Table of Contents

This is something of a summary of how catecholamines behave around adrenergic receptors. It describes catecholamine storage in vesicles, their exocytosis, presynaptic neurotransmission, and reuptake by NET ad DAT transporter proteins.

The signs, symptoms, causes and treatment of fat embolism syndrome had come up in Question 29 from the second paper of 2006. The college answer to this question was unfairly brief. An attempt to expand on this topic is made here, with the expectation that the time-poor candidate will not squander their time in reading extensively on a topic which has only infrequently merited the examiner's attention. If for whatever reason the candidate has time to squander, there are several excellent sources in the literature.

Question 4 from the first paper of 2002 invites the candidates to discuss the perioperative management of a cardiac disease patient undergoing non-cardiac surgery.  The college model answer to this 2002 question refers to the "recently published" ACC/AHA guidelines. The 2014 reiteration of these guidelines is now available, which is a massive 50 page document.  The anaesthetic trainee will be abundantly familiar with these guidelines. For them, it must be bread and butter, luxuriously coated in the warmth of cuddly risk avoidance. For the intensivist however, anything reminiscent of anaesthetic preadmission clinics and preoperative risk assessments will be met with a mixture of revulsion and despair. In that spirit, the answer to Question 4 has been offered here in as brief a form as possible.

This chapter offers a summary of the effects of catecholamine receptor activation

Question 23 from the second paper of 2008  and Question 25 from the first paper of 2006 asked the candidates to define "study power". In short,  it is the percentage chance of detecting a treatment effect if there actually is one. This is something you decide upon before commencing the trial; the higher the power value, the more patients you will need. Typically, beta is 0.8, so there is a 20% chance (1-beta) of commiting a Type 2 error , or a "false negative".

Vasopressin is an endogenously available vasoconstrictor with antidiuretic effects. "Vasopressor effects are exerted by V1 receptors, which are Gq-protein coupled receptors. Similarly to alpha-1 receptors, they increase intracellular calcium by means of increasing cAMP concentrations. V2 receptors are Gs-coupled receptors and produce the insertion of aquaporins into the apical membrane of principle cells of the collecting tubule, promoting the retention of watr.

This chapter is a summary of the pharmacological properties of milrinone. My main focus will be the differences between milrinone and dobutamine. These are the two major old-style inotropes in our arsenal; and there are situations which favour the use of one over the other.

 Dobutamine is a synthetic catecholamine. As well as a well-defined catechol group, it possesses a humongous amine substituent group, which confer upon it a high level of beta-1 selectivity. This is the result of "intelligent drug design". The first paper to describe its properties (1975) is an amazing piece of work. The authors systematically produced a whole bucketfull of catecholamines with different side chains, amine substituents, hydroxyl group arrangements, etc etc - and then tested them for cardiovascular effect. Indeed, much of what we know about the structure and function relationship of catecholamines comes from such experiments.

 Noradrenaline is an endogenous catecholamine, a sympathomimetic drug with a strong alpha-1 receptor selectivity. This chapter is a tribute to it, as it is the true workhorse of intensive care, and a drug with which one ought to become intimately familiar. It is the gateway drug to understanding the effects of catecholamines.

Amiodarone is a cardiac glycoside antiarrhythmic and inotrope which defies Vaughan Williams classification. By inhibiting Na+/K+ ATPase, digoxin increases intracellular sodium, which increases sodium-calcium exchange by the Na+/Ca2+ exchanger (INCX) during Phase 1 of the cardiac action potential. The resulting increase in intracellular calcium promotes inotropy. It also acts as a vagotonic agent, which slows conduction through the AV node, and decreases the duration of the action potential mainly by reducing the duration of Phase 2. The slope of Phase 4 is increased, promoting automaticity, but then automaticity is overall suppressed by the vagotonic effects./p>

West's Zones of the lung are physiologically distinct but anatomically blurry regions which represent different relationships between alveolar pressure, arterial pressure and venous pressure. Zone 1 is characterised by minimal perfusion (it is essentially dead space), Zone 2 is perfused intermittently, and Zone 3 has good perfusion and receives most of the blood flow. An additional fourth zone represents the region of lung which is collapsed and in which interstitial fluid pressure is the dominant Starling resistor.

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.