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Pulmonary Adjustment
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EXERCISE
Physiological
stress
ventilation is elevated
volume rate
breathing
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Mechanics of breathing
Work
tidal volumes
become less compliant at higher lung volumes elastic recoil of the lung at higher thoracic volumes Greater airway resistance due to high airflow rate airflow rate increases the resistive work of breathing through nose Minute ventilations above 40 L/min are accomplished by breathing through mouth
Inward
Increasing
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AT REST
EXERCISE
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Alveolar Ventilation
At
Can be increased to as much as 150 L/min increases to a max of 50-60% of VC or about 2.5 3 L
occurs
TV
Anatomical dead space may increase slightly due to airway distention at high lung volumes
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stimulates alveolar ventilation and cause arterial PCO2 to fall below resting levels
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ouput is increased
Increased
venous return by deeper inspiratory effort and extravascular compression by the active muscles
Both
Ventilation-Perfusion relationship
More More
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uniform regional perfusion uniform distribution of VA/QCs ventilation-perfusion ratios are close
Regional
to 1.0
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linear velocity of blood flow reduces contact time between RBC and alveolar air to less than 0.75s normally seen at rest. surface area available for diffusion mixed venous PO2and higher PCO2 creates a higher pressure gradient for diffusion
Increased Lower
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unloading at tissue is improved because of decreased tissue PO2, increased PCO2(Bohr effect), decreased pH, and increased temperature. loading at tissues is enhanced And is due to lower oxyhemoglobin levels (Haldane effect)
CO2
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Training Effects
The
physical performance improves with training an improvement in CVS and in muscle O2 metabolism rather than changes in respiratory system is the limiting factor in exercise. Physical training lowers the resting heart rate and increase SV (cardiac hypertrophy).
Mainly
CO
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O2
effect of local pH, PCO2, and temperature in the exercising muscle ability of muscle to utilise O2
oxidative capacity of the muscle is accomplished by inducing mitochondria proliferation and increasing the concentration of the oxidative enzyme, and the synthesis of glycogen and triglyceride
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Maximal
ventilation and resting ventilation do not appear to be affected by physical training ventilation at submaximal load is decreased, probably due to the lower lactic acid levels of the trained person. strength and endurance of the respiratory muscles appear to improve with training and VC are basically not affected diffusion capacity is elevated due
blood volume max CO
However,
The
TLC
Pulmonary
to:
Increased Increased
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Physiological Stresses
Decreased
ambient PO2due to the reduced total barometric pressure the fractional concentration of O2 does not change appreciably with altitude I.e. 21% or 0.21 times of total barometric pressure
However,
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Acute Effects
Deterioration of nervous system function due to hypoxia:
Sleepiness,
laziness, false sense of well-being, impaired judgment, blunted pain perception, increasing errors on simple tasks, decreased visual acuity, clumsiness, and tremors hypoxia may result in loss of consciousness or even death.
Severe
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Control of breathing
Decreased
alveolar and arterial PO2 stimulate the peripheral chemoreceptors and result in an increase of alveolar ventilation. central chemoreceptors are not responsive to hypoxia arterial PO2of 45 mmHg (at 4300 m), minute ventilation is approximately doubled.
The
At
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Arterial
PCO2 is initially normal, due to hyperventilation, PCO2 falls, causing respiratory alkalosis. hypocapnia also results in diffusion of CO2 out of the CSF, results in an increase in CSF pH. central chemoreceptors are therefore not only unresponsive to altitude hypoxia, their activity is depressed by secondary hypocapnia and alkalosis of CSF is the major stimulus for breathing???
Arterial
The
What
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Mechanics of Breathing
Hyperventilation increases the work of breathing via these mechanisms:
High
ventilatory rate may be accompanied by active expiration, resulting in dynamic compression of airways response to arterial hypoxemia, a reflex parasympathetic bronchoconstriction may occur airflow is likely to occur at elevated ventilatory rate
In
Turbulent
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Alveolar Ventilation
The
resting alveolar ventilation is approximately 20% higher than in an altitudeadapted non-native deeper inspiration and fuller expiration cause a more uniform regional distribution of alveolar ventilation collapsed or poorly ventilated alveoli will be better ventilated
The
Previously
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is an increase in CO, HR and BP due to enhanced sympathetic activity to the CVS secondary to arterial chemoreceptor stimulation and increased lung inflation (aids the VR) hypoxia cause hypoxic pulmonary vasoconstriction and with an increased sympathetic outflow to the large pulmonary vessels, results in increased mean pulmonary artery pressure (pulmonary hypertension). This greatly increased right ventricular workload intravascular hydrostatic pressure
However,
Increased
Ventilation-Perfusion relationship
Increased
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pulmonary blood flow coupled with the more uniform alveolar ventilation, the regional V/Q should be more uniform and closer to 1.0 studies showed no significant change in V/Q
However,
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pressure gradient for O2 diffusion at the lung level is decreased due to higher reduction in alveolar PO2 than the mixed venous PO2 is partly offset by increased CO and increased pulmonary pressure, which increases the blood flow.
This
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of O2 in the lung may be compromised due to low alveolar PO2 reduced arterial O2 content hypocapnia may aid in O2 loading in the lung but will interfere with O2 unloading at the tissues. main short-term compensatory mechanism for maintenance of O2 delivery is the increased CO
However,
The
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Cerebral Circulation
Hypocapnia
is a strong cerebral vasoconstrictor reduced blood flow hypoxia causes cerebral vasodilatation hyperperfusion and distention of cerebral blood vessels HACE cases of the acute mountain sickness is due to cerebral edema which elevates the intracranial pressure and distorts the intracranial structures.
However,
Most
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Excretion H+ The
are conserved
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Erythropoiesis
Occurs
days
within 3-5
Haematocrit
is increased and hence the O2-carrying capacity arterial PO2 is not increased
However,
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Increased
2,3-DPG may shift the HbO2dissociation curve to the right the fact that the Hb-O2 curve is shifted to the left is because of the more dominant effect of respiratory alkalosis
However,
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Resolution of HACE occurs at about the same time as the alleviation of the CNS symptoms. This is probably because:
Increased
Autoregulation
flow
Sympathetic
Cerebral
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The
elevated CO, HR and BP return to normal after approximately a month at high altitude be due to a decreased in sympathetic outflow pulmonary hypertension persist (hypoxic pulmonary vasoconstriction), leading to right ventricular hypertrophy
May
However,
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