Abstract

Acute respiratory acidosis results in increases in cardiac output and in systemic and pulmonary arterial blood pressures. The aim of this investigation was to determine if isoflurane modifies these effects. Nine patients (ASA II or III) scheduled for major surgery took part in the investigation. After the induction of general anesthesia, CO2 was added to the inspiratory gas mixture. After 15 min, ventilation with addition of CO2 (PaCO2 8-9 kPa) isoflurane (3%) was added. Hemodynamic measurements were made to study the effects of acute hypercapnia and the effects of isoflurane during hypercapnia. The addition of carbon dioxide resulted in increases in cardiac output, systemic and pulmonary arterial blood pressures, and right and left ventricular stroke work. The addition of isoflurane during hypercapnia decreased systemic arterial blood pressure, but pulmonary arterial blood pressure was unaffected, cardiac output and stroke volume did not change, and left but not right ventricular stroke work decreased. In conclusion, acute pulmonary hypertension induced by hypercapnia was not affected by isoflurane but, despite increased right ventricular stroke work, there were no signs of right ventricular failure.

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