This document discusses physiology related to high altitudes. It explains that atmospheric pressure and oxygen levels decrease with increasing altitude. It then covers ways the body acclimates to low oxygen levels at altitude, including increased ventilation, changes in hemoglobin affinity for oxygen, increased lung diffusing capacity, and elevated red blood cell count and hematocrit. The document also discusses acute mountain sickness that can occur from rapid ascent and chronic mountain sickness from long term high altitude living. Finally, it notes adaptations of native high altitude inhabitants.
2. At Sea level atmospheric pressure is 760 mm
of Hg and Alveolar PO2 is 104 mm of Hg
At 10,000 feet Atmospheric pressure is 523
mm of Hg and Alveolar PO2 is 67 mm of Hg
and at this point there is still 90% saturation
At 20,000 feet atmospheric pressure is 349
mm of Hg and Alveolar PO2 is 40 mm of Hg
and at this point there is 70-75% saturation.
3. Atmospheric air consists of Nitrogen, oxygen,
CO2 and water vapors.
When we ascend to high altitude although
PO2 decreases but the percent composition of
different gases remains same.
With increasing altitude main effect will be on
PO2 and PN2.
CO2 and water vapor pressure will not be
much affected.
4. Acclimatization to low PO2 at High
Altitude
1. Increased pulmonary ventilation
Low PO2 stimulates the respiration through peripheral
chemoreceptors.
Initial stimulatory affect at high altitude is not so
marked.
Reason is when there is increased ventilation; there is
increased washout of CO2 which leads to respiratory
alkalosis.
So stimulatory affect is neutralized by alkalosis.
But in about 2 -4 days there is marked increase in the
rate of pulmonary ventilation because of renal
compensation by retention of H+ and removal of
HCO3.
This change will remain as long as the person is
residing at high altitude.
5. Acclimatization to low PO2 at High
Altitude
2. Change in the affinity of Hb for oxygen:
• Left shift of curve because of alkalosis but at
the same time there is marked increase in the
formation of 2,3 DPG which shifts the curve to
right side.
• So predominantly the curve is shifted to right
side and this may affect binding of O2 at lungs
level but at tissue level it will facilitate the
release of O2.
6. Acclimatization to low PO2 at High
Altitude
3. Increased diffusing capacity of respiratory
membrane for O2:
Increased pulmonary arterial pressure, more
arteries become patent and hyperventilation
causes more expansion of lungs.
7. Acclimatization to low PO2 at High
Altitude
4. Increase in the RBC Count, Hb
concentration and Hematocrit value:
On arrival at high altitude there is erythropoietin
secretion from peritubular capillaries which
causes stimulation of erythropoiesis.
Increase in RBC count can be seen in 2-3 days.
7-10 days are taken for all stages of
erythropoiesis.
Hb level may increase to 20-22 g/dl.
Hematocrit may increase upto 60-65%.
8. Acclimatization to low PO2 at High
Altitude
5. Change in Cardiac Output:
At high altitude there is 20-30% increase initially
in cardiac output.
In some days it becomes normal and then it
may decrease.
Reason is increased RBC and Hb, there is
more transport of oxygen to tissues and
increased cardiac output is not required.
9. Acclimatization to low PO2 at High
Altitude
6. ANGIOGENESIS:
Increased number and size of blood vessels
caused by increased number of mitochondria,
increased cytochrome enzymes and increased
myoglobin.
11. If a person rapidly ascends to high altitude and starts physical
exertion immediately then it leads to acute mountain
sickness.
Features of acute mountain sickness are:
Symptoms of acute mountain sickness can start at 12,000 feet
and these include nausea, vomiting, headache, irritability,
insomnia, tachycardia and breathlessness.
At 18,000 feet these symptoms become more severe and there
may be dizziness, twitching and convulsions. Higher mental
functions may be affected, slow thought making.
Above the height of 20,000 feet coma can occur.
A person can remain conscious at the height of 23,000 feet while
inhaling air.
By inhaling pure oxygen, person can remain conscious up to the
height of 47,000 feet.
12. The features of acute mountain sickness occurs
because of acute brain edema which may be
caused by arteriolar dilatation leading to increased
capillary pressure which results in brain edema.
Acute pulmonary edema also occurs.
The exact mechanism is not known and edema fluid is
rich in proteins.
These features of acute mountain sickness
can be reversed by shifting to low altitude.
Acute mountain sickness can be avoided by
gradual ascend and avoiding physical exertion
until the person becomes acclimatized.
14. This may occur in some persons who are living at
high altitude for long period.
There is marked increase in Hematocrit and blood
viscosity.
Blood flow through tissues becomes sluggish
leading to tissue hypoxia.
There is marked pulmonary hypertension
leading to right ventricular hypertrophy and
ultimately CCF.
Then there is fall of peripheral arterial pressure.
Treatment is immediate shifting of person to low
altitude and within days to weeks the person
recovers.
16. In the valleys of Himalaya which are at 17 –
18,000 feet, in natives there process of
acclimatization start at birth.
Size of chest is larger.
Heart is larger specially right ventricle.
Enlargement of carotid bodies.
These natives can work at high altitude at same
level as the natives of sea level.
They have much more working capacity at high
altitude then low landers at high altitude.