Supplemental oxygen in cardiac emergencies

Historical overview Few controversies benefi t more from obtaining historical perspective than that of supplemental oxygen therapy, particularly in the context of cardiac emergencies. More than a century ago, it was fi rst observed that oxygen relieved pain during episodes of angina pectoris [2]. Th e explanation for this phenomenon came in 1928, when hypoxia of the myocardium was described as the cause of angina [3]. Since then, numerous reports have emphasized the potential benefi t of supplemental oxygen in patients with impaired coronary perfusion [4-6]. However, as early as in 1950, it was suggested that oxygen supplementation might be deleterious, as it prolonged electrocardiographic alterations during exercise tolerance testing [7]. In 1964, it was reported that breathing high concentrations of oxygen (85% to 90%) for at least 30 minutes in the fi rst 24 hours after myocardial infarction resulted in decreased heart rate, reduced cardiac output, and increased systemic vascular resistance [8]. In 1965, administration of 40% oxygen for 20 minutes to patients in the fi rst days following myocardial infarction resulted in a 17% decrease in cardiac output and a 5% rise in arterial blood pressure [9]. Th ree years later, it was confi rmed that high-fl ow oxygen (1-hour exposure) reduced stroke volume and cardiac output and increased arterial pressure and systemic vascular resistance in patients with myocardial infarction [10]. Around the same time, a study showed that hypoxia did not aff ect the availability of oxygen for myocardial metabolism in normal subjects until arterial oxygen saturation fell to as low as 50% [11]. Only in patients with coronary artery disease, myocardial ischemia was observed in some patients when saturations fell below 85%. Furthermore, no evidence was found that hyperoxia improved myocardial oxygen availability or attenuated myocardial ischemia in patients with coronary artery disease. In fact, in patients with severe triple-vessel disease, administration of 6 minutes of high-fl ow oxygen was demonstrated to reduce coro nary blood fl ow suffi ciently to induce myocardial ischemia [12]. In 1969, Sukumal chantra and colleagues [13] made what might turn out to be a key generic observation: owing to the disproportionate reduction in cardiac output, supplemental oxygen did not increase oxygen transport in patients with arterial oxygen satura tions of greater than 90%. Only when oxygen saturations were less than 90%, oxygen administration increased myocardial oxygen delivery [13].