High Altitude Pulmonary Edema: Hemodynamic Aspects

Abstract

Over 30 years ago hemodynamic studies on patients with high altitude pulmonary edema (HAPE) excluded the prior contention that the basic cause was left ventricular failure and correctly implicated the pulmonary circulation as the culprit. Physiological studies during the acute stage have revealed a normal pulmonary artery wedge pressure, marked elevation of pulmonary artery pressure, severe arterial unsaturation, and usually a low cardiac output. Pulmonary arteriolar (pre-capillary) resistance was elevated. A working hypothesis of the etiology of HAPE suggests that hypoxic pulmonary vasoconstriction is extensive but not uniform. The result is overperfusion of the remaining patent vessels with transmission of the high pulmonary artery pressure to capillaries. Dilatation of the capillaries and high flow results in capillary injury with leakage of protein and red cells into the alveoli. While hypoxic vasoconstriction appears to be the major cause of patchy vascular obstruction the occurrence of thrombi in the pulmonary vessels may also play a role in more severe and advanced cases. The above concept of the mechanism of HAPE has been further supported by animal studies showing pulmonary edema occurring when increased pressure and flow is produced in a portion of the pulmonary vascular bed. Clinical studies which have supported this concept include the susceptibility to HAPE of patients with an absent pulmonary artery, pulmonary edema occurring in pulmonary embolism, following removal of pulmonary arterial thrombi and following balloon dilatation of stenoses of branches of the pulmonary artery. In addition to those hemodynamic factors an increase in capillary permeability due to cell derived products resulting from capillary wall injury is an important aspect of edema formation.

Role of posterior hypothalamus in hypobaric hypoxia induced pulmonary edema

“…Even though ventilating these victims with oxygen mixed with nitric oxide (NO), administering acetazolamide and moving them to low altitudes has reduced the mortality rate (Forwand et al, 1968;Evans et al, 1976;Grissom et al, 1992;Anand et al, 1998), the pathogenesis of HAPE is still under intense investigation. Hypoxic pulmonary vasoconstriction is considered to be a prime factor in HAPE (Hultgren, 1997;Eldridge et al, 2006). Hypoxia per se causes constriction of small resistance pulmonary arteries and raises pressure in the pulmonary vasculature (Jensen et al, 1992;Sartori et al, 2007).…”

Obstructive sleep apnea at high altitude

“…Миррахимовым (1971) первично-высотной (или высокогорной) ЛАГ. Повышение ЛАД происхо-дит преимущественно за счет увеличения легочного сосудистого сопротивления, которое на высоте более 3000 м достигает уровня, вдвое превышающего норму [19][20][21]. У аборигенов высокогорья легочное сосудистое сопротивление возрастает обычно значи-тельно и ведет к закономерному формированию ЛГ с последую-щей гипертрофией правого желудочка (ГПЖ) сердца, а иногда и правожелудочковой недостаточностью.…”

Physiology in Medicine: Acute altitude exposure in patients with pulmonary and cardiovascular disease

“…It is postulated that uneven HPV elevates pressure in pulmonary capillaries, leading to stress failure (38). The factors that have been associated with an increased genetic susceptibly include a strong HPV response, abnormal increase in pulmonary artery pressure, and a reduced hypoxic ventilatory response (22,31,33).…”