high altitude deep sea diving & excercise

7/29/2019 High Altitude Deep Sea Diving & Excercise

1/18

Lecture byDr.Mohammed Sharique Ahmed Quadri

Assistant professor ,PhysiologyKFMC , Riyadh

20/12/09


2/18

Effect of High Altitude High Altitude :

Mountain climbing

Aviation Space vehicles


3/18

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 thisaltitude PO2 becomes 80 mmHg, & alveolar PO2 being

even lower at 45 mmHg

And as the arterial PO2 always equilibrated with alveolarPO2 arterial PO2 also decreases


4/18

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 blooddeclines resulting in hypoxia .

So people who rapidly ascend to high altitudes of10000 ft or more experience symptoms ofacutemountain sickness attributable to hypoxic hypoxia


5/18

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 stimulateperipheral chemoreceptors which leads to increaserespiratory rate ( hyperventilation)

As a consequence arterial PCO2 decreases producingrespiratory alkalosis .

Symptoms: fatigue , headache , nausea ,loss of appetite,difficulty of breathing & rapid heart rate & nerve dysfunction,Dizziness & incoordination .

& unacclimatized person may land in coma followed bydeath .


6/18

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 deathdue to herniation of the brain through the tentorium.

High -altitude pulmonary edema. High-altitude pulmonary edemais a patchy edema of the lungs that is related to the marked pulmonaryhypertension .

It has been argued that it occurs because not all pulmonary arterieshave enough smooth muscle to constrict in response to hypoxia, and inthe capillaries supplied by those arteries, the general rise in pulmonaryarterial pressure causes a capillary pressure increase that disrupts their

walls (stress failure).

All forms of high-altitude illness are benefited by descent to lower altitudeand by treatment with the diuretic acetazolamideIn high-altitude pulmonary edema,prompt treatment with O2 is

essentialand, if available, use of a hyperbaric chamberNifedipine, a Ca2+ channel blocker that lowers pulmonary artery pressure


7/18

Effect of High Altitude(continued)

Acclimatization to low PO2: People remaining at high altitude for days orweek or years become acclimatized to low PO2

Acclimatization is due to compensatoryresponses that occurs in body

Acute compensatory response

Long term compensatory responses


8/18

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 towardsnormal by conserving H ions


9/18


10/18

Effect of deep sea diving

Atmospheric pressure :progressivelyincreases as the diver descends under water asa result of weight of sea water

Pressure almost doubles the atmosphericpressure at the sea debt of 30 ft

As amount of gas in a solution is directly

proportional to partial pressure of the gas

Air is composed of 79% of the N2


11/18

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

But the high PN2 that occurs in deep sea diving causes moreof the N2 than normal to dissolve .that leads to N2 narcosis

N2 narcosis has characteristics similar to that of alcoholintoxication & for this reason it is called as raptures of

depth

N2 narcosis results from reduction in excitability ofneurons because of the highly lipid soluble N2dissolving in their lipid membrane & altering the ionicconductance

Diverse may experience euphoria & becomes drowsy and atstill lower depth they becomes clumsy & weak & may becomeunconciouse


12/18

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 causesN2 to quickly come out of the solution & form bubbles

in the body

Consequences depends upon amount & location of thebubbles formed ,this condition is called as

decompression sickness or bends because victimoften bends over because of joint or muscle pain .

Bubbles in pulmonary capillaries are apparently

responsible for dyspnoea that divers called "thechokes.


13/18

Effect of deep sea diving(continued)

Symptoms of decompression sickness :

nervous symptoms occurs ranging fromdizziness, paralysis ,unconsciousness

Occasionally pulmonary edema & death can alsooccur

O2 toxicity(super oxide free radicals)caused by Increase in PO2 is another

possible harmful effect of deep sea diving


14/18

Oxygen toxicity : Lung damage ConvulsionsNitrogen narcosis : Euphoria Impaired

performance

High-pressure

nervous syndrome : Tremors Somnolence

Decompression sickness : Pain Paralyses

Air embolism : Sudden death


15/18

Treatment of this disease is prompt recompression in apressure chamber, followed by slow decompression.Recompression is frequently lifesaving.

Recovery is often complete, but there may be residualneurologic sequelae as a result ofirreversible

damage to the nervous system.


16/18

The PO2 of blood f lowing intothe pulmonary capillaries falls

from 40 to 25 mm Hg or less, sothat the alveolar-capillary PO2gradient is increased and moreO2 enters the blood. Blood flow

per minute is increasedThe amount of CO2removed from each unit

of blood is increased


17/18

Exercise and Ventilation

Ventilation increases during strenuous exercise, with the depth increasingmore than the rate.

It appears that changes in PCO2 and PO2 do not play a significant role instimulating this increased ventilation. Although the precise factors whichstimulate increased ventilation during exercise are not fully understood, theyprobably include:

1. Learned responses:Ventilation increases within seconds of the beginningof exercise, probably in anticipation of exercise, a learned response.

2. Neural input from the motor cortex.: The motor areas of the cerebralcortex which stimulate the muscles also stimulate the respiratory centers.

3. Receptors in muscles and joints: Proprioceptors in moving muscles andjoints 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 exercisingmuscles, is another stimulus.


18/18

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

high altitude deep sea diving & excercise

Documents