PHYSIOLOGICAL RESPONSE TO HIGH ALTITUDE.pptx

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1. PHYSIOLOGICAL RESPONSE TO HIGH ALTITUDE PRESENTED BY:DR.VIDYA PANDA PGT 1 st year.

2. INTRODUCTION Barometric pressure falls with increasing altitude, but composition of air remain same. According to Dalton’s law: Total Pressure of Air = Sum of Partial Pressure of All Gases. P= pO 2 +pCO 2 +pN 2 +pH 2 O pH 2 O & pCO 2 determined by body so does not change with altitude. As metabolic production of CO 2 does not alter with increasing altitude, alveolar pCO 2 will not change. Only pO 2 & pN 2 changes.

3. STUDY IS IMPORTANT FOR Mountaineering Aviation & Space flight Permanent human settlement at highlands The French physiologist Paul Bert first recognized that the harmful effects of high altitude are caused by low oxygen tension.

4. ALTITUDE TYPE FROM SEA LEVEL(IN FEET) HIGH 10000-12000 FT VERY HIGH 12000-18000 FT EXTREMELY HIGH ABOVE 18000FT

5. ALTITUDE Mount Everest - 29,028 ft (8848mt)(previously 8840mt) Atmospheric Pr =255mmHg PO2= 53mmHg Inspired PO2 =44mmHg

6. PHYSIOLOGICAL RESPONSES TO HIGH ALTITUDE HYPOXIA Divided into following two--- Acute responses (accommodation) Long term responses (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

7. ACCOMODATION AT HIGH ALTITUDE Immediate reflex responses of the body to acute hypoxic exposure. A) Hyperventilation: Decrease arterial PO 2  stimulation of peripheral chemo receptors  increased rate & depth of breathing B) Tachycardia: Also stimulate peripheral chemo. Receptors  increase Cardiac Output  increase 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

8. 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

9. ACCLIMATISATION AT HIGH ALTITUDE Various physiological readjustments and compensatory mechanisms in body that reduces the effects of hypoxia in permanent residents at high altitude. It is done by- A great increase in pulmonary ventilation Increase diffusion capacity of lung Increased ability of the tissue cells to use O 2 Increased vital capacity

10. Respiratory alkalosis Cheyne-Stokes Respirations Increased erythropoietin Increased no of RBC Increased blood volume Increased Cardiac output Increased vascularity of the peripheral tissues Alkaline urine Cellular Acclimatization— Increased mitochondria Increased Cytochrome Oxidase Increased Myoglobin

11. SUSTAINED HYPERVENTILATION Such powerful ventilatory drive is also possible as- ↑sensitivity of chemo receptor to PO 2 & PCO 2 Somewhat ↓ in work of breathing  make hyperventilation easy & less tiring ↑ TLC : in high-landers  evidenced by relatively enlarged (barrel-shaped) chest ↑ventilatory capacity in relation to body mass. ↑ Diffusing capacity of lungs : due to hypoxic pulmonary vasoconstriction  Pulmonary Hypertension  ↑ no. of pulmonary capillaries

12. ↑Vascularity of the Tissues: More capillaries open up in tissues than at sea-level (normal ~25 % open & rest—remaining as‘reserve ’). Growth of new circulatory capillaries in non pulmonary tissues (angiogenesis). This combined with systemic vasodilatation(also a hypoxic response)  more O 2 delivery to tissues.

13. Physiological Polycythemia: Hypoxia induced erythropoiesis ↑Hb Conc. & RBC count (within a few wks. stay) Expansion of blood volume Hemodynamic is kept within normal limit inspite of ↑ vascularity of tissues ↑Amount of circulating Hb Inspite of ↓saturation ,O2-carrying capacity is maintained at normal limit

14. CVS Changes: Cardiac output often increases as much as 30 %immediately, then gradually return to normal in one to two weeks as the blood hematocrit increases. Capillary density in right ventricle muscle increases Cheyne-Stokes Respirations:

15. Clinical syndromes caused by high altitude (Hazard of rapid ascent) Acute mountain sickness. Chronic mountain sickness.

16. Acute mountain sickness. Occurs when person from sea level ascend to high altitude within 1-2 days for the first time Develop within 8-24 hrs & lasts for 4-8 days. More likely if : Rapid ascent Lack of acclimatization Symptoms - nausea, vomiting, headache, dizziness ,irritability, insomnia & breathlessness.

17. Cause exactly not known appears to be assoc. with Cerebral oedema (↓pO 2  arteriolar dilatation limit of cerebral autoregulatory mechs are crossed  ↑capillary pressure ↑ fluid transudation into brain tissue) or Alkalosis In the minority, more serious sequelae – high-altitude pulmonary oedema and high-altitude cerebral oedema develop. If remain untreated , it may cause— Ataxia, Disorientation, coma & Finally Death (due to tentorial herniation of the brain-tissue)

18. Treatment – High dose of Glucocorticoids. Decreasing alkalosis by giving Acetazolamide – as it decreases H+ ion excretion by kidney by inhibiting carbonic anhydrase.

19. Chronic mountain sickness. Monge’s disease Occurs in long term residents of high altitude. Develop – Polycythemia, cyanosis, malaise, fatigue & exercise intolerance. Extreme ↑Hb levels  ↑viscosity of blood  ↓ blood flow to tissues  widespread pulmonary vasoconstriction(hypoxic response)  Pul.hypertensionRVF Treatment- return to lower altitude(at sea-levels)  to prevent rapid development of fatal pulmonary oedema

20. 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.

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