Cardiorespiratory effects of inhaled nitric oxide and moderate hypercapnia in an experimental model of single ventricle

Objective

To evaluate the effects of inhaled nitric oxide and moderate hypercapnia on hemodynamics and gas exchange in an experimental model of single ventricle.

Design

Prospective, randomized, experimental study.

Setting

University research laboratory.

Subjects

Nine piglets weighing 10 to 14 kg.

Interventions

After induction of anesthesia, tracheostomy and controlled mechanical ventilation animals were instrumented with two central venous catheters and two arterial catheters. After a midline sternotomy the animals were placed on cardiopulmonary bypass and subjected to atrial septectomy, patch closure of the tricuspid valve, and creation of a 4 mm systemic to pulmonary arterial shunt. Before weaning from cardiopulmonary bypass ultrasonic flow probes were placed around the pulmonary artery and the descending aorta. In addition a pulmonary artery catheter was inserted into the pulmonary artery via the right ventricle. The protocol consisted of randomly assigned periods with different PaCO₂ levels (Normocapnia = PaCO₂ 40 torr, Hypercapnia I = PaCO₂ 50 torr, Hypercapnia II = PaCO₂ 60 torr,) and a period of inhaling nitric oxide (10 ppm) at normocapnia. Tidal volume was reduced to induce hypercapnia, inspiratory time and PEEP were adjusted to achieve constant mean airway pressures (Paw).

Measurements and results

Continuous hemodynamic monitoring included right atrial, mean pulmonary artery and mean systemic arterial pressures, and continuous flow recordings at the pulmonary artery and the descending aorta. In addition, arterial and central venous blood gases were measured. Data were obtained at baseline, normocapnia with and without NO-inhalation and 2 levels of hypercapnia and are given in the Table.

Conclusion

The creation of this experimental model of single ventricle resulted in a significant decrease in oxygen saturations and mean arterial pressure. Moderate hypercapnia resulted only in minimal changes in pulmonary artery pressure, pulmonary vascular resistance, and oxygen saturations. Inhaled nitric oxide decreased pulmonary artery pressure and resistance associated a slight increase in oxygen saturations.

Table 1