Table of Contents

The action potanetial of a cardiac myocyte has fie distinc phases:  Phase 0 (rapid depolarisation), Phase 1 (early repolarisation), Phase 2 (plateau), Phase 3 (repolarisation) and Phase 4 (resting membrane potential). The pacemaker cells are distinct, in that they donot have a resting potential: instead, their membranes depolarise gradually via the "funny" current (If), allowing them to cyclically self-depolarise. 

These are the physiological effects of infusing one litre of 0.9% sodium chloride solution into a patient.

In several papers (but none since 2007) the exam candidates were asked to describe the changes to the foetal circulation which occur after birth, and the various pathological states which interfere with this normal process. "The transfer from the fetal to the neonatal state is complex", says the college model answer. Fortunately, it can be summarised by saying that the normal extrauterine pattern of circulation results in the pressure-driven closure of the foramen ovale and ductus arteriosum.

The normal extrauterine pattern of circulation results in the pressure-driven closure of the foramen ovale and ductus arteriosum. Lungs are aerated with the first breaths (which purges liquid and creates and FRC). This decreased pulmonary vascular resistance; and at the same time, systemic vascular resistance is increased by clamping the umbilical cord. Right ventricular output is thereby channelled into the pulmonary circulation instead of the systemic. Increased pulmonary blood flow and increased systemic vascular resistance results in increased left atrial pressure, reversing the flow across the foramen ovale (which therefore closes immediately). Then, increased aortic pressure reverses flow across the ductus arteriosus.

The main differences between the adult and the foetal circulations is the main topic of this chapter. The foetal circulation operates at a lower pressure (MAP ~40 mmHg at term), but with a higher cardiac output for the body mass. It is hypoxic (sats ~ 65% in the left atrium) but because of the high foetal cardiac output and high haematocrit the oxygen delivery is still quite good. The foetal myocardium is immature, and as the consequence has poor Frank-Starling compensation. With the stroke volume relatively fixed, the foetus responds to haemodynamic stress by altering the heart rate.

The pulmonary circulation is a low pressure, low resistance system, and it contains much less blood than the systemic circulation (500ml vs. 4500ml). Where the systemic arterioles would vasodilate (eg. hypoxia, hypercapnia), the pulmonary arteries will do the opposite and vasodilate. The blood flow in the systemic circulation is distributed regionally according to organ system demands, using resistance arterioles to redistribute blood flow, whereas in the lung there nothing of the sort, and it can barely redistribute blood flow away from hypoxic regions. In short, the pulmonary and systemic circulatory systems are vastly different.

Actual bicarbonate is the concentration of hydrogen carbonate in the plasma. The ABG machine usually reports this as cHCO₃^-(P). It is a derived variable. One is interested in the bicarbonate value because it is the most important extracellular fluid buffer, accounting for 75% of total buffering in metabolic acid-base disturbances (the rest being performed by blood proteins, such as haemoglobin).

This topic keeps coming up in the SAQs. One notable appearance was in Question 5 from the first paper of 2010, where the candidates needed to not only identify the features, but also the causes of the partial spinal cord injury syndrome. The canonical resource for this would have to be Ch.78 from Oh's Manual, Spinal injuries by Sumesh Arora and Oliver J Flower. Specifically, on page 798, cord syndromes are discussed with enough detail to pass Question 5. If one happens to not own the Manual, one may find a similar amount of detail in the "International standards for neurological and functional classification of spinal cord injury" from 1997, and in a similar article on classifying partial cord syndromes from 2000. And if one were for some reason in need of a massive amount of detail, one might instead wish to purchase a copy of Diseases of the Spine and Spinal Cord By Thomas N. Byrne, which remains a definitive text on this subject.

This section deals with the act of forcibly taking control of somebody's cardiac conduction system. For a detailed review of this topic, I direct the gentle reader to the Operation Manual for the 5388 Medtronic Pulse Generator, as well as to this article on pulse generator engineering. The topics of discussion are pacing rate, sensitivity, output, and how to find the sensitivity and output thresholds.

This chapter is basically a set of long, enormously elaborate footnotes to the Wiggers Diagram, which describes the timing of pressure and volume changes in the chambers of the heart. In short, the cardiac cycle can be split into seven fairly predictable phases, each with their clearly defined boundaries, containing well described events which are a favourite of the CICM examiners.

In days gone by, people relied on the CVP as a simple means of predicting fluid responsiveness. But it turns out the CVP is really bad at predicting the patients' responsiveness to fluid challenges. There are too many variables governing central venous pressure. This has become evident from some high-quality evidence, and it has been known for some time. Indeed, so obvious the uselessness of CVP in this scenario, and so entrenched the practice of its use, that prominent authors have described a recent meta-analysis as a plea for common sense.

This chapter discusses the anatomy histology and electrophysiological function of the conduction system and myocardial muscle, which is what was presumably meant by the CICM syllabus item referring to structure and functional significance of the excitatory, conductive and contractile elements of the heart.

From a purely practical standpoint, it must be acknowledged that most CICM trainees will neever see or handle their patient's heart in the course of their normal sane behaviour. Ergo, the most exam-centric thing one can offer here is a textual description of cardiac anatomy, designed for easy regurgitation in the CICM written papers.

Physiological consequences of high altitude are related mainly to the hypoxic environment which is seen at altitudes greater than 2700m above sea level. Hypoxia here results in hyperventilation, tachycarrdia, increased cardiac output, a low PaCO₂ and a respiratory alkalosis. Chronic adaptation consists of increasing the haematocrit, which allows cardiac output to return to normal while maintaining a satisfactory rate of oxygen delivery to the tissues.