Secondary pulmonary arterial hypertension

Secondary pulmonary arterial hypertension may occur after major surgery and during chronic obstructive lung disease, pulmonary thromboembolism, acute respiratory distress syndrome, and septic shock. Occasionally, endstage cystic fibrosis or interstitial lung disease is responsible for decompensation of a cor pulmonale. In selected cases, pulmonary hypertension during decompensated chronic obstructive lung disease and acute respiratory failure may limit the circulatory changes adaptive for hypoxemia. In fact, hypoxic vasoconstriction in the lung is a mechanism for maintaining arterial oxygenation in poorly ventilated areas of diseased lungs. Nevertheless, this may lead to right ventricular afterload mismatch and a limitation of cardiac output reserve, whereas, in contrast, a rise in cardiac output may be necessary to maintain tissue O2 delivery in face of hypoxemia. Hence vasodilators, including nitrates, phosphodiesterase inhibitors, prostaglandins, hydralazine, ketanserin, calcium antagonists, and a-blockers, have been used in attempts to attenuate pulmonary hypertension selectively and unload the right heart. Epoprostenol appears to be a non-selective vasodilator that may lower pulmonary artery pressure and arterial oxygenation and may not increase tissue oxygen delivery. In contrast, prostaglandin E1 may have greater pulmonary vascular selectivity and less inhibitory effect on hypoxic vasoconstriction. Its administration in decompensated chronic obstructive lung disease may result in amelioration of pulmonary hypertension and increased cardiac output and tissue oxygen delivery.

Pulmonary embolism

Vasodilator therapy has been studied in animals with acute pulmonary embolism, but is not routine in patients ( Prewitt 1987). In contrast, vasodilators have been tried

, with varying responses, in patients with chronic pulmonary hypertension on the basis of recurrent emboli.

Septic shock and acute respiratory distress syndrome

During sepsis and acute respiratory distress syndrome, pulmonary vascular changes are thought to contribute to the diminished ability of the right heart, in the face of increased afterload, to generate a sufficiently high cardiac output, particularly during fluid loading, to meet increased tissue requirements in some patients ( Prewitt.. 1987). In animal studies, vasodilators have been used in attempts to lower the elevated pulmonary artery pressure during sepsis or endotoxemia ( Prew.itt . . .11987). In humans, pulmonary hypertension can be ameliorated to some extent with the serotonin antagonist ketanserin, even without a rise in the venous admixture of oxygen, suggesting a role for serotonin in the pulmonary vascular changes during human acute respiratory distress syndrome. The use of (non-selective) nitrovasodilators may only partly benefit the patient, even though they may effectively ameliorate pulmonary hypertension and unload the right heart, since tissue oxygen delivery may not increase by a limited rise in cardiac output and impaired arterial oxygenation.

Vasodilating prostaglandins have been used in attempts at selective dilatation of the pulmonary vessels ( Prewitt . . .1987). Prostaglandins may increase cardiac output, dilate pulmonary blood vessels, and maintain or increase PaO2. Side-effects of this type of drug include arterial hypotension, possibly associated with relatively poor pulmonary extraction of these drugs in critically ill patients with a damaged lung vasculature during sepsis and acute respiratory distress syndrome. Although prostaglandin E1 may have greater selectivity than epoprostenol in lowering pulmonary vascular pressures in chronic obstructive lung disease, this selectivity may be lost when the pulmonary (micro)vasculature has been damaged during sepsis and the acute respiratory distress syndrome. Other major side-effects of vasodilating prostaglandins are their immunomodulating properties, which may limit the inflammatory response in the lungs and thereby increase pulmonary gas exchange and patient survival. These immunomodulating properties mainly consist of inhibition of platelet and neutrophil activation and aggregation. Moreover, lowering pulmonary vascular pressure may help to limit microvascular fluid filtration and edema formation. For these reasons, clinical trials have been performed in patients with acute respiratory distress syndrome to evaluate the effect of prostaglandin E 1 on pulmonary variables and outcome. The effect of prostaglandin E1 on survival in acute respiratory distress syndrome remains controversial, however, since the lifesaving effects reported in early studies could not be reproduced. Later studies showed no beneficial effect of he drug on hemodynamics, oxygen balance, organ function, and survival in acute respiratory distress syndrome.

Postoperative problems

Major cardiopulmonary and vascular surgery may result in pulmonary vascular damage and hypertension. Various drugs to ameliorate this response have been evaluated, including nitroprusside, ketanserin, and prostaglandin E . but none of them has reached routine status (PiewitL1987). The pulmonary venous admixture of oxygen may increase with nitroprusside and decrease with ketanserin during similar vasodilation after major valvular surgery.

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