Printable list of all cardiothoracic SAQs

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Question 5 - 2000, Paper 1

List the theoretical advantages and disadvantages of coronary bypass grafting with and without cardiopulmonary bypass

College Answer

Coronary artery bypass grafting off bypass is now widely performed. There are numerous techniques for getting access to the grafts and heart (eg. limited thoracotomy, video assisted).

(a) Theoretical advantages include: 
•  Avoidance of  the effects of extracorporeal circulation including .. coagulation/kalikrein activation, microembolus of air and platelet clumps to cerebral circulation 
•  Avoidance of aortic cannulation with attendant risks of  arterial  embolisation of  air or atheroma 
•    Avoidance of atrial cannulation with attendant risk of atrial injury respectively 
•    Avoidance of the effects of cardioplegia including K load. fluid load, coronary air embolus 
•    Avoidance  of  risks  of  aortic  cross  clamping  including  atheroembolism. myocardial ischaemia
•  Decreased costs (less equipment, less staff)

(b) Theoretical disadvantages include: 
•  Potential for  myocardial ischaemia without the  protection of  cold cardioplegia during grafting. 
•  Unfavorable operating conditions with a beating heart increasing the risk of anastamotic bleeding, suboptimal revascularisation and myocardial ischaemia

[Information on graft patency, morbidity, mortality and quality of life from proper trials is not yet available]


Current status and future directions of minimally invasive cardiac surgery. Current Opinion in Cardiology 1999,14(5); 419·


Minimally invasive coronary bypass: a dissenting opinion. Circulation 98(6);495-7

Discussion

There is little to add to the college answer. It is rare for references to be included with it, and I will link to these papers below. The second one is available for free as full text, from Circulation.

I will quote from it:

"... just because something can be done by some surgeons does not mean that it should be done by all surgeons. "

A comparison of conventional and off-bypass CABG appears as a brief summary in the Required reading section. Additionally, LITFL have this article ("Cardiothoracic Surgery Literature Summaries") where two of the more influential on-vs-off-pump trials are thoroughly dissected. Put simply, the advantages and disadvantages are as follows:

Advantages of off-pump CABG:

  • Protection from circuit-related complications:
  • Avoidance of aortic cannulation
  • Avoidance of atrial cannulation
  • Avoidance of the effects of cardioplegia
  • Avoidance  of  risks  of  aortic  cross  clamping
  • Decreased costs (less equipment, less staff)
  • A meta-analysis in 2012 concluded that off-pump bypass "reduces the incidence of post-operative stroke by 30% and has no notable effect on mortality or myocardial infarction"

Disadvantages of off-pump CABG:

  • Potential for  myocardial ischaemia without the  protection of  cold cardioplegia during grafting.
  • Unfavorable operating conditions with a beating heart increasing the risk of anastamotic bleeding, suboptimal revascularisation and myocardial ischaemia
  • A recent meta-analysis has demonstrated that with off-pump grafts, there is an increased risk of graft occlusion with all grafts except LIMA and radial artery grafts.

References

These are the references used by the college in their answer:

Goldstein, Daniel J., and Mehmet C. Oz. "Current status and future directions of minimally invasive cardiac surgery." Current opinion in cardiology 14.5 (1999): 419.

Bonchek, Lawrence I., and Daniel J. Ullyot. "Minimally Invasive Coronary Bypass A Dissenting Opinion." Circulation 98.6 (1998): 495-497.

These are the subsequent studies which answer this question:

Khan, Natasha E., et al. "A randomized comparison of off-pump and on-pump multivessel coronary-artery bypass surgery." New England Journal of Medicine350.1 (2004): 21-28.

Afilalo, Jonathan, et al. "Off-pump vs. on-pump coronary artery bypass surgery: an updated meta-analysis and meta-regression of randomized trials." European heart journal 33.10 (2012): 1257-1267.

Zhang, Busheng, et al. "Comparison of Graft Patency Between Off-Pump and On-Pump Coronary Artery Bypass Grafting: An Updated Meta-Analysis." The Annals of thoracic surgery 97.4 (2014): 1335-1341.

Question 12 - 2000, Paper 1

Outline your postoperative management plan for a patient  who has just -returned from the operating theatre after undergoing bilateral thoracoscopic lung reduction for emphysema

College Answer

Although  not  stated  in  the  question,  it  was  expected  that  the  plan  would  only  cover  the immediate  postoperative  period. Success  of  the operation  is dependent  on  patient  selection, preparation surgical skill and ICU care.

It should include: 
(a) Airway/Breathing- the patient should be extubated as soon as possible to avoid the risks of barotrauma and nosocomial pneumonia.This is facilitated by a light general anaesthetic and thoracic epidural analgesia.                                    · 
(b) Circulation·arterial line for BP monitoring  and sampling. BP should be maintained with blood  transfusion  and  low  dose  vasoconstrictor.  Excessive  amounts  of  crystalloid  are avoided.  Maintenance fluids (eg. lml/kglhour of 5D +KCL +MgS04).                                                                                       · 
. (c) Analgesia- thoracic epidural. If ineffective PCA & regular paracetamol. (d) Drains underwater usually no suction. 
{e) Early mobilisation into chair. 
(f)  Antibiotics as per preop sputum culture or 24 hours IV cephalothin.

(g) Bronchodilators as indicated. 
(b) Investigations- CXR to check lung expansion. 
(i)  ABG to check for hypercarbia.

Discussion

This question is really about managing an intubated patient with severe COPD, who happens to have recently had major thoracic surgery.

One can approach this systematically

  • Airway
  • Breathing/ventilation
    • monitor ABGs for hypercapnea
    • Aim for SpO2 88-90% if the patient is a CO2 retainer
    • Avoid narcotics as they depress respiratory drive; use epidural anaesthesia if possible
    • ventilated with an I:E ratio with a long E phase, to permit CO2 clearance
    • Minimise PEEP and peak airway pressures to avoid barotrauma (lung capacity has been reduced by lung reduction surgery; tidal volumes should be kept low)
    • Observe chest drains for air leak
  • Circulation
    • Maintain normovolaemia, but avoid large volumes of fluid, as this may result in pulmonary oedema and force you to ventilate the patient at undesirably high pressures
  • Progress to sitting in a chair as soon as practical
  • Mobilise early, and encourage vigorous physiotherapy (chest physiotherapy can begin as soon as 1 hour post operatively)
  • Adequate analgesia is the key to success

Care for the patient recovering from lung reduction surgery is discussed with more detail in the "Required Reading" section.

References

This procedure is not frequently seen these days; to learn more about it I recommend a good review article from the ERJ:

Russi, E. W., U. Stammberger, and W. Weder. "Lung volume reduction surgery for emphysema." European Respiratory Journal 10.1 (1997): 208-218.

The anaesthetic perioperative management of these patients is deteailed here:

Hillier, J., and C. Gillbe. "Anaesthesia for lung volume reduction surgery."Anaesthesia 58.12 (2003): 1210-1219.

Question 11 - 2001, Paper 1

Following off-bypass coronary artery bypass grafting a patient returns to the ICU.  Soon after arrival   he  becomes  bradycardic   and  profoundly  hypotensive,  unresponsive  to  a  fluid challenge.  What may cause this and what is the most appropriate course of action?

College Answer

Potential causes of this scenario include:

-     pericardial tamponade

-     graft occlusion by clot/spasm/kinking/stitch

-     complete heart block

-     non-specific events: eg disconnection leading to severe hypoxia/bradycardia and myocardial ischaemia, pulmonary embolus

The most appropriate course of action is:

-     bag the patient with 100%

-     administer immediately available inotrope (aramine or adrenaline)

-     commence ECM if pulseless

-     obtain and use chest opening pack

-     internal cardiac massage

-     if the problem is not immediately amenable to therapy eg relief of tamponade,   organise cardiopulmonary bypass to rest the heart and allow exploration of the grafts.

Discussion

There is little to add to the college answer.

One would begin to manage such a patient in a similar algorithmic manner which is associated with any arrest situation. The major differences lie in the potential for open cardiac massage and return to cardiopulmonary bypass.

A systematic approach would resemble this:

  • A - ensure ETT is patent and in position
  • B - bag the patient with 100% FiO2
  • C - commence infusion of inotropes; given that the patient is bradycardic I marvel at the college's choice of metaraminol as a potential rescue agent. Adrenaline lives in the same trolley, people. Commence CPR if there is no response to this. 
    • As the drugs are being prepared for infusion, one should strongly consider pacing the patient through the epicardial leads if these are available. It is again bizarre that the college do not mention this in their model answer. A sensible rate would be about 80-100.
  • D - paralyse the patient to simplify resuscitation and decrease chest wall resistance to ventilation;
  • E - ensure the patient is not profoundly hypothermic (that could explain the bradycardia and hypotension
  • Think about the 4 Hs and 4 Ts:
    • Hypoxia could have caused the bradycardia; ensure the patient is well oxygenated by manual bag-mask ventilation
    • Electrolyte derangement can be easily excluded with ABG, and managed as apropriate (depending on the disturbance)
    • Hypothermia can be addressed by use of external warming devices, warmed fluids, or a warmed dialysis/ECMO circuit
    • Hypovolemia can be addessed with vigorous fluid resuscitation
    • Myocardial infarction due to graft failure needs to be excluded, and an ECG needs to be performed as soon as is practical
    • Tension pneumothorax needs to be excluded by careful physical examination and inspection of the chest drains
    • Cardiac tamponade may be the cause, and can be excluded rapidly with bedside TTE
    • Check whether any antiarrhytmics were accidentally given (eg. amiodarone given too fast)
  • If no immediately reversible cause is found and the patient is not responding to an infusion of adrenaline, surgeons should be contacted and a return to theatre should be organised. While waiting for this, cardiopulmonary bypass should recommence.

References

Akinnusi, Morohunfolu E., Lilibeth A. Pineda, and Ali A. El Solh. "Effect of obesity on intensive care morbidity and mortality: A meta-analysis*." Critical care medicine 36.1 (2008): 151-158.

 

Marik, Paul, and Joseph Varon. "The obese patient in the ICU." CHEST Journal113.2 (1998): 492-498.

 

Ling, Pei-Ra. "Obesity Paradoxes—Further Research Is Needed!*." Critical care medicine 41.1 (2013): 368-369.

Question 8 - 2002, Paper 1

Outline the aetiology, clinical manifestations and treatment of phrenic nerve palsy after cardiac surgery.

College Answer

Aetiology: potential contributing factors include difficult dissection, internal mammary artery dissection, excessive retraction (sternum/pericardium), use of topical cooling (eg. slush) and haematoma from internal jugular venipuncture

Clinical manifestations: Can be unilateral (esp. left) or less common bilateral. Usually manifest by respiratory difficulties.  Patient may not be able to be weaned from mechanical ventilation, or may have  significant  post-operative  requirements  for respiratory  support.                                  Persistent  collapse  and/or pneumonia may develop.   Clinical examination may reveal decreased movement on affected side, decreased breath sounds (± signs of collapse/consolidation), significant dullness to percussion, with absence of normal tidal percussion.   Radiological investigations confirm elevated hemidiaphragm (&/or collapse/consolidation), which moves paradoxically on sniff test (fluoroscopy).

Treatment: usually expectant for underlying lesion.   Supportive care plus specific treatment of complications (eg. aggressive physiotherapy, non-invasive ventilatory support).

Discussion

There are a few ways to damage the phrenic nerve during cardiac surgery:

  • Sever it completely (hence difficult dissection makes it more likely)
  • Put pressure on it accidentally (hence excessive retraction is to blame)
  • Topical cardiac cooling (the icy slush causes a neuropraxia)
  • IJ haematoma

The clinical manifestations will be unequal chest expansion, atelectasis on the affected side, an elevated hemidiaphragm on CXR, and difficult ventilation/weaning.

With inspiration, the paralysed diaphragm paradoxically retracts upwards.

Management is supportive. One has no choice but to continue ventilator support until it resolves. Diaphragmatic plication may be considered in persisting symptomatic diaphragmatic palsy.

References

Wilcox, Pearce, et al. "Phrenic nerve function and its relationship to atelectasis after coronary artery bypass surgery." CHEST Journal 93.4 (1988): 693-698.

Question 8 - 2003, Paper 1

List the causes of a sudden acute fall in systolic blood pressure to 50 mmHg one hour after an uneventful  coronary artery bypass operation.  Outline  your principles of management for each cause.

College Answer

Potential causes are many, and more than one may co-exist.  Could be divided according to causes of shock: artefactual, hypovolaemic, obstructive, cardiogenic, and distributive (with principles of management in brackets). Simple manoeuvres should be considered early (eg. raise legs to autotransfuse).

Artefactual: transducer error (check transducer: zero, level, calibration), damping of waveform
(assess damping coefficient), malfunction of NIBP.

Hypovolaemic: blood loss (observe drain tubes, CXR, dressings; give fluid ± blood products), massive diuresis (observe urine output; give fluid).

Obstructive: pericardial tamponade (observe chest drainage ± clots, high filling pressures: may need to open chest), tension pneumothorax (observe expanded hemi-thorax, listen to chest: check existing chest drains, may need needle thoracostomy and replace/insert ICC), elevated intrathoracic pressure (gas trapping: disconnect from ventilator; shivering/valsalva/fighting: sedate ± paralyse; ensure ETT not blocked).

Myocardial:  decreased contractility (ischaemia due to blockage/kinking/spasm: treat with GTN, inotropes &/or short term vasoconstrictor ± fix technical problem; sudden removal of inotropic drug: restart drug) or rhythm disturbance on monitor/ECG (brady-asystole: pace ± atropine/isopenaline/adrenaline; SVT: eg. K/adenosine; AF eg. K/Mg/amiodarone, VT eg. K/Mg/lignocaine).

Distributive: anaphylaxis (rash/bronchospasm: remove hapten, adrenaline, fluids); vasodilator excess (recent boluses/infusion too high: stop responsible drug, ± titrated dose vasoconstrictor); sympathetic block (recent bolus epidural LA: titrated dose vasoconstrictor).

Discussion

This question is a favourite. It has been repeated no less than three times.

Other incarnations of it are:

Approach to the haemodynamically unstable cardiac surgical patient  and causes of shock in the cardiac surgical patient are available in the shape of brief point-form summaries.
I reproduce some of this material here, to simplify revision:

Causes of Shock in the Post-Bypass Patient
Type of shock Cause Diagnostic strategy Management
Artifact of measurement Arterial blood pressure measurement is inaccurate Compare with non-invasive measurement and physical examination
  • Re-zero and recalibrate the arterial line
  • Resite arterial line or change the transducer
Cardiogenic Post-operative stunning of the myocardium TTE, ECG, cardiac output measurement by PiCCO or PA catheter
  • Fluid resuscitation
  • Commence inotrope infusion
  • Correct rhythm if in AF
  • Return to theatre, recommence cardiopulmonary bypass
Myocardial infarction TTE, ECG, cardiac enzymes
  • Consider IABP
  • Thrombolysis or anticoagulation likely contraindicated given recent cardiac surgery
  • Return to theatre
Obstructive Cardiac tamponade TTE, CVP trace
  • Fluid resuscitation
  • Emergency pericardiocentesis
  • Return to theatre
Massive pulmonary embolism TTE, CVP trace, ECG, CTPA
  • Consider emergency embolectomy
  • Thrombolysis or anticoagulation likely contraindicated given recent cardiac surgery
Tension pneumothorax

Physical examination;

CXR

  • Emergency decompression
  • Chest drain
Neurogenic Infarction of spinal cord due to ischaemia or embolic events Physical examination features, CT, MRI
  • Thrombolysis or anticoagulation likely contraindicated given recent cardiac surgery
  • commence vasopressor infusion
Hypovolemic Blood loss post operatively Examination of drains, FBC,
  • Replace blood products and red cells
  • Fluid resusiciation
  • Maintain normal acid-base balance and normothermia
  • return to theatre
Massive diuresis Observation of fluid balance charts
  • Replace lost fluid volume
  • Rewarm patient to normal temperature
Distributive Vasoplegia SVRI measurements by PiCCO
  • commence vasopressor infusion; consider vasopressin or methylene blue
Anaphylaxis Physical examination findings suggestive of angioedema
  • Adrenaline IM or as infusion
  • Withdrawal of the trigger substance
  • Corticosteroids and antihistamines

References

Question 3 - 2004, Paper 2

Outline your approach to the evaluation and treatment of a cardiac surgical patient who returns to your Intensive Care Unit with temporary atrial epicardial pacing wires and problems with atrial pacing.

College Answer

Evaluation of problems with atrial pacing requires careful evaluation of the rhythm strip (and/or ECG), and systematic examination of pacing leads (from patient to pacemaker, including ensuring atrial wires are connected to atrial port of pacemaker). Specific problems to be excluded include:
·           excessive sensitivity to electrical activity (resulting in inappropriate/excessive inhibition of atrial pacing). Excessive sensitivity is usually due to settings on the pacemaker, and may be confused with return of spontaneous atrial activity (including AF). Treatment is to increase the absolute value of sensitivity (making it harder to inhibit).
·           relative insensitivity to electrical activity (resulting in atrial pacing when not appropriate). Insensitivity is due to the specific setting of sensitivity (including deliberate setting of AOO mode). Treatment is to decrease absolute value of sensitivity (making it easier to inhibit).
·           inability to capture (resulting in no atrial activation). Inability to capture is usually due to some specific mechanical problem including: wires no longer connected to atrium [potentially activating ventricle, diaphragm or nothing at all], wires not tightly connected to cable, cable not connected to correct port, or setting of output too low relative to requirements. Treatment is to tighten and confirm all external connections, then increase output if possible. Bipolar leads may be tried in reverse positions, or attempt to convert to unipolar pacing. Positioning of patient may also facilitate capture (short term solution). Other specific treatments to be considered include treatment of underlying arrhythmias/bradycardias with appropriate medications.

Discussion

It is difficult to say precisely what ones management would be if the college doesn't specify what "problems" there are with the atrial pacing.

A guide to troubleshooting the pacemaker circuit is offered elsewhere.

In brief:

1) Start with the box.

  • Is it even on?
  • Is the battery dying?
  • Are the wires detached from the pulse generator?
  • Are the leads connected?
  • Was the temporary pacing wire pulled out in course of a recent pressure area care?
  • Are the epicardial electrodes displaced? Is the transvenous electrode tip wiggling uselessly in the venticle?
  • Is there any weird twitching in the chest wall muscles of the patient? Is the ventilator demonstrating some bizarre sawtooth pattern, suggesting that the diaphragm is being paced?

Ok, so the hardware is intact. if there is output failure, its not because of the leads or the battery. Move on to the software.

2) Check the sensor threshold.

  • Put the pacemaker in a VVI, AAI or DDD mode.
  • Change the rate to one which is much lower than the patients native rate.
  • Observe the sense indicator.
  • Keep increasing the sensitivity.
  • Find the sensitivity maximum - where the pacemaker is picking up NONE of the endogenous electrical activity.
  • Now keep decreasing the sensitivity.
  • Find the sensor threshold - where the sensor picks up EVERY endogenous electical event (i.e. no pacing spikes are visible)

Crank the sensitivity setting up to double the sensor threshold.

This should take care of oversensing as a cause of pacing failure.

3) Now, check the output threshold.

  • Set the pacemaker well above the native rate.
  • Start reducing the output.
  • Find the capture threshold - where a QRS complex no longer follows each pacing spike.

Crank the output to double the capture threshold.

4) Still not working?

  • Roll the patient to one side, and then another. Sometimes this influences the position of the transvenous pacing wire tip just enough to get you some capture.
  • Reverse the leads. Sometimes this works, but logically - it shouldnt.
  • Convert to unipolar pacing. Attach the negative lead to the positive electrode, and the negative lead to the subcutaneous tissue of the chest.
  • Give up. Time to pace externally while waiting for another wire to be floated, or the epicardial leads to be resited.

References

Question 8 - 2005, Paper 1

 List the causes of a sudden acute fall in systolic blood pressure  to 50 mmHg one hour after  an  uneventful   coronary  artery  bypass  operation.     Outline  your  principles  of management for each cause.

College Answer

Potential causes are many, and more than one may co-exist. Could be divided according to causes of shock: artefactual, hypovolaemic, obstructive, cardiogenic, and distributive (with principles of management in brackets).  Simple manoeuvres should be considered early (eg. raise legs to autotransfuse).

Artefactual: transducer error (check transducer: zero, level, calibration), damping of waveform (assess damping coefficient), malfunction of NIBP.

Hypovolaemic: blood loss (observe drain tubes, CXR, dressings; give fluid ± blood products), massive diuresis (observe urine output; give fluid).

Obstructive: pericardial tamponade (observe chest drainage ± clots, high filling pressures: may need to open chest), tension pneumothorax (observe expanded hemi-thorax, listen to chest: check existing chest drains, may need needle thoracostomy and replace/insert ICC), elevated intrathoracic pressure (gas trapping: disconnect from ventilator; shivering/valsalva/fighting: sedate ± paralyse; ensure ETT not blocked).

Myocardial: decreased contractility (ischaemia due to blockage/kinking/spasm: treat with GTN, inotropes &/or short term vasoconstrictor ± fix technical problem; sudden removal of inotropic drug: restart drug) or rhythm disturbance on monitor/ECG (brady-asystole: pace ± atropine/isopenaline/adrenaline; SVT: eg. K/adenosine; AF eg. K/Mg/amiodarone, VT eg. K/Mg/lignocaine).

Distributive:   anaphylaxis   (rash/bronchospasm:   remove   hapten,   adrenaline,   fluids);

vasodilator excess (recent boluses/infusion too high: stop responsible drug, ± titrated dosevasoconstrictor);     sympathetic     block     (recent     bolus     epidural    LA:     titrated    dose vasoconstrictor).

Discussion

This question is identical to Question 5 from the first paper of 2006.

References

Question 20 - 2005, Paper 1

Compare and contrast the advantages and disadvantages of Transoesophageal Echocardiography,   Angiography,  and  CT  Angiography  for  the  diagnosis  of  aortic injuries.

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.

References

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.

 

Question 25 - 2005, Paper 2

Outline the principles of management of superior vena caval obstruction.

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.

Type of SVC obstruction

Aetiology

Diagnosis

Management

Malignant

Malignant mass in thoracic inlet

History (eg. smoking)
CT
MRI
CXR

Surgical excision
SVC stenting by interventional radiology
Dexamethasone 
Radiation therapy

Non-malignant

Tuberculosis

Suspicious history, CT, CXR, aspiration and AFB/ZN stain/PCR  of the contents

Specific antituberculosis therapy
Surgical relief of obstruction
SVC stenting by interventional radiology

Abscess

CT, CXR, aspiration and gram stain / culture of the contents

Surgical drainage
Appropriate antibiotics

Goitre

CXR, CT, TFTs, biopsy of the mass

Surgical excision
Thyroid-suppressing medication eg. carbimazole
SVC stenting by interventional radiology

Thrombus

History of IJ CVC
CT with contrast, ultrasound

Antioagulation; clot retrieval by interventinal radiology procedure, or surgical embolectomy

Fibrosing mediastinitis

CT;
History of mediastinitis or mediastinal radiotherapy

Surgical relief of obstruction
SVC stenting by interventional radiology

Aortic aneurysm

Ct with contrast; TOE

Surgical management of aneurysm;
SVC stenting by interventional radiology

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.

References

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

Question 5 - 2006, Paper 1

List the causes of a sudden acute fall in systolic blood pressure  to 50 mmHg one hour after  an  uneventful   coronary  artery  bypass  operation.     Outline  your  principles  of management for each cause.

College Answer

A list of causes was requested, as were principles of management for each cause.

Potential causes are many, and more than one may co-exist. These could be listed according to causes of shock; one such approach to cover potential causes is: artefactual, hypovolaemic,obstructive, cardiogenic, and distributive. Principles of management are listed in brackets following each cause. Simple manoeuvres should always be considered early (eg. raise legs to autotransfuse). Artefactual: transducer error (check transducer: zero, level, calibration), damping of waveform (assess damping coefficient), malfunction of NIBP.

Hypovolaemic: blood loss (observe drain tubes, CXR, dressings; give fluid ± blood products), massive diuresis (observe urine output; give fluid).

Obstructive: pericardial tamponade (observe chest drainage ± clots, high filling pressures: may need to open chest), tension pneumothorax (observe expanded hemi-thorax, listen to chest: check

existing chest drains, may need needle thoracostomy and replace/insert ICC), elevated intrathoracic pressure (gas trapping: disconnect from ventilator; shivering/Valsalva/fighting: sedate ± paralyse; ensure ETT not blocked).

Myocardial: decreased contractility (ischaemia due to blockage/kinking/spasm: treat with GTN, inotropes &/or short term vasoconstrictor ± fix technical problem; sudden removal of inotropic drug: restart drug) or rhythm disturbance on monitor/ECG (brady-asystole: pace ± atropine/isoprenaline/adrenaline; SVT: eg. K/Mg/adenosine; AF eg. K/Mg/amiodarone, VT eg. K/Mg/lignocaine or amiodarone).

Distributive: anaphylaxis (rash/bronchospasm: remove hapten, adrenaline, fluids); vasodilator excess (recent boluses/infusion too high: stop responsible drug, ± titrated dose vasoconstrictor); sympathetic block (recent bolus of epidural Local Anaesthetic: titrated dose vasoconstrictor); too profound for a systemic inflammatory response.

Discussion

This question closely resembles  Question 13  from the first paper of 2012 and Question 13.1 from the first paper of 2009.

Relevant reading includes:

A systematic approach to this question would resemble this:

Type of shock Cause Diagnostic strategy Management
Artifact of measurement Arterial blood pressure measurement is inaccurate Compare with non-invasive measurement and physical examination
  • Re-zero and recalibrate the arterial line
  • Resite arterial line or change the transducer
Cardiogenic Post-operative stunning of the myocardium TTE, ECG, cardiac output measurement by PiCCO or PA catheter
  • Fluid resuscitation
  • Commence inotrope infusion
  • Correct rhythm if in AF
  • Return to theatre, recommence cardiopulmonary bypass
Myocardial infarction TTE, ECG, cardiac enzymes
  • Consider IABP
  • Thrombolysis or anticoagulation likely contraindicated given recent cardiac surgery
  • Return to theatre
Obstructive Cardiac tamponade TTE, CVP trace
  • Fluid resuscitation
  • Emergency pericardiocentesis
  • Return to theatre
Massive pulmonary embolism TTE, CVP trace, ECG, CTPA
  • Consider emergency embolectomy
  • Thrombolysis or anticoagulation likely contraindicated given recent cardiac surgery
Tension pneumothorax

Physical examination;

CXR

  • Emergency decompression
  • Chest drain
Neurogenic Infarction of spinal cord due to ischaemia or embolic events Physical examination features, CT, MRI
  • Thrombolysis or anticoagulation likely contraindicated given recent cardiac surgery
  • commence vasopressor infusion
Hypovolemic Blood loss post operatively Examination of drains, FBC,
  • Replace blood products and red cells
  • Fluid resusiciation
  • Maintain normal acid-base balance and normothermia
  • return to theatre
Massive diuresis Observation of fluid balance charts
  • Replace lost fluid volume
  • Rewarm patient to normal temperature
Distributive Vasoplegia SVRI measurements by PiCCO
  • commence vasopressor infusion; consider vasopressin or methylene blue
Anaphylaxis Physical examination findings suggestive of angioedema
  • Adrenaline IM or as infusion
  • Withdrawal of the trigger substance
  • Corticosteroids and antihistamines

References

Question 22 - 2006, Paper 1

Outline  the  indications  for and  the  potential  complications  of Intra-Aortic Balloon Pump (IABP) insertion.

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

References

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.

 

Question 18 - 2006, Paper 2

A 63 year old male smoker undergoes routine coronary artery bypass surgery. He remains ventilated on 10 cmH2O PEEP and FiO2  60% the following morning with a PaO2 of 63 mmHg.  Outline your diagnostic and therapeutic approach

College Answer

3 - 4 key features
•    Hypoxaemia post-cardiac surgery is common, most commonly due to basal atelectasis, but need to consider other possibilities such as pneumothorax, haemothorax, acute lung injury, airflow obstruction, pneumonia. Intra-cardiac shunt and PE unlikely unless specific history.
•    Diagnosis by history (?smoker, chronic lung disease), examination (asymmetry of movement, air entry), search for posterior basal bronchial breath sounds (common) and chest radiograph (basal atelectasis may not be obvious on CXR – but can be on clinical exam), CT scan shows much more atelectasis but rarely justified
•    Drain pneumothorax/haemothorax, bronchodilators for airflow obstruction, may need antibiotics for infection, consider ‘marginal’ extubation – often well tolerated in CABG patients but this patient probably too hypoxaemic. Basal atelectasis need time and try recruitment with specific manoeuvres and or higher level PEEP if tolerated (likely to depress BP so need careful supervision)

Discussion

Causes of hypoxia in the post-bypass patient are explored in a brief summary hidden among the "Required Reading" notes for the topic of cardiothoracic ICU. They are separated into four major groups:

Mechanical problems

  • Pneumothorax
  • Haemothorax
  • Endotracheal tube migration
  • Mucus plugging the bronchus
  • Blood clot plugging the bronchus
  • Phrenic nerve palsy

Pulmonary oedema

  • Post-bypass ARDS (as a circuit-related SIRS complication)
  • Poor LV function
  • Anaphylaxis-associated increase in pulmonary vascular permeability

Intrapulmonary shunt

  • Atelectasis (due to surgical handling, or incomplete reinflation of the left lung)
    • There is a 70% chance of atelectasis, particularly of the left lower lobe.
    • Chest wall compliance will be poor
    • Pain will be an issue limiting tidal volumes
    • Again, phrenic nerve palsy
  • Inhibition of hypoxic pulmonary vasoconstriction( by GTN or nitroprusside)

Intracardiac shunt

  • Unveiling of a previously silent septal defect by an increase in right sided pressures

A systematic approach is called for:

  • Increase FiO2 to ensure satisfactory oxygenation
  • examine patient and ventilator, looking for evidence of decreased lung compliance or increased resistance to airflow
  • auscultate the chest, looking for evidence of atelectasis, consolidation, pneumothorax or unequal air entry suggestive of ETT malposition
    • address these by increasing PEEP, changing I:E ratio, paralysing the patient or administering bronchodilators
  • ECG looking for evidence of PE or right ventricular infarction
  • CXR, looking for
    • pneumothorax/hemothorax
    • atelectasis
    • ETT dislodgement into the right main bronchus
    • acute lung injury/ARDS
  • Search of history for evidence of chronic lung disease eg. COPD or pulmonary fibrosis

References

Ng, Calvin SH, et al. "Pulmonary dysfunction after cardiac surgery." CHEST Journal121.4 (2002): 1269-1277.

Tenling, Arne, et al. "Atelectasis and gas exchange after cardiac surgery."Anesthesiology 89.2 (1998): 371-378.

Question 13 - 2007, Paper 1

Compare and  contrast the advantages and  limitations  of the intra-aortic balloon  pump  (IABP)  and  ventricular assist  devices (VAD). (You  may tabulate your answer).                 

College Answer

IABP

VAD

Can be inserted percutaneously  in ICU  or CCU

While percutaneous insertion is possible, frequently require
anaesthesia and  a surgeon for insertion and removal.

Indications

Used post cardiac surgery /
cardiogenic                  shock following an infarct

Frequently  used   in   post 
cardiac surgical patients.
Used   as     a     bridge     to transplantation.

Logistics

Intensivists  more  familiar
with  IABP

Can   be  used during transport

Less familiar  with  VAD, 
greater degree  of complexity, more  difficult to use during transport

Anticoagulation

Usually     no       need      for anticoagulation

Need for anticoagulation

Not effective in the setting of      CI       <      1.2       and 
tachyarrhythmias

Greater control on  overall
cardiac output  as  well  as
Rt    and     Lt     ventricular output

Complications

Lower       limb       ischemia,
hematoma,   aortic   trauma are complications

Bleeding,             infection,
hemolysis, device failure

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:

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

LV Assist Device vs Intra-Aortic Balloon Counterpulsation
 

IABP

VAD

Indications

No choice but pump

  • Failure to come off bypass
  • Severe aortic stenosis
  • Mitral regurgitation
  • Ventricular septal defect 

Probably harmless, but probably not useful

  • High-risk PCI patients (pre-op) - IABP-SHOCK II
  • High-risk pre-CABG patients (low LVEF)
  • Cardiogenic shock while waiting for PCI (i.e. bridge to definitive intervention)
  • Pulmonary oedema in spite of maximal medical management

Totally experimental

  • Takotsubo cardiomyopathy
  • Neurogenic stress cardiomyopathy of subarachnoid haemorrhage

Known to be pointl

Firm indications:

  • Failure to come off bypass
  • Cardiogenic shock
  • Cardiac arrest
  • Fulminant myocarditis

Potential indications:

  • High risk CABG patients (pre-op)
  • High-risk PCI patients (pre-op)

Contraindications

Absolute contraindications

  • Aortic regurgitation
  • Aortic aneurysm
  • Aortic dissection
  • Severe sepsis
  • Uncontrolled coagulopathy

Relative contraindications

  • Atherosclerosis and arterial tortuosity
  • Left ventricular outflow tract obstruction
  • Contraindications to anticoagulation
  • Aortic regurgitation
  • Aortic aneurysm
  • Aortic dissection
  • Severe sepsis
  • Uncontrolled coagulopathy
  • Left heart thrombus

Advantages

  • Bedside insertion
  • Familiarity among ICU staff
  • Less invasive
  • Flow is pulsatile; organ perfusion benefits
  • Able to compensate for all cardiac function (i.e. useful in the setting of asystole)
  • May remain in situ for longer than the IABP
  • Contrary to the college answer above ("more difficult to use during transport") most patients with VADs can be mobilised normally (Mohiyaddin, 2018)

Disadvantages

  • Useless if the cardiac index is less than 1.5
  • Insertion may be frustrated by poor peripheral arterial anatomy
  • Non-pulsatile flow; poor organ perfusion
  • Requires sternotomy for insertion (for most except the TandemHeart device, which can be inserted percutaneously)
  • Unfamiliarity among ICU staff

Anticoagulation

May not require anticoagulation

Requires mandatory anticoagulation

Complications

  • 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
  • Infection is the major cause of morbidity; something like 50% of the implanted devices get infected.
  • The LV gets (understandably) irritated by the presence of an LVAD, and in 25% of patients ventricular arrhythmias develop
  • Thrombi form on the walls of the device in spite of anticoagulation, and 10-16% of people have thrombotic complications.
  • Some degree of haemolysis and thrombocytopenia occur in everybody

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

References

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.

Question 20 - 2007, Paper 1

List the advantages and disadvantages of the following pacemaker modes:
AAI, VVI, DDD.(You  may tabulate your answer).

College Answer

Mode

Advantages

Disadvantages

AAI

a) Requires a single lead, 
b) AV synchronicity maintained,
c) Able to assess ST
changes,

a) Unable to use in AF,
b) Ventricular bradycardia may occur in the presence of a high grade AV block, 
c) Instability of a single atrial lead,
d) Higher risk of perforation of thin atrial wall

VVI

a) Requires a single lead,
b) Useful in the presence of AF and high grade AV block,

a) AV synchronicity is lost 
b) Unable to assess ST changes 
c) Loss of atrial kick .

d) Risk of pacemaker syndrome

DDD

a) AV synchronicity maintained
b) Useful in the presence of AF and high grade AV block
c) Heart rate responsiveness

a) Pacemaker mediated endless-loop tachycardia
b) Pacemaker syndrome if incorrectly setup
c) May not be able to assess ST changes

Discussion

Little can be added to the college answer. Advantages and disadvantages of various pacing modes enjoy a more thorough discussion elsewhere. And... there are fair few modes. 

A Comparison of Single and Dual Chamber Pacing Modes
Pacing Mode Description Advantages Disadvantages
AOO asynchronous atrial pacing.
  • Only one lead required
  • Preserves AV synchrony in the presence of an intact AV node
  • Protects against interference by diathermy
  • contraindicated in the presence of intrinsic cardiac rhythms. 
  • If the rate is not high enough, you will have an underlying rhythm competing with the pacemaker.
  • Useless if the AV node is dysfunctional
  • Useless in the presence of AF
  • Increased risk of perforating the thin atrial wall
AAI atrial demand pacing
  • Only one lead required
  • Preserves AV synchrony in the presence of an intact AV node
  • Only paces on demand; allows intrinsic rhythm while the rate is high enough
  • Useless if the AV node is dysfunctional
  • Useless in the presence of AF
  • Increased risk of perforating the thin atrial wall
AAT atrial pacing
  • Only one lead required
  • Preserves AV synchrony in the presence of an intact AV node
  • Useful for testing atrial sensing (using the pacing spike)
  • Useless if the AV node is dysfunctional
  • Useless in the presence of AF
  • Unproductive in general (paces in response to normal atrial contraction, while the atrium is in a refractory period); thus, not a useful permanent mode
  • Increased risk of perforating the thin atrial wall
VOO asynchronous ventricular pacing
  • Only one lead required
  • Protects against interference by diathermy
  • Asynchronous AV contraction
  • May result in the R - on - T phenomenon
  • Difficult to assess ST changes (LBBB-like QRS morphology)
VVI ventricular demand pacing
  • Only one lead required
  • Only paces on demand; allows intrinsic rhythm while the rate is high enough
  • Asynchronous AV contraction
  • Difficult to assess ST changes (LBBB-like QRS morphology)
VVT ventricular pacing
  • Useful for testing ventricular sensing (using the pacing spike)
  • Asynchronous AV contraction
  • Unproductive in general (paces in response to normal ventricular contraction, while the ventricle is in a refractory period); thus, not a useful permanent mode
  • Difficult to assess ST changes (LBBB-like QRS morphology)
  • Possibility of "endless loop" tachycardia
VAT atrial sensing, ventricular pacing
  • AV synchrony is preserved
  • "Pacemaker syndrome" is thus avoided
  • Advantageous in patients with normal atrial activity and a dysfunctional AV node
  • Two leads required
  • Bundle of His is bypassed
  • Difficult to assess ST changes (LBBB-like QRS morphology)
  • Increased risk of perforating the thin atrial wall
DDD dual chamber demand pacing
  • AV synchrony is preserved
  • "Pacemaker syndrome" is thus avoided
  • Advantageous in patients with normal atrial activity and a dysfunctional AV node
  • Versatile mode, with hemodynamic advantage 
  • Two leads required
  • Bundle of His is bypassed
  • Possibility of "endless loop" tachycardia
  • Increased risk of perforating the thin atrial wall

References

Gillis, Anne M., et al. "HRS/ACCF expert consensus statement on pacemaker device and mode selection." Journal of the American College of Cardiology 60.7 (2012): 682-703.

Question 28 - 2007, Paper 1

List the extracoporeal therapies used in the critically ill and outline the indications for their use.

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.

Extracorporal Therapies in the ICU and their Indications
Therapy Indications
Dialysis
  • Oliguria with volume overload
  • Oliguria is relative; urine output may be high and still inadequate in clearing the fluid.
  • Uremia with symptoms
  • Hyperkalemia ( K+ over 6.0)
  • Metabolic acidosis due to renal failure (pH < 7.2)
  • Removal of dialysable drugs/toxins
  • Control of electrolytes
  • Control of body temperature
Hemoperfusion
  •  There is severe life-threatening intoxication with substances which are not going to be well removed by the liver or kidneys.
  • There is an impairment of liver and kidneys, preventing clearance.
  • If a toxin is equally well cleared by hemodialysis and hemoperfusion, then hemodialysis is preferred, because it will also correct any underlying acid-base disturbance
ECMO
  • Cardiac arrest (in certain settings)
  • Failure to wean from cardiopulmonary bypass
  • Cardiogenic shock
  • Hypoxic respiratory failure
  • Hypercapneic respiratory failure
ECCO2R
  • Hypercapnic respiratory failure with adequate oxygenation
MARS
  • Fulminant hepatic failure with encephalopathy, awaiting transplant
Plasma exchange
  • HELLP syndrome
  • Multiple sclerosis
  • HIV-related neuropathy
  • Pemphigus
  • Coagulation inhibitors
  • DIC
  • Overwhelming sepsis syndromes eg meningococcaemia
  • Reye’s syndrome
  • Paraquat poisoning
  • A more complete summary of indications is available elsewhere
LVAD/RVAD
  • Cardiogenic shock
  • Cardiac arrest
  • Fulminant myocarditis
  • Failure to wean off bypass

References

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

 

LITFL page

Question 10 - 2008, Paper 1

A 56 year old woman 1 hr post cardiac surgery has a high blood pressure in the ICU. Give likely causes for her high blood pressure and the potential complications this may cause in the early post operative period.

College Answer

Causes: 
Previous hypertension
Pain
Inadequate analgesia or sedation vs paralysis
Measurement error
Hypercarbia
Endotracheal tube intolerance
Wrong dosing of inotropes/vasopressors
Blocked IDC
Post AVR for AS

Potential complications:

Bleeding from aortic cannulation site
Generalised ooze 
Heart failure 
Myocardial ischaemia 
Arrhythmias
Graft dislodgement 
Extension of a dissection 
Hypertensive crises

Discussion

Apparently, hypertension can occur in 15-40% of post-cardiac surgery patients. It receives a little less interest than hypotension. Note how the college answer has few points which are actually specific to cardiothoracic surgery. And where is hypothermia? That surely plays a role.

The college answer then goes on to mention arrhythmias and hypertensive crises as potential complications. I would have added the effects of increased afterload on myocardial oxygen consumption, the additional stress on new valve components, increase of pre-existing mitral regurgitation, increased sedation demands and thus potentially a delay of extubation, and complications related to the use of antihypertensive polypharmacy.

Anyway; the complete list of causes and consequences looks like this:

Causes

  • Pain
  • Inadequate sedation in a partially paralysed patient
  • Pre-existing hypertension, and the perioperative cessation or regular medications
  • Artifactual hypertension (measurement error)
  • Unintelligent use of vasopressors
  • The sudden improvement of aortic flow following the repair of a stenotic aortic valve, which exposes the systemic circulation to being bullied by a massively hypertrophied left ventricle.

Consequences

  • Increased bleeding risk - particularly from the aortic cannulation site
  • Extension of an arterial dissection
  • Increased afterload and thus increased LV workload
    • Thus, increased risk of ischaemia
    • Increased risk of cardiac failure due to decompensated LV failure
  • Increased stress on grafted valves or repaired aortic root
  • Worsening of existing mitral regurgitation
  • Increased need for sedation
  • Bleeding from aortic cannulation site

References

Estafanous, Fawzy G., and Robert C. Tarazi. "Systemic arterial hypertension associated with cardiac surgery.The American journal of cardiology 46.4 (1980): 685-694.

Roberts, A. J., et al. "Systemic hypertension associated with coronary artery bypass surgery. Predisposing factors, hemodynamic characteristics, humoral profile, and treatment." The Journal of thoracic and cardiovascular surgery 74.6 (1977): 846-859.

Question 12 - 2008, Paper 1

This ECG trace was taken from a 68 year old man, one hour following aortic valve replacement for aortic stenosis. Atrial and ventricular epicardial pacing wires are in place, and the pacing mode is DDD.

a) . What problem is demonstrated?

b). Outline the steps that you could take to address the problem.

The problem is resolved, and normal DDD pacing resumes. One hour later another
ECG trace is taken.

c). What problem is demonstrated?

d). What precipitated the problem?

e). Outline the pathophysiological mechanism of this problem

College Answer

a) . What problem is demonstrated?
•    Intermittent failure of ventricular capture.


b). Outline the steps that you could take to address the problem.
•     Increase the ventricular output
•     Check the connections to the pacemaker and pacing connector leads
•     Reverse the polarity of the pacing to the ventricle
•     Replace pacemaker box and pacing connector leads
•     Unipolar pacing, with a cutaneous pacing stitch. This may fix the problem if one lead is faulty.
•     Chronotropic therapy eg isoprenaline
•     Alternative pacing method: transcutaneous, transvenous
•    Open the chest and replace the epicardial wires

c). What problem is demonstrated?
•     Pacemaker mediated tachycardia

d). What precipitated the problem?
•    A ventricular ectopic

e). Outline the pathophysiological mechanism of this problem
•    The dual chamber pacemaker is forming part of a re-entry circuit. A ventricular ectopic has triggered retrograde conduction along the patient’s conducting system. The resulting P-wave has been sensed by the atrial lead of the pacemaker, and this has triggered ventricular pacing. The paced ventricular impulse has triggered retrograde conduction along the patient’s normal conducting system, and the cycle continues.

Discussion

Elaborate detail is given elsewhere to the troubleshooting of a temporary pacemaker circuit. None of the college answers are surprising or requiring of any additional research. Failure of capture, at least, is a common enough occurrence that most people would have some intuitive grasp of how to answer it in writing.

References

Reade, M. C. "Temporary epicardial pacing after cardiac surgery: a practical review." Anaesthesia 62.3 (2007): 264-271.

Reade, M. C. "Temporary epicardial pacing after cardiac surgery: a practical review: Part 2: Selection of epicardial pacing modes and troubleshooting."ANAESTHESIA-LONDON- 62.4 (2007): 364.

Gammage, Michael D. "Temporary cardiac pacing." Heart 83.6 (2000): 715-720.

Question 13.1 - 2009, paper 1

A 52 yr old patient  presents to the Emergency Department with acute  coronary syndrome and cardiogenic shock. He receives 300mg aspirin, 600mg clopidogrel and a tirofiban infusion is initiated.  The angiogram shows left main stem occlusion– and he is referred urgently to cardiac surgery. The tirofiban infusion is ceased. On return from theatre, there is 400ml/ hr blood loss for the first 3 hours.

13.1     List 5 causes of early post-operative bleeding in this patient.

College Answer

Causes

 

1 Surgical bleeding
2 Hypothermia
3 Inadequate reversal of heparinisation
4 Pre-existing platelet dysfunction - pharmacological or pathological
5 Dilutional coagulopathy
6 Thrombocytopoenia - due to trauma of bypass circuit

 

Discussion

This question closely resembles Question 13 from the 1st paper of 2012.

Bleeding complications following coronary artery bypass grafting and complications attributed to the cardiopulmonary bypass circuit are abundantly explored elsewhere.

References

Question 3.2 - 2009, Paper 2

A 65 year old man is admitted to your ICU following emergency percutaneous coronary stenting after an anterior STEMI complicated  by cardiogenic shock.

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

b) What are the physiologic consequences of this?

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".

References

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

 

Question 4 - 2009, Paper 2

4.1       Outline the potential  effects of an intercostal catheter inserted into the left chest and attached to an underwater seal drain following a left pneumonectomy. The drain is unclamped and attached to an underwater seal drain.

4.2       Explain how you would manage this situation.

College Answer

Using an underwater seal drain is inappropriate following a pneumonectomy.
A drain attached to an underwater seal will cause air to be removed from the left chest. There is no lung to expand to fill the space so the mediastinum will move to the left. This results in rapid distortion of major veins and reduced venous return. This causes reduced cardiac output and hypotension.

The situation can be prevented by immediate clamping or when mediastinal shift has occurred letting air back into the chest (by disconnecting the UWSD) resolves the situation or consider active injection of air / intermittent unclamping. It would also be necessary to contact the surgeon to ascertain how the UWSD had come to be attached.

Discussion

This is a question about a complication which is uncommon precisely because everybody is so familiar with it.

If you keep sucking air out of a pneumonectomised chest, you will cause mediastinal shift, kinking of the greater vessels, and hemodynamic collapse. Its the physiological equivalent of a tension pneumothorax.

The simple act of letting air back into the chest cavity tends to be enough to resolve this issue.

The suggestion that we then call the surgeons and interrogate them about why they mismanaged their patient is a deliciously ICU-typical response. That's why everyone hates us.

So.. why would you put a dangerous death-tube into a person's chest when you know it will cause some sort of complication, particularly a complication exciting enough to appear in the SAQs?

Well, it turns out there are good reasons for it.

The whole post-pneumonectomy chest tube issue is discussed in slightly greater detail in the brief scribble summary about the care for the post-pneumonectomy patient,  in the "Required Reading" section for the Cardiothoracic ICU topic area.

 

References

Weissberg, Dov. "Post-Pneumonectomy Chest Tubes." Texas Heart Institute Journal 29.2 (2002): 155.

Question 7.1 - 2009, Paper 2

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

b)         List three (3) complications of ECMO.

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:

 

References

Question 10.1 - 2009, Paper 2

This ECG trace was taken from a 68 year old man, one hour following aortic valve replacement for aortic stenosis. Atrial and ventricular epicardial pacing wires are in place, and the pacing mode is DDD.

a)          What problem is demonstrated?

b)         Outline the steps that you could take to address the problem.

College Answer

a)          What problem is demonstrated?

Intermittent failure of ventricular capture.

b)         Outline the steps that you could take to address the problem.

•       Increase the ventricular output
•       Check the connections to the pacemaker and pacing connector leads
•       Reverse the polarity of the pacing to the ventricle
•       Replace pacemaker box and pacing connector leads
•       Unipolar pacing, with a cutaneous pacing stitch. This may fix the problem if one lead is faulty.
•       Chronotropic therapy eg isoprenaline
•       Alternative pacing method: transcutaneous, transvenous
•       Open the chest and replace the epicardial wires

Discussion

Apart from the  brief summary of this topic, one can also review an extensive rambling digression about troubleshooting the temporary pacemaker circuit.

If one is for whatever reason unwilling to wade through that swamp of self-indulgent gibberish, one might have to settle for a short answer.

Thus:

Failure to capture means either you are using too little current, or your lead is in a stupid position (i.e. not anywhere near the ventricular wall). The latter you can do nothing about.
The former remains within your control.

Thus, the first step is to increase the pacemaker output.

If you are already using the maximum amount of current, there are several possibilities:

  • The wire tips have overgrown with fibrinous filth, and need to be replaced
  • The myocardium is resistant to pacing because of electrolyte derangement, recent defibrillation, or antiarrhytmic drugs interfering in the process.
  • The area of myocardium which the electrode is touching has infarcted and no longer does anything for anybody.

One can try to reverse the polarity of the electrodes in this situation to see if this helps. Alternativly, one can try to convert the bipolar circuit to a unipolar circuit.

One can try to reverse the polarity of the elctrodes in this situation to see if this helps. Alternativly, one can try to convert the bipolar circuit to a unipolar circuit.

 

References

Question 8.3 - 2010, Paper 2

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

OBSERVATIONS:

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

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

*LEFT ATRIUM: Mildly enlarged.

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

Aortic valve area

Left ventricular outflow tract:

0.68cm2

0.55 m/s; 

(2 – 4)

(0.8 – 1.2)

Maximum velocity 
Velocity time integral (VTI)

8.58 cm;

Aortic valve     Maximum velocity

2.93 m/s;

(<2.0)

Velocity time integral (VTI)

43 cm;

Max pressure gradient 

Mean pressure gradient

34 mm Hg 

18 mm Hg

(<16) 

(<10)

Dimensionless severity index (DSI)

0.19

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

College Answer

Severe aortic stenosis  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.

References

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

 

 

Question 8.2 - 2010, Paper 2

Examine the ECG rhythm below. The patient was being paced AAI . What is the problem with the pacing?

Image provided in examination paper

College Answer

Oversensing. In this case myopotentials are sensed.

Discussion

The image above is from the below-referenced book on pacemaker physiology.

Its a mere diagram. These exotic rhythm disturbances are hard to find examples of.

Essentially, oversensing in AAI is the pacemaker mistaking some muscle potentials as atrial activity, and inhibiting itself. The result is a missed beat.

References

A good Google book on this subject is available for all to see:

Cardiac Pacing for the Clinician by Kusumoto and Goldschlager.

 

Question 11 - 2010, Paper 2

Outline   the  role  of  ECMO   (Extracorporeal   membrane   oxygenation)   as  a supportive strategy in the critically ill.

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.

References

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.

Question 13 - 2010, Paper 2

Outline the advantages and disadvantages of a CT scan, Transoesophageal echocardiography,   MRI  and  an  aortogram  for  the  evaluation  of  suspected aortic dissection.

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:

Imaging Modalities for the Evaluation of Aortic Dissection
Imaging modality Advantages Disadvantages
Aortogram
  • High sensitivity (86-88%) and specificity (75-94%)
  • Can detect blocked coronaries in Type A dissection
  • Can assess valves
  • May allow endoluminal repair during the same procedure, expertise permitting
  • Not easily available
  • Large contrast load
  • Time consuming
  • Ineffective in detecting intramural haematoma 
    (the contrast cannot get in there!)
  • Potential for false negative results when a thrombosed false lumen prevents contrast entry
  • Slightly lower sensitivity and specificity than TOE, CT or MRI; has been largely replaced by them.
CT
  • Easily available
  • High sensitivity (83-94%) and specificity (87-100%)
  • Information about end-organ ischaemia
  • Imaging of the vascular tree allows planning of surgical or endovascular approach
  • ECG-gated CT = cardiac motion artifact is abolished
  • Able to exclude conditions which mimic aortic dissection
  • Contrast exposure
  • No information about the valves
  • Risk of transfer to CT
  • Motion artifact could be an issue in ungated studies
MRI
  • High sensitivity and specificity (95-100% for both)
  • Contrast is less nephrotoxic
  • Information about end-organ ischaemia
  • Imaging of the vascular tree allows planning of surgical or endovascular approach
  • Occasionally allows assessment of aortic valve pathology, coronary arteries and the LV
  • Significant risk of transfer
  • Not easily available
  • Certain patient groups excluded (eg. recent trauma with surgical staples)
  • Often fails to characterize the relationship of an intimal flap and aortic root structures, specifically the coronary arteries
TOE
  • Can assess valves
  • Decent sensitivity (35-80%) and specificity(39-96%)
  • Performed at the bedside- no risk of transfer
  • Contrast not required
  • Allows detection of tamponade
  • Allows assesment of proximal coronary arteries
  • Able to detect intramural haematoma
  • Invasive
  • Accuracy is operator dependent
  • Requires sedation
  • May cause hypertension
  • Limited by a blind spot caused by interposition of the trachea and left main bronchus between the oesophagus and aorta
  • Unable to visualise the abdominal aorta
CXR
  • Rapidly available
  • Immediate evidence of widened mediastinum
  • A completely normal CXR in low risk patients may be meaningful as a means of excluding dissection
  • Inadequately sensitive (~71%)
  • Rarely able to exclude dissection in most patients

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.

 

References

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.

 

Question 15 - 2010, Paper 2

The   following   questions   refer   to   implantable   cardiac   pacemakers   and implantable cardiac defibrillators.

a)         What is the effect of applying a magnet to these devices?

b)         What information can you gain from a chest X-Ray in a patient with an implantable cardiac device?

c)         What are the advantages of DDD pacing compared to VVI pacing?

d)         List 4 benefits of cardiac resynchronisation therapy.

College Answer

a)         What is the effect of applying a magnet to these devices?

ICD:  it turns off antiarrhythmic programme but has no affect on backup pacemaker
Pacemaker: It defaults to asynchronous mode or a fixed rate. Rate depends on battery life.

b)         What information can you gain from a chest X-Ray in a patient with an implantable cardiac device?

•    Single v dual chamber
•    Biventricular or left ventricular (cardiac resynchronisation)
•    Lead displacement or injury
•    Number of devices present

c)         What are the advantages of DDD pacing compared to VVI pacing?

•  AV synchronisation maintained
•  Avoids pacemaker syndrome
•  Reduced incidence of AF
•  Possible decreased thrombotic events

d)         List 4 benefits of cardiac resynchronisation therapy.

•  improved LVEF,CO and haemodynamics
•  improved exercise tolerance
•  decreased NYHA class
•  decreased hospitilisation
•  improved quality of life

Discussion

a) is pretty straightforward as far as pacemaker questions go. Generally speaking, most of them will respond to magnet exposure by becoming asynchronous, i.e. they will start pacing without sensing. AICDs will stop defibrillating. This is good to know if you are palliating a patient with an implanted device, and you don't want to have the defib firing randomly in the last few minutes of their life.

Of course, there is no standard among the manufacturers regarding what precisely should happen when the magnet is applied. Medtronic and Boston Scientific models will pace asynchronously; St Jude will cycle through some pre-programmed protocol which typically involves recording and storing an ECG, and Biotronic devices will do something completely random, depending on model and battery life. A good article about these idosyncratic behaviours is available on Medscape.

b) is also pretty straightforward. Immediately, on a chest Xray you can see how many leads there are, and you can guess from the size of the battery whether the device is also set up to defibrillate. Fractured leads and leads which have become grossly dislodged will also become obvious.

c) is a little more complicated. VVI mode of pacing is an older mode and is not optimised to deliver the best cardiac output, because it completely ignores the atrial contribution. If the atrial kick disappears altogether, the VVI box will make no attempt to compensate for this. In fact, the retrograde conduction of ventricular pacing tends to cause the atrium to contract in a profoundly stupid fashion, during ventricular systole and against a closed valve. This loss of atrioventricular synchrony is called "pacemaker syndrome".

DDD on the other hand is more sensitive to the needs of the ailing myocardium. Not only aresymptoms of the patients better with DDD (supporting the concept of hemodynamic advantage) but the risk of AF is decreased because there is a constant and reliable single source of electrical stimulus in the atrium.

d) is even more complicated, and asks for some indepth understanding of CRT. A good review article of the technique is available. The benefits of CRT for heart failure are discussed in a 2007 meta-analysis; bottom line is that CRT improves NYHA grade, and it may improve mortality (though some think this may be due to the built-in AICD function and the prevention of sudden cardiac death by these devices). The problem is, you have to have LBBB, severe heart failure and several other hideous criteria in order to benefit, which means that only 5-10% of people actually qualify for this treatment.

Relevant Required Reading chapters include:

References

BYRD, CHARLES L., et al. "DDD pacemakers maximize hemodynamic benefits and minimize complications for most patients." Pacing and Clinical Electrophysiology 11.11 (1988): 1911-1916.

Channon, K. M., et al. "DDD vs. VVI pacing in patients aged over 75 years with complete heart block: a double-blind crossover comparison." QJM 87.4 (1994): 245-251.

Strik, Marc, et al. "Cardiac resynchronization therapy." Circ J 75.6 (2011): 1297-1304.

Tang, Anthony SL, et al. "Cardiac-resynchronization therapy for mild-to-moderate heart failure." New England Journal of Medicine 363.25 (2010): 2385-2395.

McAlister, Finlay A., et al. "Cardiac Resynchronization Therapy for Patients With Left Ventricular Systolic DysfunctionA Systematic Review." Jama 297.22 (2007): 2502-2514.

Question 3 - 2011, Paper 1

A 60 year old man presents with a history of vomiting followed by the sudden onset  of  chest  pain  a  few  hours  ago.  On  examination   he  has  surgical emphysema over his neck and chest and evidence of a left pleural effusion.

Discuss your management of this patient.

College Answer

Initial management
Check ABCs and resuscitate if necessary
More extensive history and examination to look for other causes of surgical emphysema (eg CVC, barotrauma, pneumothorax), chest pain (eg pneumothorax, pulmonary embolus, musculoskeletal) and pleural effusion.
Look for signs of sepsis, shock and hypoxia.
Admit to highly monitored area in view of high risk of rapid clinical deterioration. NBM

Investigations
Contrast CT abdo chest and neck / gastrograffin swallow (avoid barium) CXR: pleural effusion, ± pneumomediastinum,  ± pneumothorax
Pleural fluid: presence of food particles, pH<6 and high amylase concentration indicative of oesophageal rupture but amylase may be high in pancreatitis.
Culture of pleural fluid Blood culture oesophagoscopy

Definitive treatment
Broad spectrum antibiotics including anaerobic cover plus antifungals
Pleural drainage
Early (within 24 hr) thoracotomy and repair or endoscopic placement of stent depending on whether patient shows signs of sepsis. Surgery preferred for septic patients, conservative if contained perforation.

Discussion

Why, this is a wonderful question on Boerhaave's syndrome. "Discuss your management for the patient with oesophageal perforation".

Immediate management

  • Attention to ABCs and correction of immediately identified lifethreatening features
  • Detailed history and thorough physical examination
  • Assessment of airway patency and intubation as needed
  • Maintenance of normoxia with supplemental oxygen
  • Maintenance of normotension with fluid resuscitation and vasopressors as needed
  • Analgesia and sedation
  • Attention to broad-spectrum antibiotic cover, including antifungal agents

Investigations:

  • CXR looking for pneumomediastinum
  • CT chest with contrast
  • Gastrograffin swallow (not barium)
  • Intercostal catheter to drain pleural effusion and analyse it, looking for acidity (suggestive of gastric contents) and food particles

Specific Management

  • Thoracoscopic or open surgical management;
  • alternatively, endoscopic stent placeemnt
  • alternatively, conservative antibiotic-based management and supportive care in ICU

References

Curci, JOSEPH J., and MARC J. Horman. "Boerhaave's syndrome: The importance of early diagnosis and treatment." Annals of surgery 183.4 (1976): 401.

Teh, Elaine, et al. "Boerhaave's syndrome: a review of management and outcome." Interactive cardiovascular and thoracic surgery 6.5 (2007): 640-643.

Skinner, David B., Alex G. Little, and Tom R. DeMeester. "Management of esophageal perforation." The American Journal of Surgery 139.6 (1980): 760-764.

Question 16 - 2011, Paper 1

A 72 year old male with known triple vessel coronary disease has returned to the ICU following an uncomplicated  coronary artery bypass grafting (CABG). An   intraoperative   transoesophageal   echo   showed   good   left   ventricular systolic  function  and no significant  valvular dysfunction.  Mediastinal  drains have  been  inserted  and  there  is  minimal  blood  loss.  Thirty  minutes  after return to the ICU his BP falls to 70/40 mmHg.

  • Give the 4 most likely causes for this.
  • Outline your immediate management

The patients BP stabilises and 2 hours later you are called to review him since he has developed significant shivering. List 4 possible treatment options

On day 1, the patient is extubated and stable. You are shown the following ECG:

What does it show? What treatment is required?

1 hour later, quite unexpectedly,  the patient  has a VF cardiac  arrest.  What are your principles of management?

College Answer

.       A 72 year old male with known triple vessel coronary disease has returned to the ICU following an uncomplicated  coronary artery bypass grafting (CABG). An   intraoperative   transoesophageal   echo   showed   good   left   ventricular systolic  function  and no significant  valvular dysfunction.  Mediastinal  drains have  been  inserted  and  there  is  minimal  blood  loss.  Thirty  minutes  after return to the ICU his BP falls to 70/40 mmHg.

Give the 4 most likely causes for this.

•    Artifactual due to inaccurate monitoring system
•     Hypovolaemia
•    Vasodilatation associated with re-warming
•    Vasodilatation associated with drugs (anti-hypertensives, vasodilators, sedation
•    Anaphylaxis
•     Pneumothorax
•    Cardiac tamponade

Outline your immediate management

•    Check monitoring system
•    Fluid bolus
•    Stop vasodilators
•    Consider use of a short acting vasopressor such as metaraminol
•    If not responding  to fluid and short acting vasopressors  consider a catecholamine infusion such as noradrenaline
•    Cease any potential allergens

The patients BP stabilises and 2 hours later you are called to review him since he has developed significant shivering. List 4 possible treatment options

•    Increase sedation / analgesia
•    Consider paralysis
•    Increase external warming
•    Consider pethidine

On day 1, the patient is extubated and stable. You are shown the following ECG:

What does it show?

•    Diffuse concave ST elevation suggestive of pericarditis

What treatment is required?

•    If the patient is asymptomatic, then no treatment is required

1 hour later, quite unexpectedly,  the patient  has a VF cardiac  arrest.  What are your principles of management?

•    Basic ALS. Immediate defibrillation, ensure airway and ventilate with 100% oxygen
•    Contact the cardiothoracic team immediately and prepare for possible sternotomy
•    Internal cardiac massage and internal defibrillation if re-sternotomy on the ICU

Discussion

The first part of the question calls for differentials for shock.

Relevant reading for this includes the following chapters:

The management of "shivering" in the ICU is somewhat more complicated. In this setting, one can assume that the patient is shivering because the process of their awakening has been faster than the process of their rewarming. The increased oxygen demand of the body can give rise to increased demand on the wounded myocardium, and this is to be avoided. Sedation, paralysis and more vigorous rewarming is the sensible solution. Pethidine is known to control rigors, and in one article it was used as a rescue agent to control post-bypass shivering before the authors resorted to pancuronium. Apparently, dexamethasone is another valid alternative.

In our study group, we were grateful to the contribution of one member, who sensibly pointed out that it would be worthwhile to take the patient's temperature before jumping to conclusions regarding the cause of their shivering. This broadens the range of management techniques (one might find themselves giving paracetamol instead of curare toxins, which is a markedly different approach).

References

Guffin, Anita, Dominique Girard, and Joel A. Kaplan. "Shivering following cardiac surgery: Hemodynamic changes and reversal." Journal of cardiothoracic anesthesia 1.1 (1987): 24-28.

Ralley, Fiona E., et al. "The effects of shivering on oxygen consumption and carbon dioxide production in patients rewarming from hypothermic cardiopulmonary bypass." Canadian journal of anaesthesia 35.4 (1988): 332-337.

Yared, Jean-Pierre, et al. "Dexamethasone decreases the incidence of shivering after cardiac surgery: a randomized, double-blind, placebo-controlled study."Anesthesia & Analgesia 87.4 (1998): 795-799.

 

Question 17 - 2011, Paper 1

Critically evaluate the  use of sodium bicarbonate therapy in Diabetic Ketoacidosis

College Answer

Critically   evaluate   the   use   of   sodium   bicarbonate   therapy   in   Diabetic
Ketoacidosis

•    Definition of DKA and it pathophysiological consequences
•    The possible rationale for the use of sodium bicarbonate
o   Severe acidaemia (generally pH < 7.10 although no hard data)
o   Severe hyperkalemia
o   Bicarbonate loss from Renal or GI tract
•    The possible problems of giving sodium bicarbonate
o   Worsening of intracellular acidaemia
o   Hypokalaemia & Hypernatraemia
o   Large bolus of hypertonic solution
•    No  evidence   for  the  use  of  HCO3-    to  treat  acidaemia,   or  improve   cardiac contractility. In fact many different texts have different values for the cut off pH which
requires treatment, suggesting no real consensus.
•    The   correction   of   the   acidaemia   is   achieved   by   correcting   the   underlying pathophysiology with fluids and insulin
•    Some evidence for the use of HCO3-  in hyperkalaemia,  as a temporising measure, assuming underlying renal function is maintained
•    Theoretical potential for giving HCO3-  with renal wasting of HCO3-  or GI loss if delta ratio is <1 (usual for DKA)
•    Evidence suggesting that HCO3- is associated with worse outcome, however this in paediatrics, in patients who presented sicker (lower PaCO2 and higher urea on presentation).  However this does not assume causality and paediatric patients can compensate for longer.
•    Despite the lack of evidence it would appear that most intensivists have a personal cut-off pH at which they consider giving HCO3-

Discussion

The "critically evaluate" questions should be approached in a structured manner.

Introduction

  • DKA is a systemic illness associated with impaired glucose metabolism due to a lack of insulin (in IDDM) or due to insulin resistance (NIDDM). The decreased oxidative phosphorylation of glucose leads to a switch in metabolism, favouring lipolysis and the use of fatty acids for the purpose of ketone body synthesis. The ketone bodies dissociate into a conjugate base and hydrogen ion, acting as acids and thereby inducing acidosis.

Rationale for this practice

  • Sodium bicarbonate is an alkaline compound used to correct metabolic acidosis; it acts as an exogenous source of bicarbonate buffer, and titrates the pH of the body fluids.
  • The administration of bicarbonate in metabolic acidosis is expected to reverse the physiological disadvantages of acidosis, including cardiovascular instability
  • Ketones in DKA are lost in the urine and therefore cannot be metabolised (which would absorb the H+ ion ) - the urinary loss of ketones therefore represents the urinary loss of bicarbonate, and exogenous bicarbonate needs to be given to replace this.

Advantages

  • Return of pH to normality = restoration of normal cellular enzyme function
  • Normalisation of pH also restores normal catecholamine receptor-ligand affinity relationships, resulting in the improvement of haemodynamic performance.
  • Administration of Na+ cations results in an increase of the strong ion difference, which maintains the improvement in pH.
  • In the event of severe hyperkalemia, sodium bicarbonate administration causes a intracellular shift of potassium, which may be useful in the context of DKA.

Disadvantages

  • Return of pH to normality may be unnecessary, as many intracellular mechanisms of compensation for acidosis function optimally in the presence of acidosis. For instance, ketone body and lactate metabolism are delayed by bicarbonate administration.
  • The administration of hyperosmolar solution may result in fluid shifts of significant magnitude, particularly dangerous in those patients who have significant cardiac comorbidities.
  • The administration of a large volume of sodium bicarbonate to an already hypokalemic patient may result in worsening hypokalemia and cardiac arrest
  • Sodium bicarbonate may be converted to CO2 and internalised into cells, where it may counterproductively cause an intracellular acidosis.
  • Sodium bicarbonate may be rapidly turned into CO2 by the act of buffering, and thus may increase PaCO2 contributing to respiratory acidosis.
  • Oveshoot may occur, resulting in metabolic alkalosis
  • The alkalinisation of body fluid will result in a decrease in the ionised fraction of Ca++ leading to tetany and muscle spasm
  • Rapid correction of acidosis with bicarbonate may impair oxygen delivery to tissues resulting in tissue hypoxia (by counteracting the rightward shift of the oxyhemoglobin dissociation curve, which is the result of acidosis).

Evidence against the use of bicarbonate in DKA

Own practice

  • The only situations in which I personally would give bicarbonate for DKA:
    • Haemodynamic instability with escalating vasopressor requirements, coupled with a blood gas pH of less than 7.00
    • A serum bicarbonate level which is approaching 0, suggesting that the endogenous buffer systems are all but depleted.

References

This LITFL article offers a balanced and concise overview of this topic.

Chua, Horng Ruey, Antoine Schneider, and Rinaldo Bellomo. "Bicarbonate in diabetic ketoacidosis-a systematic review.Annals of intensive care 1.1 (2011): 1-12.

Hale, P. J., J. Crase, and M. Nattrass. "Metabolic effects of bicarbonate in the treatment of diabetic ketoacidosis." British medical journal (Clinical research ed.) 289.6451 (1984): 1035.

Soler, N. G., et al. "Potassium balance during treatment of diabetic ketoacidosis with special reference to the use of bicarbonate." The Lancet300.7779 (1972): 665-667.

Duhon, Bryson, et al. "Intravenous sodium bicarbonate therapy in severely acidotic diabetic ketoacidosis." Annals of Pharmacotherapy 47.7-8 (2013): 970-975.

Okuda, Y. U. K. I. C. H. I., et al. "Counterproductive effects of sodium bicarbonate in diabetic ketoacidosis." The Journal of Clinical Endocrinology & Metabolism 81.1 (1996): 314-320.

Question 26.2 - 2011, Paper 1

Examine the trace from a patient with a pacemaker  in the DDD mode.   What problem is seen with this pacemaker?

College Answer

Failure to sense the atrium

Discussion

The pacing spike seen after a normal P wave suggests the pacemaker has failed to detect normal atrial activity. The rhythm strip I used up there comes from a Medscape article.

References

Wiegand, Uwe KH, et al. "Diagnosis of atrial undersensing in dual chamber pacemakers: impact of autodiagnostic features.Pacing and clinical electrophysiology 22.6 (1999): 894-902.

 

Question 1 - 2011, Paper 2

List the complications and their likely underlying mechanisms specifically related to cardiopulmonary bypass that may be seen in the Intensive Care Unit following cardiac surgery.

College Answer

Respiratory complications
  • Left lower lobe collapse (poor re-inflation post bypass, phrenic nerve injury)
  • Increased pulmonary vascular resistance (protamine)
  • Acute lung injury (SIRS)
Cardiovascular complications
  • Myocardial stunning or infarction (inadequate myocardial protection)
  • Coronary graft ischaemia (air embolism)
  • Right ventricular dysfunction (pulmonary hypertension related to protamine)

Hypoperfusion and end-organ ischaemia related to non-pulsatile flow and/or air/atheroma embolism

Neurological complications
  • Cerebrovascular events, watershed infarcts, neurocognitive dysfunction (low flow, thromboembolism)
  • Phrenic nerve palsy (use of cold cardioplegia ‘slush’)
Renal complications
  • Dysfunction related to ischaemia and SIRS
 
Gastro-intestinal complications
  • Splanchnic ischaemia (low flow, thromboembolism)
  • Hepatitic dysfunction, acalculous / gangrenous cholecystitis, pancreatitis (hypoperfusion, SIRS)
Haematological complications
  • Coagulopathy (effects of hypothermia and dilutional coagulopathy, residual heparinisation, activation of coagulation cascade during bypass)
  • Anaemia (haemodilution, blood loss in the circuit)
  • Platelet dysfunction (bypass circuit)
  • Haemolysis (bypass circuit)
Metabolic complications
  • Hypothermia (intra-operative cooling and delayed re-warming)
  • Insulin resistance and hyperglycaemia (hypothermia)
  • Electrolyte abnormalities (haemodilution, post-pump diuresis)
Immune-mediated complications
  • Activation of coagulation cascade (blood contact with non-biological surfaces and blood-gas interface)
  • SIRS (leucocyte and complement activation, cytokine release and expression of adhesion molecules stimulated by contact with bypass circuit)
  • Allergic reactions to protamine

Discussion

There is no more complicated discussion here, other than a rearrangement of the above answer into a different set of headings. The question was relatively straightfrward. The references below illuminate this topic adequately, and if I were pressed for time I would use the UpToDate articles. The poor pass rate suggests to me that many candidates have not had the pleasure of working in a post-op cardiothoracic setting.

In addition to the lazy effort below, I have written my own notes on the complications one might anticipate after cardiac surgery.

Complications due to mechanics of the bypass circuit
  • Hemodilution
  • Haemolysis
  • Blood loss into the circuit
Complications due to SIRS (complement and coagulation cascade activation caused by exposure of blood to circuit components and open surgical wounds)
  • Coagulopathy due to coagulation cascade activation and clotting factor depletion
  • Platelet dysfunction and platelet depletion
  • Renal failure due to SIRS
  • Acute lung injury due to SIRS, “pump lung”
Complications due to circuit anticoagulation and its reversal:
  • Bleeding from residual heparin
  • Heparin-induced thrombocytopenia
  • Anaphylaxis to protamine
  • Increased pulmonary resistance due to protamine
  • Right ventricular failure due to protamine-induced pulmonary hypertension
Complications due to prolonged hypothermia:
  • Heart block
  • Ventricular and atrial arrhythmias
  • Hyperglycaemia (decreased insulin production as well as insulin insensitivity)
  • Decreased tubular resorption in the kidney (thus diuresis)
  • Phrenic nerve palsy (“cold slush cardioplegia”)
Complications due to prolonged ischaemia
  • Renal failure due to ATN
  • Myocardial infarction
  • Encephalopathy and neurocognitive deterioration
  • Hepatic dysfunction and delayed drug clearance
  • Pancreatitis
  • Splanchnic ischaemia
Complications due to mechanics of the surgery
  • Atelectasis (especially of the  LLL) due to mechanical compression
Complications due to intraoperative embolism of clot, air or atheroma
  • Myocardial infarction
  • Stroke
  • Splanchnic ischaemia
  • Limb ischaemia

References

Ray Raper's chapter in Oh's manual (pp.285) had surprisingly little about the complications of bypass. Thankfully, there are exhaustingly complete reference books:

Complications in cardiothoracic surgery: avoidance and treatment, Little A.G, Merril W.H. - 2007, 2nd ed. Chapter 4 by Creswell and Karis.

Cardiopulmonary bypass- Principles and Practice, Gravlee G.P. and Davis R.F -2007 (3rd ed.)

These are very thick books to read for just one past paper question.

Thus, and most importantly for the time-poor but dollar-rich ICU public, UpToDate contains a couple of excellent summary pieces on cardiac and non-cardiac complications of CABG.

 

 

Question 26.4 - 2011, Paper 2

On examination of a critically ill patient who was in respiratory distress, the following signs were noted:

  • Tachypnoea
  • SpO2 88%
  • Trachea shifted to the left
  • Reduced air entry and dullness to percussion in the infraclavicular and axillary areas on the left side.

a) What is the likely lung pathology?

b) List 3 causes of this pathology in critically ill patients.

College Answer

a) What is the likely lung pathology?
Left lung collapse


b) List 3 causes of this pathology in critically ill patients.
Right bronchial intubation
Mucus plugging – left main bronchus
Obstructive lesions left main bronchus.

Discussion

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

a) What is the likely lung pathology?
There can really be only one sort of pathology which causes a retraction of the mediastinum towards the silent lung. Atelectasis of the whole lung has somehow occurred.


b) List 3 causes of this pathology in critically ill patients.

The Required Reading chapter on the care for the post-pneumonectomy patient includes a brief section with this list of differentials. It was not the most appropriate place to put this list, but there was nowhere else to put it.

In brief, these are the causes of a silent hemithorax with mediastinal shift towards the quiet side, in a patient who is in respiratory distress:

  • Right bronchial intubation
  • Occlusion of a main bronchus:
    • Sputum plugging
    • Inhaled object
    • Migrated tracheal or bronchial stent
    • Large blood clot in massive haemoptysis
    • Tumour
  • Post pneumonectomy patient whose left chest drain has been left on suction.
  • Phrenic nerve injury with a paralysed hemidiaphragm
 

References

Clinical Examination of the Critically Ill Patient, 3rd edition by L.I.G. Worthley - which can be ordered from The Book Depository

Clinical Examination: whatever edition, by Talley and O'Connor.

Iyer, Anand, and Sumit Yadav. "Postoperative Care and Complications After Thoracic Surgery." (2013).

Question 19 - 2012, Paper 1

  • Briefly, outline the concepts behind intra-aortic balloon counterpulsation (IABCP)
  • 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?
  • What methods can be used to trigger the IABCP?
  • 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? 

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?

labelled diagram of IABP 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.

References

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.

Question 5.3 - 2012, Paper 1

Figure 4:

What two abnormalities are shown in the pressure tracing? 

College Answer



d) Abnormalities 
• Early balloon inflation 
• Early balloon deflation

 

Discussion

This is a pattern recognition question which relies on the candidate's familiarity with troubleshooting equipment.

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:

early IABP deflation fails to improve LV afterload

References

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.

Question 13 - 2012, Paper 1

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

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

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

a) Outline your differential diagnosis for his hypotension

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

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

College Answer

a) Differential diagnosis for hypotension

  • Artefactual 
  • Preload – intravascular volume depletion (eg blood loss, rewarming), medication effect (eg 
    propofol), anaphylaxis, vasoplegia 
  • Contractility – arrhythmia, myocardial ischaemia, valvular dysfunction, hypoxia, pacing wire 
    problem 
  • Afterload – pericardial tamponade, tension pneumothorax, elevated intrathoracic pressure 
  • Outflow tract obstruction

b) Causes of post-operative bleeding and management

  • Excessive bleeding is usually due to one or more of the following factors:
    • incomplete surgical hemostasis
    • residual heparin effect after cardiopulmonary bypass
    • platelet abnormalities (platelet dysfunction and thrombocytopenia – from bypass, antiplatelet agents etc)
    • hypothermia
    • postoperative hypertension
    • clotting factor depletion
    • hemodilution (dilutional thrombocytopenia and coagulopathy)
  • Initial management
    • Assess airway, breathing, circulation.
    • PEEP 10
    • Look for potential underlying causes (as above).
    • Measure ACT and formal coagulation profile. If ACT/APTT raised, consider Protamine. 
    • Consider platelet transfusion early if antiplatelet agent in days prior to surgery or platelet dysfunction considered likely contributor. 
    • Manage hypertension with titratable agent (eg GTN, SNIP) 
    • Correct hypothermia 
    • FFP if INR and/or APTT raised. Platelet transfusion if thrombocytopenia.
    • Transfusion of packed red blood cells may also be necessary to replace blood loss. Optimal transfusion strategy, including the level below which RBC transfusion clearly improves outcomes, is uncertain (eg TRACS trial).
    • Notify cardiothoracic surgeon early if concerned. Pre-existing protocol (including guidelines for notification) useful.
    • If haemodynamically unstable from blood loss, or if bleeding persists despite above measures, consider re-thoracotomy.
    • Use of DDAVP and Factor 7 controversial. 

Discussion

This question revisits the topic of post-cardiothoracic surgery complications. Ruesch and Levy, in their chapter from Practical Approach to Cardiac Anaesthesia have nice point-form guides which calmly deal with the stressful situation of haemodynamic instability after bypass. (in general, that book is awesome). I have made my own notes on this subject, but I claim no special expertise in it. There I categorise the differential diagnosis for hypotension in the post-bypass patient, as well as the various steps one needs to take in assessing the medical and surgical causes of bleeding.

In general, it is good to organise the answer to these in the system of "measurement error, preload, contractility, afterload, rate and rhythm"; or any other system (any is better than none).

Thus:

Causes of post-cardiotomy instability, organised by alphabetical mnemonic order

A - Artifactual; art line is incorrectly zeroed

B - Tension pneumothorax

C - Cardiac tamponade

   - Myocardial ischaemia

   - Acute valvular failure (eg. of grafted valve)

   - LVOT obstruction

   - Post-bypass myocardial depression

   - Arrhythmia (eg. AF)

D - Excess sedative (eg propofol)

E - Post-bypass hypocalcemia

F - Inadequate preload - need more fluid

...Or: excessive preload in the failing left heart - causing diastolic dysfunction of the left heart

G - Arterial embolism of the mesenteric vessels (chaos ensues)

H - Haemorrhage - inadequately reversed heparinisation or DIC

   - could be into pericardial sack or pleural space

I - Anaphylaxis; reaction to anaesthetic agents

   - Vasoplegia due to circuit-induced SIRS

Causes of post-cardiotomy instability, organised by affected hemodynamic variable

  • Preload
    • Inadequate intraoperative fluid
    • Haemorrhage
    • Valve failure (mitral / tricuspid)
  • Rate
    • Bradycardia (or excessive tachycardia!)
  • Rhythm
    • AF or other arrhythmia
  • Contractility
    • Post-bypass myocardial depression
    • Myocardial ischaemia
  • Afterload
    • Artifact: art line is incorrectly zeroed
    • LVOT obstruction
    • Anaphylaxis
    • Vasoplegia
    • Valve failure (aortic or pulmonic)

Post-cardiothoracic surgical bleeding complications

Excessive bleeding is usually due to one or more of the following factors:

  • incomplete surgical hemostasis
  • residual heparin effect after cardiopulmonary bypass
  • platelet abnormalities (platelet dysfunction and thrombocytopenia – from bypass circuit consumption , antiplatelet agents etc)
  • hypothermia
  • postoperative hypertension
  • clotting factor depletion
  • haemodilution (dilutional thrombocytopenia and coagulopathy)

Immediate management

  • Maintain  SpO2 ~ 100%
  • Adjust positive pressure, with two goals in mind:
    • Enhancement of preload by controlling the intrathoracic venous flow
    • Enhancement of afterload by increasing LV transmural pressure
    • Perhaps some sort of tamponade effect - the college answer recommends a PEEP of 10, which ( a reader has helpfully pointed out) probably comes from Ilabaca et al (1980).
  • Assess the drains to make sure they are not blocked
  • Maintain satisfactory diastolic pressure with noradrenaline and/or vasopressin
  • Give a fluid bolus
  • Check for a cardiovertable rthythm disturbance
  • Consider increasing pacing rate to 90
  • Organise a TOE or TTE to assess the need for inotropes
  • Check bloods and TEG to see what further factors/platelets the patient might require
  • Alert the surgeons to the deterioration, in case you need to reopen the chest

References

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

André, Arthur C. St, and Anthony DelRossi. "Hemodynamic management of patients in the first 24 hours after cardiac surgery." Critical care medicine 33.9 (2005): 2082-2093.

Estafanous, Fawzy G., and Robert C. Tarazi. "Systemic arterial hypertension associated with cardiac surgery.The American journal of cardiology 46.4 (1980): 685-694.

Roberts, A. J., et al. "Systemic hypertension associated with coronary artery bypass surgery. Predisposing factors, hemodynamic characteristics, humoral profile, and treatment." The Journal of thoracic and cardiovascular surgery 74.6 (1977): 846-859.

Ilabaca, Patricio A., John L. Ochsner, and Noel L. Mills. "Positive end-expiratory pressure in the management of the patient with a postoperative bleeding heart." The Annals of thoracic surgery 30.3 (1980): 281-284.

Question 19 - 2012, Paper 2

Discuss the potential mechanical strategies for supporting myocardial function in a 45-year-old man presenting with cardiogenic shock post-revascularisation for an acute anterior myocardial infarction. In your answer include the physiological rationale for each strategy.

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:

 Mechanical Haemodynamic Support Strategies
Strategy Advantages Limitations

Positive pressure ventilation:
the use of positive pressure to decrease LV preload and afterload (by manipulating transmural pressure)

  • Easy to apply
  • Minimally invasive
  • Added benefit of improved oxygenation and gas exchange
  • Invasive ventilation has the added benefit of anaesthesia +/- paralysis, which decreases whole-body oxygen demand
  • Preload reduction may result in hypotension in the volume-depleted patient
  • Increased intrathoracic pressure increases RV afterload, exacerbating right heart failure
  • Positive pressure may result in barotrauma and volutrauma
  • All the risks of mechanical ventilation apply, eg. VAP
Temporary transcutaneous pacing:
  • Requires minimal skill to apply
  • Minimally invasive
  • Cardiac output will increase in proportion to
  • Requires a substantial amount of analgesia and sedation
  • Uncomfortable for the patient
  • May cause significant tissue damage
  • Not a long-term solution
  • Poor A-V synchrony
Temporary transvenous pacing
  • Comparatively easy to insert
  • Dual-chamber pacing may improve A-V synchrony and restore the "atrial kick".
  • Not only does it work in bradycardia, but also by "overdrive pacing" in tachycardia, where the slowed heart rate allows for longer diastolic filling
  • Requires some expertise to manage and troubleshoot
  • Invasive, with all the risks of large-bore central venous access
  • Generally, one can only pace the ventricle, which means A-V synchrnoy will be lost; the "atrial kick" may be sorely missed by patients with severe valve dysfunction
Cardiac resynchronisation therapy: biventricular pacing
  • Restores synchrony to ventricular contraction in patients with severe heart failure
  • There is strong evidence that CRT reduces mortality and hospitalisation  (i.e. it is superior to AICD or medical therapy).
  • Requires specialist skill to insert and adjust; hardly an emergency procedure
  • To benefit, one must have LBBB, a wide QRS, and an LVEF less than 35%.
  • Generally, only about 5-10% of heart failure patients will benefit
  • There is a "heterogeneity of effect" in patients  who do not meet the recognised criteria (read: it does them no good)
Intra-aortic balloon pump:
  • Decreases LV afterload
  • Improves coronary arterial filling in diastole
  • Improves forward flow though defective mitral valves
  • Nowadays, little adjustment is required (automatic timing is usually satisfactory)
  • "Severe" cardiogenic shock is still not very well investigated, and there may be an unrecognised  mortality benefit in this group.
  • Violently invasive
  • Requires a certain level of expertise to place correctly.
  • Significant complications are associated with its use, including a non-zero rate of death and limb loss.
  • The mortality benefit in most patients might either be marginal or altogether absent, depending on what you read. Certainly, the IABP-SHOCK II trail did not demonstrate any survival improvement.
  • Does not benefit the right ventricle.
  • Contraindicated in aortic regurgitation
  • Poor effect in AF, particularly rapid AF
Ventricular assist devices:
  • Decreases myocardial workload
  • Offers a bridge to heart transplantation
  • Effective temporary support for myocardial stunning
  • May afford a period of outpatient management
  • Highly invasive
  • Requires surgical expertise to implement
  • Requires significant anticoagulation
  • Substantial risk of infection (50%)
  • In spite of anticoagulation, there is a significant risk of thrombosis
VA- ECMO
  • Not only decreases myocardial workload- it may take over all of the circulatory workload.
  • Attends to both circulation and gas exchange
  • Easier to implement (percutaneous technique does not require surgical expertise)
  • Highly invasive
  • Requires expertise to implement
  • Requires significant anticoagulation
  • In spite of anticoagulation, there is a significant risk of thrombosis
  • All the complications of large-bore arterial and venous access

Less relevant local links include the following:

References

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.

Question 7 - 2013, Paper 1

Discuss the role of nor-adrenaline in the management of hypotension post cardiac surgery.

College Answer

Introduction

Hypotension following cardiac surgery is a common and important problem. Appropriate management includes correct diagnosis of the underlying problem and definitive treatment of the cause as well as supportive care.

Rationale

Primarily alpha agonist (vasoconstriction) with increasing beta actions (ino/chronotrophy) as dose increases. 
Has a short half- life and so given as continuous intravenous infusion and easily titratable. Increases blood pressure mainly by increase in diastolic BP and so increasing MAP and also increasing coronary artery perfusion pressure

Reflex bradycardia with lower doses may also allow increased time for diastole and so increased ventricular filling and coronary artery perfusion

Pros

Appropriate for post- pump vasodilation / SIRS response to CBP – a common cause of post cardiac surgery hypotension

There is less risk of the Beta adrenergic side effects of adrenaline such as tachyarrhythmias, hyperlactataemia and hyperglycaemia.

It has the potential advantage of increasing DBP and myocardial perfusion and subsequently contractility in context of ischaemia.

Familiar agent in ICU setting

Cheap and widely available (not all countries e.g. South Africa)

Cons

Must be used with caution as a single agent in scenarios where preload or contractility is not optimal.

I.e. exclude / correct hypovolaemia, tamponade and treat poor myocardial function appropriately

Excessive use can result in end-organ hypoperfusion.

Own practice.

Any reasonable practice and justification acceptable.

Summary

Nor-adrenaline is useful drug in this situation when hypotension due to vasodilation or reduced coronary perfusion pressure but important to ascertain and treat the underlying cause.

Discussion

The above answer does not call for a superior level of pharmacological insight. "Any reasonable practice and justification acceptable" they say.

Noradrenaline in general is well discussed elsewhere.

A brief discussion of the role of noradrenaline in the post-cardiotomy setting can be found in the  "Required Reading" section concerned with cardiothoracic intensive care.  Highlights include the following:

Rationale

  • Hypotension in the post-cardiothoracic surgery patient can be due to a multitude of factors.
  • Noradrenaline theoretically addresses at least some of them, namely:
    • Improves preload (by venoconstriction)
    • Improves vasoplegia (by arterioconstriction)
    • Improves cardiac contractility (β-1receptor effect increases with increasing dose)
    • Improves diastolic filling of coronary arteries (by increasing diastolic pressure)
    • Improves diastolic filling of the ventricles (by producing a reflex bradycardia)

Advantages of noradrenaline

  • Cheap, by the standards of a developed country
  • Short half life: easily titrated
  • Relatively pure α-1 agonist effect; thus, no lactic acidosis due to its use
  • Relatively linear dose-response relationship; predictable effects.

Disadvantages of noradrenaline

  • Expensive, by the standards of a developing country (dopamine is still in use in many places owing to its gentle effect on the ICU budget)
  • Increased afterload increases LV workload and decreases subendocardial perfusion, potentially worsening ischaemia
  • In hypotension due to cardiogenic shock, noradrenaline will do little to improve blood pressure
  • Temporary improvement in hemodynamic variables may obscure another cause of hemodynamic instability, eg. haemorrhage, infarction or cardiac tamponade.

Evidence for its use

References

Maas, Jacinta J., et al. "Cardiac Output Response to Norepinephrine in Postoperative Cardiac Surgery Patients: Interpretation With Venous Return and Cardiac Function Curves*." Critical care medicine 41.1 (2013): 143-150.

Hajjar, L., et al. "Vasopressin Versus Norepinephrine for the Management of Shock After Cardiac Surgery (VaNCS study): a randomized controlled trial." Critical Care17.Suppl 2 (2013): P222.

Antman EM, Anbe DT, Armstrong PW, Bates ER, Green LA, Hand M, Hochman JS, Krumholz HM, Kushner FG, Lamas GA, Mullany CJ, Ornato JP, Pearle DL, Sloan MA, Smith SC Jr, Alpert JS, Anderson JL, Faxon DP, Fuster V, Gibbons RJ, Gregoratos G, Halperin JL, Hiratzka LF, Hunt SA, Jacobs AK. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction). Circulation. 2004; 110: 588–636.

Question 28 - 2013, Paper 1

The following ECG trace was taken from a 68-year-old male, one hour following aortic valve replacement for aortic stenosis.
Atrial and ventricular epicardial pacing wires are in place, and the pacing mode is DDD.

ECG

  • What problem is demonstrated?
  • Outline the steps that you would take to address the problem.

The problem is resolved and normal DDD pacing resumes. One hour later another ECG trace is taken.

ECG

  • What new problem is demonstrated?
  • Briefly outline the underlying pathophysiological mechanism.
 

College Answer

a)

Intermittent failure of ventricular capture.

b)

  • Increase the ventricular output
  • Check the connections to the pacemaker and pacing connector leads
  • Reverse the polarity of the pacing to the ventricle
  • Replace pacemaker box and/or pacing connector leads
  • Unipolar pacing with cutaneous pacing stitch
  • Pharmacological therapy eg isoprenaline
  • Alternative pacing method – transcutaneous, transvenous
  • Open chest and replace epicardial wires

c)

Pacemaker mediated tachycardia.

d)

The dual chamber pacemaker is forming part of a re-entry circuit. A ventricular ectopic has triggered retrograde conduction along the patient’s conducting system. The resulting P-wave has been sensed by the atrial lead of the pacemaker, and this has triggered ventricular pacing. The paced ventricular impulse has triggered retrograde conduction along the patient’s normal conducting system, and the cycle continues.

Discussion

a)

There are two pacing spikes. DDD mode pacing is clearly detecting an absence of either atrial or ventricular spontaneous activity. Indeed if you look at what happens when it fails to capture, the patient native rhythm looks eerily like asystole. The atrium seems to respond (there is a little bump of atrial contraction after each atrial spike) but there is a failure of AV conduction.

b)

To troubleshoot this problem, one ought to use a systematic approach. LITFL again come to the rescue with an excellent summary of troubleshooting steps.

One could summarise it thus:

  • Put external pacing pads on the patient. You want an alternative pacing method to be immediately available if everything goes tits-up.
  • Check the box.
    • Is the battery running out? (Typically, a pacing box can last 40 days or so on one 9V alkaline battery)
  • Check the circuit
    • is the patient still "plugged in" to the pacing box?
  • Check the pacing wires
    • Is the CXR available to check whether their position has changed?
    • Are the wires attached properly?
  • Check the patient
    • Correct electrolytes
  • Increase the ventricular output
    • Max is about 25mA
  • Reverse the polarity of the leads
    • this might improve the situation - for some reason the negative electrode develops fibrosis first. Swapping them around can sometimes improve conduction.
  • Connect the previously positive epicardial lead to the negative TPM cable, and use an external pacing stitch as the positive lead. This way, you use the (hopefully) still fresh lead to pace the patient in a "unipolar" fashion.
  • Start isoprenaline. Hopefully this makes the myocardium more responsive to pacing, or at least the native rate might improve.
  • Pace externally or transvenously - float a temporary pacing wire into the patient; abandon the epicardial leads as useless.
  • Open the chest and resite the epicardial wires - this is an extreme solution.

c) and d) refer to the phenomenon of "endless loop tachycardia" where the pacemaker triggers its own atrial sensor by having the ventricular lead's signal conducted into the atria by a reentry circuit. These are hilarious. The rate is dictated by the size of the circuit, so the closer the atrial sensing lead to the reentry point, the more rapid the tachycardia. You can usually terminate these by putting a magnet on the pacemaker (forcing it to pace asychronously, totally ignoring the atria).

How do you recognise this? Well, the rate is going to be about 125-50 (judging by the rhythm strip) so one can assume that if the pacemaker seems to be initiating it, it must be malfunctioning in some way.

References

Reade, M. C. "Temporary epicardial pacing after cardiac surgery: a practical review: Part 2: Selection of epicardial pacing modes and troubleshooting."ANAESTHESIA-LONDON- 62.4 (2007): 364.

FURMAN, SEYMOUR, and JOHN D. FISHER. "Endless loop tachycardia in an AV universal (DDD) pacemaker.Pacing and Clinical Electrophysiology 5.4 (1982): 486-489.

Question 1 - 2013, paper 2

A 76-year-old female is admitted to the ICU following elective aortic and mitral valve replacement. Transoesophageal echo assessment at the end of surgery showed an ejection fraction of 20%. Her preoperative creatinine was 340 μmol/L. Total bypass time was 240 minutes. On arrival in ICU the patient has the following indices;

  • Temperature 35°C
  • Atrial pacing (AAI) 80/min
  • Systemic blood pressure 85/55 mmHg
  • Pulmonary artery pressure 60/30 mm Hg
  • Cardiac index 1.5 litres.min.m-2
  • Systemic vascular resistance 1700 dyn.sec.cm--5
  • Pulmonary artery wedge pressure 10 mmHg
  • Central venous pressure 8 mmHg
  • The patient is currently on adrenaline 4μg/min by infusion.

a) List the specific clinical and haemodynamic issues for this patient on admission to ICU.

b) Outline your management of these issues.

College Answer

a) The main clinical and haemodynamic issues identified are:
Elderly female patient post double valve surgery.
Pre-existing renal impairment.
Long bypass time.

Systemic hypotension (MAP 65 unlikely to be adequate for this patient).
Low output state (CI, EF post bypass).
Increased afterload / vascular impedance (SVR).
Probable fluid responsiveness (PAWP, CVP).
Moderate pulmonary hypertension.
Low core temperature.

b) This patient is high risk (female, age, long bypass time, pre-existing renal impairment, low EF). Management consists of:

  • Re-warming.
  • Judicious fluid replacement as she re-warms.
  • Improved volume state may augment CI but given poor EF unlikely to be sole intervention needed.
  • Titration of adrenaline infusion, aiming for CI > 2.2
  • Bedside echo to evaluate effect of fluid and increased adrenaline, exclude tamponade and check valve function (mitral regurgitation can increase PAP and decrease cardiac output).
  • Consideration of other vasoactive agents (dobutamine, milrinone, levosimendan) or IABP insertion if persisting low output state.
  • Assess adequacy of pacing and consider changing mode to A-V pacing (heart block common after AVR) and /or increasing rate to 90 bpm.
  • Correct post-op coagulopathy and replace blood losses to maintain Hb > 80 G/L. Surgical review if significant blood loss via drains.
  • Evaluation of any other cause of low output state e.g. tension pneumothorax, dynamic hyperinflation.
  • Close monitoring of renal function and early institution of renal replacement therapy if oligo-anuric or rising creatinine.
  • Consideration of inhaled nitric oxide to reduce pulmonary hypertension and RV afterload.

Discussion

This patient they have given you is slightly unwell. I have reformulated the answer into a systematic approach to this problem. The answer below is question-specific (as they generally should be) - a generic approach to the haemodynamically unstable cardiac surgical patient is discussed elsewhere.

  • Issues
    • Cardiogenic shock
    • Hypovolemia
    • Pulmonary hypertension
    • Hypothermia
  • Assessment
    • Examination, including dynamic manoeuvres to assess for fluid responsiveness
    • ECG to exclude STEMI
    • CXR to exclude pneumothorax
    • Arterial blood gas
    • Mixed venous blood gas
    • Formal TTE to examine valve function and sclude tamponade
  • Management
    • Re-warm patient
    • Sedate and paralyse patient to decrease whole-body oxygen demand
    • Maintain Hb ~ 80 and SpO2 ~ 100% to maintain satisfactory tissue oxygen delivery
    • Maintain heart rate and rhythm control with pacing and antiarrhymic drugs (eg. amiodarone); consider increasing rate to 90
    • Optimise RV preload: give fluid bolus 20-40ml/kg
    • Increase RV + LV contractility with milrinone or levosimendan
    • Decrease RV and LV afterload with milrinone or levosimendan (pulmonary and systemic vasodilation)
    • Decrease mycoardial workload with IABP especially if there is evidence of ischaemia with inotorope use
    • Maintain satisfactory diastolic pressure with noradrenaline

References

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

André, Arthur C. St, and Anthony DelRossi. "Hemodynamic management of patients in the first 24 hours after cardiac surgery." Critical care medicine 33.9 (2005): 2082-2093.

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.

Goepfert, Matthias SG, et al. "Goal-directed fluid management reduces vasopressor and catecholamine use in cardiac surgery patients." Intensive care medicine 33.1 (2007): 96-103.

Question 10.2 - 2013, paper 2

A 75-year-old male is a patient in your ICU, day three following an elective oesophagectomy.

Examine the photograph provided.

drain

a) What complication has occurred?

b) What is your management of this complication?

College Answer

a) Chylothorax secondary to thoracic duct damage.

NB: Both parts needed for whole mark.

b) Conservative management with drainage, octreotide and TPN. Surgical management with pleurodesis or thoracic duct ligation

Discussion

The picture abode is of a drain with chyle in it, which was not part of the original college paper. Indeed, nobody knows what precisely the college depicted in their version.

I have attempted to provide the candidate with a picture which has in it an unambiguously creamy opaque fluid, sitting in some obvious chest drain tubing.

And yes, chylothorax is a frequent complication of oesophagectomy.

Diagnosis of chylothorax:

Management of chylothorax

References

Fahimi, Hossein, et al. "Current management of postoperative chylothorax." The Annals of thoracic surgery 71.2 (2001): 448-450.

Fujita, Takeo, and Hiroyuki Daiko. "Efficacy and Predictor of Octreotide Treatment for Postoperative Chylothorax After Thoracic Esophagectomy." World Journal of Surgery (2014): 1-7.

Seriff, NATHAN S., et al. "Chylothorax: diagnosis by lipoprotein electrophoresis of serum and pleural fluid." Thorax 32.1 (1977): 98-100.

Hillerdal, G. "Chylothorax and pseudochylothorax." European Respiratory Journal 10.5 (1997): 1157-1162.

Shah, Rachit D., et al. "Postesophagectomy chylothorax: incidence, risk factors, and outcomes." The Annals of thoracic surgery 93.3 (2012): 897-904.

Merigliano, Stefano, et al. "Chylothorax complicating esophagectomy for cancer: a plea for early thoracic duct ligation." The Journal of thoracic and cardiovascular surgery 119.3 (2000): 453-457.

Valentine, Vincent G., and Thomas A. Raffin. "The management of chylothorax." CHEST Journal 102.2 (1992): 586-591.

Nair, Sukumaran K., Matus Petko, and Martin P. Hayward. "Aetiology and management of chylothorax in adults." European journal of cardio-thoracic surgery 32.2 (2007): 362-369.

Hashim, Sami A., et al. "Treatment of chyluria and chylothorax with medium-chain triglyceride." New England Journal of Medicine 270.15 (1964): 756-761.

Question 29 - 2013, paper 2

A patient in the Intensive Care Unit develops complete heart block with hypotension and has a temporary transvenous pacing wire inserted.

b) Define the pacing threshold and describe how you would test and set it.

c) Describe how you would check the pacing sensitivity.

c) What is the purpose of setting the pacing sensitivity?

The bedside nurse informs you that the output has been increased markedly over the course of his shift to maintain capture.

d)  What reversible factors might cause this problem?

College Answer

a)

  • This is the minimum amount of current (in mA) required to initiate depolarization of the paced chamber.
  • Set rate paced rate 10 above HR (to ensure patient’s rhythm is over ridden minimizing risk of R on T) and set to full demand mode (i.e. high sensitivity- low mV) and output current of 5mA.
  • Decrease output until 1:1 capture is lost.
  • Slowly increase output till 1:1 capture is regained. This is the pacing (stimulation) threshold.
  • The final setting is usually double the pacing threshold.

b)

  • This is only checked when the patient has an intrinsic rhythm which affords some cardiovascular stability.
  • Set the pacemaker rate10 below patients intrinsic rate
  • Set the output to a very low value e.g., 0.1mA
  • Setting the pacemaker to asynchronous mode by turning the sensitivity to its lowest value (highest mV setting) AFTER setting the output current to its lowest value (e.g. 0.1mA) so as to not capture but trigger the pacing indicator.
  • The sensitivity is the gradually increased (lower mV) until the pacemaker senses the patients intrinsic HR and the pacing indicator no longer illuminates but the sensing indicator does.
  • This is the sensing threshold.
  • The final setting is usually half this determined value.

c)

  • This tests the ability of the pacemaker to sense the patient’s intrinsic cardiac activity when one is present so that the pacemaker does not deliver an inappropriate stimulus in competition with the patient intrinsic rate when it is functioning in demand mode.
  • Prevents R on T phenomena

d)

  • Poor wire placement, movement of the wire
  • Acid Base abnormalities,
  • Hypo or Hyperkalaemia,
  • Hyperglycaemia,
  • Drugs e.g. B blockers, calcium antagonists.

Discussion

In general, the details of sensitivity and output settings of the temporary pacemaker  are discussed in the section concerned with mechanical haemodynamic support. In order to simplify revision and to reduce the total volume of reading, a brief guide to troubleshooting the pacemaker circuit  is also available.

 

b) Define the pacing threshold and describe how you would test and set it.

The college answer is sufficiently succinct. "This is the minimum amount of current (in mA) required to initiate depolarization of the paced chamber". It is otherwise known as the capture threshold.

Basically, you set the pacing rate to higher than the patient's native rate, and then down-titrate the current of the output until you lose capture. The point at which you barely capture is the pacing threshold. You may want to set the current to somewhere above this (say, double), to ensure capture.

c) Describe how you would check the pacing sensitivity.

Pacing sensitivity is checked by adjusting the sensitivity setting up, and then down. First, you need to set the pacemaker at a heart rate lower than the native rate. Then, increase the sensitivity setting until the pacemaker no longer senses (and starts to pace asynchronously). Then, you adjust it down (until no pacing occurs whatsoever). This lowermost sensitivity is the sensor threshold.

c) What is the purpose of setting the pacing sensitivity?

Well, if the pacemaker is sensing appropriately, it wont compete with the native pacemakers, and you wont get R on T phenomena.

The bedside nurse informs you that the output has been increased markedly over the course of his shift to maintain capture.

d)  What reversible factors might cause this problem?

There are numerous reasons why the pacemaker might need higher current to capture.

The college answer is appropriate and brief.

  • Wire malposition
  • Electrolyte derangement
  • Hypoglycaemia
  • Antiarrhytmics

"Reversible" is the key. No marks would be given to the man who mentions fibrin deposition.

References

Reade, M. C. "Temporary epicardial pacing after cardiac surgery: a practical review." Anaesthesia 62.3 (2007): 264-271.

Reade, M. C. "Temporary epicardial pacing after cardiac surgery: a practical review: Part 2: Selection of epicardial pacing modes and troubleshooting."ANAESTHESIA-LONDON- 62.4 (2007): 364.

Gammage, Michael D. "Temporary cardiac pacing." Heart 83.6 (2000): 715-720.

Sanders, Richard S. "The Pulse Generator." Cardiac Pacing for the Clinician. Springer US, 2008. 47-71.

Question 23 - 2014, Paper 1

A 39-year-old female is admitted to a tertiary centre and intubated and ventilated for severe Legionella pneumonia. Two days after admission to ICU she remains profoundly hypoxaemic (PaO2/FiO2 = 55), despite optimising ventilatory support and appropriate antimicrobial therapy.

a) Outline the factors that would influence your decision whether or not to institute extra-corporeal membrane oxygenation (ECMO) in this patient.

b) Outline the relative merits of veno-venous (V-V) and veno-arterial (V-A) ECMO for this patient.

College Answer

a)
ECMO is indicated for potentially reversible life-threatening cardiac and/or respiratory failure unresponsive to conventional support, buying time for recovery from the underlying condition and specific treatment to take effect.
This patient meets criteria for ECMO with a potentially reversible condition (Legionella pneumonia) and P/F < 60 and age < 65 years.

Alternative treatment strategies
 Ensure all other strategies have been tried – (e.g. - recruitment manoeuvres, prone positioning, NO/inhaled prostacyclin, diuresis, etc.)
 Exclude easily treated reversible problem e.g. pneumothorax, mucous plugging
 Ensure optimisation of haemodynamics, consider measurement of adequacy of DO2
Exclude contra-indications / relative contra-indications – severe pre-existing organ dysfunction, presence of other severe co-morbidities e.g. advanced malignancy, co-existing irreversible lung/cardiac pathology, and presence of bleeding disorder.
Available resources – appropriate level of expertise with trained staff to insert catheters, set up, monitor and troubleshoot ECMO circuit, and adequate equipment.
(Reference to meeting unit/regional criteria for institution of ECMO, or similar, are an acceptable answer.)

b)
Choice of V-V or V-A ECMO will depend on co-existing cardiogenic shock. V-A ECMO provides complete cardio-respiratory support, whereas V-V ECMO only provides respiratory support. If profound septic shock with myocardial depression and EF<25%, V-A ECMO indicated. If adequate cardiac function then V-V ECMO indicated otherwise significant native blood pulmonary blood flow and cardiac output results in relatively hypoxic perfusion of upper body compared with lower half.
V-V ECMO also avoids risks of serious arterial injury, has less severe consequences in case or air or clot embolization, and as a low-pressure system may prolong circuit life.
Animal studies suggest preservation of pulmonary blood flow with V-V ECMO may improve recovery from lung sepsis compared with V-A ECMO.

Discussion

For a 10 mark question, this college model answer seems somewhat barren. One might expect at least a bit of a digression into ECMO. Applications of ECMO and literature regarding the use of ECMO are discussed elsewhere. In brief:

Indications for ECMO

In order to qualify for this level of critical care, one must be special in the following ways:

  • The condition must be reversible; OR the patient qualifies for a heart/lung transplant
  • The conventional management strategies have failed.

The following situations call for ECMO:

  • Cardiac arrest (in certain settings)
  • Failure to wean from cardiopulmonary bypass
  • Cardiogenic shock
  • Hypoxic respiratory failure
  • Hypercapneic respiratory failure

Contraindications for ECMO

  • Contraindications to anticoagulation: recent surgery, uncontrolled bleeding, intracranial haemorrhage
  • Irreversible condition
  • Contraindications for heart/lung transplant

Caveats to ECMO

Before subjecting a patient to such a perversely unnatural therapy, one ought to satisfy onself that every "conventional" strategy has failed. These include:

  • Recruitment manoeuvres
  • prone positioning
  • NO/inhaled prostacyclin
  • diuresis
  • Fluid resuscitation and optimised PEEP to improve V/Q matching

The latter point needs to be expanded. Often people with severe hypoxic respiratory failure are on a high PEEP, with the aim of recruiting more alveoli. Unfortunately this pressure is often transmitted to healthy lung regions which results in overdistension, and basically creates a large Zone 1 (of Wests' Zones). At the same time the blood flow which would have gone to these well-aerated regions will be distributed to collapsed lung regions, where the high PEEP does not reach -i.e. increasing shunt. The effect is of worsening hypoxia and hypercapnia with increasing PEEP ( a larger Zone 1 and a larger physiological dead space).. The solution is to reduce the PEEP and give some fluid boluses, so that the right heart can deliver blood into these previously poorly perfused lung regions.

Veno-venous vs veno-arterial ECMO

Each has advantages and disadvantages.

  • VA ECMO has the advantage of providing complete cardiorespiratory support, and is therefore applicable in patients with very poor cardiac function (LVEF less than 25%)
  • VA ECMO has the disadvantage of large-bore arterial puncture, which is a major problem. VV ECMO has less vascular access issues, but is only indicated for patients with good myocardial function.

In summary, the evidence:
 

These abovementioned rules are fairly elastic. Specifically, where it comes to concerns regarding vascular access complications, it is now unclear whether VA ECMO is truly more dangerous. Similarly, where it comes to severe haemodynamic compromise, it is unclear whether VV ECMO is truly pointless.

  • In neonatal respiratory failure, back in 1996, Knight et al found that the frequency of intravascular thrombosis was significantly lower in patients receiving venovenous ECMO, and that otherwise things which were felt to be contraindications (eg. severe cardiac failure) weren't real barriers to successful VV ECMO.
  • A 2000 review agreed with this in principle, but failed to discern any difference in the rate of complications in the neonatal/paediatric population.
  • A more recent 2015 conference abstract also failed to find any difference in complications among adults.

References

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.

Davies, Andrew, et al. "Extracorporeal membrane oxygenation for 2009 influenza A (H1N1) acute respiratory distress syndrome." JAMA: the journal of the American Medical Association 302.17 (2009): 1888-1895.

Stub, Dion, et al. "Refractory cardiac arrest treated with mechanical CPR, hypothermia, ECMO and early reperfusion (the CHEER trial)." Resuscitation 86 (2015): 88-94.

Thourani, Vinod H., et al. "Venoarterial extracorporeal membrane oxygenation (VA-ECMO) in pediatric cardiac support." The Annals of thoracic surgery 82.1 (2006): 138-145.

Kolman, D., et al. "Clinical Outcomes In Patients With Advanced Cardiopulmonary Failure Who Were Treated With Either Veno-Arterial (va) Or Veno-Venous (vv) Extra-Corporeal Membrane Oxygenation (ecmo)." Am J Respir Crit Care Med 191 (2015): A4559.

Knight, Gail R., et al. "A comparison of venovenous and venoarterial extracorporeal membrane oxygenation in the treatment of neonatal respiratory failure." Critical care medicine 24.10 (1996): 1678-1683.

Zahraa, Jihad N., et al. "Venovenous versus venoarterial extracorporeal life support for pediatric respiratory failure: are there differences in survival and acute complications?." Critical care medicine 28.2 (2000): 521-525.

Kolman, D., et al. "Clinical Outcomes In Patients With Advanced Cardiopulmonary Failure Who Were Treated With Either Veno-Arterial (va) Or Veno-Venous (vv) Extra-Corporeal Membrane Oxygenation (ecmo)." Am J Respir Crit Care Med 191 (2015): A4559.

Bombino, Michela, Sara Redaelli, and Antonio Pesenti. "Newer indications for ECMO: pulmonary embolism, pulmonary hypertension, septic shock and trauma." ECMO-Extracorporeal Life Support in Adults. Springer Milan, 2014. 179-192.

Butt, W., and G. MacLaren. "Extracorporeal membrane oxygenation and sepsis." Crit Care Resusc 2007; 9: 76–80

Question 2 - 2015, Paper 1

List the complications and their likely underlying mechanisms specifically related to cardiopulmonary bypass that may be seen in the ICU following cardiac surgery.

College Answer

a) 

Effects related to blood contact with non-biologic surfaces and blood-gas interfaces

  • Activation of coagulation cascade- consumptive coagulopathy, thromboembolic phenomena, haemolysis, 
rarely TTP.
  • Systemic inflammatory response syndrome due to leucocyte and complement activation, cytokine release 
and expression of adhesion molecules- vasodilatory shock, fever, acute lung injury, liver dysfunction, 
multiorgan dysfunction.
  • Platelet dysfunction

b) 

Effects related to non-pulsatile flow

  • Renal dysfunction
  • Cerebrovascular events, watershed infarcts, neurocognitive dysfunction
  • Splanchnic ischaemia

c) 

Effects related to haemodilution

  • Dilutional coagulopathy, anaemia.
  • Electrolyte abnormalities

d) 

Effects of hypothermia

  • Coagulopathy
  • Decreased tissue oxygen delivery
  • Insulin resistance and hyperglycaemia

e)

Effects of heparin and protamine

  • Residual heparinisation leading to bleeding
  • Increased pulmonary vascular resistance and right ventricular dysfunction from protamine, allergic 
reactions to protamine

f)

Effects related to aortic manipulation (cross-clamping and proximal grafts)

  • Systemic embolisation with potential for neurologic, mesenteric and renal dysfunction.
  • Difficulty with myocardial protection resulting in postoperative myocardial dysfunction (especially right-sided) due to stunning or infarction

g) 

Other

  • Left phrenic nerve palsy (surgical injury, use of cold cardioplegia “slush”)
  • Left lower lobe collapse (poor re-inflation post bypass, phrenic nerve injury)

Additional comments:

Candidates who failed did not address complications specific to CP bypass and/or did not describe the underlying mechanisms. Some answers were poorly structured with a tendency to repeat points. The above answer template is not the only way to structure the answer, for example the complications could be classified by body system affected.

Discussion

There are several different ways to answer ths, as has been pointed out by the examiners. The previous (identical) incarnation of this SAQ was Question 1 from the second paper of 2011; in their model answer the college had classified the complications by organ system.  Both approaches are available for revision, presented as tables in the chapter on complications attributed to the cardiopulmonary bypass circuit. Below, the revising candidate can see a tabulated form of the alternative college answer from 2011.

Complications of Cardiopulmonary Bypass
Organised According to Organ Systems
Organ System Complication Aetiology
Respiratory Left lower lobe collapse Phrenic nerve neuropraxia, due to cold slush cardioplegia
Poor reinflation following restoration of circulation
Pulmonary hypertension Due to increased pulmonary vascular resistance (protamine)
Acute Lung Injury SIRS due to bypass circuit-associated complement activation
Cardiovascular Myocardial stunning Due to direct effects of cardiotomy and cardioplegia
Myocardial infarction Coronary graft ischaemia (air embolism)
RV dysfunction Due to pulmonary hypertension related to protamine
Arrhythmias Due to electrolyte disturbances and hypothermia
Heart block Due to hypothermia or direct conduction system trauma
Systemic MODS Hypoperfusion and end-organ ischaemia related to non-pulsatile flow and/or air/atheroma embolism
Neurological Stroke All thought to be due to the sluggish low-flow state following the recommencement of bypass, as well as due to air emboli microemboli and possibly microemboli from the bypass circuit itself
Watershed infarcts
Neurocognitive impairment
Electrolytes and
Endocrine
Hypothermia Due to intra-operative cooling and delayed re-warming
Hyperglycaemia Due to hypothermia-related insulin resistance
Due to circulating endogenous catecholamines
Electrolyte derangement Haemodilution
Renal Post-op diuresis "Cold diuresis" due to intra-operative cooling and delayed re-warming
Post-op renal failure Low flow, and thromboembolic events
Electrolyte derangement Haemodilution
Gastrointestinal Splanchnic ischaemia Low flow, and thromboembolic events
Hepatic dysfunction
Pancreatitis
Haematological Coagulopathy Due to consumption of clotting factors by the bypass circuit
Due to residual anticoagulation
Due to dilutional coagulopathy
Platelet dysfunction Due to antiplatelet agents, and due to the SIRS response
Anaemia Due to haemodilution and haemolysis
Haemolysis Due to mechanical destruction by the bypass pump, as well as due to MAHA and SIRS
Metabolic Hypothermia Due to intra-operative cooling and delayed re-warming
Hyperglycaemia Due to hypothermia-related insulin resistance
Due to circulating endogenous catecholamines
Immune Coagulation cascade activation Due to blood contact with non-biological surfaces and blood-gas interface
SIRS Due to complement activation by circuit components
Anaphylaxis A reaction to protamine

References

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

André, Arthur C. St, and Anthony DelRossi. "Hemodynamic management of patients in the first 24 hours after cardiac surgery." Critical care medicine 33.9 (2005): 2082-2093.

Ray Raper's chapter in Oh's manual (pp.285)

Complications in cardiothoracic surgery: avoidance and treatment, Little A.G, Merril W.H.  2007, 2nd ed. Chapter 4 by Creswell and Karis.

Cardiopulmonary bypass- Principles and Practice, Gravlee G.P. and Davis R.F -2007 (3rd ed.)

UpToDate contains a couple of excellent summary pieces on cardiac and non-cardiac complications of CABG.

Question 24 - 2015, Paper 1

Outline the advantages and disadvantages of a CT scan, transoesophageal echocardiography (TOE), MRI and an aortogram for the evaluation of suspected aortic dissection.

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
  • “Blind spot” arising from left main bronchus
  • 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, esp. for haemodynamically unstable patient on IV infusions
  • Limited applicability (claustrophobia, pacemakers etc. )

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

References

Question 28 - 2015, Paper 2

A 76-year-old female is admitted to the ICU following elective aortic and mitral valve replacement. Trans-oesophageal echo assessment at the end of surgery showed an ejection fraction of 20%. Her preoperative creatinine was 340 μmol/L. Total bypass time was 240 minutes. On arrival in Intensive Care Unit the patient has the following indices:

  • Temperature    35oC
  • Atrial pacing (AAI)    80/min
  • Systemic blood pressure    85/55 mmHg
  • Pulmonary artery pressure    60/30 mmHg
  • Cardiac index     1.5 L/min/m2
  • Systemic vascular resistance indexed (SVRI)    1700 dyn.sec.cm-5
  • Pulmonary artery wedge pressure    10 mmHg
  • Central venous pressure    8 mmHg

a)    List the specific clinical and haemodynamic issues for this patient on admission to ICU. (30% marks)

b)    Outline your management of these issues.    (70% marks)

College Answer

a)
The main clinical and haemodynamic issues identified are:

Elderly female patient post double valve surgery. Pre-existing renal impairment.

Long bypass time.

Systemic hypotension (MAP 65 unlikely to be adequate for this patient). Low output state (CI, EF post bypass).

Increased afterload / vascular impedance (SVR). Probable fluid responsiveness (PAWP, CVP).

Moderate pulmonary hypertension. Low core temperature.

b)

This patient is high risk (female, age, long bypass time, pre-existing renal impairment, low EF). Management consists of:

Re-warming.

Judicious fluid replacement as she re-warms.

Improved volume state may augment CI but given poor EF unlikely to be sole intervention needed.

Titration of adrenaline infusion, aiming for CI > 2.2

Bedside echo to evaluate effect of fluid and increased adrenaline, exclude tamponade and check valve function (mitral regurgitation can increase PAP and decrease cardiac output).

Consideration of other vasoactive agents (dobutamine, milrinone, levosimendan) or IABP insertion if persisting low output state.

Assess adequacy of pacing and consider changing mode to A-V pacing (heart block common after AVR) and /or increasing rate to 90 bpm.

Correct post-op coagulopathy and replace blood losses to maintain Hb > 80 G/L. Surgical review if significant blood loss via drains.

Evaluation of any other cause of low output state e.g. tension pneumothorax, dynamic hyperinflation.

Close monitoring of renal function and early institution of renal replacement therapy if oligo-anuric or rising creatinine.

Consideration of inhaled nitric oxide to reduce pulmonary hypertension and RV afterload.

Additional Examiners’ Comments:

Some answers for the management plan were very superficial with generic statements with inadequate detail e.g. “consider changing pacemaker settings”, ”order bedside echo” and lacking a consultant level approach.

Discussion

This question is nearly identical to Question 1 from the second paper of 2013, except this patient is not on adrenaline infusion 4μg/min. Also, for some reason, the college decided to change the systemic vascular resistance variable. In the 2013 version, the patient is said to have an SVR value of 1700 dyn.sec.cm-5, which is well above the reference range (800-1200). This is surely a case of overconstricted raised afterload, and the college comment in 2013 makes sense ("Increased afterload / vascular impedance (SVR)"). For some reason, in 2015 the college decided to make that parameter to SVRI, but without changing the variable. Because SVRI has a reference range of 1970-2390 dynes-sec/cm5/m2 , this parameter now suggests the patient is slightly vasodilated and requires more pressors. This would be fine if the examiners had not cut-and-pasted thir comments to Question 1 from the second paper of 2013 into this model answer. Thus, "Increased afterload / vascular impedance (SVR)" no longer makes any sense.

In the fine tradition of mindlessly cut-and-pasting, the discussion section from Question 1 from the second paper of 2013 is reproduced below wth minimal modification.

  • Issues
    • Cardiogenic shock
    • Hypovolemia
    • Pulmonary hypertension
    • Hypothermia
  • Assessment
    • Examination, including dynamic manoeuvres to assess for fluid responsiveness
    • ECG to exclude STEMI
    • CXR to exclude pneumothorax
    • Arterial blood gas
    • Mixed venous blood gas
    • Formal TTE to examine valve function and sclude tamponade
  • Management
    • Re-warm patient
    • Sedate and paralyse patient to decrease whole-body oxygen demand
    • Maintain Hb ~ 80 and SpO2 ~ 100% to maintain satisfactory tissue oxygen delivery
    • Maintain heart rate and rhythm control with pacing and antiarrhymic drugs (eg. amiodarone); consider increasing rate to 90
    • Optimise RV preload: give fluid bolus 20-40ml/kg
    • Increase RV + LV contractility with milrinone or levosimendan
    • Decrease RV and LV afterload with milrinone or levosimendan (pulmonary and systemic vasodilation)
    • Decrease mycoardial workload with IABP especially if there is evidence of ischaemia with inotorope use
    • Maintain satisfactory diastolic pressure with noradrenaline

A generic approach to the haemodynamically unstable cardiac surgical patient is discussed elsewhere.

References

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

André, Arthur C. St, and Anthony DelRossi. "Hemodynamic management of patients in the first 24 hours after cardiac surgery." Critical care medicine 33.9 (2005): 2082-2093.

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.

Goepfert, Matthias SG, et al. "Goal-directed fluid management reduces vasopressor and catecholamine use in cardiac surgery patients." Intensive care medicine 33.1 (2007): 96-103.

Question 2 - 2016, Paper 1

You are assessing a patient on the first post-operative day following an aortic valve replacement. There are atrial and ventricular epicardial wires in place and the patient is being paced at 90/min in a DDD mode.

a) Define sensitivity with respect to cardiac pacing.      (20% marks)

b) Describe the steps that you would perform to check and set sensitivity.            (30% marks)

c) In addition to checking sensitivity, what other daily checks would you perform in regards to the temporary pacing system?          (20% marks)

d) The patient becomes completely pacemaker dependent and the pacemaker suddenly completely fails to pace.
List the actions you would perform to troubleshoot the pacemaker.

(30% marks)

College Answer

The ‘sensitivity’ (as numerically represented on the pacing generator) is the minimum current that the pacemaker is able to sense. A lower number thus corresponds to a greater sensitivity. 

 b) 

This is only checked when the patient has an intrinsic rhythm which affords some cardiovascular stability. 

  • Set the pacemaker rate 10 below patients intrinsic rate
  • Set the output to a very low value e.g., 0.1mA
  • Setting the pacemaker to asynchronous mode by turning the sensitivity to its lowest value (highest mV setting) after setting the output current to its lowest value (e.g. 0.1mA) so as to not capture but trigger the pacing indicator.
  • The sensitivity is then gradually increased (lower mV) until the pacemaker senses the patients intrinsic HR and the pacing indicator no longer illuminates but the sensing indicator does. This is the sensing threshold. The final setting is usually half this determined value

OR also acceptable-

  • Gradually decrease sensitivity (with output set to low value and pacemaker set to 10 below intrinsic rate) and watch for sensing flash on box to disappear. Final setting is usually half this value.

c)

  • Underlying heart rate
  • Capture threshold
  • Appropriate pacing mode for the patient
  • Impulse generator- battery
  • (Maximum tracking rate, AV interval, post ventricular atrial refractory period (PVARP) should be noted, but do not require daily checks once set)

d)

  • Increase output to maximum (20mA)
  • Select VOO (fixed ventricular pacing) to overcome inappropriate over sensing
  • Check all leads/connections/batteries
  • Replace impulse generator if faulty
  • Consider reversing the polarity on the v wires
  • Consider percutaneous lead through skin

Discussion

a)

Sensitivity of a pacemaker electrode is the minimum myocardial voltage required to be detected as a P wave or R wave, measured in mV.  The lower the number, the higher the sensitivity, which leads to some confusion (when one asks to increase the sensitivity, one decreases  the sensitivity mV value).

b)

How to check and set sensitivity:

  • Put the pacemaker in a VVI, AAI or DDD mode (i.e. endogenous cardiac activity should inhibit the pacemaker.)
  • Set the output as low as possible; you don't want to have any R on T phenomena - you only need to see the pacing spikes.
  • Change the rate to one which is much lower than the patients native rate
  • Increase the sensitivity value until no cardiac activity is sensed
  • Now, keep decreasing the sensitivity until the pacemaker senses every p-wave or QRS interval.
  • This minimal sensitivity value is the sensitivity threshold.
  • most of the time, you tend to leave the sensitivity turned down to half of the sensitivity threshold to ensure that the cardiac electrical activity will be sensed even if the electrode tip overgrows with filth.
  • If you turn the sensitivity value down any more than that, you risk oversensing. Oversensing is described in greater detail elsewhere; briefly, it is an inappropriate inhibition of pacing in response to some sort of trivial non-cardiac signals, like the friendly hum of the nearby microwave.

c)

Daily maintenance checks of the temporary pacemaker:

Care for the epicardial wires:

  • Pacing wires must be dressed at least every 72 hours
  • When handling epicardial pacing wires, gloves should always be worn to prevent microelectrocution
  • Wires not in use should be rolled up in sterile gauze
  • Wires in use should be securely taped to the patient's abdomen

Minimum daily box and wire assessment:

  • Wound site assesment
  • Pacing wire connection check
  • Measure and document the wire length every nursing shift
  • Note position of wires on daily CXR
  • Check the impulse generator battery

Minimum daily paced patient assessment:

  • 12-lead ECG
  • Underlying rhythm and rate check (turn off the pacemaker for a few seconds)
  • Sensitivity check
  • Pacing threshold check
  • Pacing mode review (is it appropriately selected?)

Occasional (non-daily) checks:

  • Maximum tracking rate:the maximum atrial rate at which a pacemaker will deliver a ventricular pacing stimulus following each sensed atrial beat; i.e. if the atria are going at 130bpm and the pacemaker's MTR is set at 120, it will not pace any more frequently than 120.
  • AV interval: the interval following a paced or sensed atrial beat allowed before a ventricular pacing impulse is delivered. I.e. how long the pacemaker waits until it decides that the beat was not conducted through the AV node.
  • Post ventricular atrial refractory period (PVARP) is a pacemarker refractory period, intended primarily to prevent sensing of retrograde P waves; it prevents the pacemaker from sending another impulse too close to the last QRS, so as not to produce an R-on-T phenomenon.

d)

Why is the pacemaker not pacing?

First, check the patient. Are they now in asystole, or otherwise haemodynamically compromised? If not, the pacemaker can be checked.

Start with the box.

  • Is it even on?
  • Is the battery dying?
  • Are the wires detached from the pulse generator?
  • Are the leads connected?
  • Was the temporary pacing wire pulled out in course of a recent pressure area care?
  • Are the epicardial electrodes displaced? Is the transvenous electrode tip wiggling uselessly in the venticle?
  • Is there any weird twitching in the chest wall muscles of the patient? Is the ventilator demonstrating some bizarre sawtooth pattern, suggesting that the diaphragm is being paced?

Ok, so the hardware is intact. if there is output failure, its not because of the leads or the battery. Move on to the software.

First check the sensor threshold.

  • Put the pacemaker in a VVI, AAI or DDD mode.
  • Change the rate to one which is much lower than the patients native rate.
  • Observe the sense indicator.
  • Keep increasing the sensitivity.
  • Find the sensitivity maximum - where the pacemaker is picking up NONE of the endogenous electrical activity.
  • Now keep decreasing the sensitivity.
  • Find the sensor threshold - where the sensor picks up EVERY endogenous electical event (i.e. no pacing spikes are visible)

Crank the sensitivity setting up to double the sensor threshold.

This should take care of oversensing as a cause of pacing failure.

Alternatively, as the college recommend, you can simply set the pacemaker in VOO mode.
No sensing - no oversensing.

Now, check the output threshold.

  • Set the pacemaker well above the native rate.
  • Start reducing the output.
  • Find the capture threshold - where a QRS complex no longer follows each pacing spike.

Crank the output to double the capture threshold.

Still not working?

  • Roll the patient to one side, and then another. Sometimes this influences the position of the transvenous pacing wire tip just enough to get you some capture.
  • Reverse the leads. Sometimes this works, but logically - it shouldnt.
  • Convert to unipolar pacing. Attach the negative lead to the positive electrode, and the negative lead to the subcutaneous tissue of the chest.
  • Give up. Time to pace externally while waiting for another wire to be floated, or the epicardial leads to be resited.

References

Reade, M. C. "Temporary epicardial pacing after cardiac surgery: a practical review." Anaesthesia 62.3 (2007): 264-271.

Reade, M. C. "Temporary epicardial pacing after cardiac surgery: a practical review: Part 2: Selection of epicardial pacing modes and troubleshooting."ANAESTHESIA-LONDON- 62.4 (2007): 364.

Gammage, Michael D. "Temporary cardiac pacing." Heart 83.6 (2000): 715-720.

Sanders, Richard S. "The Pulse Generator." Cardiac Pacing for the Clinician. Springer US, 2008. 47-71.

Kirk, Malcolm. "Basic principles of pacing." All You Wanted to Know (2008): 1.

Hayes, David L., and Paul A. Levine. "Pacemaker timing cycles." Cardiac pacing and ICDs. Blackwell Publishing Malden (MA), 2002. 265-321.

Question 6 - 2016, Paper 1

A 76-year-old female is admitted to the ICU following elective aortic and mitral valve replacement. Transoesophageal echo assessment at the end of surgery showed an ejection fraction of 20%. Her preoperative creatinine was 340 gmol/L. Total bypass time was 240 minutes. On arrival in ICU the patient has the following indices:

Temperature

35°C

Atrial pacing (AAI)

80/min

Systemic blood pressure

85/55 mmHg

Pulmonary artery pressure

60/30 mm Hg

Cardiac index

1.5 litres.min.m 2

Systemic vascular resistance

1700 dyn.sec.cm 5

Pulmonary artery wedge pressure

10 mmHg

Central venous pressure

8 mmHg

The patient is currently on adrenaline

4 μg/min by infusion

a) List the specific clinical and haemodynamic issues for this patient on admission to ICU. (40% marks)

b) Outline your management of these issues. (60% marks)

College Answer

The main clinical and haemodynamic issues identified are:

  • Elderly female patient post double valve surgery
  • Pre-existing renal impairment
  • Long bypass time
  • Systemic hypotension (MAP 65 unlikely to be adequate for this patient)
  • Low output state (CI, EF post bypass).
  • Increased afterload / vascular impedance (SVR).
  • Probable fluid responsiveness (PAWP, CVP).
  • Moderate pulmonary hypertension.
  • Low core temperature

This patient is high risk (female, age, long bypass time, pre-existing renal impairment, low EF). Management consists of:

  • Re-warming
  • Judicious fluid replacement as she re-warms
  • Improved volume state may augment CI but given poor EF unlikely to be sole intervention needed
  • Titration of adrenaline infusion, aiming for CI >2.2
  • Bedside echo to evaluate effect of fluid and increased adrenaline, exclude tamponade and check valve function (mitral regurgitation can increase PAP and decrease cardiac output)
  • Consideration of other vasoactive agents (dobutamine, milrinone, levosimendan) or IABP insertion if persisting low output state
  • Assess adequacy of pacing and consider changing mode to A-V pacing (heart block common after AVR) and /or increasing rate to 90 bpm
  • Correct post-op coagulopathy and replace blood losses to maintain Hb > 80 G/L. Surgical review if significant blood loss via drains
  • Evaluation of any other cause of low output state e.g. tension pneumothorax, dynamic hyperinflation
  • Close monitoring of renal function and early institution of renal replacement therapy if oligo-anuric or rising creatinine
  • Consideration of inhaled nitric oxide to reduce pulmonary hypertension and RV afterload

Discussion

This question is identical to Question 28 from the second paper of 2015, and nearly identical to Question 1 from the second paper of 2013 except this patient is not on adrenaline infusion 4μg/min. The discussion section from those questions is therefore reproduced below.

  • Issues
    • Cardiogenic shock
    • Hypovolemia
    • Pulmonary hypertension
    • Hypothermia
  • Assessment
    • Examination, including dynamic manoeuvres to assess for fluid responsiveness
    • ECG to exclude STEMI
    • CXR to exclude pneumothorax
    • Arterial blood gas
    • Mixed venous blood gas
    • Formal TTE to examine valve function and sclude tamponade
  • Management
    • Re-warm patient
    • Sedate and paralyse patient to decrease whole-body oxygen demand
    • Maintain Hb ~ 80 and SpO2 ~ 100% to maintain satisfactory tissue oxygen delivery
    • Maintain heart rate and rhythm control with pacing and antiarrhymic drugs (eg. amiodarone); consider increasing rate to 90
    • Optimise RV preload: give fluid bolus 20-40ml/kg
    • Increase RV + LV contractility with milrinone or levosimendan
    • Decrease RV and LV afterload with milrinone or levosimendan (pulmonary and systemic vasodilation)
    • Decrease myocardial workload with IABP especially if there is evidence of ischaemia with inotorope use
    • Maintain satisfactory diastolic pressure with noradrenaline

A generic approach to the haemodynamically unstable cardiac surgical patient is discussed elsewhere.

Weirdly, both this question and  Question 28 from the second paper of 2015 had approximately the same pass rate (95% vs. 94%). However, in 2015 examiners felt the need to make disparaging comments about the candidates (eg. " answers for the management plan were very superficial with generic statements "). Clearly, we have learned from our mistakes this time around, and have made a series of profound and specific statements.

References

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

André, Arthur C. St, and Anthony DelRossi. "Hemodynamic management of patients in the first 24 hours after cardiac surgery." Critical care medicine 33.9 (2005): 2082-2093.

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.

Goepfert, Matthias SG, et al. "Goal-directed fluid management reduces vasopressor and catecholamine use in cardiac surgery patients." Intensive care medicine 33.1 (2007): 96-103

Question 16 - 2016, Paper 2

You are called to review an 86-year-old female, with severe pleuritic chest pain and difficulty breathing following dilation of an oesophageal stricture. Her CT thorax scan confirms an oesophageal perforation.

Outline your management of this problem, including the options for definitive treatment.

College answer

This is an emergency situation. Leakage of oesophageal and gastric contents results in a severe necrotising mediastinitis with sequelae of septic shock, multi-

organ failure and death. Mortality is about 20% and probably higher in this age group.

The principles of management are:

  • Resuscitation
  • Supportive care including haemodynamic monitoring
  • Broad-spectrum antibiotics
  • Control of extra-luminal contamination
  • Analgesia
  • Nil by mouth
  • Plan for definitive treatment to close or bypass the perforation
  • Nutritional support
  • Ensure adequate oxygenation and ventilation
    • NIV and bag-valve-mask assisted ventilation contra-indicated
    • If severely hypoxic or shocked needs intubation (unless palliative approach appropriate)
  • Haemodynamic support with fluid resuscitation and vasopressor support as indicated. Cautious fluid replacement in 86-year-old with echo or other haemodynamic monitoring guidance. 
    Monitoring including A-line and CVC and transfer to ICU/HDU
  • Early broad-spectrum antimicrobials to cover gram positives, gram negatives and anaerobes, e.g.Tazocin, Meropenem. May need addition of Vancomycin if MRSA likely and consider anti-fungal if immunocompromised or long stay in hospital
  • Drainage of pleural and mediastinal collections (source control) with surgical and/or interventional radiology assistance
  • Analgesia – opiates and adjuncts as needed
  • Strictly nil by mouth
  • Surgical opinion
  • Treatment options
    • Operative
      • Surgical repair
      • Oesophagectomy
      • Oesophageal diversion
    • Non-operative- Covered oesophageal stent –appropriate if early diagnosis, contained perforation and limited extra-luminal soilage
    • Conservative approach -antibiotics and feeding tube (jejunostomy) ± drains
  • Nutrition – likely to need TPN if poor baseline state of nutrition. NJ tube or jejunostomy can be sited at time of stent placement or surgical repair
  • Follow-up imaging –CT gastrograffin swallow
  • Consider treatment limitations with advanced age if significant co-morbidities, underlying inoperable cancer.

An acceptable answer for a pass mark included the following elements:

Resuscitation
Antimicrobial therapy
Surgical and non-surgical options
Nutrition


Additional Examiners' Comments:
Most  candidates  were  able  to  describe  surgical  and  non-surgical  options  for  definitive  treatment. However  candidates  who  did  not  pass  provided  superficial  answers  with  insufficient  detail.  Most candidates  addressed  the  ABCs  but  did  not  address  the  specific  issues  for  the  case.  For  example, issues  such  as  consideration  of  nutrition,  keeping  the  patient  nil  by  mouth,  analgesia  and  treatment limitations were commonly missed in the answers. Some candidates did not appreciate the need for resuscitation

Discussion

Immediate management

  • Attention to ABCs and correction of immediately identified lifethreatening features
  • Detailed history and thorough physical examination
  • Assessment of airway patency and intubation as needed
  • Maintenance of normoxia with supplemental oxygen
  • Maintenance of normotension with fluid resuscitation and vasopressors as needed
  • Analgesia and sedation
  • Attention to broad-spectrum antibiotic cover, including antifungal agents

Investigations:

  • CXR looking for pneumomediastinum
  • CT chest with contrast
  • Gastrograffin swallow (not barium)
  • Intercostal catheter to drain pleural effusion and analyse it, looking for acidity (suggestive of gastric contents) and food particles.

Specific Management

  • Thoracoscopic or open surgical management;
  • alternatively, endoscopic stent placeemnt
  • alternatively, conservative antibiotic-based management and supportive care in ICU
  • alternatively, palliative care

Supportive management:

  • TPN: they won't be eating for a while
  • Broad-spectrum antibiotics (tazocin is a fine choice)
  • Proton pump inhibitors to encourage the process of oesophageal repair
  • Eventually, these people end up having surgery - but it is delayed until the empyema or mediastinal abscess are well-circumscribed.

Idiosyncratic ICU issues

  • No positive pressure without intubation: even high flow nasal prongs can blow gas into the mediastinum. Thus, no bag-mask ventilation with intubation. All of these patients should be getting an RSI-like induction.

Social issues

  • This is an iatrogenic complication. Full open disclosure must be carried out
  • A family discussion of the possible outcome must take place, ideally led by the team of perforators.
  • The mortality- irrespective of the management approach - will be in the order of 40% (Biancari et al, 2014)

References

Curci, JOSEPH J., and MARC J. Horman. "Boerhaave's syndrome: The importance of early diagnosis and treatment." Annals of surgery 183.4 (1976): 401.

Teh, Elaine, et al. "Boerhaave's syndrome: a review of management and outcome." Interactive cardiovascular and thoracic surgery 6.5 (2007): 640-643.

Eroǧlu, Atilla, et al. "Esophageal perforation: the importance of early diagnosis and primary repair." Diseases of the Esophagus 17.1 (2004): 91-94.

Patton, Anthony S., et al. "Reevaluation of the Boerhaave syndrome: A review of fourteen cases." The American Journal of Surgery 137.4 (1979): 560-565.

Movsas, S. "Spontaneous Rupture of the Oesophagus Is Conservative Treatment Ever Justified?." Thorax 21.2 (1966): 111-114.

Bolooki, H. O. O. S. A. N. G., et al. "Spontaneous rupture of the esophagus: Boerhaave's syndrome." Annals of surgery 174.2 (1971): 319.

Curci, JOSEPH J., and MARC J. Horman. "Boerhaave's syndrome: The importance of early diagnosis and treatment." Annals of surgery 183.4 (1976): 401.

Teh, Elaine, et al. "Boerhaave's syndrome: a review of management and outcome." Interactive cardiovascular and thoracic surgery 6.5 (2007): 640-643.

Eroǧlu, Atilla, et al. "Esophageal perforation: the importance of early diagnosis and primary repair." Diseases of the Esophagus 17.1 (2004): 91-94.

Bhatia, Pankaj, et al. "Current concepts in the management of esophageal perforations: a twenty-seven year Canadian experience." The Annals of thoracic surgery 92.1 (2011): 209-215.

Spapen, J., et al. "Boerhaave's Syndrome: Still a Diagnostic and Therapeutic Challenge in the 21st Century." Case reports in critical care 2013 (2013).

Biancari, Fausto, et al. "Current treatment and outcome of esophageal perforations in adults: systematic review and meta-analysis of 75 studies." World journal of surgery 37.5 (2013): 1051-1059.

Hasan, Shafqat, Ali NA Jilaihawi, and Dhruva Prakash. "Conservative management of iatrogenic oesophageal perforations—a viable option." European journal of cardio-thoracic surgery 28.1 (2005): 7-10.

Biancari, F., et al. "Treatment of esophageal perforation in octogenarians: a multicenter study." Diseases of the Esophagus 27.8 (2014): 715-718.

Question 4 - 2017, Paper 1

Discuss the potential mechanical strategies for supporting myocardial function in a 45-year-old male presenting with cardiogenic shock post-revascularisation for an acute anterior myocardial infarction.

In your answer include the physiological rationale for each strategy.

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 preload 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, oygenated 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

This question is virtually identical to Question 19 from the second paper of 2012. To simplify revision and sabotage SEO, this table is copied here without any alteration.

 Mechanical Haemodynamic Support Strategies
Strategy Advantages Limitations

Positive pressure ventilation:
the use of positive pressure to decrease LV preload and afterload (by manipulating transmural pressure)

  • Easy to apply
  • Minimally invasive
  • Added benefit of improved oxygenation and gas exchange
  • Invasive ventilation has the added benefit of anaesthesia +/- paralysis, which decreases whole-body oxygen demand
  • Preload reduction may result in hypotension in the volume-depleted patient
  • Increased intrathoracic pressure increases RV afterload, exacerbating right heart failure
  • Positive pressure may result in barotrauma and volutrauma
  • All the risks of mechanical ventilation apply, eg. VAP
Temporary transcutaneous pacing:
  • Requires minimal skill to apply
  • Minimally invasive
  • Cardiac output will increase in proportion to
  • Requires a substantial amount of analgesia and sedation
  • Uncomfortable for the patient
  • May cause significant tissue damage
  • Not a long-term solution
  • Poor A-V synchrony
Temporary transvenous pacing
  • Comparatively easy to insert
  • Dual-chamber pacing may improve A-V synchrony and restore the "atrial kick".
  • Not only does it work in bradycardia, but also by "overdrive pacing" in tachycardia, where the slowed heart rate allows for longer diastolic filling
  • Requires some expertise to manage and troubleshoot
  • Invasive, with all the risks of large-bore central venous access
  • Generally, one can only pace the ventricle, which means A-V synchrnoy will be lost; the "atrial kick" may be sorely missed by patients with severe valve dysfunction
Cardiac resynchronisation therapy: biventricular pacing
  • Restores synchrony to ventricular contraction in patients with severe heart failure
  • There is strong evidence that CRT reduces mortality and hospitalisation  (i.e. it is superior to AICD or medical therapy).
  • Requires specialist skill to insert and adjust; hardly an emergency procedure
  • To benefit, one must have LBBB, a wide QRS, and an LVEF less than 35%.
  • Generally, only about 5-10% of heart failure patients will benefit
  • There is a "heterogeneity of effect" in patients  who do not meet the recognised criteria (read: it does them no good)
Intra-aortic balloon pump:
  • Decreases LV afterload
  • Improves coronary arterial filling in diastole
  • Improves forward flow though defective mitral valves
  • Nowadays, little adjustment is required (automatic timing is usually satisfactory)
  • "Severe" cardiogenic shock is still not very well investigated, and there may be an unrecognised  mortality benefit in this group.
  • Violently invasive
  • Requires a certain level of expertise to place correctly.
  • Significant complications are associated with its use, including a non-zero rate of death and limb loss.
  • The mortality benefit in most patients might either be marginal or altogether absent, depending on what you read. Certainly, the IABP-SHOCK II trail did not demonstrate any survival improvement.
  • Does not benefit the right ventricle.
  • Contraindicated in aortic regurgitation
  • Poor effect in AF, particularly rapid AF
Ventricular assist devices:
  • Decreases myocardial workload
  • Offers a bridge to heart transplantation
  • Effective temporary support for myocardial stunning
  • May afford a period of outpatient management
  • Highly invasive
  • Requires surgical expertise to implement
  • Requires significant anticoagulation
  • Substantial risk of infection (50%)
  • In spite of anticoagulation, there is a significant risk of thrombosis
VA- ECMO
  • Not only decreases myocardial workload- it may take over all of the circulatory workload.
  • Attends to both circulation and gas exchange
  • Easier to implement (percutaneous technique does not require surgical expertise)
  • Highly invasive
  • Requires expertise to implement
  • Requires significant anticoagulation
  • In spite of anticoagulation, there is a significant risk of thrombosis
  • All the complications of large-bore arterial and venous access

Though strictly speaking it is a "mechanical haemodynamic support strategy", the author still could not bring himself to include manual cardiac compressions in the list above.

References

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.

Brignole, Michele, et al. "2013 ESC Guidelines on cardiac pacing and cardiac resynchronization therapy." European heart journal (2013): eht150.

Question 18 - 2017, Paper 1

A 78-year-old female is admitted to ICU following aortic valve replacement for severe aortic stenosis.Her co-morbidities include ischaemic heart disease, peripheral vascular disease, hypertension, type 2 diabetes, emphysema and chronic kidney disease.

The operation was prolonged and difficult requiring repair of a right ventricular injury and emergency coronary artery bypass graft. The patient required adrenaline, noradrenaline and an intra-aortic balloon pump to separate from cardiopulmonary bypass.

At 4 hours post-operatively, she becomes progressively more hypotensive with increasing noradrenaline doses. List the potential causes for her shock state.       (60% marks)

With respect to severe aortic stenosis, list the available alternatives to open valve replacement, with the respective advantages and disadvantages. (40% marks)

College answer

a)

Hypovolaemic • Bleeding

Cardiogenic • Acute MI • Graft obstruction • Diastolic dysfunction • RV failure • Pacing problem • Pulmonary hypertension

Distributive • Long bypass time • Occult sepsis (e.g. GI tract ischaemia) • Relative adrenal dysfunction • Nutritional deficiency

Obstructive • Pericardial tamponade • Left Ventricular Outflow Tract Obstruction • Prosthetic valve obstruction • Tension Pneumothorax (may be loculated due to previous surgery) • IABP failure / dyssynchrony/ malposition

Combination of above e.g. Aortic dissection

b)

Medical management only +/- palliation. Considered if prognosis of comorbidities is worse than natural history of AS. Avoids risks of surgery.

Medical management + balloon valvuloplasty. BAV may provide some symptomatic benefit albeit at the risk of complications from femoral vessels/ annular rupture. May also be useful diagnostically to see if dyspnoea improves.

TAVI – femoral access probably unlikely to be possible due to PVD, transapical or transoartic much higher risk but possible. Less invasive.

Discussion

When you fix an aortic stenosis and it all goes well, frequently the patient will become hypertensive instead,  which is clearly not what we see here. The table of potenstial reasons for shock is offered below, and it is similar to what is offered in the chapter about approaching the haemodynamically unstable post-pump patient

Causes of cardiovascular instability after bypass

Immediately recognisable on direct inspection

  • Artifactual - check your lines, zero to recalibrate
  • Anaphylaxis
  • Arrhythmia, eg. AF
  • Valve failure - eg. mitral regurgitation of sudden onset

Immediately recognisable on routine investigations

  • Myocardial ischaemia should not be left unrecognized
  • Pneumothorax or tension pneumothorax
  • Cardiac tamponade
  • Haemorrhage
  • LV outflow tract obstruction

Excluded by inspection and investigations

  • Rewarming-related vasodilation
  • Excessive sedation with propofol
  • Post-bypass vasoplegia
  • Post-bypass myocardial depression

In light of the offered scenario, several of these possibilities are more likely than the others:

  • Vasoplegic shock (long by pass time, more circuit exposure, and with the background history of hypertension one might confabulate that she might have been on an ACE-inhibitor chronically).
  • Cardiac tamponade (due to right ventricular injury)
  • Right heart failure due to cardiotomy 
  • Post-bypass myocardial depression (coronary arteries need to be grafted as an emergency procedure, and the background contains enough ischaemic heart disease; on top of that the college tell us that an IABP was required to wean off bypass)
  • Myocardial infarction post-operatively
  • Tension pneumothorax (the history of emphysema makes ruptured bullae more likely)

Alternatives to open valve surgery can be listed, but the "advantages/disadvantages" question is an opening to a tabulated response. The best literature reference for this would probably be something like the UpToDate article, which gives you a choice between surgery, TAVI and conservative medical therapy. The 2016 article by Fattouch et al is also a good overview (and free).

Alternatives to Open-Heart Valve Surgery

Alternative

Advantages

Disadvantages

Transfemoral
transcatheter aortic valve implantation

  • Shorter duration of hospital stay than sternotomy
  • Better pain relief
  • Comparable outcomes in matched populations (Cao et al, 2013)
  • Requires an experienced centre
  • Requires good quality femoral vessels
  • Still fairly invasive
  • Periprocedural CPR is a commonplace occurrence 
  • Unsuitable in some populations, eg. HOCM or if there is unrevascularised coronary artery disease
  • Evidence in support of TAVI is poor among good surgical candidates

Transapical transcatheter aortic valve implantation 

  • Possible even when femoral vessels are heavily calcified
  • Similar mortality rate to transfemoral approach
  • Better placement; less paravalvular leak than transfemoral (Murashita et al, 2016)
  • More invasive
  • Risk of tamponade and VT
  • No advantage in terms of mortality of ejection fraction

Balloon valvuloplasty

  • Smaller catheter required than for TAVI (i.e. able to gain access through 
  • Older technique: more experience
  • Less invasive than TAVI
  • Can reduce the risk of subsequent TAVI or AVR by improving haemodynamics (i.e. as a "bridge")
  • Potential of stroke is greatest
  • Stenosis resolves, but now regurgitation develops
  • May be poorly tolerated haemodynamically
  • Inevitably leads to restenosis (van den Brand, 1992)

Conservative management

  • Non-invasive
  • May be well suited to patients with low activity levels (eg. nursing home patients)
  • Survival is poor: 69% at one year
  • Progression of the disease is unaffected
  • Symptom control is likely going to be poor

References

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

André, Arthur C. St, and Anthony DelRossi. "Hemodynamic management of patients in the first 24 hours after cardiac surgery." Critical care medicine 33.9 (2005): 2082-2093.

Rodés-Cabau, Josep, et al. "Transcatheter aortic valve implantation for the treatment of severe symptomatic aortic stenosis in patients at very high or prohibitive surgical risk: acute and late outcomes of the multicenter Canadian experience.Journal of the American College of Cardiology 55.11 (2010): 1080-1090.

Alkhouli, Mohamad, et al. "Morbidity and Mortality Associated With Balloon Aortic Valvuloplasty." Circulation: Cardiovascular Interventions 10.5 (2017): e004481.

Linke, Axel, et al. "Treatment of aortic stenosis with a self-expanding transcatheter valve: the International Multi-centre ADVANCE Study."European heart journal 35.38 (2014): 2672-2684.

Schymik, Gerhard, et al. "Long-term results of transapical versus transfemoral TAVI in a real world population of 1000 patients with severe symptomatic aortic stenosis.Circulation: Cardiovascular Interventions 8.1 (2015): e000761.

Cao, Christopher, et al. "Systematic review and meta-analysis of transcatheter aortic valve implantation versus surgical aortic valve replacement for severe aortic stenosis.Annals of cardiothoracic surgery 2.1 (2013): 10-23.

Murashita, Takashi, et al. "Clinical Outcomes After Transapical and Transfemoral Transcatheter Aortic Valve Insertion: An Evolving Experience."The Annals of thoracic surgery 102.1 (2016): 56-61.

Keeble, Thomas R., et al. "Percutaneous balloon aortic valvuloplasty in the era of transcatheter aortic valve implantation: a narrative review." Open Heart3.2 (2016): e000421.

van den Brand, Marcel, et al. "Histological changes in the aortic valve after balloon dilatation: evidence for a delayed healing process." British heart journal 67.6 (1992): 445-449.

Fattouch, Khalil, Sebastiano Castrovinci, and Patrizia Carità. "Aortic valve stenosis: treatments options in elderly high-risk patients." Journal of geriatric cardiology: JGC 13.6 (2016): 473-474.

Question 19 - 2018, Paper 2

A 52-year-old male is undergoing a right pneumonectomy for squamous cell carcinoma. 
  
a) What pre-operative respiratory assessments would be helpful to assess his risks for the 
    surgery and post-operative course?                               (20% marks)  
 
b)    Outline your post-operative management for this patient with regards to: 
 
i.    Analgesia  
 
ii.    Fluid management                                    (40% marks) 
 
Three days after the operation he re-presents to ICU with new onset shortness of breath and hypotension, requiring intubation and mechanical ventilation 
 
c)    Give a differential diagnosis for his deterioration. Outline how you would manage his 
    ventilation. 
 

College answer

a)    What pre-operative respiratory assessments would be helpful to assess his risks for the surgery and post-operative course?  
•    CXR and ABG’s 
•    FEV 1 and diffusing capacity for carbon monoxide (DLCO) 
•    Calculated predicted postoperative (PPO) FEV 1 and PPO DLCO  
•    6-minute walk test 
 
b)    Outline your management for this patient with regard to: 
i
. Post-operative Analgesia: Multimodal approach to analgesia 
•    Satisfactory analgesia can be achieved with i.v. opioids; however, their beneficial effects might be counterbalanced by the risk of respiratory depression, mild attenuation of the cough reflex, and diaphragm elevation due to bowel distension. 
•    The Opioid-sparing effect of a Regional techniques and avoidance of possible side effects of systemic analgesics may be advantageous in increasing tidal volume and vital capacity, and improving diaphragm activity- Epidural, Para vertebral analgesia, Intrathecal and intercostal block. 
•    Nonsteroidal anti-inflammatory drugs, especially Ketorolac may be used to supplement opioid analgesia. These drugs work synergistically with opioids and have no respiratory depressive effects. Disadvantages include platelet and renal dysfunction. Concern over renal dysfunction in patients in whom restrictive fluid administration is the norm means NSAID’s are often avoided. 
•    Ketamine, gabanoids 
•    Paracetamol at recommended doses, along with rescue doses of Tramadol, may be proposed as a valid analgesic regimen 
 
iii. Post-operative fluid management 
•    Patients routinely extubated post op and may need minimal iv fluids 
•    Potential risk of postoperative lung injury with liberal fluid administration. 
 
c)  
Give a differential diagnosis for his deterioration?  
•    Surgical Complication: 

  • Haemothorax
  • Pneumothorax 
  • Prolonged air leak/Bronchopulmonary fistula 

•    Infectious causes

  •  Aspiration pneumonia
  • Hospital acquired pneumonia  
  • Empyema 

•    Other complication: 

  • Atelectasis
  • Pulmonary oedema
  • PE 

 
Outline how you would manage his ventilation 
Mechanical ventilation may increase the risk of bronchial stump disruption, bronchopleural fistula, persistent air leakage, and pulmonary infection. 
•    Protective ventilatory settings with small tidal volumes (Vts) and positive end-expiratory pressure (PEEP) should be applied to reduce the risk of ventilator-induced lung injury 
•    Prolonged mechanical ventilation may be associated with a significant risk for pneumonia every effort should be made to promote fast weaning from invasive airways. 
•    Acceptable rather than normal ABG targets 
•    Single lung ventilation may be required if there is a bronchopulmonary fistula 
 

Discussion

Pre-operative assessment for the patient undergoing pneumonectomy: based on UpToDate, the 2013 ACCP clinical practice guidelines and the 2001 BTS guidelines 

  • Spirometry: FEV1 of less than 80% of predicted suggests that there will be complications
  • Actual diffusing capacity: DLCO of less than 80% of expected also predicts complications
  • Post-operative FEV1 (calculated):  post-op FEV1 of less than 30% of predicted is associated with increased risk of mortality
  • Post-operative DLCO (calculated): post-op DLCO of less than 30% of predicted is associated with increased risk of mortality
  • Arterial O2 and CO2 are abbreviated as "ABG" in the college answer but in fact these parameters ae not particularly useful (for example, because of improved V\Q matching the arterial Omay actually improve post pneumonectomy, making it a pointless preoperative risk marker).
  • Exercise testing can be performed for the marginal patients. This can take the shape of stair-climbing, the "shuttle test", integrated cardiopulmonary exercise testing (which measures VO2) and the "six minute walk test" mentioned in the CICM model answer. 

Post-operative management:

Analgesia

  • Analgesia needs to be sophisticated and multimodal:
    • Regional block (paravertebral seems to be favoured over thoracic epidural- Powell et al, 2011)
    • Opiates
    • Opiate-sparing agents (eg. NSAIDs and paracetamol)
    • Addition of ketamine and neuropathic pain management agents (gabapentin, tricyclic antidepressants, etc) could have an advantage

Fluid management

  • Fluid management needs to reflect the changes in the pulmonary circulation:
    • The right heart has suddenly increased afterload by 50-60%
    • The pulmonary veins have suddenly increased pressure by 50-60%
    • Increased pressure can cause capillary damage, increasing their leakyness
    • The overall upshot of all these is a propensity to pulmonary oedema
    • The management recommendation is to keep their fluid balance neutral or negative as much as possible

Causes of early deterioration with haemodynamic instability and dyspnoea:

  • Vascular causes
    • Myocardial infarction
    • Pulmonary embolism
  • Infectious causes
    • Hospital-acquired pneumonia
    • Post-pneumonectomy empyema
    • Sputum plug
  • Drug-related causes
    • Epidural analgesia overdose
    • Epidural haematoma complications
    • Excess opiates
  • Surgical complications
    • Bleeding complications (haemothorax)
    • Bronchial stump breakdown (pneumothorax)
    • Bronchopleural fistula
    • Chylothorax (thoracic duct injury)

"Outline how you would manage his ventilation" is a strangely worded question, as the answer would be strongly dependent on what the causes of the respiratory failure is. Let us try to answer this as if it did not matter why the patient was being ventilated. The basic principles (from Lytle et al, 2008) would be:

  • Smaller tidal volumes: 
  • Lower positive pressure: avoid bronchial stump barotrauma; minimise PEEP.
  • Rapid weaning and early extubation: most studies have found a significantly increased risk of BPF if ventilation continues (Toufektzian et al, 2015)
  • NIV appears to be associated with fewer complications

References

Toufektzian, Levon, et al. "Does postoperative mechanical ventilation predispose to bronchopleural fistula formation in patients undergoing pneumonectomy?." Interactive cardiovascular and thoracic surgery 21.3 (2015): 379-382.

Lytle, Francis Theodore, and Daniel R. Brown. "Appropriate ventilatory settings for thoracic surgery: intraoperative and postoperative." Seminars in cardiothoracic and vascular anesthesia. Vol. 12. No. 2. Sage CA: Los Angeles, CA: SAGE Publications, 2008.

Brunelli, Alessandro, et al. "Physiologic evaluation of the patient with lung cancer being considered for resectional surgery: diagnosis and management of lung cancer: American College of Chest Physicians evidence-based clinical practice guidelines." Chest 143.5 (2013): e166S-e190S.

British Thoracic Society Society of Cardiothoracic Surgeons of Great Britain Ireland Working Party."Guidelines on the selection of patients with lung cancer for surgery." Thorax 56.2 (2001): 89-108.

ATS Committee on Proficiency Standards for Clinical Pulmonary Function Laboratories. "ATS statement: guidelines for the six-minute walk test." Am J Respir Crit Care Med 166 (2002): 111-117.

Powell, E. S., et al. "A prospective, multicentre, observational cohort study of analgesia and outcome after pneumonectomy." British journal of anaesthesia 106.3 (2011): 364-370.

Slinger, Peter. "Update on anesthetic management for pneumonectomy." Current Opinion in Anesthesiology 22.1 (2009): 31-37.

Mesbah, A., J. Yeung, and F. Gao. "Pain after thoracotomy." Bja Education 16.1 (2016): 1-7.

Bialka, Szymon, et al. "Comparison of different methods of postoperative analgesia after thoracotomy—a randomized controlled trial." Journal of thoracic disease 10.8 (2018): 4874.

Question 5 - 2019, Paper 1

a)    Define a chylothorax.    (10% marks)

b)    Outline how you would diagnose it and the principles of management.    (90% marks)
 

College answer

Definition – A chylothorax is an accumulation of chyle (lymphatic fluid of intestinal origin) in the pleural space. It is caused by a disruption or obstruction of the thoracic duct or its tributaries - resulting in leakage of chyle into the pleural space. (1 mark-any reasonable definition)

Diagnosis (4 marks-this degree of detail not required)

The diagnosis of chylothorax is considered when a pleural effusion occurs in an appropriate clinical context. (1 mark) The aetiology of a chylothorax includes malignancy, iatrogenic injury

– thoracic or neck surgery especially oesophagectomy, trauma – blunt/penetrating or forceful emesis, associated with infection – tuberculosis – or with disease states – sarcoidosis or amyloidosis.

The gold standard for the diagnosis of a chylothorax is detection of the chylomicron content of pleural fluid. (2 marks) Chylomicrons are large lipid globules that belong in chyle – to find them in pleural fluid is always abnormal. This can be done by electrophoresis or by the less reliable method of fat staining.

Other features of a pleural effusion that suggest the diagnosis of chylothorax are a milky colour, high protein and LDH content and high triglyceride content. These signs are not as reliable as the gold standard and may miss the diagnosis especially in fasting patients. (1 mark)

A ‘fat challenge’ - looking for the presence of milky pleural exudate after consuming fat, and CT with lymphangiography are fewer practical ways of diagnosing chylothorax in the ICU.

Management (5 marks-reasonable outline, this degree of detail not required)

  1. Conservative management – the aim of all conservative management is to decrease chyle formation and allow the lymphatic defect to close (1 mark)
  • A ‘low fat’ diet, or at least one with predominantly medium chain triglycerides (0.5 mark)
  • Rare - a somatostatin or octreotide infusion or thoracic duct embolization (0.5 mark)
  • Use of TPN
  1. Treatment of the underlying condition – for example, sarcoidosis or lymphoma (1 mark)
  2. Surgical management – should be considered for all large chylothoraces, especially those associated with malnutrition or immunosuppression (1 mark)
  • ligation of the thoracic duct (0.5 mark)
  • pleurodesis (0.5 mark)
  • pleurovenous/pleuroperitoneal shunting - less frequently
     

Discussion

Of all historic CICM college answers, none have come closer to achieving a standard of transparency which would be expected from serious adult education.  The inclusion of a prescriptive marking rubric is to be applauded.

a) The definition of chylothorax:

  • Chylothorax is a pleural collection of fluid, where the fluid is positively identified as chyle by the presence of chylomicrons

b) Diagnosis and management of chylothorax:

Diagnostic methods (from Maladonado et al, 2009):

  • Gold standard: differential electrophoresis of pleural fluid to confirm chylomicrons
  • Sudan Red stain of chylomicrons in pleural fluid
  • Clinical identification of milky pleural fluid
  • Protein and LDH  in the pleural fluid is usually high
  • Pleural fluid triglyceride level is usually high
  • Fasting test and fat challenge (chylomicrons are only found in the circulation within 3 hours of eating and they disappear in the fasted state)
  • CT and lymphangiography 

Management (Bender et al, 2015):

  • Conservative measures:

  • Surgical options:

    • Thoracic duct ligation (just proximal to the aortic hiatus)

    • Talc pleurodesis

    • Percutaneous lymphography and embolisation

    • Pleuroperitoneal shunt - where, for whatever reason, thoracic duct ligation is impossible

References

Fahimi, Hossein, et al. "Current management of postoperative chylothorax." The Annals of thoracic surgery 71.2 (2001): 448-450.

Fujita, Takeo, and Hiroyuki Daiko. "Efficacy and Predictor of Octreotide Treatment for Postoperative Chylothorax After Thoracic Esophagectomy." World Journal of Surgery (2014): 1-7.

Seriff, NATHAN S., et al. "Chylothorax: diagnosis by lipoprotein electrophoresis of serum and pleural fluid." Thorax 32.1 (1977): 98-100.

Hillerdal, G. "Chylothorax and pseudochylothorax." European Respiratory Journal 10.5 (1997): 1157-1162.

Shah, Rachit D., et al. "Postesophagectomy chylothorax: incidence, risk factors, and outcomes." The Annals of thoracic surgery 93.3 (2012): 897-904.

Merigliano, Stefano, et al. "Chylothorax complicating esophagectomy for cancer: a plea for early thoracic duct ligation." The Journal of thoracic and cardiovascular surgery 119.3 (2000): 453-457.

Valentine, Vincent G., and Thomas A. Raffin. "The management of chylothorax." CHEST Journal 102.2 (1992): 586-591.

Nair, Sukumaran K., Matus Petko, and Martin P. Hayward. "Aetiology and management of chylothorax in adults." European journal of cardio-thoracic surgery 32.2 (2007): 362-369.

Hashim, Sami A., et al. "Treatment of chyluria and chylothorax with medium-chain triglyceride." New England Journal of Medicine 270.15 (1964): 756-761.

Maldonado, Fabien, et al. "Pleural fluid characteristics of chylothorax." Mayo Clinic Proceedings. Vol. 84. No. 2. Elsevier, 2009.

Light, Richard W., et al. "Pleural effusions: the diagnostic separation of transudates and exudates."Annals of Internal Medicine 77.4 (1972): 507-513.

McGrath, Emmet E., Zoe Blades, and Paul B. Anderson. "Chylothorax: aetiology, diagnosis and therapeutic options." Respiratory medicine 104.1 (2010): 1-8.

Shah, Rachit D., et al. "Postesophagectomy chylothorax: incidence, risk factors, and outcomes." The Annals of thoracic surgery 93.3 (2012): 897-904.

Ngan, H., M. Fok, and J. Wong. "The role of lymphography in chylothorax following thoracic surgery."The British journal of radiology 61.731 (1988): 1032-1036.

Buyukcelik, Mithat, et al. "An unusual cause of pleural effusion, urinothorax in a child with urinary stone disease." Pediatric Nephrology 20.10 (2005): 1487-1489.

Cellan-Jones, C. J., and William Murphy. "Traumatic chylothorax." British medical journal 2.4165 (1940): 590.

Watts, Stephen H. "Traumatic chylothorax." Annals of surgery74.6 (1921): 691.

Mishin, Igor, Gheorghe Ghidirim, and Marin Vozian. "Acute spontaneous chylous peritonitis: report of a case." Journal of Gastrointestinal & Liver Diseases 19.3 (2010).

Bender, Bradley, Vijayashree Murthy, and Ronald S. Chamberlain. "The changing management of chylothorax in the modern era." European Journal of Cardio-Thoracic Surgery 49.1 (2015): 18-24.

Guillem, Philippe, et al. "Etilefrine use in the management of post-operative chyle leaks in thoracic surgery." Interactive Cardiovascular and thoracic surgery 3.1 (2004): 156-160.

Itkin, Maxim, et al. "Nonoperative thoracic duct embolization for traumatic thoracic duct leak: experience in 109 patients." The Journal of thoracic and cardiovascular surgery 139.3 (2010): 584-590.

Question 8 - 2019, Paper 1

a)    List four predisposing conditions and four precipitating factors which may lead to the occurrence of dynamic left ventricular outflow tract obstruction in critically ill patients.
(40% marks)

b)    What specific cardiovascular clinical signs on physical examination may be present in a patient with left ventricular dynamic outflow obstruction?    (20%marks)

c)    What are the principles of medical treatment in a patient with shock secondary to dynamic outflow obstruction?    (40% marks)
 

College answer

a)    Predisposing conditions
Hypertrophic cardiomyopathy
Left ventricular hypertrophy (e.g. Hx of hypertension or aortic stenosis)
Post AVR or TAVI for aortic stenosis
Post MVR

Precipitating factors
Hypovolaemia
Vasodilatation e.g. anaesthesia, sepsis, nitrates, liver failure
Tachycardia/arrhythmias
Inotropic agents
 
b)    Ejection systolic murmur lower left sternal edge which may vary in intensity over time as the gradient changes
An associated MR murmur is common
Signs of low CO syndrome i.e. hypotension, oliguria, lactic acidosis, end organ hypoperfusion
LVF signs

c)    Fluid loading
–increase preload
Vasocontrictors (preferably without b effect i.e. phenylephrine / vasopressin) increase afterload without increasing heart rate
Negative inotrope / chronotrope e.g. b blockade
–control heart rate
–manage arrhythmias
Treat underlying conditions

Examiners Comments:

This was generally answered well. Candidates who did poorly didn't know how to manage patients with outflow tract obstruction and recommended dangerous therapies including inotropic therapy and vasodilator agents.

Discussion

Given that this was "generally answered well",  one might assume that a detailed breakdown of the subject is probably superfluous and that only cosmetic changes could be made to enhance the already excellent college answer. That is reasonably accurate. Unfortunately, the same cannot be said for the question. Specifically, the distinction between "predisposing conditions" and "precipitating factors"  is difficult to parse. Is a mitral valve replacement a "condition" or a "factor"?  If it's a predisposing condition, then why isn't liver failure a predisposing condition? Confusion prevails. In order to make sense of this, "predisposing conditions" here are interpreted as "structural factors" and precipitating factors are interpreted as "functional factors".

Predisposing conditions

  • HOCM
  • Concentric LV hypertrophy
  • Eccentric septal hypertrophy
  • Systolic anterior motion of the mitral valve (SAM)
  • Structural causes of anterior mitral valve leaflet or apparatus position
    • Redundant anterior leaflet
    • Redundant posterior leaflet
    • Papillary muscle displacement 
    • Prosthetic valve placement
  • Infiltrative cardiac disease
    • Cardiac amyloid
    • Fabry disease
    • Danon disease
    • Friedrich ataxia
    • Cardiac oxalosis
    • Mucopolysaccharidoses
    • Sarcoidosis

Precipitating factors

  • Insufficient diastolic filling pressure
    • Hypovolemia
    • Atrial fibrillation
  • Insufficient diastolic filling time
    • Tachycardia
    • SVT or VT
  • Insufficient afterload
    • Vasodilation due to sepsis
    • Vasodilator drugs, eg. nitrates or general anaesthetics
  • Excessive contractility
    • Inotrope drugs
    • Stress
    • Pain
    • Anxiety
    • Exercise

Clinical features include:

  • Haemodynamic instability associated with stress
  • Ejection systolic murmur, louder with Valsalva (whereas AS becomes softer)
  • MR murmur
  • Brockenbrough–Braunwald-Morrow phenomenon: "a paradoxical decrease in the arterial pulse pressure and an associated increase in the LV systolic pressure in the beat following a PVC" (Trevino & Buergler, 2014). 
  • Brisk arterial pulse with rapid systolic rise and rapid drop-off
  • Characteristic "spike and dome" appearance of the aortic pressure trace

Management consists of targeting the following parameters:

  • Preload: keep it high-normal. 
  • Rate: keep it slow. 
  • Rhythm: keep it sinus. 
  • Contractility: bring it down. Negative inotropes are often called for, eg. beta-blockers
  • Afterload: keep it high. Use vasopressors with minimal beta effect (eg. vasopressin or phenylephrine)

References

Walmsley, Robert. "Anatomy of left ventricular outflow tract." British heart journal 41.3 (1979): 263.

Vilcant, Viliane, and Ofek Hai. "Left Ventricular Outflow Tract Obstruction." StatPearls [Internet]. StatPearls Publishing, 2018.

Halpern, Ethan J., et al. "Characterization and normal measurements of the left ventricular outflow tract by ECG-gated cardiac CT: implications for disorders of the outflow tract and aortic valve." Academic radiology 19.10 (2012): 1252-1259.

Ibrahim, Michael, et al. "Modern management of systolic anterior motion of the mitral valve." European Journal of Cardio-Thoracic Surgery 41.6 (2012): 1260-1270.

Kobayashi, Sayuki, et al. "Causes of an increased pressure gradient through the left ventricular outflow tract: a West Coast experience." Journal of echocardiography 16.1 (2018): 34-41.

Pennacchini, Ermelinda, et al. "Distinguishing hypertension from hypertrophic cardiomyopathy as a cause of left ventricular hypertrophy." The Journal of Clinical Hypertension17.3 (2015): 239-241.

A Kelshiker, Mihir, et al. "Basal septal hypertrophy." Current cardiology reviews 9.4 (2013): 325-330.

Seward, James B., and Grace Casaclang-Verzosa. "Infiltrative cardiovascular diseases: cardiomyopathies that look alike." Journal of the American College of Cardiology 55.17 (2010): 1769-1779.

Yang, Ji Hyun, et al. "Dynamic left ventricular outflow tract obstruction without basal septal hypertrophy, caused by catecholamine therapy and volume depletion." The Korean journal of internal medicine 23.2 (2008): 106.

Sanderson, J. E., et al. "Left ventricular filling in hypertrophic cardiomyopathy. An angiographic study." Heart 39.6 (1977): 661-670.

Hong, Joon Hwa, Hartzell V. Schaff, and Rick A. Nishimura. "Fixed versus dynamic subaortic stenosis: Hemodynamics and resulting differences in Doppler echocardiography and aortic pressure contour.The Journal of thoracic and cardiovascular surgery 151.3 (2016): 883.

Sen-Chowdhry, Srijita, et al. "Update on hypertrophic cardiomyopathy and a guide to the guidelines." Nature Reviews Cardiology 13.11 (2016): 651.

Chan, Wan L., et al. "Effect of preload change on resting and exercise cardiac performance in hypertrophic cardiomyopathy." The American journal of cardiology 66.7 (1990): 746-751.

Gilligan, David M., et al. "Cardiac responses assessed by echocardiography to changes in preload in hypertrophic cardiomyopathy.American Journal of Cardiology 73.4 (1994): 312-315.

Shah, P. M., R. Amarasingham, and C. M. Oakley. "Haemodynamic effects of changes in blood volume in hypertrophic obstructive cardiomyopathy." British heart journal27.1 (1965): 83.

Cross, Cecil E., and Peter F. Salisbury. "Functional subaortic stenosis produced in animals." The American journal of cardiology 12.3 (1963): 394-398.

Hadjimiltiades, Stavros, et al. "Dynamic changes in left ventricular outflow tract flow velocities after amyl nitrite inhalation in hypertrophic cardiomyopathy." American heart journal 121.4 (1991): 1143-1148.

Sherrid, Mark V., Gretchen Pearle, and David Z. Gunsburg. "Mechanism of benefit of negative inotropes in obstructive hypertrophic cardiomyopathy." Circulation 97.1 (1998): 41-47.

Poliac, Liviu C., Michael E. Barron, and Barry J. Maron. "Hypertrophic cardiomyopathy." Anesthesiology: The Journal of the American Society of Anesthesiologists 104.1 (2006): 183-192.

Panduranga, Prashanth, et al. "Dynamic left ventricular outflow tract obstruction complicating aortic valve replacement: A hidden malefactor revisited." Saudi journal of anaesthesia 4.2 (2010): 99.

Tsuruta, Hikaru, et al. "Incidence, predictors, and midterm clinical outcomes of left ventricular obstruction after transcatheter aortic valve implantation." Catheterization and Cardiovascular Interventions 92.4 (2018): E288-E298.

Guler, Niyazi, Cenap Ozkara, and Aytac Akyol. "Left ventricular outflow tract obstruction after bioprosthetic mitral valve replacement with posterior mitral leaflet preservation." Texas Heart Institute Journal 33.3 (2006): 399.

Dahhan, Ali, et al. "Hypotension due to dynamic left ventricular outflow tract obstruction after percutaneous coronary intervention.Texas Heart Institute Journal 38.6 (2011): 723.

Trevino, Alejandro R., and John Buergler. "the BroCkenBrouGh–BraunWald–MorroW siGn." Methodist DeBakey cardiovascular journal 10.1 (2014): 34.

Pagani, Francis. "A lesson in the power of observation." The Journal of thoracic and cardiovascular surgery 156.4 (2018).

BROCKENBROUGH, EDWIN C., EUGENE BRAUNWALD, and ANDREW G. MORROW. "A hemodynamic technic for the detection of hypertrophic subaortic stenosis." Circulation 23.2 (1961): 189-194.

Goodwin, J. F., et al. "Obstructive cardiomyopathy simulating aortic stenosis." British heart journal 22.3 (1960): 403.

Slama, Michel, Christophe Tribouilloy, and Julien Maizel. "Left ventricular outflow tract obstruction in ICU patients." Current opinion in critical care 22.3 (2016): 260-266.

Question 23 - 2019, Paper 2

A 74-year-old male has been intubated for respiratory failure developing two weeks after oesophagectomy for adenocarcinoma. He has no other significant past medical history.

After intubation, an audible air leak was apparent. Urgent bronchoscopy demonstrated a fistula between the proximal left main bronchus and the oesophago-gastric anastomosis.

Outline the principles and priorities in the management of this patient.
 

College answer

Overall approach and perspective (2 marks) 2 = Clear understanding that:
This is a life-threatening complication requiring early expert assistance with surgical and anaesthetic support.
Priorities are stabilization and facilitation of urgent return to theatre for surgical repair +/- stenting. High mortality even with optimal treatment.

1= Mentions these elements but without clear understanding of urgency and/or need for definitive repair. i.e. unable to be confident that candidate would communicate and coordinate effectively.

Management of airway and ventilation

Airway (3 marks)
 
Articulates main principles to support oxygenation, minimise leak by minimising airway pressures and isolate lungs prior to surgical repair.

3= Outlines the need to isolate L and R lungs prior to surgical repair.
Demonstrates clear understanding of potential approaches and the need for expert skill and consideration of clinical stability e.g. size of leak/presence of complications etc.
e.g. Ultimately likely to need for R sided DLT to enable surgical repair if oxygenation stable and appropriate equipment available (bronchoscopy etc.), ideally in theatre with surgeon present to deal with potential complications.
May need to urgently selectively intubate RMB to manage massive leak in emergency setting especially if initial intubation was difficult.
High risk of pneumothorax and/or empyema requiring pleural drainage.

2= Principles and priorities safe but lacking finer detail or clinical perspective

1= Basic understanding or listing or options without guiding principles and clinical perspective. Not clear the candidate would safely manage themselves.

Ventilation (2 marks)

2= Ventilatory strategy should include aiming for spontaneous ventilation if possible and techniques for minimizing airway pressures (e.g. low/no PEEP).
Need to consider/monitoring for likely respiratory complications (pneumothorax, hydro-pneumothorax, empyema).
1= mentions only one of clear ventilatory strategy  or knowledge of complications.    Alternatively, superficial comment on both.

Sepsis (1 mark)

1= Mentions likely complications of pneumonia, empyema and subsequent systemic sepsis. Need for cultures (esp. blood, bronch specimens) and appropriate broad-spectrum antibiotics. (half mark if one element missing)

Supportive Care (2 marks)
2= sensible concise priorities for supportive care and clear mentions need to communicate with and offer support to family.
e.g.
Haemodynamics - large bore IV access, art-line, CVC if time allows. Planning for potential need for vasopressors.
Cease feeding, NG on free drainage if present to minimise gastric dilation and/or contamination of lung via fistula.
Elevate bed
Communication with family early to inform and prepare for potential poor outcome and provide support as required.

1= some sensible elements but lacking clinical perspective or failure to mention family communication.

Discussion

Management priorities:

  1. Stabilise the patient (control ABCD)
  2. Organise definitive management, which will be surgical, bronchoscopic or endoscopic
  3. Prepare the family for the worse

As usual, the management can be divided into "supportive" and "specific".

Supportive management:

  • Airway management:
    • Intubate the patient with a right-sided  double lumen tube
    • Ideally do this in theatre, with an upper GI and thoracic surgen present. The risk here is that potentially, you will place the tube in such a violently stupid way that the bronchio-oesophageal tear is extended. The  consequence may be massive pneumomediastinum and an unventilatable patient with rapidly falling blood pressure due to greater vessel compression. 
  • Ventilator management
    • With a single lumen tube:
      • Account for large leak: use a pressure-control mode
    • With a double lumen tube:
      • Use differential lung ventilation
      • Ventilate the "good" lung with normal one-lung ventilation
      • Ventilate the "bad" lung with some modest  PEEP (~ 5-8) and zero inspiratory pressure (i.e. CPAP)
  • Sedation and analgesia
    • ​​​​With a double lumen tube, ideally the patient should be paralysed and sedated to prevent tube dislodgement and to facilitate differential lung ventilation
    • With a single lumen tube, spontaneous respiratory activity should be encouraged and sedation should be minimised
  • Gastrointestinal/nutritional management:
    • If this is feasible,place an NGT endoscopically and allow it to vent freely or place it on low wall suction
    • Most likely, this is not feasible, and the whole anastomotic site should be left well alone  
    • Feed the patient parenterally 
    • Use liberal PPI  therapy (perhaps an infusion of pantoprazole)
  • Management of infection
    • One can almost guarrantee that some infectious process will take place, 
      • in the lung (aspirtation)
      • in the chest cavity (collection)
      • in the abdominal cavity
    • Thus, empiric antibiotics should probably be commenced, and these should ideally be broad enough to cover upper GI anaerobes. You can always stop them again in a couple of days, when the antimicrobial stewardship people start mocking you openly in the corridors.
  • Management of family expectations
    • The outcome for these scenarios is almost uniformly bad, particularrly wherre a malignancy is involved

Specific management resembles the oesophageal perforation options mentioned above, with the exception of all the bronchoscopic stuff:

  • Bronchoscopic repair
    • Bronchial stent
  • Gastroscopic repair options
    • self-expanding esophageal stainless steel-covered metal stents (SEM)
  • Surgical repair options
    • Resection and diversion (i.e. oesophagus is externalised in the neck; one essentially disconnects the upper GI tract from the lower)
    • Resection and re-anastomosis (the latter is risky)
    • Conservative management (i.e. after having a look and the placement of a NG tube, the patient returns to ICU for conservative and palliative management)


 

References

Hasan, Shafqat, Ali NA Jilaihawi, and Dhruva Prakash. "Conservative management of iatrogenic oesophageal perforations—a viable option." European journal of cardio-thoracic surgery 28.1 (2005): 7-10.

Biancari, F., et al. "Treatment of esophageal perforation in octogenarians: a multicenter study." Diseases of the Esophagus 27.8 (2014): 715-718.

Spalding, Alanson R., Donald P. Burney, and Robert E. Richie. "Acquired benign bronchoesophageal fistulas in the adult." The Annals of thoracic surgery 28.4 (1979): 378-383.

Kalmár, Katalin, et al. "Non-malignant tracheo-gastric fistula following esophagectomy for cancer." European journal of cardio-thoracic surgery 18.3 (2000): 363-365.

Lolley, David M., et al. "Management of malignant esophagorespiratory fistula.The Annals of thoracic surgery 25.6 (1978): 516-520.

Shamji, Farid M., and Richard Inculet. "Management of malignant tracheoesophageal fistula." Thoracic surgery clinics 28.3 (2018): 393-402.

Question 29 - 2020, Paper 1

In relation to cardiac surgery:

a)    What are the complications of aortic cross clamping and cardiopulmonary bypass that may affect the post-operative ICU management?    (80% marks)

b)    What are the major risks from internal mammary artery grafting? (10% marks)

c)    What are the major risks from radial artery grafting? (10% marks)
 

College answer

a)

Respiratory complications:

  • Left lower lobe collapse (poor re-inflation post bypass, phrenic nerve injury)
  • Increased pulmonary vascular resistance (protamine)
  • Acute lung injury (SIRS)
  • Pulmonary oedema
  • ?pneumothorax

Cardiovascular complications

  • Myocardial stunning or infarction (inadequate myocardial protection)
  • Coronary graft ischaemia (air embolism)
  • Right ventricular dysfunction (pulmonary hypertension related to protamine)
  • Hypoperfusion and end-organ ischaemia related to non-pulsatile flow and/or air/atheroma embolism from cross clamping
 
  • Aortic dissection from cross clamping

Neurological complications

    • Cerebrovascular events, watershed infarcts,
    • neurocognitive dysfunction (low flow, thromboembolism)
    • Phrenic nerve palsy (use of cold cardioplegia ‘slush’)

Renal complications

  • Dysfunction related to ischaemia (non-pulsatile flow) and SIRS

Gastro-intestinal complications

  • Splanchnic ischaemia (low flow, thromboembolism)
  • Hepatitic dysfunction, acalculous / gangrenous cholecystitis, pancreatitis (hypoperfusion, SIRS)

Haematological complications

  • Coagulopathy (effects of hypothermia and dilutional coagulopathy, residual heparinisation, activation of coagulation cascade during bypass)
  • Anaemia (haemodilution, blood loss in the circuit)
  • Platelet dysfunction (bypass circuit) Haemolysis (bypass circuit)
  • Bleeding from aortic cannulation site Metabolic complications
  • Hypothermia (intra-operative cooling and delayed re-warming)
  • Insulin resistance and hyperglycaemia (hypothermia)
  • Electrolyte abnormalities (haemodilution, post-pump diuresis)

Immune-mediated complications

  • Activation of coagulation cascade (blood contact with non-biological surfaces and blood-gas interface)
  • SIRS (leucocyte and complement activation, cytokine release and expression of adhesion molecules stimulated by contact with bypass circuit)
  • Allergic reactions to protamine

ALTERNATIVE TEMPLATE BASED ON PATHOPHYSIOLOGY

  1. Effects related to blood contact with non-biologic surfaces and blood-gas interfaces
    • Activation of coagulation cascade- consumptive coagulopathy, thromboembolic phenomena, haemolysis, 
rarely TTP.
    • Systemic  inflammatory  response  syndrome  due  to  leucocyte  and   complement  activation, cytokine release 
and expression of adhesion molecules- vasodilatory shock, fever, acute lung injury, liver dysfunction, 
multiorgan dysfunction.
    • Platelet dysfunction
  1. Effects related to non-pulsatile flow
    • Renal dysfunction
    • Cerebrovascular events, watershed infarcts, neurocognitive dysfunction
    • Splanchnic ischaemia
  1. Effects related to haemodilution
    • Dilutional coagulopathy, anaemia.
    • Electrolyte abnormalities
 
  1. Effects of hypothermia
    • Coagulopathy
    • Decreased tissue oxygen delivery
    • Insulin resistance and hyperglycaemia
  1. Effects of heparin and protamine
    • Residual heparinisation leading to bleeding
    • Increased pulmonary vascular resistance and right ventricular dysfunction from protamine, allergic 
reactions to protamine
  1. f) Effects related to aortic manipulation (cross-clamping and proximal grafts)
    • Systemic embolisation with potential for neurologic, mesenteric and renal dysfunction.
    • Aortic dissection from cannulation site
    • Bleeding from bypass cannulation site
    • Difficulty      with      myocardial      protection      resulting      in      postoperative myocardial dysfunction (especially right-sided) due to stunning or infarction
  1. g) Other
    • Left phrenic nerve palsy (surgical injury, use of cold cardioplegia “slush”)
    • Left lower lobe collapse (poor re-inflation post bypass, phrenic nerve injury)

b)

Artery spasm/kinking/thrombosis - resultant myocardial ischaemia/LVF

Increased risk of sternal devascularisation-> sternal non-union and infection especially with bilateral IMA grafts

Increased post-op bleeding with bilateral IMA harvesting Aneurysm/pseudo-aneurysm of artery formation

c)

Spasm -> cardiac ischaemia

Arm complications-> haematoma/haemorrhage, infection, motor impairment (usually temporary), sensory impairment, pain, distal ischaemia (rare)

Examiners Comments:

Answers generally lacked structure and detail.

Discussion

Complications of Cardiopulmonary Bypass
Organised According to Physiological Derangement
Aetiology Physiological derangement
Bypass circuit mechanism Hemodilution
Haemolysis (mechanical)
Blood loss into the circuit
SIRS due to bypass
SIRS due to bypass Coagulopathy due to coagulation cascade activation and clotting factor depletion
Platelet dysfunction and platelet depletion
Renal failure due to SIRS
Acute lung injury due to SIRS, "pump lung"
Anticoagulation and reversal Bleeding from residual heparin
Heparin-induced thrombocytopenia
Anaphylaxis to protamine
Increased pulmonary resistance due to protamine
Right ventricular failure due to protamine-induced pulmonary hypertension
Prolonged hypothermia Heart block
Ventricular and atrial arrhythmias
Hyperglycaemia (decreased insulin production as well as insulin insensitivity)
Decreased tubular resorption in the kidney (thus diuresis)
Phrenic nerve palsy (“cold slush cardioplegia”)
Prolonged ischaemia Renal failure due to ATN
Myocardial infarction
Encephalopathy and neurocognitive deterioration
Hepatic dysfunction and delayed drug clearance
Pancreatitis
Splanchnic ischaemia
Mechanics of surgery Atelectasis (especially of the  LLL) due to mechanical compression
Embolic complications Myocardial infarction
Stroke (eg. air or cholesterol emboli)
Splanchnic ischaemia
Limb ischaemia

Complications of internal mammary artery grafting (von Segesser et al, 1990)

  • Spasm of the graft may occur (whereas with SVG, it will not)
  • Potendial devascularisation of the chest wall may increase the risk of sternal wound dehiscence
  • Wound complications are thought to be more common with bilateral IMA grafting
  • Pneumothorax is more likely
  • Prenic nerve paresis is more likely
  • Chylothorax may occur duet to thoracic duct injury
  • Subclavian steal may develop

Complications of radial artery grafting (Budillon et al, 2003; Buxton et al, 1996)

  • Donor arm weakness in ~ 0.7%
  • Cutaneous paraesthesia in ~ 3.7%
  • Potential for hand ischaemia
  • Spasm of the graft may occur (whereas with SVG, it will not)

References

André, Arthur C. St, and Anthony DelRossi. "Hemodynamic management of patients in the first 24 hours after cardiac surgery." Critical care medicine 33.9 (2005): 2082-2093.

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.

von Segesser, Ludwig K. "Complications of Internal Mammary Artery Grafting." Arterial Grafting for Myocardial Revascularization. Springer, Berlin, Heidelberg, 1990. 102-108.

Budillon, Alessandro Maria, et al. "Complications after radial artery harvesting for coronary artery bypass grafting: our experience." Surgery 133.3 (2003): 283-287.

Buxton, Brian, et al. "The radial artery as a bypass graft." Current opinion in cardiology 11.6 (1996): 591-598.

Question 19 - 2020, Paper 2

With regards to veno-arterial extra-corporeal membrane oxygenation (VA-ECMO):

a)    List six major conditions for which VA-ECMO is indicated.    (40% marks)

b)    List four contraindications for VA-ECMO.    (40% marks)

c)    List four life threatening complications of VA-ECMO.    (20% marks)
 

College answer

Not available.

Discussion

This weird question asked for lists, which means that it would have been theoretically possible to score full marks with fourteen lines of text.

a) Six major conditions for which VA-ECMO is indicated:

  • Failure to wean from cardiopulmonary bypass
  • Cardiogenic shock of any cause
  • Cardiac arrest from a reversible cause (i.e. ECPR)
  • Bridge to cardiac transplant or LVAD
  • Graft failure following cardiac transplantation
  • Perioperative support for surgery requiring cardiac arrest or cardiopulmonary bypass

b) Four contraindications for VA ECMO:

  • Contraindications to anticoagulation: recent surgery, uncontrolled bleeding, intracranial haemorrhage, DIC (eg. sepsis, Ebola)
  • Irreversible condition
  • Contraindications for heart/lung transplant
  • Major immunosuppression (eg. bone marrow transplant)

c) Four life-threatening complications for VA ECMO:

  • LV distension and pulmonary haemorrhage (with VA ECMO)
  • Cardiac chamber thrombosis (with VA ECMO)
  • Bleeding complications (eg. intracranial haemorrhage)
  • Embolic phenomena (air bubbles,  clots)

References

All, literally all of this comes from the ELSO documentation.

Specifically, the ELSO Guidelines General v1.4 were of the greatest use.

Question 2 - 2021, Paper 1

A 71-year-old male is transferred to your ICU following a mechanical aortic valve replacement and coronary artery bypass surgery. The anaesthetist reports that he came off bypass readily, has not required any inotropic support, and has epicardial pacing wires in situ. However, shortly after arrival his blood pressure falls to 60/30 mmHg.
a) Outline your differential diagnosis for his hypotension. (20% marks)
b) List four likely causes of excessive post-operative bleeding in this setting. (20% marks)
c) Outline your immediate management. (60% marks)

College answer

Not available.

Discussion

This question is basically the same as Question 13 from the first paper of 2012, which demonstrates to exam candidates that they need to reach at least ten years back into historical papers in order to capture all potential repeat SAQs. 

Differential diagnosis for this hypotension can be organised in a number of different ways (see the discussion section of Question 13), but the one which 

  • Preload
    • Inadequate intraoperative fluid
    • Haemorrhage
    • Valve failure (mitral / tricuspid)
  • Rate
    • Bradycardia (or excessive tachycardia!)
  • Rhythm
    • AF or other arrhythmia
  • Contractility
    • Post-bypass myocardial depression
    • Myocardial ischaemia
  • Afterload
    • Artifact: art line is incorrectly zeroed
    • LVOT obstruction
    • Anaphylaxis
    • Vasoplegia
    • Valve failure (aortic or pulmonic)

Considering this was weighted only 20% of the total mark, one should be expected to produce a laconic pointform list rather than a paragraph of text, which means the use of this classification system might be a bit excessive. 

Four likely causes of excessive post-operative bleeding in this setting:

One could pick any from the following list of factors:

  • incomplete surgical haemostasis
  • residual heparin effect after cardiopulmonary bypass
  • platelet abnormalities (platelet dysfunction and thrombocytopenia – from bypass circuit consumption, antiplatelet agents etc)
  • hypothermia 
  • postoperative hypertension
  • clotting factor depletion
  • haemodilution (dilutional thrombocytopenia and coagulopathy)

Immediate management here would have to be structured and detailed to earn full marks. Examples of what that means abound in the past papers, but the best one is probably again in the college answer to Question 13 from the first paper of 2012. A mutant version of that structure is offered here:

  • Maintain  SpO2 ~ 100%
  • Adjust positive pressure, with two goals in mind:
    • Enhancement of preload by controlling the intrathoracic venous flow
    • Enhancement of afterload by increasing LV transmural pressure
    • Perhaps some sort of tamponade effect - the college answer recommends a PEEP of 10, which ( a reader has helpfully pointed out) probably comes from Ilabaca et al (1980).
  • Assess the drains to make sure they are not blocked
  • Maintain satisfactory diastolic pressure with noradrenaline and/or vasopressin
  • Give a fluid bolus
  • Check for a cardiovertable rthythm disturbance
  • Consider increasing pacing rate to 90
  • Organise a TOE or TTE to assess the need for inotropes
  • Check bloods and TEG to see what further factors/platelets the patient might require
  • Alert the surgeons to the deterioration, in case you need to reopen the chest

References

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

André, Arthur C. St, and Anthony DelRossi. "Hemodynamic management of patients in the first 24 hours after cardiac surgery." Critical care medicine 33.9 (2005): 2082-2093.

Estafanous, Fawzy G., and Robert C. Tarazi. "Systemic arterial hypertension associated with cardiac surgery.The American journal of cardiology 46.4 (1980): 685-694.

Roberts, A. J., et al. "Systemic hypertension associated with coronary artery bypass surgery. Predisposing factors, hemodynamic characteristics, humoral profile, and treatment." The Journal of thoracic and cardiovascular surgery 74.6 (1977): 846-859.

Ilabaca, Patricio A., John L. Ochsner, and Noel L. Mills. "Positive end-expiratory pressure in the management of the patient with a postoperative bleeding heart." The Annals of thoracic surgery 30.3 (1980): 281-284.

Question 19 - 2021, Paper 1

You are called to review an 86-year-old female, with severe pleuritic chest pain and difficulty breathing following dilation of an oesophageal stricture. Her CT thorax scan confirms an oesophageal perforation.

Outline your management of this problem, including the options for definitive treatment.

College answer

Not available.

Discussion

This question is virtually identical to Question 16 from the second paper of 2016.

Immediate management

  • Attention to ABCs and correction of immediately identified life-threatening features
  • Detailed history and thorough physical examination
  • Assessment of airway patency and intubation as needed
  • Maintenance of normoxia with supplemental oxygen
  • Maintenance of normotension with fluid resuscitation and vasopressors as needed
  • Analgesia and sedation
  • Attention to broad-spectrum antibiotic cover, including antifungal agents

Investigations:

  • CXR looking for pneumomediastinum
  • CT chest with contrast
  • Gastrograffin swallow (not barium)
  • Intercostal catheter to drain pleural effusion and analyse it, looking for acidity (suggestive of gastric contents) and food particles.

Specific Management

  • Thoracoscopic or open surgical management;
  • alternatively, endoscopic stent placement
  • alternatively, conservative antibiotic-based management and supportive care in ICU
  • alternatively, palliative care

Supportive management:

  • TPN: they won't be eating for a while
  • Broad-spectrum antibiotics (Tazocin is a fine choice)
  • Proton pump inhibitors to encourage the process of oesophageal repair
  • Eventually, these people end up having surgery - but it is delayed until the empyema or mediastinal abscess are well-circumscribed.

Idiosyncratic ICU issues

  • No positive pressure without intubation: even high flow nasal prongs can blow gas into the mediastinum. Thus, no bag-mask ventilation with intubation. All of these patients should be getting an RSI-like induction.

Social issues

  • This is an iatrogenic complication. Full open disclosure must be carried out
  • A family discussion of the possible outcome must take place, ideally led by the team of perforators.
  • The mortality- irrespective of the management approach - will be in the order of 40% (Biancari et al, 2014)

References

Curci, JOSEPH J., and MARC J. Horman. "Boerhaave's syndrome: The importance of early diagnosis and treatment." Annals of surgery 183.4 (1976): 401.

Teh, Elaine, et al. "Boerhaave's syndrome: a review of management and outcome." Interactive cardiovascular and thoracic surgery 6.5 (2007): 640-643.

Eroǧlu, Atilla, et al. "Esophageal perforation: the importance of early diagnosis and primary repair." Diseases of the Esophagus 17.1 (2004): 91-94.

Patton, Anthony S., et al. "Reevaluation of the Boerhaave syndrome: A review of fourteen cases." The American Journal of Surgery 137.4 (1979): 560-565.

Movsas, S. "Spontaneous Rupture of the Oesophagus Is Conservative Treatment Ever Justified?." Thorax 21.2 (1966): 111-114.

Bolooki, H. O. O. S. A. N. G., et al. "Spontaneous rupture of the esophagus: Boerhaave's syndrome." Annals of surgery 174.2 (1971): 319.

Curci, JOSEPH J., and MARC J. Horman. "Boerhaave's syndrome: The importance of early diagnosis and treatment." Annals of surgery 183.4 (1976): 401.

Teh, Elaine, et al. "Boerhaave's syndrome: a review of management and outcome." Interactive cardiovascular and thoracic surgery 6.5 (2007): 640-643.

Eroǧlu, Atilla, et al. "Esophageal perforation: the importance of early diagnosis and primary repair." Diseases of the Esophagus 17.1 (2004): 91-94.

Bhatia, Pankaj, et al. "Current concepts in the management of esophageal perforations: a twenty-seven year Canadian experience." The Annals of thoracic surgery 92.1 (2011): 209-215.

Spapen, J., et al. "Boerhaave's Syndrome: Still a Diagnostic and Therapeutic Challenge in the 21st Century." Case reports in critical care 2013 (2013).

Biancari, Fausto, et al. "Current treatment and outcome of esophageal perforations in adults: systematic review and meta-analysis of 75 studies." World journal of surgery 37.5 (2013): 1051-1059.

Hasan, Shafqat, Ali NA Jilaihawi, and Dhruva Prakash. "Conservative management of iatrogenic oesophageal perforations—a viable option." European journal of cardio-thoracic surgery 28.1 (2005): 7-10.

Biancari, F., et al. "Treatment of esophageal perforation in octogenarians: a multicenter study." Diseases of the Esophagus 27.8 (2014): 715-718.

Question 24 - 2021, Paper 1

With respect to chylothorax in the critically ill:

a)    Define chylothorax.    (10% marks)

b)    Outline how it should be diagnosed.    (40% marks)

c)    Describe the principles of management.    (50% marks)

College answer

Not available.

Discussion

This question is virtually identical to Question 5 from the first paper of 2019, except in 2019 diagnosis and management were rolled together into one big question worth 90% of the marks. If one inspects the marking rubric from 2019, one will note that the marks are allocated in the same way.

a) The definition of chylothorax:

  • Chylothorax is a pleural collection of fluid, where the fluid is positively identified as chyle by the presence of chylomicrons

b) Diagnosis of chylothorax:

Diagnostic methods (from Maladonado et al, 2009):

  • Gold standard: differential electrophoresis of pleural fluid to confirm chylomicrons
  • Sudan Red stain of chylomicrons in pleural fluid
  • Clinical identification of milky pleural fluid
  • Protein and LDH  in the pleural fluid is usually high
  • Pleural fluid triglyceride level is usually high
  • Fasting test and fat challenge (chylomicrons are only found in the circulation within 3 hours of eating and they disappear in the fasted state)
  • CT and lymphangiography 

c) Management of chylothorax from Bender et al (2015):

  • Conservative measures:

  • Surgical options:

    • Thoracic duct ligation (just proximal to the aortic hiatus)

    • Talc pleurodesis

    • Percutaneous lymphography and embolisation

    • Pleuroperitoneal shunt - where, for whatever reason, thoracic duct ligation is impossible

References

Fahimi, Hossein, et al. "Current management of postoperative chylothorax." The Annals of thoracic surgery 71.2 (2001): 448-450.

Fujita, Takeo, and Hiroyuki Daiko. "Efficacy and Predictor of Octreotide Treatment for Postoperative Chylothorax After Thoracic Esophagectomy." World Journal of Surgery (2014): 1-7.

Seriff, NATHAN S., et al. "Chylothorax: diagnosis by lipoprotein electrophoresis of serum and pleural fluid." Thorax 32.1 (1977): 98-100.

Hillerdal, G. "Chylothorax and pseudochylothorax." European Respiratory Journal 10.5 (1997): 1157-1162.

Shah, Rachit D., et al. "Postesophagectomy chylothorax: incidence, risk factors, and outcomes." The Annals of thoracic surgery 93.3 (2012): 897-904.

Merigliano, Stefano, et al. "Chylothorax complicating esophagectomy for cancer: a plea for early thoracic duct ligation." The Journal of thoracic and cardiovascular surgery 119.3 (2000): 453-457.

Valentine, Vincent G., and Thomas A. Raffin. "The management of chylothorax." CHEST Journal 102.2 (1992): 586-591.

Nair, Sukumaran K., Matus Petko, and Martin P. Hayward. "Aetiology and management of chylothorax in adults." European journal of cardio-thoracic surgery 32.2 (2007): 362-369.

Hashim, Sami A., et al. "Treatment of chyluria and chylothorax with medium-chain triglyceride." New England Journal of Medicine 270.15 (1964): 756-761.

Maldonado, Fabien, et al. "Pleural fluid characteristics of chylothorax." Mayo Clinic Proceedings. Vol. 84. No. 2. Elsevier, 2009.

Light, Richard W., et al. "Pleural effusions: the diagnostic separation of transudates and exudates."Annals of Internal Medicine 77.4 (1972): 507-513.

McGrath, Emmet E., Zoe Blades, and Paul B. Anderson. "Chylothorax: aetiology, diagnosis and therapeutic options." Respiratory medicine 104.1 (2010): 1-8.

Shah, Rachit D., et al. "Postesophagectomy chylothorax: incidence, risk factors, and outcomes." The Annals of thoracic surgery 93.3 (2012): 897-904.

Ngan, H., M. Fok, and J. Wong. "The role of lymphography in chylothorax following thoracic surgery."The British journal of radiology 61.731 (1988): 1032-1036.

Buyukcelik, Mithat, et al. "An unusual cause of pleural effusion, urinothorax in a child with urinary stone disease." Pediatric Nephrology 20.10 (2005): 1487-1489.

Cellan-Jones, C. J., and William Murphy. "Traumatic chylothorax." British medical journal 2.4165 (1940): 590.

Watts, Stephen H. "Traumatic chylothorax." Annals of surgery74.6 (1921): 691.

Mishin, Igor, Gheorghe Ghidirim, and Marin Vozian. "Acute spontaneous chylous peritonitis: report of a case." Journal of Gastrointestinal & Liver Diseases 19.3 (2010).

Bender, Bradley, Vijayashree Murthy, and Ronald S. Chamberlain. "The changing management of chylothorax in the modern era." European Journal of Cardio-Thoracic Surgery 49.1 (2015): 18-24.

Guillem, Philippe, et al. "Etilefrine use in the management of post-operative chyle leaks in thoracic surgery." Interactive Cardiovascular and thoracic surgery 3.1 (2004): 156-160.

Itkin, Maxim, et al. "Nonoperative thoracic duct embolization for traumatic thoracic duct leak: experience in 109 patients." The Journal of thoracic and cardiovascular surgery 139.3 (2010): 584-590.

Question 26 - 2021, Paper 1

A 74-year-old male has been intubated for respiratory failure developing two weeks after oesophagectomy for adenocarcinoma. He has no other significant past medical history. After intubation, an audible air leak was apparent. Urgent bronchoscopy demonstrated a fistula between the proximal left main bronchus and the oesophago-gastric anastomosis.

Outline the immediate management priorities and the priorities for the ongoing ICU management of this patient.

College answer

Not available.

Discussion

This question is identical to Question 23 from the second paper of 2019.

Management priorities:

  1. Stabilise the patient (control ABCD)
  2. Organise definitive management, which will be surgical, bronchoscopic or endoscopic
  3. Prepare the family for the worse

As usual, the management can be divided into "supportive" and "specific".

Supportive management:

  • Airway management:
    • Intubate the patient with a right-sided  double lumen tube
    • Ideally do this in theatre, with an upper GI and thoracic surgen present. The risk here is that potentially, you will place the tube in such a violently stupid way that the bronchio-oesophageal tear is extended. The  consequence may be massive pneumomediastinum and an unventilatable patient with rapidly falling blood pressure due to greater vessel compression. 
  • Ventilator management
    • With a single lumen tube:
      • Account for large leak: use a pressure-control mode
    • With a double lumen tube:
      • Use differential lung ventilation
      • Ventilate the "good" lung with normal one-lung ventilation
      • Ventilate the "bad" lung with some modest  PEEP (~ 5-8) and zero inspiratory pressure (i.e. CPAP)
  • Sedation and analgesia
    • ​​​​With a double lumen tube, ideally the patient should be paralysed and sedated to prevent tube dislodgement and to facilitate differential lung ventilation
    • With a single lumen tube, spontaneous respiratory activity should be encouraged and sedation should be minimised
  • Gastrointestinal/nutritional management:
    • If this is feasible,place an NGT endoscopically and allow it to vent freely or place it on low wall suction
    • Most likely, this is not feasible, and the whole anastomotic site should be left well alone  
    • Feed the patient parenterally 
    • Use liberal PPI  therapy (perhaps an infusion of pantoprazole)
  • Management of infection
    • One can almost guarrantee that some infectious process will take place, 
      • in the lung (aspirtation)
      • in the chest cavity (collection)
      • in the abdominal cavity
    • Thus, empiric antibiotics should probably be commenced, and these should ideally be broad enough to cover upper GI anaerobes. You can always stop them again in a couple of days, when the antimicrobial stewardship people start mocking you openly in the corridors.
  • Management of family expectations
    • The outcome for these scenarios is almost uniformly bad, particularrly wherre a malignancy is involved

Specific management resembles the oesophageal perforation options mentioned above, with the exception of all the bronchoscopic stuff:

  • Bronchoscopic repair
    • Bronchial stent
  • Gastroscopic repair options
    • self-expanding esophageal stainless steel-covered metal stents (SEM)
  • Surgical repair options
    • Resection and diversion (i.e. oesophagus is externalised in the neck; one essentially disconnects the upper GI tract from the lower)
    • Resection and re-anastomosis (the latter is risky)
    • Conservative management (i.e. after having a look and the placement of a NG tube, the patient returns to ICU for conservative and palliative management)

References

Hasan, Shafqat, Ali NA Jilaihawi, and Dhruva Prakash. "Conservative management of iatrogenic oesophageal perforations—a viable option." European journal of cardio-thoracic surgery 28.1 (2005): 7-10.

Biancari, F., et al. "Treatment of esophageal perforation in octogenarians: a multicenter study." Diseases of the Esophagus 27.8 (2014): 715-718.

Spalding, Alanson R., Donald P. Burney, and Robert E. Richie. "Acquired benign bronchoesophageal fistulas in the adult." The Annals of thoracic surgery 28.4 (1979): 378-383.

Kalmár, Katalin, et al. "Non-malignant tracheo-gastric fistula following esophagectomy for cancer." European journal of cardio-thoracic surgery 18.3 (2000): 363-365.

Lolley, David M., et al. "Management of malignant esophagorespiratory fistula.The Annals of thoracic surgery 25.6 (1978): 516-520.

Shamji, Farid M., and Richard Inculet. "Management of malignant tracheoesophageal fistula." Thoracic surgery clinics 28.3 (2018): 393-402.

Question 13 - 2021, Paper 2

a)    Explain the medical management of a patient with confirmed Type B aortic dissection.
(60% marks).

b)    List the indications for consideration of non-medical management of this condition.
(40% marks)

College answer

Not available.

Discussion

The question asked "explain", not "list", which means a bit of discourse is called for:

Medical management:

  • Overall management goals:
    • Decrease aortic wall stress 
    • Thus, reduce the risk of rupture
    • Decrease the risk of propagation of the dissection flap
    • Maintain the perfusion of compromised organs
  • Haemodynamic objectives which serve these goals: 
    • Decrease cardiac contractility (dP/dT)
    • Decrease blood pressure
    • Decrease heart rate
  • Options to achieve these goals:
    • Labetalol infusion (15mg bolus, then 5mg/hr)
    • Alternatively, esmolol, verapamil, diltiazem
    • Once contractility and rate control is achieved,
      vasodilators can also be used (nitroprusside, clevidipine, etc)
    • Analgesia +/- sedation to decrease sympathetic output
  • Endpoints of therapy:
    • Systolic blood pressure 100-120 mmHg
    • HR < 70
    • Improved surrogate measures of organ perfusion

Indications for surgical management:

  • Complicated Type B dissection:
    • Features suggesting instability:
      • Aortic rupture
      • Refractory hypertension
      • Aortic total diameter of > 4.5 cm
      • Extension of dissection on repeat imaging
    • Ischaemia:
      • Visceral and renal ischaemia
      • Lower extremities ischaemia
      • Spinal cord ischaemia
    • Malperfusion:
      • Paraparesis or paraplegia
      • Abdominal pain, nausea, or diarrhea
      • Renal failure or LFT derangement
  • Uncomplicated Type B dissection
    • Can usually be managed conservatively
    • If the aorta is dilated (>4cm) or the false lumen is large (>22mm), surgical management may still be preferred to prevent long-derm aneurysmal degeneration

References

Aggarwal, Bhuvnesh, and Chad E. Raymond. "Therapeutic goals in patients with acute aortic dissection: management before surgery." Journal of the American College of Cardiology 65.15 (2015): 1599-1600.

Hiratzka, Loren F., et al. "2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with thoracic aortic disease." Journal of the American College of Cardiology 55.14 (2010): e27-e129.

Goldfinger, Judith Z., et al. "Thoracic aortic aneurysm and dissection." Journal of the American College of Cardiology 64.16 (2014): 1725-1739.

Evangelista, Arturo, et al. "Insights from the international registry of acute aortic dissection: a 20-year experience of collaborative clinical research." Circulation 137.17 (2018): 1846-1860.

Tran, T. Paul, and Ali Khoynezhad. "Current management of type B aortic dissection." Vascular health and risk management 5 (2009): 53.

Harky, Amer, et al. "Systematic review and meta-analysis of acute type B thoracic aortic dissection, open, or endovascular repair." Journal of vascular surgery 69.5 (2019): 1599-1609.

Question 16 - 2021, Paper 2

Regarding Deep Hypothermic Circulatory Arrest (DHCA) during cardiac surgery:

a)    Explain the rationale for DHCA.    (30% marks)

b)    List six indications for DHCA.    (30% marks)

c)    Outline the adverse effects of DHCA that may be encountered in ICU post DHCA.
(40% marks)
 

College answer

Not available.

Discussion

References

Question 17 - 2021, Paper 2

a)    Outline the surgical differences between the following operations for carcinoma of the oesophagus:

  1. 3 Stage (modified McKeown) Oesophagectomy.
  2. Ivor Lewis Oesophagectomy.
  3. Transhiatal Oesophagectomy.    
    (15% marks)

b)    List the complications of the above procedures that are of relevance to the ICU management.
(60% marks)

c)    Outline specific post-operative management strategies of an oesophagectomy patient that reduce mortality and morbidity.    (25% marks)
 

College answer

Not available.

Discussion

a) Surgical differences between the following operations, for 15% of the marks, would have to be relatively brief:

  • 3 Stage (modified McKeown) oesophagectomy
    • Right thoracotomy 
    • Midline laparotomy
    • Left neck incision
  • Ivor Lewis oesophagectomy: 
    • Right thoracotomy 
    • Midline laparotomy
  • Transhiatal oesophagectomy
    • Midline laparotomy only

b) Complications:

  • Pain
  • Recurrent laryngeal nerve injury
  • Respiratory complications:
    • Surgical complications:
      • Tracheobronchial tree injury
      • Thoracic duct injury, leading to chylothorax (1-5% risk)
    • Early post-operative complications:
      • Atelectasis
      • Pneumothorax
    • Delayed post-operative complications
      • Hospital-acquired pneumonia
      • Pleural effusion
      • airway-gastric fistulae
  • Anastomotic leak
  • Circulatory complications
    • Immediate:
      • Haemorrhage due to retraction or dissection
      • Traction injuries to the heart or pericardium
      • Atrial fibrillation (very common - up to 40%)
    • Delayed:
      • Herniation of abdominal contents into the chest, via a loosened diaphragmatic hiatus
      • Sepsis and septic shock
  • Gastrointestinal complications
    • Early:
      • Ileus
      • Delayed gastric emptying and gastric outlet obstruction (due to vagotomy and "anatomic rearrangement", to borrow a turn of phrase from Flanagan et al, 2016). 
    • Late:
      • "Dumping syndrome": where hyperosmolar gastric contents is propelled abruptly into the small bowel, causing sudden bursts of insulin release, diarrhoea, nausea, and haemodynamic compromise (tachycardia and hypotension). 
      • Decreased peristalsis due to vagotomy
      • Gastric reflux (this is an expected complication,  in the sense that everybody gets it)
      • Oesophageal stricture

c) Post-operative strategies that reduce morbidity and mortality:

  • Early extubation
  • Prevention of AF: early use of enteral beta-blockers
  • Strategies to prevent morbidity from anastomotic leak, from Vetter & Gutschow (2020):
    • Gastric decompression by NG tube 
    • Intravenous proton pump inhibitors (eg. pantoprazole)
    • Early nutrition
    • Early detection of leak (vigilant monitoring +/- radiological swallow studies)
    • Avoidance of hypotension
    • Avoidance of CPAP
  • Strategies to prevent pneumonia: 
    • Multimodal analgesia: epidural, regional block, plus systemic opioids via PCA, plus potentially a co-analgesic like ketamine
    • Early mobility and chest physiotherapy
    • Early swallowing assessment: aspiration pneumonia is a major contributor to morbidity, so to identify at-risk patients early would be beneficial. Ideally, this should incorporate nasendoscopy and evaluation of vocal cord function, as laryngeal nerve palsy is very common. ​​​​​​​

References

Flanagan, Jennifer C., et al. "Esophagectomy and gastric pull-through procedures: surgical techniques, imaging features, and potential complications." Radiographics 36.1 (2016): 107-121.

Paul, Subroto, and Raphael Bueno. "Section VI: complications following esophagectomy: early detection, treatment, and prevention." Seminars in thoracic and cardiovascular surgery. Vol. 15. No. 2. WB Saunders, 2003.

Grimminger, Peter, et al. "Diagnosis, assessment, and management of surgical complications following esophagectomy." Annals of the New York Academy of Sciences 1434.1 (2018): 254-273.

Mboumi, Igor Wanko, Sushanth Reddy, and Anne O. Lidor. "Complications after esophagectomy." Surgical Clinics 99.3 (2019): 501-510.

Oxenberg, Jacqueline. "Prevention and management of complications from esophagectomy." Esophageal cancer and beyond. London: IntechOpen (2018): 29-47.

Imai, Takeharu, et al. "Immediate extubation after esophagectomy with three-field lymphadenectomy enables early ambulation in patients with thoracic esophageal cancer." Esophagus 15.3 (2018): 165-172.

Smith, Heather, et al. "A review and analysis of strategies for prediction, prevention and management of post-operative atrial fibrillation after non-cardiac thoracic surgery." Journal of thoracic disease 10.Suppl 32 (2018): S3799.

Vetter, Diana, and Christian A. Gutschow. "Strategies to prevent anastomotic leakage after esophagectomy and gastric conduit reconstruction." Langenbeck's Archives of Surgery (2020): 1-9.