Isoflurane Attenuates Baroreflex Control of Heart Rate in Human Neonates

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Abstract
Clinical studies have suggested that baroreflex regulation of heart rate may be more affected by inhalational anesthetics in human neonates or young animals than in adults. To test this hypothesis, baroreceptor reflex control of heart rate was studied in eight neonates during administration of 1 MAC isoflurane. The neonates were hemodynamically stable and their lungs were mechanically ventilated. No other anesthetic was used. Mean (.+-. SD) correlated gestational age was 39.4 .+-. 2.0 weeks and mena weight was 2,710 .+-. 430 g. The pressor response was tested with the use of phenylephrine and the depressor response with nitroglycerin. Changes in heart rate (R-R interval) were plotted against the changes in systolic arterial pressure, and the slope of the linear portion of this relationship was used to define the baroreflex response. Both baroresponses measured in awake neonates varied widely between patients. With administration of approximately 1 MAC isoflurane, the pretest mean systolic arterial pressure decreased by about 30% (P < 0.01), whereas mean heart rate values remained unchanged compared with control awake values. During isoflurane administration, the mean (.+-. SD) pressor response decreased to 23% of control mean (.+-. SD) pressor response decreased to 23% of control awake values (11.2 .+-. 7.7 ms/mmHg vs. 2.6 .+-. 3.7 ms/mmHg P < 0.01) and the depressor response to 28% of control (4.3 .+-. 3.2 ms/mmHg vs. 1.2 .+-. 0.8 ms/mmHg; P < 0.05). These changes can be attributed to a significant resetting of heart rate itself (calculated as the change in R-R interval at a constant pressure). The threshold pressures expressed in percentage of corresponding pretest pressures were not changed by isoflurane, indicating that the sensitivity of the baroreceptors was unchanged. The significant depression of baroreflex control of heart rate may impair the ability of neonates to compensate for rapid changes in systemic arterial pressure and to maintain an adequate cardiac output during hypovolemia.