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. of these gradientsratio VA/Q C (where Q C is pulmonary capillary blood flow) isgreatest at the top of the lung and lowest at the bottom (Fig.13.14), and ventilation and perfusion are best matched in themiddle portion. Because resting pulmonary blood flow isapproximately 5 L/min (equal to cardiac output of the systemic circulation). and. alveolar ventilation is also approximately 5 L/min, VA/Q C is approximately 1 in this middleregion, less than 1 at the base of the lung, and more than 1toward the apex.. .Dead Space and Shunt: Extremes of VA/Q C ImbalanceDead space and shunt flow are extremes of imbalance. Alveolithat are ventilated but not perfused constitute physiologicaldead space. .
(as opposed to anatomical dead space). In deadspace, VA/Q C = ∞. In contrast to dead space (ventilationwithout perfusion), shunt flow represents perfusion withoutventilation. In other words, shunted blood returning to theleft heart has not been exposed to ventilated alveoli.
If alveolarcapillaries are perfused in an area of the lung that is not ventilated (for example,an airway is blocked) physiological.. whenshunt is present (VA/Q C = 0). Shunt can also be anatomical(bypassing the alveoli). In addition to blood flow originatingin the pulmonary arteries, the pulmonary veins receive someflow from the bronchopulmonary (bronchial) circulation,which originates from the systemic circulation and perfusestissues in the conducting zone of the lungs. Thus, blood fromthe bronchopulmonary circulation returning to the left heartis not oxygenated.
The venous admixture of oxygenated anddeoxygenated blood resulting from anatomical shunt accountsfor most of the small alveolar-to-systemic arterial PO2 gradient (A-a PO2 gradient) in healthy subjects (6 to 9 mm Hg).161. .While VA/Q C varies even within normal lungs, ventilation–perfusion imbalances are a central issue in pulmonary pathophysiology (discussed in various contexts in following pages).HYPOXEMIAHypoxemia (low PaO2) may result from one of five causes, allof which reflect problems related to ventilation, perfusion, ordiffusion.
In the simplest case, ventilation (breathing) in anatmosphere with low PO2 (for example, at high altitude) willcause hypoxemia that can be corrected by breathing air withhigher PO2. A second cause of hypoxemia is hypoventilation.With insufficient ventilation (for example, with shallow breathing), PACO2 rises and PAO2 falls, due to inefficient exchangeof alveolar air with the atmosphere. Consequently, hypoxemiaand hypercapnea (high PaCO2) result. Hypoxemia of this typecan be corrected by adjusting respiratory rate and tidal volume,or breathing air containing a high concentration of oxygen.Diffusion abnormalities are a third cause of hypoxemia. Poordiffusion (for example, due to thickening of the alveolarcapillary membrane) will produce hypoxemia with an elevatedalveolar-to-systemic arterial PO2 gradient (A-a PO2 gradient);this abnormal gradient occurs because PO2 is not fully equilibrated between alveolar air and the blood leaving alveolarcapillaries.
Although hypoxemia will be corrected by administration of 100% oxygen, the A-a PO2 gradient will remainelevated.Shunt flow also produces hypoxemia. In the presence of shuntflow, venous admixture of oxygenated and deoxygenatedblood produces an elevated A-a PO2 gradient. In congenitalabnormalities of the heart in which right-to-left shunting ofblood occurs through atrial or ventricular septal defects, largeA-a PO2 gradients may be seen.
Airway obstruction also resultsin shunt flow and increased A-a PO2 gradient. Hypoxemia(low arterial PO2) caused by shunt flow can be differentiatedfrom hypoxemia caused by other defects by measurement ofPaO2 before and after several minutes of breathing of 100%oxygen. Neither the hypoxemia nor the A-a PO2 gradient associated with shunt flow can be fully corrected by breathing100% oxygen, due to venous admixture of shunt flow tooxygenated blood.Ventilation–perfusion imbalance is a fifth cause of low PaO2.As discussed earlier, gradients in ventilation and perfusionproduce some degree of ventilation–perfusion imbalance evenin a healthy subject in the standing position, and regionalventilation–perfusion imbalances contribute to the normal,small A-a gradient PO2.
If the imbalance is abnormally pronounced, mixing of blood from areas of the lung that are wellperfused but underventilated with blood from other areas(where ventilation and perfusion are better balanced) causesan exaggerated A-a PO2 gradient and hypoxemia. This type ofhypoxemia can be corrected by administration of 100%oxygen.Respiratory PhysiologyA. Conditions with low ventilation/perfusion ratioNo ventilation,normal perfusionHypoventilation,normal perfusionB.
Conditions with high ventilation/perfusion ratioNormal ventilation,no perfusion (physiologic dead space)ooVentilation or bloodflow/unit lung vol.dflow/QCBl(perVentilNormal ventilation,hypoperfusionationfusVA162VA/QCratioion)BottomBoth ventilation and blood flow are gravitydependent and decrease from bottom to topof lung. Gradient of blood flow is steeperthan that of ventilation, so ventilation/perfusionratio increases up lung.Top..Figure 13.14 Ventilation–Perfusion (VA/Q C) Relationships In the standing position, the effectsof gravity result in gradients in both perfusion and ventilation of the lung from base to apex. Because. . theperfusion gradient is steeper than the ventilation gradient, the ratio of ventilationto perfusion, VA/Q C, is.
.lowest at the bottom of the lung and greatest at the top of the lung (B). VA/Q C is also affected by variousother conditions affecting ventilation and perfusion (A and B).163CHAPTER14The Mechanics of BreathingThe physical forces resulting in ventilation of the lungs areanalogous to those creating blood flow in the cardiovascularsystem. A pressure gradient is required, and in the case of thelung, the gradient is created by movement of the chest walland diaphragm. Flow of air occurs against the resistance ofthe airways, analogous to the resistance of blood vessels.However, factors affecting pressure, flow, and resistance arecomplex, and often different, in the two systems.
This chapterdetails the physical forces involved in ventilation of the lungsand some of the changes that take place in disease.Mechanically, the lungs and chest wall can be conceptualized as a respiratory pump, acting in unison to producepressures required to generate airflow. Flow is driven by thepressure gradient between the alveolar space and the mouthopening, produced by the elastic properties of the system andactivity of respiratory muscles.
An additional characteristic ofthis pump is airway resistance (Raw), defined by the formula:R aw =( PA − PATM )rate of airflowwhere PA is alveolar pressure and PATM is atmospheric pressure.This formula can be rearranged to:BASIC MECHANICS OFTHE VENTILATORY APPARATUSVentilation occurs as a result of mechanical forces associatedwith the chest wall and lungs. Both the lungs and the chestwall are elastic; that is, they passively recoil after being distended.
Elastic recoil pressure is the pressure caused by distension. Functionally, the chest wall includes the diaphragmand abdominal muscles in addition to the rib cage. The visceral pleura (outer lining) of the lungs apposes the parietalpleura of the chest wall, and the small, fluid-filled spacebetween the pleurae, the pleural cavity, contains only a fewmilliliters (mL) of fluid. The muscles of breathing are illustrated in Figure 14.1. The diaphragm is the major muscle forinspiration during normal, quiet breathing. As it contractsand its domes descend, the thoracic space is enlarged, decreasing alveolar pressure and resulting in inward flow of airthrough the airways. During more active ventilation, forexample during exercise, the intercostal muscles have greaterinvolvement in inspiration, elevating the ribs and expandingthe chest as they contract.
Expiration is a passive processduring normal, quiet breathing and results from passiverecoil of the lungs. During active breathing, various musclesof the abdominal wall, along with some of the intercostalmuscles, contribute to the force, resulting in expiration.Elastic Recoil of the Chest Wall and LungsThe interactions between the forces of the chest wall and lungsduring normal, quiet breathing are illustrated in Figure 14.2.In the context of elastic properties of the system at all lungvolumes, from functional residual capacity (FRC; the volumeof air in the lungs after normal, quiet expiration) to total lungrate of airflow =( PA − PATM )R awThis formula is analogous to the formula for blood flow (Q =ΔP/R, where ΔP is the pressure gradient along which flowoccurs, and R is the resistance to flow).capacity (TLC), chest wall and lung forces are illustrated inFigure 14.3.
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