Hypoxic pulmonary vasoconstriction: clinical implications

Abstract

@ERSpublicationsHPV is an adaptation for fetal development and affords some advantage in optimising gas exchange in adults http://ow.ly/Uh54oHypoxic pulmonary vasoconstriction (HPV) and its mechanism of action continue to be of great interest to clinicians and physiologists. SOMMER et al. Fetal origin of HPVHPV originates in the fetus [3]. Vasomotor tone can be detected in the human fetal pulmonary circulation in the last trimester of pregnancy [4]. HPV contributes significantly to the high pulmonary vascular resistance (PVR) in the fetus (only 10-15% of right ventricular outflow goes to the lungs) [5], mainly because pulmonary artery and alveolar fluid oxygen tension (PO 2 ) levels are considerably lower (18 mmHg) than they are after birth; also, the fetal pulmonary arteries are more muscularised (this regresses in the neonatal period). The low PO 2 in the fetal pulmonary artery, versus that in the fetal aorta, is due to "streaming" in the right ventricle, whereby oxygen-poor blood from the tissues enters via the superior vena cava and is directed to the pulmonary circulation; oxygen-enriched blood (via the placental vein) enters from the inferior vena cava and passes into the left ventricle via the foramen ovale.At birth, the lungs expand with air from the first breath, alveolar liquid is reabsorbed, the alveolar PO 2 (PAO 2 ) increases dramatically, which reduces HPV, and vasodilators such as nitric oxide and prostacyclin (also called prostaglandin I 2 (PGI 2 )) are synthesised and released [5]. All these factors combine to reduce PVR five-fold (for a review, see GAO and RAJ [3]). Pulmonary artery pressure falls from about 50 to 20 mmHg and pulmonary blood flow increases three-fold. This remarkable transition at birth is, in large part, due to the inhibition of HPV. HPV clearly has a role to play in the latter third of fetal development in helping to adjust the distribution of the combined ventricular outputs in the most favourable manner for organ growth and development. HPV occurs in almost all vertebrates [1]. How useful or otherwise is its persistence into post-natal life? HPV in the normal post-natal lungIn adult mammals, the pulmonary arteriolar ( pre-acinar) vessels constrict when local PAO 2 is reduced, and dilate when it increases. This occurs over a wide PAO 2 range, from 40 to 150 mmHg [6,7]. The response is attenuated by local hypocapnia [8] or a rise in pulmonary artery pressure [9], and is augmented by a rise in local carbon dioxide tension (PCO 2 ) [8]. In experimental models (dog [10] or sheep [8]), inspired PO 2 was lowered in one or more lobes and blood flow diversion measured. With a calculated reduction in alveolar ventilation (V′A) of 70%, affecting 10-20% of total lung units, HPV reduced local blood flow by 45-50% [8,10]. If 50% of the lung was "hypoxic", the reduction was 30% [8], presumably because of the attenuating

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Comparative study of cardiac function between two populations in Latin America using the transthoracic echocardiogram: Atahualpa, Ecuador, and Mexico City, Mexico

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Estudio comparativo de la función cardíaca en dos poblaciones de América Latina mediante el ecocardiograma transtorácico: Atahualpa, Ecuador y Ciudad de México, México

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