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Pulmonary Adjustment to Various Activities

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Pulmonary Adjustment

Exercise High Altitude

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EXERCISE
Physiological

stress

Increased O2 demand CO2 production

Increased Minute tidal

ventilation is elevated

volume rate

breathing

Factors affecting Pulmonary Ventilation

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Mechanics of breathing
Work

of breathing increased during exercise because

Larger Alveoli

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

rest is about 5-6 L/min

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

at the expense of IRV

Anatomical dead space may increase slightly due to airway distention at high lung volumes

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Arterial Partial Pressure

Arterial

PO2is relatively constant

Arterial PCO2also stays relatively constant until :

Significant H+directly

increase in plasma lactic acid levels

stimulates alveolar ventilation and cause arterial PCO2 to fall below resting levels

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Pulmonary Blood Flow

Increased pulmonary blood flow is due to:
Cardiac

ouput is increased

Increased

venous return by deeper inspiratory effort and extravascular compression by the active muscles

Both

mean pulmonary artery pressure and left in pulmonary vascular resistance

atrial pressure increase, however

Decrease Recruitment Distention

of pulmonary blood vessels in upper regions of the lung of pulmonary vessels

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

Diffusion through the alveolar-capillary barrier

The diffusing capacity for both O2 and CO2 is increased due to:
Increased

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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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O2 and CO2 Transport

O2

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

delivery to the tissues is increased and

may be due to:

Increased Increased Improved

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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Pulmonary Blood Flow

There

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,

Diffusion through the alveolar capillary barrier

Partial

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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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O2 and CO2 transport

Loading

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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Renal compensation for respiratory alkalosis

Occurs

within a day of base is increased

Excretion H+ The

are conserved

mechanism is not able to restore the normal blood pH

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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

reabsorption of CSF (myogenic) of cerebral blood

Autoregulation

flow
Sympathetic

mediated vasoconstriction (takes several days to develop) vessels produced less NO

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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