Table of Contents

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.

Potency is the concentration (EC₅₀) or dose (ED₅₀) of a drug required to produce 50% of that drug’s maximal effect. Efficacy is the maximum effect which can be expected from this drug (i.e. when this magnitude of effect is reached, increasing the dose will not produce a greater magnitude of effect). A drug, when occupying the receptor, may produce a complete response, or no response, or some partial response. Intrinsic activity is the drug's maximal efficacy as a fraction of the maximal efficacy produced by a full agonist of the same type acting through the same receptors under the same conditions.

This virus was asked about in  Question 21 from the second paper of 2010. In that specific instance, the college had asked about infection in the immunocompetent host. Oh's Manual only discusses cytomegalovirus in the context of organ or bone marrow transplants, as well as pediatric pneumonia and encephalitis. One my need to resort to Harrison's (Ch. 182) for more details. A brief summary of what a CICM trainee is expected to know about CMV has been cobbled together from this chapter, as well as from articles such as this piece by Gandhi et al (2004). CMV among the immunocompetent ICU population is also explored in this 2008 JAMA paper, andits complications are detailed in this excellent CID article from 1997.

Often, the college asks the candidates to discuss diseases with a significant community prevalence which have some sort of serious impact on the ICU management of affected patients. it makes sense to expect final-stage CICM trainees to be able to discuss SLE or scleorderma, and the attention directed at these diseases is understandable. On the other hand, there are occasionally questions in the Fellowship Exam which cannot be explained by this framework. There is a group of rare diseases which have only ever appeared once and which can reasonably be expected to never appear again. These are grouped here in no particular order, basically because there is nowehere else to put them.

This topic is a constant feature of CICM Fellowship SAQs. The questions usually take the shape of "Here's a blood film; it's abnormal. What's wrong with the patient? Give differentials." Probably the most favourite topic is macrocytosis (i.e. "what are the different causes of macrocytosis"). Nucleated red cells, rouleaux formations and inclusion bodies have also made several appearances.

The college perpetually want the candidates to compare various "weakening" disease states to Guillain-Barre Syndrome. In Question 10 from the first paper of 2013, the examiners had asked the candidates to compare its features with those of critical illness polyneuropathy. In Question 20 from the first paper of 2016, GBS was compared to myasthenia gravis.  GBS is discussed in greater detail elsewhere. It also receives a thorough LITFL treatment; so does critical illness polyneuropathy.

PRES, posterior reversible leukoencephalopathy syndrome, hypertensive encephalopathy, reversible posterior cerebral oedema syndrome and hyperperfusion encephalopathy are all terms used to describe the same neuroradiology findings, which might be caused by a variety of totally different pathological processes. But, all those processes end up causing white matter oedema in a bilateral (usually posterior) distribution, which shines with an obvious increased signal intensity on an  MRI T2-weighted image. The management for most of these conditions is the same (i.e. nothing specific) and the intensivist is invariably left in an unsatisfying position of the coma babysitter, waiting for this supposedly reversible condition to turn the corner so the patient can be extubated.

A short list of arterial vascular access complications would include pain, thrombosis, infection, haematoma and nerve compression, air embolism and vessel damage. Vessel damage may lead to stricture and prevent future AV fistula formation for haemodialysis. Pseudo-aneurysms may form; bowels may be perforated by femoral insertion attempts. Arterial dissection may occur and arteriovenous fistulae may form. The risk of major complications is roughly 1 % for all sites, and is influenced more by the number of attempts and catheter diameter than anything else. 

The upper airway is structurally designed to humidify the respiratory gas mixture by increasing the turbulence of inspired gas. The mucosa and the air exchange heat and moisture with each other, such that the air at the level just below the carina becomes 100% humidified and heated to body temperature. This process remains highly efficient within a broad range of ambient temperatures and humidity values; however pathological states (tachypnoea, increased cardiac output) can increase the rate of heat and water loss via the respiratory tract

The discussion in this chapter revolves around the physiological effects of losing 1 litre of total body water. However, we are rarely confronted with a situation where this occurs in isolation. More often than not,  body water is lost together with electrolytes (by spilling on to the surgeon, or by leaking out as sweat, or by diuresis). Though the initial focus is on the movement of fluids and electrolytes, this digression-prone author then also detours into the physiological consequences of dehydration in a broader sense.