Cardiothoracic CRQs

Short explanation

Basal atelectasis would not contribute to hypotension. Carbon dioxide embolus, anaphylaxis and sepsis could all partly explain the above picture. However, the history suggests the presence of a right-to-left shunt, secondary to a chronic left-to-right shunt causing elevated right-sided pressures.

Long explanation

Eisenmenger’s syndrome occurs when a chronic left-to-right shunt results in progressively worsening pulmonary hypertension until the shunt reverses. It can be caused by any systemic pulmonary communication, including atrial and ventricular septal defects, patent ductus arteriosus, and other congenital cardiac defects.

In the case described, in the initial period post induction the patient appears to have had a surge in sympathetic stimulation, likely caused by laryngoscopy. This maintenance of systemic afterload ensures that blood continues to flow from left to right. The subsequent introduction of pneumoperitoneum causes multiple changes in cardiorespiratory physiology. The most important of these in this situation are the need for higher inspiratory inflation pressures to maintain tidal volumes and oxygenation, and the absorption of carbon dioxide. Both of these cause an increase in pulmonary vascular resistance, which will increase the propensity for switching shunt direction. In addition to this, the universal vasodilatory effect of general anaesthesia causes a reduction in systemic vascular resistance that facilitates this further.

In this life-threatening situation the treatment is to remove precipitants of pulmonary hypertension (hypoxia, hypercarbia, acidosis, high ventilatory pressures) and to give a systemic vasoconstrictor (e.g. metaraminol, phenylephrine) to reverse the direction of shunt.

Lovell AT. Anaesthetic implications of grown-up congenital heart disease. Br J Anaesth 2004; 93: 129–39.

Telford R, Murphy P. Cardiovascular disease. In Allman KG, Wilson IH, eds., Oxford Handbook of Anaesthesia, 3rd edn. Oxford: Oxford University Press, 2011.

Short explanation

The physiological implications of a Fontan type of circulation may be extreme. Blood flow from the systemic venous circulation through the lungs is entirely passive, so factors that increase pulmonary vascular resistance can dramatically reduce pulmonary blood flow. This will result in a rise in central venous pressure and inadequate filling of the systemic ventricle, leading to a reduction in cardiac output. Hypovolaemia is therefore also poorly tolerated. Laparoscopy can be undertaken provided abdominal pressures are limited. Poor analgesia and positive-pressure ventilation may result in increased pulmonary vascular resistance and therefore decreased pulmonary blood flow.

Long explanation

The Fontan operation, first described in 1971, is the surgical solution to complex congenital heart defects where a biventricular solution is not possible. It effectively involves connection of both venae cavae directly (or via conduits) onto the right pulmonary artery, usually as a staged procedure. The blood supply to the lungs becomes passive, and therefore dependent on central venous pressure.

The principles of anaesthetising such patients are broadly therefore:

• ensure adequate venous pressure to maintain pulmonary blood flow (central venous pressure as measured by an internal jugular line gives a measure of mean pulmonary artery pressure)
• avoid precipitants of raised pulmonary vascular resistance (hypoxia, hypercarbia, acidosis, inadequate analgesia/anaesthesia, vasoactive medications, excessive intrathoracic pressure)
• avoid significant reduction in myocardial contractility

In addition it is worthwhile remembering that many patients have a residual fenestration between the venous system and the remnant of the right atrium. This means that they will have a right to left shunt. For patients undergoing procedures with elevated risk of gas or fat embolus, percutaneous closure may be considered preoperatively. In the absence of such an intervention, meticulous care must be taken to avoid introduction of air into intravenous lines. The potentially slow flow of venous blood also gives significant risk of venous thrombosis, so many patients will be anticoagulated, requiring careful perioperative management.

The requirement for intraoperative positive-pressure ventilation is not absolute. Whilst it may help avoid hypoxia and hypercarbia, it will inevitably increase mean intrathoracic pressure, and thus increase pulmonary vascular resistance.

Similarly, laparoscopic procedures can be undertaken, provided intra-abdominal pressures are limited to 10 mmHg, and excessive hypercarbia is avoided (ventilatory strategy must ensure a low mean airway pressure).

Day case surgery may be suitable for specially selected patients undergoing short procedures with minimal bleeding risk. Conversely, patients undergoing major surgery should be nursed in an intensive care environment.

Lovell AT. Anaesthetic implications of grown-up congenital heart disease. Br J Anaesth 2004; 93: 129–39. Available online at http://bja.oxfordjournals.org/content/93/1/129.full (accessed 6 January 2012).

Nayak S, Booker PD. The Fontan circulation. Contin Educ Anaesth Crit Care Pain 2008; 8: 26–30. Available online at ceaccp.oxfordjournals.org/content/8/1/26 (accessed 6 January 2012).

Short explanation

One of the disadvantages of the bronchial blocker is that ventilation of the blocked side cannot be achieved without losing isolation of the two lungs. They are single-lumen tubes, commonly used in paediatric thoracic surgery when a double-lumen tube (DLT) is too large or difficult to insert.

Long explanation

Although bronchial blockers may only be something you have read about, they are still a popular exam topic. It is worth knowing a bit about them and what types of surgery they are used for, and also having an understanding of how they are inserted. It would be a good idea to ‘play with’ a bronchial blocker and a double-lumen tube (DLT) prior to the exam if you are not familiar with them.

Bronchial blockers (or endobronchial blockers) can be used in thoracic surgery to isolate a portion of the lung. They are usually inserted under direct vision via a bronchoscope or passed blindly via a tracheal tube. The bronchial blocker is a single-lumen tube with a balloon-tipped endoluminal catheter. The catheter is advanced into either of the main bronchi under bronchoscopic vision and the bronchial lumen is occluded by inflating the balloon. The central lumen of the bronchial blocker permits suction and insufflation with oxygen. The main disadvantage of the bronchial blocker is that ventilation of the blocked side cannot be achieved without losing isolation of the two lungs.

Other techniques used to provide one-lung anaesthesia or isolation of one lung include the use of a DLT and endobronchial intubation with a single-lumen tube. This method may be the quickest and simplest technique to use in an emergency situation, as the anaesthetist is likely to be more familiar with the equipment and able to perform endobronchial intubation rapidly. Normally, an uncut endobronchial tube will naturally intubate the right main bronchus, but a left main bronchus intubation can be performed by turning the patient’s head to the right and inserting the tube with the concavity of the tube facing posteriorly.

Eastwood J, Mahajan R. One-lung anaesthesia. Br J Anaesth CPED Rev 2002; 2: 83–7. Available online at ceaccp.oxfordjournals.org/content/2/3/83 (accessed 6 December 2011).

Yentis S, Hirsch N, Smith G. Anaesthesia and Intensive Care A–Z: an Encyclopaedia of Principles and Practice, 3rd edn. Edinburgh: Butterworth-Heinemann, 2004.

Short explanation

Intra-aortic balloon pumps are defibrillator-safe. PEEP increases lung volume and therefore increases transthoracic impedance. Saline-soaked swabs will shunt current flow outside of the chest and could be dangerous. Defibrillator pad site has not been shown to affect the chances of successful defibrillation. Emergency sternotomy could cause fatal injury to the heart.

Long explanation

Arrhythmias are a recognised complication of repeat median sternotomy. All patients undergoing this type of surgery should have external defibrillator pads attached prior to surgical draping, and internal paddles available. Intra-aortic balloon pumps are used in patients that are prone to arrhythmias, and thus are defibrillator-safe. However, manufacturers previously recommended that during resuscitation of such patients counterpulsation trigger is switched to arterial pressure-related, as the ECG may have significant interference during this period (most machines now automatically switch to the ‘clearest’ mode).

Successful defibrillation depends on achieving adequate current across the myocardium – note that only 4% of the total current passes through the myocardium; the rest passes through the chest wall and other structures. Changes in lung volume, including the application of PEEP, have been shown to affect transthoracic impedance (by small amounts – 1.5% increase for 5 cmH₂O PEEP) and therefore potentially the current flow across the myocardium. However, some modern defibrillator systems assess transthoracic impedance dynamically to adjust shock parameters, so this may not affect the chances of successful defibrillation.

Saline-soaked swabs have previously been used to provide coupling between the electrodes and the chest wall and to reduce impedance. However, their use in between electrode sites provides a pathway to shunt current outside of the chest. This not only potentially reduces the chances of successful defibrillation, but may even allow dangerous arcing of the shock, and thus it is not recommended.

There is no convincing evidence that electrode site makes a difference to the chances of successful defibrillation – though many authors would advocate changing electrode placement if repeated failure occurs (difficult in this situation!). Clearly the initial siting of the electrodes is dictated by the surgical field, with apex-right infrascapular sites often preferred.

Urgent sternotomy in this case might increase the chances of successful defibrillation, but at the cost of causing devastating injury to the heart (which may be adherent to the underside of the sternum), and thus is not advocated as initial management in this situation.

Kerber RE, Deakin CD, Tacker WA. Transthoracic defibrillation. In Paradis NA, Halperin HR, Kern KB, et al., eds., Cardiac Arrest: the Science and Practice of Resuscitation Medicine, 2nd edn. Cambridge: Cambridge University Press, 2007.

Deakin CD, McLaren RM, Petley GW, Clewlow F, Dalrymple-Hay MJ. Effects of positive end-expiratory pressure on transthoracic impedance: implications for defibrillation. Resuscitation 1998; 37: 9–12.

Short explanation

Neither glycopyrronium nor dobutamine will increase heart rate in someone who is pacemaker-dependent. Dobutamine may increase contractility but can cause vasodilation. Changing anaesthetic concentrations is unlikely to be helpful. Application of a magnet has variable effects. External pacing will increase heart rate, improving blood pressure in aortic regurgitation.

Long explanation

Pacemakers are becoming increasingly common in the anaesthetic population. In spite of this, there remains significant uncertainty as to how to manage patients with such devices. The Medicines and Healthcare products Regulatory Agency (MHRA) has therefore issued guidelines on the perioperative management of pacemakers and implantable cardioverter-defibrillators.

Preoperatively, information should be sought as to the type of device and functionality, indication for insertion and current level of function (including patient dependency). For elective procedures, the advice of a pacing clinic should be sought as to what interventions may need to be undertaken pre/intra/postoperatively – this may include reprogramming or switching off various functions. Obviously emergency procedures should not be delayed if this is not possible. In the case presented here, it is likely that the pacemaker entered ‘sleep mode’, whereby the pacing is set at a lower rate during the time when the patient is normally asleep.

Intraoperatively it is important to ensure that there is an alternative method available for maintaining cardiac contraction (e.g. external or transvenous pacing). The application of a magnet has variable effects on the function of pacemakers depending on programming and therefore should not be the first course of action.

In the above example the low blood pressure is potentially a feature of the low heart rate in conjunction with aortic regurgitation. (Remember the old adage for the anaesthetic management of patients with aortic regurgitation – ‘fast and forward’.) The quickest reliable method of increasing the heart rate is to ‘overdrive’ pace using external pads. Glycopyrrolate will have little effect on the heart rate unless it is a dual-chamber (DDD) pacemaker inserted for complete AV block – which is not the case here, in view of the lack of P waves. Dobutamine will similarly not affect the heart rate, although increased contractility may increase the cardiac output. This may not necessarily improve the hypotension because of its vasodilatory effects. Decreasing the inspired fraction of volatile agent may improve the blood pressure, but this is unlikely to be achieved in conjunction with an increase in the rate of a potent analgesic infusion.

Postoperatively, in an emergency case such as this, the device should be checked at the earliest possible opportunity.

MHRA guidance available online at www.mhra.gov.uk/home/groups/dts-bi/documents/websiteresources/con2023451.pdf (accessed 28 November 2011).

Short explanation:

Factors giving increased risk of stroke perioperatively include history of previous stroke, female gender, mitral regurgitation.  Some studies show that as little as 27% of perioperative strokes occur intra-operatively.  Neither intraoperative pharmacological nor physiological management strategies have been reliably shown to alter neurological outcome.

Long explanation:

The area of postoperative brain injury following cardiac surgery has been subject to significant research.  There has been little decrease (and possibly some increase) in  the incidence over the last few decades – possibly due to increasing age and preoperative morbidity of cardiac surgery patients.  The incidence of stroke has been reported at between 1.5-5.5%, encephalopathy between 6 and 32%, and that of neurocognitive dysfunction, which is very common initially but decreases over time, between 10 and 30% even at 6 months.

Perhaps surprisingly, the avoidance of cardiopulmonary bypass has little impact on the incidence of neurological morbidity (though it may alter the timing, with on-pump cases potentially suffering earlier strokes)

No specific intraoperative pharmacological or physiological intervention has been reliably shown to improve neurological outcome, although aspirin, if given in the first 48 hours may reduce neurological morbidity.  This is supported by evidence that suggests between 50 and 73% of perioperative strokes occur in the postoperative period – thus suggesting intraoperative anaesthetic management may have limited scope for reducing the incidence.

Risk factors for perioperative stroke are broadly similar to those for stroke within the general population, with previous stroke, age >65 years, diabetes, hypertension, atrial fibrillation (AF), and smoking. Additionally aortic atherosclerosis, female gender, renal failure, the presence of an intra-aortic balloon pump, aortic stenosis and mitral regurgitation (at least in part because of increased risk of postoperative AF) all increase the risk.

Cook D. Cerebral morbidity in adult cardiac surgery. In Ghosh S, Falter F, Cook D eds. Cardiopulmonary Bypass. Cambridge. Cambridge University Press. 2009; 153-66

Stearns JD, Hogue CW. Neurological complications. In Klein A, Vuylsteke A and Nashef SAM eds. Core Topics in Cardiothoracic Critical Care. Cambridge, Cambridge University Press. 2008; 352-61

Short explanation

NICE guidelines issued in 2008 recommend that antibiotics should not routinely be given as prophylaxis, even to patients at high risk of developing infective endocarditis

Long explanation

Infective endocarditis (IE) is rare, but has a significant associated morbidity and mortality (up to 20%). Some forms of congenital heart disease carry with them an increased risk of IE. Interventional procedures are known to cause bacteraemia, and thus the assumption follows that this will increase the risk of IE in those with predisposing conditions. However, this assumption is not backed up by evidence.

The recent NICE guidelines pertaining to antibiotic prophylaxis make the following observations:

• there is no consistent association between having an intervention, dental or non-dental, and the development of IE
• regular tooth brushing almost certainly presents a greater risk of IE than a single dental procedure because of repetitive exposure to bacteraemia with oral flora
• the clinical effectiveness of antibiotic prophylaxis is not proven
• antibiotic prophylaxis against IE for dental procedures may lead to a greater number of deaths through fatal anaphylaxis than a strategy of no antibiotic prophylaxis, and is not cost-effective.

Therefore it is recommended that antibiotic prophylaxis not be routinely given to prevent IE in patients at risk undergoing dental and non-dental procedures.

Lovell AT. Anaesthetic implications of grown-up congenital heart disease. Br J Anaesth 2004; 93: 129–39.

National Institute for Health and Clinical Excellence. Prophylaxis Against Infective Endocarditis: Antimicrobial Prophylaxis Against Infective Endocarditis in Adults and Children Undergoing Interventional Procedures. NICE Clinical Guideline 64, March 2008. Available online at www.nice.org.uk/CG064 (accessed 28 November 2011).

Short explanation:

Arterial line filters are used to reduce microemboli, but they filter aggregates greater than 40 micrometres.  The average erythrocyte is 6-8 micrometres in diameter and 2 micrometres thick, thus a 2 micrometre filter would prevent the passage of red blood cells.  All the other statements are correct.

Long explanation:

The cardiopulmonary bypass circuit was first successfully used in the 1950s.  Since then, despite advances in equipment and safety, the fundamental principles remain the same, with the aim of supplying oxygenated blood to the systemic circulation whilst operating on a non-beating heart.

Blood is drained under gravity from cannulae placed in the right atrium or a large vein(s) into a (cardiotomy) reservoir.  From here it is filtered to remove debris, and then pumped (via either a roller, or centrifugal pump) through an oxygenator and heat exchanger.  This blood is then passed back, under pressure from the pump to the arterial cannula which is placed in a large artery.  Blood also enters the cardiotomy reservoir from suction catheters used by the surgeon, and a vent suction catheter placed in the heart to keep it empty. Oxygenated blood may also be used as part of the cardioplegia solution used to initiate and maintain diastolic arrest of the heart during surgery.

Various filters are also incorporated into the circuit to improve safety and serve other purposes.  These include a gas line filter (prevent bacterial contamination of the gases flowing through the membrane oxygenator), arterial line filter (removing microemboli), leukodepletion, and cell salvage filters.  In addition to this a haemofilter (also ultrafilter or haemoconcentrator) can be added to the circuit to manage hyperkalaemia, acidosis or to increase the haematocrit if the circulating volume is adequate.

The cardiopulmonary bypass machine requires a gas supply to supply oxygen +/- air to the oxygenator (usually a hollow fibre membrane oxygenator).  A standard anaesthetic vaporiser can be placed in line with this system to deliver anaesthesia to the patient via this surrogate pulmonary system.

Below is a diagrammatic representation of the configuration of a cardiopulmonary bypass circuit. (insert fig 1.1 from page 2 reference below)

Chilton V, Klein A Equipment and monitoring.  In Ghosh S, Falter F, Cook D eds. Cardiopulmonary Bypass. Cambridge. Cambridge University Press. 2009; 1-22

Short explanation:

Pump blood flow does not directly determine cerebral blood flow, although it does influence mean arterial blood pressure, which is the major determinant. Haematocrit affects both the viscosity and oxygen carrying capacity of the blood. Cerebral metabolism and arterial carbon dioxide tensions directly affect vascular tone.

Long explanation:

Cerebral blood flow = Mean arterial blood pressure / Cerebral vascular resistance

The most important factors in cerebral blood flow (CBF) during cardiopulmonary bypass are therefore:

1. Mean arterial blood pressure – the single most important factor. It has been shown that below around 55 mm Hg cerebral blood flow is compromised
2. Factors affecting the cerebral vascular resistance – these include:

-Haematocrit (the reduction in haematocrit as a result of the haemodilution that occurs causes a significant increase in CBF)

-Cerebral metabolism (CMRO₂) and arterial carbon dioxide tension – both of which have direct effects on cerebral vascular tone.

In addition to these factors temperature also has an effect – with a 10 degree centigrade decrease in temperature resulting in a 50% reduction in both CMRO₂ and CBF.  Below 27 degrees centigrade the relationship becomes more complex because of a cold related vasoparesis.

Pump blood flow (analogous to cardiac output) only has an effect on the cerebral blood flow if it results in a decrease in the mean arterial blood pressure (i.e. if the systemic vascular resistance is not adequate to maintain the pressure).  The lack of pulsatility of blood flow has not been shown to have any effect.

Cook D. Cerebral morbidity in adult cardiac surgery. In Ghosh S, Falter F, Cook D eds. Cardiopulmonary Bypass. Cambridge. Cambridge University Press. 2009; 153-66

Short explanation

Citrate-phosphate-dextrose, whilst having minor anticoagulant activity due to calcium chelation, is included in cardioplegic solutions to reduce ionic calcium levels and thus reduce calcium influx (proposed to play a major role in reperfusion injury).

Long explanation

One of the vital aspects of cardiac surgery is the preservation of viable myocardium. During on-pump cardiac surgery the aim is to ensure minimum coronary ischaemia. This has been achieved using numerous methods, including intermittent cross-clamping on a beating heart, cross-clamping and fibrillation, and most commonly diastolic arrest using cardioplegia.

The energy, and therefore oxygen requirements, of the non-beating, non-fibrillating heart are far lower, and therefore ischaemia is less pronounced. Cardioplegia can be given anterograde (via the coronary arteries) and/or retrograde (via the coronary sinus – less protective to the right ventricle because of its venous drainage). It can be given intermittently or continuously.

Cardioplegia solutions vary considerably in composition and temperature of administration, but their overriding aim is to achieve cessation of electromechanical activity and prevent myocardial cell damage. They are divided into those that resemble extracellular or intracellular fluid in ionic composition, and those that are crystalloid- or blood-based.

Potassium is an essential feature in all cardioplegic solutions, inducing rapid diastolic cardiac arrest via membrane depolarisation. The solution may also contain additional components, such as dextrose, citrate (to reduce ionised calcium levels) and buffering agents such as bicarbonate and tris-hydroxymethylaminomethane (THAM). Procaine is included in some solutions to counteract the vasoconstrictive effects of particulate contaminants, and mannitol is a free-radical scavenger. So called ‘substrate-enhanced’ cardioplegia contains glutamate and aspartate, required for the function of the Krebs cycle (and depleted in both acutely and chronically ischaemic hearts).

Below are examples of the composition of commonly used cardioplegia solutions.

(See Tables 7.1 and 7.2, pg 83-4 from Cardiopulmonary Bypass, Ghosh S et al. CUP 2009)

Athanasuleas C, Buckberg GD. Myocardial protection and cardioplegia. In Ghosh S, Falter F, Cook DJ, eds., Cardiopulmonary Bypass. Cambridge: Cambridge University Press, 2009; pp. 80–91.

Short explanation

Coronary vasomotor tone is effectively dictated by local metabolism, with little nervous system input. Arterial oxygen extraction is significantly higher than for the rest of the body at 70–80%. Isoflurane is a coronary vasodilator. Sympathetic stimulation has a similar effect in normal coronaries, but results in vasoconstriction with coronary artery disease.

Long explanation

The heart has the highest oxygen consumption of all the organs of the body. The resting blood supply of 250 mL per minute can multiply up to fivefold during exercise. Anatomically the heart receives blood via the coronary arteries, which are direct branches from the proximal aorta. Venous drainage is via the coronary sinus and anterior cardiac vein, which drain into the right atrium, and the Thebesian veins, which drain directly into the chambers.

Coronary perfusion is determined by:

1. The coronary perfusion pressure (itself determined by the difference between the aortic diastolic pressure and the left ventricular end-diastolic pressure for the left ventricle). Providing this is within a given range, coronary blood flow is maintained by autoregulatory mechanisms.

2. The heart rate, which in turn dictates the diastolic time: slower heart rate = greater perfusion.

3. The diameter of the supplying blood vessels. This is highly dependent on local metabolic effects. In addition, autoregulatory mechanisms, elements of humoral control and drugs all have an effect. Autonomic nervous supply has some limited effect. The diameter may be significantly limited by atherosclerotic deposits within the walls. In the presence of such deposits, the vasodilatory effect of the sympathetic nervous becomes a vasoconstrictory response to maintain perfusion pressure. Isoflurane causes vasodilation, affecting distal more than proximal vessels. This is the basis for the theoretical coronary steal phenomenon proposed, whereby dilation of distal vessels causes preferential diversion away from areas with obstructive lesions.

The importance of maintaining coronary blood flow becomes all the more relevant when considering the fact that the oxygen extraction ratio of coronary blood is significantly higher than that of other tissues – up to 80% (vs. 25% for most others).

Ramathan T, Skinner H. Coronary blood flow. Contin Educ Anaes Crit Care Pain 2005; 5: 61–4. Available online at ceaccp.oxfordjournals.org/content/5/2/61 (accessed 28 November 2011).

Short explanation

The relative indications for use of a double-lumen tube (DLT) are generally to improve surgical access, which is true for all of the above apart from open surgery on the left main bronchus. In this case single lung isolation is necessary to assist with control of ventilation.

Long explanation

This subject is a favourite of the examiners and can be asked at any stage during the final FRCA examination. It is a good idea to have seen a double-lumen tube (DLT) used, or at least to have handled one and to understand how they work. It is also useful to have an understanding of how they are sized. There are a number of subjects that can be discussed when talking about DLTs and one-lung ventilation, so it is worth having a good general overview of these topics. The indications for one-lung anaesthesia is a commonly asked question and a very simple one to answer. The wording of this question is not very good and I’m sure some candidates will be arguing that you do not have to use a DLT, you could use a bronchial blocker technique – but that is not an option given here, and it is quite clear that the question is testing whether or not you know the absolute and relative indications for one-lung anaesthesia.

The indications for being able to provide one-lung anaesthesia (and the commonest technique used in this country is by means of a DLT) can be split into absolute and relative. The absolute indications are generally to facilitate the isolation of one lung from another to assist with ventilation (such as in a bronchopleural fistula or surgical repair of a main bronchus) or to avoid contamination (from haemorrhage or infection). Another absolute indication is unilateral bronchopulmonary lavage.

The relative indications are generally related to improving surgical access in thoracic surgery (such as oesophagectomy, lobectomy, mediastinal surgery or pneumonectomy) or non-thoracic surgery (such as spinal surgery). Another relative indication is in a patient with severe hypoxaemia due to unilateral lung disease.

As well as the indications for one-lung anaesthesia, you may be asked about the physiology of one-lung anaesthesia, the complications (especially hypoxaemia) and the preoperative assessment of the thoracic surgical patient.

Eastwood J, Mahajan R. One-lung anaesthesia. Br J Anaesth CPED Rev 2002; 2: 83–7. Available online at ceaccp.oxfordjournals.org/content/2/3/83 (accessed 6 December 2011).

Short explanation

All of the statements are true apart from the first. There is no good evidence for this. In fact, bronchial blockers (or endobronchial blockers) have a natural tendency to dislodge and cause airway obstruction. Hypoxaemia and cardiac arrest associated with malpositioning and airway obstruction have been reported.

Long explanation

This is a question of comparing the advantages and disadvantages of two recognised techniques for facilitating one-lung ventilation (OLV), so a brief overview of the pros and cons of both is needed.

When lung resection is not required, or if there are no issues with cross-contamination (e.g. pleural surgery, lung biopsy, oesophagectomy), either a double-lumen tube (DLT) or a bronchial blocker may be utilised for OLV. In this situation, bronchial blockers may be the preferred device. Examples include situations when:

• the patient is already intubated (with a single-lumen tracheal tube) before operation on the critical care unit.
• the patient is to be ventilated after operation with a single-lumen tracheal tube.
• a DLT is relatively short in a very tall patient, and thus lung isolation cannot easily be achieved.
• there is difficulty with laryngoscopy and hence placement of a DLT.
• minor airway injuries associated with a DLT are to be obviated. It has been shown in a randomized controlled trial that postoperative hoarseness and vocal cord lesions occur significantly more frequently with DLTs than with bronchial blockers.

Bronchial blockers have a natural tendency to dislodge and cause airway obstruction. Hypoxaemia and cardiac arrest associated with malpositioning and airway obstruction have been reported.

There are a number of different bronchial blockers on the market, available in a range of sizes, each with disadvantages and advantages. It is worth seeing which type is available in your hospital and being familiar with the technique of insertion and when they can be used.

Ng A, Swanevelder J. Hypoxaemia during one-lung anaesthesia. Contin Educ Anaesth Crit Care Pain 2010; 10: 117-122. Available online at ceaccp.oxfordjournals.org/content/10/4/117 (accessed 6 December 2011).

Yentis S, Hirsch N, Smith G. Anaesthesia and Intensive Care A–Z: an Encyclopaedia of Principles and Practice, 3rd edn. Edinburgh: Butterworth-Heinemann, 2004.

Short Answer

The transplanted heart should be considered to be fully denervated. Therefore atropine and glycopyrronium will have no effect. The effect of ephedrine is reduced and unpredictable. 100 μg of isoprenaline is a too large a dose. Adrenaline will act directly on the heart.

Long Answer

The number of cardiac transplants in the UK has fallen to less than 100 annually. However, with 70% survival at 5 years there is an increasing pool of patients who may present for non-cardiac surgery in non-specialist centres. Anaesthetists need to be aware of the implications of managing such patients, including the physiology of the transplanted heart and the effects of immunosuppressive and other medications.

The transplanted heart is devoid of innervation (controversy exists around potential late re-innervation). As a result of the lack of vagal input the resting heart rate is higher, around 95 beats per minute. The normal autonomic reflexes are absent – there is little beat-to-beat variation (e.g. sinus arrhythmia), no reflex tachy/bradycardia to hypo/hypertension, and no response to Valsalva/carotid sinus massage. As a result of denervation acute hypovolaemia is poorly tolerated. Responses to agents acting directly on the heart (e.g. on β-adrenoreceptors – adrenaline, isoprenaline, β-blockers) are similar. Vagolytic agents (e.g. atropine) will have no effect, and agents with indirect sympathetic effects will have variable effects.

Immunosuppression increases the risks of infection in these patients, and aseptic technique must be meticulously followed. In addition to the well-known effects of steroids, immunosuppressive therapy may also cause renal dysfunction and resultant hypertension. Accelerated coronary artery disease in heart transplant patient results in a 40% incidence at 5 years – it is important to bear this in mind even in young patients.

There is little evidence of superiority in terms of anaesthetic techniques. But it is important to bear in mind the relative paucity of response of the transplanted heart to the rapid vasodilation associated with both subarachnoid/epidural blockade and rapid intravenous induction.

Costanzo MR, Naftel DC, Pritzker MR, et al. Heart transplant coronary artery disease detected by coronary angiography: a multiinstitutional study of preoperative donor and recipient risk factors. Cardiac Transplant Research Database. J Heart Lung Transplant 1998; 17: 744–53.

Royal College of Surgeons of England Clinical Effectiveness Unit and NHS Blood and Transplant. UK Cardiothoracic Transplant Audit: end of year report, August 2010. Available online at www.rcseng.ac.uk/surgical_research_units/ceu/docs/UK_Cardiothoracic_Transplant_Audit_report_2010.pdf (accessed 28 November 2011).

Telford R, Murphy P. Cardiovascular disease. In Allman KG, Wilson IH, eds., Oxford Handbook of Anaesthesia, 3rd edn. Oxford: Oxford University Press, 2011.

Short explanation:

VVI pacemakers are inhibited by intrinsic ventricular activity. Polyfocal ectopics caused by wire insertion may result in significant compensatory pauses, thus resulting in activation of pacing (if only temporarily). Glycopyrronium will increase sino-atrial node activity, thus increasing intrinsic heart rate – this will decrease rather than increase rate of pacing output.

Long explanation:

The classification of pacemakers is essential knowledge for the FRCA. A VVI pacemaker therefore paces the ventricle, senses the ventricle and it's activity is inhibited by the presence of intrinsic activity.  As such in a patient in sinus rhythm with normal atrio-ventricular (AV) conduction pacemaker activity will be inhibited (note if the intrinsic rate is lower that the set rate of the pacemaker there will still be some pacing activity).  This equally applies to an SVT with normal AV conduction. A premature ventricular complex ('ectopic') will be sensed in the same way as the transmitted atrial impulses are – as ventricular activity, and the result will again be inhibition.  A seldinger wire inserted too far during central venous catheterisation may elicit ectopic electrical activity from either the atria or ventricle.  Initiation of a premature ventricular complex may result in a fully compensatory pause which exceeds the duration of the normal interval between QRS complexes. So whilst the ectopic itself will inhibit pacemaker activity, it's presence may result in a subsequent activation of pacemaker function secondary to a prolonged delay afterwards.  The chances of this occurring are potentially increased by the presence of multiple ectopics.  Glycopyrronium bromide is an anticholinergic, which by virtue of this action  in the presence of normal AV conduction this will result in an increase in heart rate. In the absence of normal AV conduction, there may be little change in the heart rate, but regardless there will be either a decrease or little change in pacemaker activity.

Allen, M. (2006), Pacemakers and implantable cardioverter defibrillators. Anaesthesia, 61: 883–890.

Mackay, J. Arrowsmith JE. (2004)  Core Topics in Cardiac Anaesthesia. Cambridge University Press.

Short explanation:

Bipolar is preferred to monopolar diathermy, although the use of either should be undertaken with caution.  The effect of a magnet on modern devices is variable.  ECG monitors with a 'paced' mode may falsely interpret a pacing spike as a QRS complex. There is no evidence of inhalational or IV anaesthetics  affecting pacemaker threshold.

Long explanation: 

Pacemakers are becoming increasingly common in the anaesthetic population – in spite of this there remains significant uncertainty in how to manage patients with such devices.  As such the MHRA have issued guidelines on the perioperative management of pacemakers and implantable cardioverter defibrillators.

Device manufacturers either contraindicate or give strong warnings against the use of surgical diathermy in the presence of such a device (this is of course at least to protect themselves against litigation).  This is however not always practical, and as such the risks and benefits of use should be weighed up on an individual basis.  Should the decision be taken to use diathermy, standard precautions apply: use should be limited to short bursts, the return electrode for monopolar should be sited as distant as possible, if inhibition occurs this should be conveyed immediately to the surgeon.

Preoperatively information should be sought as to the type of device and functionality, indication for insertion and current level of function (including patient dependency).  For elective procedures, the advice of a pacing clinic should be sought as to what interventions may need to be undertaken pre/intra/postoperatively – this may include reprogramming or switching off various functions.

Intraoperatively it is important to ensure that there is an alternative method available for maintaining cardiac contraction (eg transvenous/temporary external pacing).  In addition it is important to monitor the heart carefully throughout – both electrically (ECG) and mechanically (pulse oximetry +/- invasive blood pressure).  ECG monitors with a 'paced' mode may mistakenly interpret a pacing spike for a patient QRS complex.  Should this occur in conjunction with an increase in capture threshold, it is possible that the monitor could read the heart rate as that of the pacemaker, when the patient is asystolic.

Postoperatively, for the emergency case, the device should be checked at the earliest possible opportunity

MHRA guidance available at http://www.mhra.gov.uk/home/groups/dts-bi/documents/websiteresources/con2023451.pdf (accessed 15^th September 2011)

Short explanation:

Standard TEG does not measure platetet dysfunction caused by anti-platelet therapy – given the history this is a plausible explanation. Residual heparin effect is unlikely given the TEG, aprotinin is no longer widely available, and tranexamic acid will not treat platelet dysfunction.  Lab bloods will take a significant time to get results and platelet count gives no information on function.

Long explanation:

Thromboelastography (sometimes known as TEG – this is a registered trademark) measures the visco-elastic properties of whole blood during, and after clot formation.  This real-time profiling provides a global assessment of haemostatic function from initiation to early fibrinolysis.  It can thus be used to guide therapy and blood product transfusion.

The thromboelastogram is interpreted using the following measurements:

The trace produced is actually a single trace, but with a mirror image reflected about it's 'y-axis' midpoint.

The R (reaction time) is the time from the start of the test until the width of the trace is 1mm. This represents the time until fibrin is formed.  This is prolonged in clotting factor deficiency, anticoagulants and thrombocytopenia

The K time follows the R time, and is the time until the amplitude reaches 20mm. It represents the rate of reaction, and is dependent on both platelets and fibrinogen

The α angle is the angle created by a tangent to the curve at the R time and the midline.  It is a measure of the rate of clot formation, and is affected by deficiency in number or function of any aspect of the haemostatic mechanism.

The MA (maximum amplitude) is the maximum width of the curve.  It is a measure of the overall strength of clot formed, and is dependent on the platelet numbers and function, and the fibrin that links them.

LY30 (30 minute lysis) or EPL (Estimated Percent Lysis) is a the rate of decline of the curve to baseline.  It can be used to determine the stability of the clot (if rapid, indicates significant fibrinolysis)

A patient who has received recent doses of aspirin and clopidogrel will be likely to have a significant degree of platelet dysfunction, even before CPB.  These effects are not readily shown by standard TEG (although special re-agent cups are available).  So transfusing platelets is a very reasonable thing to do in this situation.  Protamine will reverse any residual heparin effect, but in the presence of a normal TEG without heparinase this is not a priority.  Aprotinin is no longer used following the BART study, and this is a large dose.  Tranexamic acid is an anti-fibrinolytic that is frequently used in cardiac surgery, but is not the drug of choice in this case.  Laboratory bloods do not give instant results and give no information on platelet function, the likely culprit of bleeding in this case.

Willmott, CHA. Arrowsmith, JE. Point of Care Testing. In Klein A, Vuylsteke A and Nashef SAM eds. Core Topics in Cardiothoracic Critical Care. Cambridge, Cambridge University Press. 2008. 117-126

Short explanation:

A prolonged R time that is normalised with heparinase suggests residual heparin effect.  FFP would not necessarily reverse this.  In the stable patient protamine sulphate is a suitable treatment, urgent re-exploration is not yet indicated. Clamping the drains could be fatal.  Heparinase is not currently used.

Long explanation:

Thromboelastography (sometimes known as TEG – this is a registered trademark) measures the visco-elastic properties of whole blood during, and after clot formation.  This real-time profiling provides a global assessment of haemostatic function from initiation to early fibrinolysis.  It can thus be used to guide therapy and blood product transfusion.

The thromboelastogram is interpreted using the following measurements:

The trace produced is actually a single trace, but with a mirror image reflected about it's 'y-axis' midpoint.

The R (reaction time) is the time from the start of the test until the width of the trace is 1mm. This represents the time until fibrin is formed.  This is prolonged in clotting factor deficiency, anticoagulants and thrombocytopenia

The K time follows the R time, and is the time until the amplitude reaches 20mm. It represents the rate of reaction, and is dependent on both platelets and fibrinogen

The α angle is the angle created by a tangent to the curve at the R time and the midline.  It is a measure of the rate of clot formation, and is affected by deficiency in number or function of any aspect of the haemostatic mechanism.

The MA (maximum amplitude) is the maximum width of the curve.  It is a measure of the overall strength of clot formed, and is dependent on the platelet numbers and function, and the fibrin that links them.

LY30 (30 minute lysis) or EPL (Estimated Percent Lysis) is a the rate of decline of the curve to baseline.  It can be used to determine the stability of the clot (if rapid, indicates significant fibrinolysis)

In the given example, a prolonged R time that corrects with heparinase (an enzyme which inactivates heparin) is likely to be as a result of residual heparin effect.  This can be rapidly ameliorated by giving protamine, which should be readily available in the above situation.  It is important to note that protamine has been documented, paradoxically, to have adverse effects on both coagulation and platelet function, so it is important not to give an excessive dose.  Giving FFP here would not necessarily correct this.  Clamping the drains could result in tamponade and therefore is dangerous.  Heparinase would reverse the abnormality, if less effectively than protamine, but it's use is not currently recommended.  Initiation of cardiopulmonary bypass following heparinase utilisation would require potentially massive doses of heparin.  Ultimately this patient may require blood product transfusion, and potentially even return to theatre, but initial therapy with protamine is the most appropriate early management.

Mallet SV, Cox DJA: Thrombelastography; a Review Article. Br J Anaes 1992; 69: 307-313(s)

Willmott, CHA. Arrowsmith, JE. Point of Care Testing. In Klein A, Vuylsteke A and Nashef SAM eds. Core Topics in Cardiothoracic Critical Care. Cambridge, Cambridge University Press. 2008. 117-126

Short explanation

SAM can cause left ventricular outflow tract obstruction, and transoesophageal echocardiography is a reliable method of diagnosing the condition. Therapy involves volume loading, vasopressor therapy, cessation of inotropes/inodilators and cautious use of β-blockers, and it may require repeat repair/replacement of the valve.

Long explanation

Systolic anterior motion (SAM) of the mitral valve occurs in up to 10% of patients undergoing mitral valve annuloplasty, but can occur in patients undergoing non-cardiac surgery as a result of the haemodynamic changes induced by general and regional anaesthesia.

During systole the excessive valve tissue of one (usually anterior) or both leaflets is dragged towards the ventricular septum, causing dynamic left ventricular outflow tract obstruction and potentially causing mitral regurgitation. The further the leaflet is dragged towards the septum, the higher the pressure gradient becomes. This pressure gradient determines the velocity of the blood past the leaflet, which in turn determines the ‘drag’ on the mitral valve leaflet. Thus the situation is amplified by itself. This can result in severe cardiovascular compromise. The condition is exacerbated by hypovolaemia (empty ventricle) and systemic vasodilation (increased pressure gradient).

Transoesophageal echocardiography is a reliable method of not only diagnosing, but also guiding therapy, as haemodynamic changes can be tracked following interventions.

Initial therapy involves ensuring adequate volume status, increasing systemic afterload, either by the use of vasopressors or by cessation of inodilatory agents, or both. Starting an inodilator such as enoximone in this case could prove disastrous. Once adequate filling has been assured, some would advocate the use, in some patients, of β-blockers to reduce heart rate (increasing time for ventricular filling) and contractility. In severe cases unresponsive to this medical management, repeat valve repair, or valve replacement, is required.

Guarracino, F. Mitral valve repair. In Feneck R, Kneeshaw J, Ranucci M, eds.. Core Topics in Transesophageal Echocardiography. Cambridge: Cambridge University Press, 2010; pp. 268–74.

Charls LM. SAM: systolic anterior motion of the anterior mitral valve leaflet post-surgical mitral valve repair. Heart Lung 2003; 32: 402–6.

Short explanation

There is no evidence to suggest differing energy strategies affect likelihood of cardioversion in AF using biphasic waveforms. CPR prior to shock has not been universally proven to improve outcome. Multiphasic defibrillators are not yet available. Electrode type may affect transthoracic impedance, but not enough to warrant specific electrode recommendations.

Long explanation

There have been significant changes in the last few years in the recommendations on the conduct of resuscitation and the use of associated equipment. Guidance is now justified by a stronger evidence basis.

The guidelines recognise that previously CPR was interspersed with numerous pauses – and that this was detrimental to the flow of blood during cardiac arrest. With the established knowledge that the chances of successful defibrillation decreased with increasing duration of cardiac arrest, it followed that a period of restoration of blood flow (i.e. CPR) preceding attempted defibrillation might increase the chances of success. This has not been supported, however, by the available evidence (although the indication is that for longer periods of cardiac arrest a period of CPR first may be beneficial).

Equipment has changed in line with this, with older monophasic hand-held paddle type defibrillators being replaced by biphasic models with self-adhesive electrodes. The biphasic waveform originated from the need to decrease the energy requirements of the implantable device due to the battery size limitations. It has subsequently found favour with all types of device, because of evidence of lower shock energy requirement, higher cardioversion/defibrillation success rates and potentially lower levels of myocardial damage and dysfunction. There is little evidence, however, to suggest that a particular or strategy or energy level is more appropriate than any other in the electrical cardioversion of atrial fibrillation. Multiphasic defibrillation patterns have been used in animal tests and appear to show a further decrease in energy level requirements, and less myocardial dysfunction – the next generation of defibrillators may contain such technology if human data confirm these findings.

The advent of self-adhesive pads has generated research into the best coupling media. Multiple compounds have been studied: saline, hypertonic saline, silver/silver chloride. Whilst this has shown that there can be up to a 20% difference in transthoracic impedance (an important factor dictating current flow across myocardium and hence probability of defibrillation), this has not led to preferential recommendation of one type over another.

The advantages of the use of self-adhesive pads include convenience, lower risk of electrical injury to others and lower risk of fire. There are numerous case reports of fires being caused by arcing between paddle electrodes in the presence of high local oxygen concentrations. Manikin studies have shown that a self-inflating bag may be left attached to an endotracheal tube without increasing local oxygen concentration. In addition, airflow systems in a theatre environment decrease this possibility further.

Jacobs I, Sunde K, Deakin CD, et al. 2010 international consensus on cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendations. Part 6: Defibrillation. Circulation 2010; 122: S325–37.