RESPIRATORY SYSTEM (EFFECT OF EXERCISE & OTHER FACTORS ON RESPIRATION) Dr. Mohammed Sharique Ahmed Quadri Assistant Prof. physiology Al maarefa college.

RESPIRATORY SYSTEM(EFFECT OF EXERCISE & OTHER FACTORS ON

RESPIRATION)

Dr. Mohammed Sharique Ahmed Quadri Assistant Prof. physiology

Al maarefa college 1

بسم الله الرحمن الرحيم

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Effect Of Exercise On Respiration• Alveolar Ventilation increases 20-fold during heavy

exercise to keep pace with increased demand of O2 uptake and CO2 output.

• Big three chemical factors that is decreased PO2, increased PCO2 and increased H+ does not play major role.

• During exercise, ventilation increases at the onset of exercise within seconds, long before arterial blood gases could become important influences on respiratory centre which requires minutes.

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Factors Increasing Ventilation During Exercise

• Reflexes originating from joints and muscle receptors during exercise reflexly stimulate the respiratory center.

• Increase in body temperature during exercise stimulates ventilation.

• Increased Epinephrine release during exercise stimulates ventilation.

• Impulses from cerebral cortex, at the onset of exercise stimulates medullary respiratory neuron.

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Cyanosis

• Cyanosis is a blue coloration of skin and mucous membranes.

• It results when reduced Hemoglobin in capillary blood is more than 5g/100ml of blood.

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Hypoxia

• Example for each type of Hypoxia.• Hypoxic Hypoxia occurs in lung disease, at high

altitude.• Anemic Hypoxia occurs in Anemia and CO

Poisoning.• Circulatory Hypoxia or Stagnant Hypoxia occurs

in slow circulation e.g. Cardiac failure.• Histotoxic Hypoxia occurs when tissues are not

able to use O2. It occurs in Cyanide Poisoning.

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{CLINICAL ASPECT} Sudden Infant Death Syndrome [SIDS]

• In SIDS, Apnea occurs [stoppage of breathing] and patient is unable to recover from Apnea period and death occurs.

• SIDS or crib [cot] death – It is the leading cause of death in the first year of life, usually

2-4 months old infant is found dead in his or her cot for no apparent reason.

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{CLINICAL ASPECT} Sudden Infant Death Syndrome [SIDS]

Cause is not clear but different possibilities are put forward:

• Baby forgets to breath – as respiratory control mechanism are immature either in brain stem or chemoreceptors are poorly developed.

• Abnormal lung development .• Aspiration of gastric [stomach] juice containing

Helicobacter pylori.• Combination of factors maybe involved.

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{CLINICAL ASPECT} Sudden Infant Death Syndrome [SIDS]

Other Observations In SIDS• Sleeping position of baby – 40% increased

incidents of SIDS is associated with sleeping on the abdomen rather than on the back or side.

• Infants whose mother smoked during pregnancy are more likely to die of SIDS.

Respiratory adjustment to High Altitude, Deep Sea Diving

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 & hypocapnia induces alkalosis.

Acute mountain sickness:

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)

As a consequence arterial PCO2 decreases producing respiratory 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 by death .

Delayed Effects of High Altitude • High -altitude cerebral edema and In high-altitude cerebral

edema, the capillary leakage progresses to coma and death.

• High -altitude pulmonary edema. High-altitude pulmonary edema is a patchy edema of the lungs that is related to the marked pulmonary hypertension . pulmonary arteries 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.

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 essential—and, 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 long term compensatory responses that occurs in body

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 almost doubles the atmospheric pressure 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

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

• Decompression sickness can be prevented by ascending slowly to the surface .

• Treatment 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.

References

• Human physiology by Lauralee Sherwood, seventh edition

• Text book physiology by Guyton &Hall,11th edition

• Text book of physiology by Linda .s contanzo,third edition