cleared renally
    • Sepsis
    • Atrial fibrillation
    • Post-cardioversion 
    • Cardiac trauma 
    • Pulmonary embolism 
    • Acute stroke
    • Intracranial haemorrhage
    • Severe burns
    • Rhabdomyolysis (particularly during recovery)
    • Skeletal muscle damage in glycogen storage disease
    • Defective assay (cross-reactivity with skeletal troponin isoforms)
 

References

This article has a nice graph of cardiac biomarker concentrations over time after an infarct:
Wu et al; National Academy of Clinical Biochemistry Standards of Laboratory Practice: Recommendations for the Use of Cardiac Markers in Coronary Artery Diseases. Clinical Chemistry 45:7 1104 –1121 (1999)

There is a CICM fellowship question regarding the critical appraisal of troponin in the ICU population.

The ECS and AHA statement referred to in the college answer is this article published in Circulation in 2007:

(Kristian Thygesen et al; Universal Definition of Myocardial Infarction. Circulation 2007, 116:2634-2653

This article from Current Opinion in Critical care (2004) discusses the various causes of raised troponin among ICU patients:


Ammann et al,Troponin as a risk factor for mortality in critically ill patients without acute coronary syndromes. Journal of the American College of Cardiology Volume 41, Issue 11, 4 June 2003, Pages 2004–2009

The fact that troponin rise among the critically ill population is associated with a poorer prognosis is supported by this study:


Gunnewiek et al. Cardiac troponin elevations among critically ill patients. Current Opinion in Critical Care: October 2004 - Volume 10 - Issue 5 - pp 342-346

Liu, Michael, et al. "Prognostic Value of Initial Elevation in Cardiac Troponin I Level in Critically Ill Patients Without Acute Coronary Syndrome." Critical care nurse 35.2 (2015): e1-e10.

Ahmed, Amna N., et al. "Prognostic significance of elevated troponin in non-cardiac hospitalized patients: A systematic review and meta-analysis." Annals of medicine 46.8 (2014): 653-663.

Ammann, P., et al. "Elevation of troponin I in sepsis and septic shock." Intensive care medicine 27.6 (2001): 965-969.

Landesberg, Giora, et al. "Troponin elevation in severe sepsis and septic shock: the role of left ventricular diastolic dysfunction and right ventricular dilatation." Critical care medicine 42.4 (2014): 790-800.

Smith, Andria, et al. "Elevated cardiac troponins in sepsis: what do they signify?." West Virginia Medical Journal 105.4 (2009): 29-33.

Tiruvoipati, Ravindranath, Nasreen Sultana, and David Lewis. "Cardiac troponin I does not independently predict mortality in critically ill patients with severe sepsis." Emergency Medicine Australasia 24.2 (2012): 151-158.

Suarez, Keith, et al. "TROPONIN TESTING IN PATIENTS HOSPITALIZED FOR SEPSIS IS ASSOCIATED WITH INCREASED CARDIOVASCULAR TESTING AND LENGTH OF STAY." Journal of the American College of Cardiology 67.13 (2016): 451.

Sheyin, Olusegun, et al. "The prognostic significance of troponin elevation in patients with sepsis: a meta-analysis." Heart & Lung: The Journal of Acute and Critical Care 44.1 (2015): 75-81.

Hunter, J. D., and M. Doddi. "Sepsis and the heart." British journal of anaesthesia 104.1 (2009): 3-11.

Vieillard-Baron, Antoine, et al. "Actual incidence of global left ventricular hypokinesia in adult septic shock." Critical care medicine 36.6 (2008): 1701-1706.

Donzé, Jacques D., et al. "Impact of sepsis on risk of postoperative arterial and venous thromboses: large prospective cohort study." BMJ 349 (2014): g5334.

Korff, Susanne, Hugo A. Katus, and Evangelos Giannitsis. "Differential diagnosis of elevated troponins." Heart 92.7 (2006): 987-993.

Wens, Stephan CA, et al. "Elevated Plasma Cardiac Troponin T Levels due to Skeletal Muscle Damage in Pompe Disease." Circulation: Genomic and Precision Medicine (2016): CIRCGENETICS-115.

Sribhen, Kosit, Rewat Phankingthongkum, and Nilrat Wannasilp. "Skeletal muscle disease as noncardiac cause of cardiac troponin T elevation." Journal of the American College of Cardiology 59.14 (2012): 1334-1335.

Question 26.3 - 2011, Paper 2

List 4 causes of a diastolic murmur over the apical area.

College Answer

Mitral stenosis
Severe mitral regurgitation (flow murmur)
Significant left to right shunt (VSD)
Austin-Flint murmur of aortic regurgitation
Carey-Coombs murmur

Discussion

This question interrogates one's knowledge of the highly regarded Talley and O'Connor manual of physical examination.

I have used this book to revisit the issue of physical examination in some detail.

In Talley and O'Connor, there is a particular table which this question references. To be precise, it is Table 3-9 in the 6th edition ("Cardiac murmurs").

The mitral stenosis, VSD and severe MR are well known and require little thought from the candidate.

Not so, for the other two.

Specifically, the Carey Coombs murmur is discussed. Not "Carey-Coombs" as the college puts it, but Carey Coombs, named after Dr C.F. Coombs from Bristol. Anyway, its a "short mid-diastolic rumble" which disappears with resolving valvular disease.

The Austin-Flint murmur is not hyphenated either - and it is named after Austin Flint, who was a damn genius and generally deserves to have his murmur spelled correctly in official college papers. Its a murmur of the aortic regurgitation jet hitting the apex of the left ventricle in diastole. The great man himself, with lucid clarity described the murmur in his seminal article:

"“Oftener rough than soft. The roughness is often peculiar. It is a blubbering sound, resembling that produced by throwing the lips or the tongue into vibration with the breath of respiration.” 

Its poetry. In fact, the whole article is awesome. It is peppered with terms like "amphoric resonance" and "puerile respiration", which have since become lost in this era of trans-thoracic echocardiography.

 

References

Clinical Examination of the Critically Ill Patient, 3rd edition by L.I.G. Worthley - which can be ordered from our college here.

Clinical Examination: whatever edition, by Talley and O'Connor. Can be acquired any damn where.

Flint, Austin. Compendium of Percussion & Auscultation, and of the Physical Diagnosis of Diseases Affecting the Lungs and Heart. W. Wood & Company, 1870.

Question 14 - 2012, Paper 1

Question 13 and Question 14 both relate to the following clinical scenario:

A 71-year-old man is transferred to your intensive care unit following a mechanical aortic valve replacement and coronary artery bypass surgery.

The anaesthetist reports that he came off bypass readily, has not required any inotropic support, and has epicardial pacing wires in situ. However, shortly after arrival his blood pressure falls to 60/30.

Question 13 was as follows:

a) Outline your differential diagnosis for his hypotension

His blood pressure improves rapidly with a fluid bolus, and examination is otherwise unremarkable. However, he is noted to lose 250ml of blood from his mediastinal drains over the next 30 minutes.

b) List 4 likely causes of, or contributors to, excessive post-operative bleeding in this setting, and outline your immediate management.

Question 14 continues from the above.

Twenty four hours later, he develops a new-onset tachycardia as shown in the ECG below. (again, the college has removed the images from their paper, but I have found an alternative (hopefully equivalent) image)

a) What is your interpretation of the ECG?

b) Outline your initial management of the tachycardia

c) List 3 primary non-cardiovascular causes of the above tachycardia.

College Answer

a) What is your interpretation of the ECG?

Atrial fibrillation (vent rate approx. 170) LAD

LVH

Lateral T inversion.

b) Outline your initial management of the tachycardia

  • Attention to airway, breathing and circulation.
  • Identify and rectify reversible factors as above
  • Fluid bolus if hypovolaemic
  • Correct electrolyte abnormalities
  • Check pacemaker
  • Treat pain
  • Consider MgSO4
  • Assess for haemodynamic compromise.
    • If significant haemodynamic compromise, early mechanical cardioversion.
    • If tolerating arrhythmia haemodynamically, options are rate-control or pharmacological cardioversion.
    • Rate-control – IV Digoxin or beta-blocker
    • Pharmacological cardioversion – Amiodarone, Sotalol, Class 1A or 1C

c) List 3 primary non-cardiovascular causes of the above tachycardia.

  • Hyperthyroidism
  • Alcohol binge
  • Sepsis /Pneumonia
  • Carbon monoxide poisoning
  • Association with Friedrich’s ataxia although this is due to a cardiomyopathy. 

Discussion

Though the previous question for this scenario was more related to the consequences of cardiothoracic surgery, this question focuses on the generic features of managing AF in the ICU. 

First of all, let us lament again the absence of ECG images from the papers. I had to steal my material from this source. If their lawyers ever contact me, I will be very upset.

Now, lets examine the college answer for the management of AF. 

The first seven points are hardly sophisticated. This seems to have required a registrar-level answer.

  • Attention to airway, breathing and circulation.
  • Identify and rectify reversible factors as above
  • Fluid bolus if hypovolaemic
  • Correct electrolyte abnormalities
  • Check pacemaker
  • Treat pain
  • Consider MgSO4​

No geniuses needed here.

The next section deals with the discrimination between haemodynamically stable and haemodynamically unstable AF.  This refers to the arrhythmia algorithm in the pre-arrest management section of the ARC ALS Handbook, and is therefore based on ILCOR Guidelines. The ARC book is not available online, but the UK version thankfully is.  Again - its nothing special; you shock the unstable ones, and the stable ones give you plenty of time to debate the choice of rhythm or rate control medications.

As for the non-cardiac causes of AF- only 3 are asked for; however the list is enormous. This British publication contains Table 1.2 (on page 6) briefly lists 6 causes. To the college answer, they would add lung cancer, pulmonary embolism, and pleural effusion. Much larger tables of causes exist in the atrial fibrillation chapter of the Required Reading section for cardiology. To simplify revision, they are reproduced below:

Causes of Atrial Fibrillation Organised by System

Vascular:

  • Myocardial infarction
  • Pulmonary embolism
  • Pulmonary hypertension
  • Subarachnoid haemorrhage

Infectious:

  • Sepsis
  • Myocarditis
  • Pericarditis
  • Infective endocarditis

Neoplastic:

  • Cardiac mass, eg. myxoma

Drug-induced:

  • Catecholamines
  • Alcohol
  • Caffeine

Idiopathic:

  • Infiltrative disease, eg. amyloidosis
  • Age-related fibrotic changes

Idiopathic:

  • Infiltrative disease, eg. amyloidosis
  • Age-related fibrotic changes

Congenitial:

  • Atrial septal defect
  • Familial AF

Autoimmune:

  • Autoimmune myocarditis

Traumatic:

  • Cardiac contusion
  • Cardiac surgery

Endocrine/environmental:

  • Hypothermia
  • Hyperthyroidism
  • Haemochromatosis/iron overload
  • Phaeochromocytoma
  • Electrolyte derangement
Causes of Atrial Fibrillation Organised by Pathophysiology

Catecholamine excess

  • Exogenous (eg. adrenaline infusion)
  • Endogenous:
    • Subarachnoid haemorrhage
    • Stress
    • Phaeochromocytoma
    • Thyrotoxicosis (indirectly)

Atrial distension

  • Pulmonary hypertension:
    • Obstructive sleep apnoea
    • Pulmonary embolism
    • Primary pulmonary hypertension
    • Pulmonic valve disease
  • Septal defects
  • Valvular disease, including infective endocarditis

Abnormality of conducting system

  • Congenital cardiac disease, eg. septal defect
  • Infiltrative cardiac disease, eg. amyloidosis
  • Ischaemic heart disease
  • Age-related fibrotic changes
  • Haemochromatosis/iron overload
  • Hypothermia

Increased atrial automaticity

  • Alcohol
  • Caffeine
  • Catecholamines
  • Electrolyte derangement
  • Myocarditis

References

Frederick A. Hensley, Jr., M.D., Donald E. Martin, M.D.,  Glenn P. Gravlee, M.D. A Practical Approach to Cardiac Anaesthesia, 3rd ed. Sibylle A. Ruesch and Jerrold H. Levy. CHAPTER 9. The Postcardiopulmonary Bypass Period: A Systems Approach. 2003 by LIPPINCOTT WILLIAMS & WILKINS

 

National Collaborating Centre for Chronic Conditions (Great Britain). "Atrial fibrillation: national clinical guideline for management in primary and secondary care." Royal College of Physicians, 2006.

Question 23.1 - 2012, Paper 1

A 45 year old woman is admitted with hyperosmolar hyperglycaemic non-ketotic coma (HONK). A routine ECG is performed. 

  • What does it show?
  • What is your treatment of this problem? 

College Answer

  • Flattening of P waves & peaked T waves consistent with hyperkalaemia.
  • Treatment of hyperkalaemia:
    • Intravenous calcium based on K levels
    • Bicarbonate
    • Insulin/? Dextrose if she has HONK
    • Resonium / beta 2 agonists
    • Investigate for cause
    • Renal function/electrolytes

Discussion

The referenced article takes good care of the latter. The former is immediately recogniseable and requires little further discussion.

Again, I extend my thanks to LITFL for making public their awesome and massive ECG library.  

References

Weisberg, Lawrence S. "Management of severe hyperkalemia." Critical care medicine 36.12 (2008): 3246-3251. 

Question 23.2 - 2012, Paper 1

A 72 year old male presents with a fractured neck of femur following a syncopal episode. He is now well and has an ECG prior to his surgical procedure. 

 What does it show?
 What could be the cause of his fall and what is the management of the findings you have identified in the ECG?

College Answer

  • Tri-fascicular block
  • Cause:
    • Complete heart block.
  • Management:
    • Correct electrolyte and endocrine abnormalities (e.g. K+, thyroid function tests)
    • Consider influence of drug therapies such as digoxin, calcium channel antagonists
    • Investigate for ischaemic heart disease
    • Referral to cardiology unit for further evaluation (?permanent pacemaker)

Discussion

If you are working though these questions systematically in reverse chronological order, this will all sound very familiar. Old man, fall, trifascicular block... This question is a repeat.

Instead of replicating the discussion entry here,  one could refer the gentle reader to the most recent incarnation of this question (Question 18.1 from the first paper of 2013). However, in this incarnation of the SAQ, the college say that the cause was complete heart block. The ECG is borrowed from the LITFL library.

In this ECG, there is:

  • Right bundle branch block
  • Left axis deviation (Left anterior fascicular block)
  • Complete heart block

In summary, for a trifascicular block:

  • RBBB should not have any axis deviation
  • If there is RBBB and the QRS in leads I and aVF is not upright, you must assume there is some sort of fascicle block.
  • A left axis deviation suggests the anterior fascicle has failed;
  • Right axis deviation means the posterior fascicle has failed

The AHA/ACCF/HRS recommend anybody with that much conductive tissue disease get a pacemaker. Other possible contributing causes need to be addressed, which could include AV blocker drugs (beta-blockers, calcium channel blockers, digoxin) and electrolyte derangement.

References

Tracy, Cynthia M., et al. "2012 ACCF/AHA/HRS Focused Update of the 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines." Journal of the American College of Cardiology 60.14 (2012): 1297-1313.

Surawicz, Borys, et al. "AHA/ACCF/HRS Recommendations for the Standardization and Interpretation of the ElectrocardiogramPart III: Intraventricular Conduction Disturbances A Scientific Statement From the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society Endorsed by the International Society for Computerized Electrocardiology." Journal of the American College of Cardiology53.11 (2009): 976-981.

Question 23.3 - 2012, Paper 1

A 22 year-old-female presents following voluntary ingestion of 20 g of amisulpride (an atypical antipsychotic / anti-depressant). 

ECG 1:

ECG 2:

You are given the following ECG (ECG 1) and notice the changes seen on the second ECG tracing (ECG 2) whilst you are reviewing the patient.

  • What is the primary abnormality seen on the first ECG?
  • What is the abnormality seen on the ECG tracing (ECG 2)?
  • What is the most likely cause of this abnormality?
  • What is the management of this problem? 

College Answer

  • .Prolonged QT.
  • Torsades de pointes.
  • QT prolongation secondary to amisulpride intoxication.
  • Resuscitation with respect to ABC
    • Correct abnormalities and administer electrolytes
      • Intravenous magnesium sulfate
      • Treatment of hypokalemia
    • Consideration of acute cardiac pacing
    • Monitoring

Discussion

With the amisulpride being mentioned in the text, one anticipates both a long QT and torsades.

The 12-lead ECG above is actually from a paywall-protected MJA article about the dangers of QT prolongation in amisulpride toxicity.One can see the faint penstrokes of the MJA authors, where they clearly either measured or calculated the QT in their ECG.

It would be unforgiveable to omit the reference to LITFL, and particularly to their page on QT interval estimation.

As for torsades de pointes, it is a fairly straightforward answer.

  • Confirm cardiac arrest
  • Proceed with normal basic and advanced life support algorithm (for shockable rhythm) with emphasis on the use of lots and lots of magnesium sulfate.
  • If the patient is not arrested but is haemodynamically unstable, you attempt a DC cardioversion as you would for any broad-complex arrhythmia
  • If the patient is stable and able to tolerate this arrhythmia (which is unlikely) one may attempt to addess it chemically, with something like a magnesium sulfate bolus.
    • Additionally, you may want to avoid amiodarone.
    In some contaxts (eg. quinidine overdose) it may be reasonable to also give sodium bicarbonate, to increase the protein-bound fraction of the drug.  Authors of case reports on amisulpride toxicity (eg. Karunasekara et al, 2012) also seem to be giving bicarbonate to their patients as a means of improving their cardiovascular stability, by modifying pH until their catecholamine receptors actually have a chance to bind their ligands.
     
  • Then, one may wish to take some preventive measures:
    • In congential long QT syndrome, you typically decrease the heart rate with beta blockers. NOT SO for drug-induced long QT. These people need to go faster. Pacing or isoprenaline maybe required if they constantly have episodes of torsades.

References

John, Sally, Phebe O'Mullane, and Sophie Gosselin. "Amisulpride deliberate self-poisoning causing severe cardiac toxicity including QT prolongation and torsades de pointes." Med J Aust 184.7 (2006): 354-356.

 

Roden, Dan M. "Antiarrhythmic drugs: from mechanisms to clinical practice."Heart 84.3 (2000): 339-346.

 

Ayad, Ramy F., et al. "Causes and management of drug-induced long QT syndrome." Proceedings (Baylor University. Medical Center) 23.3 (2010): 250.

Gowda, Ramesh M., et al. "Torsade de pointes: the clinical considerations." International journal of cardiology 96.1 (2004): 1-6.

Karunasekara, Niroshini, Michael Wilcox, and Nigel Tufft. "Cardiovascular management of amisulpride overdose." Journal of the Intensive Care Society 13.2 (2012): 160-162.

Question 30.3 - 2012, Paper 2

Report on the abnormalities on the following ECG:

College Answer

Right bundle branch block

Q waves in leads II III and AVF and T wave inversion in III and AVF indicative of old inferior infarct

>2 mm ST segment elevation in leads V2 and V3 and ST elevation in leads V4 and V5 indicating STEMI

Discussion

As the above ECG was combed out of random Google searches rather than CICM gospel, it does not contain Q waves.

It is, however, an example of RBBB with an anterior STEMI.

A vigorous discussion of the difficulties of this diagnosis (given that anteriorly the T waves are "apropriately discordant" in RBBB) occurs at the EMS12Lead blog. In short, the key seems to be to find the J-point (the transition from QRS into ST) and to demonstrate that it is above the isoelectric line

References

Pelter, Michele M., and Mary G. Adams. "ST segment changes in right bundle branch block." American Journal of Critical Care 14.4 (2005): 341-342.

Question 30.4 - 2012, Paper 2

The following is the ECG of a 61-year-old man in ICU following aortic valve replacement for endocarditis.

What does this ECG show?

College Answer

Complete heart block.

Discussion

This question is straightforward.  Any additonal discussion of such an effortless pattern recognition exercise would yet further degrade the quality of this already bloated resource.

References

Question 30.1 - 2012, Paper 2

This is the ECG of a 62-year-old man undergoing treatment for acute lymphoblastic leukaemia who presented with shortness of breath.

  • What are the abnormalities on this ECG?
  • What is the likely cause of his symptoms?

College Answer

a)

Atrial fibrillation

Low voltage complexes

Electrical alternans

b)

Pericardial effusion

Discussion

This of course is not the canonical CICM ECG, it is one which I found by Googling "AF with electrical alternans". Thus, the complexes are not actually "low volage". The presence of alternans is obscured by the irregularity of the AF, but it is still present, particularly if you look at leads V1 and V2.

In ideal conditions, electrical alternans should look like this:

electrical alternans in pericardial effusion

If the rightful owner of this image ever comes forward and demands I take it down, I will be forced to generate this electrical phenomenon in myself. 

References

Usher, Bruce W., and Richard L. Popp. "Electrical alternans: Mechanism in pericardial effusion." American heart journal 83.4 (1972): 459-463.

 

Question 14.2 - 2013, Paper 1

In each part of this question, list clinical examination findings for each of the two underlined conditions that would help you to distinguish between them:

  • Aortic regurgitation or mitral stenosis as the cause of a patient’s diastolic murmur.

College Answer

Aortic regurgitation

  • Collapsing pulse / wide pulse pressure
  • Decrescendo murmur heard over left 3rd intercostal space parasternally
  • Murmur loudest sitting forward in expiration
  • Signs associated with large pulse volume and peripheral vasodilation; eg Corrigans, De Musets. Quinckes, Duroziez.
  • Evidence of associated conditions; Infective endocarditis, ankylosing spondylitis, other seronegative arthropathies, Marfans.
  • Soft 2nd heart sound
  • 3rd heart sound
  • Displaced apex beat
  • Signs of LV failure

Mitral stenosis

  • Malar flush
  • Atrial fibrillation
  • Small pulse pressure
  • Loud 1st heart sound
  • Opening snap
  • Low-pitched, rumbling diastolic murmur over apex loudest in left lateral position
  • Pulmonary hypertension

Discussion

This question comes straight from Talley and O'Connor.

Specifically, the part of Chapter 3 (The Cardiovascular System) titled "Correlation of physical signs and cardiovascular disease". The sections dealing with aortic regurgitation and mitral stenosis make several statements to distinguish the two murmurs.

Unfortunately, its not as though there is a summary of it anywhere, nor is there any sort of table with the features of the various murmurs, which one might use as a quick reference. In fact the college answer is the closest thing to a summary of this issue.

Fortunately, before all these new-fangled gadgets came about, there were real physicians, who knew how to auscultate a praecordium. I have an 1958 article which contains precisely this sort of table, comparing the two murmurs according to their features. Together with the UpToDate page on heart sounds, this table has formed the basis of my "model answer". For more details, one may refer to the Circulation Research article by Sabbah et al (1976). In Aubrey Leatham's 1954 article for the Lancet, one may also find various causes of split heart sounds. Another important reference is  Walker's Clinical Methods, in which  Crowley's Chapter 27 is dedicated entirely to diastolic mumurs.

 
Features which Distinguish Aortic Regurgitation from Mitral Stenosis
Feature Aortic regurgitation Mitral stenosis
Rhythm usually sinus usually AF
First heart sound Normal S1 Loud S1
Second heart sound Soft S2 (A2) Normal S2 (M2)
Additional sounds Third heart sound (S3) Opening snap
Pulse quality Collapsing pulse Small pulse pressure
Where is it loudest 3rd intercostal space, parasternally Apex
When is it loudest Sitting forward, during expiration In a left lateral position
Pitch, quality Decrescendo low-pitched, rumbing
Associated findings

Signs of LV failure,

displaced apex beat

"Malar flush"
Coexisting disease Infective endocarditis, ankylosing spondylitis, other seronegative arthropathies, Marfans. Pulmonary hypertension

In case anybody is interested, here are the eponymous signs of aortic regurgitation which were mentioned by the college. If any of you young people are wondering why you (probably) have never heard of these, it is because they are almost completely useless.

Corrigans sign: a "jerky" carotid pulse: full expansion, followed by complete collapse. You're palpating the pressure of the left ventricle, essentially. It's named after a 19th century Irishman. It indicates a severe aortic incompetence. 

de Musset's sign which the college answer has spelled incorrectly is  a visible nodding of the head in time with arterial pulsation in patients with severe aortic insufficiency. It is named after an aortically insufficient French poet.

Quincke's sign, otherwise known as Quincke's pulse, is a nail sign: it is seen when the nailbed is blanched. The pale nail bed flashed red and white as capillary refill is restored. It can also be seen in the absence of any aortic problems, in patients who have sclerodactily.

Duroziez's sign is elicited by listening over the femoral artery with the bell of the stethoscope. It is supposed to be a double murmur. According to some recent evidence, it has almost 100% specificity. There is supposed to be both a systolic and a diastolic bruit, as blood rushes into - and then rapidly out of - the femoral artery.

References

Nicholas Joseph Talley, Simon O'Connor; Clinical Examination: A Systematic Guide to Physical Diagnosis (7th ed)

SEGAL, JACK P., W. PROCTOR HARVEY, and MICHAEL A. CORRADO. "The Austin Flint murmur: its differentiation from the murmur of rheumatic mitral stenosis." Circulation 18.5 (1958): 1025-1033.

Leatham, Aubrey. "Splitting of the first and second heart sounds." The Lancet 264.6839 (1954): 607-614.

Sabbah, HANI N., and PAUL D. Stein. "Investigation of the theory and mechanism of the origin of the second heart sound." Circulation research 39.6 (1976): 874-882.

Saberi, Asif, and Saeed A. Syed. "Corrigan’s sign." Hospital Physician (1999): 29.

DAVIES, M., and A. Hollman. "de Musset sign." Heart 82.3 (1999): 262.

Norton, S. A. "Keratoderma with pseudo-Quincke's pulse." Cutis 62.3 (1998): 135-136.

Sapira, J. D. "Quincke, de Musset, Duroziez, and Hill: some aortic regurgitations." Southern medical journal 74.4 (1981): 459-467.

Luisada, Aldo A. "On the pathogenesis of the signs of Traube and Duroziez in aortic insufficiency. A graphic study." American Heart Journal 26.6 (1943): 721-736.

BLUMGART, HERRMAN L., and A. CARLTON ERNSTENE. "Two mechanisms in the production of Duroziez's sign: their diagnostic significance and a clinical test for differentiating between them." Journal of the American Medical Association 100.3 (1933): 173-177.

Question 18.1 - 2013, Paper 1

The following ECG (labelled ECG 1) has been sent by fax from a doctor at a small rural hospital seeking advice. The ECG is that of a 78-year-old male presenting with a fractured neck of femur following a fall.

ECG

  • List the abnormalities shown on the ECG.
  • What cardiac complication may this patient develop?
  • What advice will you give the rural doctor?

College Answer

a)

Trifascicular block i.e. 1st degree heart block, left axis deviation, RBBB.

b)

Complete heart block.

c)

Establish cause of fall – mechanical or related to possible syncope. Continued cardiac monitoring. 
Referral to cardiology and transfer to centre with facilities for insertion TPW.

Discussion

Well, the ECG in the question above is the the canonical ECG from the CICM paper (seeing as they have removed them) but one which I have found on the glorious LITF archive of ECGs.

The moral of the story is that RBBB should not have any axis deviation, so if you see RBBB and the QRS in leads I and aVF is not upright, you must assume there is some sort of fascicle block. A left axis deviation suggests the anterior fascicle has failed; right axis deviation means the posterior fascile is at fault. I have a thing about that.

And yes, these tend to degenerate into complete heart block. In fact the AHA/ACCF/HRS recommend anybody with that much conductive tissue disease get a pacemaker. And they whinge interminably about the inappropriateness of using crudely unscientific terms like "bifascicular" and "trifascicular".

Then, for some reason, the college recommends temporary pacing wires be inserted.

For myself, I cannot understand. Surely, if this patient were transferred to a tertiary hospital, the facilities there would be appropriate for an urgent PPM insertion?

In any case, we all agree he needs a pacemaker so he doesn't break his other hip.

References

Tracy, Cynthia M., et al. "2012 ACCF/AHA/HRS Focused Update of the 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines." Journal of the American College of Cardiology 60.14 (2012): 1297-1313.

Surawicz, Borys, et al. "AHA/ACCF/HRS Recommendations for the Standardization and Interpretation of the ElectrocardiogramPart III: Intraventricular Conduction Disturbances A Scientific Statement From the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society Endorsed by the International Society for Computerized Electrocardiology." Journal of the American College of Cardiology53.11 (2009): 976-981.

Question 18.2 - 2013, Paper 1

The following ECG (labelled ECG 2) is that of a haemodialysis patient presenting with pulmonary oedema.

  • What test will you do to confirm the likely underlying diagnosis?
  • What is your immediate management for this condition?

College Answer

a)

Potassium level

b)

Counteract cardiotoxic effects of hyperkalaemia

  • Calcium chloride
  • Sodium bicarbonate

Shift potassium into the cells

  • Dextrose and insulin
  • Beta agonists

Remove potassium (and water)

  • Urgent haemodialysis

Discussion

This is a pattern-recognition ECG question requiring little discussion.

The abnormality is obvious, and the question hints at the solution by mentioning hemodialysis.

Interestingly, chronically hyperkalemic patients on hemodialysis dont seem to have a classical presentation of ECG changes, making it difficult for their physician to predict a hyperkalemic arrest.

References

Montague, Brian T., Jason R. Ouellette, and Gregory K. Buller. "Retrospective review of the frequency of ECG changes in hyperkalemia." Clinical Journal of the American Society of Nephrology 3.2 (2008): 324-330.

Weisberg, Lawrence S. "Management of severe hyperkalemia." Critical care medicine 36.12 (2008): 3246-3251.

Question 18.3 - 2013, Paper 1

The following ECG (labelled ECG 3.) is that of an 83-year-old female found by her neighbour collapsed on the bathroom floor.

  • List the abnormalities shown on the ECG.
  • What do these abnormalities indicate?

College Answer

a)

Profound bradycardia

J (Osborn) waves

Atrial fibrillation

Shivering artefact

LVH

b)

Hypothermia

Discussion

The ECG I used above comes from LITFL and was not part of the CCIM paper.

I was luckty to find it; and it contains everything in the college answer, including LVH by voltage criteria and even shivering artifact.

References

Montague, Brian T., Jason R. Ouellette, and Gregory K. Buller. "Retrospective review of the frequency of ECG changes in hyperkalemia." Clinical Journal of the American Society of Nephrology 3.2 (2008): 324-330.

Weisberg, Lawrence S. "Management of severe hyperkalemia." Critical care medicine 36.12 (2008): 3246-3251.

Question 18.1 - 2014, Paper 1

A 65-year-old male presents to the Emergency Department (ED) with persisting chest pain for one week, following an acute severe episode that lasted for two hours. His 12-lead ECG, (ECG 1), taken on presentation to ED, is shown below.

a) Describe the ECG changes.

b) What is the most likely diagnosis?

The patient develops worsening chest pain and becomes more tachypnoeic and hypotensive.
c) Give two likely causes for this deterioration.

College Answer

a)
 Atrial fibrillation with a controlled ventricular response
 Right Bundle Branch Block
 Q-waves V1- V5 and which are wide
 Left axis deviation
 ST elevation anterior and inferior
 ST depression in aVL
b)
 Recent transmural anterior MI with resulting ventricular aneurysm
c)
 Aneurysm rupture
 Septal rupture causing a VSD
 Cardiac tamponade
 Papillary muscle rupture
 Re-infarction
 (Pulmonary embolus)

 

Discussion

The ECG above has been stolen shamelessly from Dr Smith's ECG Blog, where it is discussed in glorious detail. Obviously, one would find it difficult to reproduce the exact ECG which the college had in their paper. The one I have stolen is interpreted by Dr Smith in the following fashion:

There is RBBB, but without the usual rSR' in right precordial leads.  [There is some left axis deviation as well, probably a left anterior fascicular (hemi-) block.]  The initial r-wave is gone, so that there are QR-waves (diagnostic of myocardial infarction, whether old or acute).  There is ST elevation (which is never normal in RBBB).  The negative T-wave makes it very unlikely that this acute MI, but it could be either subacute or old. 

 

References

Question 18.2 - 2014, Paper 1

A 45-year-old male has been admitted to the hospital for investigation of syncope. He has a MET call for another syncopal episode. His 12 lead ECG is shown below (ECG 2).



a) Describe the ECG changes.
 
b) What is the most likely diagnosis?
 
c) What is the underlying pathophysiology?
 
d) List four clinical situations that can worsen this condition.

College Answer

a)
 Coved ST segment elevation V1 – V2 > 2 mm.
 Subsequent negative T wave in the same leads.
b)
 Brugada syndrome (Type 1).
c)
 A mutation in the cardiac sodium channel gene.
d)
 Fever.
 Myocardial ischaemia.
 Medications
o E.g. Flecainide, Amitriptyline, Lithium, Bupivacaine, Propofol, Alcohol.
 Hypokalaemia.
 Hypothermia.
 Cardioversion.

Discussion

The criteria for the diagnosis of Brugada syndrome as well as  are explored to a fascinating depth by Edward Burns in his article for LITFL. The time-poor exam candidate will be interested in only the answers to this question:

Clinical criteria:

  • Characteristic ECG changes
    • "Coved" ST elevation:  the QRS complex finishes high, and the ST-segment slopes diagonally to form an inverted T-wave in V1 and V2
    • Inverted T waves
  • Also, one of the following:
    • documented polymorphic VT or VF
    • Family history of sudden cardiac death before the age of 45
    • Characteristic ECG changes in family members
    • Syncope
    • Induceable VT
    • Nocturnal agonal respiration

Clinical situations which can worsen this condition:

  • Ischameia
  • Hyperthermia or hypothermia
  • Hypokalemia
  • Cardioversion
  • Drugs:
    • Class 1 antiarrhythmics
    • Beta blockers and calcium channel blockers
    • Alpha-agonists
    • Nitrates
    • Cocaine and alcohol
    • Cholinergic agonists, eg. the "stigmine" drugs

References

Berne, Paola, and Josep Brugada. "Brugada syndrome 2012." Circulation Journal 76.7 (2012): 1563-1571.

Question 18.3 - 2014, Paper 1

A 75-year-old female admitted to the ICU with community-acquired pneumonia suddenly develops a tachycardia. Her 12 lead ECG is shown below (ECG 3).

a) What is the diagnosis? Justify your answer.
b) Name two co-existing diseases in critically ill patients where this condition is commonly seen.

College Answer

a)
 Multifocal atrial tachycardia
 Irregularly irregular rhythm rate > 100 bpm
 Multiple P wave morphologies

b)
 COPD
 Congestive cardiac failure

Discussion

The above-displayed ECG comes from the LITFL page on multifocal atrial tachycardia.

The cardinal features are irregularity and a plethora of different P-wave morphologies.

You need to have

  • Tachycardia (HR >100)
  • Irregular rate
  • Variability in P wave morphology

The same findings with a normal heart rate does not qualify for MAT, because it's not tachycardia; you have to call that a "wandering atrial pacemaker".

The CICM question also asked for associated diseases.  In adults, MAT is almost uniformly associated with COPD. Not only are the atria stretched by pulmonary hypertension, but the proarrhythmic bronchodilators also make for an irritable myocardium.  In the paediatric population the differentials are more broad, including bronchiolitis, croup, bronchomalacia, etc.

References

Bradley, David J. "Multifocal atrial tachycardia." DEVELOPMENTS IN CARDIOVASCULAR MEDICINE 257 (2006): 135.

LiPSON, MANUEL J., and SHAPUR NAIMI. "Multifocal Atrial Tachycardia (Chaotic Atrial Tachycardia) Clinical Associations and Significance." Circulation 42.3 (1970): 397-407.

Question 6.1 - 2014, paper 2

A 45-year-old man presents to the Emergency Department with worsening shortness of breath. His ECG is shown below


 

a) Describe the main ECG abnormality?

b) What is the likely lesion?

c) What cardiac management is required?

College Answer

a) Deep symmetrical inverted T waves in V2-V4

b) Critical stenosis of the LAD

c)  Coronary angiography + / - stenting
 Anti-platelet therapy
 Anti-coagulation
 Beta-blockade
 ACE inhibitor
 Statin

Discussion

The image above, depicting the  "Wellens WellenSign", was shamelessly stolen from Dr Leonard Gettes' excellent site. Not a great deal more to say there, really. Even a person unfamiliar with the eponymous sign will write "myocardial ischaemia" and receive marks (though less of them).

References


Engelen, Domien J., et al. "Value of the electrocardiogram in localizing the occlusion site in the left anterior descending coronary artery in acute anterior myocardial infarction." Journal of the American College of Cardiology 34.2 (1999): 389-395.

De Zwaan, Chris, Frits WHM Bär, and Hein JJ Wellens. "Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction." Professor Hein JJ Wellens. Springer Netherlands, 2000. 245-252.

Question 6.2 - 2014, paper 2

A 25-year-old male presents to hospital with atypical chest pain. His ECG is shown below

a) Describe the ECG abnormalities?

b) What are the most likely differentials in this patient for these ECG changes?

College Answer

a)  Widespread concave ST elevation, most prominent in the mid- to left precordial leads (V2-5)
 Notching or slurring at the J-point
 Prominent, slightly asymmetrical T-waves that are concordant with the QRS complexes

b) Pericarditis
 Benign early replolarisation

Discussion

The image above, depicting some pericarditis-like changes, was shamelessly stolen from an excellent LITFL page on pericarditis.

Generally speaking, ECG changes associated with acute pericarditis are diffuse ST segment elevation and PR interval depression.

These changes frequently mimic acute myocardial infarction. Also early repolarisation can look exactly like this. The latter is a stable lifelong appearance, whereas both of the former are evolving pathologies; one might be able to confidently say that serial ECGs will discriminate between them. Additionally, various authors have identified some sophisticated methods by means of which one might be able to tell the difference.

References


Marinella, MARK A. "Electrocardiographic manifestations and differential diagnosis of acute pericarditis." American family physician 57.4 (1998): 699-704.


Ginzton, LEONARD E., and MICHAEL M.  Laks. "The differential diagnosis of acute pericarditis from the normal variant: new electrocardiographic criteria." Circulation 65.5 (1982): 1004-1009.
 

Question 6.3 - 2014, paper 2

A 50-year-old female presents to hospital having been involved in a motor vehicle crash. She was the driver and was trapped by the legs requiring extrication.

a) Describe the ECG changes?

b) What is the explanation for the ECG changes?

c) What is the immediate pharmacological management?

College Answer

a)  Broad complex rhythm, not typical of a BBB pattern.
     Left axis deviation
     Absent P waves

b)  Hyperkalaemia due to rhabdomyolysis

c)  Intravenous calcium
    Intravenous sodium bicarbonate
    Salbutamol / dextrose-insulin

Discussion

The image above was shamelessly stolen from an excellent LITFL page on ECG chages in hyperkalemia.

References

Question 17.1 - 2014, paper 2

With reference to transthoracic echocardiography (TTE) in the critically ill:

a) Outline the potential uses of TTE in the management of a patient in cardiac arrest.

b) Which TTE view is the most appropriate to use during cardiac arrest resuscitation?

College Answer

a)
1) enable rapid diagnosis of potentially treatable causes of cardiac arrest e.g. PE, tamponade, hypovolaemia
2) guide interventions undertaken during cardiac arrest e.g. guide needle placement for
pericardiocentesis
3) assess response to therapy e.g. IVC diameter post fluid bolus in hypovolaemia

b)
Subcostal view (below the xiphoid sternum) – can be done without interfering with CPR.

Discussion

Which is the most appropriate view? Plainly the subcostal view; it would be insane to interfere with CPR by trying to shove the probe on the chest.

Rationale for the use of TTE during an arrest

  • Cardiac arrest is caused by numerous aetiologies, of which only a few can be diagnosed by virtue of rhythm analysis or history and examination.
  • Many of the "non-shockable" causes of cardiac arrest can be identified or confirmed by TTE, including the following:
    • Cardiac tamponade (RV collapse in systole, large effusion)
    • Massive PE (RV diltation, empty LV, D-shaped septum)
    • Hypovolemia (empty chambers, collapsed IVC)
    • Tension pneumothorax (chest US rather than cardiac echo)
  • Other basic tools of assessment are already in routine use (eg. SpO2 monitoring and EtCO2 monitoring)

Advantages of intra-arrest TTE

  • Non-invasive
  • More effective in determining cardiac activity than palpation of central pulses
  • May be effective in identifying a shockable rhythm when the ECG is impossible or unhelpful
  • Allows US guidance of remedial procedures, eg. pericardiocentesis
  • Allows real-time monitoring of the effectiveness of fluid resuscitation
  • Allows the identification of regional wall motion abnormalities during periods of ROSC, which might result in an earlier decision to proceed with angiography
  • Non-experts can be easily trained to perform brief focused TTE.

Disadvantages of intra-arrest TTE

  • Intrudes upon team attention (it is another screen to mindlessly watch)
  • Takes focus off resuscitation
  • Requires significant skill to perform
  • Images may be of poor quality in many circumstances
  • Uninformative images may be misinterpreted and inaccurate management decisions could be made.
  • So far, there has been no evidence of improved outcome
  • It may result in an unacceptable interruption to CPR. in't Veld et al (2017) and Clattenburg et al (2018) found that the use of ultrasound prolonged off-the-chest pauses from an average of 11 seconds to 17 seconds, with the additional six seconds being wasted on image acquisition. Most interestingly, the ultrasonography pause was longer when the operator was also leading the arrest. 

Evidence and consensus guidelines regarding intra-arrest TTE

  • Memtsoudis et al (2006) - 22 of non-cardiac surgical patients who had an unexpected cardiac arrest; the use of TOE in the operating theatre was evaluated. Of the 22, 18 had major changes made to their management on the basis of TOE findings. In-hospital survival was 32%.
  • Blyth et al (2012) - meta-analysis of TTE as predictor of survival in cardiac arrest. 11 papers with a total of 558 patients were included. Intra-arrest TTE which demonstrated cardiac inactivity was strongly associated with the inability to restore spontaneous circulation. There was also a small, nonzero chance of ROSC with a motionless heart: 2.4% of patients with a motionless left ventricular wall would go on to achieve ROSC.. Pooled sensitivity was 91% and specificity was 80%. Research such as this is frustrated by unclear methodology: was the TTE performed in the first minute of CPR, or in the fortieth minute? Most people would agree that there is a difference in the way you would interpret the findings.
  • Anderson et al (2014) - swine model of cardiac arrest; ultrasound-guided compressions improved coronary perfusion pressure, because the rescuers were able to see how well (or poorly) they were compressing the left ventricle.
  • Flato et al (2015) - observational cohort of 49 ICU patients. TTE changed management in 51% and there was a surprising number of "pulseless" patients who actually had cardiac activity on TTE. These patients actually had a much better rate of ROSC (~70%) in comparison to the truly pulseless patients who had no cardiac motility (who had ROSC rates of around 20%). The authors concluded that intra-arrest TTE can identify potentially salvageable patients.

Support for this practice among published  guidelines

  • ARC Guideline 11.6 (2010) gives a Class B recommendation to the use of ultrasound in cardiac arrest, but on the basis of weak (Level IV) evidence.
  • Intensive Care Society recommends "Focused Intensive Care Echo"(FICE) to be among the basic competencies for intensivists.
  • ASEP/ASE consensus statement (2010)  recommends FOCUS ( focused cardiac ultrasound ) in a complimentary diagnostic role.
  • ILCOR (2015) demur making any recommendation, saying that it "may be considered" as an adjunct only where "a qualified sonographer is present and use of ultrasound does not interfere" with CPR.

References

Price, Susanna, Shahana Uddin, and Tom Quinn. "Echocardiography in cardiac arrest." Current opinion in critical care 16.3 (2010): 211-215.
Zafiropoulos, Andreas, et al. "Critical Care Echo Rounds: Echo in cardiac arrest." Echo Research and Practice 1.2 (2014): D15-D21.

Flato, Uri Adrian Prync, et al. "Echocardiography for prognostication during the resuscitation of intensive care unit patients with non-shockable rhythm cardiac arrest." Resuscitation 92 (2015): 1-6.

Anderson, Kenton L., et al. "Ultrasound Guided Chest Compressions Over the Left Ventricle During Cardiopulmonary Resuscitation Increases Coronary Perfusion Pressure and Return of Spontaneous Circulation in a Swine Model of Traumatic Cardiac Arrest." Circulation 130.Suppl 2 (2014): A15853-A15853.
Memtsoudis, Stavros G., et al. "The usefulness of transesophageal echocardiography during intraoperative cardiac arrest in noncardiac surgery." Anesthesia & Analgesia 102.6 (2006): 1653-1657.

Blyth, Lacey, et al. "Bedside focused echocardiography as predictor of survival in cardiac arrest patients: a systematic review." Academic Emergency Medicine 19.10 (2012): 1119-1126.

Labovitz, Arthur J., et al. "Focused cardiac ultrasound in the emergent setting: a consensus statement of the American Society of Echocardiography and American College of Emergency Physicians." Journal of the American Society of Echocardiography 23.12 (2010):

in't Veld, Maite A. Huis, et al. "Ultrasound use during cardiopulmonary resuscitation is associated with delays in chest compressions." Resuscitation 119 (2017): 95-98.

Clattenburg, Eben J., et al. "Point-of-care ultrasound use in patients with cardiac arrest is associated prolonged cardiopulmonary resuscitation pauses: a prospective cohort study." Resuscitation 122 (2018): 65-68.

Michels, Guido, and Roman Pfister. "Point-of-care ultrasound use in patients with cardiac arrest: More harmful than useful?." Resuscitation 124 (2018): e21.

Atkinson, Paul R., et al. "Does Point-of-care Ultrasound Use Impact Resuscitation Length, Rates of Intervention, and Clinical Outcomes During Cardiac Arrest? A Study from the Sonography in Hypotension and Cardiac Arrest in the Emergency Department (SHoC-ED) Investigators." Cureus 11.4 (2019).

Question 17.2 - 2014, paper 2

With reference to transthoracic echocardiography (TTE) in the critically ill:

The four images shown on pages 4 and 5 are TTE images taken from two patients during resuscitation from cardiac arrest.

Figures 1a and 1b are from patient 1 (shown on page 4). Figures 2a and 2b are from patient 2 (shown on page 5).

For each TTE image:

i. Describe the main abnormalities.

ii. Give the underlying diagnosis.

College Answer

For Patient 1
1) Very large pericardial effusion
2) Right ventricular compression.
Cardiac tamponade

For Patient 2
1) Grossly dilated right ventricle (and atrium in fig 4)
2) D-shaped septum
3) Underfilled left heart
Massive pulmonary embolus

Discussion

The TTE stills depicted above are not the canonical CICM paper images; instead I have scraped them together from various Google searches, from authors who have tagged them as "labelled for reuse".

The images are easily recognisable and I will not expand on this beyond wat is said in the college answer and explained in the chapter on peri-arrest TTE.

References

Price, Susanna, Shahana Uddin, and Tom Quinn. "Echocardiography in cardiac arrest." Current opinion in critical care 16.3 (2010): 211-215.


Zafiropoulos, Andreas, et al. "Critical Care Echo Rounds: Echo in cardiac arrest." Echo Research and Practice 1.2 (2014): D15-D21.

Flato, Uri Adrian Prync, et al. "Echocardiography for prognostication during the resuscitation of intensive care unit patients with non-shockable rhythm cardiac arrest." Resuscitation 92 (2015): 1-6.

Anderson, Kenton L., et al. "Ultrasound Guided Chest Compressions Over the Left Ventricle During Cardiopulmonary Resuscitation Increases Coronary Perfusion Pressure and Return of Spontaneous Circulation in a Swine Model of Traumatic Cardiac Arrest." Circulation 130.Suppl 2 (2014): A15853-A15853.
Memtsoudis, Stavros G., et al. "The usefulness of transesophageal echocardiography during intraoperative cardiac arrest in noncardiac surgery." Anesthesia & Analgesia 102.6 (2006): 1653-1657.

Blyth, Lacey, et al. "Bedside focused echocardiography as predictor of survival in cardiac arrest patients: a systematic review." Academic Emergency Medicine 19.10 (2012): 1119-1126.

Labovitz, Arthur J., et al. "Focused cardiac ultrasound in the emergent setting: a consensus statement of the American Society of Echocardiography and American College of Emergency Physicians." Journal of the American Society of Echocardiography 23.12 (2010):

Question 6 - 2015, Paper 1

Outline the key issues in the management of acute right ventricular failure in an ICU patient with moderate to severe pulmonary hypertension.

College Answer

Goal / Principle Additional detail to be provided
Treat triggering factors Infection, anaemia, arrhythmias, comorbidities, PE,
MI, acidosis
Maintain oxygenation Supplemental Oxygen to maintain sats >90%
Avoid Intubation if possible.
Consider Echo +/ - PA Catheter risks
Establish adequate
monitoring
ECG, Arterial line, Oxygen Sats, CVP,
Echocardiography vs PA Catheter
Kidney function: Urine Catheter, Serum Creatinine,
Liver congestion: AST, ALT, Bilirubin, Lactate
Optimise fluid balance Fluids if hypovolaemia is present , diuretics if excess fluid is
present
Reduce RV afterload IV Prostanoids: Epoprostinil, iloprost
IV or Oral PDE-5 inhibitors (sildenafil)
Inhaled vasodilators (nitric oxide)
Endothelin receptor antagonists (ERAs) eg bosantan
Optimise Cardiac output Milrinone, Levosimendan,
Optimise Systemic
perfusion pressure
Norepinephrine or Vasopressin
Liaison with Pulmonary
Hypertension Centre
Surgical options: Pulmonary thrombendarterectomy /
balloon atrial septostomy / ECMO / Ventricular assist device /
Heart/lung transplant / Palliation

Additional comments:
Candidates who scored well showed an in-depth understanding of the applied physiology and consequences of the various therapeutic options. Candidates who scored poorly omitted key points.
 

Discussion

A reader has pointed out an excellent review article by Hoeper et al (2018) which covers this in some detail. 

Management of preload

  • Diuretics
  • Fluid restriction
  • Venodilators
  • Aldosterone antagonists
  • Beta-blockers
  • Maintenance of sinus rhythm and atrial systolic contribution
  • Pacing to maintain AV synchrony

Management of afterload

  • Normoxia
  • Normocapnea
  • Normal acid-base balance (especially avoidance of acidosis)
  • Avoidance of excessive positive respiratory pressures
  • Pulmonary vasodilators
    • Nitric oxide
    • Prostacycline

Increase contractility

  • Inotropes
    • Digoxin
    • Dobutamine
    • Milrinone
    • Levosimendan
  • Cardiac resychronisation
  • Supportive hormones and micronutrients (cortisol, insulin, calcium, glucagon, thyroxine, thiamine etc)

Increase cardiac output by unnatural means:

  • LVAD
  • ECMO (eg. VA ECMO or PA-LA support)
  • Increase the pacemaker rate

Decrease the organism's demand for cardiac output

  • Hypothermia
  • Paralysis/sedation

References

Hoeper, Marius M., et al. "Intensive care, right ventricular support and lung transplantation in patients with pulmonary hypertension." European Respiratory Journal 53.1 (2019).

Lahm, Tim, et al. "Medical and surgical treatment of acute right ventricular failure." Journal of the American College of Cardiology 56.18 (2010): 1435-1446.

Balanos, George M., et al. "Human pulmonary vascular response to 4 h of hypercapnia and hypocapnia measured using Doppler echocardiography." Journal of Applied Physiology 94.4 (2003): 1543-1551.

Griffiths, Mark JD, and Timothy W. Evans. "Inhaled nitric oxide therapy in adults." New England Journal of Medicine 353.25 (2005): 2683-2695.

Benedetto, Maria, et al. "Inhaled nitric oxide in cardiac surgery: Evidence or tradition?." Nitric Oxide 49 (2015): 67-79.

Question 30.1 - 2015, Paper 1

The following ECG (ECG 1) was recorded in a 25-year-old patient in ICU who was alert and conscious with a blood pressure of 100/50 mmHg.

What rhythm is demonstrated?

Give the reasons for your answer.

(40% marks)

(the college has not released their ECGs; the image above was appropriated from LITFL without any explicit permission but in the spirit of FOAM)

College Answer

The ECG is consistent with a diagnosis of SVT with aberrant conduction for the following reasons:

There are no capture or fusion beats
There is no concordance in the chest leads
The QRS complexes are relatively narrow (under 160ms)
The patient’s age makes the diagnosis of an atrial origin more likely

Discussion

This image comes from the LITFL page on distinguishing VT from SVT with aberrancy. As such, it is well suited to this SAQ. The reason for wanting to know the difference is that potentially a patient in VT will become very unstable if AV-nodal blockers like adenosine are given.

Is this VT or SVT with Aberrant Conduction? How do I know?

Supraventricular tachycardia

Historical features

  • Young age
  • Previous SVTs terminated with adenosine

ECG changes

  • Same RBBB or LBBB pattern as the patient's normal ECG
  • WPW on pre-tachycardia ECG
  • Responds to vagal manoeuvres

Ventricular tachycardia

Historical features

  • Old age
  • Ischaemic heart disease, MI
  • HOCM, long QT, Brugada

ECG changes

  • No typical RBBB or LBBB morphology
  • Bizarre axis deviation
  • Very broad complexes (>160ms)
  • AV dissociation (P rate is different to QRS rate)
  • Capture beats — occasional normal QRS complexes
  • Fusion beats — a normal and a wide QRS superimposed on top of one another
  • Concordance:         all the chest lead QRSs point in the same direction
  • Brugada’s sign –  From onset of QRS complex to nadir of S-wave is > 100ms
  • Josephson’s sign – Notching near the nadir of the S-wave
  • Left ear of RSR complex is higher than right

References

From "the ECG made easy", by Hampton (2003), and ECGs shamelessly stolen from Life in The Fastlane without any sort of permission, but in the non-commercial spirit of free education

One may turn to the ARC guidelines for management of supraventricular tachycardias (guideline 11.9), which suggests (Class A evidence) that in a stable patient, vagal manoeuvres ought to be tried and then adenosine may be used unless contraindications exist. An unstable patient may also have a trial of adenosine while a defibrillator is being acquired, or while the chest is being shaved etc.....

As their reference for this set of guidelines, the ARC quote the ACC's statement.

Question 30.2 - 2015, Paper 1

The following ECG (ECG 2) was recorded in a 40-year-old female admitted with severe trauma.

a)  List the abnormalities

b)  What is the underlying diagnosis?

c) List four pharmacological strategies for treatment of the demonstrated ECG abnormalities.

(40% marks)

(the college has not released their ECGs; the image above was appropriated from LITFL without any explicit permission but in the spirit of FOAM)

College Answer

a)            Irregular rhythm
               Absent P waves
               Bizarre widened QRS complexes
               Peaked T waves

b)            Hyperkalaemia secondary to rhabdomyolysis

c)            NaHCO 3
               CaCl2
               Dextrose/insulin
               Frusemide
               Salbutamol
               (Resonium)

A note from the author: if I am correct in my interpretation of Chris Nickson's image filename, the serum potassium in the ECG above was 9.2 mmol/L.

Discussion

Previous appeances of hyperkalemia include  Question 6.3 from the second paper of 2014, Question 18.2 from the first paper of 2013, and Question 23.1 from the first paper of 2012.

Characteristic features (if on were called upon to describe them) include the following:

  • Broad QRS complexes
  • Peaked T waves
  • No typical bundle branch block pattern
  • Left axis deviation
  • Long PR interval (if P waves are even visible)
  • Absent P waves (merged with QRS)
  • Absent T-waves (merged with QRS)
  • Ultimately, a "sine wave" ECG, which is where the P, T and QRS all merge into some sort of horrific mutant waveform. Cornelius et al (2010) published an ECG of this sort, taken from a woman with a K+ of 9.3.

References

From "the ECG made easy", by Hampton (2003), and ECGs shamelessly stolen from Life in The Fastlane without any sort of permission, but in the non-commercial spirit of free education

Cornelius, Brian G., Angela Cornelius, and Bobby Desai. "Identification of Sine Wave in Early Suspicion of Hyperkalemia." Western Journal of Emergency Medicine: Integrating Emergency Care with Population Health 11.1 (2010).

Question 30.3 - 2015, Paper 1

The following ECG (ECG 3) was recorded from a 62-year-old woman presenting with syncopal episodes

What are the abnormalities?

(20% marks)

(the college has not released their ECGs; the image above was appropriated from LITFL without any explicit permission but in the spirit of FOAM)

College Answer

Type 2 (Wenckebach) second degree heart block

Slow transition across the chest leads (? Old anteroseptal infarct)

Discussion

Little discussion is possible in this routine pattern recognition exercise. The syncopal woman has a PR interval which gradually gets longer and longer over several beats, until a P wave is not followed by a QRS complex, indicating a failure of conduction through the AV node. This is a second degree heart block, or Mobitz heart block; specifically it is a Mobitz type I (Whereas a Mobitz type II is an intermittent failure of AV conduction without PR prolongation).

The Wenckebach phenomenon referred to by the college is a Mobitz Type 1 second degree heart block, which makes their answer weird. A Type 2 second degree heart block is also an eponymous phenomenon (Hay block), and is nothing like a Wenckebach block.

Heart blocks of all sorts are discussed in greater detail elsewhere.

References

From "the ECG made easy", by Hampton (2003), and ECGs shamelessly stolen from Life in The Fastlane without any sort of permission, but in the non-commercial spirit of free education

2012 ACCF/AHA/HRS Focused Update of the 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines

Question 2 - 2015, Paper 2

a)    List four assessments of the RIGHT ventricle that can be made on transthoracic echocardiography. (20% marks)

b)    List four clinical signs of right heart failure.    (20% marks)

c)    Classify the causes of pulmonary hypertension with examples.    (60% marks)

College Answer

a)

RV size: LV size on apical 4-chamber view RV diameter


RV wall thickness


Tricuspid annular plane systolic excursion (TAPSE) or S-PRIME on apical 4-chamber view


Right ventricular systolic pressure gradient to right atrium using tricuspid regurgitation (TR) jet. Ventricular septal motion (D-shaped septum) that can indicate pressure or volume overload


Tissue Doppler and E/E’ ratios

b)

Elevated Jugular venous pressure

Right ventricular heave

Right ventricular third heart sound

Pleural effusion


Peripheral oedema Enlarged liver edge Ascites

c)

1. Pulmonary arterial hypertension (PAH)

Idiopathic PAH, Heritable-genetic disease, Drugs and toxins induced: appetite suppressants e.g. fenfluramine, Associated with systemic disease: Connective tissue diseases e.g. scleroderma, HIV infection, Porto-pulmonary hypertension

2. Pulmonary hypertension due to left heart disease

Systolic dysfunction, Diastolic dysfunction, Valvular disease: Mitral stenosis, Mitral Regurgitation, Congenital abnormalities

3. Pulmonary hypertension due to lung diseases and/or hypoxia

Chronic obstructive pulmonary disease, Interstitial lung disease, Sleep-disordered breathing, Alveolar hypoventilation disorders, Chronic exposure to high altitude

4. Chronic thromboembolic pulmonary hypertension

5. PH with unclear and/or multifactorial mechanisms

Hematological disorders: myeloproliferative disorders, Systemic disorders: sarcoidosis, vasculitis, Metabolic disorders: glycogen storage disease, Others: tumour obstruction, fibrosing mediastinitis, chronic renal failure on dialysis

Additional Examiners’ Comments:

Some candidates provided more than four answers for parts a) and b) and it should be noted that only the first four answers are considered. Part c) in general was poorly answered and many candidates confused acute elevations in pulmonary pressure with the disease entity of pulmonary hypertension.

Discussion

a) For the RV parameters detectable with TTE, I went to the 2010 ASE Guidelines for the echocardiographic assessment of the right heart in adults.

In brief, the assessable parameters are:

  • RV dimensions
  • RA dimensions
  • RVOT dimensions
  • RV wall thickness
  • IVC dimensions
  • RV systolic function
    • Several parameters: RIMP, TAPSE, 2D RV FAC, 2D RV ejection fraction (EF), three-dimensional (3D) RV EF, tissue Doppler–derived tricuspid lateral annular systolic velocity (S'), and longitudinal strain and strain rate.
  • RV diastolic function
    • Various parameters: E/A ratio, deceleration time, the E/e' ratio, and RA size
  • Pulmonary systolic pressure/RSVP

b) Clinical signs of right heart failure are difficult to find in any one single resource.

  • Features attributable to pulmonary hypertension
    • Loud P2(may be palpable)
    • Narrowly split S2
    • Tricuspid murmur
    • Diastolic murmur of pulmonary regurgitation
  • Features attributable to RV hypertrophy
    • Prominent wave in the JVP
    • Right-sided fourth heart sound (augmented by inspiration)
    • Left parasternal heave
    • Downward subxiphoid thrust.
  • Features attributable to RV dilatation and decompensated failure
    • Prominent v wave in the significantly raised JVP
    • Right-sided third  heart sound (augmented by inspiration)
    • Peripheral oedema
    • Ascites
    • Hepatomegaly (which may be pulsatile)
    • Signs of LV failure, eg. pulmonary oedema (due to out-bowing of the intraventricular septum, and LV diastolic failure resulting from this)

c)

The list used by the college answer is the updated 2013 Dana Point classification, which can be found in the Siomonneau article in Table 1.

Classification of Pulmonary Hypertension
 

Pulmonary Arterial Hypertension

  • Idiopathic
  • Herediary or congenital
    • Familial PAH
    • BMPR2 mutations (a member of the transforming growth factor β signaling family)
    • Congenital systemic-to-pulmonary shunts
    • Eisenmenger syndrome
  • Drug and toxin induced
    • Definite association: aminorex, fenfluramine, dexfenfluramine, toxic rapeseed oil
    • Possible association: cocaine, phenylpropanolamine, St Johns Wort, chemotherapy agents, SSRIs
  • Associated with connective tissue disease
    • Systemic sclerosis
    • SLE
    • Sjogren syndrome
    • polymyositis
    • rheumatoid arthritis
  • Associated with HIV infection
    • clinical, hemodynamic, and histologic characteristics similar to those seen in idiopathic PAH
  • Portopulmonary hypertension
    • 2% to 6% of patients with portal hypertension have PAH
    • Pulmonary vascular resistance (PVR) is usually normal in these cases
Left heart disease
  • LV failure
  • Mitral valve disease
  • Congenital or idiopathic cardiomyopathies, eg. HOCM
Lung disease or hypoxia
  • Idiopathic pulmonary fibrosis (by virtue of fibrosis)
  • Chronic hypoxia:
    • Alveolar hypoxia as a result of lung disease, eg. COPD or pulmonary fibrosis
    • Alveolar hypoxia due to impaired control of breathing (eg. OSA)\
    • Alveolar hypoxia due to residence at high altitude
Thromboembolism
  • obstruction of pulmonary arterial vessels by thromboemboli, tumors, or foreign bodies
Pulmonary hypertension due to unclear or multifactorial aetiologies
  • polycythemia vera
  • essential thrombocythemia
  • chronic myeloid leukemia
  • Chronic haemolytic anaemia
    • ​​​​​​​sickle cell disease (SCD)
    • thalassemia
    • hereditary spherocytosis
    • stomatocytosis
    • microangiopathic hemolytic anemia
  • sarcoidosis
  • Langerhans histiocytosis
  • glycogen storage diseases
  • Gaucher disease
  • mediastinal fibrosis
  • Schistosomiasis
    • Embolic obstruction of pulmonary arteries by schistosoma eggs
    • local vascular inflammation as a result of impacted schistosoma eggs

References

Simonneau, Gérald, et al. "Updated clinical classification of pulmonary hypertension." Journal of the American College of Cardiology 54.1s1 (2009): S43-S54.

Rudski, Lawrence G., et al. "Guidelines for the echocardiographic assessment of the right heart in adults: a report from the American Society of Echocardiography: endorsed by the European Association of Echocardiography, a registered branch of the European Society of Cardiology, and the Canadian Society of Echocardiography." Journal of the American Society of Echocardiography 23.7 (2010): 685-713.

Question 14.1 - 2015, Paper 2

The following ECG (ECG 1) is from a 35-year-old male who presents with paroxysmal tachycardia.

a)    Describe this ECG.    (30% marks)

b)    What would be the possible pharmacological options if his tachycardia were to recur? (20% marks)

College Answer

a)
Wolf-Parkinson-White syndrome

short PR interval, less than 3 small squares (120 ms)

slurred upstroke to the QRS indicating pre-excitation (delta wave) broad QRS

secondary ST and T wave changes

b)

IV procainamide or amiodarone is preferred, but any class Ia, class Ic, or class III antiarrhythmic can be used (Digoxin, Verapamil contraindicated)

Discussion

the ECG features of WPS are:

  • The PR interval is short (less than 0.12 seconds)
  • There is a delta wave (a slurred upstroke of the QRS complex)
  • Wide QRS (because the delta wave widens it)
  • ST Segment and T wave discordant changes: T waves point in the opposite direction to the QRS.
  • Pseudo-Q waves: negatively deflected delta waves in the inferior / anterior leads
  • prominent R wave in V1-3 (mimicking posterior infarction).

What can we say about the safety of AV nodal blockers in WPW?

  • Theoretically, AV nodal blockers should be safe in WPW-associated SVT, be it antidromic or orthodromic. If one thinks for a minute about the epidemiology of SVT, one will come to the conclusion that a large proportion of SVT is in fact caused by WPW or some other sort of preexcitaton syndrome, which is usually not known at the time of their first presentation. Many of these people get adenosine, which then reveals their delta waves to the horrified emergency personnel. Most of them do not die of VF. On the basis of this, we may conclude that it is probably reasonably safe.
  • Practically, antidromic SVT in WPW may be difficult to discriminate from AF or VT. Broad complexes and 300+ heart rates could be anything in WPW. Sure, it could be supraventricular, and respond to adenosine. Or it could be AF, and turn into VF. Or it could be VT, which will not benefit from an AV nodal blocker, in which case you have wasted precious time.

On this basis, the authorities tend to recommend the use of Class I or Class III agents instead of AV nodal blockers. The model answer to Question 3.1 from the first paper of 2009 lists procainamide and amiodarone as first-line agents, whereas digoxin and verapamil are contraindicated. Digoxin decreases the refractory period of the accessory pathway and verapimil tends to accelerate the ventricular response to AF by a similar mechanism. Since 2009, public opinion has also drifted away from amiodarone. As an acute infusion it is basically a beta-blocker with some AV nodal specificity. It is therefore the wrong drug for acute management of WPW SVT; or rather, it will probably be safe in the narrow-complex-obviously-orthodromic population, with the aforementioned caveats. In the long term, it becomes more useful, as its Class III and Class I effects begin to develop, slowing conduction down the accessory pathway.

Thus, generally speaking many of the AV node  blockers are at least relatively contraindicated in WPW with AF, and in AVRT unless it is confidently known to be orthodromic AVRT.  The table below has been compiled with the use of the belowlisted references and the UpToDate article on this topic

Pharmacological Peculiarities of WPW
Arrhythmia Drugs contraindicated Drugs Recommended
Orthodromic AVRT -
  • Adenosine
  • Verapamil
  • Diltiazem
  • Procainamide
  • Amiodarone
Antidromic AVRT
  • Adenosine
  • Verapamil
  • Diltiazem
  • β-blockers
  • Digoxin
  • Procainamide
  • Flacainide
  • Propafenone
  • Amiodarone
AF
  • Adenosine
  • Verapamil
  • Diltiazem
  • ß-blockers
  • Digoxin
  • Procainamide
  • Ibutilide
  • Dofelitide
  • Flecainide
  • Amiodarone




     
  •  
  •  

References

Redfearn, D. P., et al. "Use of medications in Wolff-Parkinson-White syndrome." Expert opinion on pharmacotherapy 6.6 (2005): 955-963.

Winter, C., R. Nagappan, and S. Arora. "Potential dangers of the Valsalva manoeuvre and adenosine in paroxysmal supraventricular tachycardia-beware preexcitation." Critical Care and Resuscitation 4.2 (2002): 107.

Question 14.2 - 2015, Paper 2

a)    Describe the abnormalities.    (15% marks)
b)    List the potential complications of this condition.    (15% marks)

College Answer

a)

  • ST elevation in leads II, III and aVF Q waves II, III and aVF
  • Reciprocal ST depression in aVL, V5-6
  • Consistent with inferior STEMI

b)

  • Bradycardia and heart block (2nd and 3rd degree)
  • Posterior infarction
  • Right ventricular infarction

Discussion

The image of the inferior STEMI above was acquired illegally, from some unknown source, via Google.

localisation of coronary artery territories

ST elevation in leads II, III and aVF and depression in aVL and V5-6 corresponds to a RCA or LCx territory "inferior infarct". One ought to expect some involvement of the nodes. Specifically, the sinoatrial node (RCA) and the AV node (LCx) should be affected.

In general, the best references for this come from Edward Burns, via LITFL. Specifically, his entry on inferior STEMI is superb. There is no way one could improve on it, even for an author in the habit of duplicating LITFL's efforts.

References

Question 14.3 - 2015, Paper 2

A 65-year-old truck driver, with a history of COPD, has the following ECG (ECG 3).

Describe the ECG.    (20% marks)

College Answer

Atrial flutter: ventricular response of around 150 bpm (atrial fibrillation acceptable but less marks)
Left Axis Deviation
Poor R wave progression
Partial intra ventricular conduction defect

Discussion

As usual, the college has removed their ECG images. The image above comes from www.torreyekg.com.

No interpretation is offered there. The axis seems vaguely leftward, but in the example I have provided there is no conduction delay or poor R wave progression.

Also, it is hard to believe that the ordinarily hard-assed CICM would accept atrial fibrillation as the interpretation of a regular tachycardia.

References

Question 16 - 2016, Paper 1

a) List five clinical signs of severity in chronic aortic regurgitation. (25% marks)

b) What are the indications for surgery for chronic aortic regurgitation? (25% marks)

c) List five causes of a pathological systolic murmur over the precordium and briefly list their auscultatory characteristics. (50% marks)

College Answer

a) Any five of:        

  • Collapsing pulse/wide pulse pressure
  • Length of decrescendo diastolic murmur
  • LV third heart sound
  • Soft A2
  • [Austin Flint (mid-diastolic) murmur]
  • Left ventricular failure
  • Displaced apex beat

b)             

  • Symptoms- exertional angina, dyspnoea on exertion, syncope.
  • Worsening LV failure (falling ejection fraction)
  • Progressive LV dilatation on serial echocardiography (LV end systolic dimensions >5.5 cm)

c) Any five of:                                                                                         

  • Aortic Stenosis-diamond-shaped (crescendo-decrescendo), heard best at the right upper sternal border, radiates to the right supraclavicular area, and to the carotids
  • Mitral regurgitation-blowing, harsh, holosystolic murmur heard best at the apex, usually radiates to the axilla or back.
  • Pulmonary stenosis- diamond-shaped systolic, heard best at the left upper sternal border, may radiate to back
  • Tricuspid regurgitation-harsh, holosystolic murmur heard best at the left lower sternal border.
  • Subaortic stenosis/HOCM-harsh, diamond-shaped, mid-systolic murmur heard best at the left sternal border
  • Mitral Valve Prolapse-mid-systolic click followed by a brief crescendo-decrescendo murmur, usually best at the apex
  • Ventricular Septal Defect- holosystolic murmur, best heard over lower left sternal border, with radiation to the right lower sternal border 
  • Atrial Septal Defect- mid-systolic flow murmur best heard over the “pulmonic area” of the chest, and may radiate into the back followed by fixed split S2.
  • Patent Ductus Arteriosus- To & fro machinery murmur (systolic and diastolic)

Discussion

a)

One might expect that deatures suggestive of severity in chronic AR would be mainly features related to the effect of AR on cardiac function, not just generic features of AR

  • LV dilatation (displaced apex, diffuse hyperdynamic impulse)
  • Congestive cardiac failure (low blood pressure, peripheral oedema)
  • Poor exercise tolerance
  • Signs of widened pulse pressure (see below)
  • An S3, suggestive of poor LV function

Generic features of AR are as follows:

  • Signs of widened pulse pressure:
    These were mentioned in Question 14.2 from the first paper of 2013
    • Corrigans sign: a "jerky" carotid pulse: full expansion, followed by complete collapse. You're palpating the pressure of the left ventricle, essentially. It's named after a 19th century Irishman. It indicates a severe aortic incompetence.
    • de Musset's sign which the college answer has spelled incorrectly is  a visible nodding of the head in time with arterial pulsation in patients with severe aortic insufficiency. It is named after an aortically insufficient French poet.
    • Quincke's sign, otherwise known as Quincke's pulse, is a nail sign: it is seen when the nailbed is blanched. The pale nail bed flashed red and white as capillary refill is restored. It can also be seen in the absence of any aortic problems, in patients who have sclerodactily.
    • Duroziez's sign is elicited by listening over the femoral artery with the bell of the stethoscope. It is supposed to be a double murmur. According to some recent evidence, it has almost 100% specificity. There is supposed to be both a systolic and a diastolic bruit, as blood rushes into - and then rapidly out of - the femoral artery.
  • These are mentioned in UpToDate:
    • Traube's sign – A pistol shot pulse (systolic and diastolic sounds) heard over the femoral arteries.
    • Mueller's sign – Systolic pulsations of the uvula.
    • Becker's sign – Visible pulsations of the retinal arteries and pupils.
    • Hill's sign – Popliteal cuff systolic pressure exceeding brachial pressure by more than 20 mmHg with patient in the recumbent position.
    • Mayne's sign – More than a 15 mmHg decrease in diastolic blood pressure with arm elevation from the value obtained with the arm in the standard position.
    • Rosenbach's sign – Systolic pulsations of the liver.
    • Gerhard's sign – Systolic pulsations of the spleen. 
  • Chacteristic auscultatory findings:
    • Soft S1
    • Soft A2
    • An S3 if LV function is severely depressed
    • A systolic ejection sound due to abrupt aortic distension

b)

Indications for valve replacement, as given in the 2014 AHA/ACC guidelines, are as follows:

  • Symptomatic patients:
    • When the AR is Stage D, i.e with a dilated LV, Doppler jet width ≥65% of LVOT and holodiastolic flow reversal in the proximal abdominal aorta
  • Asymptomatic patients:
    • LVEF <50%
    • Normal LVEF, but with significant LV dilatation (end-systolic diameter > 50mm or end-diastolic diameter >65mm)
    • None of the above, but about to undergo cardiac surgery anyway (for some other reason)

c)

Causes of systolic murmurs and their characteristic auscultatory findings:

Cause of murmur Auscultatory characteristics
Tricuspid regurgitation
  • Right of sternum, or left sternal edge
  • Louder on inspiration
  • Does not radiate to the carotids
Aortic stenosis
  • Radiates to the carotids
  • Louder on expiration
  • Quieter with isometric hand grip
  • Quieter with Valsalva
Mitral regurgitation
  • Loud S3
  • Soft or absent S1
  • Maximal at apex
  • Radiates to axilla
  • Pan-systolic
  • Louder with isometric hand grip
  • Quieter with Valsalva
Atrial septal defect
  • Fixed split P2
  • Louder on inspiration
HOCM
  • Loudest at left sternal edge
  • No click
  • S4 is present
  • Quieter with isometric hand grip
  • Louder with Valsalva

References

Nicholas Joseph Talley, Simon O'Connor; Clinical Examination: A Systematic Guide to Physical Diagnosis (7th ed)

SEGAL, JACK P., W. PROCTOR HARVEY, and MICHAEL A. CORRADO. "The Austin Flint murmur: its differentiation from the murmur of rheumatic mitral stenosis." Circulation 18.5 (1958): 1025-1033.

Leatham, Aubrey. "Splitting of the first and second heart sounds." The Lancet 264.6839 (1954): 607-614.

Sabbah, HANI N., and PAUL D. Stein. "Investigation of the theory and mechanism of the origin of the second heart sound." Circulation research 39.6 (1976): 874-882.

Saberi, Asif, and Saeed A. Syed. "Corrigan’s sign." Hospital Physician (1999): 29.

DAVIES, M., and A. Hollman. "de Musset sign." Heart 82.3 (1999): 262.

Norton, S. A. "Keratoderma with pseudo-Quincke's pulse." Cutis 62.3 (1998): 135-136.

Sapira, J. D. "Quincke, de Musset, Duroziez, and Hill: some aortic regurgitations." Southern medical journal 74.4 (1981): 459-467.

Luisada, Aldo A. "On the pathogenesis of the signs of Traube and Duroziez in aortic insufficiency. A graphic study." American Heart Journal 26.6 (1943): 721-736.

BLUMGART, HERRMAN L., and A. CARLTON ERNSTENE. "Two mechanisms in the production of Duroziez's sign: their diagnostic significance and a clinical test for differentiating between them." Journal of the American Medical Association 100.3 (1933): 173-177.

Nishimura, Rick A., et al. "2014 AHA/ACC guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines." Journal of the American College of Cardiology 63.22 (2014): e57-e185.

Question 26.1 - 2016, Paper 1

Please note: The following ECGs have all been recorded at 25 mm/sec and gain setting of 10 mm/mVe 26.1

A 54-year-old female walks into the Emergency Department complaining of palpitations for the past hour Her ECG is shown on page 8 (Figure 1). She has no electrolyte abnormalities.

a) Describe the rhythm disturbance. (20% marks)

b) How would you treat this rhythm disturbance? (10% marks)

c) Name two anti-arrhythmic drugs that are contra-indicated for this rhythm disturbance. (20% marks)

College Answer

a)

Atrial fibrillation with an accessory pathway                                                                                  

AF / SVT with aberrant conduction acceptable answer.(The rapid rate precludes AF with bundle branch block so no marks should be given for AF with bundle branch block).

b)

Electrical cardioversion (flecainide, ibutilide, propafenone acceptable).

c)

Digoxin, calcium channel blocker, beta-blockers, amiodarone, adenosine or other agents that preferentially block AV node and not accessory pathway.

Discussion

a)

This is WPW, in AF. The conduction rate is roughly 1:1.5; the QRS rate is about 180 to 200. It is hard to tell that its irregularly irregular. The QRS complexes will be a mixture of pre-excited delta-waving ones, and normal-looking narrow ones. If the accessory pathway has a short refractory period, it will conduct more often and therefore there will be more broad complexes than narrow ones. The shorter the refractory period of the accessory pathway, the broader the QRS. And the broader the QRS, the greater the chance of this thing degenerating into ventricular fibrillation.

b)

Management of this acute arrhythmia has several options:

  • vagal manoeuvres
  • AVOID ASV node blocking drugs such as adenosine, digoxin, beta blockers and calcium channel blockers
  • Procainamide, ibutilide or amiodarone are the only antiarrhytmics useful in WPW
  • DC synchronised cardioversion

Flecainide or propafenone are used in long term management. Amiodarone also OK - but the side effect profile in long term use is not very nice for younger patients.

c)

What can we say about the safety of AV nodal blockers in WPW?

  • Theoretically, AV nodal blockers should be safe in WPW-associated SVT, be it antidromic or orthodromic. If one thinks for a minute about the epidemiology of SVT, one will come to the conclusion that a large proportion of SVT is in fact caused by WPW or some other sort of preexcitaton syndrome, which is usually not known at the time of their first presentation. Many of these people get adenosine, which then reveals their delta waves to the horrified emergency personnel. Most of them do not die of VF. On the basis of this, we may conclude that it is probably reasonably safe.
  • Practically, antidromic SVT in WPW may be difficult to discriminate from AF or VT. Broad complexes and 300+ heart rates could be anything in WPW. Sure, it could be supraventricular, and respond to adenosine. Or it could be AF, and turn into VF. Or it could be VT, which will not benefit from an AV nodal blocker, in which case you have wasted precious time.

On this basis, the authorities tend to recommend the use of Class I or Class III agents instead of AV nodal blockers. The model answer to Question 3.1 from the first paper of 2009 lists procainamide and amiodarone as first-line agents, whereas digoxin and verapamil are contraindicated. Digoxin decreases the refractory period of the accessory pathway and verapimil tends to accelerate the ventricular response to AF by a similar mechanism. Since 2009, public opinion has also drifted away from amiodarone. As an acute infusion it is basically a beta-blocker with some AV nodal specificity. It is therefore the wrong drug for acute management of WPW SVT; or rather, it will probably be safe in the narrow-complex-obviously-orthodromic population, with the aforementioned caveats. In the long term, it becomes more useful, as its Class III and Class I effects begin to develop, slowing conduction down the accessory pathway.

References

Wellens, Hein JJ, and Dirk Durrer. "Effect of digitalis on atrioventricular conduction and circus-movement tachycardias in patients with Wolff-Parkinson-White syndrome." Professor Hein JJ Wellens. Springer Netherlands, 2000. 63-68.

Gulamhusein, S. A. J. A. D., et al. "Acceleration of the ventricular response during atrial fibrillation in the Wolff-Parkinson-White syndrome after verapamil."Circulation 65.2 (1982): 348-354.

Munger, T. M., et al. "A population study of the natural history of Wolff-Parkinson-White syndrome in Olmsted County, Minnesota, 1953-1989."Circulation 87.3 (1993): 866-873.

Svenson, ROBERT H., et al. "Electrophysiological evaluation of the Wolff-Parkinson-White syndrome: problems in assessing antegrade and retrograde conduction over the accessory pathway." Circulation 52.4 (1975): 552-562.

Narula, Onkar S. "Wolff-Parkinson-White Syndrome A Review." Circulation 47.4 (1973): 872-887.

and, somewhat more recently...

Scheinman, Melvin M. "History of Wolff‐Parkinson‐White Syndrome." Pacing and clinical electrophysiology 28.2 (2005): 152-156.

Keating, L., F. P. Morris, and W. J. Brady. "Electrocardiographic features of Wolff-Parkinson-White syndrome." Emergency medicine journal 20.5 (2003): 491-493.

 

Question 26.2 - 2016, Paper 1

Please note: The following ECGs have all been recorded at 25 mm/sec and gain setting of 10 mm/mVe 26.1

A 64-year-old male is admitted to the ICU following coronary artery bypass surgery. His rhythm strip and central venous pressure waveform is shown on page 9 (Figure 2).

Give the likely cause of the abnormality shown.        (20% marks)

College Answer

Epicardial (atrial & ventricular) pacing leads reversed. 

Discussion

The image used here is from an article by Aktas et al (2007), where this phenomenon is discussed. Specific feature is the fact that pacer spikes both precede and follow each QRS complex (one is the atrial lead pacing the ventricle, the other is the ventricular lead pacing the atrium after the ventricle has already depolarised).

Additional information can be derived from the (not to scale) CVP waveform:

atrioventricular lead reversal CVP waveform

The first wave is the ventricular contraction, which ejects blood out of the tricuspid valve before it closes (as the atria had not contracted yet, the annulus is not "tight" enough). The second ave is the poor atriumcontracting against a closed tricuspid valve, which increases the venous pressure.

References

Aktas, Mehmet K., Abrar H. Shah, and Toshio Akiyama. "Atrioventricular Pacemaker Leaf Reversal." Journal of Arrhythmia 23.1 (2007): 69-72.

Question 26.3 - 2016, Paper 1

Please note: The following ECGs have all been recorded at 25 mm/sec and gain setting of 10 mm/mVe 26.1

Describe the ECG shown on page 10 (Figure 3). (20% marks)

List four conditions that are associated with the axis abnormality seen in this ECG. (10% marks)

College Answer

a)

  • Rightward QRS axis 
  • Peaked P waves in the inferior leads > 2.5 mm (P pulmonale) with a rightward P-wave axis (inverted in aVL)
  • Clockwise rotation of the heart with a delayed R/S transition point (transitional lead = V5). Right ventricular hypertrophy criteria present Right axis deviation of +110° or more.
  • Dominant R wave in V1 (> 7 mm tall or R/S ratio > 1).
  • Dominant S wave in V5 or V6 (> 7 mm deep or R/S ratio < 1).
  • QRS duration < 120 ms (i.e. changes not due to RBBB).
  • Right ventricular strain pattern = ST depression / T wave inversion in the right precordial (V14) and inferior (II, III, aVF) leads.
  • Deep S waves in the lateral leads (I, aVL, V5-V6).

b) Right ventricular hypertrophy

  • Left posterior hemi block
  • Lateral myocardial infarction
  • Acute right heart strain
  • Drug toxicity (e.g. TCAs)

Discussion

This is an ECG of RV hypetrophy stolen from LITFL.

Edward Burns gives the following electrocardiographic features:

Diagnostic criteria

  • Right axis deviation of +110° or more.
  • Dominant R wave in V1 (> 7mm tall or R/S ratio > 1).
  • Dominant S wave in V5 or V6 (> 7mm deep or R/S ratio < 1).
  • QRS duration < 120ms (i.e. changes not due to RBBB).

Supporting criteria

  • Right atrial enlargement (P pulmonale).
  • Right ventricular strain pattern = ST depression / T wave inversion in the right precordial (V1-4) and inferior (II, III, aVF) leads.
  • S1 S2 S3 pattern = far right axis deviation with dominant S waves in leads I, II and III.
  • Deep S waves in the lateral leads (I, aVL, V5-V6).

Other abnormalities caused by RVH 

Right bundle branch block (complete or incomplete).

References

Question 25.1 - 2016, Paper 2

The ECG shown on page 11 (Figure 1) is from a 41-year-old female admitted for management of anorexia.

a) List the ECG abnormalities. (10% marks)

b) Give the underlying cause. (10% marks)

c) List four other ECG abnormalities that may be seen in this condition. (10% marks)

College answer

a)  
ST depression 
T    wave flattening and inversion 
U    waves  
Long QT/QU interval (fusion of T and U waves) 
 
b)    Hypokalaemia 
 
c)    
P wave amplitude increased (>2.5 mm in limb leads, >1.5 mm in chest leads) 
P wave width increased (>120 msec) 
PR interval prolonged (>200 msec) 
Supraventricular ectopics 
Ventricular ectopics 
Atrial fibrillation 
Atrial flutter 
Atrial tachycardia 
Torsade de pointes 
 

Discussion

The ECG above was stolen from the LITFL archive.

ECG findings of hypokaelmia:

  • Ventricular tachycardia: classically, torsades de pointes
  • Atrial tachycardias
  • PR interval prolongation (>200 msec)
  • P wave amplitude increased (>2.5 mm in limb leads, >1.5 mm in chest leads) - a "pseudo-P-pulmonale" pattern
  • P wave width increased (>120 msec)
  • u-waves (thpough these are not unique to hypokalemia: they are associated with LVH, bradycardia and may occasionally be a normal variant)
  • T-wave inversion
  • Ectopics (ventricular and atrial)

References

Norgard, Nicholas, Amanda McEvoy, and Thomas Madejski. "Influence of Pharmacologic Agents and Electrolytes on ECGs." Clinical Exercise Electrocardiography (2015): 173.

Question 25.2 - 2016, Paper 2

The ECG shown on page 12 (Figure 2) is that of a 26-year-old patient who collapsed while playing football.

a) Describe the ECG abnormalities. (5% marks)

b) Give the likely diagnosis. (5% marks)

c) What other features would you look for on examination of the cardiovascular system? (20% marks)

College answer

a)    LVH with strain pattern. 
 
b)    Hypertrophic obstructive cardiomyopathy (HOCM). 
 
c)    Late systolic murmur / midsystolic murmur at left lower sternal edge and apex (due to LVOT obstruction).  Pansystolic murmur at apex due to mitral regurgitation (LVOT obstruction lead to pressure effect on anterior mitral valve leaflet causing systolic anterior motion and mitral regurgitation). 
 

Discussion

Image stolen from the LITFL LVH page.

References

Question 25.3 - 2016, Paper 2

The ECG shown on page 13 (Figure 3) is that of a 76-year-old male presenting with acute appendicitis requiring surgery. He is haemodynamically stable.

a) Comment on this ECG. (20% marks)

The anaesthetist would like a temporary pacing wire placed before surgery.

b) What is your advice? (20% marks)

College answer

a)    Secondary degree AV block, Mobitz type 1 
 
b)    Patients with Mobitz type 1 block who are asymptomatic and haemodynamically stable do not require a pacing wire. If unstable then atropine could be tried. Transcutaneous or transvenous pacing is then indicated. Reversible causes like myocardial ischaemia, high vagal tone or drugs (beta blockers, Ca channel blockers or digoxin) should be sought and corrected.  

Additional Examiners' Comments: 
There were a number of common difficulties candidates encountered. The main one was lack of knowledge in this area, and the main gap was in recognising the second-degree AV block – type 1.  Many of the answers were 'scattergrams' of all the ECG patterns/phrases the candidates could remember – sometimes contradictory! Another systemic problem seemed to be time allocation. A number of candidates missed whole parts of the question or answered part 3 with less care and attention than parts 1 and 2. 

 

Discussion

Image stolen from the LITFL page on this heart block

References

2012 ACCF/AHA/HRS Focused Update of the 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines

Question 6 - 2017, Paper 1

A 64-year-old female patient has been ventilated in your ICU for 36 hours with septic shock and is receiving significant doses of noradrenaline and vasopressin. On the morning review you note her troponin level is elevated to over 10 times the normal range for your institution.

How do you interpret the raised troponin level in this setting?        (40% marks)

Outline your assessment and management plan specific to the raised troponin level. (60% marks)

College answer

a) Interpretation of raised troponin- should not be used in isolation in this patient. The measured 
value of troponin is high and should not be ignored or dismissed. If unexpected, repeat the 
test. Symptoms of chest pain are not easy to elicit in the ventilated patient. Troponin leak in 
this setting may be due to myocarditis associated with sepsis, acute cardiomyopathy.
Takotsubo disease given high dose vasopressor or a STEMI or NSTEMI or right ventricular 
disease. Elevated troponin in renal failure should also be considered if relevant. Elevated 
troponins are associated with poor outcomes in septic patients.

b) Management plan- Comprehensive clinical assessment especially cardiovascular and 
haemodynamic assessment. Look for recent, rapid increase in vasopressor requirement, 
signs of cardiogenic shock. Review ECG for any evidence of STEMI or other new changes, 
Review CXR for new pulmonary oedema/heart failure. Echo- transthoracic or if available TOE 
is mandatory to look for any regional wall motion abnormalities that may be new. Evidence of 
global changes on echocardiography may indicate acute cardiomyopathy e.g. Myocarditis. 
Look for classic changes of Takatsubo’s.
Further management will be determined by ECG and echo findings. Cardiology review, 
anticoagulation, careful consideration of thrombolysis or angioplasty if STEMI or regional 
changes on echo with consideration given to haemodynamic instability and challenges of 
transfer and management in cardiac catheter lab. Role of IABP in global hypokinesis related 
to acute cardiomyopathies. 
Troponin increases in septic patients is thought to be associated with poor prognosis 

Additional Examiners’ Comments:
Candidates were not expected to reproduce the template, but to demonstrate a reasonable and 
structured approach to the issue.

Discussion

Interpretation of a raised troponin in septic shock:

  • It may be totally meaningless:
    • Cardiac troponins are elevated in 85% of patients with sepsis in the absence of acute coronary syndrome.
    • Overinterpretation can increase the cost and duration of hospital stay (Suarez et al, 2016)
  • It may represent an acute coronary syndrome:
    • Sepsis is a high-output cardiac failure state, and may unmask some sort of (previously subclinical) coronary artery disease.
    • Any proinflammatory state can give rise to an increased risk of MI (Donzé et al, 2014)
  • It may identify patients with septic cardiomyopathy:
    • Significant myocardial depression is observed in up to 60% of septic patients (Vieillard-Baron et al , 2008)
    • This may be associated with a raised troponin
    • A raised troponin does not identify patients who need inotropes
  • It may be a predictor of increased mortality:
    • Raised troponin predicts increased mortality,  with a risk ratio of around 1.9. (Sheyin et al, 2015)

Assessment and management plan:

  • History
    • Detailed interrogation of the bedside records to determine whether any critical events had taken place recently, eg. sudden increase in vasopressor doses or episodes of unexplained tachycardia
    • Exploration of the past medical history, specifically looking for previous history of ischaemic heart disease
  • Examination, to look for...
    • New murmurs
    • Features more consistent with cardiac failure than with distributive shock, eg. oedema, pulsatile liver, displaced apex beat, elevated JVP, cool extremities.
  • ECG, to look for...
    • Changes associated with ischaemia, eg. ST segments and T waves
    • New bundle branch block
    • Arrhythmia, eg. new onset AF
  • Biochemistry
    • ABG, to assess for metabolic acidosis (as this can cause myocardial depression)
    • Electrolyte values, to exclude embarrassingly correctable causes of low cardiac output eg. severe ionised hypocalcemia or hypophosphataemia
    • A repeat troponin value, and serial measurements to follow
  • TTE, to assess
    • Global systolic function
    • Regional wall motion
    • Valve function
    • Diastolic function
  • Management:
    • This would depend on the findings of the abovelisted investigations.
    • If the TTE is essentially normal, it may be that no further management is required beyond regular aspirin.
    • If there is global systolic dysfunction, inotropes may be called for. At this stage, one may decide to use some sort of advanced haemodynamic monitor (eg. PA catheter, PiCCO etc) so that one may be better able to titrate their vasoactive drugs.
    • If there are ECG changes and/or regional wall motion abnormalities, one may be able to make a diagnosis of acute MI. This poses several treatment options:
      • Conservative management with antiplatelet drugs and heparin infusion (which may be impossible in the context of severe sepsis, where DIC has already made the patient thrombocytopenic and coagulopathic)
      • Angiography and revascularisation (risky in the context of severe sepsis, particularly insofar as stent deployment is concerned)
      • Coronary artery bypass grafting (essentially out of the question given the severe shock state)

References

Ahmed, Amna N., et al. "Prognostic significance of elevated troponin in non-cardiac hospitalized patients: A systematic review and meta-analysis." Annals of medicine 46.8 (2014): 653-663.

Ammann, P., et al. "Elevation of troponin I in sepsis and septic shock." Intensive care medicine 27.6 (2001): 965-969.

Landesberg, Giora, et al. "Troponin elevation in severe sepsis and septic shock: the role of left ventricular diastolic dysfunction and right ventricular dilatation." Critical care medicine 42.4 (2014): 790-800.

Smith, Andria, et al. "Elevated cardiac troponins in sepsis: what do they signify?." West Virginia Medical Journal 105.4 (2009): 29-33.

Tiruvoipati, Ravindranath, Nasreen Sultana, and David Lewis. "Cardiac troponin I does not independently predict mortality in critically ill patients with severe sepsis." Emergency Medicine Australasia 24.2 (2012): 151-158.

Suarez, Keith, et al. "TROPONIN TESTING IN PATIENTS HOSPITALIZED FOR SEPSIS IS ASSOCIATED WITH INCREASED CARDIOVASCULAR TESTING AND LENGTH OF STAY." Journal of the American College of Cardiology 67.13 (2016): 451.

Sheyin, Olusegun, et al. "The prognostic significance of troponin elevation in patients with sepsis: a meta-analysis." Heart & Lung: The Journal of Acute and Critical Care 44.1 (2015): 75-81.

Hunter, J. D., and M. Doddi. "Sepsis and the heart." British journal of anaesthesia 104.1 (2009): 3-11.

Vieillard-Baron, Antoine, et al. "Actual incidence of global left ventricular hypokinesia in adult septic shock." Critical care medicine 36.6 (2008): 1701-1706.

Donzé, Jacques D., et al. "Impact of sepsis on risk of postoperative arterial and venous thromboses: large prospective cohort study." BMJ 349 (2014): g5334.

Question 15.1 - 2017, Paper 2

A 69-year-old male presents with a fractured neck of femur following a syncopal episode. He is now well and has an ECG (Figure 1 shown on page 14) prior to his surgical procedure.

a) What does the ECG show? (10% marks)

trifascicular block

b) What complication is likely to have led to his fall, and how would you manage it? (20% marks) 

College answer

a)

Tri-fascicular block                                          
 
    b)                                                          
•    Cause – Complete heart block 
•    Management – 
o    Correct electrolyte and endocrine abnormalities (e.g. K+, thyroid function tests)
o Consider influence of drug therapies such as digoxin, calcium channel antagonists
o Investigate for ischaemic heart disease 
o    Referral to cardiology unit for further evaluation (?permanent pacemaker) 
 

Discussion

That ECG has just enough movement artifact on it to look "genuine". It is in fact not the original college image (because lawyers, etc) but comes from the authors' own collection, from a patient with a right bundle branch block, LAFB and a PR interval so prolonged that the ECG machine misinterpreted it as AF. The patient also had a serum potassium of around 6.6 mmol/L, which was unhelpful. 

Management of trifascicular block with syncope? The 2008 ACC/AHA/HRS guidelines and their  2012 focused update both recommend:

  • Exclude drugs as the influence on AV conduction (eg. β-blockers)
  • Exclude electrolyte disturbances
  • Consider the prolonged PR interval as the herald of a complete heart block
  • Consider the syncope a sign that intermittent complete heart block is occurring 
  • The presence of syncope and even mere bifascicular block upgrades the class for recommendation for PPM insertion from Class IIa to Class I ("Benefit >>> risk")

References

Question 15.2 - 2017, Paper 2

The ECG (Figure 2 shown on page 15) is of a haemodialysis patient presenting with pulmonary oedema.

hyperkalemia - K+ 7.9 mmol/L

c) What test will you do to confirm the likely underlying diagnosis? (10% marks)

d) What is your immediate management for this condition? (20% marks) 

College answer

c)    Potassium level                                              
 
d)    Counteract cardiotoxic effects of hyperkalaemia                     
•    Calcium chloride 
•    Sodium bicarbonate 
        Shift potassium into the cells 
•    Dextrose and insulin 
•    Beta agonists 
      Remove potassium (and water) 
•    Urgent haemodialysis 
 

Discussion

Classical ECG features of hyperkalemia:

  • Broad QRS complexes 
  • Peaked T waves 
  • No typical bundle branch block pattern 
  • Left axis deviation
  • Long PR interval (if P waves are even visible)
  • Absent P waves (merged with QRS)
  • Absent T-waves (merged with QRS)
  • Ultimately, a "sine wave" ECG.

Montague (2008) found that these were generally unreliable.  The ECG used here is not from the college paper, but rather represents the ECG of an end stage renal failure patient presenting with syncope. The serum potassium level was 7.9.

Management of hyperkalemia is discussed elsewhere. In brief, it consists of the following strategies:

Stabilize myocardial cell membrane:

  • Calcium chloride (10%): 6.8 mmol (10ml) over 2-5 minutes
  • Hypertonic saline (3%): apparently, this has been show to reverse the ECG changes of hyperkalemia, only when there is concurrent hyponatremia.

 Shift potassium into cells:

  • Sodium bicarbonate: 50-100mmol/L, over 5 minutes
  • 50ml of 50% dextrose with 10 units of Actrapid insulin
  • Salbutamol: 2-4 ×salbutamol nebs (5mg each)

Promote potassium excretion:

  • Frusemide 40 to 80 mg IV
  • Cation-exchange resin: AHA recommend "kayexelate", which is the same sodium polystyrene sulfonate which is marketed as "Resonium" in Australia.
    "15 to 50 g per oral or per rectum" is recommended in the AHA text, along with sorbitol (to promote rapid transit, one assumes). Oh's Manual suggests a flat dose of 50g, and does not mention sorbitol.
  • Dialysis is ultimately the most effective clearance mechanism

References

Lavonas, Eric J., et al. "Part 10: Special Circumstances of Resuscitation 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care." Circulation 132.18 suppl 2 (2015): S501-S518.

Weisberg, Lawrence S. "Management of severe hyperkalemia." Critical care medicine 36.12 (2008): 3246-3251.

Montague, Brian T., Jason R. Ouellette, and Gregory K. Buller. "Retrospective review of the frequency of ECG changes in hyperkalemia." Clinical Journal of the American Society of Nephrology 3.2 (2008): 324-330.

Question 15.3 - 2017, Paper 2

The ECG (Figure 3 shown on page 16) is from a 35-year-old male who presents with paroxysmal tachycardia.

e) What condition is demonstrated? Describe the characteristic features. (30% marks)

f) What would be the possible pharmacological options if his tachycardia were to recur?
(10% marks) 

College answer

e)    Wolf-Parkinson-White syndrome                                 
•    short PR interval, less than 3 small squares (120 ms) 
•    slurred upstroke to the QRS indicating pre-excitation (delta wave) 
•    broad QRS 
•    secondary ST and T wave changes 
 
f)    IV procainamide or amiodarone is preferred, but any class Ia, class Ic, or class III antiarrhythmic can be used      
 

Discussion

The ECG features of WPS are:

  • The PR interval is short (less than 0.12 seconds)
  • There is a delta wave (a slurred upstroke of the QRS complex)
  • Wide QRS (because the delta wave widens it)
  • ST Segment and T wave discordant changes: T waves point in the opposite direction to the QRS.
  • Pseudo-Q waves: negatively deflected delta waves in the inferior/anterior leads
  • prominent R wave in V1-3 (mimicking posterior infarction).

Management of SVT in this condition:

  • Vagal manoeuvres
  • AVOID AV node blocking drugs such as adenosine, digoxin, beta blockers and calcium channel blockers
  • Procainamide, ibutilide or amiodarone are the only antiarrhytmics useful in WPW. And amiodarone is probably not useful acutely. 
  • DC synchronised cardioversion

Flecainide or propafenone are used in long term management. Amiodarone also OK - but the side effect profile in long term use is not very nice for younger patients. 

In summary, about the management of acute SVT in WPW:

  • Theoretically, AV nodal blockers should be safe in WPW-associated SVT, be it antidromic or orthodromic. If one thinks for a minute about the epidemiology of SVT, one will come to the conclusion that a large proportion of SVT is in fact caused by WPW or some other sort of preexcitaton syndrome, which is usually not known at the time of their first presentation. Many of these people get adenosine, which then reveals their delta waves to the horrified emergency personnel. Most of them do not die of VF. On the basis of this, we may conclude that it is probably reasonably safe.
  • Practically, antidromic SVT in WPW may be difficult to discriminate from AF or VT. Broad complexes and 300+ heart rates could be anything in WPW. Sure, it could be supraventricular, and respond to adenosine. Or it could be AF, and turn into VF. Or it could be VT, which will not benefit from an AV nodal blocker, in which case you have wasted precious time.

On this basis, the authorities tend to recommend the use of Class I or Class III agents instead of AV nodal blockers. The model answer to Question 3.1 from the first paper of 2009 lists procainamide and amiodarone as first-line agents, whereas digoxin and verapamil are contraindicated. Digoxin decreases the refractory period of the accessory pathway and verapimil tends to accelerate the ventricular response to AF by a similar mechanism. Since 2009, public opinion has also drifted away from amiodarone. As an acute infusion it is basically a beta-blocker with some AV nodal specificity. It is therefore the wrong drug for acute management of WPW SVT; or rather, it will probably be safe in the narrow-complex-obviously-orthodromic population, with the aforementioned caveats. In the long term, it becomes more useful, as its Class III and Class I effects begin to develop, slowing conduction down the accessory pathway.

In general:

Pharmacological Peculiarities of WPW
Arrhythmia Drugs contraindicated Drugs Recommended
Orthodromic AVRT  
  • Adenosine
  • Verapamil
  • Diltiazem
  • Procainamide
  • Amiodarone
Antidromic AVRT
  • Adenosine
  • Verapamil
  • Diltiazem
  • β-blockers
  • Digoxin
  • Procainamide
  • Flecainide
  • Propafenone
  • Amiodarone
AF
  • Adenosine
  • Verapamil
  • Diltiazem
  • ß-blockers
  • Digoxin
  • Procainamide
  • Ibutilide
  • Dofelitide
  • Flecainide
  • Amiodarone

In case you were wondering, WPW patients die sudden cardiac deaths when they develop AF, which is conducted rapidly and erratically through their aberrant pathway, producing VF (Obeyeseker et al, 2012)

Some might ask: why don’t the college want us to just give adenosine for what is likely to be standard narrow-complex-obviously-orthodromic arrhythmias? AHA and UpToDate agree: you treat them as per usual. However, the problem is that you can never exactly know that the SVT is definitely orthodromic. As far as is possible to tell, the recommendation to use procainamide is there as a guideline-maker’s safeguard to protect patients against a mistakenly unrecognised antidromic SVT. They say, “AV node-specific blocking drugs such as adenosine, verapamil, and beta blockers should be avoided unless the tachycardia is definitely known to be antidromic AVRT.” As one can never definitely know that the tachycardia is, to always use the safe agent seems like the right option. To do otherwise may invite weird bedside arguments about the width of QRS complexes.  

With regards to amiodarone, as an acute infusion it is basically a beta-blocker with some AV nodal specificity. It is therefore the wrong drug for acute management of WPW SVT; or rather, it will probably be safe in the narrow-complex-obviously-orthodromic population, with the aforementioned caveats. In the long term, it becomes more useful, as its Class III and Class I effects begin to develop, slowing conduction down the accessory pathway.

References

Wellens, Hein JJ, and Dirk Durrer. "Effect of digitalis on atrioventricular conduction and circus-movement tachycardias in patients with Wolff-Parkinson-White syndrome." Professor Hein JJ Wellens. Springer Netherlands, 2000. 63-68.

Gulamhusein, S. A. J. A. D., et al. "Acceleration of the ventricular response during atrial fibrillation in the Wolff-Parkinson-White syndrome after verapamil."Circulation 65.2 (1982): 348-354.

Munger, T. M., et al. "A population study of the natural history of Wolff-Parkinson-White syndrome in Olmsted County, Minnesota, 1953-1989."Circulation 87.3 (1993): 866-873.

Svenson, ROBERT H., et al. "Electrophysiological evaluation of the Wolff-Parkinson-White syndrome: problems in assessing antegrade and retrograde conduction over the accessory pathway." Circulation 52.4 (1975): 552-562.

Narula, Onkar S. "Wolff-Parkinson-White Syndrome A Review." Circulation 47.4 (1973): 872-887.

and, somewhat more recently...

Scheinman, Melvin M. "History of Wolff‐Parkinson‐White Syndrome." Pacing and clinical electrophysiology 28.2 (2005): 152-156.

Keating, L., F. P. Morris, and W. J. Brady. "Electrocardiographic features of Wolff-Parkinson-White syndrome." Emergency medicine journal 20.5 (2003): 491-493.

Obeyesekere, Manoj, et al. "Risk of sudden death in Wolff-Parkinson-White syndrome: how high is the risk?." (2012): 659-660.

Luigi Di Biase, M. D., Edward P. Walsh, and Bradley P. Knight. "Treatment of symptomatic arrhythmias associated with the Wolff-Parkinson-White syndrome." UpTo Date

Question 15.2 - 2018, Paper 1

A 45-year-old male post-cholecystectomy for acute gangrenous cholecystitis complains of palpitations.

a) Interpret this ECG.    (10% marks)
b) Outline your management principles.    (40% marks)
 

College answer

a) 
This ECG shows a broad complex, regular tachycardia at a rate of 230 with no apparent P waves. This could be either a VT or SVT with aberrant conduction. 
 
b) 
Check effect of this tachycardia on the patient’s haemodynamics: BP, perfusion, SpO2 
If haemodynamics compromised treat urgently with synchronized cardioversion following ALS principles and guidelines. 
 
If haemodynamics not compromised: 
Check a previous ECG for evidence of a conduction defect 
Correct electrolyte abnormalities 
Move patient to a monitored environment (CCU/ICU) 
Slow rate down with adenosine. If this is a SVT with aberrancy we might see underlying rhythm/conduction abnormality. VT will not slow down with adenosine. Anti-arrhythmic therapy: Amiodarone if unsure re VT?SVT 
 

Discussion

That ECG comes from the ACLS Medical training website blog, from a June 2016 post titled "SVT with Aberrancy or Ventricular Tachycardia?"  It is remarkably similar to the official college ECG  because the college examiners must have performed the same Google image search. 

The blog post comments on this image: 

"There is a regular wide complex tachycardia at a rate of about 230 without sinus P waves. There is a LBBB pattern in lead V1. However, we would not consider this to be a “typical” LBBB pattern due to the normal axis in the frontal plane and the presence of a small S-wave in lead I."

The management according to the ALS algorithm (ARC Guideline 11.9) depends on whether the patient is compromised by this rhythm. "Compromised" in this context means "about to die" or "already dead". The immediate assessment would be to check for signs of life and a pulse. The patient in the SAQ does not sound as if he requires immediate CPR, because he is complaining of palpitations. One would therefore look for the following features to determine the need for synchronised cardioversion:

  • Systolic BP < 90 mmHg
  • Heart rate > 150/min
  • Chest pain
  • Heart failure
  • Drowsiness or confusion

If none of these are present, one has some time to think, have a cup of coffee while looking over the old ECGs, and argue with the CCU staff about whose job it is to look after this patient ("but he's surgical!"). Certainly, SVT with aberrancy might be an explanation for this, but the ARC recommends treating all such broad complex tachycardias as VT, because treating an SVT as VT is less likely to cause deterioration than treating VT as SVT. Given that it is regular, the official ARC recommendation is to give amiodarone 300mg over 20-60 minutes, followed by an infusion of 900mg over 24 hours. Amiodarone is a good "broad spectrum antiarrhythmic", as it treats both VT and SVT. Lam & Saba (2002) also point out that procainamide is indicated, but may not be suitable because it causes hypotension with rapid administration (moreover it is not available in Australia). The ARC do not mention adenosine in their pathways for broad-complex tachyarrhythmias.

The blog post which serves as the source for this ECG appears to be reporting a real patient case. They gave the patient 150mg amiodarone over 10 minutes. "A rhythm change is noted and the following 12-lead ECG is obtained":

"Now there is sinus tachycardia with virtually identical QRS morphology ... It is safe to conclude that this patient had a conduction defect at baseline, which is what caused the complexes to be wide during the tachycardia." 

References

Lam, Patrick, and Samir Saba. "Approach to the evaluation and management of wide complex tachycardias." Indian pacing and electrophysiology journal 2.4 (2002): 120.

Question 5 - 2018, Paper 2

List the findings, advantages and disadvantages of the following methods of assessment in a patient with right ventricular failure secondary to pulmonary hypertension: 
 
a)    Clinical bedside Assessment.                           (30% marks) 
 
b)    Transthoracic Echo.                                         (40% marks) 
 
c)    Pulmonary Artery Catheter.                             (30% marks) 

College answer

Findings:

  • Raised JVP with prominent A wave, pulsatile liver. 
  • Loud P2, RV/parasternal heave
  • TR murmur
  • Bilateral Peripheral edema
  • Hypotension if severe 

Advantages

  • Quick
  • Simple
  • Cheap
  • Non-invasive

Disadvantages

  • Poor reproducibility
  • Often difficult in ICU – immobility of patient, equipment, dressings etc
  • May be impaired by patient habitus
  • Non-quantitative
  • Continuous monitoring impractical

Transthoracic Echo                              

  Clinical Assessment

Findings 

  • ECHO: TR, long axis cavity size, short axis septal kinetics, apex loses triangular shape, 
  • RV size compared to LV size, 
  • loss of inspiratory collapse of IVC, dilation of PA
  • RVSP > 25 for acute 
  • TAPSE <16mm

Advantages

  • Non -invasive
  • Qualitative and quantitative
  • Can give other information relevant to clinical state
  • Record and retrieve results

Disadvantages

  • Expertise required
  • Expensive equipment
  • Inter operator variability
  • Unable to perform continuous monitoring
  • Often difficult in ICU – immobility of patient, equipment, dressings etc
  • May be impaired by patient habitus

Pulmonary Artery Catheter                             

 Findings

  • Right heart failure: high CVP, low CI, high PVR
  • Elevated pulmonary artery pressures (PAPm >25mmHg)

 Advantages

  • Continuous monitoring 
  • Gold standard for pulmonary hypertension measurement
  • Quantitative measurement
  • No inter operator variability
  • Can give other information relevant to clinical state
  • Therapeutic uses – iv access, pacing
  • Record and retrieve results

 Disadvantages

  • Invasive
  • Risk of serious complications – infection, bleeding, pneumothorax, vessel rupture 
  • Drift of measurements
  • Complex, now unfamiliar in many units
  • Time limited – should not be left in for > 72 hours

Discussion

Like virtually every other question which asks people to discuss and compare the advantages and disadvantages of something, this one would benefit from a tabulated answer in point-form, as this is much easier for the examiner to mark. The worst possible thing one could do is try to answer this in a block of flowing prose. 

Thus:

Diagnostic Strategies in Right Heart Failure
Modality and findings Advantages Disadvantages

Clinical examination:

  • Raised JVP
  • Pulsatile liver. 
  • Loud P2
  • RV heave
  • TR murmur
  • Oedema 

(for more detail, see above)

  • Quick
  • Simple
  • Cheap
  • Non-invasive
  • Good specificity
  • Poor sensitivity
  • Poor reproducibility
  • Non-quantitative
  • Made complex by ICU environment
  • Difficult in cardiac surgery/open chest

Transthoracic echo

  • TR
  • Chamber size
  • Septal kinetics
  • Apex shape 
  • IVC dynamic collapse
  • Dilation of PA
  • RVSP > 25 for acute 
  • TAPSE <16mm
  • Non -invasive
  • Qualitative and quantitative
  • Can give other information relevant to clinical state
  • Record and retrieve results
  • Serial examinations possible
  • "Operator-dependent" accuracy
  • Requires an ultrasound machine
  • Unable to perform continuous monitoring
  • Impaired by ICU environment: position, drains, dressings

PA catheter

  • High CVP
  • Low cardac output
  • High PA pressure
  • High PVR
  • Gold standard for right heart assessment
  • Quantitative measurement
  • No inter-operator variability
  • Can give other information relevant to clinical state
  • Therapeutic uses – IV access, pacing
  • Record and retrieve results
  • Invasive
  • Risk of serious complications 
  • Measurement subject to assumptions and errors (particularly with TR)
  • Drift of measurements
  • Complex, now unfamiliar in many units
  • Time limited – should not be left in for > 72 hours

References

Question 23.1 - 2018, Paper 2

A 37-year-old male has presented to the Emergency Department with a 12-hour history of central crushing chest pain. He was taken to Catheter Lab by the cardiologists who have referred him to ICU 12 hours later due to hypotension, and confusion. His ECG (ECG 23.1) is shown on page 9, and laboratory results are presented below.   

Parameter

Patient Value

Adult Normal Range

FiO2

6L Hudson Mask

pH

7.36

7.35 – 7.45

pO2 

162 mmHg (21.6 kPa)

pCO2

36.7 mmHg (4.89 kPa)

35.0 – 45.0 (4.60 – 6.00)

SpO2

99%

Bicarbonate 

20.1 mmol/L*

22.0 – 26.0 

Base Excess 

-4.4 mmol/L*

-2.0 – +2.0 

Lactate 

5.1 mmol/L*

0.5 – 1.6

Sodium 

148 mmol/L*

135 – 145 

Potassium 

4.8 mmol/L

3.5 – 5.0

Chloride 

115 mmol/L*

95 – 105

Glucose 

28.0 mmol/L*

3.5 – 6.0

Aspartate aminotransferase (AST)

3252 U/L*

< 35

Alanine aminotransferase (ALT)

6378 U/L*

< 35

Alkaline phosphatase (ALP)

58 U/L

30 – 110

-Glutamyl transferase (GGT)

32 U/L

< 40

Prothrombin time (PT)

29.8 seconds*

12.0 – 15.0

International normalized ratio (INR)

2.9*

0.8 – 1.1

Activated Partial Thromboplastin Time (APTT)

> 170.0 seconds*

25.0 – 37.0

Creatinine 

140 U/L*

45 – 90

(actual ECG image removed by examiners)

Dr Smith's ECG Blog

  1. Describe the ECG (ECG 23.1 on page 9) changes.                                     (20% marks) 
  1. Give a rationale for the biochemical abnormalities.                                     (20% marks)
  1. What is the most likely diagnosis?                                                             (10% mark)

College answer

a) Describe the ECG changes Bradycardia 
ST elevation in Leads II, III and aVF (inferior MI acute) also in lateral leads. ST elevation also in anterior leads, I aVL (Lateral) have ST depression. 
Compete Heart Block 
 
b) Give a rationale for the biochemical abnormalities 
Metabolic acidosis with elevated Lactate, either cardiogenic shock or related to bradycardia. Lactate is relatively high considering normal pH and only minor reduction in bicarb – potentially catecholamine infusion or hepatic injury 
Elevated liver enzymes AST and ALT probably associated with hepatic congestion Elevated INR and APTT associated with hepatic congestion, or therapeutic interventions

Corrected Na is elevated, hyperglycaemia may be underlying diabetes or stress response.

Mildly elevated Creatinine 140 secondary to hypotension, and/or contrast post angiography.

May also be pre-existing. 
 
c) What is the most likely diagnosis? 
Cardiogenic shock due to Acute right ventricular Infarction with hepatic congestion, or shock related to bradycardia 
 

Discussion

Though the ECG image was removed by the examiners, and souvenir exam papers becoming forbidden to trainees (as of this paper), it is impossible to determine which Google search the examiners used to get their images. Fortunately, within fifteen seconds one is able to conjure an ECG with the described abnormalities, from Dr Smith's ECG blog. Stephen W. Smith describes it thus:

"Rhythm: There is a regular, narrow complex bradycardia, with ventricular rate of ~43 bpm. There appear to be P-waves at irregular intervals, but without relationship to the QRS.  Thus, there is third degree (complete) AV block.  The escape is narrow, thus junctional or from the bundle of HIS.  

QRST: The QRS is narrow, so any ST-T abnormalities are primary: there is significant ST elevation in leads II, III, and AVF, with reciprocal ST depression in leads I and AVL, all suggestive of an inferior STEMI. Note that the ST elevation in lead III is greater than that in lead II, but that this is not specific for culprit artery (RCA vs. Left Circumflex).  However, there is ST elevation in lead V1, the furthest right pre-cordial lead, which lies directly over the RV free wall and highly suggests a Right Ventricular MI"

This context serves to demystify the rest of the interpretation. Rationale for the rest of the abnormalities is as follows:

  • There is virtually no A-a gradient, probably because this sort of MI does not tend to produce florid pulmonary oedema (A-a = (0.30 × 713)-(36.7 / 0.8) - 162 = 6 mmHg).
  • There is no acidaemia or alkalaemia
  • There is a metabolic acidosis, which is mild (SBE -4.4)
  • The respiratory compensation is appropriate (expected CO2 is 36.3 mmHg if you use the Copenhagen method, or (1.5 × 20.1)+8 = 38.1 mmHg by Winter's formula).
  • The anion gap is raised if you calculate it with potassium (17.7) or normal without it (12.9). The delta ratio is therefore either 0.23 or 1.46 (because the bicarbonate change was so small). Because lactate is raised (5.1), one would be probably more inclined to trust the potassium-inclusive result, as it fits better into the "liver, lactate, HAGMA" narrative. 
  • Speaking of the LFTs, they are profoundly deranged, with a predominantly hepatotoxic patter, colloquially referred to as a "transaminitis". The large AST elevation can be in part attributed to the myocardial myocyte death.
  • Synthetic liver function is deranged, with elevated PT/INR and APTT.
  • The creatinine is raised (140) which the college have attributed to contrast post angiography ("He was taken to Catheter Lab").
  • There is otherwise unexplained hyperglycaemia, which given the state of cardiogenic shock could be due to anything, including the stress response and catecholamine release.

In summary, the most likely explanation which covers the ECG and biochemistry is cardiogenic shock due to right ventricular infarction, with hepatic congestion. 

References

Question 27 - 2018, Paper 2

Outline the therapeutic options with rationale for the treatment of right ventricular dysfunction in an ICU patient. 

College answer

Optimise preload:  
By titrating fluid if hypovolaemic or diurese or dialyse off volume if required.  
Most conditions that lead to RV dysfunction in the ICU are due to increased afterload & an enlarging RV may worsen coronary perfusion as well as impede LV filling through ventricular interdependence. Hence reducing RV excessive preload can both reduce RV stretch and function as well as improving the performance of the LV. 
In those specific circumstances where RV output is impaired due to contractile dysfunction e.g. in the setting of a normal afterload, a higher preload is needed to maintain forward flow. e.g. RV infarction 
 
Improving contractility  
 
General measures to improve contractility: 
Avoid over stretch of the RV free wall with optimisation of preload and afterload.  
Maintenance of Sinus rhythm – correct electrolytes, acidaemia, use of anti-dysrhythmics, and if needed AV sequential pacing. 
 
Pharmacological approaches: 
1.    Noradrenaline improves coronary perfusion in the RV but will increase pulmonary vascular resistance (PVR); however, the overall impact is that noradrenaline has been shown be helpful in RV dysfunction 
2.    Adrenaline improves RV contractility without increasing (PVR) 
3.    Milrinone (50mcg/kg bolus -> 0.2-0.8mcg/kg/min) a PD3 inhibitor improves inotropy and promotes vasodilatation (systemic and pulmonary). Can be associated with hypotension so paired with noradrenalin.  
4.    Dobutamine -can be paired with noradrenaline but can cause tachyarrhythmias 
5.    Levosimendin is a calcium sensitiser and can improve RV function in left heart disease. 
 
Mechanical devices to support the RV: whist we treat the underlying cause. These include: ECMO; RV assist devices/Impella.  
 
Afterload reduction  
Excessive afterload plays some role in nearly all cases of acute RV failure. 
Reduction best achieved by a range of general measures and specific pharmaco-therapies including pulmonary vasodilators. 
 
General measures to improve hypoxia hypercarbia and acidosis 
1.    Oxygen therapy  
2.    Lung protective mechanical ventilation using the lowest effective plateau pressure tidal volume and PEEP whilst avoiding hypoxia and hypercarbia.  
e.g. Vt 4-6ml/kg Ideal BW; minimise PEEP; P plat < 30 mmHg; treat hypercarbia, acidosis. (PVR lowest at FRC) 
3.    Avoidance of hypothermia  
4.    Treatment of thromboembolic disease if acute cor pulmonale from PE. 
 
Pulmonary Vasodilators   
Several classes of drug in this setting and all have the potential to cause systemic hypotension and blunt hypoxic pulmonary vasoconstriction and can worsen VQ mismatch. 
 
a)    Inhaled nitric oxide 20-40ppm; rapid onset short offset short half-life is the inhaled vasodilator of choice in the critically ill. Has been shown to improve RV ejection fraction and end-diastolic volume in these patients, improve pulmonary hemodynamics and mixed venous oxygen saturation in patients with acute RV failure. 
 
b)    Inhaled prostacyclin analogues have been shown to be   effective in post cardiac surgery patients with pulmonary hypertension, refractory hypoxaemia or right heart dysfunction. 
  
Examiners’ Comments: 
 
The level of detail in template was not required. Discussion of preload optimisation, contractility and pulmonary vasodilation was required for a pass. 

 

Discussion

This is the second question on right heart failure in the same paper, the other being  Question 5  (focusing on the investigations for right heart failure). Management of RV dysfunction is discussed in (much) greater detail elsewhere, and so the nitty-gritty of it are omitted from this discussion section because under the stress of years of (many) RV failure questions that section has hypertrophied to a completely unmanageable thickness, to the point where it no longer functions as a revision resource for the time-poor candidate.

In summary:

  • Preload management:
    • Acute failure: increase preload to CVP 8-12 mmHg
    • Chronic failure: decrease preload to CVP 8-12 mmHg 
    • Titrate using PA catheter (CO measurements)
  • Afterload management:
    • Prevent pulmonary vasoconstriction:
      • Keep PEEP 6-10 cm H2O
      • Keep SpO2 >92%
      • Keep PaCO2 35-45 mmHg
      • Keep pH 7.35-7.45
      • Avoid high dose noradrenaline
        • But: keep systemic BP at least above pulmonary BP
    • Increase pulmonary vasodilation:
      • Nitric oxide
      • IV or inhaled prostacycline
      • Bosentan, ambrisentan
      • Sildenafil, tadalafil
      • Riociguat
  • Contractility:
    • Dobutamine, for where PA pressure is normal
    • Milrinone, for where PA pressure is raised
    • Levosimendan, for where you really need a cardiac output boost
  • Rate
    • ​​​​​​​60-100 appears to be a safe range (no specific diastolic benefit with low rates, no specific diastolic disadvantage with high rates)
  • Rhythm
    • ​​​​​​​​​​​​​​Sinus rhythm might be favoured in RV failure due to acute RV infarction (where there is no preexisting pulmonary hypertension).

References

Haddad, François, et al. "Right ventricular function in cardiovascular disease, part II: pathophysiology, clinical importance, and management of right ventricular failure." Circulation 117.13 (2008): 1717-1731.

Brida, Margarita, Gerhard-Paul Diller, and Michael A. Gatzoulis. "Systemic right ventricle in adults with congenital heart disease: anatomic and phenotypic spectrum and current approach to management." Circulation 137.5 (2018): 508-518.

Kucher, Nils, et al. "Double-chambered right ventricle." Circulation 103.21 (2001): e105-e106.

Tonelli, Adriano R., et al. "Peripheral pulmonary artery stenosis as a cause of pulmonary hypertension in adults." Pulmonary circulation 5.1 (2015): 204-210.

Blake, Hu A., Robert J. Hall, and William C. Manion. "Anomalous pulmonary venous return." Circulation 32.3 (1965): 406-414.

Takach, Thomas J., et al. "Sinus of Valsalva aneurysm or fistula: management and outcome." The Annals of thoracic surgery 68.5 (1999): 1573-1577.

Vavuranakis, Manolis, Charles A. Bush, and Harisios Boudoulas. "Coronary artery fistulas in adults: incidence, angiographic characteristics, natural history." Catheterization and cardiovascular diagnosis 35.2 (1995): 116-120.

Kulasegaram, Kulamakan, et al. "The alignment imperative in curriculum renewal." Medical teacher (2018): 1-6.

Marcus, Frank I., et al. "Diagnosis of arrhythmogenic right ventricular cardiomyopathy/dysplasia: proposed modification of the task force criteria." Circulation 121.13 (2010): 1533-1541.

Gorter, Thomas M., et al. "Right ventricular dysfunction in heart failure with preserved ejection fraction: a systematic review and meta‐analysis." European journal of heart failure18.12 (2016): 1472-1487.

Gorter, Thomas M., et al. "Right heart dysfunction and failure in heart failure with preserved ejection fraction: mechanisms and management. Position statement on behalf of the Heart Failure Association of the European Society of Cardiology." European journal of heart failure 20.1 (2018): 16-37.

Zamora, Rolando, James H. Moller, and Jesse E. Edwards. "Double-outlet right ventricle: anatomic types and associated anomalies." Chest 68.5 (1975): 672-677.

Mant, Jonathan, et al. "Systematic review and individual patient data meta-analysis of diagnosis of heart failure, with modelling of implications of different diagnostic strategies in primary care." (2009).

Voelkel, Norbert F., et al. "Right ventricular function and failure: report of a National Heart, Lung, and Blood Institute working group on cellular and molecular mechanisms of right heart failure." Circulation 114.17 (2006): 1883-1891.

Ventetuolo, Corey E., and James R. Klinger. "Management of acute right ventricular failure in the intensive care unit." Annals of the American Thoracic Society 11.5 (2014): 811-822.

Vlahakes, Gus J., Kevin Turley, and J. I. E. Hoffman. "The pathophysiology of failure in acute right ventricular hypertension: hemodynamic and biochemical correlations." Circulation 63.1 (1981): 87-95.

Dell'Italia, L. J., et al. "Comparative effects of volume loading, dobutamine, and nitroprusside in patients with predominant right ventricular infarction." Circulation 72.6 (1985): 1327-1335.

Bart, Bradley A., et al. "Cardiorenal rescue study in acute decompensated heart failure: rationale and design of CARRESS-HF, for the Heart Failure Clinical Research Network." Journal of cardiac failure 18.3 (2012): 176-182.

Patil, Nitin Tanajirao. "Strategies in patients with right ventricular failure on mechanical ventilation." Indian Journal of Respiratory Care 7.1 (2018): 22.

Schmitt, Jean-Marie, et al. "Positive end-expiratory pressure titration in acute respiratory distress syndrome patients: impact on right ventricular outflow impedance evaluated by pulmonary artery Doppler flow velocity measurements." Critical care medicine 29.6 (2001): 1154-1158.

Lahm, Tim, et al. "Medical and surgical treatment of acute right ventricular failure." Journal of the American College of Cardiology 56.18 (2010): 1435-1446.

Kiely, David G., Robert I. Cargill, and Brian J. Lipworth. "Effects of hypercapnia on hemodynamic, inotropic, lusitropic, and electrophysiologic indices in humans." Chest 109.5 (1996): 1215-1221.

Sylvester, J. T., et al. "Hypoxic pulmonary vasoconstriction." Physiological reviews 92.1 (2012): 367-520.

Zamanian, Roham T., et al. "Management strategies for patients with pulmonary hypertension in the intensive care unit." Critical care medicine 35.9 (2007): 2037-2050.

Carvalho, Carlos Roberto Ribeiro, et al. "Temporal hemodynamic effects of permissive hypercapnia associated with ideal PEEP in ARDS." American journal of respiratory and critical care medicine 156.5 (1997): 1458-1466.

Rudolph, A. M., and Stanley Yuan. "Response of the pulmonary vasculature to hypoxia and H+ ion concentration changes." The Journal of clinical investigation 45.3 (1966): 399-411.

Bousvaros, George A. "Effects of norepinephrine on human pulmonary circulation." British heart journal 24.6 (1962): 738.

Bhorade, Sangeeta, et al. "Response to inhaled nitric oxide in patients with acute right heart syndrome." American journal of respiratory and critical care medicine 159.2 (1999): 571-579.

Charl, J., et al. "Inhaled prostacyclin is safe, effective, and affordable in patients with pulmonary hypertension, right heart dysfunction, and refractory hypoxemia after cardiothoracic surgery." The Journal of thoracic and cardiovascular surgery127.4 (2004): 1058-1067.

Ferrario, Maurizio, et al. "Hemodynamics of volume loading compared with dobutamine in severe right ventricular infarction." American Journal of Cardiology 74.4 (1994): 329-333.

Kerbaul, François, et al. "Effects of norepinephrine and dobutamine on pressure load-induced right ventricular failure." Critical care medicine 32.4 (2004): 1035-1040.

Eichhorn, Eric J., et al. "Differential effects of milrinone and dobutamine on right ventricular preload, afterload and systolic performance in congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy." American Journal of Cardiology 60.16 (1987): 1329-1333

Hansen, Mona Sahlholdt, Asger Andersen, and Jens Erik Nielsen-Kudsk. "Levosimendan in pulmonary hypertension and right heart failure." Pulmonary circulation 8.3 (2018): 2045894018790905.

Kleber, Franz X., et al. "Repetitive dosing of intravenous levosimendan improves pulmonary hemodynamics in patients with pulmonary hypertension: results of a pilot study." The Journal of Clinical Pharmacology 49.1 (2009): 109-115.

Qiu, Jiayong, et al. "Efficacy and safety of levosimendan in patients with acute right heart failure: a meta-analysis." Life sciences 184 (2017): 30-36.

Dubin, Anne M., et al. "Electrical resynchronization: a novel therapy for the failing right ventricle." Circulation 107.18 (2003): 2287-2289.

Skhiri, Mehdi, et al. "Evidence-based management of right heart failure: a systematic review of an empiric field." Revista Española de Cardiología (English Edition) 63.4 (2010): 451-471.

Question 30.3 - 2018, Paper 2

List four clinical signs of severity in chronic aortic regurgitation.          (40% marks) 

College answer

•    Collapsing pulse/wide pulse pressure  
•    Length of decrescendo diastolic murmur  
•    LV third heart sound  
•    Soft A2  
•    Austin Flint (mid-diastolic) murmur  
•    Left ventricular failure  
•    Displaced apex beat  
 

Discussion

This question closely resembles the first part of Question 16 from the first paper of 2016, which expected the candidates to "list five clinical signs of severity in chronic aortic regurgitation. (25% marks)". The college answer here is a direct cut-and-paste. The author, emboldened by this, has reproduced the discussion section for Question 16 below, with neither useful modification nor any sense of shame. 

One might expect that features suggestive of severity in chronic AR would be mainly features related to the effect of AR on cardiac function, not just generic features of AR

  • LV dilatation (displaced apex, diffuse hyperdynamic impulse)
  • Congestive cardiac failure (low blood pressure, peripheral oedema)
  • Poor exercise tolerance
  • Signs of widened pulse pressure (see below)
  • An S3, suggestive of poor LV function

Generic features of AR are as follows:

  • Signs of widened pulse pressure:
    These were mentioned in Question 14.2 from the first paper of 2013
    • Corrigans sign: a "jerky" carotid pulse: full expansion, followed by complete collapse. You're palpating the pressure of the left ventricle, essentially. It's named after a 19th century Irishman. It indicates a severe aortic incompetence.
    • de Musset's sign which the college answer has spelled incorrectly is  a visible nodding of the head in time with arterial pulsation in patients with severe aortic insufficiency. It is named after an aortically insufficient French poet.
    • Quincke's sign, otherwise known as Quincke's pulse, is a nail sign: it is seen when the nailbed is blanched. The pale nail bed flashed red and white as capillary refill is restored. It can also be seen in the absence of any aortic problems, in patients who have sclerodactily.
    • Duroziez's sign is elicited by listening over the femoral artery with the bell of the stethoscope. It is supposed to be a double murmur. According to some recent evidence, it has almost 100% specificity. There is supposed to be both a systolic and a diastolic bruit, as blood rushes into - and then rapidly out of - the femoral artery.
  • These are mentioned in UpToDate:
    • Traube's sign – A pistol shot pulse (systolic and diastolic sounds) heard over the femoral arteries.
    • Mueller's sign – Systolic pulsations of the uvula.
    • Becker's sign – Visible pulsations of the retinal arteries and pupils.
    • Hill's sign – Popliteal cuff systolic pressure exceeding brachial pressure by more than 20 mmHg with patient in the recumbent position.
    • Mayne's sign – More than a 15 mmHg decrease in diastolic blood pressure with arm elevation from the value obtained with the arm in the standard position.
    • Rosenbach's sign – Systolic pulsations of the liver.
    • Gerhard's sign – Systolic pulsations of the spleen. 
  • Chacteristic auscultatory findings:
    • Soft S1
    • Soft A2
    • An S3 if LV function is severely depressed
    • A systolic ejection sound due to abrupt aortic distension

References

Nicholas Joseph Talley, Simon O'Connor; Clinical Examination: A Systematic Guide to Physical Diagnosis (7th ed)

SEGAL, JACK P., W. PROCTOR HARVEY, and MICHAEL A. CORRADO. "The Austin Flint murmur: its differentiation from the murmur of rheumatic mitral stenosis." Circulation 18.5 (1958): 1025-1033.

Leatham, Aubrey. "Splitting of the first and second heart sounds." The Lancet 264.6839 (1954): 607-614.

Sabbah, HANI N., and PAUL D. Stein. "Investigation of the theory and mechanism of the origin of the second heart sound." Circulation research 39.6 (1976): 874-882.

Saberi, Asif, and Saeed A. Syed. "Corrigan’s sign." Hospital Physician (1999): 29.

DAVIES, M., and A. Hollman. "de Musset sign." Heart 82.3 (1999): 262.

Norton, S. A. "Keratoderma with pseudo-Quincke's pulse." Cutis 62.3 (1998): 135-136.

Sapira, J. D. "Quincke, de Musset, Duroziez, and Hill: some aortic regurgitations." Southern medical journal 74.4 (1981): 459-467.

Luisada, Aldo A. "On the pathogenesis of the signs of Traube and Duroziez in aortic insufficiency. A graphic study." American Heart Journal 26.6 (1943): 721-736.

BLUMGART, HERRMAN L., and A. CARLTON ERNSTENE. "Two mechanisms in the production of Duroziez's sign: their diagnostic significance and a clinical test for differentiating between them." Journal of the American Medical Association 100.3 (1933): 173-177.

Nishimura, Rick A., et al. "2014 AHA/ACC guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines." Journal of the American College of Cardiology 63.22 (2014): e57-e185.

Question 1 - 2019, Paper 1

You are attending a rapid response call (RRC) for a 60-year-old male who is hypotensive following coronary angiography and angioplasty.

a)    What is your differential diagnosis for the hypotension?    (20% marks)

b)    List the findings from the history, examination and investigations that would help determine the cause of the hypotension.    (30% marks)

c)    Outline your management priorities.    (50% marks)
 

College answer

Diagnoses

Pericardial collection with tamponade

Stent occlusion

Coronary dissection or rupture

Evolving MI

Anaphylaxis

Effects of sedation and respiratory depression

Blood loss from cannulation site or retroperitoneal haematoma (femoral access)

Pulmonary oedema

Arrhythmias including heart block

History

-known allergies

-indication for procedure

-procedure performed, anatomical site of access, ease of procedure, coronary anatomy and disease, stents deployed

-medications given (anticoagulants, antiplatelets, vasodilators, inotropes or vasoconstrictors, sedatives, hypnotics etc)

-current symptoms (chest or abdo pain, SOB, dizziness etc)

Examination

-signs of cardiogenic shock (cold, clammy, diaphoretic, altering mentation, pulmonary oedema etc)

-signs of tamponade (soft HS / Elevated JVP and distended neck veins / pulsus paradoxus)

-Assess access sites especially groin and look for signs of local or retroperitoneal bleeding

-signs of anaphylaxis e.g. wheeze, flushing etc.

Blood pressure, heart rate and rhythm, respiratory rate, signs of respiratory distress, heart sounds

Investigations

ECG and echo mandatory

-ECG: new or ongoing ST elevation may indicate thrombus, stent occlusion or coronary dissection. Inferior MI may lead to 2/3rd degree heart block, and ongoing ischaemia may result in ventricular arrhythmias.

-Echocardiography looking or pericardial effusion/tamponade, which may be the result of coronary artery perforation, or cardiac perforation. Also looking for regional wall motion abnormalities or new VSD, cardiac function etc.

-Bloods including blood gas and troponin; drop in Hb, elevated lactate, significant hypoventilation etc Chest x-ray if signs of respiratory distress

Management priorities

Should focus on stabilisation of ABC and correction of reversible causes.

Haemorrhage should be excluded as quickly as possible, as should a contrast or other drug reaction. Judicious fluid challenge and use of inotropic agents/vasopressors to achieve a safe blood pressure. The need for urgent return to the Cath Lab or proceeding to the operating theatre should be decided on as soon as possible. In the absence of local haemorrhage or another clear precipitant, and after the deployment of stents, return to the Cath Lab is almost mandated to exclude stent occlusion/dissection

The need for intubation should be very carefully assessed, as the procedure carries

significant risk in the setting of severe hypovolemia or cardiac tamponade. Oxygen should be given, and judicious use of CPAP may help with pulmonary oedema although this may worsen RV dysfunction/tamponade physiology etc

Temporary pacing (transvenous or percutaneous) as indicated. Anti-arrhythmics such as amiodarone should be given as required.

Examiners Comments:

Often unstructured general resuscitation answers without reference to the specific clinical scenario. The crucial possibilities of reinfarction and cardiac tamponade were missed by many candidates as were the potential need for specific therapies. Unfortunately, some candidates spent a lot of time writing on very general aspects.

Discussion

Though the college list pulmonary oedema in their list of differentials, it is unclear how this is supposed to produce hypotension. Rather, it is an expected epiphenomenon seen in association with cardiogenic shock.

The list of differentials can be divided into categories:

  • Complications of the anaesthetic
    • Anaphylaxis (eg. to the contrast)
    • Cardiodepressant effect of general anaesthetics
    • Local anaesthetic toxicity
  • Complications of the procedure
    • Cardiac tamponade
    • Coronary artery dissection or perforation
    • Aortic injury
    • Stent thrombosis
    • Retroperitoneal haematoma
    • Intestinal ischaemia due to cholesterol emboli
  • Complications of the underlying disease
    • Cardiogenic shock due to ischaemia
    • Brady or tachyarrhythmia
  • Unrelated catastrophic event
    • Pulmonary embolism
    • Sepsis

"List the findings from the history, examination and investigations that would help determine the cause of the hypotension" they asked. This is a potentially massive time-wasting exercise for 30% of the marks. Because minimal history is given (60 years old, male, post angio), the possible answer may be quite broad. The college examiners have done quite a good job of listing the most informative examination findings in this model answer. In short, the following broad categories of question need to be asked to help determine the cause of the hypotension":

Presenting history

  • R​​​​​eason for angiography
  • Anaesthetic and procedure history (eg. which drugs did they give?)
  • Pre-procedure course (i.e. were they already in shock?)

Past history

  • Allergies
  • Medications (eg. anticoagulated?)

Examination findings and symptoms

  • Features of anaphylaxis (urticarial rash, wheeze, etc)
  • Features of cardiogenic shock (chest pain, cool extremities, shortness of breath, creps in the chest, etc)
  • Features of cardiac tamponade (pulsus paradoxus, raised JVP, etc)
  • Features of aortic dissection (back pain, differential limb pulses, abdominal pain)
  • Features of retroperitoneal haematoma (abdominal pain, distension, obvious haematoma)

Investigations:

  • ECG (STEMI, arrhythmias)
  • TTE 
  • CXR (tamponade)
  • ABG (haemoglobin, lactate)
  • Coags

Management priorities, one would have to say, depend entirely on what one finds during the process of investigating the cause of the hypotension. One would have rather different priorities in dealing with cardiac tamponade as compared to anaphylaxis. Because of this, it would have been difficult for the trainees to offer anything but "unstructured general resuscitation answers".  Moreover, though the college complained about generic responses lacking in elements specific tot he scenario, they also recommended the trainees to focus on "stabilisation of ABC and correction of reversible causes", which is as generic as it gets. With these conflicting directives, the following answer attempts to walk a fine line between specifics and generalities.

A - Assess the need for immediate airway control (eg. in context of contrast anaphylaxis)

B - Establish adequate oxygenation 

C - Correct hypotension:

   - Confirm that vascular access is secure

   - Administer short-acting vasopressor, eg. metaraminol

   - Assess the need for fluid resuscitation (eg. is the patient already in pulmonary oedema?)

   - Assess the need for immediate return to the cath lab or operating theatre (ECG looking for MI)

D - Address the patients' pain and distress

E - Correct any urgently lifethreatening electrolyte derangements (eg. give magnesium if the patient is having polymorphic VT)

H - Assess the need for blood products and coordinate urgent surgical referral if a retroperitoneal haematoma is discovered

References

Tavakol, Morteza, Salman Ashraf, and Sorin J. Brener. "Risks and complications of coronary angiography: a comprehensive review." Global journal of health science 4.1 (2012): 65.

Question 24.2 - 2019, Paper 1

What clinical signs on physical examination would you expect in a non-ventilated patient with a right ventricular infarct?    (25% marks)

College answer

  • Clinical signs would include the triad of hypotension, elevated JVP and clear lung fields
  • Pulsus paradox
  • Kussmaul’s sign (elevation of JVP on inspiration)
  • Right sided gallop S3/4.

Examiner's comments:

Part b was answered poorly - candidates listed the signs of right ventricular failure, not of a right ventricular infarct.

Discussion

The signs of right heart failure, which we were not supposed to specifically mention, would surely develop with a right sided infarct, and therefore reveal it to be right sided. 

"The clinical triad of hypotension, clear lung fields, and elevated jugular venous pressure in a patient with an inferior infarction is virtually pathognomonic for right ventricular infarction." However, the triad has a sensitivity of 25% (Kinch et al; 1994). Other signs may include:

  • Kussmaul's sign
  • Distended neck veins
  • Tricuspid regurgitation
  • Gallop rhythm
  • AV dissociation (i.e. conduction abnormalities)

Anyway: features of right heart failure will not have time to develop with acute infarction, but here they are anyway:

  • Features attributable to pulmonary hypertension
    • Loud P2(may be palpable)
    • Narrowly split S2
    • Tricuspid murmur
    • Diastolic murmur of pulmonary regurgitation
  • Features attributable to RV hypertrophy
    • Prominent a  wave in the JVP
    • Right-sided fourth heart sound (augmented by inspiration)
    • Left parasternal heave
    • Downward subxiphoid thrust.
  • Features attributable to RV dilatation and decompensated failure
    • Prominent wave in the significantly raised JVP
    • Right-sided third  heart sound (augmented by inspiration)
    • Peripheral oedema
    • Ascites
    • Hepatomegaly (which may be pulsatile)
    • Signs of LV failure, eg. pulmonary oedema (due to out-bowing of the intraventricular septum, and LV diastolic failure resulting from this)

References

Lorell, Beverly, et al. "Right ventricular infarction: clinical diagnosis and differentiation from cardiac tamponade and pericardial constriction.The American journal of cardiology43.3 (1979): 465-471.

Kinch, Jack W., and Thomas J. Ryan. "Right ventricular infarction." New England Journal of Medicine 330.17 (1994): 1211-1217.

Question 30.1 - 2019, Paper 1

A 60-year-old female who has presented to the Emergency Department with breathlessness is referred to you. Her ECG is shown on page 11 (ECG 30.1).

a)    Describe the important features of this ECG.    (40% marks)

b)    List the likely differential diagnoses in this patient.    (20% marks)
 

ECG 30.1

cor pulmonale and RVH.jpg

College answer

a)    Describe the important features of this ECG (40% marks)
Sinus tachycardia
Right axis deviation
Peaked P waves
Upright R in avR
R wave in V1,
poor R wave progression (RVH)
 
b)    List the likely differential diagnoses in this patient. (20% marks)

Massive Pulmonary Embolus

Pulmonary arterial hypertension (various aetiologies, including underlying connective tissue disorders, porto-pulmonary hypertension, primary pulmonary hypertension)

Conditions causing cor pulmonale (including COPD, Interstitial lung disease, OSA/obesity hypoventilation syndrome)

Discussion

Judging by the differentials, this was an ECG demonstrating some sort of acute or chronic right heart strain. The image comes from Chapter 7 of Clinical Electrocardiography: A Simplified Approach by Goldberger et al (2017). The interpretation for this figure is:

"A tall R wave (as part of an Rs complex) with an inverted T wave caused by right ventricular overload is seen in leads V1 to V5 (also in II, III, and aVF) from a patient with right ventricular hypertrophy (RVH) that was multifactorial. Marked right axis deviation is also present because the R wave in lead III is much taller than the R wave in lead II. In fact, the RVH is so severe that the R wave progression pattern is actually reversed (rS in V6). The negative but prominent P wave in V1 is probably due to right atrial overload, with slightly peaked P waves in leads II, III, and aVF."

The differentials for RV hypertrophy are broad:

  • Due to pulmonary hypertension
    • Acute PE
    • Chronic thromboembolic pulmonary hypertension
    • Chronic hypoxic lung disease, eg. pulmonary fibrosis or connective tissue disease
    • Pulmonectomy
    • Connective tissue disease
    • Secondary pulmonary hypertension, eg. due to mitral valve disease or diastolic heart failure
  • Due to structural cardiac disease
    • Atrial septal defect
    • Ventricular septal defect
    • Eisenmenger syndrome
    • Stenosis of the pulmonic valve or pulmonary artery
    • Anomalous pulmonary venous return
    • RV hypertrophy due to hyperthyroidism

References

Goldberger, Ary L., Zachary D. Goldberger, and Alexei Shvilkin. "Chapter 7 - Atrial and Ventricular Enlargement"; in:  Clinical Electrocardiography: A Simplified Approach E-Book: A Simplified Approach. Elsevier Health Sciences, 2017.

Question 30.2 - 2019, Paper 1

A 36-year-old female with history of alcohol abuse presents with nausea, vomiting and palpitations. Her ECG is shown on page 12 (ECG 30.2).

a)    What is the major abnormality in this ECG?    (20% marks)

b)    List three differential diagnoses for the ECG abnormality.    (20% marks)
 

ECG 30.2

long qt

College answer

a)    What is the major abnormality in this ECG (20% marks)
Prolonged QT

b)    List 3 differential diagnoses for the ECG abnormality (20% marks – 5% marks each)
-    Electrolyte abnormality
o    Hypokalaemia
o    Hypocalcaemia
o    Hypomagnesaemia
-    Drugs (many)
o    E.g. Amitriptyline, amiodarone, erythromycin, droperidol, haloperidol, risperidone,
-    Thyroid – hypo/hyper
-    Myocardial – heart failure, ischaemia, myocarditis
-    Congenital
 

Discussion

This ECG is on loan from the Jill Squires collection, with many thanks to her.  The QTc of this patient was 585 msec according to the automated QT-correcting algorithm. 

Differentials, according to Harrigan & Chan (2009), include:

Non-drug-related causes

  • Hypokalemia
  • Hypocalcemia
  • Hypomagnesemia
  • Hypothermia
  • Thiamine deficiency
  • Cardiac ischaemia

Drugs (also see www.qtdrugs.org)

  • Cardiac agents
    • Anti-arrhythmics (Type Ia, Ic, and III)
    • Calcium channel-blockers (some) (e.g. bepridil, isradipine, nicardipine)
  • Anti-psychotic agents
    • Phenothiazines (some) (e.g. thioridazine, mesoridazine)
    • Butyrophenones (e.g. haloperidol, droperidol)
  • Anti-depressants (some) (e.g. tricyclics, fluoxetine, sertraline, venlaflaxine)
  • Anti-infective agents
  • Fluoroquinolones (some) (e.g. sparfloxacin, gatifloxacin, moxifloxicin)
  • Macrolides (some) (e.g. erythromycin, clarithromycin)
  • Miscellaneous (pentamidine, amantadine, tetracyclines, foscarnet, quinine, chloroquine)
  • Neurologic agents
    • Carbamazepine, fosphenytoin, sumatriptan, zolmitriptan, naratriptan
  • Organophosphates
  • Gastrointestinal agents (e.g. cisapride, ipecac, octreotide, dolasetron)
  • Other (e.g. cocaine, diphenhydramine, methadone, tacrolimus, tamoxifen, probucol, tizanidine, salmeterol)

References

Harrigan, Richard A., and Theodore C. Chan. "| What is the ECG differential diagnosis of a prolonged QT interval?." Critical Decisions in Emergency and Acute Care Electrocardiography. Oxford, UK: Wiley‐Blackwell, 2009. 479-482.

Question 12 - 2019, Paper 2

A 64-year-old female patient has been ventilated in your ICU for 36 hours with septic shock and is receiving significant doses of noradrenaline and vasopressin. On the morning review you note her troponin level is elevated to over 10 times the normal range for your institution.

a)    How do you interpret the raised troponin level in this setting?    (40% marks)

b)    Outline your assessment and management plan specific to the raised troponin level.
(60% marks)
 

College answer

Interpretation of raised troponin- should not be used in isolation in this patient. The measured value of troponin is high and should not be ignored or dismissed. If unexpected, repeat the test. Symptoms of chest pain are not easy to elicit in the ventilated patient. Troponin leak in this setting may be due to myocarditis associated with sepsis, acute cardiomyopathy, Takotsubo disease given high dose vasopressor or a STEMI or NSTEMI or right ventricular disease. Elevated troponin in renal failure should also be considered if relevant. Elevated troponins are associated with poor outcomes in septic patients.

Management plan- Comprehensive clinical assessment especially cardiovascular and haemodynamic assessment. Look for recent, rapid increase in vasopressor requirement, signs of cardiogenic shock. Review ECG for any evidence of STEMI or other new changes, Review CXR for new pulmonary oedema/heart failure. Echo- transthoracic or if available TOE is mandatory to look for any regional wall motion abnormalities that may be new. Evidence of global changes on echocardiography may indicate acute cardiomyopathy e.g. Myocarditis. Look for classic changes of Takatsubo’s.

Further management will be determined by ECG and echo findings. Cardiology review, anticoagulation, careful consideration of thrombolysis or angioplasty if STEMI or regional changes on echo with consideration given to haemodynamic instability and challenges of transfer and management in cardiac catheter lab. Role of IABP in global hypokinesis related to acute cardiomyopathies.

Troponin increases in septic patients is thought to be associated with poor prognosis

Discussion

This question is identical to Question 6 from the first paper of 2017, and so is this answer:

What could this raised troponin mean?

  • It may be totally meaningless:
    • Cardiac troponins are elevated in 85% of patients with sepsis in the absence of acute coronary syndrome.
    • Overinterpretation can increase the cost and duration of hospital stay (Suarez et al, 2016)
  • It may represent an acute coronary syndrome:
    • Sepsis is a high-output cardiac failure state, and may unmask some sort of (previously subclinical) coronary artery disease.
    • Any proinflammatory state can give rise to an increased risk of MI (Donzé et al, 2014)
  • It may identify patients with septic cardiomyopathy:
    • Significant myocardial depression is observed in up to 60% of septic patients (Vieillard-Baron et al , 2008)
    • This may be associated with a raised troponin
    • A raised troponin does not identify patients who need inotropes
  • It may be a predictor of increased mortality:
    • Raised troponin predicts increased mortality,  with a risk ratio of around 1.9. (Sheyin et al, 2015)

Assessment and management plan:

  • History
    • Detailed interrogation of the bedside records to determine whether any critical events had taken place recently, eg. sudden increase in vasopressor doses or episodes of unexplained tachycardia
    • Exploration of the past medical history, specifically looking for previous history of ischaemic heart disease
  • Examination, to look for...
    • New murmurs
    • Features more consistent with cardiac failure than with distributive shock, eg. oedema, pulsatile liver, displaced apex beat, elevated JVP, cool extremities.
  • ECG, to look for...
    • Changes associated with ischaemia, eg. ST segments and T waves
    • New bundle branch block
    • Arrhythmia, eg. new onset AF
  • Biochemistry
    • ABG, to assess for metabolic acidosis (as this can cause myocardial depression)
    • Electrolyte values, to exclude embarrassingly correctable causes of low cardiac output eg. severe ionised hypocalcemia or hypophosphataemia
    • A repeat troponin value, and serial measurements to follow
  • TTE, to assess
    • Global systolic function
    • Regional wall motion
    • Valve function
    • Diastolic function
  • Management:
    • This would depend on the findings of the abovelisted investigations.
    • If the TTE is essentially normal, it may be that no further management is required beyond regular aspirin.
    • If there is global systolic dysfunction, inotropes may be called for. At this stage, one may decide to use some sort of advanced haemodynamic monitor (eg. PA catheter, PiCCO etc) so that one may be better able to titrate their vasoactive drugs.
    • If there are ECG changes and/or regional wall motion abnormalities, one may be able to make a diagnosis of acute MI. This poses several treatment options:
      • Conservative management with antiplatelet drugs and heparin infusion (which may be impossible in the context of severe sepsis, where DIC has already made the patient thrombocytopenic and coagulopathic)
      • Angiography and revascularisation (risky in the context of severe sepsis, particularly insofar as stent deployment is concerned)
      • Coronary artery bypass grafting (essentially out of the question given the severe shock state)

References

Ahmed, Amna N., et al. "Prognostic significance of elevated troponin in non-cardiac hospitalized patients: A systematic review and meta-analysis." Annals of medicine 46.8 (2014): 653-663.

Ammann, P., et al. "Elevation of troponin I in sepsis and septic shock." Intensive care medicine 27.6 (2001): 965-969.

Landesberg, Giora, et al. "Troponin elevation in severe sepsis and septic shock: the role of left ventricular diastolic dysfunction and right ventricular dilatation." Critical care medicine 42.4 (2014): 790-800.

Smith, Andria, et al. "Elevated cardiac troponins in sepsis: what do they signify?." West Virginia Medical Journal 105.4 (2009): 29-33.

Tiruvoipati, Ravindranath, Nasreen Sultana, and David Lewis. "Cardiac troponin I does not independently predict mortality in critically ill patients with severe sepsis." Emergency Medicine Australasia 24.2 (2012): 151-158.

Suarez, Keith, et al. "TROPONIN TESTING IN PATIENTS HOSPITALIZED FOR SEPSIS IS ASSOCIATED WITH INCREASED CARDIOVASCULAR TESTING AND LENGTH OF STAY." Journal of the American College of Cardiology 67.13 (2016): 451.

Sheyin, Olusegun, et al. "The prognostic significance of troponin elevation in patients with sepsis: a meta-analysis." Heart & Lung: The Journal of Acute and Critical Care 44.1 (2015): 75-81.

Hunter, J. D., and M. Doddi. "Sepsis and the heart." British journal of anaesthesia 104.1 (2009): 3-11.

Vieillard-Baron, Antoine, et al. "Actual incidence of global left ventricular hypokinesia in adult septic shock." Critical care medicine 36.6 (2008): 1701-1706.

Donzé, Jacques D., et al. "Impact of sepsis on risk of postoperative arterial and venous thromboses: large prospective cohort study." BMJ 349 (2014): g5334.

Question 15.1 - 2019, Paper 2

A 60-year-old male is complaining of breathlessness of sudden onset two months previously.

There is no associated chest pain.

What are the abnormalities on the ECG and what is the likely diagnosis?    (25 % marks)
 

ECG-Ventricular-Aneurysm.jpg

College answer

Q waves in leads V1-V4 (Previous MI?)
Elevated ST segments and inverted T waves in V2-V5
 
Inverted T waves in aVL
Likely diagnosis is left ventricular aneurysm

Examiners Comments:

Many candidates appear to have examined the ECG, drawn a conclusion and then retrofitted findings to support that. Confabulation in answers was common. Acceptance in marking was made of relatively amorphous answers (e.g. "anterior" as opposed to specific leads) but even with this, lack of specificity was common. Many candidates ignored the highly pertinent history that was given, showing a lack of clinical context/Bayesian thinking.

Discussion

This image was shamelessly stolen from LITFL, where - one can be reasonably sure - the examiners also turn when they Google for ECG images. This one comes from the specific entry on LV aneurysm

For the record, the ECG features listed by LITFL are as follows:

  • ST elevation seen > 2 weeks following an acute myocardial infarction.
  • Most commonly seen in the precordial leads.
  • May exhibit concave or convex morphology.
  • Usually associated with well-formed Q- or QS waves.
  • T-waves have a relatively small amplitude in comparison to the QRS complex (unlike the hyperacute T-waves of acute STEMI).

References

Question 15.2 - 2019, Paper 2

You have been asked to review a 50-year-old female who has collapsed at work.

a)    What are the abnormalities on the ECG?    (25 % marks)

b)    What is the rhythm?    (25 % marks)
 

ECG-Atrial-flutter-1-1-block-1024x553.jpg

College answer

Narrow complex tachycardia, rate around 300bpm

Absent p waves
ST segment depression V4-V6

Atrial flutter with 1:1 conduction.

Examiners Comments:

Many candidates appear to have examined the ECG, drawn a conclusion and then retrofitted findings to support that. Confabulation in answers was common. Acceptance in marking was made of relatively amorphous answers (e.g. "anterior" as opposed to specific leads) but even with this, lack of specificity was common. Many candidates ignored the highly pertinent history that was given, showing a lack of clinical context/Bayesian thinking.
 

Discussion

This image was shamelessly stolen from LITFL. It is a rapid (rate of 300) sinus tachycardia with some ST segment depression which likely represents some degree of demand ischaemia. The only other thing this could be is a super-rapid AVNRT with orthodromic conduction.

References

Question 15.3 - 2019, Paper 2

You are reviewing an 80-year-old female admitted to the Emergency Department after a fall and head injury. Her ECG is shown on page 15

RBBB%20%2B%20LPFB_0.jpg

What are the abnormalities? (25 % marks)

College answer

Right axis deviation

Right bundle branch block

Bifasicular block.

Examiners Comments:

Many candidates appear to have examined the ECG, drawn a conclusion and then retrofitted findings to support that. Confabulation in answers was common. Acceptance in marking was made of relatively amorphous answers (e.g. "anterior" as opposed to specific leads) but even with this, lack of specificity was common. Many candidates ignored the highly pertinent history that was given, showing a lack of clinical context/Bayesian thinking.
 

Discussion

This image was shamelessly stolen from the website which is clearly identified on the watermark. The authors described it thus:

"Sinus tachycardia with a rate of 113. The QRS is wide at 158 ms. There is a monophasic R-wave in lead V1. There is a right axis deviation with qR complexes in the inferior leads and rS complexes in the high lateral leads"

LIFT lists ECG features of RBBB:

  • Broad QRS > 120 ms
  • RSR’ pattern in V1-3 (‘M-shaped’ QRS complex)
  • Wide, slurred S wave in the lateral leads (I, aVL, V5-6)

LIFT also lists features of LAFB:

  • Left axis deviation (usually between -45 and -90 degrees)
  • Small Q waves with tall R waves (= ‘qR complexes’) in leads I and aVL
  • Small R waves with deep S waves (= ‘rS complexes’) in leads II, III, aVF
  • QRS duration normal or slightly prolonged (80-110 ms)
  • Prolonged R wave peak time in aVL > 45 ms
  • Increased QRS voltage in the limb leads

References

Question 15.1 - 2020, Paper 1

The ECG shown on page 13 (ECG 15.1) is from a 36-year-old male patient who presented with syncope.

ECG-Brugada-Syndrome-Type-1-2-1024x492.jpg
a)    Describe the abnormalities. (20% marks)

b)    What is the likely diagnosis? (10% marks)

c)    What is the treatment for this condition? (5% marks)
 


 

College answer

a)    Incomplete RBBB and ST elevation in anterior leads
b)    Brugada syndrome
c)    AICD
 

Discussion

This image was stolen from LITFL, where the examiners also shop for their ECGs. There is no evidence of an AICD in the image (as that was hard to find). The ECG demonstrates the classic "coved ST segment elevation" in V1-V3,  followed by a negative T wave.


 

References

Question 15.2 - 2020, Paper 1

The ECG shown on page 14 (ECG 15.2) is from a 74-year-old female admitted for monitoring after facial surgery. There is no chest pain.

Wellens-Syndrome-Type-B-Pattern.jpg

 
a)    Describe the abnormalities. (25% marks)

b)    What is the underlying diagnosis? (10% marks)
 


 

College answer

a)

  • Deep TWI anterior leads
  • Left axis deviation
  • Moderate voltage criteria for LVH
  • ST abnormalities
  • Prolonged QTc

b)

Critical LAD stenosis (Wellens syndrome) 
 

Discussion

This image was stolen from LITFL, as they all tend to be. According to Rhinehart et al (2002), via that LTFL entry (which is gloriously detailed), the criteria for Wellen's syndrome are:

  • Deeply-inverted or biphasic T waves in V2-3 (may extend to V1-6)
  • Isoelectric or minimally-elevated ST segment (< 1mm)
  • No precordial Q waves
  • Preserved precordial R wave progression
  • Recent history of angina
  • ECG pattern present in pain-free state
  • Normal or slightly elevated serum cardiac markers

References

Rhinehardt, Joseph, et al. "Electrocardiographic manifestations of Wellens' syndrome." The American journal of emergency medicine 20.7 (2002): 638-643.

Question 15.3 - 2020, Paper 1

The ECG shown on page 15 (ECG 15.3) is from a 47 year-old female with breast cancer who presented with shortness of breath.

 ECG_massive_pericardial_effusion-768x410.jpg
a)    Describe the abnormalities. (20% marks)

b)    What is the likely underlying diagnosis? (10% marks)
 


 


 

College answer

a)

  1. Low voltage QRS complexes
  2. Electrical alternans
  3. Tachycardia
b) Pericardial effusion

Discussion

This ECG was stolen from the LITFL page on ECG changes in massive pericardial effusion. The alternans is most clearly visible in the rhythm strip, which is V1. 

References

Usher, Bruce W., and Richard L. Popp. "Electrical alternans: mechanism in pericardial effusion." American heart journal 83.4 (1972): 459-463.

Question 16 - 2020, Paper 2

The following questions relate to targeted critical care transthoracic echocardiography (Level 1 haemodynamic assessment) performed in the ICU.

a)    In a patient with suspected pericardial tamponade:

i.    Which view on transthoracic echocardiography would you use to assess the heart and why?    (10% marks)

ii.    Describe three features of pericardial tamponade that you would expect to see in this view.    (30% marks)

b)    In a patient with a history of ischaemic heart disease who is cold, clammy and hypotensive, describe how you would assess left ventricular systolic function in the parasternal short axis (PSSA) view.    (30% marks)

c)    In a previously healthy patient with a traumatic leg amputation, describe how you would assess volume status in the subcostal view.    (30% marks)
 

College answer

Not available.

Discussion

a)

i. Subxiphoid view is the single best view, if you could only choose one view:

  • It is available while CPR is in progress, 
  • It is convenient to perform this in a supine patient, and
  • The most dependent portion of the heart is nearest to your probe, and that is where the effusion is most likely to be

ii. Features of tamponade in this view:

  • Dilated inferior vena cava
  • Right atrial collapse in systole
  • Diastolic collapse of right atrium and right ventricle
  • Hepatic vein flow reversal
  • Septal "bounce"

Theoretically, one could also list "a visible pericardial effusion", and that would accurate, but would probably score no marks because of obviousness.

b) A patient with a history of ischaemic heart disease who is cold, clammy and hypotensive? Surely it could not be cardiogenic shock? It's hard to know why that extra sentence was added. Also, the parasternal short axis is specified. From Mitchell et al (2019):

  • Linear dimensions (change in the LV cavity size on M-mode)
  • Wall motion abnormalities, scanning from base to apex
  • Ejection fraction by biplane disk summation

Also, though they might not be assessing LV systolic function strictly speaking, the PSAX view gives you an assessment of the ventricular size and wall thickness. 

c) Volume assessment on the subcostal view could be performed using:

  • Chamber volumes (ie. qualitatively collapsed looking ventricles, "kissing walls")
  • Size of the IVC: <10mm diameter suggests that the patient will respond well to a fluid challenge, but overall the static diameter of the IVC is not especially predictive of anything (Desai & Garry, 2018)
  • Distensibility index of IVC, in mechanically ventilated patients: the percentage variation of the IVC during inspiration verses expiration. 18% variation is 90% sensitive (Barbier et al, 2004)
  • Collapsibility index of SVC, in spontaneously breathing patients: the percentage variation of the IVC during expiration divided by the maximum diameter. 

References

Question 30.1 - 2020, Paper 2

A 69-year-old female has been admitted to the ICU for monitoring, after an uncomplicated laparoscopic cholecystectomy. Her routine admission ECG is shown on page 12 (ECG 30.1).

long qt

a)    Describe the ECG and the diagnosis.    (25% marks)

b)    Name three drugs that could contribute to the manifestation of this ECG pattern. (15% marks)
 

College answer

Not available.

Discussion

The already challenging process of finding ECGs which the college remove from their published papers (so they can reuse them) has been rendered even more challenging in the Cursed Second Paper of 2020 which was returned to the candidates without any official answers. So: this SAQ sounds like it might have involved some kind of QT interval prolongation, but let's face it, it could have been any of these drug-induced ECG changes.

So:

a) this is QT interval prologation  (it is about 512 msec in its uncorrected state, or 585 corrected for heart rate).

b) 

Drugs which cause this (also see www.qtdrugs.org)

  • Cardiac agents
    • Anti-arrhythmics (Type Ia, Ic, and III)
    • Calcium channel-blockers (some) (e.g. bepridil, isradipine, nicardipine)
  • Anti-psychotic agents
    • Phenothiazines (some) (e.g. thioridazine, mesoridazine)
    • Butyrophenones (e.g. haloperidol, droperidol)
  • Anti-depressants (some) (e.g. tricyclics, fluoxetine, sertraline, venlaflaxine)
  • Anti-infective agents
  • Fluoroquinolones (some) (e.g. sparfloxacin, gatifloxacin, moxifloxicin)
  • Macrolides (some) (e.g. erythromycin, clarithromycin)
  • Miscellaneous (pentamidine, amantadine, tetracyclines, foscarnet, quinine, chloroquine)
  • Neurologic agents
    • Carbamazepine, fosphenytoin, sumatriptan, zolmitriptan, naratriptan
  • Organophosphates
  • Gastrointestinal agents (e.g. cisapride, ipecac, octreotide, dolasetron)
  • Other (e.g. cocaine, diphenhydramine, methadone, tacrolimus, tamoxifen, probucol, tizanidine, salmeterol)

References

Lionte, Catalina, Cristina Bologa, and Laurentiu Sorodoc. "Toxic and drug-induced changes of the electrocardiogram." Advances in Electrocardiograms: Clinical Applications. 1st ed. Rijeka, Croatia: InTech (2012): 271-96.

Question 30.2 - 2020, Paper 2

A 76-year-old male presented to Emergency Department with chest pain.

 from LITFL

a)    Describe the ECG shown on page 13 (ECG 30.2).    (15% marks)

b)    Describe the anatomical lesion/s resulting in these ECG changes and the mechanism of the changes in the aVR lead.    (25% marks)
 

College answer

Not available.

Discussion

The already challenging process of finding ECGs which the college remove from their published papers (so they can reuse them) has been rendered even more challenging in the Cursed Second Paper of 2020 which was returned to the candidates without any official answers. So: this SAQ sounds like it might have involved ST changes in aVR, detailed by Robert Buttner and Ed Burns from LITFL. The image itself orginates from johnsonfrancis.org.

So:

a) The ECG changes in this tracing:

  • ST elevation in aVR
  • ST depression in other leads, most prominent in I, II and V4-V6

b) The anatomical lesion is proximal LAD occlusion, resulting in basal ischaemia.

The mechanism, to quote directly from Johnson Francis:

"ST segment elevation in aVR in proximal left LAD occlusion before first septal is thought to be due to transmural ischemia of the basal part of the septum. Injury current of basal part of septum is directed towards right shoulder and aVR."

References

Question 30.3 - 2020, Paper 2

A 57-year-old male patient is admitted to the ICU with urosepsis secondary to an obstructed urinary tract. He is haemodynamically stable with no chest pain. His ECG is shown on page 14 (ECG 30.3).

LITFL

a) What is the most likely diagnosis, and the immediate pharmacological therapy?    (20% marks)
 

College answer

Not available.

Discussion

The already challenging process of finding ECGs which the college remove from their published papers (so they can re-use them) has been rendered even more challenging in the Cursed Second Paper of 2020 which was returned to the candidates without any official answers. Fifty seven? UROSEPSIS? What the hell could this mean? The imagination runs wild. Surely, you think to yourself, this must have been some kind of electrolyte abnormality which gives rise to urinary calculi as well as to a clearly obvious ECG abnormality, and which has some emergency pharmacological treatment? Hypercalcemia fits that description. This ECG from the Atlas of Electrocardiography via LITFL has a shortened QT interval, which is characteristic of this condition. Bisphosphonates, calcitonin and IV hydration would be the immediate pharmacological steps.

References

Question 2 - 2021, Paper 2

Discuss the use of trans-oesophageal echocardiography (TOE) in the ICU. Use the following headings in your answer: rationale for use, data obtained, and how it assists clinical management, associated risks, and limitations.

College answer

Not available.

Discussion

The act of helping the trainees structure their answer by offering specific headings is laudable, as without it this question could have easily turned into a trap for people who misunderstood the depth of what is expected (for example, from reading the first sentence, one would not immediately develop the impression that one needs to discuss the risks. 

"Rationale for use" of TOE can probably be interpreted as "scenarios which call for the use of TOE instead of TTE", as that would make the greatest amount of sense. A "rationale for use" which includes all the various applications of cardiac sonography would not be a sensible way to answer. Thus:

  • Superior resolution for imaging posterior cardiac structures
  • Does not interfere with CPR
  • Does not require an intact chest wall (thus, suitable for assessing patients with severe anterior chest wall burns, extensive rib fractures, and patients following cardiac surgery).

Data obtained

  • Stuctural data:
    • Intracardiac shunts and septal defects
    • Valve structure and function
    • Vegetations
    • Aortic dissection
    • Intracardiac thrombus
    • Guidance for procedures, eg. ECMO cannula positioning
  • Functional data:
    • Some contractility and systolic function data (though TTE is better for this)
    • Preload sensitivity (respiratory phasic size variation of the SVC)
    • Shunt flow 
    • Doppler analysis of pulmonary venous inflow
    • Cardiac tamponade effects
    • Cardiac motility and efficacy of resuscitation efforts during cardiac arrest

How it assists clinical management

  • Directs haemodynamic management (eg. by identifying fluid responsive patients)
  • Directs duration of antibiotic therapy (by identifying vegetation)
  • Assesses the success of procedures (eg. TAVI, ECMO cannulation)
  • Helps estimate risk of stroke prior to cardioversion of a patient in AF
  • Assists decisionmaking in cardiac arrest (where LV wall movement are absent, the patient is  highly unlikely to achieve ROSC).

Associated risks

  • Each procedure has a small but non-zero risk of major complications, including oesophageal perforation, endotracheal tube dislodgement, and death.
  • The nasogastric tube is often in the way, and ends up being removed. It then needs to be reinserted, with attendent complications.
  • In the non-intubated patient, the use of sedation carries its own risks.

Limitations

  • Invasive
  • Potential risk of cross-infection
  • Probes are expensive and experts who can use them are even more expensive
  • Many contraindications, eg. oral or oesophageal surgery, upper GI anastomosis, oesophageal stricture or diverticulum, severe coagulopathy, etc
  • TTE is a better modality for assessment of the apex as well as LV and RV function

References

Cheitlin, Melvin D., et al. "ACC/AHA/ASE 2003 guideline update for the clinical application of echocardiography." A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/ASE Committee to Update the 1997 Guidelines for the Clinical Application of Echocardiography). American College of Cardiology Foundation and American Heart Association (2003).

Roscoe, Andrew, and Tim Strang. "Echocardiography in intensive care."Continuing Education in Anaesthesia, Critical Care & Pain 8.2 (2008): 46-49.

Douglas, Pamela S., et al. "ACCF/ASE/ACEP/ASNC/SCAI/SCCT/SCMR 2007 Appropriateness Criteria for Transthoracic and Transesophageal Echocardiography⁎: A Report of the American College of Cardiology Foundation Quality Strategic Directions Committee Appropriateness Criteria Working Group, American Society of Echocardiography, American College of Emergency Physicians, American Society of Nuclear Cardiology, Society for Cardiovascular Angiography and Interventions, Society of Cardiovascular Computed Tomography, and the Society for ...." Journal of the American College of Cardiology 50.2 (2007): 187-204.

Mayo, Paul H., Mangala Narasimhan, and Seth Koenig. "Critical care transesophageal echocardiography." Chest 148.5 (2015): 1323-1332.

Question 9 - 2021, Paper 2

Outline your approach to the assessment and management of atrial fibrillation in the critically ill patient

College answer

Not available.

Discussion

Cause of AF in ICU is usually non-structural, reversible, and non-cardiac (i.e. related to the cause of the non-cardiac critical illness). Common causes in the ICU include:

  • Catecholamine excess, whether exogenous (eg. adrenaline infusion) or endogenous (SAH, stress, pheochromocytoma, thyrotoxicosis)
  • Atrial distension (Pulmonary hypertension, OSA, PE, septal defects, valvular disease)
  • Abnormality of conducting system: 
    • Congenital cardiac disease, eg. septal defect
    • Infiltrative cardiac disease, eg. amyloidosis
    • Ischaemic heart disease
    • Age-related fibrotic changes
    • Haemochromatosis/iron overload
    • Hypothermia
  • Increased atrial automaticity / irritation
    • Drugs: Alcohol, caffeine, catecholamines
    • Electrolyte derangement
    • Myocarditis

Thus:

Assessment of the cause and consequences of AF

  • History, looking for features of OSA, ischaemic heart disease, pulmonary hypertension, prior episodes ("paroxysms") of AF, or recently ceased antiarrhythmic medications
  • Clinical examination, looking for evidence of heart failure
  • 12-lead ECG, looking for ischaemia
  • Blood biochemistry, looking for electrolyte derangement
  • Troponin, looking for ischaemia or myocarditis
  • Thyroid function tests, looking for hyperthyroidism
  • Scrutiny of the ICU monitoring equipment, to determine the duration of AF, to see if it coincides with some specific event (eg. the insertion of a line where the guidewire became unusually adventurous)
  • CXR, to look for radiological signs of atrial dilatation or cardiomegaly
  • TTE, to assess the effect on cardiac function

Assessment of the risk of stroke from AF

  • Duration of AF: if it started in the ICU, this should be easy to determine from the monitoring systems.
  • Risk stratification tools, such as the  CHA2DS2-VASc scoring system, can help determine the risk of stroke (A score of 1 equates to a risk of 1.3%; the maximum score is 9, with an associated stroke risk of 15.2%.)
  • TOE, looking for clots in the right atrial appendage, would be helpful if cardioversion is contemplated

Management options

  • Addressing the cause:
    • Management of the primary pathology (eg. shock state, sepsis, PE, MI, etc)
    • Correction of correctable predisposing causes (eg. hypoxia, acidosis, electrolyte derangement)
  • Cardioversion :
    • best suited to recent-onset AF (with the first 48 hours), or where TOE has demonstrated the absence of clot in the left atrial appendage
    • Should be considered in scenarios where the AF has produced a substantial haemodynamic disadvantage
    • Usually, in the ICU population, this is ineffective in the medium-term, as the pathology which is driving the AF first needs to resolve before sinus rhythm can be sustained.
    • Chemical (eg. amiodarone, IV magnesium, beta-blockers) and electrical cardioversion have a similar risk profile
    • In general, rate control and rhythm control have similar outcome effects, but rate control seems to have some advantage in the outpatient cohort
  • Rate control
    • Aim to reduce the rate to 80-100
    • Best suited for patients who are not hemodynamically compromised, and in whom the duration of the AF is unknown
    • Amiodarone or vernakalant are first-line for haemodynamically unstable patients
    • Beta-blockers are the first line for haemodynamically stable patients
    • Cardioselective calcium channel blockers such as verapamil or diltiazem are an alternative for people for whom beta-blockers are not appropriate (eg. asthma, COPD, peripheral vascular disease)
    • Digoxin in the ICU is generally less effective, but might be a better option for patients with poor LV function, as it has a subtle inotropic effect
  • Anticoagulation
    • Options include unfractionated heparin infusion, LMWH, warfarin or a DOAC such as dabigatran rivaroxaban or apixaban
    • If you are going to anticoagulate, anticoagulation with something should continue for at least 3 weeks before and 4 weeks after their TOE-cardioversion.

References

Wyse, D. G., et al. "A comparison of rate control and rhythm control in patients with atrial fibrillation." The New England journal of medicine 347.23 (2002): 1825-1833.

Van Gelder, Isabelle C., et al. "A comparison of rate control and rhythm control in patients with recurrent persistent atrial fibrillation." New England Journal of Medicine 347.23 (2002): 1834-1840.

Jörg Carlsson, J., et al. "Randomized trial of rate-control versus rhythm-control in persistent atrial fibrillation: The Strategies of Treatment of Atrial Fibrillation (STAF) study." Journal of the American College of Cardiology 41.10 (2003): 1690-1696.

Hohnloser, Stefan H., et al. "Rhythm or rate control in atrial fibrillation—Pharmacological Intervention in Atrial Fibrillation (PIAF): a randomised trial." The Lancet 356.9244 (2000): 1789-1794.

Yoshida, Takuo, et al. "Epidemiology, prevention, and treatment of new-onset atrial fibrillation in critically ill: a systematic review." Journal of intensive care 3.1 (2015): 19.

Caldeira, Daniel, Cláudio David, and Cristina Sampaio.  "Rate versus rhythm control in atrial fibrillation and clinical outcomes: updated systematic review and meta-analysis of randomized controlled trials." Archives of cardiovascular diseases 105.4 (2012): 226-238.

ARTUCIO, HERNAN, and MAXIMO PEREIRA. "Cardiac arrhythmias in critically ill patients: epidemiologic study." Critical care medicine 18.12 (1990): 1383-1388.

Reddy, Madhu, et al. "VERNAKALANT FOR RAPID CARDIOVERSION OF RECENT ONSET ATRIAL FIBRILLATION: A META-ANALYSIS." Journal of the American College of Cardiology 63.12_S (2014).

Morrison, Laurie J., et al. "Part 8: advanced life support 2010 international consensus on cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendations." Circulation 122.16 suppl 2 (2010): S345-S421.

Arrigo, Mattia, Dominique Bettex, and Alain Rudiger. "Management of Atrial Fibrillation in Critically Ill Patients." Critical Care Research and Practice 2014 (2014).

Kanji, Salmaan, et al. "Epidemiology and management of atrial fibrillation in medical and noncardiac surgical adult intensive care unit patients." Journal of critical care 27.3 (2012): 326-e1.

Kanji, Salmaan, et al. "Treatment of new-onset atrial fibrillation in noncardiac intensive care unit patients: A systematic review of randomized controlled trials*." Critical care medicine 36.5 (2008): 1620-1624.

January, Craig T., et al. "2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation." Circulation (2014): CIR-0000000000000041.

Sibley, Stephanie, and John Muscedere. "New-onset atrial fibrillation in critically ill patients." Canadian respiratory journal 22.3 (2015): 179-182.

Herzog, Eyal, et al. "Pathway for the Management of Atrial Fibrillation and Atrial Flutter.Critical pathways in cardiology16.2 (2017): 47-52.

Question 23.1 - 2021, Paper 2

An 85-year-old male presents to the Emergency Department following a collapse. There was no loss of consciousness. His ECG (ECG 23.1) is shown on page 9.

[it shown here. This page 9.] 

ECG

a)    List the major abnormalities.    (5% marks)

b)    List the likely aetiologies for these abnormalities.    (20% marks)

c)    List the potential cardiac complication is this patient.    (5% marks)
 

College answer

Not available.

Discussion

The college answer, let alone the ECG image, are not available at the time of writing, making this a hilarious exercise in trying to guess what the examiners were thinking. What condition has "major abnormalities" on ECG, causes octogenarians to collapse without passing out, has several possible aetiological causes and is associated with cardiac complications?

Well, reader, that could be damn near anything. The list could include:

  • Conduction abnormalities, eg. complete heart block
  • Ischaemia
  • Arrhythmias, eg. AF or VT
  • Implantable device malfunction
  • Electrolyte disturbance

It probably would not include inherited channelopathies and weird conduction disorders like WPW syndrome or arrhythmogenic RV cardiomyopathy, because the patient is 85. 

Fortunately, Kate Wagner from Jonathan Begley's study group found the exact ECG 

that was used for this paper, in Wikipedia of all places. It was apparently this Mobitz Type II block. That means this elderly man had a Stokes-Adams attack. Thank you, Wagner et al. If Deranged Physiology had merch, some would have been sent your way.

Thus:

a) Major abnormalities: 

  • RBBB
  • Mobitz Type II AV block
  • Tachycardia (sinus rate is ~ 100)

b) Likely etiologies:

  • Ischaemic heart disease
  • Anterior MI
  • Age-related degenerative change (Lenègre-Lev disease)
  • Cardiac surgery, eg. mitral valve repair

c) Cardiac complications:

  • Sudden P-wave asystole
  • Progression to complete heart block

References

Question 23.2 - 2021, Paper 2

A 48-year-old male presented with chest pain. His ECG (ECG 23.2) is shown on page 10.

https://litfl.com/vt-versus-svt-ecg-library/#:~:text=their%20previous%20ECGs-,example%202,-%3Cimg%20data-attachment

a)    List the abnormal ECG findings.    (15% marks)

b)    List two likely differential diagnoses consistent with these ECG finidngs.    (10% marks)

c)    Explain how to differentiate these two differential diagnoses using ECG criteria.    (20% marks)
 

College answer

Not available.

Discussion

The college answer and ECG image were both not available at the time of writing, so it is impossible to accurately reconstruct the original ECG, but judging from the question, it would have to have been either a question about Brugada criteria or Sgarbossa criteria. Seeing as the differentials generated by the application of Sgarbossa criteria are boring (they're infarcting, or they're not infarcting), the author settled on Brugada. The ECG is an example of VT from the LITFL page on broad complex tachycardias (example 2, to be precise).

So, 

a) Major abnormalities:

  • Tachycardia (rate almost 200)
  • Broad QRS complexes (~150 msec)
  • Extreme "northwest" axis

b)  Two differentials:

  • VT
  • SVT with bundle branch block

c) how to differentiate these two differential diagnoses using ECG criteria:

  • Brugada criteria:
    • Absence of RS complex in all precordial leads
    • R to S interval more than 100 msec in one precordial lead
    • AV dissociation (P waves and QRS complexes at different rates)
    • Morphology criteria for VT present in V1-2 and V6
      • LBBB pattern:
        • Initial R more than 40ms
        • Slurred or notched downwards leg of S wave in leads V1 or V2
        • Beginning of Q to nadir QS >60 ms in V1 or V2
        • Q or QS in V6
      • RBBB pattern:
        • Monofasic R or qR in V1
        • R taller than R' (rabbit-ear sign)
        • rS in V6
    • If any of these criteria are satisfied, VT is present
    • In this case,
      • AV dissociation is present, random P waves can be seen in V1

References

Question 23.3 - 2021, Paper 2

A 35-year-old male is brought to the Emergency Department after an out-of-hospital cardiac arrest. His ECG (ECG 23.3) is shown on page 11.

a)    What was the likely underlying rhythm at the time of the arrest? Please provide your reasoning.
(10% marks)

b)    List three likely aetiologies for these abnormalities.    (15% marks)

College answer

Not available.

Discussion

The college answer and ECG image were both not available at the time of writing, so it is impossible to accurately reconstruct the original ECG. This could have also been long QT syndrome (this time a congenital one, because the patient is young) but because we've already used that for another question in this paper, this one had to be something else. Let's go with Brugada syndrome. This ECG is recycled from Question 18.2 from the first paper of 2014.

a) The most likely rhythm would have been polymorphic VT or VF, as that is one of the diagnostic criteria for Brugada syndrome, and the ECG demonstrates characteristic ECG changes:

  • "Coved" ST elevation:  the QRS complex finishes high, and the ST-segment slopes diagonally to form an inverted T-wave in V1 and V2
  • Inverted T waves

b) Three possible aetiologies here are:

References

Berne, Paola, and Josep Brugada. "Brugada syndrome 2012." Circulation Journal 76.7 (2012): 1563-1571.

Hauer, R. N. W. "Brugada Syndrome or Brugada Mimicry?." Cardiac Arrhythmias 2003. Springer, Milano, 2004. 335-338.

Aksu, Uğur, et al. "Massive pulmonary embolism mimicking electrocardiographic pattern of Brugada syndrome." The American journal of emergency medicine 34.5 (2016): 933-e1.

Mehta, Sahil, et al. "Hypercalcemia due to rhabdomyolysis mimicking Brugada syndrome." Pacing and clinical electrophysiology 32.11 (2009): e14.

Question 22 - 2022, Paper 1

a)    Outline the WHO classification system for the causes of pulmonary hypertension.
(30% marks)

b)    Discuss measures to optimise right ventricular function in a patient with known pulmonary hypertension who is intubated for pneumonia.    (70% marks)
 

College answer

Not available.

Discussion

a) 

In brief, the WHO recognises  5 major groups of disease which fall under the pulmonary hypertension heading:

  1. Pulmonary arterial hypertension 
  2. Pulmonary hypertension due to left heart disease
  3. Pulmonary hypertension due to lung disease or hypoxia
  4. Pulmonary hypertension due to chronic PE​​
  5. Pulmonary hypertension due to "unclear multifactorial mechanisms"

These "PH WHO" groups are also known as the Dana Point classification system, so named because the original 2008 symposium on pulmonary hypertension was held in Dana Point, Ca.  

b)

Management of right heart failure 

  • Preload management:
    • Acute failure: increase preload to CVP 8-12 mmHg
    • Chronic failure: decrease preload to CVP 8-12 mmHg (this is the most likely scenario, as they are telling us the patient has known pulmonary hypertension). Thus, the options are:
      • Diuretics (potentially as an infusion)
      • Dialysis for fluid removal (potentially even SCUF)
    • The exact preload is difficult to find, is individual, and is best titrated by using  a PA catheter (CO measurements) or serial TTE/TOE
  • Afterload management:
    • Prevent pulmonary vasoconstriction:
      • Keep PEEP 6-10 cm H2O
      • Keep SpO2 >92%
      • Keep PaCO2 35-45 mmHg
      • Keep pH 7.35-7.45
      • Avoid high dose noradrenaline; prefer to use vasopressin
        • But: keep systemic BP at least above pulmonary BP
      • Position the patient with the "good" lung dependent to encourage blood flow into a more compliant system
    • Increase pulmonary vasodilation:
      • Nitric oxide
      • IV or inhaled prostacycline
      • Bosentan, ambrisentan
      • Sildenafil, tadalafil
      • Riociguat
  • Contractility:
    • Milrinone, for where PA pressure is raised
    • Levosimendan, for where you really need a cardiac output boost
    • Dobutamine is probably not the best choice, but can be resorted to if the patient is in renal failure and cannot tolerate the systemic vasodilation from the other agents

References

Simonneau, Gérald, et al. "Updated clinical classification of pulmonary hypertension." Journal of the American College of Cardiology 54.1s1 (2009): S43-S54.

Simonneau, Gerald, et al. "Updated clinical classification of pulmonary hypertension." Journal of the American College of Cardiology 62.25 (2013): D34-D41.

Galiè, Nazzareno, et al. "2015 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension." European heart journal (2015): ehv317.

Haddad, François, et al. "Right ventricular function in cardiovascular disease, part II: pathophysiology, clinical importance, and management of right ventricular failure." Circulation 117.13 (2008): 1717-1731.

Ventetuolo, Corey E., and James R. Klinger. "Management of acute right ventricular failure in the intensive care unit." Annals of the American Thoracic Society 11.5 (2014): 811-822.

Patil, Nitin Tanajirao. "Strategies in patients with right ventricular failure on mechanical ventilation." Indian Journal of Respiratory Care 7.1 (2018): 22.