Indices of vagal and sympathetic activity were studied in 30 elderly males, to elucidate their possible roles in causing hypotension during spinal analgesia. The technique of spinal analgesia and the regimen of intravenous fluids were standardised. An index of vagal activity was derived from the degree of heart rate variation (successive RR interval change) on ECG recordings. Sympathetic activity was evaluated by changes in the skin conductance (SCR) of 15 patients. Analgesia to pinprick reached a median dermatome level of T5-6 (range T2-T10) by 15 min. Hypotension was correlated with the level of analgesia, and was more likely when spinal analgesia was higher than T5. There was no correlation between vagal activity and the degree of hypotension. The depression of skin conductance responses was not correlated with the degree of hypotension nor with vagal activity. Vagal efferent activity, measured at the heart, does not seem to play a causative role in hypotension occurring during spinal analgesia.
The extent of sympathetic blockade in 36 patients, who had been given extradural analgesia, was studied by means of the skin conductance response (SCR). The SCR was also studied in six healthy volunteers who received, in a cross-over fashion, infusions of physiological saline (placebo) and saline containing mepivacaine. Two more volunteers were given saline containing bupivacaine. Extradural analgesia caused a partial blockade of sympathetic activity. The higher the level of analgesia the greater the degree of inhibition of the SCR. Complete blockade of the SCR or only a weak response in the foot was obtained in the majority of cases when the level of analgesia reached a dermatome level of T4 or higher. There was no significant relationship between the degree of motor blockade of the lower extremities and the intensity of blockade of the SCR. Extradural injection of 2% mepivacaine had a greater effect on the SCR than did 0.5% bupivacaine. There was no indication that infusion of mepivacaine or bupivacaine in volunteers, whose blood levels were as high as or higher than those likely to be produced during extradural analgesia, affected the SCR.
We investigated the bar graph on a pulse oximeter as an indicator of peripheral blood flow. Because blood flow is known to increase in the lower extremities during spinal analgesia, we chose patients receiving spinal analgesia as the experimental model. Although they are indirect indicators, we used laser Doppler readings and skin temperature to reflect peripheral blood flow. These measurements were made from each patient's foot and hand before and after spinal analgesia and were compared with the deflection on the pulse oximeter bar graph. After subarachnoid injection of bupivacaine, laser Doppler readings from the foot increased to 620 +/- 120% (P less than 0.05) of the control reading. The pulse oximeter signal amplitude increased from 5.2 +/- 0.4 to 9.4 +/- 0.3 bars (P less than 0.05) and mean skin temperature increased from 24.6 +/- 0.5 to 31.2 +/- 0.8 degrees C (P less than 0.05). No changes were noted in readings obtained from the hand. A Nellcor N-200 pulse oximeter may be used to evaluate the effect of sympathetic nerve block as indicated by an increase in peripheral blood flow.
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