INTRODUCTION: Acute heart failure (AHF) is characterized by inadequate cardiac output (CO), congestive symptoms, poor peripheral perfusion and end organ dysfunction. Treatment often includes a combination of diuretics, oxygen, positive pressure ventilation, inotropes and vasodilators or vasopressors. Lactate is a marker of illness severity but is also an important metabolic substrate for the myocardium at rest and during stress. We tested the effects of half-molar sodium lactate infusion on cardiac performance in AHF. METHODS: A prospective, randomized, controlled, open label, pilot clinical trial in 40 patients fulfilling two out of three criteria for AHF: 1) left ventricular ejection fraction (LVEF) < 40%, 2) acute pulmonary oedema or respiratory failure of predominantly cardiac origin requiring mechanical ventilation, 3) receiving vasopressor/inotropic support. Patients in the intervention group received 3 ml/kg bolus over 15 min of half-molar sodium lactate followed by 1 ml/kg/h continuous infusion for 24 h. The control group received only 3 ml/kg bolus of Hartman's solution without continuous infusion. The primary outcome was CO assessed by transthoracic echocardiography 24 hours post randomization. Secondary outcomes included a measure of right ventricular systolic function (tricuspid annular plane systolic excursion-TAPSE), acid base, electrolyte and organ function parameters along with length of stay and mortality. RESULTS: The infusion of half-molar sodium lactate increased CO from 4.05 +/- 1.37 L/min to 5.49 +/- 1.9 L/min, (P < 0.01) and TAPSE from 14.7 +/- 5.5 mm to 18.3 +/- 7 mm, (P = 0.02). Plasma sodium and pH increased (136 +/- 4 to 146 +/- 6 and 7.40 +/- 0.06 to 7.53 +/- 0.03, respectively, both P < 0.01) while potassium, chloride and phosphate levels decreased. There were no significant differences in the need of vasoactive therapy, respiratory support, renal or liver function tests, duration of ICU and hospital stay or 28 and 90 day mortality. CONCLUSIONS: Infusion of half-molar sodium lactate improved cardiac performance and led to metabolic alkalosis in AHF patients without any detrimental effect on organ function.Trial registration: Clinicaltrials.gov NCT01981655.