Vasopressin, But Not Norepinephrine, Causes Ventriculoarterial Mismatch In Experimental Post Ischemic Cardiogenic Shock

Introduction In agreement with existing guidelines, inotropic and vasopressor support is given routinely in cardiogenic shock (CS). However, there is a lack of scientific evidence supporting the efficacy and safety of such treatment. Hypothesis Vasoconstrictors given in cardiogenic shock will increase the ventriculoarterial mismatch and thus lead to reduced cardiac output Methods In a closed chest pig model we tested the inodilator (dobutamine, Dobut) alone and combined with either an inoconstrictor (norepinephrine, NE) or a pure vasopressor (arginine vasopressin, AVP). In anesthetized animals, CS was induced by coronary microembolization under fluoroscopic guidance. Hemodynamic indices were obtained by Swan-Ganz catheters, left ventricular pressure-volume catheters and echocardiography, and the ventriculoarterial coupling calculated. Results In the normal heart, Dobut (2ug/kg/min) enhanced ventriculoarterial energy transfer, shown as a decreased Ea/Ees (ratio of arterial and ventricular elastance), 1.0 ± 0.1 to 0.8 ± 0.1, and an increased preload recruitable stroke work (PRSW), 53 ± 5 to 63 ± 2. This was further enhanced by NE (100 ng/kg/min) to 0.7 ± 0.1 and 79 ± 6. In contrast, adding AVP (0.001 u/kg/min) resulted in an increased Ea/Ees (1.0 ± 0.1) and decreased PRSW (56 ± 8) compared to Dobut alone (a two fold increase in systemic vascular resistance (SVR), concomitant with no elevation in contractility). In post ischemic CS, energy transfer from the ventricle to the arterial system (Ea/Ees 1.8 ± 0.2, PRSW 26 ± 2 and Ejection fraction 42 ± 6 %) was partly restored by Dobut (1.4 ± 0.2, 46 ± 2 and 47 ± 6%) unaffected by further adding NE (1.5 ± 0.2, 53 ± 2 and 45 ± 5%), but impaired after adding AVP (2.0 ± 0.1, 43 ± 1 and 34 ± 4%). Consequently, Dobut improved the shock by increasing cardiac output (CO) and SVO2 from 74 ± 3 ml/kg and 37 ± 2% to 103 ± 8 ml/kg and 49 ± 3%. Adding NE resulted in a further improvement of CO (125 ± 9 ml/kg) and SVO2 (59 ± 4%). In contrast AVP further worsened the shock state by decreasing CO (70 ± 6 ml/kg) and SVO2 (45 ± 5%) compared to Dobut alone. Conclusion A pure afterload increasing substance in acute ischemic hearts with cardiogenic shock aggravate the shock state by causing a ventriculoarterial mismatch.