Hypotension in OB Spinal Anesthesia, Dr. H. Chang

Helen A. Chang, DO

Article:
Hypotension in obstetric spinal anesthesia: a lesson from pre-eclampsia. G. Sharwood-Smith and
G.B. Drummond. British Journal of Anesthesia. 2009, 102 (3): 291-294.

Summary:
Vasopressors are oftentimes used to prevent hypotension after spinal anesthetics for cesarean section. Why expectant mothers become hypotensive may be due to several theories:

1. Spinal anesthesia almost always causes hypotension in normal pregnancy

2. Cardiac output can be reduced by aortocaval compression in the supine position from decreased venous return

3. A marked bradycardia with concomitant reduction in cardiac output and severe hypotension can occur suddenly

Many studies and therapies have been proposed to elude why drastic changes in hemodynamics may occur. There is no escape from the fact that therapies based on the concept of caval compression do not reliably prevent hypotension after a spinal technique. Compliance is more important than resistance in the venous system. Venous capacitance and its regulation in pregnancy are important in understanding the hemodynamic response to spinal anesthesia.

Sensors that normally autoregulate arterial pressure (carotid sinus and aorta) are part of the baroreflex pathway. Why does this reflex fail to maintain arterial pressure after spinal anesthesia in pregnancy? Answer is possibly seen in the pathophysiology of pre-eclampsia. In pre-eclampsia, vascular epithelium is damaged by placental-derived proteins, leading to an imbalance between pro-/anti-angiogenic growth factors. This results in persistent vasoconstriction. Sympathomimetic vasopressors to sustain arteriolar tone have become the most important strategy for safe spinal anesthesia in contemporary practice. This still holds despite the theory of caval occlusion as the culprit  for hypotension following a spinal in normal pregnancy