Pulmonary Hemodynamics during Induction of Anesthesia

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Abstract
Changes in pulmonary hemodynamics and acid-base balance were recorded during induction of anesthesia using either i.v. administration of a barbiturate [sodiumeniboma] (28 patients) or inhalation of N2O-O2-halothane (12 patients). The 2 types of induction resulted in equal elevations of pressures within the pulmonary circulation. The increase, proportional on the 2 sides of the heart, was most pronounced immediately before endotracheal intubation. Cardiac index decreased before and during intubation but subsequently increased to levels above control values. Systemic blood pressure increased more during barbiturate than during inhalation induction. Changes in acid-base balance were similar during the 2 types of induction: arterial blood PCO2 [blood CO2 tension] and PO2 [blood O2 tension] increased, pH decreased and standard bicarbonate remained unchanged. Changes in pulmonary arterial mean pressure and central venous pressure were correlated with changes in PaCO2 [arterial CO2 tension]. Pulmonary capillary filtration pressure (i.e., pulmonary capillary wedge pressure minus plasma colloid osmotic pressure) was negative in every patient before anesthesia. During induction of anesthesia, filtration pressures became positive in half the patients. Observed changes in circulation may have been caused by hypercapnia alone or by a combination of hypercapnia and vascular reflexes associated with instrumentation during intubation. The increased strain on the heart during induction of anesthesia may lead to cardiac failure in patients with diminished cardiac reserve.

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