8,000 – 12,000 12,000 – 18,000

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 )

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


• 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.

•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

In feet (metre) In mm of Hg 0 (i.e.sealevel) Upto 10,000 (3,000) 10,000 – 15,000 (3,000 – 4,500) 15,000 – 20,000 (4,500 – 6,000) 160 110 in % ~ 97 % ~ 90 %

Stages (if any) NIL Usually none, +/- some nocturnal visual reduction ( of indifference) Mod. Hypoxic symptoms cardiorespiratory manifestaions & early CNS involvements ( of reaction) Severe hypoxic symp  aggravated CNS involvement (of disturbance)


~ 80 %


< 70 %

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 .


 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

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

•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: open up in tissues than at • More capillaries
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: not • A few individuals do
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: people experience a • Above 10,000 ft (3,000 m) most

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 breathingarrest, 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:understood but two processes are believed to • Still not well
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 2,3DPG 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:occurring in a low-lander, who ascends • Symptom-complex
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)

 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:  in some long term high• aka Monge’s disease

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: Disease &/or Hypertension, • Obstructive Pul.
• 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.


• 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.

• 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!!!

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