Hypoxia following etorphine administration in goats (Capra hircus) results more from pulmonary hypertension than from hypoventilation

BACKGROUND: Etorphine, a potent opioid agonist, causes pulmonary hypertension and respiratory depression. Whether etorphine-induced pulmonary hypertension negatively influences pulmonary gas exchange and exacerbates the effects of ventilator depression and the resultant hypoxemia is unknown. To determine if these effects occurred we instrumented twelve goats with peripheral and pulmonary arterial catheters to measure systemic and pulmonary pressures before and after etorphine administration. Concurrent cardiopulmonary and arterial blood gas variables were also measured. RESULTS: Etorphine induced hypoventilation (55% reduction to 7.6 ± 2.7 L.min(−1), F((11,44)) = 15.2 P < 0.0001), hypoxia (<45 mmHg, F((11,44)) = 8.6 P < 0.0001), hypercapnia (>40 mmHg, F((11,44)) = 5.6 P < 0.0001) and pulmonary hypertension (mean 23 ± 6 mmHg, F((11,44)) = 8.2 P < 0.0001). Within 6 min of etorphine administration hypoxia was twice (F((11,22)) = 3.0 P < 0.05) as poor than that expected from etorphine-induced hypoventilation alone. This disparity appeared to result from a decrease in the movement of oxygen (gas exchange) across the alveoli membrane, as revealed by an increase in the P(A-a)O(2) gradient (F((11,44)) = 7.9 P < 0.0001). The P(A-a)O(2) gradient was not correlated with global changes in the ventilation perfusion ratio (P = 0.28) but was correlated positively with the mean pulmonary artery pressure (P = 0.017, r(2) = 0.97), indicating that pulmonary pressure played a significant role in altering pulmonary gas exchange. CONCLUSION: Attempts to alleviate etorphine-induced hypoxia therefore should focus not only on reversing the opioid-induced respiratory depression, but also on improving gas exchange by preventing etorphine-induced pulmonary hypertension.