Ventilationperfusion mismatch

V/Q mismatch is responsible for most of the hypoxemia encountered in the intensive care environment, including hypoxemia in chronic obstructive pulmonary

disease, pulmonary embolism, pulmonary edema, and interstitial lung disease (Rodriguez-Roisjn and Wagner 1990). VlQ mismatch is illustrated by comparing the two plots in Fig 3, which shows a normal subject and a subject with VlQ maldistribution. The V/Q distribution for any lung unit must fall somewhere on the curve shown in FiQ.,4 in a patient breathing room air. The curve for a specific patient will vary depending on the mixed venous partial pressure of oxygen and the oxygen concentration of the inspired gas.



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Fig. 4 The relationship between partial pressures of oxygen and carbon dioxide and ventilation-perfusion ratio at various points in the lung in a patient breathing room air: RQ, respiratory quotient. (Reproduced with permission from Nuoo.(19,93,),.)

As the degree of VlQ maldistribution increases, the deleterious effect on oxygenation increases for two reasons. The first is that with VlQ maldistribution, a greater

percentage of the cardiac output passes through lung units with VlQ ratios that are lower than normal (perfusion in excess of ventilation) so that less well saturated blood makes a greater contribution to total pulmonary blood flow. The second reason is related to the sigmoid shape of the hemoglobin dissociation curve; the oxygen

content of blood from lung units with low VlQ ratios exerts a greater effect on the mean saturation of blood flowing into the left side of the heart as demonstrated in Fig 5.

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Oj ïHÙMiflWn Cijnrfh

Q 200 Aco eoo fln^ (nml-lgi

Q 200 Aco eoo fln^ (nml-lgi

Fig. 5 Shunt while breathing pure oxygen. Note that the addition of a small amount of shunted blood significantly reduces the arterial partial pressure of oxygen. (Reproduced with permission from West... .(.1,9.9.8.)..)

Ventilation-perfusion relationships are primarily determined by regional perfusion characteristics, and hypoxic pulmonary vasoconstriction actively regulates VlQ

a distribution (Marshall et al 1994). In normal conditions, hypoxic pulmonary vasoconstriction acts to reduce blood flow to lung regions with low VlQ ratios, and thereby improve the efficiency of gas exchange. Under certain pathological conditions, it is impaired or abolished by sepsis and trauma and by vasoactive mediators, such as prostaglandins, leukotrienes, cytokines, and platelet activating factor, or drugs, such as sodium nitroprusside and nitroglycerin, and blood flow to poorly ventilated lung increases with resulting hypoxemia.

Conversely, when the pulmonary vascular bed is partially obliterated (emphysema) or occluded (pulmonary embolism), pulmonary artery pressures can rise to the point that hypoxic pulmonary vasoconstriction is 'overcome' and is generally ineffective in redistributing blood flow. The failure of hypoxic pulmonary vasoconstriction

to divert flow from atelectatic or consolidated lung results in VlQ mismatch and hypoxemia.

Finally, the combination of systemic hypoxemia and low mixed venous PO2 is a potent stimulus for generalized hypoxic pulmonary vasoconstriction, causing increased pulmonary artery resistance and the potential for right heart failure. Pulmonary embolism and acute respiratory distress syndrome are two diseases in which this commonly occurs, and in this setting hypoxic pulmonary vasoconstriction is diffuse and maladaptive in contrast with its actions in pneumonia or atelectasis where it is regional and beneficial.

It is difficult to distinguish between the contributions of true shunt and those of VlQ maldistribution, and in many clinical situations the two effects are combined.

However, analysis of the isoshunt diagram in Fig. 6 provides some general insights into the behavior of the two lesions. VlQ maldistribution results in hypoxemia because the spread of alveolar oxygen tensions is uneven. However, when breathing 100 per cent oxygen, the alveolar oxygen tension is almost homogeneous ■ ■

irrespective of the VlQ distribution and venous admixture is equal to true shunt. An estimate of the VlQ effect can be obtained by comparing the venous admixture when breathing 100 per cent oxygen with that at some lower fractional inspired oxygen concentration (FiO 2), and is approximately equal to the difference between the venous admixture on low FiO2 and that on 100 per cent oxygen.

Fig. 6 Isoshunt diagram showing the percentage of shunt blood flow for different values of inspired and arterial oxygen concentration. (Reproduced with permission from Nunn_ (1993).)

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