Arterial Hypoxemia and Distribution of Pulmonary Perfusion after Uncomplicated Myocardial Infarction^1–3

Abstract

__________________________________________________ ___To assess the consequences of myocardial infarction on the lung, pulmonary gas exchange and distribution of pulmonary perfusion and ventilation were studied after uncomplicated myocardial infarction in 35 patients in whom no clinical or radiographic evidence of congestive failure was apparent. Studies were performed in some of the patients during the first and third weeks after infarction and in 7 patients 2 to 6 months later.During the first week, the mean arterial oxygen tension was decreased to 72 mm Hg and the mean alveolar-arterial oxygen tension gradient increased to 47 mm Hg; both values improved in the convalescent phase. The mean arterial oxygen tension was 447 mm Hg and the mean alveolararterial oxygen tension gradient was 203 mm Hg while breathing 100 per cent oxygen during the first week after infarction; both values returned to normal in the 2-to 6-month follow-up studies. Distribution of pulmonary perfusion was abnormal in the first week. There was diminution of the normally occurring vertical gradient of perfusion in the lung, with relative hypoperfusion of lung base, increased perfusion of lung base, and increased perfusion of the apex. This abnormality returned toward normal in the follow-up period.No other hemodynamic abnormalities were demonstrated. The underlying mechanism of both hypoxemia and perfusion maldistribution appeared to be fluid accumulation in the lung interstitium secondary to transient left ventricular failure at the time of acute myocardial infarction.

Clinical Significance of Hypoxemia without Congestive Heart Failure in Patients Presenting with Acute Myocardial Infarction

“…The diagnosis of AMI was made on the basis of finding the typical clinical symptoms, electrocardiographic and echocardiographic changes and an increased serum creatinine kinase (CK) concentration. Of the 196 patients, 62 (48 men and 14 women) who met the following criteria were enrolled in the study: admission within 12 h after infarction [1], Killip group I [10] physical findings regarding the chest on admission [2], a mean pulmonary capillary wedge pressure (PCWP) of less than 18 mm Hg on admission [3], emergency coronary angiography had been performed on admission [4], the absence of clinical manifestations of respiratory disease [5], the absence of congestive heart failure and respiratory disease by chest radiograph [6], and the absence of previous coronary artery bypass grafting [7].…”

“…Once interstitial pulmonary edema develops and hypoxemia results, the production of endothelium-derived relaxing factor is inhibited [17], which leads to hypoxic pulmonary vasospasms and an increase in the ventilation-perfusion imbalance [17,18]. The investigation of the distribution of pulmonary blood flow using xenon-133 in patients with AMI and a normal PCWP, a normal cardiac output, and the absence of pulmonary congestion has shown a relative shift of the blood flow from the base to the apex of the lungs [5,6]. Al Bazzaz and Kazemi [6] have investigated pulmonary gas exchange, perfusion, and ventilation in 21 patients with AMI who had hypoxemia despite the absence of heart failure.…”

“…The investigation of the distribution of pulmonary blood flow using xenon-133 in patients with AMI and a normal PCWP, a normal cardiac output, and the absence of pulmonary congestion has shown a relative shift of the blood flow from the base to the apex of the lungs [5,6]. Al Bazzaz and Kazemi [6] have investigated pulmonary gas exchange, perfusion, and ventilation in 21 patients with AMI who had hypoxemia despite the absence of heart failure. They have concluded that one third of the increment in the alveolar arterial oxygen tension difference (AaDO 2 ) was due to increased pulmonary venoarterial shunting, and that the ventilation-perfusion imbalance was the cause of the remaining two thirds of the increment.…”

“…The reduction in arterial oxygen tension is thought to correlate well with the severity of pulmonary vascular congestion [1,2]. However, hypoxemia occasionally develops in the acute phase of myocardial infarction (MI) despite the absence of overt clinical or hemodynamic manifestations of left ventricular pump failure and pulmonary edema [3][4][5][6]. This hypoxemia has been reported to be a result of mild interstitial pulmonary edema caused by transient left heart failure immediately after infarction [3,7].…”

Physiologic Changes Associated with Increasing Pulmonary Wedge Pressures in the Dog

“…Since at a Pc of 28 mmHg or above, gross physiological changes take place, most studies of pulmonary edema have concentrated upon events occurring at these greatly elevated pressures [21,23,28,32], Yet, it is of obvious clinical and theoretical importance to identify subtle physiological changes which may occur at sub-clinical levels of pressure . Although other investigators have alluded to events occurring at a Pc pressure of 28 mmHg and below [3,41,45], no one to our knowledge has systematically studied in vivo physiologic changes which may be applicable to clinical situations.…”