Role of pulmonary vasodilators in pulmonary hypertension

The most obvious effect of pulmonary hypertension is that it increases the right ventricular pressure, workload, and oxygen consumption, and so may lead to right ventricular failure. As the blood flow to the right ventricle occurs during both systole and diastole it is important to maintain a high systemic pressure to minimise myocardial ischaemia. A second problem resulting from a high pulmonary artery pressure is that it may cause high pressure pulmonary oedema by increasing the pressure in the precapillary vessels. Pulmonary venous hypertension also causes oedema and in both situations severe arterial hypoxaemia may result. Pulmonary embolism and other conditions causing chronic hypertension may cause a maldistribution of blood flow as a result of changes in arteriolar resistance. Localised reductions in flow result in non-perfused alveoli and an increase in alveolar dead space, but the concomitant increases in pressure may also oppose the effects of hypoxic vasoconstriction, which redistributes flow away from underventilated areas of lung, and so may also increase arterial hypoxaemia.

It will be apparent that there are many causes of pulmonary hypertension, and that a number may be present in any one patient. For example, in chronic obstructive airway disease the hypertension may be caused by alveolar hypoxia and hypercapnia, destruction of the vascular bed, polycythaemia (which increases blood viscosity), gas trapping, and water retention (which increases the static pressure throughout the circulation). Although little can be done to alter the size of the vascular bed, all the other causes are amenable to treatment. The effects of treatment will, however, depend on the magnitude and reversibility of the factors involved in each patient. Similarly in ARDS it seems probable that in the early stages pulmonary hypertension is predominantly caused by vasoconstriction from hypoxia and endogenous mediators, augmented by a reduction in the vascular bed as a result of alveolar collapse, and obstruction of small vessels by leucocytes, although in the later stages medial hypertrophy, thrombosis, and interstitial fibrosis dominate the scene. Again, the relative importance of each factor in the individual patient is difficult to determine. Many of the putative mediators are very short lived and difficult to measure, and there is no good animal model of ARDS. As a number of therapeutic strategies currently employed are designed to reduce pulmonary vasomotor tone, it is necessary to consider some of the implications of this type of therapy.

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