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  • High-altitude-physiology

    1. 1. HIGH ALTITUDEPHYSIOLOGY Dr Raghuveer Choudhary Associate Professor Dept. of Physiology Dr S.N.Medical College ,Jodhpur
    2. 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
    4. 4. STUDY IS IMPORTANT FOR:1) Mountaineering2) Aviation & Space flight3) 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. 5. 1% Oth er 21 % O2 78 % N2 The French physiologist Paul Bert first recognized that the harmful effects760 mm Hg of high altitude are caused by low oxygen tension. 47 --- mm/Hg 95 --- 190 --- 380 --- 523 --- 760 ---
    6. 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. 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. 8. PHYSIOLOGICALYCRITICAL ALTITUDES:•Upto 10,000 ft (3,000m)”safe zone of rapidascent”classicallydefines ‘high altitude’•At 18,000 ft (5,500 m) upper limit of permanenthuman inhabitation•Above 20,000 ft (6,000m)  life is endangeredwithout supplementaloxygen•From 40,000 ft(12,000 m) Ozone layer starts
    9. 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. 10. CHARACTER & DEGREE OF HYPOXIC EFFECTSWITH INCREASING ALTITUTUDE DEPENDSUPON:•Level of thealtitude•Rate of ascent•Duration ofexposure at highaltitude
    11. 11.  COMMON HYPOXIC EFFECTSWITH DIFFERENT ALTITUDES:ALTITUDE INSPIRED Hb- EFFECTSLEVEL AIR PO2 SATURATIONIn 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 fatigue15,000 – 20,000 70 < 70 % Severe hypoxic symp  aggravated CNS(4,500 – 6,000) involvement Seizures and muscle twitchingAbove 20,000 & Further falls below 60 % Unconsciousness & alarmingonwards deterioration survival impossible without supplemental O2 (critical survival altitude)
    12. 12. WARNING!When hemoglobin saturation falls below 60%serious cellular dysfunction occurs; and if prolonged, can cause death
    13. 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. 14. PHYSIOLOGICAL RESPONSES TOHIGH 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 hypoxiaAcclimatizationRefers to changes in body tissues in response to long term exposure to hypoxia
    15. 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 breathingB) Tachycardia:Also d/t peripheral chemo. Response  CO  oxygen delivery to the tissues
    16. 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. 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. 18. ACCLIMATIZATION AT HIGH ALTITUDE:•Delivery of atmospheric O2 to the tissues normallyinvolve 3 stages---with a drop in PO2 at each stage.•When the starting PO2 is lower than normal, bodyundergoes 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 toadjust by certain physiological adaptations..
    19. 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. 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. 21. C)↑Vascularity of theTissues: 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. 22. E) Physiological Polycythemia:
    23. 23. F) CVS Changes:• adequate restoration of tissue O2 supply gradual reversal of the hyperdynamic activity (occurred during initial accommodative period)  ↑performance & ↓discomfort.
    24. 24. MALADAPTATIONS AT HIGHALTITUDE: do not• A few individualssmoothly adapt  developserious manifestations  warrantreturn to lower levels• Even those having alreadyAdapted  may deteriorate,if stationed above 16,000 ftfor more than 3-4 days.• Four relatively common &specific clinical forms discussed--
    25. 25. A)General Deterioration:• Mildest & most common form.• Even in already acclimatized subs.• Gradual loss of well-being, c/blaziness, loss of appetite & weight,passing of loose, greasy stools.• Takes 2-4 wks to recover afterreturning to lower levels.• Usually not occur at altitudesbelow 16,000 ft.
    26. 26. Cheyne-StokesRespirations: 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. 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. 28. •Acute Mountain Sickness:•Cause exactly not known appears to be assoc.with Cerebral oedema (↓pO2  arteriolardilatation limit of cerebral autoregulatory mechsare crossed  ↑cap.pressure ↑fluid transudationinto brain tissue) or AlkalosisIn the minority, more serious sequelae – high-altitude pulmonary oedema and high-altitudecerebral oedema develop.
    29. 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 tentorialherniation of thebrain-tissue)
    30. 30. B) High Altitude PulmonaryOedema (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. 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. 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. 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. 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. 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. 36. MEDICAL CONDITIONS AGGRAVATED ATHIGH 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. 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, persons 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. 38. A Gamow bag in action during equipment practice on the Apex 2 Expedition.
    39. 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