Inhaled NO

Inhaled NO relaxes smooth muscles in arteries and veins in a similar way to endogenous NO by activating soluble guanylate cyclase and increasing cyclic guanosine 3',5'-monophosphate. Since NO is inactivated by hemoglobin as soon as it enters the blood stream, the dilatory effect of low concentrations of inhaled NO is restricted to the pulmonary vasculature of ventilated lung areas (T.a.ble 2). Thus elevated pulmonary artery pressure is selectively decreased in various diseases. In addition, the ratio of PaO2to FiO2 may increase in patients with a high intrapulmonary shunt (Rossaint. .et.a[ 1993).

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Table 2 Advantages and disadvantages of inhaled NO

Table 2 Advantages and disadvantages of inhaled NO

In patients with acute respiratory distress syndrome, the increase in ratio of PaO2 to FiO2 and the decrease in pulmonary artery pressure may be associated with increases in right ventricular ejection fraction and a decrease in right ventricular volume. In contrast with intravenous epoprostenol, which has a similar but greater effect, inhaled NO does not usually increase cardiac output in this group of patients. However, in some patients suffering from severe acute respiratory distress syndrome, inhaled NO may cause an increased right ventricular ejection fraction which will be followed by a rise in cardiac index.

In congenital heart disease, pulmonary hypertension may result from increased pulmonary blood flow or from pulmonary venous obstruction resulting in hypertrophy and hyperplasia of pulmonary artery smooth muscle and pulmonary vasoconstriction. After corrective cardiac surgery the pulmonary vascular bed may be unable to regress sufficiently to accommodate the postoperative hemodynamic changes and this may lead to right ventricular failure. This is a common cause of death after surgical correction of congenital heart diseases with a left to right shunt. In order to determine the vasodilatory capacity of the pulmonary vascular bed and thereby predict the postoperative risk of life-threatening suprasystemic pulmonary hypertension, NO inhalation has been used during preoperative cardiac catheterization. Inhaled NO exhibits a far greater vasodilatory effect than hyperoxic breathing. Moreover, adding NO inhalation to the routine testing protocol for pulmonary vascular reactivity during preoperative cardiac catheterization allows identification of patients with preserved vascular reactivity who did not respond to infused epoprostenol or inhaled pure oxygen but did respond to inhaled NO. If preoperative inhaled NO produces pulmonary vasodilatation, this gas may be used to relieve severe postoperative pulmonary hypertension. Inhaled NO has recently been used to treat moderate and severe pulmonary hypertension in children undergoing open-heart surgery. In some cases NO inhalation caused not only a reduction in pulmonary artery pressure, but also an increase in pulmonary blood flow resulting in a simultaneous decrease in PaCO2, improvements in arterial oxygenation, progressive weaning from epinephrine (adrenaline), and reversal of oligoanuria.

In patients with pulmonary hypertension undergoing cardiac surgery, inhaled NO decreased pulmonary artery pressure and pulmonary vascular resistance but did not affect central venous pressure, cardiac output, or systemic hemodynamics. These observations are in agreement with those made in patients suffering from chronic pulmonary hypertension, demonstrating that inhalation of 40 ppm NO did not increase cardiac output despite a decrease in pulmonary vascular resistance and a constant central venous pressure. Inhaled NO does not, in general, appear to influence right ventricular function in patients with chronic pulmonary hypertension despite its effect on pulmonary vascular resistance. However, a small number will derive benefit. In patients receiving circulatory support with a ventricular assist device, 20 ppm NO decreased pulmonary artery pressure and pulmonary vascular resistance, as well as increasing PaO2, arterial pressure, and mixed venous oxygen saturation. These alterations may reflect improved right ventricular function and increased cardiac output from the natural heart. Thus inhaled NO may improve systemic hemodynamics when right ventricular failure and an elevated pulmonary vascular resistance are limiting factors.

Inhaled NO has also been evaluated in the pre- and postoperative treatment of patients receiving orthotopic heart transplantation. Pulmonary hypertension is a common preoperative feature. An increased pulmonary vascular resistance may induce right ventricular failure after implantation of the donor heart. Therefore the extent of the elevated pulmonary vascular resistance as well as the prospect of pharmacological treatment should be evaluated preoperatively in transplant candidates. If reversibility is shown, patients can be accepted for orthotopic heart transplantation; otherwise, heart-lung transplantation may be considered more suitable. NO inhalation has also been used as a bridge to heart-lung transplantation to manage right ventricular failure with concurrent systemic hypoperfusion. After heart transplantation, NO inhalation appears superior to epoprostenol infusion if pulmonary hypertension and right ventricular failure are associated with systemic hypotension.

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