Response to inhaled nitric oxide in patients with acute right heart syndrome

Inhaled nitric oxide (iNO), a selective pulmonary vasodilator, has been sho wn to decrease pulmonary artery pressures but not increase cardiac output i n hemodynamically stable patients with a variety of causes of pulmonary hyp ertension. The response to iNO in hemodynamically unstable patients with ac ute right heart syndrome has not been previously described. We determined t he response to iNO in 26 critically ill adult patients with acute right hea rt failure defined by echocardiographic criteria. Patients received iNO thr ough the inspiratory limb of the ventilator in increments of 10 ppm with he modynamic and gas-exchange measurements made before and after each level. W hen maximal effect was seen, iNO was discontinued to compare parameters wit h baseline. iNO significantly increased cardiac output (5.5 +/- 3 to 6.4 +/ - 4 L/min), stroke volume (54 +/- 27 to 65 +/- 38 mi), and mixed-venous oxy gen saturation (69 +/- 8 to 73 +/- 10%), all p < 0.01. With discontinuation of iNO, all parameters returned immediately to baseline. These parameters of improved perfusion were related to a decrease in pulmonary vascular pres sures and resistance. In a subset of approximately 50% of patients, these c hanges were substantial (> 20%) and in approximately 25% of all patients, t he improvement in hemodynamic measures permitted a decrease in other vasoac tive drug administration. The mean concentration of iNO required to achieve these effects was 35 ppm, and 85% of patients exhibiting a substantial imp rovement in hemodynamics did so at a concentration of iNO of less than or e qual to 40 ppm. Underlying causes of right heart failure and baseline hemod ynamics did not predict response to iNO, but the use of alpha-agonist catec holamines did. We conclude iNO improves hemodynamics in patients with respi ratory failure, shock, and right ventricular dysfunction. Although mortalit y was not a key end point in this pilot study, it was high for both respond ers and nonresponders to this therapy. Further evaluation of the role of iN O in this patient population is supported by these data.