Oxygen extraction is altered by endotoxin during tamponade-induced stagnant hypoxia in the dog
Zhang, H.; Vincent, J.L.
Circulatory Shock 40(3): 168-176
1993
ISSN/ISBN: 0092-6213 PMID: 8348680 Document Number: 1105
The present study used a model of cardiac tamponade to investigate the effects of endotoxin on the oxygen extraction capabilities of the body during an acute reduction in blood flow, when blood volume and arterial oxygen content were maintained. In 21 pentobarbital anesthetized, mechanically ventilated dogs, two catheters were introduced into the pericardial space to induce cardiac tamponade, and simultaneously to measure the intrapericardial pressure. Oxygen uptake (VO-2) was determined from the expired gases. Oxygen delivery (DO-2) was calculated by the product of the thermodilution cardiac index and the arterial oxygen content. Eleven dogs received 1 mg/kg Escherichia coli endotoxin, followed by generous saline infusion (20 ml/kg cntdot hr). Ten dogs served as a control group. In each dog, DO-2 was progressively reduced by pericardial saline infusion at a rate of 40 ml/hr for the first hour and 30 ml/hr thereafter. Critical O-2 delivery (DO-2crit) and critical O-2 extraction ratio (O-2ERcrit) were determined from a plot of VO-2/DO-2 for each individual dog. The DO-2crit was greater in the endotoxic than in the control group (12.1+-3.1 ml/kg cntdot min vs. 9.6+-1.6 ml/kg cntdot min; P lt 0.05). Endotoxin at the dose used did not alter VO-2 (or critical VO-2). Accordingly, O-2ERcrit was significantly lower in the endotoxic than in the control animals (47.2%+-5.7% vs. 60.3%+-10.6%; P lt 0.01). The mixed venous PO-2 levels at DO-2crit were higher in the endotoxic than in the control group (30.6+-6.1 mm Hg vs. 25.4+-5.2 mm Hg; P lt 0.05). Arterial blood lactate concentration was higher in the endotoxic than in the control dogs. There was no significant change in hemoglobin concentration throughout the study. The systemic flow-pressure relationship indicated that, for any cardiac index, the mean systemic arterial pressure was significantly lower in the endotoxic than in the control dogs. There was a significant relationship between O-2ER and systemic vascular resistance (r=0.79, P=0.02). We conclude that endotoxin alters the oxygen extraction capabilities of the whole body during an acute reduction in blood flow in the absence of significant hypovolemia. A decrease in vascular reactivity seems to be implicated in this phenomenon.
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