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Inhaled nitric oxide. Selective pulmonary vasodilation in cardiac surgical patients
G F Rich1, G D Murphy, C M Roos
1Department of Anesthesiology, University of Virginia Health Sciences Center, Charlottesville 22908.
Anesthesiology
|June 1, 1993
Summary
Inhaled nitric oxide (NO) effectively reduces pulmonary hypertension in cardiac surgery patients, both before and after cardiopulmonary bypass (CPB). This pulmonary vasodilation is proportional to baseline resistance and unaffected by CPB or nitrates.
Area of Science:
- Cardiovascular Physiology
- Pulmonary Medicine
- Anesthesiology
Background:
- Inhaled nitric oxide (NO) is a selective pulmonary vasodilator.
- Investigated NO's effect on pulmonary hypertension, considering cardiopulmonary bypass (CPB) and nitrates.
Purpose of the Study:
- To determine if inhaled NO (20 ppm) selectively reduces pulmonary artery pressure and vascular resistance.
- To assess if these effects are influenced by the degree of pulmonary hypertension, CPB, or concomitant nitrate use.
Main Methods:
- 20 cardiac surgery patients and 5 ventricular assist device (VAD) patients received 20 ppm inhaled NO for 6 minutes.
- Hemodynamic parameters, including pulmonary artery pressure and pulmonary vascular resistance (PVR), were measured before and after CPB, and in VAD patients.
Main Results:
- Inhaled NO significantly decreased pulmonary artery pressure and PVR in all patient groups (P < 0.05).
- The reduction in PVR was proportional to baseline PVR (PVRb).
- No significant changes in systemic hemodynamics or blood gases were observed, except in VAD patients where arterial oxygen tension and mean arterial pressure increased.
Conclusions:
- 20 ppm inhaled NO is a selective pulmonary vasodilator in cardiac surgical patients and those supported by a VAD.
- NO-induced vasodilation is proportional to baseline PVR and is not significantly altered by CPB, VAD support, or nitrates.