To determine physiologic responses to apnea-induced severe hypoxemia in anesthetized horses.Study design
Prospective experimental study.Animals
Six university-owned horses with a median (range) body weight of 500 (220–510) kg and aged 13.5 (0.8–24.0) years scheduled for euthanasia.Methods
Xylazine–midazolam–ketamine-anesthetized horses breathing room air spontaneously were instrumented with a facial artery catheter for pressure measurement and blood sampling, and were made apneic with atlanto-occipital intrathecal lidocaine (4 mg kg−1). Cardiopulmonary, biochemical and hematologic variables were recorded before (baseline) and every minute for 10 minutes after lidocaine injection.Results
PaO2 values were: baseline, 55 mmHg (7.3 kPa); 1 minute, 28 mmHg (3.8 kPa); 2 minutes, 18 mmHg (2.4 kPa); 3 minutes, 15 mmHg (2.0 kPa), and 4–10 minutes, (8–11 mmHg (1.1–1.5 kPa). PaCO2 values were: baseline, 50 mmHg (6.7 kPa); 1 minute, 61 mmHg (8.1 kPa), and 2–10 minutes, 64–66 mmHg (8.5–8.8 kPa). Base excess values at baseline, 1 minute and 2–10 minutes were 5.3 mmol L−1, 6.5 mmol L−1 and 7.0–8.1 mmol L−1, respectively. Pulse rates at baseline, 1 minute and 2–7 minutes were 36, 53 and 54–85 beats minute−1, respectively. Asystole occurred at 8 minutes. Pulse pressures were 50 mmHg at baseline and 1 minute, and 39 mmHg, 31 mmHg, 22 mmHg, 17 mmHg and 1–9 mmHg at 2, 3, 4, 5 and 6–10 minutes, respectively. Lactate was 0.9 mmol L−1 at baseline, progressively increasing to 1.7–2.4 mmol L−1 at 7–10 minutes. Packed cell volume increased after 7 minutes of apnea. There were no other major changes.Conclusions and clinical relevance
Apnea immediately exacerbated hypoxemia and hypercapnia and rapidly caused hemodynamic instability. Apnea in hypoxemic anesthetized horses is associated with a serious risk for progress to cardiovascular collapse.