3. Why do we need to study this topic???
1) Mountaineering
2) Aviation & Space flight
3) Permanent human settlement at highland
4. Critical Altitude
• Up to 10000 ft – no signs & symptoms, but mild hypoxia Can
acclimatize.
• So high altitude called above 10000ft
• 18,000 ft highest altitude where permanent inhabitation possible
• Above 20,000 ft hypoxia endanger life so O2 needed
• About 35,000 ft modern aircrafts fly, pressurized cabins
7. Physiological responses to high altitude
hypoxia
• Divided into following two
I) Acute responses (accommodation)
II) Long term responses (acclimatization)
Accommodation immediate reflex adjustments of respiratory and
cardiovascular system to hypoxia
Acclimatization changes in body tissues in response to long term
exposure to hypoxia
8. Accommodation
• Immediate reflex responses of the body to acute hypoxic exposure.
A) Hyperventilation: Decrease arterial PO2
stimulation of peripheral chemo receptors
increased rate & depth of breathing
B) Increased 2,3-DPG conc. in RBC: within hours, ↑deoxy-Hb conc.
locally ↑Ph
↑2,3-DPG
↓oxygen affinity of Hb
tissue O2 tension maintained at higher than normal level
9. C) Tachycardia: Also stimulate peripheral chemo receptors
increase Cardiac Output
increase oxygen delivery to the tissues
D) Neurological
• Considered as “warning signs”
• Depression of CNS feels lazy, sleepy ,headache
• ‘Release Phenomena’ like effect of alcohol, lack of coordination,
slurred speech, slowed reflexes, overconfidence
• At further height cognitive impairment, poor judgment, twitching,
convulsion & finally unconsciousness
10. Acclimatization
• Various physiological readjustments and compensatory mechanisms in body
that reduces the effects of hypoxia in permanent residents at high altitude.
• It is done by
A great increase in pulmonary ventilation
Increase diffusion capacity of lung
Increased ability of the tissue cells to use O2
Increased vital capacity
Respiratory alkalosis
11. Sustained Hyperventilation
• Prolonged hyperventilation
CO2 wash-out
respiratory alkalosis
renal compensation
alkaline urine
normalization of pH of blood & CSF
withdrawal of central chemo- mediated respiratory depression
Fading inhibition for 2-5 days
Respiratory center response to chemoreceptor with full force and
increase ventilation to five times normal
12. Increased erythropoietin
Increased no of RBC
Increased blood volume
Increased Cardiac output
Increased vascularity of the peripheral tissues
Alkaline urine
• Cellular Acclimatization
Increased mitochondria
Increased Cytochrome Oxidase
Increased Myoglobin
13. Acclimatization Schedule
• Stage 1 [9000’-12000’] 6days
• Days 1-2 : Rest, short walks,
no climb
• Days 3-4 : Slow pace walk
1.5-3 km, no steep climb
• Days 5-6 : 5 km walk, climb
300m
14. Clinical syndromes caused by high altitude
(Hazard of rapid ascent)
• High altitude pulmonary edema (HAPE)
• Acute mountain sickness.
• Chronic mountain sickness.
15. High altitude pulmonary edema (HAPO)
• Above 10000 ft.
• Seen in Persons who acclimatized to high altitude, stay at sea levels for >
2wk s& again rapidly re-ascend.
• Characteristics
(i) life-threatening form of non-cardiogenic pulmonary edema due to
aggravation of hypoxia
(ii) Not develop in gradual ascent & on avoidance of physical exertion during
first 3-4 days of exposure.
16.
17.
18. Acute mountain sickness
• Occurs when person from sea level ascend to high altitude within 1-
2 days for the first time
• Develop within 8-24 hrs & lasts for 4-8 days.
• More likely if : –Rapid ascent –Lack of acclimatization
19.
20. Acute mountain sickness
• Cause exactly not known
• appears to be assoc. with Cerebral edema
↓pO2
arteriolar dilatation
limit of cerebral autoregulatory mechanisms are crossed
↑capillary hydrostatic pressure
↑ fluid transudation into brain tissue
• If remain untreated , it may cause—Ataxia, Disorientation, coma & Finally
Death
21. Chronic mountain sickness
• Occurs in long term residents of high altitude.
• Develop – Polycythemia, cyanosis, malaise, fatigue & exercise intolerance.
Extreme ↑Hb levels
↑viscosity of blood
↓ blood flow to tissues
widespread pulmonary vasoconstriction(hypoxic response)
Rise in pulmonary arterial pressure (Pulmonary hypertension)
Right heart failure