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Cardiorespiratory effects of inhaled nitric oxide and moderate hypercapnia in an experimental model of single ventricle
Critical Care volume 3, Article number: P043 (2000)
To evaluate the effects of inhaled nitric oxide and moderate hypercapnia on hemodynamics and gas exchange in an experimental model of single ventricle.
Prospective, randomized, experimental study.
University research laboratory.
Nine piglets weighing 10 to 14 kg.
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.
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.
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Zobel, G., Dacar, D., Knez, I. et al. Cardiorespiratory effects of inhaled nitric oxide and moderate hypercapnia in an experimental model of single ventricle. Crit Care 3, P043 (2000). https://doi.org/10.1186/cc418
- Nitric Oxide
- Pulmonary Artery
- Cardiopulmonary Bypass
- Pulmonary Artery Pressure
- Pulmonary Artery Catheter