Effects of oxygen in disordered gas exchange

Oxygen delivery to the tissues depends on the oxygen content of the blood, the oxygen-hemoglobin binding characteristics, the cardiac output, and undefined factors controlling distribution and diffusion of oxygen from capillary blood. Until it becomes possible to monitor intracellular PO2 in cells perfused by the vascular bed of clinical interest, dose (FiO2)-response (intracellular PO2) relationships will remain assumptions. General relationships exist between inspired PO2 and changes in arterial PO2 that are predictable based on knowledge of the intrapulmonary mechanisms of hypoxemia.

If V/Q relationships remain normal during alveolar hypoventilation due to sedation or neuromuscular disease, alveolar PO2 will increase directly with PiO2. The alveolar gas equation, which is given in simplified form by

where BP is barometric pressure, then predicts the arterial PO2 (in mmHg). Patients with decompensated chronic bronchitis and emphysema are often admitted to the intensive care unit (ICU) with respiratory failure characterized by both hypoxemia and hypercapnia. Relatively small increases in FiO 2, often to less than 0.4, substantially correct alveolar PO2 and permit maintenance of 90 per cent oxygen saturation of hemoglobin. The arterial PO2 response varies greatly from patient to

patient depending on the pattern of breathing and the underlying disorder causing V/Q mismatching. Arterial PC02 may increase after starting oxygen therapy because of increased physiological dead-space (improved ventilation of poorly perfused regions), although neither minute ventilation nor respiratory drive decreases significantly. Increased FiO2 overcomes diffusion impairment with improvement in PaO2, because the rate of oxygen transfer from the lung to the blood varies with alveolar PO2.

Arterial P02 is less responsive to increased Fi02 when anatomical dead-space is present or when portions of the lung have extreme V/Q mismatching, which is the functional equivalent of shunt in acute respiratory distress syndrome. Application of supplemental oxygen therapy may also improve systemic oxygen delivery by increasing the oxygen content of arterial blood. Small increases in PaO2 may be amplified functionally as increases in oxygen content, which favorably affect mixed venous PO2 and tissue oxygenation. Oxygen therapy may also be of benefit in disease states characterized by systemic hypoperfusion (e.g. hemorrhagic or cardiogenic shock) even without hypoxemia. However, pharmacologically increased oxygen delivery does not improve survival in septic shock.

Oxygen delivery equipment

Equipment currently in use in the ICU allows delivery of increased levels of inspired oxygen ranging from a few per cent above that in room air to pure oxygen at atmospheric pressure. Table 1 lists oxygen therapy equipment available for non-intubated patients and the indications for each type. Although less commonly used for hypoxemia without ventilatory failure, mechanical ventilators with which the FiO 2 can be varied from 0.21 to 1.00 may be required to treat hypoxemic states refractory to oxygen therapy by face mask.

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Table 1 Oxygen delivery equipment for spontaneous breathing

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Table 1 Oxygen delivery equipment for spontaneous breathing

Physiological responses to oxygen

Physiological responses to oxygen are completely reversible on resumption of air breathing. They differ in this functional character from those resulting in the irreversible pathological changes of oxygen toxicity. The most evident physiological responses to oxygen occur in the cardiovascular system.

Oxygen breathing results in decreased pulse rate and pressure, while diastolic blood pressure increases significantly. Significant decreases in cardiac index accompany increases in peripheral vascular resistance and systolic and diastolic blood pressures. Atropine abolishes the heart rate response to oxygen, suggesting vagal control of the bradycardia. Regional circulations appear to respond variably to hyperoxia, but in general blood flow decreases with the rise in venous oxygen saturation. Patients with acute myocardial infarction breathing 40 per cent oxygen had increases in systemic blood pressure and detectable decreases in cardiac output. In acute myocardial infarction beneficial effects of oxygen appear due to increasing coronary arterial oxygen tension and decreasing myocardial oxygen consumption.

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