Effects of milrinone and epinephrine or dopamine on biventricular function and hemodynamics in right heart failure after pulmonary regurgitation

Abstract

Right ventricular failure (RVF) secondary to pulmonary regurgitation (PR) impairs right ventricular (RV) function and interrupts the interventricular relationship. There are few recommendations for the medical management of severe RVF after prolonged PR. PR was induced in 16 Danish landrace pigs by plication of the pulmonary valve leaflets. Twenty-three pigs served as controls. At reexamination the effect of milrinone, epinephrine, and dopamine was evaluated using biventricular conductance and pulmonary catheters. Seventy-nine days after PR was induced, RV end-diastolic volume index (EDVI) had increased by 33% (P = 0.006) and there was a severe decrease in the load-independent measurement of contractility (PRSW) (-58%; P = 0.003). Lower cardiac index (CI) (-28%; P < 0.0001), mean arterial pressure (-15%; P = 0.01) and mixed venous oxygen saturation (SvO2) (36%; P < 0.0001) were observed compared with the control group. The interventricular septum deviated toward the left ventricle (LV). Milrinone improved RV-PRSW and CI and maintained systemic pressure while reducing central venous pressure (CVP). Epinephrine and dopamine further improved biventricular PRSW and CI equally in a dose-dependent manner. Systemic and pulmonary pressures were higher in the dopamine-treated animals compared with epinephrine-treated animals. None of the treatments improved stroke volume index (SVI) despite increases in contractility. Strong correlation was detected between SVI and LV-EDVI, but not SVI and biventricular contractility. In RVF due to PR, milrinone significantly improved CI, SvO2, and CVP and increased contractility in the RV. Epinephrine and dopamine had equal inotropic effect, but a greater vasopressor effect was observed for dopamine. SV was unchanged due to inability of both treatments to increase LV-EDVI.

Current Interventional and Surgical Management of Congenital Heart Disease

“…Other strategies include optimal mechanical ventilation, appropriate inotropic support, careful fluid management, and avoidance of acidosis and arrhythmias. 64 Selection of inotropic support at the time of discontinuation of CPB and in the early postoperative period is largely driven by institutional experience and practice algorithms. The combination of epinephrine and milrinone are commonly used as initial drug therapy after separation from bypass.…”

“…It is not clear how inotropic-responsive a dilated and thinned RV can be, but there is evidence that milrinone and epinephrine can significantly improve cardiac index, SvO 2 (mixed venous oxygen saturation), CVP (central venous pressure), and increased RV contractility in animal models. 64 In the postoperative phase, once cardiopulmonary stability is established, it is important to wean off epinephrine and milrinone as timely as possible to avoid the potential side effects. For example, milrinone has been associated with tachyarrhythmias in the early postoperative phase after CHD surgery.…”

Hypoxic hepatitis during the perioperative period in patients with severe pulmonary disease and cor pulmonale

“…Considering the patient's underlying disease, epinephrine was the drug of choice as it has superior inotropic potency and positively influences right ventricular output. [9] Furthermore, epinephrine has an overwhelming effect on right ventricular output against increased pulmonary arterial pressure. [10]…”

Changes in overall ventricular myocardial architecture in the setting of a porcine animal model of right ventricular dilation

“…Ferreira and associates suggested this conformation to be brought upon by failure of diastolic relaxation. Hyldebrandt and co-workers assessed the current model by conductance catheter technique [ 22 ]. They found an unaltered left ventricular isovolumetric relaxation constant (tau) whereas left ventricular compliance was decreased as judged by a significant increase in the end-diastolic pressure volume relationship.…”

“…Since dilation arises from a different pathogenetic mechanism as compared to hypertophy, this raised the question as to whether such morphological changes are also to be found in the setting of right ventricular dilation. For this purpose, we have introduced a porcine model of right ventricular dilation [ 21 ] and heart failure [ 22 ]. In this study, we aimed to compare the orientations of the aggregated cardiomyocytes in the normal and dilated right ventricular myocardium.…”