A free online resource for Intensive Care Medicine.
An unofficial Fellowship Exam (CICM Part 2) preparation resource.
Deranged Physiologyis a slowly growing archive of discussions and study notes relevant (or if not relevant, then at least interesting) to the practice of intensive care medicine. The content provides an introduction to the fundamental themes in intensive care: mechanical ventilation, vasopressors, electrolyte management, hemodynamic monitoring, dialysis, and so forth. Attention is directed at equipment in intensive care, and there are attempts to revisit interesting pharmacology and physiology. The aim of this resource is to supplement the bedside teaching of senior staff, and to consolidate resources for intensive care trainees in the initial stages of their training.
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.
As the main substrate of the respiratory system are gases and vapours, it makes sense to start the discussion of respiratory physiology with this as a foundation. Humidification is discussed in greater detail in the chapters dealing with the normal physiological mechanisms of humidification and with the technological solutions used to replicate it for mechanical ventilation. For the purpose of this chapter, it will suffice to discuss the colligative properties of liquids which are relevant to the evaporation of water and anaesthetic gases.
Positive pressure ventilation affects preload, afterload and ventricular compliance. The net effect in most situations is a decrease in cardiac output. However, the effect may be beneficial in the context of decompensated heart failure, where the decreased preload and afterload result in a return to a more productive part of the Starling curve. In this rests the chief benefit of CPAP in the management of acute pulmonary oedema.
Volume of distribution is a pharmacokinetic concept which is used to describe the distribution of drugs in the body as relative to the measured concentration. In brief, it is the apparent volume into which the drug appears to be distributed when only the sample concentration is considered. It is a purely theoretical volume, which can substantially exceed the total body volume, or potentially even be infinite in size. Among many other uses, the volume of distribution (VD) plugs into loading dose calculations. It can also help you decide instantly whether your drug is going to be easily cleared by dialysis.
The arterial pressure wave travels at 6-10 metres/sec. The cannula in the artery is connected to the transducer via some non-compliant fluid-filled tubing; the transducer is usually a soft silicone diaphragm attached to a Wheatstone Bridge. It converts the pressure change into a change in electrical resistance of the circuit. This can be viewed as waveform.
The arterial pressure wave (which is what you see there) is a shockwave; it travels much faster than the actual blood which is ejected. It represents the impulse of left ventricular contraction, conducted though the aortic valve and vessels along a fluid column (of blood), then up a catheter, then up another fluid column (of hard tubing) and finally into your Wheatstone bridge transducer. A high fidelity pressure transducer can discern fine detail in the shape of the arterial pulse waveform, which is the subject of this chapter.
Historically, the arterial line waveform has appeared in the exam in several forms. The trainees have at one stage been expected to discuss broadly what sort of information can be derived from it (Question 30.2 from the second paper of 2013). Questions regarding the change of the waveform depending on its position in the vascular tree have also appeared (Question 11.1 from the first paper of 2010). More often, the college will produce an arterial waveform tracing with some abnormality (eg. AF with loss of atrial kick, or respiratory "swing" ) and then ask the trainee to identify the abnormality and give four causes.
The pulmonary circulation is a low pressure, highly elastic system, with vessel walls which are much thinner and less muscular than the systemic circuit. The pulmonary trunk divides into pulmonary arteries which can be divided into elastic (large), muscular (small) and nonmuscular (the smallest), though further subdivisions are histologically apparent. Pulmonary arteries and veins travel with bronchi, nerves and lymphatics in bronchovascular bundles, which are extensions of the visceral pleura. Pulmonary veins are thinner and more collagen-rich than pulmonary arteries. The bronchi are supplied by the systemic circulation which arises from the intercostal arteries on the right and from the aorta on the left.
There are numerous permutations of ventilator circuits, and of course ICU trainees are not expected to become familiar with all of them. The vast majority of the variants are relevant more to the anaesthetic environment, as their design is characterised by various attempts to conserve anaesthetic gas while discarding expired CO2. The breathing circuits used in Intensive Care are usually much more straightforward. This chapter has an ICUcentric focus, but the whole Mapleson family is still thoroughly explored.
This page acts as a footnote to the "Boston vs. Copenhagen" chapter from Acid-Base Physiology by Kerry Brandis. His chapter explores the epistemology of acid-base interpretation systems by means of which we might be able to determine whether a patient has a single or mixed acid base disorder; i.e. whether there is a purely metabolic or a purely respiratory disturbance, or some mixture of the two. As it happens, there are two well-accepted systems for doing this, each with its own merits and demerits. These are the Boston and Copenhagen methods of acid-base interpretation.
Many past paper SAQs have asked the candidates to identify some rash, pupuric blotching, gangrenous embolic phenomena or some other visually impressive manifestation of disease. Irritatingly, the college examiners tend to remove these images from their published papers, presumably because they plan to reuse them. Previous questions of this sort have included Question 25.1 from the first paper of 2011 (erythema multiforme), Question 20.2 from the second paper of 2008 (Stevens-Johnson syndrome) and Question 10 from the first paper of 2005 (Toxic Epidermal Necrolysis). Question 15.1 from the second paper of 2012 was more about the non-specific approach to the evaluation of a gross whole-body rash. This approach is discussed below.
Cardiac biomarkers some up frequently, but to be honest these questions have generally been referring only to troponin. Only Question 27 from the second paper of 2010 takes a broad overview of the cardiac biomarkers. The college answer to that question is a table of advantages and disadvantages, comparing oldies like CRP and ESR with CK, troponin with some exciting novel biomarkers. Since this 2010 paper, none of these exciting novel biomarkers have become commonplace.