high altitude physiology

Physiological changes and acclimatization

at high altitude

Mayank Agarwal JR III

ma.gsvm@gmail.com

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.