Critical altitudes• 10000 ft. (3000 m): high altitude
• 18000 ft. (5500 m): permanent inhabitation
• 20000 ft. (6100 m): endangered life with atmospheric air
• 46000 ft. (14000 m) : endangered life even with 100% O2
• 63000 ft. (19200 m): body fluids boil s at 37°C
Altitude (ft)
Atmospheric pressure (mm Hg)
pO2 in air mm Hg
Alveolar pCO2 mm
Hg
Alveolar pO2
mm Hg
0 760 159 40 (40) 104 (104)
10000 523 110 36 (23) 67 (77)
20000 349 73 24 (10) 40 (53)
Breathing air
Altitude (ft) Barometric pressuremm Hg
Alveolar pCO2 mm Hg
Alveolar pO2mm Hg
0 760 40 673
10000 523 40 436
20000 349 40 262
30000 226 40 139
40000 141 36 58
Breathing pure oxygen
Altitude (ft) Arterial O2 saturation on breathing air
Arterial O2 saturation on breathing pure O2
0 97 (97) 100
10000 90 (92) 100
20000 73 (85) 100
30000 24 (38) 9940000 8450000 15
• O2 saturation < 50% : unconsciousness in unacclimatised
• Breathing air at 23000 ft. O2 saturation is 50%
• Breathing pure O2 at 47000 ft. O2 saturation in 50%
Acute effects of hypoxia12,000 ft 18000 ft 23000 ftDrowsiness Seizures Coma
Lassitude Death
Mental and muscle fatigue
Sometimes headache
Occasionally nausea
Sometimes euphoria
Acclimatization • Increased pulmonary ventilation
• Increased RBC number and hemoglobin concentration
• Increased diffusion capacity
• CVS changes and increased tissue capillarity
• Cellular level changes
Increased pulmonary ventilation
• Within seconds 1.65 times increase in ventilation due to peripheral chemoreceptor stimulation (most effective at pO2<60 mm Hg)
• In 2-5 days reaches 5 times of normal, due to renal compensation of respiratory alkalosis
Increase in RBC and Hb• Erythropoietin increases promptly
• Increased RBC in circulation in 2-3 days
• Low pO2 for weeks hematocrit rises slowly from 40 to 60; whole blood Hb rises from 15gm/dl to 20 gm/dl
• Blood volume increases by 20-30%
• Increase in total body Hb by 50%
• Increase in 2,3-DPG; more oxygen delivery to tissues
Increased diffusion capacity
• Normal diffusion capacity of O2 = 21ml/mm Hg/min
• Increased pulmonary capillary blood volume
• Increase in lung air volume
• Increase in pulmonary arterial blood pressure (normal 25/8 mm Hg, mean 15 mm Hg)
CVS changes and increased tissue capillarity
• HR, CO ( 30%), and BP increases due to sympathetic stimulation
• During acclimatization, SV decreases due to decrease in plasma volume because of natriuresis and bicarbonate diuresis
• Vasodilatation
• Angiogenesis- combined effect of hypoxia and increased work load
Cellular level changes• Increased mitochondria
• Increased myoglobin
• Increased oxidative enzymes like cytochrome oxidase
Hypoxia inducible factors
Native of high altitude• Barrel shaped chest
and decreased body size high ratio of ventilatory capacity to body mass
• Cardiomegaly extra amount of CO
Work capacity• Decreased mental proficiency (decreased judgement,
memory and performance of discrete motor movements)
• Decreased work capacity of skeletal and cardiac muscles
Acute mountain sickness (AMS)
• Sickness begins from few hours up to 4 days after ascent.
• Lake Louis Scoring System: headache and at least one of the other symptoms like malaise, lethargy, loss of appetite, nausea, vomiting, dizziness and disturbances of sleep often with periodic respiration
• Normal neurologic exam and normal mental status
• Pathophysiology: hypoxemia, hypocapnia, hypoxia mediated release of neuromodulators (substance P, VEGF, bradykinin)
High altitude cerebral edema (HACE)
• Lake Louis consensus: ataxia ± altered mental status in a person with AMS; or both ataxia and mental status changes in the absence of AMS.
• raised intracranial pressure and with reversible oedema of the white matter, particularly of the corpus callosum
• Pathophysiology: hypoxia mediated cerebral vasodilatation and neuromodulator release coupled with a possible impairment of the autoregulation of cerebral blood flow, resulting in vasogenic oedema
High altitude pulmonary edema (HAPE)• Pathophysiology: uneven (non homogenous) pulmonary
vasoconstriction due to hypoxia and sympathetic overactivity
• ‘Stress failure’ of pulmonary capillaries
• Pulmonary capillary pressure rises from 7 mm Hg to more than 28 mm Hg
Chronic mountain sickness• Polycythemia increased viscosity sluggish blood
flow
• Further increase in pulmonary arterial pressure
• RVH RVF
• Hypoxia induced systemic vasodilatation hypotension
References • Guyton and Hall, 23ed
• Ganong 25ed
• Luks AM. Physiology in Medicine: A physiologic approach to prevention and treatment of acute high-altitude illnesses. J Appl Physiol (1985). 2015 Mar 1;118(5):509-19.