G. Alec Rooke, M.D., Ph.D.
Associate Professor of Anesthesiology
University of Washington, Box 356540
Seattle, WA 98195-6540
rooke@u.washington.edu

Spinal anesthesia blocks the sympathetic efferent nerves that release norepinephrine onto vascular smooth muscle, the SA node, the AV node, the conduction system and the muscle cells of the heart. The actual degree of sympathetic blockade depends on the spread of the local anesthetic. Limited spread may only block sympathetic fibers in the lower thoracic dermatomes, but rostral spread can easily extend to include the cardiac accelerator fibers (T1-T4). There is considerable debate over how much sympathetic blockade is achieved with any given level of sensory blockade, but at least one study indicates that partial sympathetic blockade can extend many dermatomes above the identified level of sensory blockade. Thus one must be prepared for possible significant hypotension with even modest levels of spinal anesthesia. Even though it may not be easily determinable, the level of sympathetic blockade is important. Although the sensory input of the baroreflex system is carried by the vagus and therefore not affected by spinal anesthesia, greater degrees of sympathetic blockade will eliminate a greater proportion of sympathetic nervous system outflow (sympathetic tone). Loss of sympathetic nerves will limit the ability of the baroreflex to combat hypotension not only by minimizing the portion of the body over which compensatory vasoconstriction can occur but by possibly even eliminating stimulation of the heart. Even though aging appears to have minimal effects on vasoconstriction, the aged heart does not respond to beta receptor stimulation as effectively as a young heart so there will be less of an increase in heart rate and contractility in the elderly, and therefore these mechanisms for increasing cardiac output will be less effective than in young adults. One might argue that the control of heart rate by the vagus is still operative during spinal anesthesia. Unfortunately, it appears that aging is associated with decreased vagal tone, thereby limiting vagal tone withdrawal as a means of increasing heart rate.

With a high spinal anesthetic one can anticipate that all the components of blood pressure could be compromised. Loss of sympathetically mediated vasoconstriction would decrease vascular resistance, loss of sympathetically mediated cardiac stimulation could decrease both heart rate and stroke volume by decreasing contractility (decreased ejection fraction), and loss of venous smooth muscle constriction might permit peripheral pooling of blood and lower the end-diastolic volume of a preload-dependent, aged left ventricle, further lowering stroke volume and cardiac output. The question is, do the elderly respond in an exaggerated manner compared to young adults with respect to any of these mechanisms? The answer is hampered by the lack of studies that examined both young and old subjects; but two studies performed on only elderly subjects do suggest differences when historically compared to studies of spinal anesthesia in younger, healthier subjects, where both vascular resistance and cardiac output appear to decrease by approximately 10 percent with high spinal anesthesia. ^{1,2 3} The studies on elderly subjects also observed 10 percent decreases in cardiac output, but in contrast to studies on younger subjects, systemic vascular resistance decreased by 26 percent and 21 percent in the elderly.^2,3 Such a result is not all that surprising if one believes the evidence that the elderly have increased sympathetic tone at rest and are therefore at risk for greater decreases in vascular resistance when that tone is removed by spinal anesthesia. One of the studies also examined blood distribution throughout the body and observed that the decrease in cardiac output was primarily due to a decrease in stroke volume that was, in turn, due to a 19-percent decrease in left ventricular end-diastolic volume.¹ The effect of the decrease in end-diastolic function on stroke volume and cardiac output was limited by an increase in the ejection fraction that was presumably due to afterload reduction, not an increase in contractility. During the spinal anesthetic, there were shifts in blood volume with the most important increases in volume observed in the mesentery (+6.7%) and the legs (+6%).

Given these effects of spinal anesthesia in the elderly, the next question centers around the appropriate treatment of hypotension from a spinal anesthetic. Crystalloid administration is a commonly chosen therapy, but in the elderly crystalloid is frequently insufficient by itself either prophylactically or after the hypotension develops.^2,4 Logically, it would be surprising if fluid alone was sufficient, given that it is difficult, if not impossible and dangerous, to give enough fluid to increase stroke volume to a level that could compensate for the precipitous decrease in vascular resistance. Epinephrine has been advocated, and has been extensively studied when administered as a low dose infusion (approximately 0.04 ucg/kg^-1/min^-1) during epidural anesthesia.⁵ This technique effectively supports cardiac output, usually increasing cardiac output to above prespinal levels, but does not raise blood pressure and may even lower pressure due to beta₂ receptor vasodilation. Phenylephrine or other alpha-agonists effectively increase blood pressure but may compromise cardiac output or cause coronary artery vasoconstriction. The ideal drug likely lies somewhere between epinephrine and phenylephrine, and the practitioner must use his or her own judgment as to which agent or combination of agents to use, including crystalloid.

References:

1. Rooke GA, Freund PR, Jacobson AF. Hemodynamic response and change in organ blood volume during spinal anesthesia in elderly men with cardiac disease. Anesth Analg. 1997; 85:99-105.
2. Critchley LAH, Stuart JC, Short TG, Gin T. Haemodynamic effects of subarachnoid block in elderly patients. Br J Anaesth. 1994; 73:464-470.
3. Mark JB, Steele SM. Cardiovascular effects of spinal anesthesia. Int Anesthesiol Clin. 1989; 27:31-39.
4. Coe AJ, Revanas B. Is crystalloid preloading useful in spinal anaesthesia in the elderly? Anaesthesia. 1990; 45:241-243.
5. Sharrock NE, Bading G, Mineo R, Blumenfeld JD. Deliberate hypotensive epidural anesthesia for patients with normal and low cardiac output. Anesth Analg. 1994; 79:899-904.