High-Altitude Pulmonary Edema (HAPE)

Abstract

Much of the clinical impact of acute altitude illnesses stems from fl uid accumulation in interstitial spaces and nowhere is this more apparent than in the lungs as the edema escapes into the alveoli to cause life-threatening hypoxemia. This chapter will update our knowledge of HAPE over the past decade about the vasculature, alveolar epithelium, innervation, immune response, and genetics of the lung in hypoxia, as well as prophylactic and therapeutic strategies to reduce the toll of this most common alpine life-threatening illness. 406extend to HPV, would predict greater HAPE susceptibility. Although HAPE can develop in sedentary persons, exercise [ 6 ] and its pulmonary hemodynamic consequences (discussed below) are important precipitating factors.Symptoms, signs, and physiologic changes in lung function typical of pulmonary edema [ 1 -3 , 7 ] evolve in 2-4 days after ascent, often preceded or accompanying AMS (see Chap. 20 ), but can occur later with further ascent. Arterial saturations can fall as low as 40 % and PaO 2 s in the low 20 mmHg range. HAPE in its severest stage with profound hypoxemia can lead to high-altitude cerebral edema [ 8 ]. Repeat occurrences of HAPE do not always involve infi ltrates in the same areas, which suggests that fi xed structural aspects of lung parenchyma or vessels do not account for the timing of edema or its locale [ 9 ]. A special exception is unilateral absence of a pulmonary artery, in which edema always occurs in the contralateral lung receiving the entire cardiac output [ 10 ].It has been suggested that many persons (50-75 %) may have subclinical HAPE that resolves spontaneously despite remaining at altitude [ 11 -13 ]. This incidence equals that of AMS, which itself can cause mild gas exchange impairment [ 14 ] by unknown mechanisms perhaps related to altered autonomic infl uences on the pulmonary circulation and/or airways leading to ventilation-perfusion mismatching. Subclinical HAPE may be considerably overestimated without radiography [ 15 ] because indirect measures of interstitial edema such as spirometry, closing volume, and/or transthoracic impedance can vary for other reasons related to mountaineering including intense exercise and increased cardiac output, cold/dry air-induced bronchoconstriction, and hypocapnia [ 16 ]. With radiographically mild HAPE, only modest abnormalities were detectable [ 15 ] suggesting many lung function parameters are not sensitive enough to detect small changes in interstitial fl uid and may require highresolution tissue density measurements by CT or MR imaging. Reentry HAPE occurs when longterm high-altitude residents return to high altitude following a brief low-altitude sojourn. It has a strong familial basis and affl icts children more than adults [ 17 ], perhaps due to a twofold greater magnitude of HPV in preteen children (age 6-9) compared to teenagers (age 14-16) when tested 40 h after ascent to high altitude [ 18 ]. PathophysiologyFrom its fi rst modern descriptions, pulmonary hypertension and HAPE have been inex...

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“…Studies should account for the potential effects of dietary nitrate and should include human population. Acts as a vasodilator, and directly stimulates angiogenesis and vasculogenesis Bartsch (1999) 52 Hackett et al, (2001) 53 Schoene (2004) 54 Schoene et al, (2001) 55 Swenson et al, (2002) 56 CONCLUSION: Synergistic effects of dietary (inorganic) nitrate originate from the 'nitratenitrite-nitric oxide (NO) mechanism'. Nitrate has potential therapeutic role on human health.…”

Evidence for and Against Genetic Predispositions to Acute and Chronic Altitude Illnesses

“…These high vascular pressures are believed to cause the extravasation of fluid from pulmonary capillaries to alveolar spaces, which impairs diffusion in the lung, causing severe hypoxemia (Maggiorini et al, 2001;Swenson et al, 2002). Accordingly, HAPE is characterized by fatigue, breathlessness, coughing, frothy sputum, inspiratory crackles, cyanosis, tachypnea, and tachycardia (Hackett and Roach, 2001;Schoene and Swenson, 2013). The presence of patchy alveolar infiltrates on radiographs is an objective marker for HAPE.…”

“…The onset of HAPE is generally two days after arrival at a new altitude (usually above 3000 m; Hackett and Roach, 2001;Schoene and Swenson, 2013). The risk of HAPE increases with ascent rate and the altitude attained.…”

“…Accordingly, we will focus on data obtained from genome-wide association studies (GWAS) rather than candidate gene association studies (CGAS), which were the primary source of data for previous reviews (MacInnis et al, 2010;Rupert and Koehle, 2006). The reader is directed elsewhere for reviews of basic genetic terminology (Attia et al, 2009a;MacInnis et al, 2011), genetic association studies (Attia et al, 2009b;2009c;Manolio, 2010), and the pathophysiology of altitude illness (Bartsch and Bailey, 2013;Bartsch and Swenson, 2013;Schoene and Swenson, 2013).…”

Risk of high altitude pulmonary edema and telomere length

“…HAPE is classified into various grades, varying from mild to severe, based on clinical profile, X‐ray findings and objective criteria such as heart rate and respiratory rate . Although not within the scope of the present work, the grading of cases of HAPE in their study based on severity and an analysis of the correlation of each grade with six SNPs in the telomere length‐related gene ACYP2 polymorphism could have resulted in a more valuable addition to the relatively new field of genetics in HAPE.…”