Difference between revisions of "High altitude pulmonary edema"

Line 26: Line 26:
==Clinical Features==
==Clinical Features==
*Dry [[cough]], decreased exercise performance, [[dyspnea]] on exertion, localized rales  
*Dry [[cough]], decreased exercise performance, prolonged exercise recover time, [[dyspnea]] on exertion, localized rales  
*Resting SaO2 is [[hypoxia|very low]] for the expected altitude but patients often appear clinically better than their saturation (aids in diagnosis)
*Resting SaO2 is [[hypoxia|very low]] for the expected altitude but patients often appear clinically better than their saturation (aids in diagnosis)
*Easily desaturates with exertion
*Easily desaturates with exertion

Revision as of 21:54, 22 May 2021


  • Also known as HAPE
  • Noncardiogenic pulmonary edema due to increased microvascular pressure in the pulmonary circulation
  • Most lethal of the altitude illnesses with mortality approaching 50% if descent is not completed in a timely manner [1]
  • Occurs in <1/10,000 skiers in Colorado; 2-3% of Mt. McKinley climbers
  • Typical patient is strong and fit; may not have symptoms of altered mental status before onset of HAPE
  • Most commonly noticed on the second night at a new altitude

Risk Factors

  • Heavy exertion
  • Rapid ascent
  • Cold
  • Excessive salt ingestion
  • Use of a sleeping medication
  • Preexisting pulmonary hypertension
  • Preexisting respiratory infection (children)
  • Previous history of HAPE


  • Multiple pathways but thought to be due to an exaggerated pulmonary artery pressure elevation in response to hypoxia [2] and the following hypothesis:
    • Breakdown of the alveolar/endothelial barrier leading to increased pulmonary vascular endothelial permeability
    • Normal wedge pressure, which distinguishes this pathophysiology from heart failure [3]
    • Increased intra-cranial pressure which can lead to pulmonary edema [4]

Clinical Features


  • Dry cough, decreased exercise performance, prolonged exercise recover time, dyspnea on exertion, localized rales
  • Resting SaO2 is very low for the expected altitude but patients often appear clinically better than their saturation (aids in diagnosis)
  • Easily desaturates with exertion


Differential Diagnosis

High Altitude Illnesses

Pulmonary Edema Types

Pulmonary capillary wedge pressure <18 mmHg differentiates noncardiogenic from cardiogenic pulmonary edema[5]


Chest x-ray of HAPE showing characteristic patchy alveolar infiltrates with right middle lobe predominance.



  • Clinical diagnosis

Expected SpO2 and PaO2 levels at altitude[6]

Altitude SpO2 PaO2 (mm Hg)
1,500 to 3,500 m (4,900 to 11,500 ft) about 90% 55-75
3,500 to 5,500 m (11,500 to 18,000 ft) 75-85% 40-60
5,500 to 8,850 m (18,000 to 29,000 ft) 58-75% 28-40


High altitude management algorithm.
  • Immediate descent is treatment of choice - minimize exertion
  • If cannot descend use combination of:
    • Supplemental O2 - An oxygen concentrator is often used at high altitude ski resorts after the patient is titrated down to nasal cannula. A portable oxygen tank is used for ambulation. Can completely resolve the pulmonary edema within 36-72hr
    • Hyperbaric bag - (e.g. Gamow Bag). Should not delay descent, if possible.
    • Keep patient warm (cold stress elevates pulmonary artery pressure)
    • Use expiratory positive airway pressure mask
    • Nifedipine 30mg ER q12hr (or 20mg normal-release q8hr)[7]
      • May consider the other medications listed below that are usually used for prevention


  • Admission
    • Warranted for severe illness that does not respond immediately to descent
  • Discharge
    • Progressive clinical and X-ray improvement and a PaO2 of 60mmHg or SaO2>90%
  • May re-ascend in 2-3 days if mild-moderate symptoms resolved that only required descent as the intervention


  • Nifedipine 20mg q8hr or 30mg ER q12hr while ascending is effective prophylaxis in patients with prior episodes of HAPE
  • Tadalafil 10mg BID 24hr prior to ascent OR Sildenafil 50mg q8hr
  • Salmeterol 125 mcg inhaled BID
  • Acetazolamide 125mg BID for prevention of hypoxia

See Also


  1. Lobenhoffer HP, Zink RA, et al. High altitude pulmonary edema: analysis of 166 cases. In: Brendel W, Zink RA, editors. High Altitude Physiology and Medicine. New York, NT: Springer-Verlag; 1982. pp. 219–231
  2. Bärtsch P. High altitude pulmonary edema. Med Sci Sports Exerc. 1999;31(1 Suppl):S23-27.
  3. Hultgren HN, Lopez CE, Lundberg E, Miller H. Physiologic studies of pulmonary edema at high altitude. Circulation. 1964;29(3):393-408.
  4. Ducker TB, Simmons RL. Increased intracranial pressure and pulmonary edema. 2. The hemodynamic response of dogs and monkeys to increased intracranial pressure. J Neurosurg. 1968;28(2):118-123.
  5. Clark SB, Soos MP. Noncardiogenic Pulmonary Edema. In: StatPearls. Treasure Island (FL): StatPearls Publishing; October 1, 2020.
  6. Gallagher, MD, Scott A.; Hackett, MD, Peter (August 28, 2018). "High altitude pulmonary edema". UpToDate. Retrieved May 2, 2019.
  7. Luks AM, McIntosh SE, Grissom CK, et al. Wilderness Medical Society Practice Guidelines for the Prevention and Treatment of Acute Altitude Illness: 2014 Update. Wilderness & Environmental Medicine. 2014(25): S4–S14)