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Question 22 from the second paper of 2009 asked the candidates to talk about the role of vasopressin and its analogues in the critically ill patient.  The question did not ask to critically evaluate anything; the objective was to merely outline. However, vasopressin probably merits a more detailed exploration. An extensive homage to vasopressin is available elsewhere; this chapter should only offer a brief revision of vasopressin and vasopressin-like substances.

Hepatorenal syndrome is essentially a pre-renal failure which is created by an escalating over-constriction of renal arteries, which leads to an escalating secretion of renin and angiotensin, which in turn leads to an escalating constriction of renal arteries. By definition, hepatorenal syndrome is pre-renal failure which fails to respond to fluid therapy. There are several diagnostic criteria to remember: Cirrhosis, ascites, creatinine level over 150mmol/L,    failure of this to improve after  fluid replacement and the absence of other causes of renal failure, such as nephrotoxic drugs or some sort of serious parenchymal renal disease (eg. glomerulonephritis or renal tract obstruction).

This collection of trials and guidelines about gastroenterology and hepatology has also ended up with all of general surgery in it, because there was nowhere else to put it. It is separated into "liver stuff", "gut stuff" and "general abdominal surgical stuff"as these are the broad categories into which the material has seemingly organised itself.  The CICM Second Part exam candidate will always be at risk of being expected to know about these common problems.

Acute liver failure is a major inconvenience, adversely affecting all the organ systems. Among the possible complications, one might expect ARDS, circulatory collapse from SIRS, encephalopathy and raised ICP, a metabolic acidosis, renal failure due to hepatorenal syndrome, bone marrow failure and immune suppression from a decrease in the synthesis of complement.

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?"

Diastolic heart failure, otherwise known as "heart failure with preserved ejection fraction", is a phenomenon which can be mainly attributed to a failure of ventricular diastolic relaxation, with raised end-diastolic chamber pressures. The tendency to go into "flash" acute pulmonary oedema is mainly due to the steep pressure-volume relationship of the poorly compliant ventricle. Management of this can be summarised as "keep em slow and sinus". Afterload reduction, preload reduction and heart rate control are crucial.

A at basic level, the act of discharging a patient from the ICU is an act of communication and trust, where the intensivist throws a ball and hopes that hospital and community healthcare teams will catch it. This chapter is a start of this discussion, focusing initially on the problems of discharging patients directly home.

Several past paper SAQs demand the candidate either generate a list of differentials or define a sensible approach to the assessment  and management of acute hypercapneic respiratory failure. Also related to this topic are past paper questions on the ventilation strategies in COPD.

Status epilepticus has been asked about in  Question 16 from the second paper of 2014, where it was presented wrapped in a case of subarachnoid haemorrhage. Specifically, the college wanted a demonstration of an escalating "ladder of management", as well as drug doses, strategies for weaning sedation, and some opinion about prognosis (which probably has more to do with the subarachnoid haemorrhage than with the seizures). Other questions on this topic have included Question 22 from the second paper of 2005.

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).

The contents and properties of packed red blood cells, the physiology of acute haemorrhage and the physiological responses to a moderate-volume blood transfusion are detailed in other chapters. CICM have asked about this only in Question 1 from the first paper of 2005.

Of the factors that determine the speed of onset of neuromuscular junction blockers, the potency of the agent is the most important. The larger the molar concentration of the agent in the effective dose, the faster it seems to take effect, which means the least potent agents (eg. rocuronium) are the fastest-acting. Other factors (eg. site of injection, presence of hyperkalemia or hypercalcemia, pathologies such as myasthenia gravis or stroke) play less important roles.

ICU Exit block describes the inability to discharge a patient from the ICU who is otherwise medically fit to leave. The causes of this are usually external to the ICU, and are not within their control, such as lack of ward staff or bed availability.

A physiologically difficult airway is where the patient has physiological characteristics that create a high chance of adverse events from the induction agents, ventilation or response to laryngoscopy, even though the laryngoscopy itself may be technically uncomplicated. This excellent concept separates the crude instrumentation of the larynx from the fine art of not killing the patient with your induction agents.