External DC (direct current) cardioversion for atrial tachyarrhythmias is a common cardiological procedure that has traditionally been performed with the patient under general anaesthesia. However organising anaesthetic cover for a cardioversion can sometimes be a challenging experience for the cardiologist. He/she often has to coordinate their own availability with: a starved patient, a coronary care nurse, an anaesthetist, and a trained anaesthetic assistant. This process is time consuming and may be frustrating for staff and patients when delays are encountered, and can lead to longer hospital stays with cost implications. Physicians in a variety of specialities have experience in providing safe sedation for unpleasant procedures in accordance with the many guidelines now available.¹ In cardiology the widespread use of transoesophageal echocardiography has led to familiarity in the administration of sedative drugs.^2,3

The first issue relates to the level of sedation required for this procedure. External DC cardioversion may be a very brief procedure, but is profoundly stimulating and needs anaesthesia and not merely sedation to obtund stress responses effectively and prevent recall. The pain level for external cardioversion can be equated to that of electroconvulsive therapy—which is of a similar brief duration and for which a short general anaesthetic is also given. Electrophysiology procedures and transoesophageal echocardiography are lengthier, and sedation is to reduce discomfort and allay anxiety rather than to produce anaesthesia. In the two recent studies published in this journal an unusually deep level of sedation was induced to prevent recall, as indicated by loss of eyelash reflex⁴ or a Ramsay sedation score of 5⁵ (described as a sluggish response to light glabellar tap or loud auditory stimulus).⁶ In fact, most of the patients in these studies could be described as being in the light planes of anaesthesia. This distinction has also been highlighted in the Practice guidelines for sedation and analgesia by non-anaesthesiologists.⁷ They define sedation and analgesia as a state that allows patients to tolerate unpleasant procedures while maintaining adequate cardiorespiratory function and the ability to respond purposefully to verbal command and/or tactile stimulation. They suggest that patients whose only response is reflex withdrawal from a painful stimulus are sedated to a greater degree than encompassed by sedation/analgesia—in other words, they are anaesthetised.

A third concern is that of hypoventilation and carbon dioxide retention. Intravenous anaesthetic induction agents, benzodiazepines, and opioids all cause dose related respiratory depression and eventually apnoea. Pulse oximetry measuring oxygen saturation is a monitor of hypoxia, but provides no information as to the level of arterial carbon dioxide. It is easy for inadequate ventilation (and therefore a climbing Paco₂) to be masked if the patient has supplementary oxygen. It is not suggested that supplementary oxygen should not be used, as avoiding hypoxia is vital. However, it should be recognised that when a longer duration and deeper level of sedation are used patients are likely to become significantly hypercapnoiec, which may in itself precipitate arrhythmias and deepening coma. In anaesthetic practice, spontaneously breathing anaesthetised patients routinely have their end tidal carbon dioxide levels monitored, and management instigated to prevent dangerous levels of hypercapnia developing.