Pulmonary capillaries contribute approximately 40 per cent, arteries 50 per cent, and veins 10 per cent to total pulmonary vascular resistance. Only arteries and veins actively regulate their diameters through smooth muscle cells. Physiologically, a balance exists between vasodilating agents (e.g. prostacyclin, nitric oxide) and vasoconstricting agents (e.g. thromboxane, endothelins, serotonin). In health the effects of vasodilators predominate, keeping pulmonary vascular tone low. Any increase in vasoconstrictor activity and/or decrease in vasodilator activity will cause pulmonary vasoconstriction.

Small pulmonary arteries, arterioles, and probably venules constrict as a response to alveolar hypoxia. (The problem is actually more complex. In pulmonary arteries of diameter greater than 500 pm, vascular tone is determined by arterial PO2, with maximum hypoxic pulmonary vasoconstriction occurring at 40 to 50 mmHg (5.3-6.6 kPa). In contrast, vessels of diameter less than 500 pm mainly respond to local PO2, i.e. the gradient between alveolar and mixed venous PO2.) This mechanism is called hypoxic pulmonary vasoconstriction and its molecular basis remains unclear. Hypoxic pulmonary vasoconstriction prevents non-ventilated alveoli from being perfused, thereby reducing intrapulmonary shunt and maintaining PaO2. It is particularly active in the presence of profound hypoventilation (e.g. respiratory drive impairment, sleep apnea, neuromuscular disorders) and/or ventilation-perfusion mismatch (e.g. acute respiratory distress syndrome, chronic airflow limitation).

Sleep Apnea

Sleep Apnea

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