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)O2 gradient (F(11,44) = 7.9 P < 0.0001). The P(A-a)O2 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, r2 = 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