INTRODUCTION TO VENTILATION/PERFUSION MATCHING
The student will be able to explain why the ratio of alveolar ventilation to lung vascular perfusion increases apically in lungs of an upright subject.
The student will be able to distinguish between the anatomical and physiological concepts of dead space and shunt.
The student will be able to explain the circumstances that elicit the acute hypoxic pressor response and its effect on pulmonary arterial pressure.
The student will be able to apply multiple inert gas data to distinguish normal subjects versus diseased patients with increased shunt or dead space.
The student will be able to use relevant equations to estimate alveolar versus dead space ventilations, and calculate alveolar Po2 from patient data.
In the normal upright lung, both ventilation and perfusion favor dependent lung regions (Chaps. 6 and 7). These relationships will be explored here to develop a fuller understanding of their normal ranges and perturbations having clinical importance (Fig. 8.1). Since both V̇A and Q̇ change with lung height, their alveolar ventilation perfusion ratio V̇A/Q̇ increases exponentially from lung base to apex. In this situation, V̇A/Q̇ <1 at the level of the diaphragm due to the heavy blood flow through Zone 3 capillaries. With increasing height above the heart of the upright lung, the V̇A/Q̇ ratio rapidly passes through 1.0 toward higher values that could theoretically approach infinity (ie, the denominator = 0) if apical alveolar capillaries are actually in Zone 1 conditions.
Distribution of ventilation and blood flow in the upright lung. The ventilation/perfusion ratio decreases toward the lung bases. From West, Respiratory Physiology; 2005.
Regardless of their cause, inequalities in V̇A/Q̇ have a direct bearing on the efficiency of ventilation and the adequacy of perfusion. In simplified form, the extreme range of possible situations is shown in Fig. 8.2. The structures shown represent individual alveoli and their capillaries, or entire lung lobes, with several basic principles the same. First, inspired gas is well mixed and normally provides a suitable Po2 even when diluted with alveolar air. Second, pulmonary arterial blood is also homogenous as it enters the lungs with respect to its mixed venous O2 content, CV̄o2. Under these conditions, the open airway and patent blood vessel serving the central gas exchange structure in this diagram offer no serious impediments to ventilation or perfusion, and thus its V̇A/Q̇ = 1.
Mechanisms that alter systemic Pao2 by well-matched or poorly matched ventilation and pulmonary arterial blood. Lung units with high V̇a/Q̇ (right) add relatively little O2 overall to blood because blood flow is low; such regions contribute to physiological dead space. Lung units with low V̇a/Q̇ (left) add little oxygen because they are under ventilated; such regions contribute to physiological shunt. From West, Respiratory Physiology; 2005.