3. HPV

HPV is a mechanism that diverts blood flow away from areas of the lung where the alveolar oxygen tension is low, shunting it to better ventilated zones and improving the ventilation–perfusion ratio. (Elsewhere in the circulatory system, hypoxia always results in the vasodilatation of vascular beds.)

HPV is of little importance in health, but it is more significant in disease. It explains, for example, the upper lobe diversion characteristic of left ventricular failure, as blood in the congested and hypoxaemic lower parts of the lung is diverted away. It is significant during one-lung anaesthesia

this occurs via the constriction of small arterioles; it is not neurally mediated. - in denervated lungs (following transplantation). Nor is it mediated by humoral vasoconstrictors but rather by pulmonary mixed venous oxygenation and, more importantly, by alveolar oxygenation. Larger blood vessels may be affected globally, as in the fetal pulmonary circulation in which the low PaO2 reduces pulmonary blood flow to about 15% of the cardiac output.

Onset: this is within seconds of the decrease in PaO2, and lobar blood flow may halve within minutes from its value during normoxia. The phenomenon is biphasic, with the vascular resistance returning almost to baseline before the onset of a second phase of slower and sustained vasoconstriction that reaches a plateau at 40 minutes

Mediators: the mechanisms have not been fully identified. • Nitric oxide • Endothelin • O2 sensitive K channel The pulmonary vasculature is maintained in a state of active vasodilatation to which nitric oxide may contribute, and so suppression of endothelial nitric oxide production will lead to vasoconstriction. In addition, hypoxia stimulates production of the peptide endothelin, which is the most potent vasoconstrictor yet identified in humans. It is also known that pulmonary blood vessels have oxygen-sensitive potassium channels such that the membrane potential alters in response to hypoxia, with opening of calcium channels and smooth muscle contraction. This phenomenon is not seen in the systemic vasculature.

Influences: acidosis and hypercarbia potentiate HPV, while alkalosis either attenuates or abolishes it and causes pulmonary vasodilatation.

all inhalational anaesthetics inhibit HPV. The effect is dose-dependent and is similar for all the agents apart from nitrous oxide, whose action is less potent. The dose–response curve is of typical sigmoid shape; the ED50 is just under 2 MAC, and the ED90 is around 3 MAC. At 1.3 MAC, HPV is diminished by around 30%. Intravenous induction agents have little effect

Oxygen: a high FiO2 may inhibit HPV by maintaining higher PaO2 even in underventilated alveoli

Cardiac output: any factor which depresses cardiac output will reduce mixed venous PO2 and so may enhance HPV.

Drug effects: drugs such as calcium-channel blockers, sodium nitroprusside, glyceryl trinitrate, bronchodilators, nitric oxide and dobutamine all attenuate HPV. It is potentiated by cyclo-oxygenase inhibitors, propranolol and by the respiratory stimulant almitrine. (Although not used in the UK, it acts by stimulating carotid body chemoreceptors. It also enhances the effect of HPV in situations in which it is deficient