Respiratory alkalosis (RA) continues to be used as a therapy for persistent pulmonary hypertension of the newborn. Hypothesis: Prolonged alkalosis has adverse effects on hemodynamic variables, furthermore, it can exacerbate hypoxic induced pulmonary vasoconstriction. Method: 2 groups (control n=5, and hypocapnic alkalosis, n=6) of 1-3 d old fentanyl anesthetized, vecuronium paralyzed piglets (mean weight 1.69 ± 0.11 kg) were instrumented with an arterial catheter and a flow directed thermodilution catheter to measure cardiac index (Q), mean systemic (SAP) and pulmonary (PAP) arterial pressure. Baseline values were recorded. Alveolar hypoxia was then induced to arterial O2 sats of 50-60% for 15 minutes. RA (pH 7.55-7.60) was then achieved and continued for 240 minutes by hyperventilation in the RA group, and final values were recorded. Inspired CO2 was used with hyperventilation in the control group to maintain PaCO2 35-45 mmHg and pH 7.35-7.45. Hypoxia was induced again at 15 and 240 minutes. Pulmonary and systemic vascular resistance (PVR and SVR) and stroke volume (SV) were calculated. Results: Prolonged alkalosis leads to a statistically significant 18% fall in SAP (ANOVA, p<0.05), with no effect on Q or PAP. Calculated SVR therefore decreased (0.45 ± 0.03 vs. 0.39 ±.05, p<0.05). There were no statistically significant changes in any of the variables in the control group. Both ionized calcium and serum phosphorus fell with RA (1.38 ± 0.034 and 6.9 ± 1.17 vs. 1.28 ± 0.08 and 6 ± 0.86, p<0.05) and were unchanged in the control animals. Neither acute or prolonged RA had a significant effect on hypoxic pulmonary vasoconstriction.

The hypotensive effect of prolonged hyperventilation is potentially counterproductive and detrimental. Table

Table 1
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