Seminar

1. HIGH ALTITUDE
PHYSIOLOGY
Dr Raghuveer Choudhary
Associate Professor
Dept. of Physiology
Dr S.N.Medical College
,Jodhpur

2. High Altitude Physiology
• Discussion Points
• Air pressure changes in high altitude
• Physiologic effects of low air pressure on the
body
• Diseases that can arise from low air pressure
environment

3. CATEGORISATION FOR
DESCRIPTIVE CONVENIENCE:
ALTITUDE TYPE FROM SEA-LEVEL
(In feet)
HIGH 8,000 – 12,000
VERY HIGH 12,000 – 18,000
EXTREMELY HIGH Above 18,000

4. STUDY IS IMPORTANT FOR:
1) Mountaineering
2) Aviation & Space flight
3) Permanent human settlement at highlands
 Barometric Pressure &
Height Have Inverse
Relationship:
• Primary problem at high altitude.
• Atmospheric composition of air remains almost
constant (upto ~30,000 ft) but PO2 decreases with

5. 1% Oth
er
21
%
O2
78
%
N2 The French physiologist
Paul Bert first recognized
that the harmful effects
760 mm Hg of high altitude are
caused by low oxygen
tension.
47 --- mm/Hg
95 ---
190 ---
380 ---
523 ---
760 ---

6. SIGNIFICANT ATMOSPHERIC PRESSURE
VARIATION WITH ALTITUDE:
ALTITUDE PRESSURE
(FEET) ( mm of Hg) (ATMOSPHERIC UNIT)
0 760 1
18,000 380 1/2
34,000 190 1/4
48,000 95 1/8
63,000 47 1/16

7.  BASIC CONCEPT :
• Human body is specifically designed in such a
way that it delivers adequate O2 to the
tissues only when oxygen is supplied at a
pressure close to the sea-level (P = 760 mm
Hg  PO2 =159 mm Hg)
• So, at high altitude there is hypoxic hypoxia
 tissue oxygenation suffers physiological
derangements.
• “connecting a 24 volt motor to a 6 volt
battery”—perfect comparison by J.S.Milledge.

8. PHYSIOLOGICALY
CRITICAL ALTITUDES:
•Upto 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
•From 40,000 ft(12,000 m)
 Ozone layer starts

9. Altitude
• Mount Everest
• 29,028 ft (8848mt)
• Atmospheric Pr=255mmHg
• PO2= 53mmHg
• Inspired PO2=21%x(255-47)
• =44mmHg
– Unacclimatized person
– Unconscious in 45 seconds
– Dead in 4 to 6 minutes

10. CHARACTER & DEGREE OF HYPOXIC EFFECTS
WITH INCREASING ALTITUTUDE DEPENDS
UPON:
•Level of the
altitude
•Rate of ascent
•Duration of
exposure at high
altitude

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

12. WARNING!
When hemoglobin saturation falls
below
60%
serious cellular dysfunction occurs;
and if prolonged, can cause death

13. Critical Stage
• Altitudes
Air: 20,000 feet and above
100% O2: 44,800 feet and above
• Signs: loss of consciousness,
convulsions and death

14. PHYSIOLOGICAL RESPONSES TO
HIGH ALTITUDE HYPOXIA:
• Arbitrarily Divided into following two---
I) Acute responses (aka accommodation)
II)Long term responses ( aka 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

15. ACCOMMODATION AT HIGH ALTITUDE:
 immediate reflex responses of the body
to acute hypoxic exposure.
A)Hyperventilation:
arterial PO2  stimulation of peripheral
chemoreceptors  increased rate & depth of
breathing
B) Tachycardia:
Also d/t peripheral chemo. Response  CO 
oxygen delivery to the tissues

16. Contd…..
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

17. 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

18. ACCLIMATIZATION AT HIGH ALTITUDE:
•Delivery of atmospheric O2 to the tissues normally
involve 3 stages---with a drop in PO2 at each stage.
•When the starting PO2 is lower than normal, body
undergoes acclimatization so as to—
(i)↓ pressure drop during transfer
(ii)↑ oxygen carrying capacity of blood
(iii) ↑ ability of tissues to utilize O2
•With longer stay at high altitude ,body is able to
adjust by certain physiological adaptations..

19. A)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 d/t ↑ 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

20. B) Other Respiratory Changes:
↑ TLC : esp in high-landers(natives for
generations) evidenced by relatively
enlarged (barrel-shaped) chest l/t
↑ventilatory capacity in relation to body
mass.
↑ Diffusing capacity of lungs: d/t hypoxic
pulmonary vasoconstriction  Pul.
Hypertension  ↑ no. of pulmonary
capillaries
→ existence of this effect is still

21. C)↑Vascularity of the
Tissues: open up in tissues than at sea-level
• More capillaries
(normal ~25 % open & rest—remaining as‘reserve’).
• This combined with systemic vasodilatation(also a
hypoxic response) more O2 delivery to tissues.
D) Cellular level changes:
• ↑ intracellular mitochondrial density
• ↑ conc. of cellular oxidative enzymes
• ↑ synthesis of Mb( O2-storing pigment)
→ all aimed to improve O2 utilization.

22. E) Physiological Polycythemia:

23. F) CVS Changes:
• adequate restoration of tissue O2 supply
gradual reversal of the hyperdynamic activity
(occurred during initial accommodative
period)  ↑performance & ↓discomfort.

24. MALADAPTATIONS AT HIGH
ALTITUDE: do not
• A few individuals
smoothly adapt  develop
serious manifestations  warrant
return to lower levels
• Even those having already
Adapted  may deteriorate,
if stationed above 16,000 ft
for more than 3-4 days.
• Four relatively common &
specific clinical forms discussed--

25. A)General Deterioration:
• Mildest & most common form.
• Even in already acclimatized subs.
• Gradual loss of well-being, c/b
laziness, loss of appetite & weight,
passing of loose, greasy stools.
• Takes 2-4 wks to recover after
returning to lower levels.
• Usually not occur at altitudes
below 16,000 ft.

26. Cheyne-Stokes
Respirations: most people experience a
• Above 10,000 ft (3,000 m)
periodic breathing during sleep. The pattern begins with a
few shallow breaths increases to deep sighing
respirations  falls off rapidly.
• 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.
Not considered abnormal at high altitudes. But
if occurs first during an illness (other than
Altitude illnesses) or after an injury
(particularly a head injury)  may be a sign of
a serious disorder.

27. A) Acute Mountain Sickness:
• Symptom-complex occurring in a low-lander, who
ascends to very high altitudes over 1-2 days for first
timestarts ~8-24 hrs. after arrival lasts ~4-8 d
 Typically occurs at altitude > 8000 feet
 No predeliction based on gender
 More likely if :
–Rapid ascent
–Lack of acclimatization
–c/b nausea, vomiting, headache, dizziness ,irritability,
insomnia & breathlessness.

28. •Acute Mountain Sickness:
•Cause exactly not known appears to be assoc.
with Cerebral oedema (↓pO2  arteriolar
dilatation limit of cerebral autoregulatory mechs
are crossed  ↑cap.pressure ↑fluid transudation
into brain tissue) or Alkalosis
In the minority, more serious sequelae – high-
altitude pulmonary oedema and high-altitude
cerebral oedema develop.

29. Contd……
 Symptoms can be reduced by—
• ↓Cerebral oedema by large doses of
Glucocorticoids
• ↓Alkalosis by Acetazolamide (inhibits CA↓H+ &
↑HCO3- excretion through kidneys)
 If remain untreated ,
it may cause— Ataxia,
Disorientation,coma &
Finally Death(d/t tentorial
herniation of the
brain-tissue)

30. B) High Altitude Pulmonary
Oedema (HAPO):
• Usually seen in individuals who---
(i)Engage in heavy physical work during first 3-4 days
after rapid ascent (to more than 10,000 ft)
(ii)Are already acclimatizedreturn to high altitude
after a stay of ~2wks or more at sea-level.
• Characteristics---
(i)life-threatening form of non-cardiogenic pulmonary
edema d/t aggravation of hypoxia
(ii)Not develop in gradual ascent & on avoidance of
physical exertion during first 3-4 days of exposure.

31.  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.

32. Underlying Mech. Of HAPO:
• Still not well understood but two processes are
believed to be important:
(i)↑Symp. Activity (d/t hypoxia, cold & physical
exertion)Pul.vasoconstriction ↑pulmonary
capillary hydrostatic pressures (pul.hypertension)
(ii)An idiopathic non-inflammatory increase in the
permeability of the pul. vascular endothelium
→ fluid is driven out of capillariespul.oedema
 Incidence: in unacclimatized travellers exposed
to high altitude (~4,000 m or 13,000 ft) appears to
be 1-1.6% (as per world-wide statistics)

33. Predisposing factors for HAPO:
• Sex : Women may be less prone to develop HAPO.
• Other factors, such as alcohol, respiratory
depressants, and respiratory infections  enhance
vulnerability to HAPO.
• Individual susceptibility to HAPO is difficult to
predict. The most reliable risk factor is previous
susceptibility to HAPO, & there is likely to be a
genetic basis to this condition, perhaps involving
the gene for ACE.
• Recently, scientists have found significant
correlation b/w relatively low levels of 2,3-DPG
with the occurrence of HAPO.

34. Treatment of HAPO:
• Standard & most imp to descend to lower
altitude as quickly as possible( preferably by at least
1000 metres) & 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, but
may worsen headache (if any) of AMS.

35. D)Chronic Mountain Sickness:
• aka Monge’s disease  in some long term high-
altitude residents develops slowlybasically an
aberration of normal physiological responses
• Extreme ↑Hb levels  ↑viscosity of blood  ↓
blood flow to tissues ↓tissue oxygenationc/b
malaise, mental fatigue, headache & exercise
intolerance  widespread pulmonary
vasoconstriction(hypoxic response)Pul.HtnRVF
• T/t basically involves return to lower altitude(pref .
@ sea-levels)  to prevent rapid development of
fatal pulmonary oedema

36. 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.
→ Such individuals should be cautious or
completely abstain from visits to high
altitude. All visitors to the height of 5000
m or more, should first consult their

37. GAMOW BAG:
• A clever invention that has revolutionized the field
t/t of high altitude illnesses.
• Basically a sealed chamber with a pump(wt-6.3 kg).
• The person is placed inside the bag & it is fully
inflated by pumping → effectively ↑ the conc. Of
O2 molecules simulates a descent to lower
altitude (In ~ 10 mins,it can create an "atmosphere"
that corresponds to that at 3,000 - 5,000 ft lower)
After 1-2 hrs. in the bag, person's body chemistry
will have "reset" to the lower altitude lasts for 12
hrs outside of the bag  enough time to walk them
down to a lower altitude  allow for further
acclimatizationcarried in most HA-expeditions.

38. A Gamow bag in action during equipment practice on the
Apex 2 Expedition.

39. TO SUMMARIZE……….
• At high altitude air is thin. To make up for it, the
blood gets thick, respiration ↑ & circulation
improves, provided adequate time is given & body
functions properly  still some limitations remain
 natives adapt better