ACE inhibitors and anaesthesia.

During the last decade, two angiotensin converting enzyme (ACE) inhibitors, captopril and enalapril, have become accepted into clinical practice and are regarded as effective treatments for hypertension and congestive cardiac failure.' A third agent, lisinopril, had recently become available and others are likely to be introduced in the near future. It is clear, therefore, that more patients, who are being treated with these drugs, will present for elective and emergency anaesthesia than has previously been the case. Physicians and anaesthetists must be aware of the associated implications. Severe hypertension is undoubtedly a risk factor for anaesthesia, especially if it is poorly controlled.2 Adequate control of hypertension, smooth anaesthesia, choosing agents for their desired cardiovascular properties, and awareness of potential drug interactions are essential if the risk of adverse events is to be minimized. Anaesthetic agents generally interact with antihypertensive drugs in a predictable fashion and such interactions are usually of little consequence. ACE inhibitors may pose special problems by virtue of their modes of action, namely: reduction in angiotensin II, and aldosterone formation, blockade of the effects of renin and inhibition of bradykinin breakdown. Despite the initial reduction in aldosterone levels these often return to normal and the natriuretic effect may be due to the reduction in angiotensin II. Plasma volume has generally been found to be normal although cardiac preload is reduced.4 However, it is important to realize that the renin response to haemorrhage or hypotension will be greatly attenuated and therefore normal homeostatic reflexes will be impaired. In addition, the 'normal' increase in blood pressure with surgical stimulation corresponding to an increase in renin activity will be modified.' It has come to our attention that many anaesthetists, especially junior anaesthetists, do not appreciate the potential problems associated with these agents and this is due to the paucity of clinical trials or infrequent case reports on ACE inhibitors and anaesthesia. Recently we have seen cases of severe, unexpected hypotension at induction of anaesthesia in well controlled hypertensive patients on monotherapy with captopril. This hypotension was persistent and only reversed by the infusion oflarge volumes of fluid. ACE inhibitors used to be reserved for patients with severe hypertension but are now prescribed increasingly by general practitioners for any patient with hypertension despite their not being recommended as first line treatment for hypertension.' The increasing use of ACE inhibitors as monotherapy for hypertension may increase the incidence of such adverse anaesthetic occurrences. On the positive side, when controlled hypotension is desirable during general anaesthesia, ACE inhibitors may contribute and reduce the requirements for other agents such as sodium nitroprusside,6 and thus reduce the potential for cyanide toxicity during long operations. The use of ACE inhibitors in patients with congestive cardiac failure is also increasing due to their beneficial effects on symptomatology and a reduction in mortality.7 However, hypotension may be a problem, particularly with enalapril,8 with the potential for myocardial ischaemia and this again may also be increased during induction of anaesthesia. Compared with other vasodilators, ACE inhibitors are more likely to be associated with hypoperfusion9 particularly so when their use is preceded by a diuretic. This compounds the fact-that they are, in any case, less likely to retain fluid and could conceivably increase the magnitude of the reduction ofblood pressure that may occur at induction ofanaesthesia. The blood volume is relatively reduced when these patients are compared with those treated with other vasodilators. Hypotension with captopril has been shown to be more likely if the patient is sodium and volume depleted'" and therefore prolonged fasting before elective anaesthesia may increase the incidence of hypotension. In conclusion, although ACE inhibitors are therapeutically effective, their widespread use may contribute to anaesthetic problems (and possibly to