Altitude Physiology

Altitude Physiology


ALTITUDE PHYSIOLOGY

  • High altitude has “Low atmospheric pressure”.
  • Air composition unchanged with altitude.
  • PO2 forms about 21% of atmospheric pressure at any altitude.
  • Hence, PO2 is low at high altitudes.
  • PO2 of inspired air (PiO2) is low.
  • Adequate oxygen delivery to tissues happens only at pressure close to sea level pressure.
  • If PO2 falls much below sea level, 
  • PO2 tissue oxygenation suffers (hypoxic hypoxia)
  • Consequently, physiological functions are deranged.

EFFECTS OF HIGH ALTITUDE:

  • Earliest response to fall in PO2 –
  • Hyperventilation – At altitude 3000 meters above sea level.
  • Hypoxic symptoms – At altitude of 4000 meters.
  • Becomes severe – at 5000 meters.
  • Loss of consciousness – At 6000 meters.

TYPES OF RESPONSE:

  • Acute response/Acute Transient Response/Acute Mountain Sickness.
  • Acclimatization.
  • Chronic Mountain Sickness.

I. ACUTE RESPONSE:

  • Earliest response – Hyperventilation.
  • Followed by increased cardiac output.
  • Responses include – Breathlessness & palpitation
  • Hence, referred “Acute Transient Response”/”Transient Mountain Sickness”.
  •  “Acute Mountain Sickness” – 
  • Develop after a lag of 6 hours to 4 days

1. ACUTE MOUNTAIN SICKNESS:

  • Usually develops within a day & lasts for a week.
  • Characterized by hypoxic symptoms –
  • Breathlessness.
  • Weakness.
  • Headache
  • Dizziness
  • Palpitation
  • Tachycardia.
  • Sweating
  • Dimness of vision
  • Partial sleeplessness.
  • Nausea.

May cause syndromes – 

  • High Altitude Pulmonary Edema (HAPE).
  • High Altitude Cerebral Edema (HACE).

1a. HIGH ALTITUDE PULMONARY EDEMA (HAPE):

  • Hypoxia causes pulmonary capillaries vasoconstriction causing,
  • Pulmonary hypertension → In turn, raises pulmonary capillary hydrostatic pressure.
  • Results in,
  • Distrupion of weaker capillaries walls.
  • Exudation of protein-rich fluid in lung tissues.

1b. HIGH ALTITUDE CEREBRAL EDEMA (HACE):

  • Low PO2 causes arteriolar dilation.
  • If cerebral autoregulation does not compensate,
  • Results in increased cerebral capillary pressure → Favoring increased fluid transudation into brain tissue.
II. ACCLIMATIZATION:
  • “Development of compensatory mechanisms to ward off ill-effects of low barometric pressure”.
  • Due to continued stay at high altitude.

EFFECTS:

  • Hyperventilation – Most fundamental response to hypoxia.
  • Low arterial PO2 (hypoxemia) stimulates carotid body peripheral chemoreceptors.
  • Causing hyperventilation.

But, hyperventilation washes out CO2,

  • Leading to, 
  • Arterial PCO2 fall.
  • Fall in PCO depresses respiration.
  • Via central chemoreceptor mechanism.
  • Respiratory alkalosis (increased pH). 
  • Compensated by increased renal excretion of bicarbonate.
  • Thus blood carbonic acid/bicarbonate ratio & pH maintained at normal level.
  • Peripheral chemoreceptors are not affected by pH.
  • An acclimatized person maintain slight acidic CSF pH.
  • Because HCO3 pump is located at blood-brain barrier
  • Pumping out HCO3-.
  • Consequently, CSF pH is restored to normal.
  • Since central chemoreceptors are affected primarily by CSF pH
  • No longer inhibit respiration despite CO2 washout.
  • Increased respiratory chemoreceptor sensitivity causing hypoxia & CO2.
  • Eventual effect is “Increased minute volume”, primarily a result of increased tidal volume.
3. RISE OF 2,3 – DIPHOSPHOGLYCERATE (DPG) CONCENTRATION OF RBCs:
  • Increases DPG.
  • Causing “Rightward” shift of oxygen-Hb dissociation curve.
  • Resulting in increased tissue O2 delivery.

4. POLYCYTHEMIA:

  • Hypoxia stimulates “Erythropoietin” release.
  • Stimulating erythropoiesis  → Increased RBC count & hemoglobin concentration.
  • Hence, absolute polycythemia with increased red cell mass.

5. OTHER COMPENSATORY MECHANISM:

  • Increases renal alkali (HCO3) excretion.
  • Increased cardiac output immediately.
  • Returns normal within few weeks.
  • Due to increased blood hematocrit.
  • Increased lung diffusion capacity.
  • Increased vascularity of tissues.
  • Increased capillary density.
  • Enhancement of oxidative metabolism.Increased myoglobin.
  • By increased mitochondrial count & cytochrome oxidase content.

6. RELATIONSHIP Bt. WORK CAPACITY & ACCLIMATIZATION:

  • Work capacity of skeletal & cardiac muscle –
  • Decreased in unacclimatized person
  • Acclimatization improves work capacity gradually.
  • Exercise performed at high altitude hastens acclimatization process.
  • Exercise increases oxygen requirement despite low avaialability.
  • Thus, increasing duration of exercise increases work capacity.
  • Work capacity at high altitude can be increased by,
  • Increasing duration of exercise.
  • Also by reducing/maintaining workload at an optimum level corresponding to maximum oxygen uptake rate.
  • Thus all available oxygen utilized.

III. CHRONIC MOUNTAIN SICKNESS/ MONGE’S DISEASE:

  • Due to insensitive peripheral chemoreceptors to hypoxia.
  • Causes severe hypoxic symptoms.
EFFECTS:
  • Causes widespread pulmonary vasoconstriction → Eventually right ventricular failure (cor pulmonale).
Exam Question
 

ALTITUDE PHYSIOLOGY

  • PO2 is low at high altitudes.
  • PO2 of inspired air (PiO2) is low.
  • Earliest response to fall in PO2 – Hyperventilation
  • Acute mountain sickness is characterized by hypoxia-like symptoms Tachycardia.
  • High altitude pulmonary edema causes raise pulmonary capillary hydrostatic pressure.
  • During acclimatization, Hyperventilation is most fundamental response to hypoxia.
  • Low arterial PO2 (hypoxemia) stimulates carotid body peripheral chemoreceptors → Causing hyperventilation.
  • Leading to “Arterial PCO2 fall” & “Respiratory alkalosis (increased pH). 
  • Respiratory alkalosis compensated by increased renal excretion of bicarbonate.
  • Thus blood carbonic acid/bicarbonate ratio & pH maintained at normal level.
  • Peripheral chemoreceptors are not affected by pH.
  • “Increase in sensitivity of respiratory chemoreceptor mechanisms to hypoxia & CO2.
  • Eventual effect is “Increased minute volume”, as a result of increased tidal volume.
  • Acclimatization increases DPG.
  • Causing “Rightward” shift of oxygen-Hb dissociation curve.
  • Resulting in increased tissue O2 delivery.
  • Hypoxia stimulating erythropoiesis → Increased RBC count & hemoglobin concentration.
  • Hence, absolute polycythemia with increased red cell mass.
  • Other compensatory mechanisms – Increases renal alkali (HCO3-) excretion.
  • Exercise performed at high altitude hastens acclimatization process.
  • Increasing duration of exercise increases work capacity.
  • Work capacity at high altitude can be increased by,
  • Increasing duration of exercise.
  • Also by reducing/maintaining workload at an optimum level corresponding to maximum rate of oxygen uptake.
  • All available oxygen can be utilized.
  • Chronic mountain sickness/Monge’s disease can lead to right ventricular failure (cor pulmonale).
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