Spinal anaesthesia in the form of either epidural or subarachnoid block, causes inhibition of sensory, motor and autonomic fibre activity in the spinal segments affected by the local anaesthetic.
From the point of view of the patient with cardiac disease, the effects on the autonomic nervous system, both direct and reflex, are the most relevant. Vasomotor activity influences both arteriolar tone as well as venomotor tone via small, unmyelinated C-type fibres.
Preload is decreased by blood pooling in the dilated venous capacitance vessels, including the splanchnic vessels. The extent of preload reduction will depend on the existing resting venous tone, the volume status of the patient and the effectiveness of compensatory vasoconstriction in the unblocked regions of the body. This may cause a reduction in cardiac output and a fall in blood pressure which is aggravated by the decrease in systemic vascular resistance (SVR) due to arteriolar dilation.
Baroreceptor responses which would normally act to preserve perfusion pressure are limited by the amount of the vascular bed which will respond to vasoconstrictor activity. If the autonomic block affects the upper thoracic segments, particularly T1 to T4 levels, then reflex chronotropic responses will also be prevented, and a relative increase in vagal tone to the heart results. This has implications for maintenance of blood pressure and cardiac output as well as effects on the heart rhythm and conducting system (Chapter 83). It is worth noting that the upper level of autonomic block may be two or more segments higher than the measured sensory level.
Patients with heart disease are often taking medications which may obtund their ability to compensate for the circulatory changes induced by spinal anaesthesia. Beta-adrenergic blocking drugs in particular may prevent chronotropic responses to hypotension, even if the level of block is below the thoracic segments, although Reiz (1) and Stenseth (2) have found thoracic epidural anaesthesia to be safe in such patients.
Vasodilators, including nitrates, may attentuate the compensatory cardiovascular response to spinal anaesthesia, although in practice their impact is often negligible. This is particularly true in the pregnant patient at term, where vasodilators are often singularly ineffective.
References:
1. Reiz S, Haggmark S, Rydvall A, Ostman M. Beta-blockers and thoracic epidural analgesia. Cardioprotective and synergistic effects. Acta Anaesthesiol Scand. 76S:54-61; 1982
2. Stenseth R, Berg EM, Bjella L, Christensen O, Levang OW, Gisvold SE. The influence of thoracic epidural analgesia alone and in combination with general anesthesia on cardiovascular function and myocardial metabolism in patients receiving beta-adrenergic blockers. Anesth Analg 77:3; 463-468 1993