Download - High altitude physiology
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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
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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
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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
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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%
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Acute effects of hypoxia12,000 ft 18000 ft 23000 ftDrowsiness Seizures Coma
Lassitude Death
Mental and muscle fatigue
Sometimes headache
Occasionally nausea
Sometimes euphoria
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Acclimatization • Increased pulmonary ventilation
• Increased RBC number and hemoglobin concentration
• Increased diffusion capacity
• CVS changes and increased tissue capillarity
• Cellular level changes
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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
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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
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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)
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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
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Cellular level changes• Increased mitochondria
• Increased myoglobin
• Increased oxidative enzymes like cytochrome oxidase
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Hypoxia inducible factors
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Native of high altitude• Barrel shaped chest
and decreased body size high ratio of ventilatory capacity to body mass
• Cardiomegaly extra amount of CO
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Work capacity• Decreased mental proficiency (decreased judgement,
memory and performance of discrete motor movements)
• Decreased work capacity of skeletal and cardiac muscles
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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)
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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
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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
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Chronic mountain sickness• Polycythemia increased viscosity sluggish blood
flow
• Further increase in pulmonary arterial pressure
• RVH RVF
• Hypoxia induced systemic vasodilatation hypotension
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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.