Bicarbonate does not improve left ventricular contractility during resuscitation from hypovolemic shock in pigs

Lactic acidosis due to tissue hypoperfusion during hypovolemic shock may depress left ventricular contractility and further reduce the inadequate cardiac output. Bicarbonate has been used to correct the acidemia, yet the effect of this therapy on left ventricular contractility during resuscitation from hypovolemic shock is unknown. Therefore, in 12 anesthetized, mechanically ventilated pigs we measured left ventricular pressure using a Millar catheter and left ventricular volume using three pairs of ultrasonic crystals. Left ventricular contractility was assessed using the endsystolic pressure-volume relationship determined from left ventricular pressure-volume trajectories. Following phlebotomy (40% of the circulating blood volume removed for 4 ± 1 hours) and then reinfusion of all shed blood, six pigs were randomized to receive an infusion of bicarbonate (6 mEq/kg of 1 mol/L NaHCO₃) and six control pigs received an equivalent infusion of saline (6 mEq/kg of 1 mol/L NaCl). During hypovolemic shock severe lactic acidosis developed (pH 7.08 ± 0.7, lactate 9.3 ± 4.0 mmol/L) but contractility increased slightly (P ≤ .005). Our main finding is that following reinfusion of all shed blood, bicarbonate (which increased arterial pH to 7.45 ± 0.07; P ≤ .0001) did not improve left ventricular contractility. We conclude that during resuscitation from hypovolemic shock, correction of acidemia using bicarbonate does not increase left ventricular contractility.