Cardiovascular function during spinal and epidural anaesthesia: pathogenesis, prophylaxis and therapy of complications

Abstract

Summary Both spinal and epidural anaesthesia are fraught with a high risk for life-threatening cardiovascular collapse and also fatal cardiac arrests, the incidence of which is higher than with general anaesthesia. These mishaps also endanger young people with sensory block below the T4–T5 range and in spite of appropriate care according to presently accepted standards. With regard to the pathogenesis and also the prophylaxis and therapy of such events, some new information has been considered: 1. Sympathetic neurogenic control of the circulation is impaired, if not completely eliminated, when sensory blockade is above the T6 level (lumbar techniques) or below T6 (segmental thoracic epidural anaesthesia). 2. Major conduction anaesthesia prevents the renin-angiotensin system from acting, so that cardiovascular stability depends entirely on vasopressin. 3. Major conduction anaesthesia primarily reduces central blood volume and thus the heart's filling because of blood pooling in the denervated muscle and skin regions, an effect which is counteracted by vasoconstriction in the remaining innervated body regions and, in the vast majority of people, by constriction of the splanchnic vasculature. 4. Cardiovascular collapse may occur whenever the filling of the heart is further reduced, such as by blood loss, positive airway pressure, or low blood volume states as in certain forms of arterial hypertension or in bed-ridden patients, and also when the vasoconstrictor mechanism of the splanchnic circulation fails in certain individuals with an inherent dysfunction of splanchnic vasomotor control./lt The prophylaxis and therapy of cardiovascular complications during major conduction anaesthesia must primarily be aimed at stabilizing or reestablishing appropriate cardiac filling by an increase in either blood volume or vasomotor tone. There is convincing evidence that the efficacy of vasoconstrictor prophylaxis in preventing cardiovascular complications is by far superior to volume prophylaxis as currently employed. The trouble spot of major conduction blockade resides in the filling of the heart. Vasoconstrictor agents in general and catecholamines of the adrenaline-type in particular mobilize rapidly (within a few minutes at the most) substantial volumes of blood from the peripheral vasculature in favour of the heart. Vasoconstrictors are therefore the first choice for the prophylaxis and therapy of cardiovascular complications during major conduction anaesthesia. It should be remembered that cardiopulmonary resuscitation is ineffective when there is no blood in the heart.