Ventilationperfusion matching

In order to optimize gas exchange, the uptake of oxygen from the alveolar gas into the pulmonary blood, and the elimination of carbon dioxide from the pulmonary blood into the alveolar gas, a given lung unit must be equally well ventilated and perfused. In other words, the air and blood must be brought together for the exchange gases. This is referred to as ventilation-perfusion (V/Q) matching. The most effective conditions for gas exchange occur when the V/Q ratio is equal to one, or when the amount of ventilation in a lung unit is balanced, or matched, by the amount of perfusion. In this region, the mixed venous blood entering the pulmonary capillaries has a PO2 of 40

mixed venous blood PO2 = 40 PCO2= 45

blood returned to arterial system PO2 = 100 (a) Pco2 = 40

Normal lung unit V/Q = 1

mixed venous blood PO2 = 40 PCO2= 45

blood returned to arterial system PO2 = 100 (a) Pco2 = 40

Normal lung unit V/Q = 1

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

(b) Shunt (airway obstruction) V/Q<1

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

Figure 17.5 Ventilation-perfusion matching. (a) Normal lung unit. Ventilation and perfusion are matched so that the V/Q ratio is equal to one and gas exchange is optimized. Mixed venous blood low in oxygen and high in carbon dioxide enters the pulmonary capillaries. As the blood flows through these capillaries in the walls of the alveoli, oxygen is obtained and carbon dioxide is eliminated. Blood returning to the heart and the arterial system is high in oxygen and low in carbon dioxide. (b) Shunt. Airway obstruction with normal perfusion can lead to shunt (V/Q < 1). Blood flows through the lungs without obtaining oxygen or eliminating carbon dioxide. This V/Q mismatch causes hypoxemia. (c) Alveolar dead space. Obstructed blood flow with normal ventilation causes development of alveolar dead space (V/Q > 1). The partial pressures of oxygen and carbon dioxide in the alveoli are similar to those of conducting airways. This ventilation is wasted because it does not participate in gas exchange.

mmHg and a PCO2 of 45 mmHg. The alveolar gas has a PO2 of 100 mmHg and a PCO2 of 40 mmHg. Ventilation-perfusion matching results in efficient gas exchange, a PO2 of 100 mmHg and a PCO2 of 40 mmHg in the blood, leaving the capillaries and returning to the heart (see Figure 17.5, panel a).

Airway obstruction leads to a reduction in the V/Q ratio to a value less than one. In this lung unit, perfusion is greater than ventilation (see Figure 17.5, panel b). Complete airway obstruction leads to shunt, which refers to blood that enters the arterial system without passing through a region of ventilated lung. In other words, mixed venous blood travels through the pulmonary circulation without participating in gas exchange. This blood enters the pulmonary capillaries with a PO2 of 40 mmHg and a PCO2 of 45 mmHg. If the lung unit is not ventilated, then this blood exits the capillaries and returns to the heart with the partial pressures of oxygen and carbon dioxide unchanged. The addition of blood low in oxygen to the rest of the blood returning from the lungs causes hypoxemia. The degree of hypoxemia is determined by the magnitude of the shunt. As airway obstruction increases throughout the lungs, this widespread decrease in the V/Q ratio results in a greater volume of poorly oxygenated blood returning to the heart and a greater degree of hypoxemia. As discussed, airway obstruction may be caused by many factors, including bronchoconstriction, excess mucus production, airway collapse, and alveolar flooding.

Obstructed blood flow leads to an increase in the V/Q ratio to a value greater than one and, in this lung unit, ventilation is greater than perfusion (see Figure 17.5, panel c). Complete loss of blood flow leads to alveolar dead space. In this lung unit, the air enters the alveoli with partial pressures of oxygen and carbon dioxide equal to those of the conducting airways (PO2 of 150 mmHg and PCO2 of 0 mmHg). With no perfusion, oxygen is not taken up from this mixture, nor is carbon dioxide added to the mixture to be eliminated. Alveolar dead space may be caused by pulmonary thromboem-bolism, which is when a pulmonary blood vessel is occluded by a blood clot. Alveolar dead space may also occur when alveolar pressure is greater than pulmonary capillary pressure. This leads to compression of the capillaries and a loss of perfusion. Alveolar pressure may be increased by positive pressure mechanical ventilation. Pulmonary capillary pressure may be decreased by hemorrhage and a decrease in cardiac output.

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 bron-chiolar 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.

In a lung unit with low blood flow and high ventilation (alveolar dead space), the level of carbon dioxide is decreased and the level of oxygen is increased. The reduced carbon dioxide causes bronchoconstriction and a decrease in ventilation. The excess oxygen causes vasodilation and an increase in perfusion and, once again, the V/Q ratio is brought closer to one and gas exchange is improved.

Essentials of Human Physiology

Essentials of Human Physiology

This ebook provides an introductory explanation of the workings of the human body, with an effort to draw connections between the body systems and explain their interdependencies. A framework for the book is homeostasis and how the body maintains balance within each system. This is intended as a first introduction to physiology for a college-level course.

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