Lecture by Dr.

Mohammed Sharique Ahmed Quadri Assistant professor ,Physiology KFMC , Riyadh 20/12/09

Effect of High Altitude

High Altitude : Mountain climbing Aviation Space vehicles

Effect of High Altitude

Atmospheric (Barometric) pressure :progressively

declines as altitude increases.

At altitude of 18000 feet atmospheric pressure is only 380

mmHg i.e. half of the normal sea level value (760 mmHg)
As the PO2 of inspired air is 21% of atm pressure , at this

altitude PO2 becomes 80 mmHg, & alveolar PO2 being even lower at 45 mmHg
And as the arterial PO2 always equilibrated with alveolar

PO2 arterial PO2 also decreases

Effect of High Altitude(continued)

At any altitude above 10000 feet arterial PO2 falls into

steep proportion of the O2-Hb curve.

As a result % saturation of Hb in arterial blood

declines resulting in hypoxia .

So people who rapidly ascend to high altitudes of

10000 ft or more experience symptoms of acute mountain sickness attributable to hypoxic hypoxia

Acute mountain sickness:

is due to hypoxic hypoxia (in which the PO2 of the arterial blood is reduced)
This syndrome develops 8-24 hours after arrival at altitude and lasts

4-8 days

Whenever arterial PO2 reaches below 60 mmHG it stimulate

peripheral chemoreceptors which leads to increase respiratory rate ( hyperventilation) respiratory alkalosis .

As a consequence arterial PCO2 decreases producing

Symptoms: fatigue , headache , nausea ,loss of appetite,

difficulty of breathing & rapid heart rate & nerve dysfunction ,Dizziness & incoordination . & unacclimatized person may land in coma followed by death .

Delayed Effects of High Altitude

High -altitude cerebral edema and In high-altitude cerebral edema,

the capillary leakage in mountain sickness progresses to frank brain swelling, with ataxia, disorientation, and in some cases coma and death due to herniation of the brain through the tentorium. is a patchy edema of the lungs that is related to the marked pulmonary hypertension . It has been argued that it occurs because not all pulmonary arteries have enough smooth muscle to constrict in response to hypoxia, and in the capillaries supplied by those arteries, the general rise in pulmonary arterial pressure causes a capillary pressure increase that disrupts their walls (stress failure).

High -altitude pulmonary edema. High-altitude pulmonary edema

All forms of high-altitude illness are benefited by descent to lower altitude and by treatment with the diuretic acetazolamide In high-altitude pulmonary edema, prompt treatment with O2 is essentialand, if available, use of a hyperbaric chamber Nifedipine, a Ca2+ channel blocker that lowers pulmonary artery pressure

Effect of High Altitude(continued)

Acclimatization to low PO2:
People remaining at high altitude for days or

week or years become acclimatized to low PO2

Acclimatization is due to compensatory

responses that occurs in body

Acute compensatory response Long term compensatory responses

Effect of High Altitude(continued)

Acute compensatory response Increase pulmonary ventilation Increase cardiac out put Long term compensatory responses increase red blood cells Increase 2,3DPG (RBC) Increase no capillaries with in the tissues Increase mitochondria in tissue cells Kidney restores the arterial pH towards normal by conserving H ions

Effect of deep sea diving

Atmospheric pressure :progressively

increases as the diver descends under water as a result of weight of sea water pressure at the sea debt of 30 ft

Pressure almost doubles the atmospheric As amount of gas in a solution is directly Air is composed of 79% of the N2

proportional to partial pressure of the gas

Nitrogen narcosis :
At sea level N2 is poorly soluble in tissue fluid

But the high PN2 that occurs in deep sea diving causes more of the N2 than normal to dissolve .that leads to N2 narcosis
N2 narcosis has characteristics similar to that of alcohol

intoxication & for this reason it is called as raptures of depth

N2 narcosis results from reduction in excitability of

neurons because of the highly lipid soluble N2 dissolving in their lipid membrane & altering the ionic conductance
Diverse may experience euphoria & becomes drowsy and at

still lower depth they becomes clumsy & weak & may become unconciouse

Decompression sickness :
If the divers who has been submerged long enough for a

significant amount of N2 to dissolve into tissue ,suddenly rises to surface ,rapid reduction in PN2 causes N2 to quickly come out of the solution & form bubbles in the body
Consequences depends upon amount & location of the

bubbles formed ,this condition is called as decompression sickness or bends because victim often bends over because of joint or muscle pain .
Bubbles in pulmonary capillaries are apparently

responsible for dyspnoea that divers called "the chokes.

Effect of deep sea diving(continued)

Symptoms of decompression sickness :
nervous symptoms occurs ranging from

dizziness, paralysis ,unconsciousness

Occasionally pulmonary edema & death can also

occur
O2 toxicity(super oxide free radicals)

caused by Increase in PO2 is another possible harmful effect of deep sea diving

 Oxygen toxicity

Nitrogen narcosis
High-pressure

: Lung damage Convulsions : Euphoria Impaired performance

nervous syndrome : Tremors Somnolence Decompression sickness : Pain Paralyses Air embolism : Sudden death

 Treatment of this disease is prompt recompression in a

pressure chamber, followed by slow decompression. Recompression is frequently lifesaving.

Recovery is often complete, but there may be residual

neurologic sequelae as a result of irreversible damage to the nervous system.

The amount of CO2 removed from each unit of blood is increased

The PO2 of blood flowing into the pulmonary capillaries falls from 40 to 25 mm Hg or less, so that the alveolar-capillary PO2 gradient is increased and more O2 enters the blood. Blood flow per minute is increased

Exercise and Ventilation

Ventilation increases during strenuous exercise, with the depth increasing more than the rate. It appears that changes in PCO2 and PO2 do not play a significant role in stimulating this increased ventilation. Although the precise factors which

stimulate increased ventilation during exercise are not fully understood, they probably include: 1. Learned responses:Ventilation increases within seconds of the beginning of exercise, probably in anticipation of exercise, a learned response. 2. Neural input from the motor cortex.: The motor areas of the cerebral cortex which stimulate the muscles also stimulate the respiratory centers. 3. Receptors in muscles and joints: Proprioceptors in moving muscles and joints stimulate the respiratory centers. 4. Increased body temperature: An increase in body temperature stimulates the respiratory centers. 5. Circulating epinephrine and norepinephrine:secreted by the adrenal medulla stimulates the respiratory centers. 6. pH changes due to lactic acid: Lactic acid, produced by exercising muscles, is another stimulus.

References
Text book of physiology by Guyton & Hall review of medical physiology by william F.Ganang Text book of physiology by Linda .S .Costanzo third

edition