It was Landry et al.¹ who first reported the use of vasopressin in critically ill adults in septic shock when high doses of inotropic pressor therapy had failed to maintain an adequate blood pressure. The systemic inflammatory response syndrome is in several ways comparable to septic shock, being an acute manifestation occurring after cardiac surgical procedures. It consists of severe persistent systemic vasodilation, with massive redistribution in the flows of blood leading to hypoperfusion of the major vascular beds, resulting eventually in multi-organ failure. The severe vasodilation often proves refractory to traditional vasoactive drugs, and can be fatal.^2–4 It has now been suggested that vasopressin should be used in such cases when the patients are unresponsive to high doses of catecholamines,^1–4 arguing that the combined effects of low doses of vasopressin, namely systemic vasoconstriction and pulmonary vasodilation, should prove advantageous, particularly in the presence of right ventricular failure.^{4, 5} We describe our recent experience using this combination, since little information exists concerning patients who are unresponsive to conventional therapy after suffering the systemic inflammatory response syndrome complicated by severe right ventricular failure following cardiac surgery.

Case report

A 33-year-old woman, with an echocardiographic diagnosis of a large atrial septal defect and right ventricular infundibular and pulmonary valvar stenosis, underwent surgical repair. This included closure of the atrial septal defect with an autologous pericardial patch, resection of all three dysplastic pulmonary valvar leaflets, and enlargement of the right ventricular outflow tract with a transjunctional pericardial patch without resection of any muscular bands. The patient was weaned easily from cardio-pulmonary bypass, and was transferred to the intensive care unit in stable haemodynamic condition. Due to a residual gradient of 75 millimetres of mercury, measured across the right ventricular outflow tract by echocardiographic interrogation on the first postoperative day, the patient was returned to the operating room for resection of residual muscle bands obstructing the right ventricular outflow tract, and placement of a larger pericardial patch further to widen the right ventricular outflow tract. After this second intervention, the postoperative course was complicated by a systemic inflammatory response syndrome, including fever at 38.5 degree Celsius, systemic hypotension, sinus tachycardia, oliguria, and need for mechanical ventilation. The count of white blood cells was 12,700 per cubic millimetre.

The patient initially received 3 litres of intravenous fluids and inotrops (Fig. 1) without any haemodynamic improvement. The cardiac output was measured by thermodilution and haemodynamic changes were continuously monitored.

Figure 1. Time related changes of haemodynamic parameters before and after the infusion of vasopressin. : vasopressin infusion started; ; vasopressin infusion stopped. The modified inotropic index* (Rosenzweig et al.) is equal to dopamine (micrograms per kilogram per minute) plus dobutamine (micrograms per kilogram per minute) plus epinephrine (100 times micrograms per kilogram per minute) plus norepinephrine (100 times micrograms per kilogram per minute) plus milrinone (10 times micrograms per kilogram per minute).

After 6 hours, we encountered signs of right ventricular failure, believed to be caused in part by the necessary resection of the multiple obstructing and hypertrophied muscle bands within the right ventricular outflow tract, and also by an increased pulmonary vascular resistance secondary to the severe inflammatory response after bypass, with capillary leak, pulmonary endothelial dysfunction and increased extravascular pulmonary water. At this point, the right atrial pressure had increased to 22 millimetres of mercury, and the right ventricular end-diastolic pressure was 17 millimetres of mercury. Left ventricular function seemed to be preserved, with the left ventricular ejection fraction being 52 pecent, and a pulmonary capillary wedge pressure of 11 millimetres of mercury.

We commenced treatment with vasopressin at a dose of 0.0003 units per kilogram per hour, which produced an immediate and sustained haemodynamic improvement (Fig. 1), as evidenced by an increase in systemic resistance, reduction in total pulmonary resistance and central venous pressure, and an increase in urine output from 1.5 to 5.6 millilitres per kilogram per hour. Subsequently, we were able to reduce all other inotropes (Fig. 1). The intravenous infusion of vasopressin was discontinued after 39 hours. The patient was then extubated on the fifth postoperative day, and was discharged from the intensive care unit on the tenth postoperative day. An echocardiogram performed prior to discharge from hospital confirmed complete closure of the atrial septal defect, showing only a mild residual gradient across the right ventricular outflow tract of 16 millimetres of mercury.