Temporary unilateral pulmonary artery occlusion: a method for controlling Swan-Ganz catheter-induced hemoptysis.

A patient undergoing mitral and aortic valve replacement suffered catheter-induced pulmonary artery trauma and massive hemoptysis during weaning from cardiopulmonary bypass. Hemorrhage ceased when the ipsilateral pulmonary artery was occluded. Forty-eight hours later the temporary band was removed, and the patient did well without further bleeding.

Catheter-induced pulmonary artery hemorrhage. Diagnosis and management in cardiac operations.

Three case reports describing catheter-induced pulmonary artery hemorrhage in patients having cardiac operations are presented--a 0.2% incidence of this complication. One patient exsanguinated and died, another survived after undergoing an emergency lobectomy, and the third escaped without surgical intervention. As a result of this experience and the recommendations in the literature, we have developed and describe herein a rational therapy for this highly lethal complication.

Nitroprusside and mitral stenosis.

The cardiovascular effects of an intravenous nitroprusside infusion were evaluated intraoperatively in seven patients with pure mitral stenosis and seven patients with predominant mitral stenosis. Prior to therapy the adverse hemodynamic consequences of light anesthesia and surgical stimulation were evident in all patients: systemic and/or pulmonary hypertension were present, systemic vascular resistance was twice normal, and cardiac function was depressed. Nitroprusside consistently reduced systemic vascular resistance and systemic arterial as well as pulmonary arterial and wedge pressures, but cardiac index increased only when severe pulmonary hypertension and/or some mitral regurgitation coexisted with mitral stenosis. In the group with predominant mitral stenosis, cardiac index increased from 1.8 to 2.1 L/min/m2 with nitroprusside (p < 0.05). In three individuals who demonstrated severe pulmonary hypertension (one with pure mitral stenosis and two with predominant mitral stenosis), nitroprusside induced an increase of almost 50% in cardiac index and stroke volume. In contrast, patients with pure mitral stenosis and mild pulmonary hypertension showed little change in cardiac index or stroke volume. It is concluded that nitroprusside can safely be used to control systemic or pulmonary hypertension during anesthesia and surgery in patients with mitral stenosis and that if severe pulmonary hypertension and/or mitral regurgitation coexist with mitral stenosis, cardiac function will also improve.

Comparison of intraoperative nitroprusside unloading in mitral and aortic regurgitation.

To compare the hemodynamic effect of vasodilator therapy on different regurgitant lesions, we infused sodium nitroprusside intraooperatively in 12 patients with mitral regurgitation and 15 with aortic regurgitation. During the critical period preceding establishment of cardiopulmonary bypass, both groups had developed intense vasoconstriction and cardiac decompensation. All demonstrated improved cardiac function with vasodilator therapy; however, the degree of improvement with nitroprusside differed in the two groups. Stroke volume increased 10 ml. per beat per meter squared in those patients with aortic regurgitation and only 6 ml. per beat per meter squared in those with mitral regurgitation (p less than 0.05). The percent increase in stoke volume induced by nitroprusside was inversely correlated to the preoperative left ventricular ejection fraction (r = 0.44, p less than 0.02). Patients with aortic regurgitation had lower preoperative left ventricular ejection fractions than those with mitral regurgitation (0.53 versus 0.63, p less than 0.02). Therefore, we conclude that patients with aortic regurgitation derived greater intraoperative hemodynamic benefit from unloading with nitroprusside, because they came to surgery with greater impairment of left ventricular contractility. Although nitroprusside improved cardiac function in both groups, only the patients with aortic regurgitation achieved normal pulmonary artery pressure (17 torr) and pulmonary vascular resistance (2.1 units) as a result of unloading. Those with mitral regurgitation continued to have pulmonary hypertension (28 torr) and increased pulmonary vascular resistance (3.9 units) despite vasodilator therapy. Thus the data suggest that patients with mitral regurgitation derived less hemodynamic benefit from intraoperative nitroprusside therapy because they were also limited by right ventricular dysfunction and a less responsive pulmonary vasculature.