Printable list of all cardiology SAQs

College Answer

A case of near electromechanical dissociation  in a 58 year old man. This could be caused by hypovolaemic shock. anaphylaxis or cardiogenic shock etc. Therefore the candidate should have started with a comprehensive approach and be directed to specific problems.

(a) An outline is requested but it should contain some rationale. eg:

•  A/B if the patient is breathing and talking apply a 100% oxygen mask. If not. bag with face mask and high·flow (h.   LOC may improve rapidly with BP restoration, but if not, intubation and ventilation will be necessary.

•  Quickly assess the patient's volume status (JVP visible?, veins engorged). Establish best venous access  possible (peripheral IV. external jugular, femoral). If the patient appears hypovolaemic. commence bolus of fluid. Continue fluid boluses until filling  pressures appear adequate as judged by rise in NP, CVP (or PAOP) or occurrence of worsening respiratory distress(? pulmonary.oedema).

•  If the patient is not hypovolaemic on arrival or remains hypotensive despite achieving adequate filling pressures give 1mg increments of araminc and commence an inoconstrictor infusion.

•     As soon as possible insert an intra·arterial cannula. It is possible that the central BP is adequate.

Meanwhile, a primary survey should be undertaken to determine the cause and a detailed history sought. Life-threatening injuries arc excluded. The patient is quickly examined from head to foot for signs of anaphylaxis (erythema, wheals etc), cardiac failure or tamponade (venous congestion, raised JVP). Tension pneumothorax or sepsis (hot. flushed, local signs) etc.

Investigations and initial treatments should be guided by the history and signs eg. intercostal catheter.pericardio--centesis.·

Discussion

This 58 year old gentleman is about to have a PEA arrest. Perhaps "moribund" is probably not a very precise medical term, but according to the all-knowing oracle of Wikipedia it refers to a "literal or figurative state of near death", which is appropriate to describe a man with a barely palpable rapid pulse.

However difficult to palpate, the pulse is still palpable.

The patient has not yet arrested.

One's priorities, then, are to assess this patient, rapidly determine the cause of his hemodynamic instability, and reverse the immediately reversible factors.

Perhaps he has not arrested yet. Still, the 4 Hs and 4Ts apply:

• Hypoxia
• Hypovolemia
• Hyper/hypokalemia
• Hyper/hypothermia
• Tension pneumothorax
• Tamponade (i.e. cardiac tamponade)
• Toxins (eg. anaphylactic reaction or intoxication)
• Thrombus (eg. a PE or MI)

Thus, a stepwise approach to this problem would be something resembling the following:

1) Ensure personal safety

2) Perform a basic peri-arrest primary survey

• Immediate assessment to diagnose cardiac arrest
  • Are they awake?
  • If they appear unconscious, shake them and ask "Are you alright?"
  • If they are unresponsive, look listen and feel for respiratory effort.
  • If the patient is unconscious, unresponsive, and is not breathing, call for help and start CPR.
    Otherwise, move on with the structured approach to prevent cardiac arrest
• Airway:
  • Assess patency: best done by interrogating the patient. If he provides coherent answers to your questions, his ABCs are unlikely to be desperately compromised. If he does not, one should secure his airway - initially usig unsophisticated techniques (jaw thrush, chin lift), progressing through airway adjuncts to intubation as needed.
  • Look for presence of vomit or foreign body
  • Prepare to progress to intubation
• Breathing
  • Observe respiratory rate
  • maintain oxygenationintially with high flow oxygen via tight-fitting reservoir mask. A high flow nonrebreather mask not only delivers around 75% FiO₂, it also allows one to assess respiratory function by observing the expiratory fogging of the clear plastic, and one can hook up an end-tidal capnometer to it to detect expired CO₂.
  • progress to bag-mask ventilation if respiratory arrest occurs
  • Auscultate the chest, percuss it, palpate for surgical emphysema
  • Investigate with ABG and urgent CXR
  • Specific differentials to consider before moving on with the survey:
    • Massive PE (distended neck veins, cyanosis, tachycardia and hypotension)
    • Acute severe asthma (silent hyperexpanded chest, the hint of wheeze)
    • Tension pneumothorax (unequal air entry, deviated trachea, hyper-resonant chest)
    • Massive haemothorax or effusion (unequal air entry, deviated trachea, dull percussion note over the hemithorax)
    • Pulmonary oedema (pink frothy sputum, coarse gurling creps)
• Circulation
  • Ensure large-bore IV access
  • Measure the blood pressure non-invasively and attach ECG leads for monitoring
  • administer IV fluids as bolus
  • administer readily available vasopressors, eg. metaraminol in order to maintain cerebral perfusion
  • assess for sources of bleeding
  • ABG or FBC to assess Hb, and need for transfusion
  • rapid bedside TTE to assess cardiac chamber volume and contractility
  • Specific differentials to consider before moving on with the survey:
    • Extremes of hypovolemia (collapsed veins, empty chambers, slow capillary refill, dry mucosae, cool extremities, weak rapid pulse)
    • Haemorrhagic shock ( exactly as above but also deathly pallor)
    • Cardiac tamponade (distended neck veins, muffled heart sounds, electrical alternans on ECG)
    • Peri-arrest arrhythmia (eg. VT or SVT)
    • Severe sepsis (mottled skin, fever, hyperdynamic circulation with hypotension)
  • A fluid bolus would be an appropriate reaction in any case. A hand-operated pump giving set with a litre of crystalloid should be set up. Ideally, one should prepare for invasive arterial blood pressure monitoring.
• Disability/neurology
  • Assess for signs of intracranial catastrophe by performing a brief neurological examination, including pupils and muscle tone/reflexes
  • Test BSL: ensure normoglycaemia
  • Specific differentials to consider before moving on with the survey:
    • Intracranial catastrophe (pupils, focal signs)
    • Seizure (increased tone, exaggerated reflexes, gaze deviation, clonus)
    • Extreme hypoglycaemia
    • Hyperglycaemic coma
    • Extremes of electrolyte derangement (eg. a sodium of 90 or 190)
    • Hepatic encephalopathy
• Exposure/examination
  • Assess for sources of bleeding
  • Examine for features of anaphylaxis
  • Check temperature; ensure normothermia

ARC Guideline 11.2: Protocols for Advanced Life Support

Additionally, the ARC ALS2 manual contains several chapters dealing with pre-arrest scenarios such as this one.

College Answer

(b) This provides some help.but is not definitive. Possible causes still include pulmonary embolus. hypovolaemia from bleeding DU. myocardial infarction etc. A progression from simple/quick investigations to more complex but specific/diagnostic investigations should be outlined. There should have beeo a sense of appropriate priorities.

If there are signs of GIT bleed with hypovolaemia, then fluid resuscitation, NG tube insertion, endoscopy, FBC and coag screen will be indicated  along with anti-ulcer therapy and perhaps surgery.

If there are signs of acute myocardial infarction. in the setting of recent DU, angiogram and angioplasty would be a preferable course perhaps after urgent echo.

If there are signs of massive pulmonary embolus (right  heart failure), and initial tests are supportive (right heart strain on ECG, oligaemic lung on CXR, distended RV on echo), a spiral CT would be indicated with commencement of IV heparin

Discussion

This part of this multi-part question offers some explanation as why the patient is "moribund". In essence, it narrows the differentials generated by the "4 Hs and 4 Ts" approach, which one can use to systematically organise one's diagnostic approach to this peri-arrest scenario in the first part of this question.

In detail:

• Hypoxia is possible due to pulmonary oedema or atelectasis
• Hypovolemia is a differential, given the history of GI bleeding
• Hyper/hypokalemia is now less likely
• Hyper/hypothermia is also less likely
• Tension pneumothorax is unlikely given the history
• Tamponade (i.e. cardiac tamponade) cannot be excluded but again, does not fit the history
• Toxins (eg. anaphylactic reaction or intoxication) cannot be ruled out, especially given the recent surgery and thus the potential oral antibiotic therapy
• Thrombus (eg. a PE or MI) is a definite possibility - particularly the PE - given the recent history of orthopaedic surgery

Thus, one would organise the following investigations:

• Routine bloods to measure urea and haemoglobin, to investigate the possibility of a GI bleed
• CXR to exclude pneumothorax, atelectasis and APO, as well as to look for subdiaphragmatic gas associated with a perforated duodenal ulcer
• TTE to investigate myocardial contractility and to look for regional wall motion abnormalities associated with MI. Even a low-skilled interpreter will also be able to rapidly rule out cardiac tamponade and right ventricular dilatatation associated with massive PE.
• CTPA to exclude massive PE; the CT will also capture a portion of the upper GI tract giving more information regarding the state of affairs in the duodenum.
• Upper GI endoscopy would be the gold standard to investigate and manage duodenal bleeding, and one should contact a gastroenterologist to organise this.

The following specific management could be commenced while awaiting results:

• High flow oxygen therapy
• Volume resuscitation
• PPI infusion

Seeing as both bleeding and thrombosis are a part of the differentials, anticoagulation/thrombolysis should be thought about but left until investigations reveal more about the cause of this shock state.

College Answer

{d) Ideally, intubate and ventilate with 100%  02, turn  up the noradrenaline, repeat fluid bolus, commence CPR if indicated and transfer immediately to the OT for surgery. In the absence of cardiac surgery 'facilities, one is left with a Trendelenberg operation by a general surgeon or continued medical therapy or risk lysis.

Discussion

This is a question regarding the management of a PEA arrest.

Another question - Question 15 from the first paper of 2011 - discusses the management steps, but with a different history of presentation. The steps are generic, and I will reproduce them here to simplify revision. Additionally, PEA is discussed in greater detail in the answer to Question 8 from the second paper of 2004.

Thus:

1) Confirm cardiac arrest

2) Call for help

3) Commence BSL (CPR) until help arrives;

• 100 compressions per minute
• Compression to a depth of 1/3rd of the anterior-posterior chest diamweter
• Asynchronous ventilation of 8-10 breaths per minute if intubated, otherwise 30 compressions to 2 breaths.
• Ensure the ETT is not malpositioned (chest examination, end tidal CO₂ or calorimetry)

4) With help arriving, follow the non-shockable pathway of the ALS algorithm, which consists of CPR and 1mg adrenaline every 2nd cycle.

4) Work on resolving the cause of the arrest, using the "four Hs and four Ts" as a general guide.

The index of ARC guidelines is available from the ARC website.

It contains the relevant algorithm for managing a non-shockable rhythm.

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.

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.

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.

College Answer

Pulseless VT: managed as per cardiac arrest protocol (immediate unsyncbronised defibrillation [up to 3 sequential  shocks  if  necessary],  followed  by CPR  intubation/IV/oxygen, consider antiarrhythmics  (lignocaine, amiodarone, potassium and magnesium], administer  adrenaline 1 mg every 3 minutes, exclude reversible causes [5Hs and 5Ts].

VT with a pulse: if deteriorates or unstable haemodynamically manage as for pulseless VT.If stable administer  oxygen/obtain  IV  access  and  rapidly  exclude  reversible  factors  (including   wire catheter in RV, hypokalaemia,  hypomagnesaemia, others  as indicated  by a systematic  review to exclude  other  reversible  causes.  Drug  therapy  according  to  scenario  but  useful  drugs include lignocaine (for ischaemia/post  cardiac surgery: 1-1.5  mg/kg IV then infusion), procainamide  (50 mglmin to max of 17 mglk.g),sotalol (l mglkg) or amiodarone (5 mg/kg over 20 minutes).

Discussion

The question draws on the candidate's knowledge of recent resuscitation guidelines.

The ARC has a pretty straightforward view of these sort of tachyarrhythmias. If it is hemodynamically usntable, you shock it. If it is haemodynamically stable, you can afford to think about drugs. If it is without pulse, the patient is dead and you should proceed according to the ALS algorithm for shockable rhythms (nowadays we dont do those three shocks anymore).

Thus:

• Acute management:
  • VT with pulse:
    • haemodynamically stable:
      • control arrhythmia with antiarrhytmic medications
      • Amiodarone is now the preferred agent (ARC guideline 11.9, 2009)
      • 300mg amiodarone over 20-60 minutes, followed by an infusion of 900mg over 24 hrs
      • Class 1a agents like lignocaine are a reasonable alternative, particularly if the QT interval is prolonged.
    • Haemodynamically unstable:
      • Synchronised cardioversion
      • If this does not work, give 300mg amidoarone over 10-20min, and then attempt cardioversion again
      • Follow this with 900mg amiodarone over 24 hours.
  • Pulseless VT:
    • consider a praecordial thump
    • commence CPR
    • progress according to ILCOR ALS algorithm for shockable rhythms
• Prevention of recurrence:
  • correct electrolyte disturbance
  • rule out cardiac ischaemia as cause
  • cease arrhythmogenic medications
  • address mechanical causes of VT: for example, PA catheter or very low CVC tips

Pellegrini, Cara N., and Melvin M. Scheinman. "Clinical management of ventricular tachycardia." Current problems in cardiology 35.9 (2010): 453-504.

Hazinski, Mary Fran, et al. "Part 1: Executive Summary 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations." Circulation 122.16 suppl 2 (2010): S250-S275.

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?

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.

College Answer

a)         The roles of the team leader include:

1)   Ensure  that  the  priorities  of  management  are  carried  out  effectively  and  efficiently.

Coordinate defibrillation, intubation cannulation and drug administration

2)   Help  establish  a  diagnosis  by  ECG  and  physical  examination  and  by  obtaining  all available history from hospital notes and bystanders.

3)   Check resuscitation status ( ?DNR) and prognosis

4)   Order investigations

5)   Reassess response to treatment

6)   Communicate with admitting consultant

7)   Ensure family is notified

8)   Organise post resuscitation care

b)         Priorities of cardiac arrest management may be best listed by drawing a sensible algorithm

(preferably AHA 2000 0r ILCOR 1999). The list should include

-     immediate basic life support

-     rapid rhythm diagnosis

-     defibrillation for VF, intubation/adrenaline for asystole or PEA

-     continued drug and defibrillation management

-     effective post –resuscitation care

Discussion

According to the ARC statement, the team leader is responsible for: 

• Directing and co-ordinating the resuscitation attempt 
• The safety of the resuscitation team at the cardiopulmonary arrest
• Ending the resuscitation attempt when indicated, often in consultation with other resuscitation team members and medical staff otherwise in charge of the patient
• Documentation (including audit forms) and for communication with the relatives and other healthcare professionals involved in the patient's management 
• Organising resuscitation team debriefing.

To this, one might add the following responsibilities:

• Assessing the rhythm and evaluating the need for defibrillation
• Ensuring the correct application of ALS and BLS
• Establishing a diagnosis for the cause of the arrest
• Ordering the appropriate investigations
• Ensuring minimal interruptions to CPR
• Allocating roles to the rescuers, and coordinating their efforts.
• Recruiting external resources (eg. cardiologists, ICU staff, cardiothoracic surgeons) into the resuascitation effort
• Communicating with family and the primary admitting consultant

ARC statement: Standards for Resuscitation: Clinical Practice and 
Education

Hunziker, Sabina, et al. "Teamwork and leadership in cardiopulmonary resuscitation." Journal of the American College of Cardiology 57.24 (2011): 2381-2388.

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)

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.

College Answer

Rapidly expanding area, answer needs covering of various areas.

Evidence to support use: comatose survivors after cardiac arrest had improved neurological survival (recent PRCT NEJM X 2); controversial/equivocal for severe head injuries (GCS 3-8), certainly demonstrated to decrease ICP; early evidence to support use in stroke and perhaps myocardial infarction; anecdotal evidence to support cooling to at least normothermia (eg. management of malignant hyperpyrexia); experimental for ARDS; use as adjuvant to minimise cerebral insult (prophylaxis) in the operating theatre during cardiac surgery (deep hypothermic circulatory arrest) and some neurosurgical procedures.

Technique: need to define temperature (eg. 32-33 degrees C), method to cool (blankets, surface cooling, intravenous device), and duration of therapy (eg. 12-24 hours or days).

Potential problems: immune suppression (increased infections), risks bleeding, vasoconstriction, shivering (necessitating neuromuscular paralysis and adverse effects of immobility).

Discussion

This question is identical to Question 20 from the second paper of 2006.

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.

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.

College Answer

Obvious initial priorities are airway, breathing and circulation, but aware of the fact that there may be some limitations placed on the resuscitative efforts. If no formal documentation is immediately available, it is appropriate to aggressively resuscitate (as usual, without delay) until appropriate information is obtained.

Endotracheal intubation is almost certainly indicated (immediately if unable to protect airway, or after a short period of cardiovascular resuscitation). Rhythm assessment is required to rapidly exclude reversible rhythm disorder. Fluids should be administered (type and amount over time should be discussed), and a vasopressor (bolus ± infusion) may be appropriate when hypovolaemia has been excluded.

Major differential to be considered includes hypovolaemia and sepsis (abdominal, respiratory) but other causes must be considered (including pulmonary embolus, myocardial infarction, anaphylaxis, adrenal insufficiency etc.).

Early administration of broad spectrum antibiotics &/or corticosteroids should be considered.

Discussion

...Should this patient even come to ICU?

Oh well, you can work that out after you have violently resuscitated her, amiright?

Initial assessment, with attention to ABCs with simultaneous brief history and rapid focused examination

• 1) Ensure personal safety

  2) Perform a basic peri-arrest primary survey

• Immediate assessment to diagnose cardiac arrest
  • Are they awake?
  • If they appear unconscious, shake them and ask "Are you alright?"
  • If they are unresponsive, look listen and feel for respiratory effort.
  • If the patient is unconscious, unresponsive, and is not breathing, call for help and start CPR.
    Otherwise, move on with the structured approach to prevent cardiac arrest
• Airway:
  • Assess patency: best done by interrogating the patient. If he provides coherent answers to your questions, his ABCs are unlikely to be desperately compromised. If he does not, one should secure his airway - initially usig unsophisticated techniques (jaw thrush, chin lift), progressing through airway adjuncts to intubation as needed.
  • Look for presence of vomit or foreign body
  • Prepare to progress to intubation
• Breathing
  • Observe respiratory rate
  • maintain oxygenationintially with high flow oxygen via tight-fitting reservoir mask. A high flow nonrebreather mask not only delivers around 75% FiO₂, it also allows one to assess respiratory function by observing the expiratory fogging of the clear plastic, and one can hook up an end-tidal capnometer to it to detect expired CO₂.
  • progress to bag-mask ventilation if respiratory arrest occurs
  • Auscultate the chest, percuss it, palpate for surgical emphysema
  • Investigate with ABG and urgent CXR
  • Specific differentials to consider before moving on with the survey:
    • Massive PE (distended neck veins, cyanosis, tachycardia and hypotension)
    • Acute severe asthma (silent hyperexpanded chest, the hint of wheeze)
    • Tension pneumothorax (unequal air entry, deviated trachea, hyper-resonant chest)
    • Massive haemothorax or effusion (unequal air entry, deviated trachea, dull percussion note over the hemithorax)
    • Pulmonary oedema (pink frothy sputum, coarse gurling creps)
• Circulation
  • Ensure large-bore IV access
  • Measure the blood pressure non-invasively and attach ECG leads for monitoring
  • administer IV fluids as bolus
  • administer readily available vasopressors, eg. metaraminol in order to maintain cerebral perfusion
  • assess for sources of bleeding
  • ABG or FBC to assess Hb, and need for transfusion
  • rapid bedside TTE to assess cardiac chamber volume and contractility
  • Specific differentials to consider before moving on with the survey:
    • Extremes of hypovolemia (collapsed veins, empty chambers, slow capillary refill, dry mucosae, cool extremities, weak rapid pulse)
    • Haemorrhagic shock ( exactly as above but also deathly pallor)
    • Cardiac tamponade (distended neck veins, muffled heart sounds, electrical alternans on ECG)
    • Peri-arrest arrhythmia (eg. VT or SVT)
    • Severe sepsis (mottled skin, fever, hyperdynamic circulation with hypotension)
  • A fluid bolus would be an appropriate reaction in any case. A hand-operated pump giving set with a litre of crystalloid should be set up. Ideally, one should prepare for invasive arterial blood pressure monitoring.
• Disability/neurology
  • Assess for signs of intracranial catastrophe by performing a brief neurological examination, including pupils and muscle tone/reflexes
  • Test BSL: ensure normoglycaemia
  • Specific differentials to consider before moving on with the survey:
    • Intracranial catastrophe (pupils, focal signs)
    • Seizure (increased tone, exaggerated reflexes, gaze deviation, clonus)
    • Extreme hypoglycaemia
    • Hyperglycaemic coma
    • Extremes of electrolyte derangement (eg. a sodium of 90 or 190)
    • Hepatic encephalopathy
• Exposure/examination
  • Assess for sources of bleeding
  • Examine for features of anaphylaxis
  • Check temperature; ensure normothermia

College Answer

Timing and the information expected is required. Immediate investigations should include ECG monitoring (for rhythm and ST segment assessment), arterial blood gases (oxygenation, carbon dioxide and acid base status), full blood examination (Hb, WCC) and electrolytes (including renal function and lactate). Blood cultures should be taken as soon as possible. Less urgent (minutes) investigations include chest and abdominal radiographs, ECG, and consideration of further abdominal investigations (eg. CT scan).

More specific investigations may be indicated according to the clinical suspicion. Consider exclusion of pulmonary embolus (CT angiogram, transoesophageal echo), severe myocardial dysfunction (PA catheter, echocardiography), baseline cortisol (before administer corticosteroids).

Discussion

Immediate investigations

• ABG
• CXR
• FBC, EUC, CMP, LFT, group and screen, blood cultures (as well as any other relevant body fluid)
• ECG

Investigations in the short-medium term

• CTPA and CT abdomen (to look for major postoperative bleeding, as well as rule out PE)
• Formal TTE to assess cardiac function in detail
• random cortisol level

College Answer

The major determinants of survival after a cardiac arrest are cardiac (arrhythymias and myocardial function) and neurological. Accuracy of assessment of prognosis of both factors increases with time. No techniques have 100% positive predictive value, or more importantly 100% negative predictive value.

•    Cardiovascular techniques of most value are the response to therapy (including thrombolysis or angioplasty) and echocardiography.
•    Neurological survival is best predicted by neurologic examination (again increasing certainty with time). Early poor prognostic signs (eg at 24 hours post-arrest) are fixed,unreactive pupils and extensor or absent motor response to painful stimuli (if not paralysed or deeply sedated). Brain death criteria are rarely met. Further refinement of prognosis may be achieved with investigations such as Somato-Sensory Evoked Potentials or EEG. CT is notoriously unreliable. MRI will detect more abnormalities, as it is a more sensitive test (though studies relating appearance to outcome are lacking).

Discussion

This question closely resembles Question 4 from the second paper of 2013: "Describe the clinical signs and investigations available to predict poor neurological outcome in comatose survivors of cardiac arrest. Include in your answer the factors that may confound the interpretation of these signs and investigations."

College Answer

Immediate management should be according to an appropriate ACLS protocol (including confirmation of  lack  of  central  pulse,  management  according  to  rhythm,  vasoconstrictor and external cardiac compression as appropriate, confirm placement of ETT [check position and ETCO2]; search for and correct reversible factors especially vasodilatation, profound hypoxaemia, excessive ventilation and hyperkalaemia [suxamethonium plus chronic muscle wasting).  Other management includes ongoing supportive care of ICU patient (eg. further communication and discussion with family, pressure care, DVT and stress ulcer prophylaxis, cultures and antibiotics if appropriate, etc.)

Discussion

This question consolidates within itself the answers to Question 6 from the first paper of 2006,Question 8 from the second paper of 2004 and Question 14 from the second paper of 2003, which ask about the management of PEA and VF.

Also, this scenario closely resembles Question 18.1 from the first paper of 2010, which asks the candidate for causes of cardiac arrest in a recently intubated tetraplegic patient.

The question states that the patient becomes pulseless, meaning that cardiac output is lost, but it mentions nothing about the underlying rhythm. Thus, the answer should focus on the systematic application of BLS and ALS, as well as the generation of differential diagnoses for the causes of such an arrest.

Thus:

Firstly, one assumes that cardiac arrest has been confirmed as "the cessation of cardiac mechanical activity as confirmed by the absence of signs of circulation".

Thus, first one should commence CPR, with the registrar asynchonously ventilating the patient via the newly inserted ETT.

Then, one should get more help by pressing the alarm button.

When help arrives, one should immediately call for defibrillator pads to be applied. As soon as possible, the underlying rhythm should be assessed, with the defibrillator charging while CPR is in progress.

While waiting for this rhythm check, one should systematically evaluate the situation:

A) - endotracheal position of the ETT should be confirmed by end-tidal capnography

B) - bag ventilation should continue at a CPR-asynchronous rate of 8-10 breaths per minute with 100% FiO₂, using conservative tidal volumes.

C) - CPR should continue at a rate of 100 compressions per minute, ideally with a rotating queu of staff ready to take over from fatigued rescuers. IV access should be expanded upon (I am assuming a cannula at least was available, if thio/fentanyl/sux were used to induce the patient). Through this line, a fluid bolus should be administered via a hand-pumped giving set.The patient must have been monitored while intubation was taking place, and the monitor should offer a log of periarrest rhythm changes one could peruse to determine the pre-arrest rhythm.

D) A BSL should be collected to rule out hypoglycaemia.

E) An ABG should be collected, to rule out hyperkalemia due to suxamethonium, or hypokalemia due to other causes.

The drug chart and obs chart should be quickly reviewed, and a quick examination should be performed, to excluded hypothermia and anaphylaxis as causes of the arrest.

Once the underlying rhythm is established, one can determine whether to defibrillate (for a shockable rhythm) or to give adrenaline (for a non-shockable rhythm, which in this scenario is more likely).

The 4 Hs and 4 Ts should be considered:

• Hypoxia (thus, oesophageal intubation or delayed oxygenation)
• Hypovolemia (thus, cardiovascular collapse due to vasodilation by an induction agent like propofol, or due to the autonomic dysfunction of spinal cord injury)
• Hyper/hypokalemia (thus, the effects of suxamethonium)
• Hyper/hypothermia (probably irrelevant in this case)
• Tension pneumothorax (due to overvigorous bag-mask ventilation, or due to tracheobronchial disruption by violent use of the bougie)
• Tamponade (unlikely in this setting)
• Toxins (eg. anaphylactic reaction to induction agents)
• Thrombus (eg. PE or MI)

ARC Guideline 11.2: Protocols for Adult Advanced Life Support

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.

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

College Answer

Ventricular fibrillation requires an initiating stimulus in a susceptible myocardium. VF can be induced in a previously normal myocardium as a result of electrical stimulation (electrocution, lightning) or by trauma (commotio cordis).  The myocardium can be made more susceptible by the presence of hypoxaemia (e.g. respiratory arrest), electrolyte disturbances (low K and Mg), altered autonomic and vagal inputs, and mechanical stimuli (e.g. wire or catheter in RV).  The myocardium may be abnormally susceptible due to congenital (e.g. conduction abnormalities) or acquired disorders (including ischaemia, hypertrophy, myocarditis, pro-arrhythmic drugs, etc).

Principle of management include early defibrillation, but in concert with correction of any correctible cause (e.g. wire, electrolytes, hypoxaemia etc), support of the cardio-respiratory state with adequate basic life support, and restoration of an appropriate metabolic milieu to support a normal rhythm.  This latter approach may require performance of cardiopulmonary resuscitation, and administration of specific anti-arrhythmic drugs.   Defibrillation is performed with either monophasic (200/200/360J) or biphasic (150/150/150J) defibrillator waveforms in a series of up to three sequential shocks. Subsequent monophasic shocks should be administered at maximal dose.

Discussion

This question is identical to Question 6 from the first paper of 2006.

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.

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

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).

College Answer

Electro-mechanical dissociation refers to a clinical state in which the patient has an ECG compatible with a normal output but has no palpable pulse. Various ways have been proposed to assist practitioners to remember the sort of conditions that could be responsible for EMD (eg. 10 step zigzag sequence [Kloeck 1995], 4Hs and 4Ts [ILCOR 2000]). Specific conditions that should be considered (history, examination, and investigation, with specific management) include:
·           Hypoxia (ensure 100% oxygen),
·           Hypovolaemia (administer fluids, stop haemorrage, clamp bleeding vessels),
·           Hypo/hyperthermia (ensure adequately warmed if severely hypothermic, or cooled
[eg. with dantrolene for malignant hyperpyrexia])
·           Hypo/hyper-kalemia and other metabolic disorders (exclude abnormalities in K , Mg , Ca ; severe acidosis: consider HCO3)
·           Tamponade (drain pericardial collection, release ventilation induced intra-thoracic pressure)
·           Tension Pneumothorax (needle thoracostomy then chest tube),
·           Toxins/Poisons/Drugs (consider all recently administered drugs for allergy and/or anaphylaxis [adrenaline, fluids, oxygen, remove hapten], excessive vasodilatation or cardiac depression [consider antidotes: isoprenaline {betablockers}, Ca {Ca channel blockers}, HCO3 for Na channel blockers {especially tricyclic anti-depressants}) ·           Thrombosis Pulmonary/Coronary (consider thrombolytics, urgent surgery)

Discussion

PEA is a situation where one is presented with organised electrical activity (i.e. a potetially perfusing rhythm) in the absence of cardiac output. The old term (electro-mechanical dissociation) is no longer in use.

A good systematic framework for this is the "Four Hs and four Ts" mnemonic:

• Hypoxia
• Hypovolemia (or distributive shock)
• Hyper/hypokalemia
• Hyper/hypothermia
• Tension pneumothorax
• Tamponade
• Toxins
• Thrombus

Thus, one may start by saying that the management of such a situation, whatever the cause, should begin with cardiopulmonary resuscitation.

Specific management then depends on the cause.

Thus:

• Hypoxia in an arrest is usually well-managed with adequate bag-mask ventilation and high concentration of supplied oxygen
• Hypovolemia and distributive shock can be ameliorated by the administration of fluids
• Potassium disturbances will be discovered whent he first ABG returns from the blood gas machine, and these can be managed routinely
• Tension pneumothorax can be suspected from history, and confirmed by examination. Management consists of decompression.
• Cardiac tamponade is also suggested by history and examination findings. Management consist of emergency pericardicentesis
• Toxins are suggested by history and characteristic examination findings, eg. pinpoint pupils, the rashj of anaphylaxis, etc. Management consists of administering an antidote, if it is available.
• Thrombosis - in the context of arrest-inducing massive PE - can be suspected from history; confirmation relies on the presence of an ultrasound machine and a skilled operator. Management consists of intra-arrest thrombolysis. For coronary thrombosis, this may not be a viable option.

Everyone has heard of the 4Hs and 4 Ts, but what the hell is this 10-step zigzag sequence? Apparently, it was described by Walter J.G. Kloeck in 1995. The article is not available to me, and the abstract is uninformative, but this entry in JournalGems confirms that this 10-step mnemonic is in fact the same 4 Hs and 4 Ts with an extra H (hypoglycaemia) and an extra T (separating PE and MI). One could also argue that we could extend the mnemonic further, and end up with 20 Hs and 20Ts, but one ought to remember that these mnemonics are used by critical care staff who have brief two minute breaks between rhythm checks to diagnose the cause of the arrest while running the show. Any complex memory device used to recall causes of arrest is only adding to their already massive cognitive load.

The index of ARC guidelines is available from the ARC website.

Kloeck, Walter GJ. "A practical approach to the aetiology of pulseless electrical activity. A simple 10-step training mnemonic." Resuscitation 30.2 (1995): 157-159.

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.

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.

College Answer

The major aortic injury is traumatic aortic rupture. This usually occurs at the aortic isthmus, between the left subclavian and the first intercostals arteries, where a few cm only of subadventitial rupture may be seen, with an associated intraluminal flap.   Other potential injuries include intimal tears, mural thrombi and aortic dissection.

All of the techniques have potential practical limitations, as they all require expert practitioners to perform, and a degree of sedation/anaesthesia. No comparative studies have evaluated management based on a particular technique. Choice will usually depend on local expertise!

The definitive test (gold standard) is still direct angiography (aortography). It requires catheter placement into the proximal aorta, and has problems associated with arterial access (eg. femoral) and arterial dye injection, but it provides better anatomical details for some areas (eg. aortic arch, brachiocephalic arteries and distal arteries).

CT angiography (usually high resolution, contrast enhanced spiral CT) has the advantages of providing other anatomical information, is more widely available, can be performed at short notice with rapid results (in trauma centres) and can be performed as part of workup for other injuries (eg. patient has other indications for chest CT).  It still requires IV contrast injection, transport to CT scan, immobilisation and expert interpretation.

Trans-Oesophageal Echocardiography is becoming more accessible at short notice as more practitioners are trained in its use.   Limitations include availability of expert practitioner (and equipment), requirement for sedation (+/- airway protection) and need for oesophageal placement of scope (in patient with unknown cervical spine status).   Artefacts may limit diagnostic accuracy (including atherosclerotic change).  Advantages include portability of procedure, rapid results with good sensitivity and specificity (comparable to spiral CT), and the ability to assess other cardiac and aortic structures (eg. in the presence of aortic dissection).

Discussion

This question closely resembles Question 13 from the second paper of 2010.

Though the question does not specify dissection, the same principles apply.

Assuming it is blunt aortic injury we are talking about, nice guidelines are available from a 2000 article in Trauma. To briefly visit this paper, aortography by direct angiography is still the gold standard, and TOE is still only supported by level 3 evidence.

Nagy, Kimberly, et al. "Guidelines for the diagnosis and management of blunt aortic injury: an EAST Practice Management Guidelines Work Group." Journal of Trauma-Injury, Infection, and Critical Care 48.6 (2000): 1128-1143.

The canonical source for this information would have to be the most recent iteration of the ACCF/AHA Guidelines for Diagnosis and Management of Patients With Thoracic Aortic Disease.

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:

• Right bundle branch block
• Different varieties of heart block
• Left anterior fascicle block
• Bifascicular and trifascicular block

Or one could review the topic properly at LITFL.

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.

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.

College Answer

Principles of management include:

Diagnose it clinically

History - dyspnoea, head fullness, cough, lines, tumour

Examination - plethoric cyanosed facies, periorbital oedema, exopthalmos, conjunctival injection, fundal venous engorgement, raised non-pulsatile JVP, lymphadenopathy, Pemberton's sign, dilated arm and chest collaterals

Look for associated features

Central airway compression, recurrent laryngeal involvement, phrenic nerve paralysis, Horner'ssyndrome, cardiac tamponade, pleural effusion

Confirm by investigation and look for cause

Thoracic neoplasm (usually bronchogenic Ca or Non Hodgkin’s Lymphoma), retrosternal thyroid,mediastinal fibrosis (post infection), thrombosis from intravascular device, aneurysm

High resolution CT is the most useful investigation. Also consider CXR, bronchoscopy/biopsy, echocardiograph, mediastinoscopy/biopsy, Magnetic Resonance Imaging

Peripheral tissue diagnosis often successful - node biopsy, sputum cytology, Bone Marrow biopsy

Treat obstruction

Steroids, Deep X-Ray Therapy, chemotherapy, surgery when indicated. Anticoagulation andthrombolytic Rx for acute catheter related thrombosis.

Support as necessary

Initial vascular access - IVC territory. Prepare for peri-operative/anaesthesia risks - CVS collapse(tamponade), central airway obstruction, laryngeal dysfunction, associated respiratory dysfunction(pleural and pulmonary involvement)

Few candidates considered the significant risk of sedating/anaesthetising patients with a mediastinal mass.

Discussion

The causes of SVC obstruction can be divided into malignant and non-malignant.

The non-malignant causes are well summarised in a nice table in the below-referenced article.

I will paraphrase it in the structured answer offered below.

Superior vena cava obstruction receives a (slightly) more detailed treatment in the "Required Reading" section, in a level of detail proportional to its value for the exam candidate.

MAURIEMARKMAN, MD. "Diagnosis and management of superior vena cava syndrome." Cleveland Clinic journal of medicine 66.1 (1999): 59.

College Answer

Several antiarrhythmic drugs are recommended in the ARC guidelines for use in VF/pulseless VT cardiac arrests and for bradycardia/asystole. However no drugs have been shown to improve long- term survival after cardiac arrests. Basic and advanced life support, early access to defibrillation and treatment of reversible causes take priority.

Guideline recommended drugs that should be considered include:

Lignocaine 1-1.5mg/kg, Amiodarone 300mg, Magnesium 5 mmol and atropine (1-3 mg).

Lignocaine is a class 1 antiarrhythmic, sodium channel blocker and has been traditionally used in VF/ pulseless VT cardiac arrest and while it is listed as first line in the ARC guidelines, the evidence for its use is limited. It should be given as a bolus for refractive VF/VT and occasionally can be used when the patient has recurrent VF/VT to prevent recurrence. Prophylactic use in AMI not complicated by arrhythmia is not recommended as there is some evidence that it may worsen overall prognosis.

Amiodarone is a complex antiarrhythmic drug with effects on sodium, potassium and calcium channels and alpha and beta blocking effects. It is an effective antiarrhythmic agent for both supraventricular and ventricular arrhythmias and it also causes less cardiac depression than other antiarrhythmics. It thus has some advantage over lignocaine. It is toxic to the tissues if it extravasates and is recommended for central venous administration but administration into an antecubital vein in the cardiac arrest situation is acceptable. Bolus injection of 300mg can be

followed by 150 mg if no effect and can be followed by infusion. Amiodarone has been shown to be better than placebo and lignocaine in terms of survival to hospital admission after out of hospital cardiac arrest due to refractory VF.

Magnesium is recommended by the ARC particularly for: Torsades de points, digoxin toxicity, and demonstrated hypokalemia/hypomagnesemia. It can be given as a 5mmol bolus which can be repeated and followed by infusion. There are no clinical studies using magnesium in this setting but it has been demonstrated to be a useful antiarrhythmic in postoperative cardiac surgical patients (Level 1 evidence).

Atropine is recommended by the ARC for use in severe bradycardia and in asystole. There are no controlled or randomised studies supporting its use. It can be given in 1 mg boluses up to 3 mg.

Discussion

This question, written in 2005, pre-dates the changes in ARC guidelines which have done away with lignocaine and atropine, leaving behind only amiodarone. This drug now occupies a shaky position after the third cycle of CPR for a shockable rhythm; the objective of using it is really to convert a defibrillation-refractory VF into one which is defibrillation-sensitive.

The evidence for its use is supported by two trials (Dorian et al 2002, and Somberg et al 2002) which found some benefit of amiodarone over lignocaine in the context of shock refractory or recurrent VT and VF. There was no benefit in survival to hospital discharge, but there was some benefit in survival to hospital admission. This better than the evidence for any other anitarrhytmic drug, and thus amiodarone remains in the guidelines ...for now.

All of this information is available in the ARC Guideline 11.5: Medications in Adult Cardiac Arrest. In brief summary, other drugs which are covered by this guidelines statement are as follows:

• Adrenaline: Favoured because retrospective studies have found an improvement in the rates of ROSC with adrenaline; however there has never been any confirmed improvement in survival associated with it.
• Calcium: Not recommended routinely; no benefit in terms of survival (6.8mmol calcium chloride as a bolus)
• Lignocaine: Not as good as amiodarone, and thus recommended only for those situations when amiodarone cannot be used (1mg/kg bolus)
• Magnesium: Recommended for torsades des pointes, but not recommended for any other situation, as there is no survival benefit. (5mmol bolus)
• Potassium: Recommended for hypokalemic arrests only (5mmol bolus)
• Sodium bicarbonate: Not recommended, as it is associated with poor short-term and long-term outcomes.
• Vasopressin: Not recommended as an alternative to adrenaline, as there is insufficient data to support its use.
• Aminophylline: There is no evidence of harm, but there is insufficient evidence to recommend its routine use.
• Thrombolytics: Recommended only in confirmed or strongly suspected massive PE as a cause of cardiac arrest, in which case one is committed to performing CPR for 60-90 minutes.

Rationale for the use of antiarrhythmic drugs in cardiac arrest

• Cardiac arrest is often the consequence of a non-perfusing arrhythmia. Ergo, an antiarrhythmic drug is the correct treatment.
• The energy required to defibrillate is decreased by acute administration of amiodarone (in dogs - Fain et al, 1987)
• The use of anti-arrhythmics may not be guided by any scientific principles, but it appears so deeply ingrained that it has become accepted as standard practice. Therefore to abjure the use of antiarrhythmics would be viewed as a substantial departure from standard practice. What would the coroner say?

Arguments against the use of antiarrhythmic drugs in cardiac arrest

• Pro-arrhythmic properties of antiarrhythmics must be taken into account; even amiodarone can produce QTc prolongation and torsade.
• The addition of extra drugs or steps to the algorithm complicates it, and makes it more difficult to teach (and to follow).
• The improvement of survival to hospital admission may not translate into any improvement in survival (in fact, none of the studies have found any improvement in survival)
• All the trials involving athiarrhythmics have compared one drug to another; there have been no placebo-controlled trials. We do not know what would happen without these drugs. Would survival rates drop sharply?

ARC Guideline 11.5: Medications in Adult Cardiac Arrest

Levine, Joseph H., et al. "Intravenous amiodarone for recurrent sustained hypotensive ventricular tachyarrhythmias." Journal of the American College of Cardiology 27.1 (1996): 67-75.

Dorian, Paul, et al. "Amiodarone as compared with lidocaine for shock-resistant ventricular fibrillation." New England Journal of Medicine 346.12 (2002): 884-890.

Skrifvars, M. B., et al. "The use of undiluted amiodarone in the management of out‐of‐hospital cardiac arrest." Acta anaesthesiologica scandinavica 48.5 (2004): 582-587.

Somberg, John C., et al. "Intravenous lidocaine versus intravenous amiodarone (in a new aqueous formulation) for incessant ventricular tachycardia." The American journal of cardiology 90.8 (2002): 853-859.

Kudenchuk, Peter J., et al. "Amiodarone for resuscitation after out-of-hospital cardiac arrest due to ventricular fibrillation." New England Journal of Medicine 341.12 (1999): 871-878.

Ong, Marcus Eng Hock, Tommaso Pellis, and Mark S. Link. "The use of antiarrhythmic drugs for adult cardiac arrest: a systematic review." Resuscitation 82.6 (2011): 665-670.

Huang, Yu, et al. "Antiarrhythmia drugs for cardiac arrest: a systemic review and meta-analysis." Crit Care 17.4 (2013): R173.

Fain, Eric S., John T. Lee, and Roger A. Winkle. "Effects of acute intravenous and chronic oral amiodarone on defibrillation energy requirements." American heart journal 114.1 (1987): 8-17.

College Answer

Causes: Ventricular fibrillation requires an initiating stimulus in a susceptible myocardium. VF can be induced in a previously normal myocardium as a result of electrical stimulation (electrocution, lightning) or by trauma (commotio cordis,  not to be confused with contusio cordis which is the systolic dysfunction resulting from blunt cardiac trauma). The myocardium can be made more susceptible by the presence of hypoxaemia (e.g. respiratory arrest), electrolyte disturbances (low K and Mg), altered autonomic and vagal inputs, and mechanical stimuli (e.g. wire or catheter in RV). The myocardium may be abnormally susceptible due to congenital (e.g. conduction abnormalities) or acquired disorders (including ischaemia, hypertrophy, myocarditis, pro-arrhythmic drugs, etc).

Principles of management: include early defibrillation, but in concert with correction of any correctible cause (e.g. wire, electrolytes, hypoxaemia etc), support of the cardio-respiratory state with adequate basic life support, and restoration of an appropriate metabolic milieu to support a normal rhythm. This latter approach may require performance of cardiopulmonary resuscitation, and administration of vasoconstrictors and specific anti-arrhythmic drugs, especially in the setting of prolonged VF. According to the ALS guidelines in place when the question was set, defibrillation is performed with an appropriate energy level for either monophasic (eg.

200/200/360J) or biphasic (eg. 150/150/150J) defibrillator waveforms in a series of up to three sequential shocks. Subsequent monophasic shocks should be administered at maximal dose.

The longer-term management, including the use of implantable defibrillators should be considered according to published guidelines.

Candidates were not penalised if they did not discuss the new guidelines (including higher energy levels for monophasic, and a single shock approach).

Discussion

This question is grounded in the ARC guidelines.

Causes of VF:

• Cardiac ischaemia
• Electrical myocardial injury
• Traumatic myocardial injury
• Irritating mechanical stimulus (eg. CVC guidewires, PA catheter)
• Myocarditis

Predisposition to VF:

• Low potassium
• Low magnesium
• Hypoxia
• Arrhythmogenic drugs eg. theophylline, sympathomimetics
• Congential and idopathic predisposition
• Prior cardiac surgery
• Cardiac chamber hypertrophy
• Severe hypothermia

Principles of management of VF:

• Cardiopulmonary resuscitation with an emphasis on uninterrupted chest compressions
• Early defibrillation - single shock
• When it is witnessed in a monitored environment and the defibrillator is readily available, three "stacked" shocks may be used.
• Correction of immediately responsible cause (eg. withdrawal of PA catheter, or immediate angiography for myocardial infarction)
• Correction of predisposing causes (eg. hypoxia, hypokalemia)
• Consideration for an automated implantable defibrilator (AICD).

ARC Guideline 11.2: Protocols for Adult Advanced Life Support

Chen, Qiuyun, et al. "Genetic basis and molecular mechanism for idiopathic ventricular fibrillation." Nature 392.6673 (1998): 293-296.

Wiggers, Carl J. "The mechanism and nature of ventricular fibrillation." American Heart Journal 20.4 (1940): 399-412.

Beck, Claude S., Walter H. Pritchard, and Harold S. Feil. "Ventricular fibrillation of long duration abolished by electric shock." Journal of the American Medical Association 135.15 (1947): 985-986.

College Answer

Indications for IABP insertion include:
•    Prophylactic (eg. cardiac surgery left main with unstable angina; or non cardiac surgery with severe Left Ventricular impairment)
•    Failure to wean from CPB
•    Cardiogenic shock – acute MR/VSD
•    Support for re-perfusion/revascularisation
•    Bridge to heart transplant

Potential complications include:
•    Limb ischemia
•    Vascular trauma, dissection
•    Infection
•    Balloon rupture
•    Bleeding

•    Thrombocytopenia
•    Malposition, vascular obstruction
•    Malfunction, failure to unwrap

Discussion

Indications for insertion and complications of use of IABPs are discussed in greater detail elsewhere.

In brief summary:

Indications for IABP use:

No choice but pump

• Failure to come off bypass
• Severe ischaemic mitral regurgitation or ventricular septal defect
  with haemodynamic compromise, while waiting for repair

Probably harmless, but probably not useful

• High risk CABG patients (pre-op)
• High-risk PCI patients (pre-op)
• Cardiogenic shock while waiting for PCI
• Pulmonary oedema in spite of maximal medical management

Totally experimental

• Takotsubo cardiomyopathy
• Neurogenic stress cardiomyopathy of subarachnoid haemorrhage
• Severe aortic stenosis with cardiogenic shock

Complications of IABP use:

• Common complications
  • Mild limb ischaemia - 2.9%
  • Balloon leak - 1.0%
  • Major limb ischaemia - 0.9%
  • Haemorrhage - 0.8%
  • Leg amputation due to ischaemia - 0.1%
• Rare complications
  • Atheromatous cholesterol emboli
  • Aortic or arterial dissection
  • Cerebrovascular accident
  • Thrombocytopenia
  • Haemolysis
  • Helium embolism

Ranucci, Marco, et al. "A Randomized Controlled Trial of Preoperative Intra-Aortic Balloon Pump in Coronary Patients With Poor Left Ventricular Function Undergoing Coronary Artery Bypass Surgery." Critical care medicine (2013). 2013 Nov;41(11):2476-83.

Theologou, Thomas, et al. "Preoperative intra aortic balloon pumps in patients undergoing coronary artery bypass grafting." Cochrane Database Syst Rev 1 (2011).

Ohman, E. Magnus, et al. "Use of aortic counterpulsation to improve sustained coronary artery patency during acute myocardial infarction. Results of a randomized trial. The Randomized IABP Study Group." Circulation 90.2 (1994): 792-799.

Gutfinger, Dan E., et al. "Aggressive preoperative use of intraaortic balloon pump in elderly patients undergoing coronary artery bypass grafting." The Annals of thoracic surgery 67.3 (1999): 610-613.

Thiele H, Zeymer U, Neumann FJ, Ferenc M, Olbrich HG, Hausleiter J, Richardt G, Hennersdorf M, Empen K, Fuernau G, Desch S, Eitel I, Hambrecht R, Fuhrmann J, Böhm M, Ebelt H, Schneider S, Schuler G, Werdan K; IABP-SHOCK II Trial Investigators: Intraaortic balloon support for myocardial infarction with cardiogenic shock. N Engl J Med 2012, 367:1287-1296

Parissis, Haralabos, et al. "The need for intra aortic balloon pump support following open heart surgery: risk analysis and outcome." J Cardiothorac Surg 5 (2010): 20.

Eagle, Kim A., et al. "ACC/AHA 2004 guideline update for coronary artery bypass graft surgery: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1999 Guidelines for Coronary Artery Bypass Graft Surgery)." Circulation 110.14 (2004): e340.

BUCKLEY, MORTIMER J., et al. "Intra-aortic balloon pump assist for cardiogenic shock after cardiopulmonary bypass." Circulation 48.1S3 (1973): III-90.

Sjauw, Krischan D., et al. "A systematic review and meta-analysis of intra-aortic balloon pump therapy in ST-elevation myocardial infarction: should we change the guidelines?." European heart journal 30.4 (2009): 459-468.

Unverzagt, Susanne, et al. "Intra-aortic balloon pump counterpulsation (IABP) for myocardial infarction complicated by cardiogenic shock." Cochrane Database Syst Rev 7 (2011).

Perera, Divaka, et al. "Elective intra-aortic balloon counterpulsation during high-risk percutaneous coronary intervention." JAMA: the journal of the American Medical Association 304.8 (2010): 867-874.

GOLD, HERMAN K., et al. "Intraaortic balloon pumping for ventricular septal defect or mitral regurgitation complicating acute myocardial infarction." Circulation 47.6 (1973): 1191-1196.

Kettner, Jiri, et al. "Utility of Intra-Aortic Balloon Pump Support for Ventricular Septal Rupture and Acute Mitral Regurgitation Complicating Acute Myocardial Infarction."The American journal of cardiology (2013).

Aksoy, Olcay, et al. "Cardiogenic shock in the setting of severe aortic stenosis: role of intra-aortic balloon pump support." Heart 97.10 (2011): 838-843.

Lazaridis, Christos, et al. "Intra-aortic balloon pump counterpulsation in the setting of subarachnoid hemorrhage, cerebral vasospasm, and neurogenic stress cardiomyopathy. Case report and review of the literature." Neurocritical care 13.1 (2010): 101-108.

Madhavan  M., Rihal  C.S., Lerman  A., Prasad  A.; Acute heart failure in apical ballooning syndrome (takotsubo syndrome/stress cardiomyopathy): clinical correlates and Mayo Clinic risk score. J Am Coll Cardiol. 57 2011:1400-1401.

Braunwald, Eugene, et al. "ACC/AHA 2002 guideline update for the management of patients with unstable angina and non–ST-segment elevation myocardial infarction—summary articlea report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on the Management of Patients With Unstable Angina)." Journal of the American College of Cardiology 40.7 (2002): 1366-1374.

Yutani, Chikao, et al. "CEREBRO‐SPINAL INFARCTION CAUSED BY ATHEROMATOUS EMBOLI." Pathology International 35.4 (1985): 789-801.

Ho, A. C., et al. "Stroke after intraaortic balloon counterpulsation associated with mobile atheroma in thoracic aorta diagnosed using transesophageal echocardiography." Chang Gung medical journal 25.9 (2002): 612-616.

Kvilekval, Kara HV, et al. "Complications of percutaneous intra-aortic balloon pump use in patients with peripheral vascular disease." Archives of Surgery 126.5 (1991): 621.

Rius, Jordi Bañeras, et al. "Resolution of Shock-Induced Aortic Regurgitation With an Intraaortic Balloon Pump." Circulation 124.4 (2011): e131-e131.

Ferguson, James J., et al. "The current practice of intra-aortic balloon counterpulsation: results from the Benchmark Registry." Journal of the American College of Cardiology 38.5 (2001): 1456-1462.

Alderman, James D., et al. "Incidence and management of limb ischemia with percutaneous wire-guided intraaortic balloon catheters." Journal of the American college of Cardiology 9.3 (1987): 524-530.

Pennington, D. Glenn, et al. "Intraaortic balloon pumping in cardiac surgical patients: a nine-year experience." The Annals of thoracic surgery 36.2 (1983): 125-131.

Cruz-Flores, Salvador, Alan L. Diamond, and Enrique C. Leira. "Cerebral air embolism secondary to intra-aortic balloon pump rupture." Neurocritical Care 2.1 (2005): 49-50.

HIROOKA, KAZUNOBU, et al. "Helium Gas Embolism caused by a Ruptured Intraaortic Balloon." Japanese Journal of Intensive Care Medicine 27.9 (2003): 867-871.

Mitchell, Simon J., et al. "Cerebral arterial gas embolism by helium: an unusual case successfully treated with hyperbaric oxygen and lidocaine." Annals of emergency medicine 35.3 (2000): 300-303.

Chockalingam, Anand, et al. "Dynamic left ventricular outflow tract obstruction in acute myocardial infarction with shock cause, effect, and coincidence." Circulation116.5 (2007): e110-e113.

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:

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.

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.

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

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)

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.

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.  

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.

College Answer

Proven role:

1)  cardiac arrest – out of hospital VF arrest improved neurological outcome and survival

32-34C

2)  Control of intracranial hypertension – Improves ICP, but no reduction in mortality

Areas under investigation

1)  Stroke patients

2)  Perinatal asphyxia

Practical issues:

a)  difficulty in achieving hypothermia rapidly

b)  shivering and the need for relaxants which can delay neurological assessment c)  Not proven for non-vf arrests

d)  Not proven for in-hospital arrests

e)  Hypothermia can cause diuresis with attendant electrolyte disorders

f)       Risk of arrhythmias

g)  Risk of infection

Discussion

In general, therapeutic hypothermia in cardiac arrest and the physiology of hypothermia overall are discussed elsewhere. This question also asks about the extended indications for therapeutic hypothermia, which are generally not very well known (being exotic and enjoying only very patchy support from the ICU senior medical community).

In late 2015, this question would be interpreted very differently, and would likely attract a slightly different answer from the candidates. A good example might resemble the college answer to Question 9 from the first paper of 2015. The discussion section for that SAQ is reproduced below, as the two questions are virtually identical, and a 2006-specific answer would be of no interest to the modern candidates.

Rationale for therapeutic hypothermia:

• Therapeutic hypothermia has been advanced a a means of improving survival and good neurological outcome following cardiac arrest.
• It has also been offered as a means of controlling intracranial hypertension which is refractory to other modalities.
• Therapeutic hypothermia modulates the activity of body proteins and electrolytes.
• This modulation is thought to have some beneficial effects in scenarios where inflammatory damage is anticipated.
• This also involves the down-modulation of the overall metabolic rate, which decreases the metabolic demands of the organism in situations where supply of metabolic substrate may be compromised.
• Decrease in oxygen consumption matches decreased demand with decreased supply in "penumbra" areas, at the watersheds, where hypoxic injury has caused oedema.\

Advantages of therapeutic hypothermia

• Decreased granulocyte migration into tissue
• Decreased cerebral oedema
• Intrinsic anticonvulsant effects of hypothermia

Well-accepted indications:

• Mild therapeutic hypothermia for survivors of cardiac arrest
• Therapeutic hypothermia for traumatic brain injury

Evidence for use in cardiac arrest:

• Pseudorandomised unblinded trial in 1996 - promising results
• Bernard et al  demonstrated a survival benefit in out of hospital VF arrest survvors
•  A recent Cochrane review supports the use of therapeutic hypothermia, finding a 1.35 risk reduction for mortality.
• The recent TTM trial  has demonstrated non-inferiority of a more conservative hypothermia (36°C) with standard temperature goals, in terms of mortality.

Evidence for use in traumatic brain injury

• EUROTHERM 3235 trial (2015): 387 patients; hypothermia was used as a second-line therapy to reduce ICP.
• No survival benefit was observed.
• Recruitment was suspended early owing to safety concerns.
• ICP control was in fact better in the hypothermia group (they required rescue therapies less frequently)
• The meta-analysis mentioned by the college is possibly  this 2013 review by Georgiou et al; except there was no benefit in mortality when only high quality trial were included.

Extended indications:

Therapeutic hypothermia in cooling of a hyperthermic patient

• Hyperthermia is associated with substantial harm, particularly if the temperature increases beyod 41°C
• Causes of such hyperthermia may be numerous, including sepsis, malignant hyperthermia, anticholinergic drug poisoning, heat stroke, and so on and so forth.
• In brief, these causes all have specific management strategies which may take time to work.
• In the interim, the temperature must be managed, so that organ damage does not occur
• Induction of hypothermia (or maintenance of controlled normothermia) by cooling the patient can be viewed as one of the indications.

Therapeutic hypothermia for subarachnoid haemorrhage

• Theoretically, TH may be protective in SAH in the same way that it is supposed to be protective in traumatic brain injury. Areas affected by ischaemia in the context of vasospasm may benefit from having a lower metabolic rate.
• TH certainly  seems to decrease the flow velocity in the MCA of subarachnoid haemorrhage patients (Seule et al, 2014), suggesting that the metabolic rate is indeed affected enough to influence cerebral blood flow.
• Animal studies have also demonstrated that hypothermia reverses vasospasm (in rats)
• In patients with "poor-grade" SAH, good functional outcome was achieved in 48% with the combination of barbiturate coma and hypothermia to 33-34°C (Gasser et al, 2003)
• A more recent case series (Seule et al, 2010) found good outcomes in 57% of  severe SAH patients who developed vasospasm.
• In contrast, Karnatovskaia et al (2014) found no difference in neurological outcome within their case series.
• No recommendation in favour of this use of TH can be made with a straight face.

Therapeutic hypothermia for super-refractory status epilepticus

• Hypothermia is known to have antiepileptic effects.
• Case series (eg. Corry et al, 2008) have demonstrated its feasibility in humans (target temperature: 31–35°C)
• Neurocritical care society guidelines for status epilepticus (Brophy et al, 2012) identified only 4 articles in the literature, and were unable to make very strong recommendations.
• The HYBERNATUS trial mentioned in the college answer is apparently ongoing, but no longer recruiting participants.

Therapeutic hypothermia for severe sepsis

• Anti-inflammatory effects of hypothermia were studied in an animal model of severe sepsis (Kwang et al, 2012).
• The hypothermic rats (30–32 °C) did better in terms of acute lung and liver injury.
• Human applications of this are limited by concern that ...firstly, a fever is an antibacterial physiological response, and secondly, that the haemodynamic instability of septic shock will be exacerbated by hypothermia.

Therapeutic hypothermia for meningitis

• Evidence of potential harm mentioned by the college in their answer was found by a 2013 RCT (Mourvillier et al). The investigators found a higher mortality in the hypothermia group.

Therapeutic hypothermia for neonatal asphyxia

• Following on from the success of TH in adult cardiac arrest, this modality has been applied to neonatal hypoxic-ischaemic encephalpathy.
• Shankaran et al (2005) performed an RCT; the group of neonates who were cooled 33.5°C for 72 hours; the rate of cerebral palsy was reduced from 19% to 15%, and mortality improved from 37% to 24%. In the long term, there was no increase in disability among hypothermia-exposed survivors when compared to surviving controls (Shankaran et al, 2012)
• TOBY trial (2014) confirmed that both survival and neurological outcome is improved

Therapeutic hypothermia for stroke

• The college answer points out that fever is associated with two-fold risk of death after haemorrhagic or ischaemic stroke. Pharmacologic methods of fever control have not shown improved outcome in stroke.
• In animal models of stroke, , mild or moderate hypothermia has been shown to decrease infarct size and lead to functional improvement when cooling was initiated within a few hours of ischemia onset (Clark et al, 2008). But... These were rats, and they were cooled to 24°C

Therapeutic hypothermia for acute hepatic encephalopathy

• This use of TH is an extension of the observation that TH reduces cerebral oedema in patients with traumatic brain injury.
• Some authors (Stravitz et al, 2008) have suggested that TH may be an effective bridge to liver transplant.
• Human case series support this assertion (Jalan et al, 1999); during their treatment there was no significant relapse of increased intracranial pressure.
• There are no RCTs, but a large-scale retrospective cohort (Karvellas et al, 2014) did not find any survival benefit.

Therapeutic hypothermia in ARDS :

• Recent studies (Zhicheng et al, 2012) have confirmed that mild hypothermia improves gas exchange, lung compliance, duration of ventilation and the levels of IL-6 in local lung tissue.
• Of particular interest is the use of hypothermia to reduce the whole-body oxygen demand in situations where even veno-venous ECMO is powerless to oxygenate the patient (Hayek et al, 2015)

Intraoperative therapeutic hypothermia

• Cardiothoracic surgery, routinely in use (including DHCA).
• Neurosurgery for aneurysm clipping: IHAST trial, 2005; no benefit ("good-grade" SAH patients)
• Vascular surgery, to protect the spinal cord during prolonged aortic cross-clamp

Suspended animation for delayed resuscitation

• In essence, this is a practice of stopping the circulation with deep hypothrmia, so as to buy time to the definitive management of the cause of the cardiac arrest.
• Animal studies have demonstrated success with up to 90 minutes of no-flow (Safar et al, 2002)
• Wu et al (2006) subjected dogs to rapid haemorrhage, and then used a 2°C saline aortic flush to achieve a brain temperature of 10°C. The dogs remained on ice for 2 hours, and were then revived on cardiopulmonary bypass.  Intact neurological outcome was achieved in 4 out of 6 dogs.

Polderman, Kees H. "Application of therapeutic hypothermia in the ICU: opportunities and pitfalls of a promising treatment modality. Part 1: Indications and evidence." Intensive care medicine 30.4 (2004): 556-575.

Seule, M., et al. "Therapeutic hypothermia reduces middle cerebral artery flow velocity in patients with severe aneurysmal subarachnoid hemorrhage." Neurocritical care 20.2 (2014): 255-262.

Gasser, Stefan, et al. "Long‐Term Hypothermia in Patients with Severe Brain Edema After Poor‐Grade Subarachnoid Hemorrhage Feasibility and Intensive Care Complications." Journal of neurosurgical anesthesiology 15.3 (2003): 240-248.

Karnatovskaia, Lioudmila V., et al. "Effect of prolonged therapeutic hypothermia on intracranial pressure, organ function, and hospital outcomes among patients with aneurysmal subarachnoid hemorrhage." Neurocritical care 21.3 (2014): 451-461.

Kim, Jong Youl, and Midori A. Yenari. "Hypothermia for treatment of stroke." Brain Circulation 1.1 (2015): 14.

Todd MM, Hindman BJ, Clarke WR, Torner JC; Intraoperative Hypothermia for Aneurysm Surgery Trial (IHAST) Investigators. Mild intraoperative hypothermia during surgery for intracranial aneurysm. N Engl J Med 2005;352:135-45.

Clark, Darren L., et al. "Comparison of 12, 24 and 48 h of systemic hypothermia on outcome after permanent focal ischemia in rat." Experimental neurology 212.2 (2008): 386-392.

Shankaran, Seetha, et al. "Whole-body hypothermia for neonates with hypoxic–ischemic encephalopathy." New England Journal of Medicine 353.15 (2005): 1574-1584.

Shankaran, Seetha, et al. "Childhood outcomes after hypothermia for neonatal encephalopathy." New England Journal of Medicine 366.22 (2012): 2085-2092.

Azzopardi, Denis, et al. "Effects of hypothermia for perinatal asphyxia on childhood outcomes." New England Journal of Medicine 371.2 (2014): 140-149.

Mourvillier, Bruno, et al. "Induced hypothermia in severe bacterial meningitis: a randomized clinical trial." JAMA 310.20 (2013): 2174-2183.

Rim, Kwang Pil, et al. "Effect of therapeutic hypothermia according to severity of sepsis in a septic rat model." Cytokine 60.3 (2012): 755-761.

Corry, Jesse J., et al. "Hypothermia for refractory status epilepticus." Neurocritical care 9.2 (2008): 189-197.

Villar, Jesus, and Arthur S. Slutsky. "Effects of induced hypothermia in patients with septic adult respiratory distress syndrome." Resuscitation 26.2 (1993): 183-192.

White, H. D., C. D. Spradley, and A. Hayek. "Therapeutic Hypothermia For Refractory Hypoxia In Acute Respiratory Distress Syndrome Undergoing Extracorporeal Membrane Oxygenation." Am J Respir Crit Care Med 191 (2015): A4570.

Zhicheng, Fang, et al. "Effect of mild hypothermia treatment on mechanical ventilation of acute respiratory distress syndrome." Modern Journal of Integrated Traditional Chinese and Western Medicine 29 (2012): 002.

Stravitz, R. Todd, et al. "Therapeutic hypothermia for acute liver failure: toward a randomized, controlled trial in patients with advanced hepatic encephalopathy." Neurocritical care 9.1 (2008): 90-96.

Jalan, Rajiv, et al. "Moderate hypothermia for uncontrolled intracranial hypertension in acute liver failure." The Lancet 354.9185 (1999): 1164-1168.

Karvellas, C., et al. "A multicenter retrospective cohort analysis of therapeutic hypothermia in acute liver failure." Critical Care 18.Suppl 1 (2014): P200.

Wu, Xianren, et al. "Induction of profound hypothermia for emergency preservation and resuscitation allows intact survival after cardiac arrest resulting from prolonged lethal hemorrhage and trauma in dogs." Circulation 113.16 (2006): 1974-1982.

College Answer

Discussion

I love it when they invite you to tabulate your answer.

Among the things worth mentioning is the horrific rate of infectious complications with the VAD (up to 50% of patients have an LVAD-associated infection) and the fact that its not merely anticoagulation, but insane anticoagulation that is required (APTT target is 150-200).

It is difficult to compare the two therapies, of course. An IABP is a supportive treatment to assist the recovering cardiac patient. The VAD is essentially a mechanical heart. There are reports of people who were awake, and asystolic, with a VAD in situ.

Beyond the tabulated answer offered here, the following chapters may be meaningful:

• Mechanical haemodynamic support strategies in brief summary
• Applications of VAD in brief summary
• Indications, contraindications and complications of IABP
• A comparison of IABP and LVAD

A slightly expanded answer, with more detail, is also offered:

Even more broadly, the chapter on mechanical haemodynamic support strategies contains a comparison of several other mechanical methods of increasing cardiac output.

To the tabulated answer presented here, I would add a reference or two to aid those (like me) who have never even seen a VAD.

UpToDate has a nice chapter on VADs.

My own barebones summary of the VAD is available here. IABP receives a slightly more elaborate treatment here.

EMCrit brandishes the expertise of somebody who works with these things, and I take that seriously.

Additionally, there is an insanely colourful brochure which has device-specific recommendations.

College Answer

Basic Life Support

a)  No signs of life equals: unresponsiveness, not breathi.ng, not moviri.g normally.
Pulse check not required to commence CPR.
b)  The term" Rescue Breathing'' has replaced Expired Air resuscitation
c)  Compression ventilation ratio 30:2 for children & adults. d)  Same ratio regardless of number of rescuers
e)  Identifying the lower halfof sternum by visualizing the centre of chest, no
. need  to measure and remeasure                                .
f)  2 initial breaths, not 5.
g)  Chest compressions at 100 Imin

Advanced Life Support

.  a)  Minimise interruptions to chest compressions
b)  If unwitnessed arrest,  VF or pulseless VT,.single shock instead of stacked shocks.

c)  If witnessed arrest-up to 3 shocks may be given at the first attempt.

d)  If monophasic defibrillator-energy level360 J
e)  Ifbiphasic defibrillator-energy level200 J
f)   If unsure of device, use 200

J. After each defibrillation, 2 min of CPR before checking.pulse.

Discussion

Since the 2006 update (and this question), there has been another guideline update.

The below answer will be based on the most recent change, and thus is going to look different to the college answer from early 2007.

In summary:

Changes to BLS:

• "signs of life" changed into "unresponsive and not breathing normally"
• If unwilling to perform conventional CPR, public is encouraged to perform compression-only CPR
• Pulse check has been downgraded - it is now only for health care professionals
• "S" has been added into DRSABC - it stands for "send for help"
• CPR now commences with chest compressions rather than rescue breaths

Changes to ALS:

• Depth of compression increased to > 5 cm
• Now, we charge the defibrillator while chest compressions continue
• No longer are "stacked shocks" recommended (outside of "special circumstances")
• When amiodarone is given after the third shock, the timing is now "at the time of CPR recommencement"
• Atropine has been removed from the guidelines
• Precordial thump is no longer recommended for VF - monitored pulseless VT only
• Hyperoxia after ROSC is emphasised as a bad thing.

The ARC has a portion of their website dedicated to the past update information of their guidelines.

Specifically, one can review a summary of BLS changes and a summary of ALS changes.

The index of the new guidelines is available from the ARC website.

College Answer

1) Dialytic techniques. 
Traditional indications used for acute renal failure, are concerns about fluid overload (actual or to facilitate nutritional support), hyperkalaemia or other uncontrolled electrolyte disorders, metabolic acidosis, hyponatraemia, uraemic symptoms or elevated urea (e.g. 30 mmoJIL).

2) Dialysis or haemoftltration (e.g. with charcoal filter) can be used to increase the clearance of toxic products from the circulation (e.g. lithium, theophylline, myoglobin). 

3) Newer related extracorporeal techniques have also been developed to support liver dysfunction. 

4) ECMO - Severe respiratory failure 

5) ECC02-Severe respiratory failure 

6) Extracorporeal ventricular assist device - Severe myocardial dysfunction 

7) Plasmapheresis/filtration-meningococal infection, Guilian Barre, ITP

Discussion

This question would benefit from a tabulated answer.

Hughes, T., et al. "Novel uses of arteriovenous extracorporeal membrane carbon dioxide removal (AV-ECCO2R)–two case studies." (2013): 169-73.

LITFL page

College Answer

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.

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.

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

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.

College Answer

Diagnosis of the underlying cause of the cardiac arrest ...
(eg drug overdose vs cerebral metastatic adencarcinoma) and any serious comorbidites that may be present.
•      Time to ROSC < 10 min
•      Bystander CPR
•      Rhythm VF better than asystole
•  Neurological status (assessed at 24-72 hours)
•   requires absence of sedation or neuromuscular blocking agents
•   Pupillary response to light – absent is poor prognostic sign
•   Best motor response – absent or extensor motor response is a poor prognostic
sign
•  Biochemical evidence of neurological damage
•   Neurone specific enolase
•   S-100 neuroprotein

•  Electrophysiological evidence of neurological damage
•   Somatosensory evoked potentials

•  Cardiac status
•   Sucessful revascularisation if STEMI is underlying cause
•   Ejection fraction on ECHO

Discussion

This question closely resembles several other questions from subsequent papers:

Question 4 from the second paper of 2013: "Describe the clinical signs and investigations available to predict poor neurological outcome in comatose survivors of cardiac arrest. Include in your answer the factors that may confound the interpretation of these signs and investigations. "

Question 14 from the first paper of 2011: "Outline the value of the following in determining prognosis for neurological recovery in an adult patient admitted to ICU, after successful cardiovascular resuscitation from an out-of-hospital cardiac arrest:  Peri-arrest data, Clinical examination, Neuro-imaging, Neurophysiology, Biomarkers"

In the answers to the above questions, elaborate tables display the information which is relevant in post-arrest prognostication, discuss its prognostic value, and digress upon the various confounding factors which might fuddle one's forecasts.

The AAN report referenced below is an excellent resource for all questions of this nature.

For data largely from the pre-hypothermia era:

Wijdicks, E. F. M., et al. "Practice Parameter: Prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence-based review) Report of the Quality Standards Subcommittee of the American Academy of Neurology."Neurology 67.2 (2006): 203-210.

For daa including post-hypothermia data:

Sandroni, Claudio, et al. "Prognostication in comatose survivors of cardiac arrest: an advisory statement from the European Resuscitation Council and the European Society of Intensive Care Medicine." Resuscitation 85.12 (2014): 1779-1789.

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

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:

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.

College Answer

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).

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.

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)

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.

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.

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.

.

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.

College Answer

Treatment

1)  Depends on cause
2)  Fluid bolus +/- inotropes – usually norad
3)  Line change if indicated
4)  Broad spectrum Gram positive and gram negative cover if sepsis is deemed likely.
+/- fungal cover
5)  PRBC as required
6)  Targeted therapy for PE /anaphylaxis

Discussion

One can easily see through the thin veneer of this burns history the college gives us. This is really just a boring question about the differential causes of shock.

Thus:

• Artifactual shock
  • Art line inappropriately zeroed
  • Wrong size NIBP cuff
• Technical error
  • CVC is extravasating vasopressors
  • Vasopressor infusion was improperly prepared
• Obstructive shock
  • Cardiac tamponade
  • Tension pneumothorax
  • Pulmonary embolism
• Distributive shock
  • Septic shock - bacterial translocation from infected burns which have been disturbed
  • Anaphylactic shock - a reaction to antibiotics or anaesthetic agents
  • Propofol-related vasoplegia
• Hypovolemic shock
  • Haemorrhage intraoperatively
  • Inadequate fluid resuscitation in theatre
• Cardiogenic shock
  • Intraoperative MI
  • Cardiodepressant effect of drugs

An approach to investigation would thus consist of the following:

• Examination of the cardiorespiratory system to exclude anahylaxis, cardiac tamponade, pneumothorax and obvious haemorrhage
• ABG to assess the severity of the metabolic acidosis
• FBC to look for haemorrhage
• Mast cell tryptase
• Septic screen
• ECG to exclude perioperative MI
• CXR to look for features of cardiac failure
• TTE to exclude tamponade and to look for features of cardiac failure or right heart dilation
• CTPA to exclude PE

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.

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.

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

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).

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.

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)

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.

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

College Answer

a) Comment  on the arterial waveform and describe your reasoning.

Arterial waveform from IABP
Early inflation of balloon (augmentation occurs before dicrotic notch) Early deflation –

b) What are the physiologic consequences of this?

Incr LV wall stress, incr myocardial 02 consumption, incr LVEDV & LVEDP, worsening of mitral regurgitation, worsening of pulmonary oedema.

Discussion

a) is straightforward. It is a pattern recognition question.

Details of IABP waveform analysis are discussed elsewhere.

b) is somewhat more tricky, but the answer can be arrived at by process of logic rather than brute memory.

The early diastolic inflation increases the afterload of the contracting ventricle, which causes it to work harder. Hence the increased O₂ consumption.LV wall stress is also increased, which decreases subendocardial perfusion. End-diastolic LV pressure is increased, which increases mitral regurgitation. The failure of systolic augmentation is more of a "loss-of-benefit" father than a "gain-of-harm".

Krishna, Murli, and Kai Zacharowski. "Principles of intra-aortic balloon pump counterpulsation." Continuing Education in Anaesthesia, Critical Care & Pain9.1 (2009): 24-28.

College Answer

a)           What types of ECMO (extracorporeal membrane oxygenation) are available and what are their indications?

Veno-Arterial: Cardiogenic shock
Veno-Venous; Respiratory failure

b)         List three (3) complications of ECMO.

Bleeding, thromboembolism, infection, trauma to vesels

Discussion

This question closely resembles Question 11 from the 2nd paper of 2010.

Instead of repeating the list of indications and complications, I will instead link to summaries of ECMO topics I had prepared earlier:

• Applications of ECMO in brief summary
• Literature regarding the use of ECMO
• Routine care of the patient on ECMO
• Troubleshooting the ECMO circuit
• Manipulation of extracorporial gas exchange

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.

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.

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. A reader has pointed out (thank you Vinay) that Mobitz Type II 2nd degree AV block is could also be listed here; because it is also irregular, but is it irregularly irregular? The reader is left to consider what they mean by this statement.

College Answer

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.

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.

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.

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

College Answer

Reasons supporting the statement

Physiological:
a) In cardiac arrest heart dilates acutely. Decompression  of the heart occurs with good compressions
b) Ventilation can lead to decreased venous return
c) Passive ventilation still occurs with compression only CPR
d)  Gasping  can  provide  adequate  ventilation  and  in  presence  of  a  partial  airway obstruction may lead to increased venous return

Logistic reasons:

a) Reluctance  to perform  mouth  to mouth  by rescuers  therefore  some  people  do not attempt CPR.
b) Interruption to compressions therefore limiting their effectiveness

c) Easier to teach compression only CPR.
d) Out of hospital arrests it will minimise time to hospital.

e) Useful particularly in the setting of a single rescuer

Studies:

Mostly observational or animal. Some RCT
No difference in outcome using compression only versus standard CPRs in most studies
Evidence of value of good compressions

Against:

Most studies are observational.
Reported survival is no better with compression only therefore why change.
Data for most studies are prior to the change in recommendation   to 30:2 RATIO Ventilation is important for many arrests EG drowning/children/in hospital arrests ARC not recommend as standard practice

Present position: 
Not standard currently. Wait further studies. It can be used if rescuer is reluctant to use mouth to mouth

Discussion

This discussion is written in late 2014, with the benefit of four ensuing years of research and policy change.

Introduction

• Compression-only CPR dispenses with recommendation to interrupt CPR for breaths.

Rationale

• In cardiac arrest, ardiac output is the rate-limiting step of oxygen delivery
• Compressions create enough passive circulation for adequate gas mixing to occur
• Breath pauses in compressions may be counterproductive (as they allow cardiac output to decrease)
• Reluctance to provide mouth-to-mouth may discourage all CPR attempts in lay rescuers

Advantages

• Easier to teach
• Easier to perform as a single rescuer
• Definitely better than no CPR
• May encourage grossed-out lay rescuers to provide some CPR, rather than no CPR
• Uninterrupted compressions may be of better quality

Disadvantages

• Supporting data is mainly from animal studies
• Positive pressure ventilation may be essential in drowning, pulmonary oedema, airway obstruction, etc.

Evidence

• In 2007, two observational studies published in Circulation (Iwami, Taku, et al. and Bohm, Katarina, et al.) did not find any survival benefit (or if you rather, confirmed equivalent efficacy) for compression-only CPR.
• A 2010 RCT from NEJM compared the two strategies and again found no mortality difference.
• A larger observational study published in 2011 found some difference, favouring conventional CPR.
• A 2014 meta-analysis confirmed that there is no difference in mortality between conventional and compression-only CPR, but admitted that the issue "is unclear for the patients with noncardiac cause of arrest and with long periods of untreated arrest."

Current status of recommendations

• The ARC still recommends a 30:2 compression-ventilation ratio. "The ARC has extensively reviewed the recently published evidence and does not consider it to be of sufficient magnitude to warrant a change in the current guidelines"
• The ARC also recommends you provide compression-only CPR if you are for some reason unwilling to provide proper CPR.

The ARC have a brief FAQ on this issue, as well as a more comprehensive advisory statement.

Iwami, Taku, et al. "Effectiveness of bystander-initiated cardiac-only resuscitation for patients with out-of-hospital cardiac arrest." Circulation 116.25 (2007): 2900-2907.

Bohm, Katarina, et al. "Survival is similar after standard treatment and chest compression only in out-of-hospital bystander cardiopulmonary resuscitation." Circulation 116.25 (2007): 2908-2912.

Svensson, Leif, et al. "Compression-only CPR or standard CPR in out-of-hospital cardiac arrest." New England Journal of Medicine 363.5 (2010): 434-442.

Ogawa, Toshio, et al. "Outcomes of chest compression only CPR versus conventional CPR conducted by lay people in patients with out of hospital cardiopulmonary arrest witnessed by bystanders: nationwide population based observational study." BMJ 342 (2011).

Yao, Lan, et al. "Compression-only cardiopulmonary resuscitation vs standard cardiopulmonary resuscitation: an updated meta-analysis of observational studies." The American journal of emergency medicine 32.6 (2014): 517-523.

College Answer

Primary problem not fixed 
•    Untreated focus of infection/ inadequate  primary source control eg pancreatic abscess, infected pseudocyst
•    New  sepstic  site  eg  central  line/  hospital  acquired  pneumonia  /cholecystitis, urinary tract

Systematic Approach 
“hypovolaemic/ obstructive/ cardiac/ distributive +/- endocrine

•    Hypovolaemia  or hidden  bleeding     eg. From surgical  site/ peptic ulcer, “third space” losses (eg ascites from peritonitis)

•    Undiagnosed  or new     “obstructive  shock” :Tension pneumothorax/  Pericardial effusion/gas trapping (auto PEEP)/ pleural effusions/ pulmonary emboli

•    Severe Intra abdominal hypertension

•    Dysrhythmia eg SVT, junctional rhythm etc
•    New myocardial ischaemia
•    New/ undiagnosed cardiac valve pathology

•    Severe adrenal/ pituitary/thyroid dysfunction.
•    Drug reaction/ anaphylaxis
•    Vitamin deficiency (B1)
•    Electrolyte abnormalities such as hypophosphataemia  and hypocalcaemia (the latter particularly with pancreatitis)

Technical

•    CVL fallen out or not in a central vein / no pressors in the infusion bag
•    Measurement   error  –  eg  arterial  line  not  zeroed/under   or  over  damped, transducer height, wrong NIBP cuff size  etc

Miscellaneous

•    Radial/ central arterial monitoring discrepancy with severe vasoconstriction
•    Upper limb vascular disease (radial arterial line) or obstruction (eg dissection or aorto-occlusive disease: femoral arterial line)
•    Anti hypertensive drugs taken as part of patients usual medications

Discussion

This question is identical to Question 17 from the second paper of 2013.

College Answer

•    Oesophageal intubation
•    Hypoxic cardiac arrest (unrelated to oesophageal intubation due to delayed or unanticipated difficulty with intubation)
•    Suxamethonium induced hyperkalemia
•    Incidental PE
•    Autonomic dysfunction from the spinal injury.
•    Tension pneumothorax
•     Anaphylaxis

Discussion

This question relies on the candidate being able to generate a list of differential causes for cardiac arrest.

A good systematic framework for this is the "Four Hs and four Ts" mnemonic:

• Hypoxia (thus, oesophageal intubation or delayed oxygenation)
• Hypovolemia (thus, cardiovascular collapse due to vasodilation by an induction agent like propofol, or due to the autonomic dysfunction of spinal cord injury)
• Hyper/hypokalemia (thus, the effects of suxamethonium)
• Hyper/hypothermia (probably irrelevant in this case)
• Tension pneumothorax (due to overvigorous bag-mask ventilation, or due to tracheobronchial disruption by violent use of the bougie)
• Tamponade (unlikely in this setting)
• Toxins (eg. anaphylactic reaction to induction agents)
• Thrombus (eg. the PE which the college for some reason offer as a valid differential)

ARC Guideline 11.2: Protocols for Advanced Life Support

College Answer

•     Capnograph to check tube position and reintubate if not in the right position
•     Urgent serum K
•      ECG
•      CTPA
•      Echo
•     CXray

Discussion

A systematic approach to this question would resemble the following:

A) confirm ETT position with capnography

B) ABG to assess adequacy of oxygenation

...and CXR to rule out pneumothorax

C) ECG to assess cardiac causes (eg. STEMI)

... and TTE to assess for presence of cardiac tamponade, and to evaluate chamber filling (thus investigating hypovolemia)

D) BSL to assess blood glucose

E) ABG to assess serum potassium levels

CTPA is mentioned because PE is considered as a differential for this cardiac arrest in the college answer to the first part of this three-part question.

ARC Guideline 11.2: Protocols for Advanced Life Support

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.

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.

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.

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.

College Answer

This is PEA
•    Tension pneumothorax
•     Tamponade
•    PE
•     Hypovolemia
•     Hypothermia

Discussion

It is difficult to justify a prolonged discussion for something like this.

The image I have provided is from LITFL, and demonstrates hypothermia with a slow junctional rhythm, but really any sort of organised electrical activity would have sufficed.

College Answer

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

Pressure gradients may be low in the presence of LV dysfunction

Discussion

The aortic valve area places this person into the "critical stenosis" category, unless they are tiny. The critical stenosis threshold is 0.5cm/m².

The impairment of LV systolic function is evident from the history of SOB, as well as from the Xray findings. This person has heart failure. The man pressure gradient for the LVOT is actually only 18mmHg, which suggests that the poor bewildered ventricle cannot compensate for the narrowed valve, and can no longer generate sufficient pressure to effectively push blood into the systemic circulation. This is what the college means when they say "gradients may be low in the presence of LV dysfunction"; the implication is that the severity of stenosis is underestimated because the LV cannot produce a sufficiently powerful ejection jet for the echosonographer to measure.

This sort of low-gradient aortic stenosis is discussed with due diligence in an article from 2011.

Awtry, Eric, and Ravin Davidoff. "Low-flow/low-gradient aortic stenosis."Circulation 124.23 (2011): e739-e741.

College Answer

Indications:

ECMO is indicated as a supportive strategy for patients (adults, children and neonates) with potentially reversible acute severe heart or lung failure with a high mortality risk despite conventional therapy.

Types: Veno-venous or veno-arterial

Evidence for use of ECMO

•    ECMO has proven benefit as a supportive strategy in neonates with cardiorespiratory failure. The International Registry reports 75% survival to discharge for neonates on ECMO.

•    Recent studies have shown a benefit for the use of ECMO in adult respiratory failure but the evidence for its use in cardiac failure is still poor. CESAR Trial from the UK compared ECMO and conventional ventilation for severe acute respiratory failure in
160 patients with improved 6 month survival in the ECMO group (63% versus 47%). The Australasian experience of the 2009 influenza A (HINI) pandemic (ANZ ECMO Influenza Investigators) reported 68 patients who received ECMO with 21% mortality. All these patients met inclusion criteria for the CESAR trial.

•    ECMO also used as a rescue strategy for cardiac arrest (ECPR).
•    Several centres world-wide have experience in retrieval and transport of patients with
ECMO.

Complications

•    Circuit related
•     Anticoagulation/Bleeding
•     Sepsis
•     Death

Summary statement

•  ECMO remains a specialised strategy
•  requiring appropriate resources and personnel.
•  However its use should be limited to centres with appropriate expertise, resources and experience and facilities for transport and retrieval should be supported.

Discussion

The question has a broad scope.

Rather than offer a summary of the applications of ECMO (which is done elsewhere) I will instead offer a summary of the literature regarding the use of ECMO

ECMO in neonates:

This has been going on since before 1986. Bartlett et al reported that after the experience, 63% of his patients were "normal or near normal".

ECMO in adults

The CESAR trial from the UK is quoted in the college answer. 63% survival at 6 months was indeed a wonderful thing.Not so for cardiac failure. In one 2004 study, only 37 out of 219 patients survived to 5 year follow-up. This does not seem to have improved with time. In general, nobody over the age of 75 survived to discharge.

ECMO as CPR has initially failed to yield satisfying results. In one study from 2003, the survival rate for patients in whom VA ECMO was started during CPR was 31%. Multi-organ system failure was the culprit there. However, a more recent observational study has produced some encouraging data.These days, it is beginnging to look more and more promising. The obvious disadvantage is that you need an ED which has a circuit cycling 24/7.

UpToDate has a nice summary chapter about ECMO.

The world is sustained by the guidelines published by ELSO (the Extracorporeal Life Support Organisation)

BARTLETT, ROBERT H., et al. "Extracorporeal membrane oxygenation (ECMO) in neonatal respiratory failure." Annals of surgery 204.3 (1986): 236-245.

Peek, Giles J., et al. "Efficacy and economic assessment of conventional ventilatory support versus extracorporeal membrane oxygenation for severe adult respiratory failure (CESAR): a multicentre randomised controlled trial." Lancet (London, England) 374.9698 (2009): 1351-1363.

Doll, Nicolas, et al. "Five-year results of 219 consecutive patients treated with extracorporeal membrane oxygenation for refractory postoperative cardiogenic shock." The Annals of thoracic surgery 77.1 (2004): 151-157.

De Waha, S., et al. "Extracorporeal membrane oxygenation in refractory cardiogenic shock-the Leipzig ECMO registry." European Heart Journal 34.suppl 1 (2013): P4025.

Chen, Yih-Sharng, et al. "Analysis and results of prolonged resuscitation in cardiac arrest patients rescued by extracorporeal membrane oxygenation." Journal of the American College of Cardiology 41.2 (2003): 197-203.

Shin, Tae Gun, et al. "Extracorporeal cardiopulmonary resuscitation in patients with inhospital cardiac arrest: A comparison with conventional cardiopulmonary resuscitation*." Critical care medicine 39.1 (2011): 1-7.

Scanziani, Margherita, Leonello Avalli, and Roberto Fumagalli. "Extracorporeal Membrane Oxygenation Strategy in Cardiac Arrest." Resuscitation. Springer Milan, 2014. 109-117.

College Answer

•    CT Advantages:
•    easy availability on an emergency basis
•     high sensitivity and specificity
•    can pick up complications involving the branches ( e.g. ischaemic gut) and extent of dissection into abdominal aorta
•    easier to monitor the patient than MRI
•    detects pericardial effusion.

Disadvantages: 
•    have to move the patient
•    iodinated contrast
•    cannot assess for AR, LV function or coronaries

•    TOE Advantages:
•    bedside test
•    can detect intimal flap, true and false lumen AR, tamponade
•    assess LV function
•    no contrast needed

Disadvantages: 
•     semi-invasive
•    may need anaesthesia/intubation
•    may cause undesirable hypertension
•    not widely available
•    special expertise required

•     MRI Advantages:
•    High sensitivity and specificity
•    MR contrast (Gadolinium) has more favourable safety profile
•    can detect AR

Disadvantages: 
•    Not readily available
•    inconvenient (patient motionless for 30 minutes)
•    access and monitoring difficult
•    limited applicability (claustrophobia, pacemakers)

•     Aortography
Advantages: 
•    will detect intimal flap, AR
•    assess LV, tamponade, blocked coronaries (important for surgery in type A
dissection)

Disadvantages: 
•    not readily available
•     invasive
•    large contrast load

Discussion

The college answer can be more easily reduced into a table:

A good article on this topic is available. It illuminates some of the finer points which the college answer has omitted:

• In high risk patients, all the modalities are more or less equal in accuracy
• In moderate risk patients, positive predicitive values are >90% for CT, MRI and TOE but only 65% for aortography
• MRI is the most sensitive of the lot - in low risk patients, it picks up close to 100% of the dissections
• All four modalities have a 85% negative predictive value.

Khan, Ijaz A., and Chandra K. Nair. "Clinical, diagnostic, and management perspectives of aortic dissection." Chest Journal 122.1 (2002): 311-328.

The canonical source for this information would have to be the most recent iteration of theACCF/AHA Guidelines for Diagnosis and Management of Patients With Thoracic Aortic Disease.

College Answer

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.

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

College Answer

Consider mixed aetiology for shock
•    Cardiogenic (cardiac history, severe sepsis, rhythm)
•    Distributive shock (sepsis)
•    Obstructive  shock (PE, tamponade)  – less likely but will probably  get mentioned.
Maybe give less marks for this than the other causes

Establishing relative contribution of each to the hypotension
•    Clinical Signs
•    Distributive;  warm  and  dilated  (if  adequate  filling),  temperature,  potential  source sepsis

•     Cardiogenic
•    LVF; tachycardia, bibasal crepitations, gallop
•    RVF; JVP, hepatomegaly, oedema
•    Escalating monitoring
•    Minimal: ECG, NIBP, SpO2
•    ABP, CVP progressing to Central Venous O2 Sat / TTE / PICCO / PAC as indicated

•    Laboratory Investigations directed at cause
•    Lactate, Troponin, ECG, CXR, Sepsis screen, UA
•    Collateral history

Interventions
•    Optimise preload
•     Cardiogenic
•    Optimize preload (low from redistribution
•    Optimize contractility
•    Rhythm; rate control / normalization (cardioversion?)
•    Inotropic support
•    Dobutamine / Milrone / Levosimenden / Adrenaline / Nor Ad (increases coronary art perfusion pressure) Caution with inodilators while still hypotensive

•     IABP
•    CPAP
•    Reversible / Specific factors

•    Exclude / treat ischaemia (heparin / angio , revascularisation etc.)
•     Distributive
•    Optimize preload
•    Vasopressor support
•     Noradrenaline
•    Adjuncts: Vasopressin / Steroid (infusion or bolus)
•    Mixed pathology issues
•    Risk of Noradrenaline  alone is an increased  afterload  with worsening  cardiogenic shock / peripheral perfusion

•    Start with inotrope and then add vasopressor; dobutamine / norad combination

•    Adrenaline may a safer choice (inotrope + vasoconstriction)

Discussion

This is a question about undifferentiated shock. The question really should read "how do you assess a patient in a non-specific shock state, and maintain their organ perfusion while looking for a cause?" It would probably be useful to mention a rapid focused bedside echo. Obvious hints in terms of fever and a history of crusty coronaries have been given. The examiners would mainly be looking for a systematic approach to diagnosis and treatment, without overcommitment to any specific diagnosis.

The following is really just a rearrangement of the college answer. A standard template of shock assessment should exist; it can be applied here with minimal variation.

Immediate management:

• Attention to airway and breathing
• Establish secure venous access
• Introduce invasive monitoring tools - arterial/central line

Rapid assessment:

• Focused history to differentiate a source of sepsis, and to assess the contribution of cardiac ischaemia
• Physical examination to assess adequacy of peripheral perfusion
• ABG, ECG, CXR, cardiac enzymes, blood and urine cultures
• Rapid bedside TTE to rule out cardiac tamponade and to assess contractility
• Fluid challenge 20-40ml/kg of crystalloid, to assess fluid responsiveness - plus/minus dynamic bedside manoeuvres
• Consider advanced hemodynamic monitoring, eg. SvO2 PAC or PiCCO

Decisive management for this mixed shock state:

• Control sepsis
  • Broad spectrum antibiotics, given early
  • Consider "stress dose" steroids
• Optimise preload
  • Fluid boluses to continue, as permitted by measures of fluid responsiveness
• Optimise afterload
  • Maintain organ perfusion and coronary filling by maintaining a MAP > 65 and a reasonable diastolic pressure, using vasopressors such as noradrenaline and vasopressin
• Optimise rhythm
  • Consider early DC cardioversion if the rhythm is atrial fibrillation, to recover the "atrial kick"
• Optimise contractility
  • If there is concern regarding contractility, consider inotropes eg. dobutamine milrinone or levosimendan
• Use adjuncts to resuscitation
  • Consider IV thiamine, perticularly if there is lactic acidosis
• Reverse any reversible factors
  • Early angiography or thrombolysis
  • Surgical source control for septic foci

Jones, Alan E., et al. "Randomized, controlled trial of immediate versus delayed goal-directed ultrasound to identify the cause of nontraumatic hypotension in emergency department patients*." Critical care medicine 32.8 (2004): 1703-1708.

College Answer

a. Peri-arrest data:

Initial rhythm, bystander CPR, time to ROSC intuitively helpful and commonly considered, but have not been shown to correlate  with individual  outcome.   Co-morbidities  and pre- arrest performance status may determine overall survival.

b. Clinical Examination:

Unreliable  and of no predictive  value before 24 hours, clinical assessment  at ≥ 72 hours conventional
•    Appropriate     pre-conditions:    absence     of    sedation/relaxants,     adequate     CVS
resuscitation, normothermia, corrected biochemistry etc.
•    All data pertains to studies before the common use of therapeutic hypothermia, and the effect of this intervention  unknown.   May need longer than 72 hours to obtain reliable data from CNS examination in patients treated with induced hypothermia
•    GCS < 4, absent corneal response, absent pupillary response to light indicative of poor prognosis
•    myoclonus not sufficiently predictive to be reliable in isolation but myoclonic status epilepticus is a poor prognostic feature

c. Neuro-imaging:

•    CT may be performed early to exclude a CNS cause of arrest
•    CT  signs  of  poor  prognosis   include  qualitative   assessment,   and  quantitative assessment of white matter Houndsfield unit ratio.  Optimum timing not clear
•    MRI demonstration  of diffuse cortical lesions  or sub-cortical  lesions  is associated with poor outcome

d. Neurophysiology:

•    No neurophysiology study reliably predicts outcome at < 24 hours
•    EEG findings  of: diffuse suppression  to < 20 mV, burst suppression,  generalised seizures, diffuse periodic complexes indicate poor prognosis
•    EEG  shown  to  have  increased  false  positive  prediction  for  poor  outcome  after induced hypothermia
•    SSEP:  bilaterally  absent  cortical  responses  to  median  nerve  stimulation  seems highly accurate (0% False Positive Rate), not studied after induced hypothermia

e. Biomarkers:

•    Neurone specific enolase (NSE) most studied, some studies show 0% FPR for poor outcome, but cut-off levels vary, studies small

Discussion

With the exception of the "peri-arrest data" section, this question closely resembles Question 4 from the second paper of 2013.

The table from Question 4 is thus reproduced below, with the peri-arrest data section added, sans the confounding factors column. The whole peri-arrest data issue is better discussed in the chapter on prognostication of neurological recovery following a cardiac arrest.

Peri-arrest data:

• VF arrest has the best prognosis: 40% survive until discharge from hospital.
• PEA has a poor prognosis. 11% survive until discharge from hospital.
• Asystole has the poorest prognosis. 2% survive until discharge from hospital.
• CPR lasting >20 minutes has a poorer prognosis
• A witnessed arrest followed by bystander CPR has a better prognosis
• Increasing age of the patient and presence of comorbidities have a negative influence on prognosis.

The key features of the college answer one would be wise to remember include the following:

• Arrest characteristics (eg. time to ROSC) do not correlate with individual outcome.
• Clinical findings are unreliable within the first 24 hours.

Engdahl, Johan, et al. "Can we define patients with no and those with some chance of survival when found in asystole out of hospital?." The American journal of cardiology 86.6 (2000): 610-614.

Bunch, T. Jared, et al. "Outcomes and in-hospital treatment of out-of-hospital cardiac arrest patients resuscitated from ventricular fibrillation by early defibrillation." Mayo Clinic Proceedings. Vol. 79. No. 5. Elsevier, 2004.

Levine, Robert L., Marvin A. Wayne, and Charles C. Miller. "End-tidal carbon dioxide and outcome of out-of-hospital cardiac arrest." New England Journal of Medicine 337.5 (1997): 301-306.

Rea, Thomas D., et al. "Temporal Trends in Sudden Cardiac Arrest A 25-Year Emergency Medical Services Perspective." Circulation 107.22 (2003): 2780-2785.

Carew, Heather T., Weiya Zhang, and Thomas D. Rea. "Chronic health conditions and survival after out-of-hospital ventricular fibrillation cardiac arrest." Heart 93.6 (2007): 728-731.

Goldberger, Zachary D., et al. "Duration of resuscitation efforts and survival after in-hospital cardiac arrest: an observational study." The Lancet (2012).

Wijdicks, E. F. M., et al. "Practice Parameter: Prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence-based review) Report of the Quality Standards Subcommittee of the American Academy of Neurology."Neurology 67.2 (2006): 203-210.

Rogove, Herbert J., et al. "Old age does not negate good cerebral outcome after cardiopulmonary resuscitation: analyses from the brain resuscitation clinical trials."Critical care medicine 23.1 (1995): 18-25.

Levy, David E., et al. "Predicting outcome from hypoxic-ischemic coma." Jama253.10 (1985): 1420-1426.

Zandbergen, E. G. J., et al. "Prediction of poor outcome within the first 3 days of postanoxic coma." Neurology 66.1 (2006): 62-68.

Tapia, F. J., et al. "Neuron-specific enolase is produced by neuroendocrine tumours." The Lancet 317.8224 (1981): 808-811.

Torbey, Michel T., et al. "Quantitative analysis of the loss of distinction between gray and white matter in comatose patients after cardiac arrest." Stroke 31.9 (2000): 2163-2167.

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.

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.

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.

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.

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.

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.

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

... 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.

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.

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.

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

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.

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

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.

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

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)

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.

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:

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.

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.

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:

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.

College Answer

a) Concepts behind intra-aortic balloon counterpulsation (IABCP)

Classic concept of intra-aortic balloon counter pulsation involves inflation in synchrony with aortic valve closure at the onset of isovolumic diastole and the appearance of the dicrotic notch

This displaces blood comparable to the balloons volume into the peripheral circulation during diastole

To accomplish further unloading and to prevent interference with left ventricular ejection, balloon deflation starts prior to opening of the aortic valve and the onset of LV ejection

The classic response is thus is a lowering of the systolic pressure and augmentation of the diastolic pressure

The main benefits are a decrease in afterload and increased coronary artery perfusion with secondary improvements in hemodynamics

b)

A = Assisted systole

B = Diastolic augmentation

C = Unassisted systole

D = Unassisted aortic end-diastolic pressure

E = Dicrotic notch

F = Assisted aortic end-diastolic pressure

• Methods

• Image intensifier screening during insertion

• Length of catheter inserted should be distance from insertion point to umbilicus, plus distance from umbilicus to sternal angle

• Position on TOE should be 2 cm distal to L subclavian

• CXR to confirm position - Just above the level of the left main bronchus or 2nd or 3rd intercostal space

e) Methods can be used to trigger the IABCP

• ECG

• BP

• Pacing

e) Problem

• Balloon rupture should be suspected. IABCP catheter should be disconnected from console. It should then be removed (and replaced if it is still needed).

Discussion

IABP is discussed in greater detail elsewhere.

• Briefly, outline the concepts behind intra-aortic balloon counterpulsation (IABCP)
  • The balloon inflates in diastole, displacing aortic blood both into the systemic circulation and into the coronary arteris.
  • The ballon deflates before systole, decreasing aortic pressure
  • Diastolic augmentation thus improves coronary blood flow
  • Systolic augmentation this decreases afterload and LV workload

• Identify the points labelled A-F on the following intra-aortic balloon pump pressure-time trace?

• What methods can be used to check that the IABCP catheter is in the correct position, both during and after insertion?
  • Measurement of the length of insertion: from insertion point to umbilicus, plus distance from umbilicus to sternal angle
  • Fluoroscopy-guided insertion
  • TOE
  • CXR

Alternatively (and dangerously) one can retract the IABP until it no longer causes diminished left subclavian bloodflow.

• What methods can be used to trigger the IABCP?
  • Blood pressure
  • ECG
  • Pacemaker

• Blood is seen in the tubing connected to the gas lumen of the IABCP catheter. What problem do you suspect, and what action should be taken?
  • This means the balloon has ruptured. The IABP tends to stop pumping on its own when this happens - loss of helium pressure triggers the off-valve. The next step is to remove it.

Insertion of the IABP: a manual by MAQUET

Moulopoulos, Spyridon D., Stephen Topaz, and Willem J. Kolff. "Diastolic balloon pumping (with carbon dioxide) in the aorta—a mechanical assistance to the failing circulation." American heart journal 63.5 (1962): 669-675.

SOROFF, HARRY S., et al. "Assisted circulation II. Effects of counterpulsation on left ventricular oxygen consumption and hemodynamics." Circulation 27.4 (1963): 722-731.

Hanlon-Pena, Patricia M., and Susan J. Quaal. "Intra-aortic balloon pump timing: review of evidence supporting current practice." American Journal of Critical Care 20.4 (2011): 323-334.

Krishna, Murli, and Kai Zacharowski. "Principles of intra-aortic balloon pump counterpulsation." Continuing Education in Anaesthesia, Critical Care & Pain9.1 (2009): 24-28.

Nanas, J. N., and S. D. Moulopoulos. "Counterpulsation: historical background, technical improvements, hemodynamic and metabolic effects." Cardiology 84.3 (1994): 156-167.

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.  

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

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.

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.

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.

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.

College Answer

d) Abnormalities 
• Early balloon inflation 
• Early balloon deflation

Discussion

Unfortunately, the college has removed the images, so nobody can recognise the patterns.

The depicted pattern in (d) was probably an IABP waveform where the balloon inflated and deflated too early.

The IABP chapter has some exhaustingly detailed discussions about what this means for your myocardial workload.

As a reminder, that waveform looks like this:

Directly relevant:

Maquet educational materails: IABP timing pocket reference guide

Mildly interesting:

Papaioannou, Theodoros G., and Christodoulos Stefanadis. "Basic principles of the intraaortic balloon pump and mechanisms affecting its performance."ASAIO journal 51.3 (2005): 296-300.

College Answer

Positive End Expiratory Pressure

This can either be delivered invasively or non-invasively. By increasing the positive pressure within the thoracic cavity, venous return to the heart is reduced thereby reducing cardiac pre load to facilitate movement back to the optimal point on the Starling Curve. Also reduces afterload by reducing pressure gradient across the myocardial (left ventricular) wall. Also reduces work of breathing (reduces cardiac work) and improves PaO2 (O2 delivery to coronary blood flow).

Intra Aortic Balloon Pump

The inflation of the intra aortic balloon pump at the time of diastole increases coronary perfusion to increase cardiac contractility and reduces the after load at the commencement of systole as the balloon deflates

Pacing

Emergency transcutaneous, temporary transvenous and permanent multi-chamber pacing. Improves cardiac output by optimising the heart rate and/or synchronising A-V conduction optimising “atrial kick”. Increasing the heart rate to normal in profound bradycardia as CO = SV x HR. Overdrive pacing in tachyarrhythmias to re-establish normal conduction and then slow the heart improves cardiac output by increased ventricular filling and improved coronary artery perfusion in diastole.

Ventricular Assist Devices

This provides either a continuous or pulsatile pumping of blood from the left ventricle directly into the aorta (LVAD) or from right atrium or right ventricle directly to pulmonary artery (RVAD) or functions as both (BIVAD).

Decreases workload of the heart whilst maintaining adequate flow and blood pressure. Indicated if potentially reversible myocardial stunning or as a bridge to transplantation or for support during high-risk revascularisation procedures. In this patient as a bridge to transplantation may allow management as outpatient. Requires cardiac surgical expertise for insertion and so not available in all centres.

Veno-Arterial Extra Corporeal Membrane Oxygenation

Venous blood is extracted, oxygenated externally and then pumped and returned to the arterial system providing both oxygenation and circulation. Decreases workload of heart and lungs whilst maintaining flow, blood pressure and oxygenation. 
Requires expertise for insertion and maintenance and not available in all ICUs.

Discussion

The question specifically asks about mechanical strategies. Put away your levosimendan. Thus, apart from the "mechanical" support of positive pressure ventilation, one is left with pacing wires, the IABP, the LVAD, and VA ECMO.T hese are rather specialised devices, but thankfully Cove and MacLaren summarised the issues for us in their 2010 article which is brilliantly revelant to this question.

This article formed the core of my own tabulated summary. The abovementioned strategies are reviewed in terms of their advantages and limitations in a summary chapter from the Required Reading section (Mechanical haemodynamic support strategies in brief summary).

The table is presented below to simplify revision:

Less relevant local links include the following:

• Mechanical Haemodynamic Support -an entire section dedicated to this topic, but excessively verbose and unsuited to exam revision
• Effects of positive pressure ventilation of cardiovascular physiology
• Haemodynamic changes during a mechanical breath

Cove, Matthew E., and Graeme MacLaren. "Clinical review: mechanical circulatory support for cardiogenic shock complicating acute myocardial infarction." Crit Care 14.5 (2010): 235.

Boehmer, John P., and Eric Popjes. "Cardiac failure: mechanical support strategies." Critical care medicine 34.9 (2006): S268-S277.

Cooper, David S., et al. "Cardiac extracorporeal life support: state of the art in 2007." Cardiology in the young 17.S4 (2007): 104-115.

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:

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. 

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

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

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

College Answer

Observations and Investigations:

Clinical Signs:

• Absent brain stem reflexes.
• Myoclonic status epilepticus within the first 24 hours.

• (Generalised and repetitive myoclonus is strongly associated with poor outcome, with a reported false positive rate of 0%. Conversely, single seizures and sporadic myoclonus, do not accurately predict poor outcome.)

• Absence of pupillary responses – within days 1 to 3 after CPR.
• Absent corneal responses - within days 1 to 3 after CPR.
• Absent or extensor motor responses – after 3 days post CPR.

Electrophysiological:

EEG patterns of generalised suppression, burst suppression, or generalised periodic complexes are strongly associated with poor outcome, but the prognostic accuracy is not considered as high as SSEP.

Bilateral absence of N20 component of SSEP with median nerve stimulation within 1-3 days post CPR is strongly associated with poor outcome.

Biochemical:

Serum neuron-specific enolase levels > 33mg/L at days 1-3 strongly associated with poor outcome.

(S100, CSF CKBB are not considered accurate enough for prognostication.)

Radiological:

Imaging may reveal catastrophic intracerebral cause for the arrest.

(Diffuse swelling on CT scan is common, but predictive power not known, role of MRI/PET also unclear.)

Confounding Factors:

Induced Hypothermia – majority of studies carried out before induced hypothermia widely used. Evidence that cooling may alter interpretation of these results, but to what extent remains unclear

Time of assessment: Period of at least 72 hours post CPR recommended. Unclear how hypothermia effects this.

CT scan done too early may not show changes

Sedatives / neuro- muscular blockers 
Metabolic derangements 
Presence of shock

Organ failure

Role of “self-fulfilling prophecy” in interpreting studies

Salient points

• Absent brainstem reflexes
• Extensor motor response
• EEG
• Myoclonic status epilepticus
• SSEP
• Neuron-specific enolase
• CT brain (oedema)

Discussion

This question would benefit from a tabulated answer.