The arterial blood gas (ABG) is pH 7.35, PCO2 37 torr, and PO2 54 torr on control-mode ventilation (CMV) with a rate of 12 breaths per minute, a tidal volume of 650 mL, an FiO2 of 0.5, and a positive end-expiratory pressure (PEEP) of 5 cm H2O. Peak inspira-tory pressures (PIP) are 26 cm H2O. What are the four primary causes of hypoxemia and how are they distin-guished? Which is most likely in this patient, and how would you treat it?
The four primary causes of hypoxemia are hypoventilation, shunt, ventilation/perfusion (V/Q) mismatch, and diffusion impairment.
Hypoventilation means that there is a reduction in fresh gas flow to the alveoli such as is seen in a circuit disconnect. The hallmark feature is an increased arterial PCO2. Two basic equations relate to this condition:
where VCO2 is the CO2 produced, VA is the alveolar venti-lation, and k is a constant equal to 0.863. This means that if the alveolar ventilation is halved, the PCO2 doubles and vice versa.
where PAO2 is the alveolar partial pressure of oxygen, Patm is the atmospheric pressure, usually 760 mmHg at sea level (but in the low 600s in Denver, Colorado), PH2O is the saturated pressure of water at 37°C (47 mmHg), and RQ is the respiratory quotient, between 0.7 and 1.0 depending on the carbohydrate/lipid ratio in the diet (usually a value of 0.8 is used). This equation predicts that even severe hypoventilation may be overcome by administration of high FiO2. Thus, postoperative patients with respiratory depres-sion receiving supplemental oxygen by mask are more likely to suffer the effects of respiratory acidosis than hypoxemia.
A shunt exists when blood passes from the venous circula-tion to the arterial circulation without exposure to ventilated areas of the lung. The primary feature of a significant shunt is the failure of the PO2 to rise to normal values with the administration of oxygen. The PCO2 is not raised because the central chemoreceptor sensitivity to a rise in the PCO2 and hypoxemia will both act as a stimulus for greater ven-tilation. The degree of shunting is calculated by the shunt equation:
where .QS and .QT refer to the shunt and total pulmonary blood flows, respectively, and Cc, Ca, and Cv refer to the oxygen content of pulmonary end-capillary, arterial and mixed venous blood, respectively. Blood oxygen content is calculated as follows:
Where Hb is the hemoglobin concentration in mg/dL, SaO2 the oxygen saturation of hemoglobin, and PO2 the partial pressure of oxygen. Hemoglobin concentration and oxygen saturation are thus the main determinants of blood oxygen content, with the partial pressure of oxygen playing a comparatively small role, except in special situations such as severe anemia or hyperbaric oxygen therapy.
Ventilation/perfusion mismatch is the most common cause of hypoxemia and refers to the inefficient and incomplete transfer of gas because of mismatching of blood flow to ventilation. In practice, ventilation/perfusion mismatching is said to occur when hypoventilation, shunt, and diffusion defect (to be discussed next) are excluded from the differential diagnosis by studying the PCO2 to rule out hypoventilation, the response to oxygen adminis-tration to rule out shunt, and a lack of history and radi-ographic findings to suggest diffusion impairment.
Diffusion impairment implies that there is an incom-plete equilibrium between the gas in the alveolus and the capillary blood because of an abnormality in the normally thin-walled and easily crossed alveolar–capillary barrier. This may occur in a variety of chronic lung diseases such as interstitial fibrosis, asbestosis, and sarcoidosis. Although diffusion capacity may be measured in a pulmonary func-tion laboratory setting using carbon monoxide, bedside quantification of diffusion-limited hypoxemia using stan-dard laboratory tests is impossible.
In the case of this patient, the alveolar to arterial (A–a) gradient is 256, while the PaO2/FiO2 ratio is 108. The most likely cause of hypoxemia is V/Q mismatch. The PCO2 is normal, virtually excluding hypoventilation. Shunt can be excluded if an increase in PO2 is seen after increasing the FiO2. Several etiologies could account for the V/Q mismatch: pre-existing lung disease, fluid overload after an operation with major fluid shifts, aspiration pneumonitis, and atelec-tasis after general anesthesia with neuromuscular blockade and one-lung ventilation. Increasing the FiO2 will help raise the PO2, but an FiO2 greater than 0.6 for prolonged periods of time should be avoided, if possible, because of the risk of oxygen toxicity. Increasing the PEEP, as hemodynamically tolerated, can recruit additional alveoli, reduce the shunt component, and redistribute lung water to areas that do not participate in gas exchange. Diuresis is indicated if fluid overload is clinically suspected or confirmed by invasive monitoring.
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