Ventilation/perfusion matching

Alveolar dead space (obstructed blood flow) V/Q 1 

Ventilation-perfusion mismatch leads to hypoxemia. Reduced ventilation caused by obstructed airflow or reduced perfusion caused by obstructed blood flow leads to impaired gas exchange. Interestingly, each of these conditions is minimized by local control mechanisms that attempt to match airflow and blood flow in a given lung unit. 

Bronchiolar smooth muscle is sensitive to changes in carbon dioxide levels. Excess carbon dioxide causes bronchodilation and reduced carbon dioxide causes bronchoconstriction. Pulmonary vascular smooth muscle is sensitive to changes in oxygen levels excess oxygen causes vasodilation and insufficient oxygen (hypoxia) causes vasoconstriction. The changes in bronchiolar and vascular smooth muscle tone alter the amount of ventilation and perfusion in a lung unit to return the V/Q ratio to one. 

In a lung unit with high blood flow and low ventilation (airway obstruction), the level of carbon dioxide is increased and the level of oxygen is decreased. The excess carbon dioxide causes bronchodilation and an increase in ventilation. The reduced oxygen causes vasoconstriction and a decrease in perfusion. In this way, the V/Q ratio is brought closer to one and gas exchange is improved. 

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Explain the effects of airway obstruction and obstructed blood flow on ventilation-perfusion matching... 

The benefits of NIPPV include respiratory muscle rest, increasing alveolar ventilation, lung compliance, chemosensitivity, and ventilation/perfusion matching (4). To accomplish optimal rest, high volumes or pressure spans are used. Assist-control mode is set at volumes... 

Q13 Chandra s blood gas composition is abnormal. One factor which contributes to this is ventilation-perfusion inequality. How is alveolar ventilation normally matched to perfusion in the lung ... 

Normal ventilation- perfusion ratio. The function of the lung is to maintain P02 and PC02 within the normal range. This is accomplished by matching 1 ml mixed venous blood with 1 mL fresh air (V/Q = 1). Normally, there is less ventilation (V) than perfusion (Q), and the V/Q ratio is 0.8. 

Perfusion Perfusion occurs when blood from the pulmonary circulation is sufficient at the alveolarcapillary bed to conduct diffusion. For perfusion to occur, the alveolar pressure must be matched by adequate ventilation. Mucosal edema, secretions, and bronchospasm increase resistance to the airflow, resulting in decreased ventilation and decreased diffusion. 

Oxygen makes up 21% of air, with a partial pressure of 21 kPa (158 mm Hg) at sea level. The partial pressure drives the diffusion of oxygen thus, ascent to elevated altitude reduces the uptake and delivery of oxygen to the tissues. air is delivered to the distal airways and alveoli, the PO2 decreases by dilution with carbon dioxide and water vapor and by uptake into the blood. Under ideal conditions, when ventilation and perfusion are well matched the alveolar PO2 will be -14.6 kPa (110 mm Hg). The corresponding alveolar partial pressures of water and CO2 are 6.2 kPa (47 mm Hg) and 5.3 kPa (40 mm Hg), respectively. Under normal conditions, there is complete equilibration ( alveolar gas and capillary blood. In some diseases, the diffusion barrier for gas transport may be increased during exercise, when high cardiac output reduces capillary transit time, full equilibration may not occur, and the alveolar-end-capillary Po gradient may be increased. 

Carbon dioxide is a rapid, potent stimulus to ventilation. Inhalation of 10% CO can produce minute volumes of 75 L/min in normal individuals. Carbon dioxide acts at multiple sites to stimulate ventilation. Elevated Pco causes bronchodilation, whereas hypocarbia causes constriction of airway smooth muscle these responses may play a role in matching pulmonary ventilation and perfusion. Circulatory effects of CO result from the combination of direct local effects and centrally mediated effects on the autonomic nervous system. The direct effects are diminished contractility of the heart and vascular smooth muscle (vasodilation). The indirect effects result from the capacity of CO to activate the sympathetic nervous system these indirect effects generally oppose the local effects ofCO. Thus, the balance of opposing local and sympathetic effects determines the total circulatory response to CO. The net effect of CO inhalation is an increase in cardiac output, heart rate, and blood pressure. In blood vessels, however, the direct vasodilating actions of carbon dioxide appear more important, and total peripheral resistance decreases when the Pco is increased CO also is a potent coronary vasodilator. Cardiac arrhythmias associated with increased Pco are due to the release of catecholamines. 

For gas exchange to occur properly in the lung, air must be dehvered to the alveoK via the conducting airways, gas must diffuse from the alveoli to the capillaries through extremely thin walls, and the same gas must be removed to the cardiac atrium by blood flow. This three-step process involves (1) alveolar ventilation, (2) the process of diffusion, and (3) ventilatory perfusion, which involves pulmonary blood flow. Obviously, an alveolus that is ventilated but not perfused cannot exchange gas. Similarly, a perfused alveolus that is not properly ventilated cannot exchange gas. The most efficient gas exchange occurs when ventilation and perfusion are matched. 

Ventilation-peifiision scans may be helpful since a markedly abnormal pattern of patchy, matched ventilation and perfusion defects is often seen. Magnetic resonance imaging with hyperpolarized 3He, 99mTc-Technegas, and 133Xe dynamic SPECT have made possible the noninvasive reproducible measurement of structure-function relationship in small airways (10). 

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