Hemodynamic effects of inhaled nitric oxide in right ventricular myocardial infarction and cardiogenic shock Original Research Article

Objectives We sought to determine whether or not inhaled nitric oxide (NO) could improve hemodynamic function in patients with right ventricular myocardial infarction (RVMI) and cardiogenic shock (CS). Background Inhaled NO is a selective pulmonary vasodilator that can decrease right ventricular afterload. Methods Thirteen patients (7 males and 6 females, age 65 ± 3 years) presenting with electrocardiographic, echocardiographic, and hemodynamic evidence of acute inferior myocardial infarction associated with RVMI and CS were studied. After administration of supplemental oxygen (inspired oxygen fraction [FiO2] = 1.0), hemodynamic measurements were recorded before, during inhalation of NO (80 ppm at FiO2 = 0.90) for 10 min, and 10 min after NO inhalation was discontinued (FiO2 = 1.0). Results Breathing NO decreased the mean right atrial pressure by 12 ± 3%, mean pulmonary arterial pressure by 13 ± 2%, and pulmonary vascular resistance by 36 ± 8% (all p < 0.05). Nitric oxide inhalation increased the cardiac index by 24 ± 11% and the stroke volume index by 23 ± 12% (p < 0.05). The NO administration did not change systemic arterial or pulmonary capillary wedge pressures. Contrast echocardiography identified three patients with a patent foramen ovale and right-to-left shunt flow while breathing at FiO2 = 1.0. Breathing NO decreased shunt flow by 56 ± 5% (p < 0.05) and was associated with markedly improved systemic oxygen saturation. Conclusions Nitric oxide inhalation results in acutehemodynamic improvement when administered to patients with RVMI and CS.