HYPOXIA CAUSES APNEA DURING EPIDURAL-ANESTHESIA IN RABBITS

Background: Although pulmonary function is minimally changed by neurax ial blockade in most cases, ventilatory arrest may ensue in rare cases . The authors examined the mechanism of apnea in a rabbit model of sud den ventilatory arrest during the combination of epidural anesthesia a nd hypoxia. Methods: Rabbits were studied during alpha-chloralose seda tion and spontaneous ventilation through a tracheostomy tube. Heart ra te and mean arterial pressure were monitored by intraarterial cannulat ion, Respiratory rate and tidal volume mere measured by pneumotachogra ph. Responses were recorded during administration of oxygen at inspire d oxygen concentrations of 11% for 2.5 min and 0% for 40 s, before and after either thoracolumbar epidural blockade (0.4 ml/kg lidocaine, 1. 5%) or intramuscular lidocaine (15 mg/kg). In a third group of animals , epinephrine was given intravenously during epidural blockade to retu rn mean arterial pressure to baseline values before hypoxia. In a four th group of animals, which did not get Lidocaine, sympathetic blockade and hypotension were produced with intravenously administered trimeth aphan rather than epidural blockade. Results: Thoracolumbar epidural a nesthesia decreased mean arterial pressure from 76 +/- 4 mmHg (mean +/ - SE) to 42 +/- 2 mmHg. Apnea during hypoxia occurred in 90% of these animals (nine of ten) but in only 11% of animals (one of nine) after i ntramuscularly administered lidocaine (P < 0.01), Treatment of epidura l hypotension with epinephrine prevented apnea (zero of nine animals). Apnea during hypoxia occurred in 50% (three of six) of animals given trimethaphan. Apnea in all groups was sudden in onset, with no precedi ng decreases in respiratory rate or tidal volume. Conclusions: Epidura l anesthesia results in a narrowed margin of safety for oxygen deliver y to the brain and predisposes subjects to ventilatory arrest during h ypoxia. This results from the combined effects of decreased blood oxyg en content, which is due to decreased inspired oxygen concentration su perimposed on circulatory depression due to neural blockade.