Abstract
In a normal individual, pulmonary arterial blood is diverted from alveoli that are not being ventilated and perfuses the alveoli that are being ventilated [1, 2]. The mechanism that is responsible for this physiological shunt in blood flow is called hypoxic pulmonary vasoconstriction (HPV). When the PaO2 falls, the smooth muscle of the pulmonary arterioles contracts. The only non-oxygenated blood that enters the pulmonary veins is from the bronchial and thebesian vessels with this perfect match of ventilation and perfusion [3, 4]. With atelectasis, airway obstruction, alveolar edema and abnormalities of nitric oxide (NO) production, there can be a disruption of the pulmonary microcirculation. We will discuss the physiological processes that are responsible for HPV and how they can be disrupted by various pulmonary problems commonly encountered in the intensive care unit (ICU).
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Traber, D.L., Traber, L.D. (2002). Hypoxic Pulmonary Vasoconstriction and the Pulmonary Microcirculation. In: Vincent, JL. (eds) Intensive Care Medicine. Springer, New York, NY. https://doi.org/10.1007/978-1-4757-5551-0_8
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DOI: https://doi.org/10.1007/978-1-4757-5551-0_8
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