The document provides an overview of high altitude physiology, discussing the effects of decreased barometric pressure and oxygen levels on human health. It highlights physiological responses to hypoxia, including acute responses and acclimatization, and details common clinical syndromes such as high altitude pulmonary edema and acute mountain sickness. Additionally, it emphasizes the importance of understanding these effects for activities like mountaineering, aviation, and human settlement at high altitudes.

1. High Altitude Physiology
Dr. Ranadhi Das
ranadhi@gmail.com

2. Introduction
 Barometric pressure falls with increasing altitude, but
composition of air remain same.
 According to Dalton’s law:
Total Pressure of Air = Sum of Partial Pressure of All Gases.
 P= pO2+pCO2+pN2+pH2O
 pH2O & pCO2 determined by body so does not change
with altitude.
 As metabolic production of CO2 does not alter with
increasing altitude, alveolar pCO2 will not change.
 Only pO2 & pN2 changes.

3. Study is important for:
1) Mountaineering
2) Aviation & Space flight
3) Permanent human settlement at highlands
 The French physiologist Paul Bert first
recognized that the harmful effects of high
altitude are caused by low oxygen tension.

4. ALTITUDE TYPE FROM SEA-LEVEL (In feet)
HIGH 10,000 – 12,000
VERY HIGH 12,000 – 18,000
EXTREMELY HIGH Above 18,000

5. Barometric pressure & partial pressure
of gases.
Monday, April 24, 2017
Level of alt
Itude(Feet)
Barometric
pressure(
mmHg)
Atmospher
ic pressure
pO2(mmHg
)
Alveolar
air
pO2(mmHg
)
pCO2(mm
Hg)
% O2
saturation
of Hb
Sea level 760 159 104 40 100
5000 630 130 80 40 95
10000 520 110 60 40 90
15000 480 90 50 36 80
18000 400 80 40 30 70
20000 350 70 <40 <30 <70
40000 140 30 12 24 15

6. Physiologically critical altitudes:
• Up to 10,000 ft (3,000 m)“safe zone of rapid
ascent”classically defines ‘high altitude’
• At 18,000 ft (5,500 m)  upper limit of permanent
human inhabitation
• Above 20,000 ft (6,000 m)  life is endangered without
supplemental oxygen
• At 25,000 to30,000 ft  O2 supplement has to be started.
Called Critical Survival Altitude.
• From 40,000 ft(12,000 m)  Ozone layer starts

7. Altitude
 Mount Everest -
 29,028 ft (8848mt)(previously
8840mt)
 Atmospheric Pr=255mmHg
 PO2= 53mmHg
 Inspired PO2 =44mmHg
 Unacclimatized person ----
 Unconscious in 45 seconds
 Dead in 4 to 6 minutes

8. Facts to know:
 Commercial plane fly- 8000 ft(2400mt)
 Skydiver- 15000ft(4800mt)
 Military Aircraft fly- 59,000ft(18,000mt)
 Helicopter fly- 6000ft
 In 1936, Francis Swain of the Royal Air Force reached 15,230 m
(49,970 ft) flying a Bristol Type 138 while wearing a pressure suit.
 Two years later Italian military officer Mario Pezzi set an altitude
record of 17,083 m (56,047 ft), wearing a pressure suit in his open-
cockpit plane.
 The highest current world absolute general aviation altitude record is
37,650 meters (123,520 ft) set by Alexandr Fedotov, on 31 August
1977.

9.  Common hypoxic effects with
different altitudes:
ALTITUDE
LEVEL
INSPIRED
AIR PO2
Hb-
SATURATION
EFFECTS
In feet (metre) In mm of Hg in % Stages (if any)
0 (i.e.sea-level) 160 ~ 97 % NIL
Upto 10,000
(3,000)
110 ~ 90 % Usually none, +/- some nocturnal visual
reduction
10,000 –
15,000
(3,000 – 4,500)
98 ~ 80 % Mod. Hypoxic symptoms Drowsiness,
headaches ,Mental and muscle fatigue
15,000 –
20,000
(4,500 – 6,000)
70 < 70 % Severe hypoxic symp  aggravated
CNS involvement Seizures and muscle
twitching
Above 20,000
&
onwards
Further falls below 60 % Unconsciousness ,Failing vision,
incordination, inability to perform
mental task survival impossible
without supplemental O2 (critical
survival altitude)

10.  29,000 feet- Highest level at which aviator can fly
without O2
 34,000 feet- Highest level at which aviator can fly
with O2
 40,000 feet- Aviator can fly in pressurized cabin
with 100% O2 with pressure suit.
 64,000 feet (47mm Hg)- when water boil at normal
body temperature. Vapour density of water same as
that of water. Known as Armstrong limit.

11. Physiological responses to high altitude hypoxia:
 Divided into following two---
I) Acute responses (accommodation)
II) Long term responses (acclimatization)
Accomodation
Refers to immediate reflex adjustments of respiratory
and cardiovascular system to hypoxia
Acclimatization
Refers to changes in body tissues in response to long
term exposure to hypoxia

12. Accommodation at high altitude:
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) Tachycardia:
Also stimulate peripheral chemo. Receptors  increase Cardiac
Output  increase oxygen delivery to the tissues
C) 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

13. 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

14. Acclimatization at high altitude:
 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

15.  Respiratory alkalosis
Cheyne-Stokes Respirations
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

16. 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  net result is ↑resting pulmonary ventilation
(by ~5 folds ),primarily due to ↑ in TV (upto 50% of VC)
 Such powerful ventilatory drive is also
possible as-
(i) ↑sensitivity of chemo receptor to PO2 & PCO2
(ii) Somewhat ↓ in work of breathing  make
hyperventilation easy & less tiring

17. ↑ TLC : in high-landers evidenced by
relatively enlarged (barrel-shaped) chest
↑ventilatory capacity in relation to body mass.
↑ Diffusing capacity of lungs: due to hypoxic
pulmonary vasoconstriction  Pulmonary
Hypertension  ↑ no. of pulmonary capillaries

18. ↑Vascularity of the Tissues:
• More capillaries open up in tissues than at sea-
level (normal ~25 % open & rest—remaining
as‘reserve’).
• Growth of new circulatory capillaries in non
pulmonary tissues (angiogenesis).
• This combined with systemic
vasodilatation(also a hypoxic response) more
O2 delivery to tissues.

19. Physiological Polycythemia:
 Hypoxia induced erythropoiesis
◦ ↑Hb Conc. & RBC count (within a few wks. stay)
 Expansion of blood volume
Hemodynamic is kept within normal limit inspite of ↑
vascularity of tissues
 ↑Amount of circulating Hb
 Inspite of ↓saturation ,O2-carrying capacity is maintained
at normal limit

20. CVS Changes:
• Cardiac output often increases as much as
30% immediately, then gradually return to
normal in one to two weeks as the blood
hematocrit increases.
• Capillary density in right ventricle muscle
increases because of the combined effects of
hypoxia and excess workload on the right
ventricle caused by pulmonary hypertension
at high altitude.

21. Cheyne-Stokes Respirations:
 Above 10,000 ft (3,000 m) most people experience a periodic
breathing during sleep. Repeated sequence of gradual onset of
apnoea followed by gradual restoration of respiration.
 Respirations may cease entirely for a few secs & then shallow
breaths begin again. During period of breathing-arrest, person often
becomes restless & may wake with a sudden feeling of suffocation.
• Can disturb sleeping patterns exhausting the climber.
Acetazolamide is helpful in relieving this.

22. Clinical syndromes caused by high
altitude (Hazard of rapid ascent)
 High altitude pulmonary oedema. (HAPO)
 Acute mountain sickness.
 Chronic mountain sickness.

23. High altitude pulmonary edema
(HAPO).
 Above 10000 ft.
 Seen in
◦ 75-80% in persons doing heavy physical work in first 3-4 days
◦ Persons who acclimatized to high altitude, stay at sea levels for
> 2wks& 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.

24. HAPO Manifestations:
 Earliest indications are- ↓exercise tolerance & slow recovery from
exercise. The person feels fatigue, weakness & exertional dyspnoea .
 Condition typically worsens at night & tachycardia and tachypnea
occur at rest.
 Symptoms --Cough, frothy sputum, cyanosis, rales & dyspnea
progressing to severe respiratory distress
 Other common features-- low-grade fever, respiratory alkalosis, &
leucocytosis
 In severe cases-- an altered mental status, hypotension, and ultimately
death may result.

25. Mechanism of development of HAPO
Monday, April 24, 2017
Sympathetic activation by physical work is over
& above sympathetic stimulation by hypoxia &
cold.
Vasoconstriction
Increase in pulmonary capillary hydrostatic
pressure.(10 to 25mmHg)
Increase in capillary pressure drives the
fluid out of pulmonary capillaries
Develops Pulmonary Oedema

26. Treatment of HAPO:
 Standard & most imp to descend to lower altitude as
quickly as possible( preferably by at least 1000 meters) & to
take rest.
 Oxygen should also be given (if possible).
 Symptoms tend to quickly improve with descent, but less
severe symptoms may continue for several days.
 The standard drug treatments for which there is strong clinical
evidence are dexamethasone & CCB’s (like nifedipine).
 PDE inhibitors (e.g. tadalafil) are also effective.

27. 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
Symptoms- nausea, vomiting, headache, dizziness ,irritability,
insomnia & breathlessness.

28. • Cause exactly not known appears to be assoc. with Cerebral
oedema (↓pO2  arteriolar dilatation limit of cerebral
autoregulatory mechs are crossed  ↑capillary pressure ↑
fluid transudation into brain tissue) or Alkalosis
• In the minority, more serious sequelae – high-altitude pulmonary
oedema and high-altitude cerebral oedema develop.
• If remain untreated , it may cause— Ataxia, Disorientation, coma
& Finally Death (due to tentorial herniation of the brain-tissue)

29. Treatment –
 High dose of Glucocorticoids.
 Decreasing alkalosis by giving Acetazolamide
– as it decreases H+ ion excretion by kidney
by inhibiting carbonic anhydrase.

30. Chronic mountain sickness.
 Monge’s disease
 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)
Pul.hypertensionRVF
 Treatment- return to lower altitude(at sea-levels)  to
prevent rapid development of fatal pulmonary oedema

32. Medical conditions aggravated at high
altitude:
 Obstructive Pul. Disease &/or Hypertension,
 Congestive cardiac failure,
 Sickle cell anemia,
 Angina/Coronary artery disease,
 Cerebrovascular diseases,
 Seizure disorders, etc.