Impact of Concomitant Vasoactive Treatment in Mechanical Left Ventricular Unloading in Profound Cardiogenic Shock

PURPOSE: To compare the effect of equipotent dosages of epinephrine, dopamine, norepinephrine, and phenylephrine on left ventricular (LV) work and end-organ perfusion in a porcine model of profound ischemic cardiogenic shock (CS) supported by Impella CP. METHODS: CS was induced in 10 pigs by stepwise intracoronary injection of microspheres. After CS was induced and Impella CP support initiated, animals were treated in a blinded crossover design with norepinephrine (0.10 µg/kg/min), epinephrine (0.10 µg/kg/min) or dopamine (10 µg/kg/min) for 30 minutes each. Phenylephrine (10 µg/kg/min) was given at the end of the study for 20 minutes. LV work was estimated using a conductance catheter. Main outcome measure was LV work estimated by pressure volume area (PVA) x heart rate. End-organ perfusion was evaluated by mixed venous oxygen saturation (SVO2) from the pulmonary artery and arterial lactate levels. Multilevel mixed-effects linear regression was used to evaluate treatment effect. RESULTS: All vasoactive drugs induced a significant increase in LV work, borderline for norepinephrine by 92.4 (mmHg*mL)*103/min ⦋95%CI(-1.1, 186), p=0.053)⦌. For all catecholamines, stroke work was significantly increased, but unchanged with phenylephrine, which on the other hand caused a significant increase in potential energy by 483 mmHg*mL ⦋95%CI(195, 772), p=0.001)⦌. SVO2 increased significantly with catecholamines and decreased borderline with phenylephrine by -9 %point ⦋95%CI(-19, 0.49), p=0.063)⦌ which also increased arterial lactate levels by 2.4 mmol/L ⦋95%CI(0.89, 3.92), p=0.002)⦌. There was a trend toward lower arterial lactate levels with norepinephrine by -1.53 mmol/L ⦋95%CI(-3.15, 0.09), p=0.064)⦌ CONCLUSION: Catecholamines increased SVO2 but at the expense of increased LV work, least for norepinephrine and highest for dopamine (figure). Isolated vasoconstriction (phenylephrine) caused an increase in LV work, a decrease in SVO2 and increase in arterial lactate levels.