caval compression is not as important to the mechanism of spinal hypotension in pregnancy as previously thought, as alluded to by Sharwood-Smith and Drummond, it is important to appreciate that hypotension is only one aspect of the haemodynamic effect of spinal anaesthesia. Arterial pressure changes have traditionally been the main target for treatment because they are easy to measure. However, recently, there has been renewed interest in the investigation of changes in cardiac output, largely because of the advent of new non-invasive and minimally invasive measurement techniques. For example, Langesaeter and colleagues recently showed that phenylephrine has the potential to decrease maternal cardiac output, although the exact effects of this on placental blood flow in normal clinical circumstances are uncertain. Of similar importance, aortocaval compression may have important effects on cardiac output that may not be detected using usual intraoperative monitors. Recently, we used non-invasive haemodynamic monitors to study changes associated with aortocaval compression in nonlabouring term parturients. We found that aortocaval compression could cause significant reduction in cardiac output, but this was not necessarily accompanied by hypotension, possibly because of a compensatory increase in sympathetic tone. However, when spinal anaesthesia was induced, patients with greater changes in cardiac output from aortocaval compression had a higher incidence of hypotension and required more vasopressor to maintain their arterial pressure (unpublished data). Thus, we concur with Sharwood-Smith and Drummond that the use of tilt or other methods to attain lateral uterine displacement remains a rationale part of our management of obstetric patients. Clinicians who rely solely on monitoring of arterial pressure may under-appreciate the effects of aortocaval compression.
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