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HIGH ALTITUDE

PHYSIOLOGY

BY
CATEGORISATION FOR
DESCRIPTIVE
CONVENIENCE:
ALTITUDE FROM SEA-
TYPE LEVEL (In
feet)
HIGH 8,000 –
12,000
VERY HIGH 12,000 –
18,000
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 remains almost
constant (upto ~30,000 ft) but PO2 decreases
with increasing altitude (acc. to Dalton’s Law )
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
 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.
PHYSIOLOGICA
LY 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
CHARACTER & DEGREE OF
HYPOXIC EFFECTS WITH
INCREASING ALTITUTUDE
DEPENDS UPON:
•Level of the
altitude
•Rate of ascent
•Duration of
exposure at
high altitude
 COMMON HYPOXIC EFFECTS
WITH DIFFERENT ALTITUDES:
ALTITUDE INSPIRED Hb- EFFECTS
LEVEL AIR PO2 SATURATIO
N

In feet (metre) In mm of Hg in % Stages (if any)

0 (i.e.sea- 160 ~ 97 % NIL
level)
Upto 10,000 110 ~ 90 % Usually none, +/- some nocturnal
(3,000) visual reduction ( of
indifference)
10,000 – 98 ~ 80 % Mod. Hypoxic symptoms
15,000 cardiorespiratory manifestaions &
(3,000 – early CNS involvements
4,500) ( of reaction)
15,000 – 70 < 70 % Severe hypoxic symp 
20,000 aggravated CNS involvement
(4,500 – (of disturbance)
6,000)
PHYSIOLOGICAL
RESPONSES TO HIGH
ALTITUDE HYPOXIA:
• Arbitrarily Divided into following two---
I) Acute responses (aka accommodation)
II)Long term responses ( aka acclimatization)
• “Arbitrary” because ----
i) Acute are also beneficial for long-term coping up.
ii) Acute are modified steadily & imperceptibly in such a
way that after 2-3 days are considered as beginninng
of acclimatization .
iii) Sharpness of division depends on rate of ascent .
IMP. CONCEPTS IN
ENVIRONMENTAL PHYSIOLOGY:
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
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

D) Neurological :
• Considered as “warning signs”
• Depression of CNS  feels lazy, sleepy
,headache
• ‘Release Phenomena’ like effect of alcohol
• At further height  cognitive impairment,
twitching, convulsion & finally unconsciousness
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
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 to
60L/min),primarily d/t ↑ in TV (upto 50% of VC)

• Such powerful ventilatory drive is also
possible as-
(i)↑sensitivity of chemo- mechs to PO2 & PCO2
(ii)Somewhat ↓ in work of breathing  make easy &
less tiring
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
C)↑Vascularity of the
Tissues:
• More capillaries open up in tissues than at
sea-level (normal ~25 % at 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)
E) Physiological
Polycythemia:
F) CVS Changes:
• adequate restoration of tissue O2
supply gradual reversal of the
hyperdynamic activity (occurred
during initial accommodative period)
 ↑performance & ↓discomfort.
MALADAPTATIONS AT HIGH
ALTITUDE:
• A few individuals do not
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--
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.
Cheyne-Stokes
Respirations:
• Above 10,000 ft (3,000 m) most people experience a
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.
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.
 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.
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)
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.
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.
C) 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
• c/b nausea,vomiting,headache,irritability,insomnia &
breathlessness.
• 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 (renal shutdown inability to regulate normal
blood pH)
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)
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
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
physician.
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.
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 as implied,
natives adapt best & may wonder what
all the fuss the low-landers are making
about!!!