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.