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This third edition of the highly successful The Anaesthesia Science Viva Book contains detailed, accessible summaries of the core questions in anatomy, physiology, pharmacology and clinical measurement that may be asked in the oral section of the Final FRCA exam. In addition to comprehensive updating of all the topics, this edition includes new subject material in each of the four basic sciences, with almost 200 detailed summaries of the most relevant topics in the examination. This volume once again gives candidates an insight into the way the viva works, offering general guidance on exam technique, and providing readily accessible information relating to a wide range of potential questions. Written by a former senior examiner for the diploma of the Fellowship of the Royal College of Anaesthetists and listed as recommended reading by AnaesthesiaUK, the prime educational resource for trainee anaesthetists, it remains an essential purchase for every Final FRCA candidate.
This is a standard question but one which contains a lot of anatomical detail. It may be helpful to practise drawing a simple explanatory diagram. The viva may be linked to intracranial aneurysms and their management, and it may also touch on physiological aspects of cerebral perfusion, on the problem of cerebral vasospasm or briefly on the subject of intracranial pressure.
You will be asked about the arterial supply to the brain. The venous drainage is included below but is less likely to feature prominently in the oral.
Arterial supply (Figure 2.1)
The brain is supplied by four major vessels: two internal carotid arteries which provide two-thirds of the arterial supply, and the two vertebral arteries which deliver the remaining third. (Some texts quote an 80:20 distribution.)
The vertebral arteries give off the posterior inferior cerebellar arteries, before joining to form the basilar artery. This also provides the anterior inferior cerebellar and the superior cerebellar arteries.
The basilar artery then gives off the two posterior cerebral arteries, which supply the medial side of the temporal lobe and the occipital lobe.
The artery then anastomoses with the carotid arteries via two posterior communicating arteries.
The internal carotid arteries meanwhile give rise to the middle cerebral arteries which supply the lateral parts of the cerebral hemispheres. They also provide much of the supply to the internal capsule, through which pass a large number of cortical afferent and efferent fibres.
The carotids also give rise to the anterior cerebral arteries, which are connected by the anterior communicating artery and which supply the medial and superior aspects of the hemispheres.
The discovery of anaesthesia transformed the human condition, and unplanned awareness returns a patient to the nightmare that was surgery before anaesthesia and analgesia. Significant advances in the pharmacology and technology of anaesthesia have still not brought us much closer to a reliable means of monitoring its depth, although because awareness is such a serious complication considerable research effort has been dedicated to the search for methods of detection. Many remain research tools or are not yet in widespread use, but you should have some idea about which may in due course find their way into clinical practice.
You may be asked about the types of awareness under general anaesthesia, the commonest causes, patients particularly at risk, and possible sequelae.
Definitions: awareness can be ‘explicit’ or ‘implicit’. Explicit awareness is defined by spontaneous or prompted recall of intraoperative events, which may or may not include pain. Its accurate incidence is hard to determine, but commonly quoted figures are up to 0.2% in non-obstetric and non-cardiac anaesthesia, up to 0.4% in emergency caesarean section under general anaesthesia, and up to 1.5% in cardiac surgery. (The Royal College of Anaesthetists patient information leaflet quotes an incidence of 0.1–0.2%.)
Causes: its causes lie in equipment and its (mis)use, in pharmacology and its application, and, very rarely, in the physiology of patients.
Equipment and apparatus: awareness may result from a failure of the apparatus to deliver adequate concentrations of anaesthetic agent. The anaesthetic machine must deliver an accurate fresh gas flow via an appropriate breathing system using a vaporizer.
Pneumothorax is an important complication in anaesthesia, trauma and medicine. This viva will concentrate both on the precise mechanisms by which pneumothoraces occur and on details of recognition and management. A pneumothorax can develop rapidly into a life-threatening emergency and so you must ensure that your management is competent.
You may be asked to list some of the common causes of pneumothorax, and explain how you would confirm the diagnosis.
Traumatic: pneumothorax can follow penetrating injury, rib fracture or blast injury.
Iatrogenic (surgical): it may occur during procedures such as nephrectomy, in spinal surgery, during tracheostomy (especially in children), laparoscopy, or as a consequence of oesophageal or mediastinal perforation.
Iatrogenic (anaesthetic): pneumothorax may result from attempted central venous puncture and various nerve blocks, from barotrauma from mechanical ventilation at excessive pressures, and from high-pressure gas injector systems. Patients with emphysematous bullae are at risk.
Miscellaneous: it may occur if the alveolar septa are weakened, as described above, and is associated with many pulmonary diseases, including asthma. There are some bizarre and unusual causes: recurring catamenial pneumothorax, for example, is a spontaneous pneumothorax, usually right-sided, which occurs in phase with the menstrual cycle. (By all means impress the examiners with this information, but do not cite it first.)
Diagnosis of pneumothorax in the awake patient
Typical features (which are not invariable and which will depend on the size of the pneumothorax and whether or not it is expanding) include chest pain, referred shoulder tip pain, cough, dyspnoea, tachypnoea and tachycardia. There may be reduced movement of the affected hemithorax, hyperresonance on percussion, diminished breath sounds and decreased vocal fremitus.
The emphasis, if not the content, of the Final FRCA science viva is changing. In response to muted criticism that an otherwise good exam has been diminished by a basic science viva that at times seemed to be little more than ‘Primary Lite’, the College has introduced greater clinical focus. This has meant that many of the answers that appeared in the first edition needed some reorientation. Yet, as before, this book's prime purpose remains to give you a wide range of potential questions presented in a way that is relevant to the exam that you are facing, and organized so that the information is manageable. As before, the introduction still aims to give you some insight into how the clinical science viva works, together with some revised general guidance as to how to improve your chances of success.
The examination questions continue to be divided broadly into the four subject areas of anatomy, physiology, pharmacology and physics, although the increased clinical emphasis can mean that the distinction between the subject areas can be somewhat blurred. The anatomy question on the internal jugular vein, for example, may well include some discussion of the physiology of central venous pressure. Equally, some questions on pharmacology may encompass aspects of physiology with which there is obvious potential for overlap. This means that you may not always find all the necessary information within one single answer, but should find most of it covered in other sections.
The format of the Final FRCA examination has remained materially unchanged since its inception in 1996, and the clinical science viva continues to test ‘the understanding of basic science to the practice of anaesthesia, intensive therapy and pain management’. The College has always included the proviso that ‘it is accepted that candidates will not have acquired a detailed knowledge of every topic during the period of recognised training’, but this has on occasion contrasted uneasily with the bitter perception of at least some candidates that they had been examined almost to destruction on scientific minutiae. This perception, against a background of muted unease about this section of the exam, has been acknowledged by the College, which has decided therefore to introduce greater clinical emphasis into the science oral. The change of emphasis is relatively subtle, because both the College and its examiners remain reluctant to dilute the rigour of what for most candidates will be the last examination in anaesthesia that they are likely to take. Nevertheless, the tenor of many of the questions has now altered so that the clinical applications of the underlying science have more prominence than hitherto. The questions continue to have two parts: the basic scientific principles and their clinical application, but many of the topics will now be introduced via a clinically orientated question that is intended to reassure you that the subject does have anaesthetic relevance.
This has been the focus of fundamental research which this viva will not have time to explore in depth. The subject matter is complex and although selective effects on CNS proteins appear to offer the most complete explanation, much remains unexplained. If you can give a reasonably plausible summary of the main points, then you should have done enough to pass.
You will be asked about the theories that have been advanced to explain the action of general anaesthetics.
Compounds that cause reversible insensibility range from xenon, which is chemically unreactive and whose structure could not be simpler, to barbiturates and phenols, whose structures are both complex and dissimilar. This makes the search for a unifying theory of action with particular emphasis on a specific structure–activity relationship more difficult.
Meyer–Overton hypothesis: Meyer and Overton (separately) were the first to relate the potency of anaesthetic agents to their lipid solubility. They argued further that the onset of narcosis was evident as soon as the particular substance had attained a certain molar concentration in the lipids of the cell, and that the lipid layers of the cell membrane represented the main site of action. Much early research was based on the hypothesis that disruption of the lipid bilayer affected the function of membrane proteins and mediated an interruption of neuronal traffic. As a unifying theory however, it was undermined by the observations that temperature rises disrupt lipid membranes without inducing a state of general anaesthesia, and that there are many compounds with high lipid solubility which exert no anaesthetic effect.