Effect of bicarbonate administration on cardiac function

Abstract

In the current issue, Bersin et al [l] examined the deleterious effects of sodium bicarbonate administration on cardiac function in a well-designed study of patients with stable New York Heart Association class III or IV congestive heart failure. All patients became more hypoxic after the administration of sodium bicarbonate. This effect could not be related to volume overload, since the group receiving equal amounts of volume with sodium chloride did not show the same complication. In addition, both systemic and myocardial oxygen consumption decreased below basal levels of oxygen demand, resulting in anerobic metabolism in both circulations. The mechanisms resulting in these derangements are complex. Some patients developed myocardial ischemia. Although cardiac outputs did not change significantly from baseline values in patients with sodium chloride administration, 40% of the patients with sodium bicarbonate administration developed transient reduction of cardiac output, whereas 20% developed transient pump failure without a significant change in heart rate and systemic vascular resistance. This may indicate a decrease in myocardial contractility. The effect of bicarbonate administration on myocardial function has been examined in various studies. In denervated heart experiments, in the absence of hypoxia or acidosis, it caused a decrease in myocardial contractility [2]. However, in intact animals and humans, it resulted in an increase in myocardial contractility [3]. This effect seems to be dependent on the sympathetic nervous system, since pretreatment with propranolol unmasked the direct negative inotropic action of sodium bicarbonate [4]. In hypoxic lactic acidosis, sodium bicarbonate administration has been shown to reduce cardiac output by decreasing myocardial contractility [2]. Since the effect of catecholamines on the myocardium is blunted in the presence of acidosis, the direct negative inotropic action of sodium bicarbonate can be seen as in intact animals without hypoxia or acidosis pretreated with beta-blocking agents [4]. The negative inotropic effect of sodium bicarbonate is, in part, mediated by carbon dioxide production, resulting in a paradoxical decrease in the intracellular pH [2]. In isolated heart preparations, a triphasic effect of sodium bicarbonate can be observed [3]. In the initial phase, myocardial contractility decreases due to a worsening intracellular pH resulting from entry of carbon dioxide into the cells. In the second phase, as bicarbonate enters the cells to neutralize the effect of carbon dioxide, myocardial contractility returns to baseline. As the carbon dioxide reequilibrates with blood, there is an increase in intracellular pH in the late phase, resulting in in