Table of Contents

These are the physiological effects of infusing one litre of Hartmann's compound sodium lactate into a patient.

Question 25 from the first paper of 2010 and the near-identical Question 5 from the second paper of 2004 both asked the candidate to "critically evaluate the use of albumin" in critically ill patients.  Judging by the college answers, these questions were not after an indepth dissction of outcomes literature.  Rather, they may be better worded as "how many legitimate uses of albumin can you think of?"

It is possible to measure anatomical dead space and physiological dead space; alveolar dead space can then be determined by subtracting the first from the second. Physiological dead space can be measured using the Bohr-Enghoff method, using either alveolar CO₂ (Bohr version) or arterial CO₂ (Enghoff modification) to determine the ratio of exhaled CO₂ concentration to PACO₂ or PaCO₂. The anatomical dead space can be determined using the Fowler method, which involves using a single breath of 100% oxygen to displace all the nitrogen from the anatomical dead space.

Wolff-Parkinson-White syndrome is a relatively common preexcitation syndrome which has appeared multiple times in the Second Part CICM exam. Its appearances are usually of the same basic format. The trainees are usually posed with an ECG which bears a characteristic delta wave, and then asked to comment on the management of a tachyarrhythmia. The ECG interpretation is usually worth very few marks, because it is a boring exercise in pattern recognition for a very obvious pattern. The real test of character is in the decisionmaking around antiarrhythmic choice, when trying to address an acute SVT in these patients. As should become apparent from the discussion below, this is far from straightforward, as there does not appear to be any consistency in expert recommendations for best practice, nor in the college examiner comments.

Abnormal cardiac excitation can be classified as automatic or triggered. Abnormal automaticity is the spontaneous generation of action potentials in excitable cardiac tissues which are usually not expected to act as pacemakers (eg. Purkinje cells). Early afterdepolarisations are triggered depolarisations which occur during Phase 3, and which are promoted by anything which prolongs the repolarisation. Late afterdepolarisations are triggered depolarisations which occur during Phase 4, and which are promoted by anything that might increase the intracellular calcium.

Clinical testing for brain death is a favourite topic of the examiners. It frequently comes up in the SAQs and vivas. The most "examinable" aspects are the preconditions to testing, the precise sequence of testing, which cranial nerves are involved, and the expected findings of the apnoea test. Again, the ANZIC statement on Brain Death and Organ Donation is my primary resource for this summary.  At the time of writing, the recent edition is Version 3.2 (2013).

Under which circumstances must one be so interested in intracranial pressure, so as to introduce things into the patient's skull? This question, in a variety of permutations, is a College favourite. For instance, it has recently appeared in Question 27 of the first paper of 2014,  less recently in Question 16 of the first paper of 2009, and Question 27.2 from the first paper of 2008. The advantages and disadvantages of various ICP monitoring techniques are discussed elsewhere; this is the chapter which debates the very need for something like this.

These are the circuit of an externalised artificial cardiac conduction system. The difference between these systems is mainly impedance, and the amount of required current. A bipolar circuit has both the electrode inside the heart, with the heart muscle and intraventricular blood completing the circuit. A unipolar circuit on the other hand relies on a large amount of tissue and body fluid to complete the circuit, and therefore has a much higher impedance. In the majority of situations these days the bipolar circuit is favoured. There is much less electrical interference and substantially less current is required.

Amiodarone is a Class III antiarrhythmic with Class I, Class II and Class IV effects. Given acutely as an infusion, it mainly acts as a beta-blocker and calcium channel blocker, increasing the refractory period of the AV node and therefore counteracting supraventricular tachycardias. Prolonged therapy reveals more of a Class I and Class III effect, which decreases the velocity of action potential propagation and decreases the risk of reentry from ectopic minipacemakers. Amiodarone has uniquely tenacious pharmacokinetics, is extensively tissue bound, and has a half life measured in tens of days. ,/p>

The question, as always, is "can I give this guy more fluid?" For any given patient, there will be some sort of unique and magical volume which represents their ideal ventricular filling volume. Achieving this ideal volume results in the greatest contractility improvement and the highest cardiac output for this specific patient.

The Vaughan Williams classification of antiarrhythmic agents divides these drugs into four main classes according to the mechanism of antiarrhythmic effect. Class I are the sodium channel blockers, Class II are the beta-blockers, Class III block potassium channels and Class IV are calcium channel antagonists. Many agents fall into multiple classes, and some agents (eg. amiodarone) exhibit activity from each class.

In the CICM part II exam, this does not come up nearly as often as it does in real life. Specifically, Question 2 from the first paper of 2017 had presented the candidates with an ECG of a patient suffering from complete heart block after being dosed with both sotalol and verapamil. It was given to her by well-meaning radiology technicians who just wanted to get some nice CT images of her coronaries. The more conventional scenario for this is a patient being treated for refractory rapid atrial fibrillation, who ends up on multiple agents and becomes haemodynamically unstable from complete heart block. The college have only ever explored this in the context of a CCB/β-B cocktail, and so the majority of this chapter will be dedicated to this specific problem, and its management. Other more exotic combinations make for an interesting digression, but do not form a part of core CICM exam preparation, and can be safely ignored forever.

This chapter is related to one of the aims of Section C(i) from the 2017 CICM Primary Syllabus, which expects the exam candidate to "define and explain dose-effect relationships of drugs, including dose-response curves with reference to... graded and quantal response".