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There are two types of V/Q mismatch. Both produce dead space , regions of broken down or blocked lung tissue. Dead spaces can severely impact breathing, because they reduce the surface area available for gas diffusion. As a result, the amount of oxygen in the blood decreases, whereas the carbon dioxide level increases. Dead space is created when no ventilation and/or perfusion takes place. Anatomical dead space or anatomical shunt, arises from an anatomical failure, while physiological dead space or physiological shunt, arises from a functional impairment of the lung or arteries.
An example of an anatomical shunt is the effect of gravity on the lungs. The lung is particularly susceptible to changes in the magnitude and direction of gravitational forces. When someone is standing or sitting upright, the pleural pressure gradient leads to increased ventilation further down in the lung. As a result, the intrapleural pressure is more negative at the base of the lung than at the top, and more air fills the bottom of the lung than the top. Likewise, it takes less energy to pump blood to the bottom of the lung than to the top when in a prone position. Perfusion of the lung is not uniform while standing or sitting. This is a result of hydrostatic forces combined with the effect of airway pressure. An anatomical shunt develops because the ventilation of the airways does not match the perfusion of the arteries surrounding those airways. As a result, the rate of gas exchange is reduced. Note that this does not occur when lying down, because in this position, gravity does not preferentially pull the bottom of the lung down.
A physiological shunt can develop if there is infection or edema in the lung that obstructs an area. This will decrease ventilation but not affect perfusion; therefore, the V/Q ratio changes and gas exchange is affected.
The lung can compensate for these mismatches in ventilation and perfusion. If ventilation is greater than perfusion, the arterioles dilate and the bronchioles constrict. This increases perfusion and reduces ventilation. Likewise, if ventilation is less than perfusion, the arterioles constrict and the bronchioles dilate to correct the imbalance.
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The structure of the lungs and thoracic cavity control the mechanics of breathing. Upon inspiration, the diaphragm contracts and lowers. The intercostal muscles contract and expand the chest wall outward. The intrapleural pressure drops, the lungs expand, and air is drawn into the airways. When exhaling, the intercostal muscles and diaphragm relax, returning the intrapleural pressure back to the resting state. The lungs recoil and airways close. The air passively exits the lung. There is high surface tension at the air-airway interface in the lung. Surfactant, a mixture of phospholipids and lipoproteins, acts like a detergent in the airways to reduce surface tension and allow for opening of the alveoli.
Breathing and gas exchange are both altered by changes in the compliance and resistance of the lung. If the compliance of the lung decreases, as occurs in restrictive diseases like fibrosis, the airways stiffen and collapse upon exhalation. Air becomes trapped in the lungs, making breathing more difficult. If resistance increases, as happens with asthma or emphysema, the airways become obstructed, trapping air in the lungs and causing breathing to become difficult. Alterations in the ventilation of the airways or perfusion of the arteries can affect gas exchange. These changes in ventilation and perfusion, called V/Q mismatch, can arise from anatomical or physiological changes.
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