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Under graduate Lecture


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

High Altitude Physiology: 

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




STUDY IS IMPORTANT FOR: Mountaineering Aviation & Space flight 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 increasing altitude .

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760 mm Hg 47 --- mm/Hg 95 --- 190 --- 380 --- 523 --- 760 --- 21% O 2 78% N 2 1% Other The French physiologist Paul Bert first recognized that the harmful effects of high altitude are caused by low oxygen tension.

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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 .


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


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


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 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 ( of indifference) 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 & alarming deterioration  survival impossible without supplemental O2 (critical survival altitude)


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

Critical Stage: 

Critical Stage Altitudes Air: 20,000 feet and above 100% O 2 : 44,800 feet and above Signs: loss of consciousness, convulsions and death


PHYSIOLOGICAL RESPONSES TO HIGH ALTITUDE HYPOXIA: Arbitrarily Divided into following two--- Acute responses (aka accommodation) 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


ACCOMMODATION AT HIGH ALTITUDE: immediate reflex responses of the body to acute hypoxic exposure. 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….. 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

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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


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— ↓ pressure drop during transfer ↑ oxygen carrying capacity of blood ↑ ability of tissues to utilize O2 With longer stay at high altitude ,body is able to adjust by certain physiological adaptations ..

A)Sustained Hyperventilation:: 

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- ↑sensitivity of chemo receptor to PO2 & PCO2 Somewhat ↓ in work of breathing  make hyperventilation easy & less tiring

B) Other Respiratory Changes:: 

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 debatable!!!

C)↑Vascularity of the Tissues:: 

C)↑Vascularity of the Tissues: More capillaries open up in tissues than at sea-level ( 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.

E) Physiological Polycythemia:: 

E) Physiological Polycythemia:

F) CVS Changes:: 

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:: 

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:: 

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.

A) Acute Mountain Sickness:: 

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.

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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.


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)

B) High Altitude Pulmonary Oedema (HAPO):: 

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

HAPO Manifestations:: 

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:: 

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:: 

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:: 

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.

D)Chronic Mountain Sickness:: 

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.

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


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