The influence of esmolol on right ventricular function in early experimental endotoxic shock

Abstract

The mechanism by which heart rate (HR) control with esmolol improves hemodynamics during septic shock remains unclear. Improved right ventricular (RV) function, thereby reducing venous congestion, may play a role. We assessed the effect of HR control with esmolol during sepsis on RV function, macrocirculation, microcirculation, end‐organ‐perfusion, and ventricular‐arterial coupling. Sepsis was induced in 10 healthy anesthetized and mechanically ventilated sheep by continuous IV administration of lipopolysaccharide (LPS). Esmolol was infused after successful resuscitation of the septic shock, to reduce HR and stopped 30‐min after reaching targeted HR reduction of 30%. Venous and arterial blood gases were sampled and the small intestines’ microcirculation was assessed by using a hand‐held video microscope (CytoCam‐IDF). Arterial and venous pressures, and cardiac output (CO) were recorded continuously. An intraventricular micromanometer was used to assess the RV function. Ventricular–arterial coupling ratio (VACR) was estimated by catheterization‐derived single beat estimation. The targeted HR reduction of >30% by esmolol infusion, after controlled resuscitation of the LPS induced septic shock, led to a deteriorated RV‐function and macrocirculation, while the microcirculation remained depressed. Esmolol improved VACR by decreasing the RV end‐systolic pressure. Stopping esmolol showed the reversibility of these effects on the RV and the macrocirculation. In this animal model of acute severe endotoxic septic shock, early administration of esmolol decreased RV‐function resulting in venous congestion and an unimproved poor microcirculation despite improved cardiac mechanical efficiency.

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“…In another study by the same authors examining the effects of esmolol on RV function in an experimental model of LPS-induced septic shock, the > 30% reduction in HR induced by esmolol infusion following controlled resuscitation led to deterioration of RV function and macrocirculation, with microcirculation remaining depressed. [23] On the other hand, esmolol improved ventriculo-arterial coupling by decreasing RV end-systolic pressure. Discontinuing esmolol reversed the effects on both RV function and macrocirculation.…”

“…[22] Sheep Endotoxemia LPS Esmolol BB increased pressure dependency of renal blood flow to renal perfusion pressure by impairing renal autoregulation Van Loon et al. [23] Lamb Endotoxemia LPS Esmolol Esmolol improved VACR by decreasing the RV end-systolic pressure in a single-beat PV loop assessment Carrara et al. [41] Pig Intraperitoneal instillation of autologous feces Esmolol ivabradine Sepsis-induced cardiac dysautonomia was improved by esmolol and ivabradine, but only esmolol continued to provide benefit under norepinephrine treatment Carrara et al.…”