OXYGEN

What are the effects of diffusion defects and ventilation-perfusion mismatches on arterial oxygenation?

• Diffusion defects and ventilation perfusion mismatches cause hypoxemia, responsive to exogenous oxygen and positive pressure ventilation.

Oxygen diffuses from the alveoli to the pulmonary capillaries along a partial pressure gradient – there is less oxygen in the blood, the higher the inspired concentration of oxygen, the more rapidly the gases diffuse. For most individuals, an equilibrium position occurs early in inspiration, when the arterial blood becomes fully saturated with oxygen, and the rate of uptake of oxygen depends on capillary blood flow.

The diffusion capacity depends on the thickness of the alveolar wall, the area available for gas exchange and the partial pressure difference between the two sides. If the thickness of the wall increases – such as in pulmonary fibrosis, chronically, or pulmonary edema, acutely, the diffusion capacity is lower. Moreover, with increasing heart rate, the time for equilibration may be shorted, and the patient may become hypoxemic. The treatment is to increase the partial pressure gradient for oxygen by administering exogenous oxygen to the patient. If the patient has pulmonary edema, the surface area may be increased by increasing the transalveolar pressure (and marginalizing fluid), through administration of continuous positive airway pressure (CPAP).

Ventilation perfusion mismatch occurs along a spectrum: on one end alveoli are ventilated but not perfused (pure dead space ventilation), and on the other end alveoli are perfused but not ventilated (pure shunt). The best ventilation perfusion (V/Q) ratios occur in dependent regions of the lung, due to the preferential effect of gravity on both ventilation and perfusion. The non dependent regions are relatively better ventilated than perfused (alveolar dead space). Extensive ventilation perfusion mismatch occurs due to lung injuries, whether due to consolidation (filling alveoli with exudates), perioperative atelectasis, or “acute lung injury” where there is alveolar edema and capillary microthrombosis. Hypoxemia due to ventilation-perfusion mismatch can usually be reversed with application of supplemental oxygen. Where there is extensive atelectasis due to gas absorption (see below) or mucus plugging, the treatment is oxygen, bronchial toilet and perhaps CPAP, to recruit collapsed airways. Stiff lungs (low compliance) may induce an overwhelming workload to breathing, and additional inspiratory support may be required to reduce workload and improve V/Q matching.

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