野外與登山醫學: Summary of WMS Practice Guidelines 2024 Update 高海拔疾病預防-診斷-治療

2025-10-31 10:09AM

寫在前面, WMS高海拔疾病預防診斷治療指引是給醫師看的. 不是寫給一般民眾. 我會儘量將內容簡化讓大家能看懂

Summary of Wilderness Medical Society Practice Guidelines for the Prevention, Diagnosis and Treatment of Acute Altitude Illness: 2024 Update
George RodwayAndrew Luks－　2024年7月8日－Volume 41, Issue 3

注意. 有些文獻的風險等級是用於預測AMS發生機率. 這張圖是預測高海拔疾病發生率. 

(高海拔疾病包含AMS; AMS沒有包含其他高海拔疾病)

圖一 fig 1 

英文名詞/縮寫及中文翻譯

AAI= acute altitude illness 急性(高)海拔疾病

HAI=high altitude illness 高海拔疾病

AMS= acute mountain sickness 急性高山病

HACE=high altitude cerebral edema 高海拔腦水腫　

HAPE =high altitude pulmonary edema 高海拔肺水腫

高海拔疾病. 在不同文獻出現不同稱呼. 但都是指同一個疾病,  acute altitude illness 等於 high altitude illness 等於 altitude illness. 

建議大家在翻譯成中文時, 將AMS翻譯為急性高山病, 不要翻成急性高山症. 高海拔疾病儘量不要說成高山症. 原因是很多民眾會將高山症與急性高山症畫上等號. 導致用威而鋼預防AMS的謬誤

高山症等於AMS+HACE+HAPE+其他

高海拔疾病=高山症 high altitude illness 

高山症不等於急性高山症AMS

高山症不等於急性高山病AMS

下面中文使用GOOGLE自動翻譯

概論

前往海拔2500公尺以上的地區旅行有發生高海拔疾病AAI(acute altitude illness)的風險，包括AMS, HACE, HAPE. 雖然未適應高山環境的人在攀登到海拔2500公尺以上時會面臨高海拔疾病的風險，但由於個體對高海拔疾病的差異很大，在較低海拔也可能出現AAI。

為了指導臨床醫生並傳播最佳實踐知識，荒野醫學會（WMS）召集了一個專家小組，制定了基於循證醫學的急性高原病預防、診斷和治療指南。本文介紹了預防和治療方法，並針對每種急性高原症提出了建議。

AMS和HACE
從臨床角度來看，高海拔腦水腫是AMS的一種極其嚴重的類型；因此，可以同時採取針對這兩種疾病的預防和治療措施。

(可視為同一種疾病. AMS是早期. HACE是晚期)

AMS急性高山病/HACE高海拔腦水腫的預防
建議：預防AMS和高海拔腦水腫的方法應取決於前往高海拔地區個人的風險狀況（圖1）。首要任務是確保逐步上升到目標海拔。旅行者可以透過在中等海拔地區過夜來降低風險。例如，居住在海平面的居民前往海拔2800公尺以上的科羅拉多州度假區，可以在丹佛（海拔1600公尺）過夜。如果由於各種後勤因素導致旅行者無法逐步上升，則可以考慮藥物預防。在低風險情況下，通常不需要預防性藥物，但在中高風險情況下，除了逐步上升之外，還應考慮使用藥物（圖1）。在海拔3000米以上地區旅行時，每日睡眠海拔升高幅度不應超過500米，並且應每3-4天安排一天休息日（即不攀登至更高海拔的睡眠地點）。

丹木斯(乙醯唑胺)：丹木斯在預防急性高山病方面具有確切療效。對磺胺類藥物過敏者服用丹木斯有誘發過敏反應的風險，儘管這種風險極低。過去對磺胺類藥物有過敏性休克史或有史蒂文斯-約翰遜症候群病史者禁用丹木斯。丹木斯應在登山前一天開始服用，但即使在登山當天開始服用，仍然有效（表1）。

類固醇(地塞米松) Dexamethasone：地塞米松不像丹木斯那樣有助於適應高山環境，但它在預防AMS方面具有確切療效。只有在極高風險的情況下，例如軍事人員或搜救人員被空運到海拔 3500 公尺以上並立即進行體力活動時，才可考慮使用高於表 1 中建議劑量（每 6 小時 4 毫克）的劑量。如果使用超過 5-7 天，地塞米松應在一週內逐漸減量，而不是突然停藥。不建議兒童使用地塞米松預防AMS。地塞米松應在攀登前一天開始服用，但即使在攀登當天開始服用，仍然有效。

(類固醇種類很多. 目前高海拔研究最常用的是Dexamethasone. 其他類固醇, 例如  prednisolone 也有少量文獻說有效. 但研究證據不充足. 無法做結論)

消炎止痛藥NSAID布洛芬：在快速攀登過程中，布洛芬不建議用於預防AMS，其療效不如丹木斯或地塞米松（表 1）。但是，對於不願服用乙醯唑胺或地塞米松，或對這些藥物過敏或不耐受的人，可以使用布洛芬。

(非首選.不得以時可作為備用選項)

分階段攀登與預適應：專家小組不建議任何特定的預適應方案（即在高海拔旅行前反覆暴露於低氧環境）和分階段攀登方案（即在攀登至目標海拔前，先在中等海拔停留數日）作為預防AMS的手段。關於在低氧帳篷中進行常壓低氧暴露，只有在適當週數內定期進行足夠長時間（每天超過 8 小時）的暴露，才有可能帶來顯著的預適應益處。

其他選擇：

以下措施尚未被證實有效：

咀嚼古柯葉、

飲用古柯茶和其他古柯衍生產品；

「強制」或「過度」補水；

短期吸氧，例如前往氧吧或使用非處方氧氣輸送系統（透過吸入預充式小罐中的富氧氣體）；

其他非處方產品，例如粉末狀飲料沖劑、貼片和口服補充劑。

(利尿劑 furosemide 在2013年NEJM的高海拔疾病文獻中已經被剔除. 罹患HAPE的患者體內通常是脫水狀態. 因此利尿劑對於高海拔肺水腫無效. 且可能有害)

急性高山病/高海拔腦水腫(AMS/HACE) 的診斷
AMS的診斷是在非常特定的臨床背景下做出的，即未適應高海拔環境的低地居民在攀登至高海拔地區（通常高於 2500 公尺）後數小時至 3 天內出現不適症狀。診斷完全基於患者自述的症狀，因為身體檢查或實驗室檢查沒有特徵性發現。

AMS的症狀包括：頭痛、厭食、噁心、疲勞和頭暈。

根據更新後的路易斯湖AMS評分表（見表 2），這些指引強調頭痛在AMS診斷中的作用，而弱化睡眠障礙的重要性。

最佳的診斷方法是考慮旅行者的健康狀況和功能狀態。

在攀登至海拔高於 2500 公尺的地區後數小時至 3 天內感到不適和/或必須減少日常活動的人很可能患有AMS。

高海拔腦水腫 (HACE) 的診斷以腦病徵象(運動失調或神智改變)為先兆，包括共濟失調（通常是最早出現的臨床表現）和精神狀態改變。其他體徵包括冷漠、易怒、疲倦和無法自理，所有這些體徵都可能很輕微。未經治療的 HACE 可進展至昏迷。局部神經功能缺損並不常見，應考慮其他診斷。足跟到足尖行走可用於評估共濟失調，視乳頭水腫可確診為腦水腫。

建議的AMS/HACE 治療

方案：應注意排除症狀和體徵與 AMS 和 HACE 相似的疾病，例如腦血管意外、一氧化碳中毒、低血糖、低鈉血症、感染或創傷性腦損傷
。

高海拔肺水腫（HAPE ）的某些危急程度是根據對AMS的預測而定的，但兩種類型的AMS並不相同。任何程度的AMS或高海拔腦水腫（HACE）患者都應停止上升，並可能需要考慮下降，具體取決於病情嚴重程度和具體情況。 AMS患者症狀緩解後可恢復上升。如果症狀持續存在，切勿繼續上升或重新上升到先前達到的高度。對於任何疑似HACE患者，或儘管使用丹木斯或地塞米松治療，AMS症狀仍持續惡化的情況，都應開始下降。

對於中度至重度AMS/HACE，地塞米松被認為是比丹木斯可靠的藥物治療。如果下降不可行，也應使用補充氧氣或攜帶式高壓艙。

補充氧氣：如果條件允許，可透過鼻導管或面罩以足以緩解症狀的流量輸送氧氣，作為下降的合適替代方案。

當建議下降但不可行，或重症患者在下降過程中也應使用氧氣。血氧飽和度（SpO2）> 90% 通常足夠。

不應依賴短期使用非處方氧氣罐來達到此目的。

便攜式高壓艙：便攜式高壓艙可有效治療嚴重的高海拔疾病，但需要醫護人員持續照顧，且難以用於幽閉恐懼症或嘔吐的患者。

在許多情況下，患者病情可能會好轉，症狀緩解後即可協助撤離並下降。

在需要下降的情況下，使用便攜式高壓艙不應延誤下降。

丹木斯：應考慮使用丹木斯治療AMS（表 1）。

地塞米松：地塞米松是治療AMS非常有效的藥物。該藥物不能促進適應性訓練，因此應推遲進一步的上升，直到患者停藥且無症狀。大量的臨床經驗支持在 HACE 患者中使用地塞米松（表 1）。

高海拔肺水腫(HAPE) 

HAPE預防建議：

由於個體對高海拔的適應速度和生理反應差異很大，本文提出的上昇路線建議並不能保證所有高海拔旅行者都能預防 HAPE。

循序漸進的上昇路線是預防 HAPE 的主要方法；

上述針對AMS 和HACE 的預防建議也適用於 HAPE 的預防。

藥物預防僅適用於有 HAPE 病史的個體，尤其是多次發作者。

(不曾罹患 HAPE 的民眾不需要預防性服藥)

循序漸進的上升：上升速度與疾病發生率之間有明顯的相關性。建議採用循序漸進的上升方式來預防 HAPE。

Nifedipine 硝苯地平：硝苯地平是一種鈣離子阻斷劑，可促進血管擴張並降低肺動脈壓。應在上升前一天開始服用硝苯地平，並持續服用直至開始下降或在最高海拔停留 4 天，如果上升速度超過建議的上升速度，則可能需要持續服用長達 7 天（表 1）。

犀利士(他達拉非tadalafil)：對於已知易感且不適合服用硝苯地平的個體，他達拉非可用於預防高海拔肺水腫（HAPE）（表1）。

硝苯地平和他達拉非不宜同時使用。

(威而鋼相關研究比犀利士少. 不列為預防用藥建議)

預適應和分階段攀登：分階段攀登和預適應可能是預防HAPE的合理方法。然而，目前尚不確定達到預期效果所需的適度海拔暴露的強度和持續時間。

HAPE診斷

高海拔肺水腫 (HAPE) 的診斷需要非常特定的臨床背景——例如，未適應高原環境的低地居民攀登至海拔 ≥2500 公尺的高度——並依賴於一組特徵性症狀，包括活動性呼吸困難，且程度遠超以往在高海拔地區的經歷或同等高度下其他個體所經歷的呼吸困難。患者也可能出現乾咳、疲倦、虛弱和胸悶。隨著病情進展，患者在輕微活動或休息時即出現呼吸困難，並可能出現紫紺和咳出粉紅色泡沫痰。

如果條件允許，脈搏血氧飽和度監測可以確認是否存在與預期海拔高度不符的低氧血症。然而，在高海拔地區使用指尖血氧儀時必須格外謹慎，因為在高海拔地區，氧飽和度會隨著氧分壓的微小變化而迅速改變，且當動脈血氧飽和度低於 80% 時，儀器的準確性會下降。

在特定海拔高度下，正常的血氧飽和度可能無法精確地確定，應將其視為一個數值範圍，而非一個具體數值。因此，臨床決策不應基於一段時間內或個體間血氧飽和度的微小差異。

此外，應盡量減少導致測量誤差的因素，例如四肢冰冷、環境光線過強、血氧儀探頭不合適等。

也應考慮其他在高海拔地區引起呼吸道症狀的原因，例如氣喘、支氣管痙攣、肺炎、氣胸、肺栓塞、病毒性上呼吸道感染、心臟衰竭或心肌梗塞。高海拔肺水腫

高海拔肺水腫的治療

建議：如果懷疑或確診為HAPE，應在條件允許的情況下開始吸氧，並開始下降至較低海拔。如果下降不可行或延遲，則應繼續吸氧，或將患者置於便攜式高壓氧艙內。

發生高海拔肺水腫（HAPE）的患者，只有在HAPE症狀完全消退，且在休息和輕度運動時，無需吸氧和/或使用血管擴張劑治療，並能維持穩定的氧合狀態後，才能考慮進一步攀登更高海拔或再次攀登。

下降：

與AMS和HACE一樣，下降仍然是治療HAPE的最佳方法。

患者應嘗試下降至少1000米，或直至症狀消退。

下降過程中應盡可能減少體力消耗（例如，不攜帶背包或搭乘機動車、直升機或動物運輸），因為體力消耗會進一步增加肺動脈壓，加重水腫。

吸氧：

如有條件，在等待開始下降、無法下降以及重症患者下降過程中，應使用足夠的氧氣，使血氧飽和度（SpO2）達到90%以上或緩解症狀。

攜帶式高壓氧艙：

與急性高山症（AMS）和高海拔腦水腫（HACE）類似，當下撤不可行或延遲，或無法取得補充氧氣時，便攜式高壓氧艙可用於治療高海拔肺水腫（HAPE）。

硝苯地平(Nifedipine 鈣離子阻斷劑. 降血壓藥物)

當下撤不可能或延遲，且無法可靠地獲得補充氧氣或便攜式高壓氧治療時，應使用硝苯地平治療高海拔肺水腫（表1）。

磷酸二酯酶抑制劑：(犀利士; 威而鋼)

由於磷酸二酯酶抑制劑能夠擴張肺血管並降低肺動脈壓，因此在治療高海拔肺水腫方面具有充分的生理依據。因此，當下撤不可能或延遲，無法獲得補充氧氣或便攜式高壓氧治療，且無法使用硝苯地平時，可使用他達拉非或西地那非治療高海拔肺水腫。

(萬不得已才用威而鋼或犀利士治療 HAPE)

(在2024WMS更新的藥物表格並未將犀利士或威而鋼列入HAPE治療)

持續性呼吸道正壓通氣（CPAP）：

正壓通氣透過增加肺泡壁的跨壁壓來發揮作用，從而增加肺泡容積並改善氣體交換。當無法使用補充氧氣或肺血管擴張劑治療高海拔肺水腫（HAPE）時，或作為對單獨使用補充氧氣無反應的患者的輔助治療，可考慮使用CPAP。

合併HAPE和高海拔腦水腫（HACE）的患者：

對於合併神經功能障礙且在給予補充氧氣和氧飽和度改善後仍未迅速緩解的HAPE患者，應在治療方案中加入地塞米松，劑量與HACE的劑量相同（表1）。合併HAPE和HACE的患者，可使用硝苯地平或其他肺血管擴張劑，但需注意避免降低全身血壓。

圖1. 評估AAI風險。

Figure 1. Assessing the risk of acute altitude illness. 

病史和計​​畫攀登的特徵可用於評估攀登後發生急性高原病的風險。請在最能描述左側列中各項變數的方格內打勾。計劃攀登的風險由最右側打勾的列決定。此評估適用於未適應高原環境的人員。假設攀登從海拔低於 1200 公尺的海拔開始。先前急性高原病史並不一定意味著未來所有攀登都存在高風險，因為在後續行程中降低攀登速度或目標海拔可能有助於避免問題。透過確保適當緩慢的攀登速度，可以降低在任何給定海拔以上旅行的風險。既往急性高原病的嚴重程度可使用表 2 的資訊進行分級。

 AMS，急性高原病；HACE，高原腦水腫；HAPE，高原肺水腫。

表1. 預防及治療高海拔疾病的藥物建議劑量
1. 對於攀登至並停留於特定海拔高度的人員，到達目標海拔高度後，若遵循建議的攀登速度，則應繼續用藥2天；若攀登速度超過建議速度，則應繼續用藥2-4天。若攀登至目標海拔高度後立即下降，則可在開始下降後停止用藥。
2. 此劑量適用於低至中度風險的攀登情況。對於高風險的攀登情況，可考慮每日兩次，每次250毫克。海拔5000公尺以上的攀登，合適的劑量尚不清楚。 
3. 乙醯唑胺也可作為地塞米鬆的輔助藥物用於高山腦水腫的治療，但地塞米松仍是高山腦水腫的主要治療藥物。


4. 對於需要進行高原肺水腫預防的人員，若攀登至目標海拔並停留在該海拔，則在到達目標海拔後，若遵循建議的攀登速度，應繼續用藥4天；若攀登速度超過建議速度，則應繼續用藥4-7天。若攀登至目標海拔高度後立即下撤，則可在下撤開始後停止用藥。

表2. AMS分類

Introduction
Travel to elevations above 2500 m is associated with risk of developing one or more forms of acute altitude illness: acute mountain sickness (AMS), high altitude cerebral edema (HACE), and high altitude pulmonary edema (HAPE). Although unacclimatized individuals are at risk of high altitude illness when ascending to altitudes above 2500 m, it is possible to see acute altitude illness present at lower elevations due to a high degree of variability in responses to high altitude between individuals.

To provide guidance to clinicians and disseminate knowledge about best practices, the Wilderness Medical Society (WMS) convened an expert panel to develop evidence-based guidelines for prevention, diagnosis, and treatment of acute altitude illness. Preventive and therapeutic modalities are presented, and recommendations made for each form of acute altitude illness.

Acute Mountain Sickness and High Altitude Cerebral Edema
From a clinical standpoint, HACE represents an extremely severe form of AMS; therefore, preventive and treatment measures for the two disorders can be addressed simultaneously.

AMS/HACE Prevention
Suggested Approach: The approach to prevention of AMS and HACE should be a function of the risk profile of the individual traveling to high altitude (Figure 1). The first priority should be ensuring gradual ascent to the target elevation. Travelers can lower their risk by sleeping one night at an intermediate altitude. For example, sea level residents traveling to Colorado resort areas over 2800 m can spend one night in Denver (1600 m). If travelers are unable to ascend gradually due to various logistical factors, pharmacologic prophylaxis can be considered. Prophylactic medications are generally not necessary in low risk situations but should be considered in addition to gradual ascent for use in moderate to high risk situations (Figure 1). With travel above 3000 m, individuals should not increase the sleeping elevation by more than 500 m per day and should include a rest day (i.e. no ascent to higher sleeping elevation) every 3-4 days.

Acetazolamide: 

Acetazolamide has an established role in prevention of AMS. There is a risk, albeit extremely low, of inciting an allergic reaction in persons with sulfonamide allergy when taking acetazolamide, and the drug is contraindicated in persons with any prior anaphylactic reaction to a sulfonamide medication or a history of Stevens-Johnson syndrome. Acetazolamide should be started the day before ascent but will still have beneficial effects if started on the day of ascent (Table 1).


Dexamethasone: 

Dexamethasone does not facilitate acclimatization like acetazolamide but has an established benefit in AMS prevention. Higher doses than those recommended in Table 1 (4 mg every 6 hours) may be considered only in very high risk situations such as military or search and rescue personnel being airlifted to altitudes > 3500 m with immediate performance of physical activity. If used for longer than 5-7 days, dexamethasone should be tapered over a one week period rather than stopped abruptly. It is not recommended for AMS prevention in children. Dexamethasone should be started the day before ascent but will still have beneficial effects if started on the day of ascent.


Ibuprofen: 

Ibuprofen cannot be recommended over acetazolamide or dexamethasone for AMS prevention during rapid ascent (Table 1), however, it could be used in persons who do not wish to take acetazolamide or dexamethasone or have allergies or intolerance to these medications.


Staged Ascent and Preacclimatization: 

The panel does not endorse a particular protocol for preacclimatization (i.e., repeated exposures to hypoxia preceding high altitude travel) and staged ascent (i.e., staying at a moderate elevation for several days before ascending to the target elevation) as a means of AMS prevention. With regard to normobaric hypoxia exposure in a hypoxic tent, only sufficiently long exposures (> 8 hours per day) that can be undertaken regularly over an appropriate number of weeks are likely to offer any significant preacclimatization benefit.


Other Options: 

The following interventions have not been shown to be of benefit: chewed coca leaves, coca tea and other coca-derived products; “forced” or “over” hydration; short-term oxygen use in the form of either visits to oxygen bars or over-the-counter oxygen delivery systems by which individuals inhale oxygen-enriched gas from a small pre-filled canister; other over-the-counter products, such as powdered drink mixes, patches, and oral supplements.

AMS/HACE Diagnosis
The diagnosis of AMS is made in a very specific clinical context, that of an unacclimatized lowlander who becomes ill within several hours to 3 days following ascent to high elevations, generally >2500 m. Diagnosis is based solely on reported symptoms, as there are no characteristic findings on physical exam or diagnostic laboratory studies. Symptoms of AMS include: headache, anorexia, nausea, fatigue, and light-headedness or dizziness. In line with the updated Lake Louise Acute Mountain Sickness Score (see Table 2), these guidelines emphasize the role of headache and de-emphasize the role of sleep disruption in the diagnosis of AMS. The best approach to diagnosis is to consider the traveler’s well-being and functional status. Individuals who feel ill and/or must reduce their daily activities several hours to 3 days following ascent to elevations >2500 m likely have AMS.

The diagnosis of HACE is heralded by signs of encephalopathy including ataxia–which is often the earliest clinical finding–and altered mentation. Other signs include apathy, irritability, lassitude, and inability to provide self-care, all of which can be subtle. Untreated HACE can progress to coma. Focal neurologic deficits are unusual and should prompt consideration of other diagnoses. Heel-to- toe walking can be used to gauge ataxia, and papilledema can confirm cerebral edema.

AMS/HACE Treatment
Suggested Approach: Care should be taken to exclude disorders whose symptoms and signs resemble those seen with AMS and HACE, such as cerebrovascular accident, carbon monoxide poisoning, hypoglycemia, hyponatremia, infection, or traumatic brain injury.
這張危險分級是用於預測高海拔疾病風險. 包含 AMS. HACE. HAPE
有些文獻的危險分級是用於預測 AMS 風險
兩種並不相同.



Persons with AMS of any severity or HACE should cease ascending and may need to consider descent, depending on the severity of illness and circumstances. Individuals with AMS may resume ascending once symptoms resolve. Further ascent or reascent to a previously attained altitude should never be undertaken if there are ongoing symptoms. Descent should be initiated in any suspected HACE victim or if symptoms of AMS are worsening despite treatment with acetazolamide or dexamethasone. Dexamethasone is considered to be a more reliable pharmacological treatment for moderate to severe AMS/HACE than acetazolamide. If descent is not feasible, supplemental oxygen or a portable hyperbaric chamber should also be used.

Supplemental Oxygen: 

Oxygen, if available, delivered by nasal cannula or mask at flow rates sufficient to relieve symptoms provides a suitable alternative to descent. It should also be used when descent is recommended but not feasible or during descent in severely ill individuals. An SpO2 > 90% is usually adequate. Short-term oxygen use in the form of over-the-counter oxygen canisters should not be relied on for this purpose.


Portable Hyperbaric Chambers: 攜帶型加壓艙/袋

Portable hyperbaric chambers are effective for treating severe altitude illness but require constant tending by care providers and are difficult to use with claustrophobic or vomiting patients. In many cases, ill individuals may improve enough that they can assist with their evacuation and descend once symptoms improve. Use of a portable hyperbaric chamber should not delay descent in situations where descent is required.

Acetazolamide: 丹木斯

Acetazolamide should be considered for treatment of AMS. (Table 1).

Dexamethasone: 類固醇

Dexamethasone is very effective for treating AMS. The medication does not facilitate acclimatization, so further ascent should be delayed until the patient is asymptomatic while off the medication. Extensive clinical experience supports using dexamethasone in patients with HACE (Table 1).

Medication	Indication	Route	Dosage
Acetazolamide	AMS, HACE Prevention	Oral	125 mg every 12 h 1, 2 Pediatrics: 1.25 mg•kg-1 every 12 h (maximum 125 mg per dose)
	AMS Treatment 3	Oral	250 mg every 12 h Pediatrics: 2.5 mg•kg-1 every 12 h (maximum: 250 mg per dose)
Dexamethasone	AMS, HACE Prevention	Oral	2 mg every 6 h or 4 mg every 12 h 1 Pediatrics: Should not be used for prophylaxis
	AMS, HACE Treatment	Oral, IV, IM	AMS: 4 mg every 6 h HACE: 8 mg once then 4 mg every 6 h Pediatrics: 0.15 mg•kg-1•dose-1 every 6 h (Maximum: 4 mg per dose)
Ibuprofen	HAH Treatment	Oral	600 mg every 8 h
Nifedipine	HAPE Prevention	Oral	30 mg ER version, every 12 h or 20 mg ER version every 8 h 4
	HAPE Treatment	Oral	30 mg ER version, every 12 h or 20 mg ER version every 8 h
Tadalafil	HAPE Prevention	Oral	10 mg every 12 h 4
Sildenafil	HAPE Prevention	Oral	50 mg every 8

High Altitude Pulmonary Edema

HAPE Prevention
Suggested Approach: 

Because the rates of acclimatization and physiologic responses to high altitude vary considerably among individuals, the ascent profile recommendations presented here do not guarantee HAPE prevention in all high altitude travelers. A gradual ascent profile is the primary method for preventing HAPE; the recommendations provided above for AMS and HACE prevention also apply to HAPE prevention. Pharmacologic prophylaxis should only be considered for individuals with a history of HAPE, especially multiple episodes.

Gradual Ascent: 

There is a clear relationship between rate of ascent and disease incidence. Gradual ascent is recommended to prevent HAPE.

Nifedipine: 

A calcium channel blocker that promotes vasodilation and lowers pulmonary artery pressure, nifedipine should be started the day prior to ascent and continued either until descent is initiated or the individual has spent 4 days at the highest elevation, perhaps up to 7 days if the individual ascended faster than recommended ascent rates (Table 1).

Tadalafil: 

Tadalafil can be used for HAPE prevention in known susceptible individuals who are not candidates for nifedipine (Table 1). There is no role for concurrent use of nifedipine and tadalafil.

Preacclimatization and Staged Ascent: 

Staged ascent and preacclimatization may offer a reasonable means of HAPE prevention. However, uncertainty remains as to the magnitude and duration of moderate altitude exposure necessary to yield benefit.

HAPE Diagnosis
The diagnosis of HAPE requires a very specific clinical context–an unacclimatized lowlander ascending to elevations ≥2500 m–and relies on a characteristic set of symptoms, including dyspnea on exertion out of proportion to previous experiences at high altitude or that experienced by other individuals at the same elevation. Nonproductive cough, fatigue, weakness, and gurgling sensation in the chest may also be present. With progression, individuals become dyspneic with mild exertion or at rest and may develop cyanosis and cough productive of pink frothy sputum. 

If available, pulse oximetry can confirm the presence of hypoxemia out of proportion to that expected for a given elevation, however, care must be exercised when using fingertip oximeters at high altitude, as oxygen saturation changes rapidly in response to small changes in oxygen tensions at high altitude and device accuracy declines with arterial oxygen saturations of less than 80%. The normal oxygen saturation at a given elevation may not be known with certainty and should be viewed as a range of values, rather than a specific number. For these reasons, clinical decisions should not be based on small differences in saturation over time or among individuals. Effort should also be made to minimize factors that cause measurement errors, including cold extremities, excess ambient light, and ill-fitting oximeter probes.

Consideration should be given to other causes of respiratory symptoms at high altitude, such as asthma, bronchospasm, pneumonia, pneumothorax, pulmonary embolism, viral upper respiratory tract infection, heart failure, or myocardial infarction.

HAPE Treatment
Suggested Approach: 

If HAPE is suspected or diagnosed, oxygen should be started, if available, and descent initiated to lower elevation. If descent is infeasible or delayed, supplemental oxygen should be continued, or the individual should be placed in a portable hyperbaric chamber. Individuals who develop HAPE may consider further ascent to higher altitude or reascent only when symptoms of HAPE have completely resolved and they maintain stable oxygenation at rest and with mild exercise while off supplemental oxygen and/or vasodilator therapy.

Descent: 

As with AMS and HACE, descent remains the single best treatment for HAPE. Individuals should try to descend at least 1000 m or until symptoms resolve. They should exert themselves as little as possible while descending (e.g. travel without a pack or via motor vehicle, helicopter or animal transportation) because exertion can further increase pulmonary artery pressure and exacerbate edema formation.

Supplemental Oxygen: 

When available, supplemental oxygen sufficient to achieve an SpO2 > 90% or relieve symptoms should be used while waiting to initiate descent, when descent is infeasible and during descent in severely ill patients.

Portable Hyperbaric Chambers: 

As for AMS and HACE, portable hyperbaric chambers can be used for HAPE treatment when descent is infeasible or delayed or supplemental oxygen is unavailable.

Nifedipine:

 Nifedipine should be used for HAPE treatment when descent is impossible or delayed and reliable access to supplemental oxygen or portable hyperbaric therapy is unavailable (Table 1).


Phosphodiesterase Inhibitors: 

By virtue of their ability to cause pulmonary vasodilation and decrease pulmonary artery pressure, there is a strong physiologic rationale for using phosphodiesterase inhibitors in HAPE treatment. Therefore, tadalafil or sildenafil can be used for HAPE treatment when descent is impossible or delayed, access to supplemental oxygen or portable hyperbaric therapy is impossible, and nifedipine is unavailable.

Continuous Positive Airway Pressure (CPAP):

Positive airway pressure works by increasing transmural pressure across alveolar walls, thereby increasing alveolar volume and subsequent gas exchange. CPAP may be considered for treatment of HAPE when supplemental oxygen or pulmonary vasodilators are not available or as adjunctive therapy in patients not responding to supplemental oxygen alone.

Patients with Concurrent HAPE and HACE
For HAPE patients with neurologic dysfunction that does not resolve rapidly with administration of supplemental oxygen and improvement in the patient’s oxygen saturation, dexamethasone should be added to the treatment regimen at the doses described for HACE (Table 1). Nifedipine or other pulmonary vasodilators may be used in patients with concurrent HAPE and HACE, with care to avoid lowering systemic blood pressure.

Figure 1. 

Assessing the risk of acute altitude illness. Medical history and features of the planned ascent can be used to assess the risk of acute altitude illness after ascent. Check marks should be placed in the boxes that best describe the variables in the left-hand column. The risk of a planned ascent is determined by the farthest column to the right in which a check mark is placed. This assessment applies to unacclimatized individuals. Ascent is assumed to start from elevations <1200 m. A history of acute altitude illness does not necessarily reflect high risk with all future ascents, as a slower ascent rate or lower target elevation on subsequent trips may help avoid problems. The risk of travel above any given elevation can be mitigated by ensuring an appropriately slow rate of ascent. The severity of prior AMS can be graded using the information in Table 2. AMS, acute mountain sickness; HACE, high altitude cerebral edema; HAPE, high altitude pulmonary edema.
Table 1. Recommended Dosages for Medications Used in the Prevention and Treatment of Altitude Illness

table 1 註解
AMS: Acute mountain sickness; ER: extended release; HACE: High altitude cerebral edema; HAH: High altitude headache; HAPE: High altitude pulmonary edema
1 For individuals ascending to and remaining at a given elevation, following arrival at the target elevation, the medication should be continued for 2 days in individuals adhering to the recommended ascent rate and 2-4 days in individuals ascending faster than recommended rates. Individuals who ascend to a target elevation and immediately descend can stop the medication once descent is initiated.
2 This dose applies to low-moderate risk ascent profiles. For high-risk ascent profiles, consider 250 mg BID. The appropriate dose for ascent above 5000 m is not clear.
3 Acetazolamide can also be used at this dose as an adjunct to dexamethasone in HACE treatment, but dexamethasone remains the primary treatment for HACE.
4 For individuals requiring HAPE prophylaxis, ascending to and remaining at a given elevation, following arrival at the target elevation, the medication should be continued for 4 days in individuals adhering to the recommended ascent rate and 4-7 days in individuals ascending faster than recommended rates. Individuals who ascend to a target elevation and immediately descend can stop the medication once descent is initiated.

Table 2. Acute Mountain Sickness Classification

Category	Mild AMS	Moderate-Severe AMS	High Altitude Cerebral Edema (HACE)
Symptoms	Headache plus one or more other symptoms (nausea/vomiting; fatigue, lassitude, dizziness).   All symptoms of mild intensity	Headache plus one or more other symptoms (nausea/vomiting; fatigue, lassitude, dizziness). All symptoms of moderate-severe intensity	Worsening of symptoms seen in moderate to severe AMS
Signs	None	None	Ataxia, severe lassitude, altered mental status, encephalopathy
Lake Louise AMS Score	3-5	6-12	Not applicable

血小板低下輸血條件 Platelet Transfusion Threshold

2025-10-30 16:55
剛接到檢驗報告異常. 血小板僅12K.查詢一下輸血小板輸血條件

原則上. 若無症狀. 單純體檢或健檢發現異常

一萬以下考慮輸血小板.


Platelet Transfusion 2024 Jun 6
作者 Ankit Agarwal; Atif I. Khan; Faiz Anwer.僅節錄部分內容.
中文使用google翻譯

出血患者的血小板輸注閾值
血小板輸注閾值指導根據出血嚴重程度和臨床情況做出輸注決策。以下出血情況需要治療：

血小板計數低於 50,000 個/μL 且伴隨嚴重出血，包括瀰漫性血管內凝血；
血小板計數低於 30,000 個/μL 且出血不危及生命或不被認為是嚴重的；
血小板計數低於 100,000 個/μL 且伴有多發性創傷或顱內出血

遵循根據出血嚴重程度和具體情況制定的血小板輸注閾值，可優化患者的治療和預後。

預防性輸注閾值
當血小板計數低於特定閾值時，建議進行血小板輸注，作為特定操作前的預防措施或預防自發性出血。預防性輸注閾值如下表所示。

臨床背景	血小板輸注閾值
自發性出血預防	<10,000 /μL 有些醫師建議 < 5000 /μL 才輸
神經外科手術或眼科手術前	<100,000 /μL
大型手術前	<50,000 /μL
散播性血管內凝血	<50,000 /μL
中心靜脈置管前	<20,000 /μL [9]
硬脊膜外麻醉前	<80,000 /μL
支氣管肺泡灌洗前	<20,000-30,000 /μL [10]
內視鏡檢查前	用於治療程序  <50,000/μL 低風險診斷程序< 20,000 /μL。
分娩期間	陰道分娩時 <30,000/μL 剖腹產時 <50,000/μL  [11]
腰椎穿刺前	血癌患者 <10,000-20,000/μL 非血癌患者 40,000-50,000 /μL。

Platelet Transfusion Thresholds in Bleeding Patients

Platelet transfusion thresholds guide transfusion decisions based on severity and clinical context. The treatment is indicated in the following bleeding cases:Less than 50,000 cells/μL with severe bleeding, including disseminated intravascular coagulation
Less than 30,000 cells/μL when bleeding is not life-threatening or considered severe
Less than 100,000 cells/μL for bleeding in the context of multiple trauma or intracranial bleeding [8]

Adherence to platelet transfusion thresholds, tailored to bleeding severity and the circumstances, optimizes patient care and outcomes.

Prophylactic Transfusion Thresholds

Platelet transfusion is recommended when the platelet count falls below a certain threshold, either as a preventive measure before specific procedures or to prevent spontaneous bleeding. The prophylactic transfusion thresholds are outlined in the table below.

Clinical Context	Platelet Transfusion Threshold
Spontaneous bleeding prevention	<10,000 cells/μL Some authors recommend a threshold of 5000 cells/μL.
Before neurosurgery or ocular surgery	<100,000 cells/μL
Before major surgery	<50,000 cells/μL
Disseminated intravascular coagulation	<50,000 cells/μL
Before central line placement	<20,000 cells/μL [9]
Before epidural anesthesia	<80,000 cells/μL
Before bronchoalveolar lavage	<20,000-30,000 cells/μL [10]
Before endoscopic procedures	<50,000 cells/μL for therapeutic procedures <20,000 cells/μL for low-risk diagnostic procedures
During parturition	<30,000 cells/μL for a vaginal delivery <50,000 cells/μL for a cesarean section [11]
Before lumbar puncture	<10,000-20,000 cells/μL in hematologic malignancies <40,000-50,000 cells/μL if without a hematologic malignancy

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.

2025 AHA ACLS update 重點整理

2025-10-28 08:54AM
參考資料-大林慈濟李宜/恭主任製作的摘要 及 簡報檔案

成人呼吸道異物梗塞處理. 新增拍背的步驟. 先拍背五次. 再做哈姆立克法五次.
建議一般民眾做CPR的時候加入人工呼吸. 以前認為民眾做人工呼吸很耽誤時間. 且不容易正確操作. 加上有傳染疾病疑慮. 使得BLS推廣不易.所以推廣僅壓胸不吹氣的CPR. 
CPR時建議讓患者以正面仰躺. 但若有特殊情況也可以讓患者俯臥(面朝下)施行
嬰兒CPR之前使用的兩根手指壓胸已經移除. 因為實際執行的時候不容易到達正確深度. 建議使用單手掌跟或雙手環抱以拇指按壓
持續的多形性VT會導致心臟輸出停止. 建議立即電擊除顫. 藥物可用於預防再次發生VT, 但不可為了注射藥物而耽誤電擊去顫
胸前重擊 precardial thump 不應該使用.
特殊情況. 在心導管室. 病患受到持續性監測. 當醫師發現患者心電圖突然呈現 aststole 或 bradycardia 時. 在患者尚未完全失去意識前. 可給予胸前重擊(模擬電擊)
嬰兒及兒童接受CPR時. 若有動脈導管(通常是在ICU的患者). 可依照舒張壓評估CPR品質.
舒張壓目標 嬰兒DBP≥25 mmHg、兒童DBP≥30 mmHg
成人CPR的時候舒張壓應該要多高. 目前無一致結論. 建議用 ETCO2 潮氣末二氧化碳濃度監測 CPR 品質.

CPR過程. ETCO2目標是 > 10 mmHg.

ROSC 時. ETCO2目標是 > 35 mmHg.

For adults Guidance:

While diastolic pressure is a key surrogate for coronary perfusion pressure during CPR, the specific targets may vary and are not as clearly defined in the 2025 ACLS guidelines for adult CPR as they are for children.
It's crucial to monitor other indicators of CPR quality, such as end-tidal CO2 (EtCO2) levels, which should be at least 10 mmHg for healthcare professionals and rise to >35 mmHg after ROSC.

Adjust CPR efforts based on the overall response, including the patient's response to interventions like vasopressors.

ROSC之後. 意識未恢復的患者體溫建議維持 32-37.5度c 維持36小時. 

blood pressure control- tPA for ischemic stroke

trandate 10mg IV

check BP every 3-5 min

ACLS child 兒童定義

ACLS 關於兒童的定義是指一歲至青春期之前
In Advanced Cardiovascular Life Support (ACLS), a child is defined as a patient from 1 year of age up to the onset of puberty.

ACLS關於兒科(pediatric)定義是指嬰兒.兒童. 青少年至18歲前. 但排除新生兒 newborns. 

neonates 新生兒是指30天以下. 

For the purposes of the pediatric advanced life support guidelines, pediatric patients are infants, children, and adolescents up to 18 years of age, excluding newborns. For pediatric basic life support (BLS), guidelines apply as follows:
•Infant guidelines apply to infants younger than approximately 1 year of age.
•Child guidelines apply to children approximately 1 year of age until puberty. For teaching purposes, puberty is defined as breast development in females and the presence of axillary hair in males.
•For those with signs of puberty and beyond, adult basic life support guidelines should be followed.

Resuscitation of the neonate is addressed in “Part 5: Neonatal Resuscitation” and applies to the newborn typically only during the first hospitalization following birth. Pediatric basic and advanced life support guidelines apply to neonates (less than 30 days old) after hospital discharge.

老年人高血壓-2022年台灣高血壓治療指引

2025-10-20 11:16M

參考資料-2022台灣高血壓治療指引(只有英文版)

裡面提到 the “J-curve” phenomenon., 在血壓的部分是指. 血壓降到某個程度之下. 冠狀動脈心臟病機率反而增加. 

統合分析. 

收縮壓超標20mmHg的血管性死亡率與舒張壓超標10mgHg相近

血壓降到 115/75 以下. 不會再降低風險(不需特意將血壓降更低)

年齡60-79歲. 收縮壓維持90~144. 舒張壓維持 60-74. 死亡率最低

韓國研究. 60-95歲. 收縮壓維持 100-110. 全因死亡率或心血管疾病死亡率最低. 

血壓最低降到110/60是安全的

HYVET研究. 80歲以上. 基礎血壓 173/90. 使用 indapamide + perinfopril 將血壓降到140/80. 可降低30%非致死性中風. 降低 21% 全因死亡率

 is a placebo-controlled RCT to test the effect of antihypertensive therapy on the risk of stroke and all-cause death in very elderly patients (age  80 years) with a baseline BP of 173.0/90.8 mmHg.619 Use of indapamide, plus perindopril if necessary, decreased fatal or nonfatal stroke by 30% (p = 0.06) and all-cause death by 21% (p = 0.02) with final achieved BP of 140/80 mmHg.

2022台灣高血壓治療指引(只有英文版)
17. ELDERLY PATIENTS 

Recommendations/Keypoints  For patients aged  65 years, the SBP threshold for pharmacological therapy is  130 mmHg (COR I, LOE B).  For patients aged  65 years, the SBP target for pharmacological therapy is < 130 mmHg. (COR I, LOE B). 

In a meta-analysis of individual data from one million adults from 61 prospective studies (Prospective Study Collaboration), BP was associated strongly with the age-specific mortality rates from stroke and CHD.252 In general, a 20 mmHg difference in SBP is approximately equivalent in its hazards to a 10 mmHg difference in DBP. These relationships with vascular mortality continued steeply down as far as a SBP of 115 mmHg and a DBP of 75 mmHg, below which there was little evidence.252 All of these proportional differences in vascular mortality were about half as extreme at ages 80-89 years as at ages 40-49 years, but the annual absolute differences in risk were greater in old age.252 Similar findings were observed in the Asia Pacific Cohort Studies Collaboration,6 and a Chinese cohort study.43 In the sub-analysis of the Felodipine Event Reduction (FEVER) trial, the relative risk reduction of CV events was greater in patients aged > 65 years compared with those aged  65 years.613 Taken together, controlling BP in the elderly is very important. Isolated systolic hypertension (ISH) is more common in the elderly. The major concern in the hypertension management in the elderly is fear of the “J-curve” phenomenon that an aggressive BP lowering might t increase the risk of coronary event given that the DBP is already in the lower ranges in these elderly patients. In a cohort study of 1.25 million subjects, the lowest risk for CV disease in people aged 60-79 years was 90-114 mmHg in SBP and 60-74 mmHg in DBP, without any evidence of J-curve phenomenon above these levels.615 Among 1,235,246 individuals who participated in routine medical examinations in Korea, the lowest risk of all-cause death and ASCVD death in the elderly (age 60-95 years) was observed in the range of 100-110 mmHg in SBP, and there was no J-curve above this BP level. 

In the three most important RCTs in the elderly (age > 60 years) with ISH (SHEP, Syst-Eur, Syst-China), the risk of myocardial infarction was reduced in the treatment group compared to the placebo group.616-618 No J-curve phenomenon was observed. Therefore, it seems to be safe to decrease SBP to a level above 110 mmHg and DBP to above 60 mmHg. The Hypertension in the Very Elderly Trial (HYVET) is a placebo-controlled RCT to test the effect of antihypertensive therapy on the risk of stroke and all-cause death in very elderly patients (age  80 years) with a baseline BP of 173.0/90.8 mmHg.619 Use of indapamide, plus perindopril if necessary, decreased fatal or nonfatal stroke by 30% (p = 0.06) and all-cause death by 21% (p = 0.02) with final achieved BP of 140/80 mmHg. However, the HYVET trial is not a BP target-driven trial, and it cannot answer the question that whether the effects could be even better if lower BP levels are achieved. There were two BP target-driven trials for the elderly hypertensive patients before the SPRINT trial, the JATOS and the VALISH trials.620,621 The JATOS trial tested a SBP < 140 mmHg vs. < 160 mmHg in the Japanese elderly patients,620 while VALISH trial tested a SBP < 140 mmHg vs. < 150 mmHg in the Japanese elderly patients.621 A lower BP target, compared with a higher BP target, did not translate into better CV outcomes in both trials.620,621 However, the number of enrollment was too low to have enough power for analysis.621 In addition, follow-up durations were very short and the event rates were very low (1.1 to 1.2%/ year in JATOS, 0.82 to 0.85%/year in VALISH),620,621 making the conclusions not convincing.621 A larger trial with longer follow-up period was needed. The SPRINT trial is a recent target-driven trial and probably the most important one.622 One of the inclusion criteria was the elderly patients with age  75 years, and about 28% of the total study population of 9,361 patients were the elderly. In the pre-defined sub-analysis of the elderly patients, a BP target of < 120 mmHg (intensive treatment group), compared with a BP target of < 140 mmHg (standard treatment group), reduced the composite endpoints by 34% (95% CI: 0.51-0.85) and all-cause mortality by 33% (95% CI: 0.49-0.91).623 The overall rate of serious adverse events was not different between treatment groups. Interestingly, the incidence of orthostatic hypotension of the two treatment groups (5.0% vs. 5.7%) did not differ.624 The final achieved SBP was 123.4 mmHg vs. 134.8 mmHg, and the DBP was 62.0 mmHg vs. 67.2 mmHg.623 Similar findings were reported in a more recent sub-analysis of very elderly patients (age  80 years) in the same trial.625 The STEP trial,9 comprising exclusively of Chinese patients aged 60 to 80 years, replicates what had been observed in the SPRINT trial, and reassures the safety and effi