野外與登山醫學-大氣中的氧氣佔比21%幾乎不變

2025-10-29 11:18AM

參考資料: 維基百科-Atmosphere of Earth

氧氣是綠色的線. 可以看到在100公里以上. 才發生銳減. 

這張圖片適用於海拔85公里以上高度

因此. 在聖母峰高度以下的空氣組成. 氧氣占比幾乎不變(約21%), 但隨海拔增加. 氣壓下降. 可供人體利用的有效氧氣濃度也下降. 

野外與登山醫學-高海拔肺水腫 2023更新 from StatPearls-High Altitude Pulmonary Edema

2025-10-29

筆記: High Altitude Pulmonary Edema- 同一作者與標題. 2017年的版本

統一名詞翻譯
Dexamethasone 類固醇(地塞米松), 高海拔疾病的研究或文獻. 提到的類固醇幾乎都是指 dexamethasone(類固醇種類很多,不僅地塞米松一種)
HAI= high altitude illness 高海拔疾病(等於高山症)
AMS =acute mountain sickness 急性高山病(不等於高山症)
HAC=E high altitude cerebral edema 高海拔腦水腫
HAPE =high altitude pulmonary edema 高海拔肺水腫
Acetazolamide 丹木斯(乙酰唑胺). 一種利尿劑

Nifedipine 硝苯地平, 是一種降血壓藥物, 分類上屬於鈣離子阻斷劑CCB, 於1969年被合成，1981年在美國核准上市。  

High Altitude Pulmonary Edema(Last Update: July 17, 2023.)
Jacob D. Jensen; Andrew L. Vincent.

重點整理

1. HAPE發生於海拔2500公尺以上. 但曾有海拔2000公尺就發病的案例, 通常發生在抵達高海拔地區第2-5天. 

2. HAPE發生率與個人健康無關. 但與個人體質相關, 發生過HAPE之後. 再次復發(相似海拔及上升速率)機率達60%

3. HAPE患者, 有50%伴隨AMS, 有14%伴隨 HACE

4. HAPE患者血氧飽和度通常低於預期值10%(不同海拔.不同氣壓的預期值不同)
5. HAPE診斷通常要有兩個以上的症狀及兩個以上的徵象(首次出現於 1991
The Lake Louise Consensus on the Definition of Altitude Illness, 但並非所有文獻都這樣建議)

6. HAPE處置. 建議下降海拔1000公尺以上. 藥物或氧氣可輔助用於下降過程. 但並非用藥/給氧治療都能改善. 治療死亡率11%. 不治療死亡率50%

7. 若有充足氧氣可使用. 建議維持血氧濃度90%以上. 

8. 攜帶式加壓艙PAC可使用於無法立即下撤的患者. PAC可模擬海拔下降1000公尺的環境. 但離開PAC之後HAPE可能再發. 

9. Nifedipine 硝苯地平可作為輔助治療. 但若能下降或給氧. 不應使用 nifedipine 作為唯一治療選項. 

10. 犀利士或威而鋼可用於預防HAPE. 但預防效果並沒有優於 nifedipine. 因此預防性藥物建議首選為 nifedipine. 

11. 犀利士治療HAPE有少量研究證實. 但仍缺更大規模研究. 威而鋼目前無研究證明能治療HAPE

12. 目前並無足夠研究證明類固醇.丹木斯.氣管擴張劑.其他利尿劑能用於治療HAPE

下面中文使用google自動翻譯

(High Altitude-google翻譯成高原..我改成高海拔)

簡介
高海拔肺水腫 (HAPE) 是一種致命的嚴重高山症。 HAPE 是一種繼發於缺氧的非心源性肺水腫。它的臨床診斷特徵是疲勞、呼吸困難和勞力性乾咳。如果不及時治療，它會發展為靜止呼吸困難、羅音、發紺，未治療的HAPE死亡率高達 50%。

病因
與其他與高海拔疾病一樣，HAPE 發生在 2500 公尺以上的高度，但也可能發生在低至 2000 公尺的高度。危險因子包括由於低氧通氣反應 (hypoxic ventilatory response. HVR) 導致的個體易感性、達到的海拔高度、快速上升速度、男性、使用安眠藥、攝入過量鹽、環境寒冷溫度和劇烈體力勞動。導致肺血流量增加、肺動脈高壓、肺血管反應性增強或卵圓孔未閉等先前存在的疾病可能更容易發生 HAPE。

流行病學
HAPE 的嚴重程度取決於多種因素，包括海拔、初步識別和處理以及是否能夠獲得醫療服務。在 4500 公尺的高度，發病率為 0.6% 至 6%，在 5500 公尺的高度，發病率為 2% 至 15%，上升時間越快，發病率越高。曾經罹患 HAPE 的人復發率高達 60%。個人的健康程度並未被證實是保護因子。接受治療的死亡率可高達 11%，未接受治療的死亡率則高達 50%。高達 50% 的病例可能伴隨急性高山病 (AMS) ，高達 14% 的病例伴隨高海拔腦水腫 (HACE)。
HAPE的發生是肺血管系統對缺氧的一種反應。在高海拔環境下，人體會透過過度換氣來應付缺氧。這被稱為缺氧通氣反應 (HVR)。這種反應因人而異，並且具有遺傳因素。高海拔適應性是一種有趣的現象，通常發生在長期生活在高海拔的人身上，但對於前往高海拔的人來說並不常見。然而，了解組織氧氣輸送的原理有助於理解人們從高氣壓過渡到高海拔低壓環境時所產生的影響和適應性。海平面每公升空氣中的氧氣濃度為 21%。在 4000 公尺（約 13,200 英尺）的高度，此濃度也相同，但由於該海拔高度的氣壓降低，與海平面相比，可用氧分子數量僅剩下 63%。因此，為了充分地向組織輸送氧氣，特別是那些最需要氧氣進行有氧代謝的組織（大腦、心臟、肺、腎臟），必須進行某些適應。

有四種潛在的適應性措施可以克服​​高山缺氧的限制：(1) 靜止通氣，(2) 缺氧通氣反應，(3) 動脈血紅素氧飽和度，以及 (4) 血紅素濃度。

對安第斯山脈和西藏山脈人群的研究表明，儘管處於同一海拔高度，但不同群體之間的適應性變化不同。

西藏人群的前兩個特徵平均比安地斯山脈的艾馬拉人高出 0.5 個標準差，後兩個特徵則低出一個標準差。這項研究表明，同一海拔高度的不同人群適應高海拔壓力的方式存在遺傳傾向。

對於那些短期前往高海拔地區的人來說，每分鐘通氣量往往是來自低海拔地區的健行者適應環境的機制。一般來說，促紅血球生成素 EPO 水平需要 1 到 2 週的時間才能升高到足以引起造血和循環血紅蛋白增加的程度。當人們進入較高海拔時，每分鐘通氣量幾乎會立即增加，並隨之發生呼吸性鹼中毒。這會導致氧解離曲線左移（血紅素對氧的親和力增加）。作為對此機制的反應，腎臟開始增加質子的重吸收，從而穩定血液 pH 值。紅血球 2,3-DPG 水準在第 2 天和第 3 天開始升高。然後，血紅素-氧解離曲線右移（血紅素對氧的親和力降低）。這使得氧氣能夠更充分地輸送到組織，特別是由於攀爬和/或徒步旅行的勞累而承受更大壓力的肌肉組織。如果由於遺傳易感性或鎮靜劑導致 HVR 減弱，將導致進一步缺氧，從而引起不均勻、過度的缺氧性肺血管收縮 (HPV)。這種肺血管收縮會導致受影響肺泡的灌注增加，從而增加靜水壓力/壓力，進而增加血氣屏障的機械應力。血氣屏障受損會導致毛細血管通透性增加，並隨後導致不均勻的肺水腫。這種水腫的形成會阻礙氧氣運輸，導致HPV感染範圍更廣、病情惡化。 HPV反應引起的交感神經刺激和循環血管收縮劑會導致血管收縮，加重肺動脈高壓，並升高毛細血管壓力。如果個體缺乏對這些器官層面變化的先天適應能力，或未能識別和治療這種疾病，病情將持續存在並持續惡化。

病史和身體檢查
HAPE通常發生在抵達高地後 2 至 5 天。其發病隱匿，表現為乾咳、運動耐受性下降、胸痛及勞力性呼吸困難。如果不治療，病情可能發展為靜止性呼吸困難和嚴重的勞力性呼吸困難。咳嗽時可能咳出粉紅色泡沫痰或帶血痰。患者也可能出現羅音或哮鳴音、中樞性紫紺、呼吸急促和/或心跳過速。 SpO2 通常比該海拔預期值低 10%，考慮到患者的低氧血症程度和 SpO2 值（通常在 40% 至 70% 左右），患者的病情通常比預期要好。

評估
HAPE 的臨床診斷至少包括以下兩種症狀或主訴：胸悶或胸痛、咳嗽、靜止呼吸困難和運動耐受性下降。還可能有以下兩種檢查結果：中央發紺、囉音/哮鳴音、心跳過速和呼吸急促。如果可以，胸部 X 光檢查 (CXR) 可能顯示斑狀肺泡浸潤，縱膈/心臟大小正常，超音波可能顯示與肺水腫一致的 B 光。心電圖可能顯示電軸右偏和/或缺血的跡象。對於 CXR 顯示浸潤的患者，透過吸氧快速糾正臨床狀態和 SpO2 是 HAPE 的特徵。即使可以，實驗室檢查的作用也很有限，臨床醫生應始終考慮同時存在 AMS 和/或 HACE。

處置與治療
主要的治療方法是下降 1000 公尺或直到下降過程中症狀消失。

在下降過程中，務必盡量減少用力，因為用力可能會加重身體代謝需求引起的低氧血症，使患者病情惡化。

如果條件允許，嘗試氧氣治療可以改善症狀，並在下降過程中遇到技術困難或延誤時幫助患者緩解病情。

即便如此，無論氧氣供應情況如何，下降仍是主要的治療方法。如果條件允許，透過高流量鼻導管和麵罩輔助供氧，並將血氧飽和度滴定至高於 90% 是合理的替代方案。如果無法下降，也可以使用便攜式高壓氧艙，但這些通常需要持續護理，對於伴有急性高山病/高海拔腦水腫 (AMS/HACE) 並出現噁心嘔吐、幽閉恐懼症或精神狀態改變的患者來說，使用便攜式高壓氧艙可能比較困難。離開高壓氧艙後，症狀也有復發的風險。硝苯地平作為輔助藥物，可透過減少肺血管收縮來改善症狀，但如果可以選擇吸氧或下潛，則不應將其作為唯一治療手段。如果無法使用硝苯地平，可以使用磷酸二酯酶抑制劑，透過血管擴張來幫助降低肺動脈和毛細血管壓力。乙醯唑胺、β受體激動劑或利尿劑的作用尚未被臨床證實。

鑑別診斷：
氣喘、
支氣管炎
、黏液栓、
心肌梗塞、肺炎、氣胸、肺栓塞、上呼吸道感染。提升醫療團隊的療效

高海拔肺水腫 (HAPE) 是一種致命的嚴重高山症。 HAPE 是一種繼發於缺氧的非心源性肺水腫。其臨床特徵為疲勞、呼吸困難及勞力性乾咳。若不及時治療，病情可能發展為靜止呼吸困難、囉音、發紺，死亡率高達 50%。此病最好由內科醫生、運動醫學醫生、神經科醫生和心臟科醫生組成的跨專業團隊進行治療。預防的關鍵在於教育患者。一旦症狀消退，不再需要吸氧或血管擴張劑治療，且運動耐量較症狀發作時有所提高，患者可以考慮以適當的速度恢復上升。對於既往患有 HAPE 的患者，臨床醫生還應考慮使用硝苯地平、PDE 抑制劑或沙美特羅進行預防。

Introduction
High Altitude Pulmonary Edema (HAPE) is a fatal form of severe high-altitude illness. HAPE is a form of noncardiogenic pulmonary edema that occurs secondary to hypoxia. It is a clinical diagnosis characterized by fatigue, dyspnea, and dry cough with exertion. If left untreated, it can progress to dyspnea at rest, rales, cyanosis, and a mortality rate of up to 50%.

Etiology
Along with other illnesses related to altitude, HAPE occurs above 2500 meters but can occur at altitudes as low as 2000 meters. Risk factors include individual susceptibility due to low hypoxic ventilatory response (HVR), the altitude attained, a rapid rate of ascent, male sex, use of sleep medication, excessive salt ingestion, ambient cold temperature, and heavy physical exertion. Preexisting conditions such as those leading to increased pulmonary blood flow, pulmonary hypertension, increased pulmonary vascular reactivity, or patent foramen ovale may have a higher predisposition towards the development of HAPE.

Epidemiology
The severity of HAPE will depend on multiple factors including altitude, initial recognition and management, and access to medical care. At 4500 meters the incidence is 0.6% to 6%, and at 5500 meters the incidence is 2% to 15%, with faster ascent time correlating to a higher incidence. Those with a prior incidence of HAPE have a recurrence rate as high as a 60%. One’s level of fitness is not proven to be a protective factor. Mortality rate, when treated, can be as high as 11% and as high as 50% when untreated. Up to 50% of cases may have concomitant acute mountain sickness (AMS), and up to 14% will have concomitant high altitude cerebral edema (HACE).

Pathophysiology
The development of HAPE occurs as a response of the pulmonary vasculature to hypoxia. At altitude, the body responds to hypoxia by hyperventilation. This is known as the hypoxic ventilatory response (HVR). This response varies between individuals and has a genetic component. High altitude adaptation is an interesting phenomenon that regularly applies to individuals living at altitude for long periods of time but is not usual for those visiting altitude. Understanding the principles of tissue oxygen delivery, however, is useful when considering the effects and adaptations of those coming from higher barometric pressures to the lower pressures of high elevation. The concentration of oxygen in 1 liter of air at sea level is 21%. This concentration is the same at 4000 meters (~13,200 feet), but due to the decreased barometric pressure at this altitude, only 63% of the number of available oxygen molecules remain as compared to sea level. Thus, to adequately deliver oxygen to the tissues, particularly those that are most in need of oxygen for aerobic metabolism (brain, heart, lungs, kidneys), certain adaptations must occur.

There are four potential adaptations to overcome the constraints of high altitude hypoxia: (1) resting ventilation, (2) hypoxic ventilatory response, (3) oxygen saturation of arterial hemoglobin, and (4) hemoglobin concentration. Studies of populations in the Andes and Tibetian ranges and ranges have shown different adaptive changes between groups despite being at the same altitude. Those from Tibet had mean 0.5 standard deviations above that of the Aymara people of the Andes for the first two traits and a full standard deviation below for the latter two traits. This research suggests a genetic predisposition to how different groups of people at the same altitude may adapt to high altitude stress. For those traveling to a high altitude for a short period, minute-ventilation tends to be the mechanism by which trekkers from low altitude will acclimate. In general, it takes as much as 1 to 2 weeks for erythropoietin levels to increase enough to cause hematopoiesis and increased circulating hemoglobin. As one enters higher elevations, minute-ventilation increases almost immediately and respiratory alkalosis ensues. This causes a shift in the oxygen-dissociation curve to the left (increased affinity of oxygen by hemoglobin). In response to this mechanism, the kidneys begin increasing proton reabsorption which stabilizes the blood pH. RBC 2,3-DPG levels which begin to increase on days 2 and 3. Then, the Hgb-O2 dissociation curve shifts to the right (decreased affinity for O2 by hemoglobin). This allows for a more adequate delivery of oxygen to the tissues, particularly muscle tissues that may be under greater levels of stress due to exertion with climbing and/or trekking. If the HVR is blunted, due to genetic predisposition or sedatives, it will lead to further hypoxia causing a non-uniform, exaggerated hypoxemic pulmonary vasoconstriction (HPV). This pulmonary vasoconstriction then results in increased perfusion to affected alveoli, causing increased hydrostatic stress/pressure and thus increased mechanical stress on the blood-gas barrier. Damage to the blood-gas barrier results in increased capillary permeability and subsequent non-uniform pulmonary edema. This edema formation impedes oxygen transport, resulting in more widespread and worsening HPV. Sympathetic stimulation and circulating vasoconstrictors from the HPV response result in vasoconstriction, worsening pulmonary hypertension, and increasing capillary pressures. If an individual lacks innate adaptation to these organ level changes or the condition is not recognized and treated, the disease condition will persist and continue to worsen.

History and Physical
HAPE typically occurs 2 to 5 days after arrival at altitude. It has an insidious onset with a non-productive cough, decreased exercise tolerance, chest pain, and exertional dyspnea. Without treatment, it can progress to dyspnea at rest and severe exertional dyspnea. A cough may become productive of pink and frothy sputum or frank blood. The patient also may have rales or wheezes, central cyanosis, tachypnea, and/or tachycardia. SpO2 is often 10% less than expected for altitude, and the patient often will appear better than expected given their level of hypoxemia and SpO2 value, which typically resides around 40% to 70%.


Evaluation
HAPE's clinical diagnosis would include at least two of the following symptoms or complaints: chest tightness or pain, cough, dyspnea at rest, and decreased exercise tolerance. It also would have two of the following exam findings: central cyanosis, rales/wheezes, tachycardia, and tachypnea. If available, CXR may show patchy alveolar infiltrates with normal-sized mediastinum/heart, and ultrasound may show B-lines consistent with pulmonary edema. ECG may show signs of right axis deviation and/or ischemia. In a patient with infiltrates on CXR, rapid correction of clinical status and SpO2 with supplemental oxygen is pathognomonic of HAPE. Even if available, labs are of limited utility, and the clinician should always consider concomitant AMS and/or HACE.

Treatment / Management
The mainstay of treatment is to descend 1000 meters or until there is a resolution of symptoms with the descent. During the descent, it is important to minimize exertion as exertion may increase hypoxemia from metabolic demands of the body and worsen an individual’s condition. If available, a trial of oxygen therapy may ameliorate symptoms and help temporize the patient if the descent is technically difficult or delayed. That said, the mainstay of treatment remains descent, regardless of oxygen availability. Supplemental oxygen via a high-flow nasal cannula and facemask titrated to Sp02 greater than 90% is a reasonable alternative when available. Portable hyperbaric chambers also may be used when descent is not possible, but these typically require constant care and may be difficult for individuals experiencing nausea or vomiting, claustrophobia, or altered mental status from concomitant AMS/HACE. There also exists the risk of recurrence of symptoms after exiting from the chamber. Nifedipine improves symptoms as an adjunct by decreasing pulmonary vasoconstriction but should not be used as the sole therapy if oxygen or descent are options. Phosphodiesterase inhibitors may be used to help to decrease pulmonary artery and capillary pressure through vasodilation if nifedipine is unavailable. There is no clinically proven role for acetazolamide, B-agonist, or diuretics.

Differential Diagnosis
Asthma
Bronchitis
Mucous plugging
Myocardial infarction
Pneumonia
Pneumothorax
Pulmonary embolism
Upper respiratory tract infection

Enhancing Healthcare Team Outcomes
High Altitude Pulmonary Edema (HAPE) is a fatal form of severe high-altitude illness. HAPE is a form of noncardiogenic pulmonary edema that occurs secondary to hypoxia. It is a clinical diagnosis characterized by fatigue, dyspnea, and dry cough with exertion. If left untreated, it can progress to dyspnea at rest, rales, cyanosis, and a mortality rate of up to 50%. The condition is best managed by an interprofessional team that consists of an internist, sports physician, neurologist and cardiologist. The key to prevention is education of the patient. Individuals may consider resuming ascent at an appropriate rate once symptoms resolve and they no longer require oxygen or vasodilator therapy and have an increased exercise tolerance compared to symptom onset. Clinicians also should consider nifedipine, PDE inhibitors, or salmeterol as prophylaxis for those with a prior incidence of HAPE.