A case report describes a patient with right ventricular cardiogenic shock due to a dissected right coronary artery1. There was deterioration despite fluid, inotropic and intraaortic balloon pump therapy, followed by improvement with the introduction of inhaled nitric oxide (iNO) at 12 to 15 ppm (a selective pulmonary vasodilator), to the point where vasoactive medication was withdrawn. The cessation of iNO was associated with deterioration which resolved with its reintroduction. It was more gradually withdrawn and the patient made a good recovery.
The rationale for the use of iNO in patients with acute RV heart failure due to MI is afterload reduction without systemic hypotension.
It has been shown to improve haemodynamics in RV MI patients with cardiogenic shock in a previous case series2 (abstract below) in which its effects on pulmonary vasodilation are thought be beneficial. In RV MI with shock increased pulmonary vascular tone is postulated to result from the following mechanisms:
- A low cardiac output results in a decreased mixed venous blood oxygen content, which enhances pulmonary artery vasoconstriction.
- The intravenous infusion of alpha-adrenergic vasoconstrictors can contribute to pulmonary vasoconstriction.
- Mechanical ventilation with positive end-expiratory pressure can increase the pulmonary vascular resistance through compression of the pulmonary vasculature.
- Interstitial pulmonary edema, which may occur in some patients with coexisting LV dysfunction, can also cause pulmonary constriction
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 [F(i)O(2)] = 1.0), hemodynamic measurements were recorded before, during inhalation of NO (80 ppm at F(i)O(2) = 0.90) for 10 min, and 10 min after NO inhalation was discontinued (F(i)O(2) = 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 F(i)O(2) = 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 acute hemodynamic improvement when administered to patients with RVMI and CS.
1. Use of inhaled nitric oxide in the treatment of right ventricular myocardial infarction
Am J Emerg Med. 2011 May;29(4):473.e3-5
2. Hemodynamic effects of inhaled nitric oxide in right ventricular myocardial infarction and cardiogenic shock
J Am Coll Cardiol. 2004 Aug 18;44(4):793-8