The hemodynamic effects of prolonged respiratory alkalosis in anesthetizednewborn piglets

Objective: To test the hypothesis that prolonged alkalosis decreases cardia c output and, furthermore, exacerbates hypoxic pulmonary vasoconstriction, as respiratory alkalosis is frequently induced as a therapy for persistent pulmonary hypertension of the newborn despite a lack of controlled evidence of improved outcomes. Potential adverse effects of prolonged alkalosis hav e been demonstrated. Method: Two groups (control, n = 6, and hypocapnic alkalosis, n = 6) of 1-3 day old fentanyl-anesthetized, vecuronium-paralyzed piglets were instrumen ted to measure cardiac index (CI) and mean systemic (MAP) and pulmonary (PA P) arterial pressures. Baseline values were recorded. Alveolar hypoxia was then induced to achieve an arterial oxygen saturation of between 50 and 60 % for 15 min. Respiratory alkalosis was then induced, by increasing ventila tion to achieve a pH between 7.55-7.60, and was continued for 240 min. Insp ired carbon dioxide was used with hyperventilation in the control group to maintain pressure of arterial carbon dioxide (PaCO2) at 35-45 mmHg and pH o f 7.35-7.45. Hypoxia was induced again at 15 and 240 min. Pulmonary and sys temic vascular resistances (PVR and SVR) were calculated. Results: Prolonged alkalosis led to a significant and progressive fall in m ean MAP from 61 (SD 7) mmHg at the start of the study falling to 50 (SD 6.9 , p = 0.043), with no effect on CI. Calculated SVR decreased (0.45 SD 0.03 vs 0.36 SD 0.05). There were no statistically significant changes in any of the variables in the control group. Neither acute nor prolonged respirator y alkalosis had a significant effect on hypoxic pulmonary vasoconstriction. Conclusions: Prolonged hyperventilation leads to systemic hypotension, howe ver it does not exacerbate hypoxic pulmonary vasoconstriction.