Hypoxic pulmonary vasoconstriction

Hypoxic pulmonary vasoconstriction (HPV) was first described by von Euler and Liljestrand in 1946 and is still the only known vascular feedback control mechanism in the lung. This technique results in a redistribution of blood flow away from poorly ventilated areas into better ventilated regions, thus reducing shunt. HPV functions as a local mechanism that acts in response to alveolar hypoxia but in the smallest areas of the lung, making it an important mechanism in all situations where ventilation perfusion mismatch occurs. To be effective, HPV needs normal pulmonary areas into which blood flow can be diverted. This explains why the efficacy of the treatment depends on the area that is vasoconstricted. The effect on PaO2 is maximal when the amount of the hypoxic lung ist 30-70%. If the area in vasoconstriction is small, the influence on PaO2 is negligible. On the other hand, when most of the lung is hypoxic, there is no significant normoxic region to which the hypoxic region can divert flow. In that case it does not matter, in terms of PaO2, whether the hypoxic region has active hypoxic pulmonary vasoconstriction or not. In this situation HPV becomes a rather detrimental mechanism, because it causes an increase in pulmonary arterial pressure. At some stage a turning point, where the gain in PaO2 is lost due to an increase in right ventricular afterload, inducing a decrease in CO. The reaction is diminished by exogenous manipulations, drugs (inhalation anesthetics, direct vasodilators), endotoxin, very low PaO2 values, vasodilating mediators and changes in the acid-base balance. Acidosis and alcalosis inhibit HPV. Factors like spontaneous or mechanical ventilation, PEEP, open or closed chest, and the type of hypoxia (atelectasis or nitrogen) have no influence on HPV. The small arteries, those less than 500 mu m in diameter, were identified as the location of the hypoxic constriction. Pulmonary vascular smooth muscle cells in pure culture reversible and repeated constriction. Examination of a histological lung section emphasizes that the small arteries are closely surrounded by alveoli gas on the outside and by mixed venous blood on the inside. Thus, the response is believed to be accounted for by each smooth muscle cell in the pulmonary arterial wall responding proportionally to the local oxygen tension in its vicinity and depending on alveolar as well as mixed venous oxygen pressure. The biochemical intracellular mechanism remains unknown.