Cardiorespiratory effects of inhaled nitric oxide during acute hypercapnia with and without correction of blood pH in a acute respiratory failure in piglets

Objective

To evaluate the effects of inhaled nitric oxide on gas exchange and hemodynamic data during acute hypercapnia with uncorrected and corrected blood-pH.

Design

Prospective, randomized, experimental study.

Setting

University research laboratory.

Subjects

Ten piglets weighing 9 to 13 kg.

Interventions

After induction of anesthesia, tracheostomy and controlled mechanical ventilation animals were instrumented with two central venous catheters, a pulmonary artery and two arterial catheters, and an ultrasonic flow probe around the pulmonary artery. Acute respiratory failure was induced by the infusion of oleic acid (0.08 ml/kg) and repeated lung lavages with 0.9% NaCl (20 ml/kg). The protocol consisted of randomly assigned periods with different PaCO₂ levels (Normocapnia = PaCO₂ 40 torr, Hypercapnia I = PaCO₂ 65 torr. Hypercapnia Ic = PaCO₂, 65 torr-pH corrected, Hypercapnia II = PaCO₂ 85 torr, Hypercapnia Iic = Hypercapnia 85 torr-pH corrected). Tidal volume was reduced to induce hypercapnia, inspiratory time was prolonged to achieve constant mean airway pressures (Paw). Tham infusion was used to correct pH. At each PaCO₂-period the animals were ventilated with and without inhaled nitric oxide (10 ppm).

Measurements and results

Continuous hemodynamic monitoring included right atrial, mean pulmonary artery and mean systemic arterial pressures, and continuous flow recording at the pulmonary artery. In addition, airway pressures, tidal volumes, lung compliance and airway resistance, arterial and mixed venous blood gases were measured. Data were obtained with and without inhalation of nitric oxide at baseline, normocapnia and 2 levels of hypercapnia with and without pH correction and are given in the Table.

Conclusion

Acute hypercapnia resulted in a significant increase in pulmonary artery pressure and pulmonary vascular resistance without significantly influencing oxygenation and cardiac output. pH-correction at hypercapnic episodes decreased pulmonary artery pressure and pulmonary vascular resistance associated with a slight increase in cardiac output and oxygenation. Inhaled nitric oxide significantly reduced pulmonary hypertension induced by acute hypercapnia and significantly improved oxygenation during normocapnia and acute hypercapnia with and without acidosis.

Table 1 Table1