High altitude pulmonary oedema.
D P Hall1, K Duncan, J K Baillie
1Royal Infirmary of Edinburgh, Edinburgh, UK.
Journal of the Royal Army Medical Corps
|April 7, 2011
Summary
High altitude pulmonary oedema (HAPE) is a significant risk for those ascending to great heights. Progressive acclimatisation is key to preventing HAPE, with incidence increasing with altitude.
Area of Science:
- Altitude sickness
- Pulmonary medicine
- Epidemiology
Background:
- High altitude pulmonary oedema (HAPE) is a leading cause of death in mountainous regions.
- Accurate global incidence data for HAPE is limited due to remote case occurrences.
- Disparities in diagnostic criteria hinder consistent clinical and research application.
Purpose of the Study:
- To review the existing literature on HAPE incidence and epidemiology.
- To consolidate understanding of HAPE risk factors and prevalence at varying altitudes.
- To emphasize the importance of HAPE awareness, diagnosis, and prevention.
Main Methods:
- Systematic literature review of HAPE incidence and epidemiology.
- Analysis of reported HAPE cases across different altitudes.
- Synthesis of identified risk factors and pre-disposing elements.
Main Results:
- HAPE incidence rises with altitude: 0.01% at 2500m, 1.9% at 3600m, and 2.5-5% at 4300m.
- Key risk factors include rapid ascent, intense exercise, and attained altitude, alongside potential genetic susceptibility.
- HAPE represents the extreme of a spectrum of altitude-induced pulmonary fluid accumulation.
Conclusions:
- HAPE is a preventable condition, primarily through progressive acclimatisation.
- Increased awareness and standardized diagnosis are crucial for high-altitude visitors.
- Further research into HAPE epidemiology and genetics, potentially via databases like the International HAPE Database, is warranted.
Related Concept Videos
01:18Pulmonary Edema II: Pathophysiology
Pulmonary edema is the accumulation of fluid in the interstitial and alveolar spaces of the lungs, impairing gas exchange and oxygen delivery. It may be cardiogenic or noncardiogenic, but both reduce oxygenation and lung compliance.Cardiogenic Pulmonary EdemaCardiogenic edema results from increased hydrostatic pressure in pulmonary capillaries, usually due to left ventricular dysfunction from myocardial infarction, heart failure, or valvular disease. Ineffective cardiac pumping causes blood to...
01:21Acute Respiratory Failure-II
Type I Respiratory Failure, or hypoxemic respiratory failure, occurs when the partial pressure of oxygen (PaO2) in arterial blood falls below 60 mmHg while breathing room air without a corresponding increase in arterial carbon dioxide levels (PaCO2). This condition highlights a significant impairment in the lungs' capacity to oxygenate the blood.
The underlying physiological abnormalities that contribute to hypoxemic respiratory failure include:
The underlying physiological abnormalities that contribute to hypoxemic respiratory failure include:
01:29Pulmonary Embolism I: Introduction
Pulmonary embolism (PE) occurs when a thrombus, fat or air embolus, amniotic fluid, or tumor tissue blocks one or more pulmonary arteries. These blockages originate in the venous system or the right side of the heart.EtiologyPE primarily arises from deep vein thrombosis (DVT) and other hypercoagulable states, such as inherited thrombophilias. Additional etiological factors include venous stasis, commonly seen in obesity, and endothelial injury from surgery and trauma. Less common causes include...
01:19Pulmonary Embolism I: Introduction
A blood clot, or thrombus, is a semi-solid mass composed of fibrin, platelets, and red blood cells. When it forms within a vessel, it can obstruct blood flow, known as thrombosis. If part of the clot detaches, it becomes an embolus that can travel and block distant vessels. When this occurs in the pulmonary arteries, it causes a condition known as pulmonary embolism (PE).Origin and ImpactMost often, the embolus originates from a thrombus in the deep veins of the lower limbs, a condition called...
01:10Atelectasis II: Pathophysiology
Atelectasis develops when alveoli lose their air and collapse inward. Because lung tissue is naturally elastic, these air sacs shrink rather than remaining open. Collapsed alveoli are no longer ventilated, reducing their role in gas exchange. Blood flow may continue in these regions, creating a ventilation–perfusion mismatch. Clinical findings include decreased breath sounds, dullness to percussion, reduced chest expansion, and decreased tactile fremitus as sound transmission through collapsed...
01:23Chronic Obstructive Pulmonary Disease II: Emphysema
Emphysema, a major phenotype of chronic obstructive pulmonary disease (COPD), is characterized by irreversible destruction of alveolar walls and permanent enlargement of distal airspaces. Unlike chronic bronchitis, which primarily affects the airways, emphysema predominantly involves the lung parenchyma, where structural damage leads to airflow limitation.PathophysiologyIt most commonly results from prolonged exposure to cigarette smoke and other toxic gases, particularly cigarette smoke.