The Mechanism of Arterial Hypoxemia in Acute Myocardial Infarction

Arterial blood gases were measured before and during oxygen breathing in 34 patients with acute myocardial infarction of whom 12 exhibited the shock syndrome, 14 showed evidence of left ventricular failure, and eight had no complications. Initial mean values for Po2 of 58, 60, and 72 mm Hg, respectively, were found for the three groups. When the same patients breathed oxygen via a nasal cannula or face mask at flow rates of 8 to 12 L/min, values were 106, 128, and 160 mm Hg, respectively. In all instances hemoglobin saturation values in excess of 95% were obtained when the patient breathed oxygen.In 15 patients measurements of the oxygen saturation of right atrial blood permitted calculation of the degree of venous admixture. Saturation of mixed venous blood was found to be 34, 56, and 73% for the groups of patients, while the degree of venous admixture was calculated at 18, 27, and 23%, respectively. Furthermore, from the data obtained while the patients breathed oxygen, the magnitude of true right-to-left shunt was identical for all three groups at 11%. It was concluded that the initial pulmonary defect is similar for all patients with acute myocardial infarction, and possibly is due to elevated pulmonary venous pressure in all patients. As time progresses, however, the pulmonary defect changes according to the general progress and circulatory response of the subject. Thus, in those patients in whom general deterioration occurred, pulmonary function also deteriorated; whereas, in those who demonstrated clinical and hemodynamic improvement, pulmonary function improved progressively.