Printable list of all cardiothoracic SAQs

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 5% D +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
  • extubate onto NIV as soon as permitted by gas exchange and comfort.
  • Ideally, these people should be extubated in the operating theatre immediately following surgery
• 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.

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.

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.

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.

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.

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.

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.

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

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:

• Question 5 from the first  paper of 2006
• Question 8 from the first  paper of 2005

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:

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.

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.

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:

• Approach to the haemodynamically unstable cardiac surgical patient
• Causes of shock in the cardiac surgical patient
• Definition and classification of shock

A systematic approach to this question would resemble this:

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

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.

College Answer

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. 

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.

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

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.

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.

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.

College Answer

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.

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.

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

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.

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.

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

Cardiac Pacing for the Clinician by Kusumoto and Goldschlager.

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:

• Cardiac resynchronisation therapy (for details of CRT)
• Advantages and disadvantages of various pacing modes (for a discussion of DDD pacing, and the haemodynamic problems of pacemaker syndrome)
• A brief guide to troubleshooting the pacemaker circuit  (for magnet stuff)

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.

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

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.

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:

• Approach to the haemodynamically unstable cardiac surgical patient
• Causes of shock in the cardiac surgical patient
• Differential diagnosis and classification of shock

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).

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.

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.

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.

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

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, 2^nd ed. Chapter 4 by Creswell and Karis.

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

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

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

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).

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

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.

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.

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.

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

• Guidelines support the use of noradrenaline.The AHA still recommends it as the pharmacological agent of choice (though not by name) in cardiogenic shock with poor fluid response (level C recommendation).
• However, in shocked post-cardiac-surgery patients, at least one trial has suggested thatvasopressin is better.

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.

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:

• Lipoprotein content of pleural drain fluid
• Chylomicron content of pleural fluid
• Fasting test and fat challenge
• CT and lymphangiography may be helpful but practically speaking this could be difficult.

Management of chylothorax

• Low fat diet - or at least a diet rich in medium-chain triglycerides (hoping with reduced chyle flow the defect will close on its own)
• TPN may be required - but is not an essential part of management. If one were to use TPN, one may wish to use medium-chain fatty acids - i.e. anything with a chain length shorter than laurate (12 carbon atoms)
• It seems octreotide is an effective treatment option
• Surgical ligation is always an option, and some say it should be the first option.

​

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.

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

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.

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.

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.

College Answer

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, 2^nd ed. Chapter 4 by Creswell and Karis.

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

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

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/cm^–5/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.

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.

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.

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.

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.

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

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)

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.

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. 

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).

College answer

c)                                                          
•    Immediate VF or pacing (if indicated) before external cardiac massage – can delay ECM up to one minute to administer shock/pace 
•    No need for pulse check – observe monitored waveforms/ECG sufficient for diagnosis • Avoid adrenaline/vasopressin bolus 
•    Cease all infusions until reviewed 
•    If IABP in situ set to pressure trigger 
•    If PEA and paced, turn off pacemaker to exclude underlying VF 
•    Plan for emergency re-sternotomy, ideally within five minutes. 
 

Discussion

For a definitive resource, one should read the 2015 or 2009 ERC guidelines (they did not change much).

In short, the basic differences are:

• You do not use full dose adrenaline (rather, give smaller doses)
• You do three "stacked shocks"
• You try pacing in asystole if pacing wires are available; if they are already paced and in PEA, you turn off the pacing to "unmask" VF.
• These shocks and attempted pacing are all measures you take before  starting CPR, which is a departure from the ACLS norms.
• If you can't control a shockable rhythm with three stacked shocks, you give amiodarone immediately rather than after three cycles.
• CPR is something you do while waiting to re-open the chest. After five minutes of unsuccessful resuscitation the chest should be re-opened.
• Non-surgical staff are encouraged to re-open the chest in an emergency

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 O₂ may 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

College answer

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:

  • Low fat diet - or at least a diet rich in medium-chain triglycerides (hoping with reduced chyle flow the defect will close on its own)

  • TPN (use medium-chain fatty acids) 

  • Secretion inhibitors such as octreotide and somatostatin

  • Vasocosntrictrs, eg. etilefrine

• 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

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.

College answer

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.

College answer

a)    72-year-old female ventilated in ICU 4 hours post cardiac surgery

College answer

College answer

This question was answered well, as most candidates were able to outline sufficient potential differential diagnoses. Candidates are reminded that is a question asks for 4 likely causes, only the first four causes listed will be taken into consideration. Candidates were required to demonstrate a stepwise logical approach
to for the immediate management.

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

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)

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:

  • Low fat diet - or at least a diet rich in medium-chain triglycerides (hoping with reduced chyle flow the defect will close on its own)

  • TPN (use medium-chain fatty acids) 

  • Secretion inhibitors such as octreotide and somatostatin

  • Vasocosntrictrs, eg. etilefrine

• 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

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)

College answer

Not available.

Discussion

a) Rationale:

• Surgical access
  • The surgical approach to the replacement or repair of the aortic arch and aortic root requires that at some stage the aorta be incised and open to air.
  • It is impractical to do this with normal circulation: air emboli and blood loss would be prohibitive
  • Circulation must therefore cease while the aortic root is opened
• Organ protection
  • Hypothermia protects the organs during circulatory arrest
  • This is the result of a decreased metabolic rate
  • At 18º C, cerebral metabolic rate decreases to something like 10-15% of the normal rate seen at 37º C
  • At this temperature, complete circulatory arrest can be well tolerated for up to 30 minutes

b) Indications:

• Cardiac surgery:
  • Aortic arch reconstruction (aneurysm, rupture, dissection)
  • Pulmonary thromboendarterectomy
  • Repair of complex congenital heart defects (transposition of the great arteries, total anomalous pulmonary venous return, hypoplastic left heart syndrome)
  • Vascular reconstruction during cardiac transplant
• Non-cardiac surgery:
  • Surgery on the thoracoabdominal aorta
  • Repair of giant cerebral aneurysms
  • Resection of cerebral arteriovenous malformations
  • Resection of renal cell carcinoma with caval invasion
  • Resection of other tumors with caval invasion

c) Adverse effects:

• Respiratory complications:
  • Hypoxia due to atelectasis
  • ARDS (if prolonged bypass)
• Circulatory complications:
  • Low cardiac output states (if prolonged bypass time)
  • Arrhythmias (especially if incompletely rewarmed)
• Neurological complications:
  • Stroke (mainly embolic, and mainly in those who had more than 40 minutes of DHCA)
  • Seizures
  • Choreoathetosis (usually develops 2-6 days following the surgery; seems to be related to temperatures below 15º C)
  • Decreased cognitive function
  • Spinal cord ischaemia 
• Renal complications
  • Acute kidney injury
• Hepatic complications:
  • LFT derangement
• Haematological complications:
  • Coagulopathy 

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. ​​​​​​​

College answer

Not available.

Discussion

Advantages and disadvantages of various pacing modes is a topic that has come up in the past, specifically in the form of Question 20 from the first paper of 2007. To see it return in the 2020s is a positive sign - repeating questions about important topics is not a failure of SAQ design, but a way of emphasising important material (because assessment drives learning), and prevents a drift towards esoterica which can occur if the examiners intentionally avoid repeating SAQs.

The answer to that old SAQ is reproduced below with zero modification. 

The other (20% mark) part of this question, which relates to the troubleshooting of the pacemaker circuit, is impossible to reconstruct from the wording of the question, because "(Image removed from report.)" The post-AVR patient described in the stem could theoretically develop any range of temporary pacing wire complications. For the purpose of keeping things simple, undersensing was used here, because it fits the scenario. So:

Pacing issue:  undersensing. This is a situation where the pacemaker, instructed to inhibit itself whenever a viable P or QRS comes along, instead paces irresponsibly, ignoring normal cardiac activity. This pacemaker is in essence asynchronous.

Steps:

• Reduce the output to minimum immediately, to minimise the risk of R on T phenomenon. This should be safe, as the patient has a native rate of 60.
• Keep the rate 40, i.e. lower than the patients native rate
• Increase the sensitivity (i.e. keep reducing the sensitivity value) until no pacing spikes are seen. The value at which this happens is the sensitivity threshold.
• Reduce the sensitivity setting to half of this value, to prevent this from happening again.

College answer

Not available.

Discussion

This is a lot like Question 3 from the first paper of 2020, except that time the examiners called them "modifications". "Outline the modifications to the standard adult ALS algorithm", thy asked. This time they wanted to "discuss the key differences". It would no doubt be highly instructive to learn, what possible key differences (or modifications?) could distinguish "outline" from "discuss" enough for the examiners to change the wording, but their minds are alien and inscrutable. 

Anyway. The following "differences" can be identified:

• Differences in diagnostic thinking:
  • Hypovolemia, tension pneumothorax and cardiac tamponade are among the most common causes of cardiac arrest following cardiac surgery.
• Differences in ALS algorithm:
  • You do not use full dose adrenaline (rather, give smaller doses)
  • You do three "stacked shocks"
  • You try pacing (rate of 90, DDD) in asystole if pacing wires are available
  • If they are already paced and in PEA, you turn off the pacing to "unmask" VF.
  • These shocks and attempted pacing are all measures you take before  starting CPR, which is a departure from the ACLS norms.
  • If you can't control a shockable rhythm with three stacked shocks, you give amiodarone immediately rather than after three cycles.
  • Amiodarone is the only drug in the protocol, which makes it easy to remember. Atropine is mentioned in the college answer but it is not a part of the 2017 consensus statement recommendations.
  • The college suggests you grab the knife after one minute, but the official guidelines makers say "we recommend this within 5 minutes". In short, after five minutes of unsuccessful resuscitation the chest should be re-opened.  External CPR is pointless in all of the common causes of arrest in this scenario. Therefore, CPR is something you do while waiting to re-open the chest. 
• Differences in logistics
  • Non-surgical staff are encouraged to re-open the chest in an emergency. However:
  • Operating theatres, cardiac surgeon and cardiac anaesthetist need to be notified
  • Blood bank need to be notified to be ready for a massive transfusion
• Additional steps which are not a part of the normal adult algorithm:
  • Take the patient off the ventilator and manually ventilated them
  • Drop the PEEP to zero, to optimise preload
  • Stop the sedating infusions. With diminished cerebral perfusion, the chances of awareness are pretty minimal.  In fact, stop all the infusion (to prevent drug errors). 
  • Switch the IABP to pressure trigger mode (that way it assists CPR)

Dunning, Joel, et al. "The Society of Thoracic Surgeons Expert Consensus for the Resuscitation of Patients Who Arrest After Cardiac Surgery." The Annals of Thoracic Surgery103.3 (2017): 1005-1020.

Dunning, Joel, et al. "Guideline for resuscitation in cardiac arrest after cardiac surgery." European Journal of Cardio-Thoracic Surgery 36.1 (2009): 3-28.

College answer

Generally, well answered. Some candidates could not diagnose the issues in the first part of the question related to PA catheters adequately. The second part which was related to failure-to-capture was again well answered by most. Some candidates went into great depth about testing pacemakers, which didn't score marks and probably took a lot of time to write. Time management and answering the questions asked are two of the most important exam techniques which candidates can employ to score optimal marks for their level of knowledge.

Discussion

a) 

Those PA catheter abnormalities:

• The CVP is raised
• The PA pressure is raised, and especially the PA diastolic pressure is raised, which suggests raised LA pressure (tenuously, insofar as PADP is a surrogate for PAOP, and PAOP is a surrogate for LA pressure). 
• The cardiac index is rather high, if we accept 4.0 as the upper limit of normal. This suggests the circulation is hyperdynamic.
• The SVRI is extremely low, as the normal range of values is 1970 - 2390 dynes.sec.cm^–5.m². This suggests the patient is very vasodilated. 
• The SvO₂ of 70% is reasonably normal, which suggests that, whatever else is going on in the circulation, the tissue delivery of oxygen is not especially impaired.

In summary, the patient has well-corrected distributive shock and increased PA pressure.

b)

The most likely differential diagnosis for this is vasoplegia due to a combination of the effects of cardiopulmonary bypass and sepsis. The raised PA numbers could be attributed to a myriad possible causes (mechanical ventilation, protamine, pre-existing lung disease, what have you) but this question asked the trainees to "list the most likely differential diagnosis" and these would not necessarily make it onto that list. Incidentally, making some assumptions (eg. that PADP is virtually the same as PAOP, and that MPAP can be estimated by the same mathematical shortcuts as MAP) we can plug the other variables into the usual equation and get a PVRI of 133, which is not especially elevated.

c) The pacing spikes and the QRS complexes are completely unrelated to each other in this image (shamelessly stolen from emergencymedicinecases.com). The other abnormalities are:

• Right bundle branch block
• Junctional rhythm at rate 40
• Sensing, but failure to capture
• Diffuse deep T wave inversions

b)

Management of this would include:

• Try increasing the output to maximum
• Try reversing the leads
• Convert to unipolar pacing using a skin lead
• Remove the PA catheter from its sheath and instead float a balloon-tipped transvenous pacing wire
• Worst case scenario, pace externally or attempt to increase the junctional rate by increasing the dobutamine infusion dose 

College Answer

Syllabus topic/section:

2.1.18 Peri-operative Issues in Intensive Care – L1.

Aim:

To examine the candidate’s knowledge regarding the assessment and management of a common complication of cardiac surgery.

Discussion:
The question was generally well answered. Candidates who specifically addressed the clinical scenario (post CABG surgery, not general pericarditis presentations) and addressed each aspect of assessment (history, examination, and investigation) performed well. A reminder for candidates to be specific, if possible, with detail (such as specific ECG changes expected). Also, a reminder for candidates to refer to the glossary of terms – outline indicates some detail and explanation required, rather than a simple list.
 

Discussion

• History
  • Emergency vs. elective bypass: if the patient was already having a STEMI, they are at risk of Dressler's syndrome anyway, leaving aside the complications of cardiac surgery
  • Onset: ischaemia is more likely to be abrupt, whereas pericarditis is more likely to be slow in onset
  • Chest pain, which is made worse by leaning forward
• Examination findings
  • Haemodynamic parameters:
    • Graft failure or vasospasm would usually be associated with worsening cardiac output and organ perfusion, whereas pericarditis is usually stable
  • Fever, not otherwise explained
  • Pericardial rub on auscultation
• ECG findings
  • ​​​​​​​Specific findings of pericarditis include:
    • Concave "saddle-like" ST elevation
    • Modest magnitude of elevation, usually 0.5-1.0 mm
    • Depression of the PR interval
    • Reciprocal ST depression and PR elevation in lead aVR
    • Changes are otherwise widespread and do not obey coronary artery territories
• Biochemistry
  • ​​​​​​​Inflammatory markers (WCC< ESR, CRP) will be elevated - more so in pericarditis then in cardiac ischaemia
  • Trend of cardiac biomarkers (eg. troponin) would be downward with pericarditis and upward with ischaemia
• Imaging
  • ​​​​​​​TTE or TOE could reveal
    • new regional wall motion abnormalities, suggesting ischaemia, or
    • pericardial effusion and pericardial thickening suggestive of pericarditis
  • CXR, which could reveal pleural effusion
• Factors that make this distinction difficult:
  • ​​​​​​​The patient may still be sedated and intubated, which makes history taking and examination more challenging
  • Postoperative pain and strong analgesia makes the characteristic pain of pericarditis less discernable
  • Recent cardiac surgery (dressings drains and residual intrapericardial air) obscures classical auscultation findings
  • Intrathoracic hardware makes the CXR difficult to interpret
  • Pacing and myocardial inflammation makes the assessment of the ECG difficult
  • Biomarkers of inflammation and cardiac injury are uninformative, as they are inevitably elevated following cardiotomy

College Answer

Syllabus topic/section:

2.1.18    Peri-operative Issues in Intensive Care – L1.

Aim:
To assess the candidate’s understanding of the main issues that affect ICU care post pneumonectomy. In detail, an understanding of pathophysiological considerations affecting immediate post op ICU care, the potential early complications to look for and detailed understanding of intricacies of fluid therapy was tested.

Discussion:
Candidates are rewarded for following the glossary, being precise with listing the specific and early complications, correct handling of fluid therapy, and demonstrating an understanding of specific pathophysiological perturbations, as opposed to generic statements.
Candidates who received less marks demonstrated a poor understanding of the cardiovascular physiological changes following pneumonectomy. Those that understood the changes were able to score well for this question. Many simply stated the obvious respiratory changes of reduced FVC and tidal volume. This would be implied in the surgery itself and didn't demonstrate that candidates understand the changes that occur when a lung is removed. Examples of such changes include chylothorax, phrenic nerve/ recurrent laryngeal nerve damage, Atrial arrythmias (80% within 72 hours) and RV failure among others.

Many candidates listed general complications common to many different surgeries like infection or atelectasis (these did not score marks) rather than the specific complications of a pneumonectomy. Majority of candidates were able to provide and justify a sensible fluid management strategy.

Discussion

The middle "list" question was weighted six marks, which should alert the candidates to the importance of making a good list of only pneumonectomy-relevant complications, rather than

squandering their six points on listing generic surgical badness. 

a) Cardiorespiratory physiological effects of pneumonectomy, which, to be fair, might also sound as if they are "complications" of pneumonectomy, insofar as these are undesirable consequences of the procedure, except if one looks closely the surgical literature defines "complications" as "any deviation from the normal postoperative course". At the same time the college seemed to have wanted us to list only those physiological changes which were not barn-door-obvious, such as the decrease in FVC would be, for example. What these might have consisted of, one can not be sure, but the following list was constructed from Batirel (2021):

• Respiratory
  • Decreased carbon monoxide diffusion capacity (DLCO) by about 30%
  • Decreased maximal oxygen uptake (VO₂max) by about 30%
  • Hyperinflation of the remaining lung
• Cardiac
  • Increased RV afterload due to increased pulmonary vascular resistance
  • Increased pulmonary artery pressure
  • Change of the cardiac position within the chest cavity, with rotation and displacement of the heart, which results in the impairment of venous return

b) Complications of pneumonectomy:

• Atrial fibrillation: occurs in 10-20%
• Cardiac ischaemia: seems to occur in 1.2-3.8%
• Right ventricular failure: this is caused by the increased afterload.
• Post-pneumonectomy pulmonary oedema: incidence is about 2.5-4%. 
• Right to left shunt though a PFO
• Cardiac herneation
• Compression of the intact main bronchus due to a shift of the medistainal structures
• Hilar torsion and gangrene
• Chylothorax: the risk is between 0.7 and 2%.
• Stump breakdown and bronchopleural fistula
• Phrenic nerve damage
• Recurrent layngeal nerve damage
• Post-operative pneumonia or empyema: This seems to happen in up to 25% of patients. The major culprit is post-operative atelectasis.

c) Post operative fluid management, for two marks, would not have been an extensive outline:

• Keep the patient in a neutral or negative balance, because:
  • 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 leakiness
  • The overall upshot of all these is a propensity to pulmonary oedema

College answer

Syllabus topic/section:

2.1.4 Cardiovascular Intensive Care/ Shock: L1
2.1.18 Perioperative Issues in Intensive Care: / Cardiac surgery L1

Discussion:  

Candidates who followed the glossary instructions, listing common causes, outlining in part b) how those four causes (in part a) could be distinguished and having a structured answer using the glossary of terms for assessment in part B did well. The SAQ asked for common causes. Thiamine deficiency or metformin use is unusual 4 hours post cardiac surgery and was marked accordingly. Given the cardiac indices are normal, tamponade and cardiogenic shock are less appropriate.
The better answers considered microvascular dysfunction, post bypass syndrome, hypoxaemia, severe anaemia, causes of regional tissue ischemia, or inadequate lactate clearance such as hepatic injury ( eg with acute right heart failure), or metabolic aetiology of lactate generation such as catecholamine use which increases glycolysis.
Answers to part b) presenting the assessment of a raised lactate without relating back to their stated differential did not address the question as asked. These candidates could have improved their answer by reading the question and following the directions. Some candidates listed general historical and clinical features and investigations with no reference to how they could be used to distinguish between these causes.
For example, “long bypass time” without including any relevance to the listed causes, would have been improved by including the rationale “long bypass time with resultant microvascular dysfunction, cytokine activation and vasodilation increasing the risk of post bypass syndrome/SIRS.”

Discussion

The long blocks of text from the examiners conceal an important message, namely an example of what the marking was looking for in the answers. The total time for part (b) 

a) Four causes: the lactate is high, and the cardiac indices are normal. But how?

Let's use a system to not miss anything. Consider: "normal cardiac indices" tells you nothing about the haemoglobin or oxygenation, for example. 

• Poor tissue oxygen delivery
  • Whole body: anaemia, hypoxia
  • Regional:
    • compartment syndrome following graft harvesting,
    • distal emboli (eg. to the mesentery from the aortic cannula site)
    • Dissection of the femoral arteries (eg. from canulation for peripheral bypass)
• Increased glycolysis
  • Catecholamine excess (eg. adrenaline infusion, salbutamol nebs)
  • Increased metabolism, eg. malignant hyperthermia
• Impaired oxidative phosphorylation
  • toxins, eg. excessive propofol use, use of nitroprusside for afterload reduction
• Impaired clearance
  • Poor hepatic blood flow
  • Preexisting liver disease

To pick four of the most likely causes, one would have to have worked in a cardiothoracic ICU, or else be familiar with obscure literature like O'Connor & Fraser (2012). Such a list could look like:

• Post-bypass microvascular dysfunction (the long bypass spoken of in the examiner's comments)
• Inadequate oxygen delivery due to poor oxygen carriage: anaemia or hypoxia
• Hepatic metabolic insufficiency (either sluggish hepatic blood flow or pre-exisiting poor liver function)
• Regional circulatory occlusion, eg. something is ischaemic somewhere (let's say the mesentery)
• Increased rate of glycolysis, eg. catecholamines

Of these, catecholamines and liver problems are intrinsically unsexy, because there will be few findings to discuss, and the assessment may consist of "ask for a history of adrenaline infusion; look at adrenaline pump to examine the contents; investigate the effects of weaning the adrenaline". The remaining causes could be organised into a table, if that was the easiest way to present such information:

College answer

Syllabus topic/section:

2.1.7 Renal Intensive Care: Renal failure: L1
2.1.18 Peri-operative issues in Intensive Care: Cardiac Surgery: L1

Discussion: 

Passing this question required a structured and detailed approach to a common ICU issue.

Part a): Answers that included discussion of the actual mechanisms of renal injury scored more highly than just listing the causes or risk factors. CS-associated AKI includes both intra- and post-operative factors, so discussion of the various mechanisms of bypass-associated renal injury, intra-op hypoperfusion and postcardiotomy low CO state were all expected. Above-standard answers also included nephrotoxins, vasodilatory shock, SIRS, embolic phenomena, and/or factors associated with decreased renal reserve. A number of candidates used the pre-renal, renal and post-renal framework for part a) which actually didn’t serve very well in this question as it tended to narrow the breadth of information presented, resulted in confusion about pre-renal vs intra-renal mechanisms, or led to undue focus on renal tract obstruction (a very uncommon cause of CS-AKI). More successful structures included pre, intra and post-op mechanisms; patient, procedure and medication-related mechanisms, or listing of the mechanisms with subheadings and explanations.

Part b) required specifics of patient management in this context, rather than generic statements like “maintain the MAP or euvolaemia”. Such generic statements without including what or how MAP and euvolemia are to be maintained are beneath the standard required to demonstrate the independent practice of a trainee who will progress to a transitional fellow. Some information on the specific nephrotoxins to avoid, how to assess and manage volume status, the haemodynamic parameters to target, as well as the fluids, vasopressors or inotropes used to achieve these targets was expected for at standard. For those that covered these basics well, extended-pass answers included finer points like glycaemic control, renally adjusted drug dosing, experimental therapies and/or bundles of care. The marking rubric is included to aid the candidate’s future study.

Discussion

The examiner's use of the "pre, intra and post-op" framework to classify the mechanisms suggests that the source for their thinking could have been Yu et al (2023), where this exact template is used. Or, it is a common enough template; so it could have developed independently by parallel evolution. In either case, the suggestion that "pre, intra and post" (or "patient, pathology and procedure", or "modifiable and non modifiable") might be better options for a mechanism answer is entirely valid. Yes, post-renal failure is a thing that could happen to anyone, including cardiac surgical patients, but if one considers the matter logically, one would agree that unblocking a blocked catheter is not something that requires a CICM fellow's level of  acumen, and is therefore unlikely to be a source of high marks in the CICM Fellowship Exam.

a) Mechanisms, as a "discuss" question for 6 marks, would have needed to be about 120 words of high-density "underlying key principles ...controversies and/or advantages and disadvantages". 

• Combination of pre-existing renal frailty and perioperative insult
• Pre-existing frailty includes reduced renal reserve due to effects of old age, NIDDM, poor LVEF, high NYHA grade, chronic renal failure and acute cardiac dysfunction (eg. cardiogenic shock)
• Perioperative insult includes:
  • Poor renal perfusion
    • Decreased cardiac output
    • Hypervolemia or hypovolemia
    • Renal vasoconstriction (neurohumoural response, and due to free haemoglobin liberated by haemolysis)
    • Embolic phenomena (eg. cannulation site atheroma, air bubbles,  IABP)
  • Tubular dysfunction
    • Inflammatory cytokine-mediated renal dysfunction due to bypass (similar to sepsis)
    • Oxidative stress (ischaemia-reperfusion, hyperglycaemia)
  • Nephrotoxins
    • ACE-Is, NSAIDs, antibiotics, IV contrast
    • Normal saline

b) Preventative strategies:

• Nothing specific to cardiac surgery has ever been shown to improve outcomes; generic KDIGO nephro-protective principles apply:
  • Avoid excessive fluid resuscitation or diuresis
  • Use balanced crystallod
  • Monitoring the urine output and biochemistry
  • Aggressively correct low cardiac output state
  • Avoid nephrotoxins, eg. ACE-inhibitors, ARBs, NSAIDs, contrast and aminoglycosides
  • Adjust renally cleared drug doses
  • Aim BSL ~6-8 mmol/L
• Experimental therapies that have been tested include:
  • Corticosteroids
  • N-acetylcysteine
  • Remote ischaemic preconditioning
  • Statins
  • Sodium bicarbonate
  • Leukocyte filtration
  • Renal vasodilators (eg. fenoldopam)
  • Nitric oxide
  • Balanced crystalloid (mostly extrapolating from data that does not involve cardiac surgical patients, and which is already unclear)
  • Tight glucose control
  • Use of vasopressin instead of (and in addition to) noradrenaline

College answer

Syllabus topic/section:

2.1.4 Cardiovascular Intensive Care Shock and cardiac arrest: L1
2.1.18    Peri-operative Issues in Intensive Care - Cardiac surgery: including sternotomy for bypass grafting, valve surgery and aortic surgery: L1

Discussion: 

This question covers core/foundation knowledge and was generally completed to an adequate standard. Candidates who demonstrated a clear structure around their answer were rewarded. The better answers included a clear exploration of the elements of history, examination and Investigation that differentiated Obstructive, Vasodilatory, Hypovolaemic and Cardiogenic shock and provided specific detail to this end e.g. CXR and echo findings
Less satisfactory answers demonstrated a lack of structure and/or detail, or else significant omissions. While all candidates were able to reference the CALS approach for part b, the level of knowledge or detail provided varied.

Once again, candidates are reminded to follow the glossary of terms.

Discussion

Assessment:

• History
  • Indications/urgency of surgery
  • Duration of bypass
  • Medication, eg., ACE-I
  • Pre-op infections
  • Residual antiplatelet effects 
  • Massive diuresis  from bypass
  • TTE/TIE results (eg. LVOT obstruction?)
• Examination
  • Temperature
  • Drain output
  • Peripheral perfusion
  • PPV, SVV, cardiac indices
  • Air entry (pneumothorax? Haemothorax?)
• Investigations
  • ABG (lactate, Hb)
  • CXR (haemothorax, mediastinal widening)
  • ECG (arrhythmia, ST changes)
  • TOE to assess contractility, valve failure (mitral / tricuspid)

Cardiac arrest:

• Notify surgeons
• Assemble team - two to begin to scrub, the rest to perform ALS
• Defer chest compressions; assess rhythm
  • Three "stacked shocks" for VF
    • If you can't control a shockable rhythm with three stacked shocks, you give amiodarone immediately 
  • Pacing (rate of 90, DDD) in asystole
  • If they are already paced and in PEA, turn off the pacing to "unmask" VF.
• Do not use full dose adrenaline (rather, give smaller doses)
• After five minutes of unsuccessful resuscitation the chest should be re-opened.