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VENTILATION, which can be spontaneous (as in breathing) or artificial (as in mechanical ventilation) is the movement of AIR [Air is a mixture of gases. According to Dalton’s Law, the total pressure of a mixture of gases is the sum of the pressures of the individual gases. In dry air, at an atmospheric pressure of 760 mm HG, 78% of the total pressure is due to nitrogen molecules and 21% is due to oxygen.] between the environment and the alveoli. It is measured as the frequency of breathing multiplied by the volume of each breath. Ventilation maintains normal concentrations of oxygen and carbon dioxide in the alveolar gas and, through the process of diffusion, also maintains normal partial pressures of oxygen and carbon dioxide in the blood flowing from the capillaries.
MINUTE VENTILATION, the volume of gas ventilated in one minute, is expressed as
MINUTE VENTILATION = TIDAL VOLUME x BREATHS/MIN.
ALVEOLAR VENTILATION, the volume of gas available to the alveolar surface per minute, is expressed as
ALVEOLAR VENTILATION=
(TIDAL VOLUME–DEAD SPACE) X BREATHS/MIN
VENTILATION-PERFUSION RELATIONSHIPS |
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Ventilation and perfusion are normally matched in the lungs so that gas exchange (ventilation) nearly matches pulmonary arterial blood flow (perfusion). If mismatched, impairment of oxygen and carbon dioxide transfer results.
The concentration of oxygen (PO2) in any lung unit is measured by the ration of ventilation to blood flow:
VENTILATION/PERFUSION or V/Q
This relationship also applies to carbon dioxide, nitrogen and any other gas present.
The Ventilation – Perfusion relationship can be measured by calculating the alveolar (a) – Arterial (A) PO2 difference. PAO2 can be calculated using the equation:
PAO2 = FIO2 (Patm – PH2O) – (PaCO2/R)
at sea level, FIO2 = .21, PH20 = 47, Pbreath = 760, PaCO2 measured by lab analysis, R = 0.8
PAO2 = 150 – (PaCO2/0.8)
PaO2 is measured by lab analysis.
Normal PAO2-PaO2 gradient = 10, increasing by 5-6 per decade over 50. |
CONTROL OF VENTILATION |
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The three basic elements of the respiratory control system are: SENSORS, CENTRAL CONTROLLERS and EFFECTORS.
SENSORS: The sensors that contribute to the control of breathing include lung stretch receptors in the smooth muscle of the airway, irritant receptors located between airway epithelial cells, joint and muscle receptors that stimulate breathing in response to limb movement, and juxtacapillary (or J) receptors located in alveolar walls which sense engorgement of the pulmonary capillaries and cause rapid shallow breathing. The most important sensors are central chemoreceptors in the medulla as well as peripheral chemoreceptors in the carotid and aortic bodies. The central chemoreceptors in the medulla respond to changes in the pH of the CSF. Decreases in CSF pH produce increases in breathing (hyperventilation) whereas increases in pH result in hypoventilation. The peripheral chemoreceptors in the carotid and aortic bodies cause an increase in ventilation in response to decreases in arterial PO2, increases in arterial PCO2 and increases in arterial hydrogen concentrations (decrease in pH).
CENTRAL CONTROLLERS:Central control of breathing is achieved at the brainstem, specifically the pons and midbrain, (responsible for involuntary breathing) and the cerebral cortex (responsible for voluntary breathing).
EFFECTORS:The “effectors” are the muscles of respiration, including the diaphragm, intercostal muscles, abdominal muscles and accessory muscles such as the sternocleidomastoid
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