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 textgreater30% 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.
- Beta-blocker esmolol
- right ventricular function
- ventricular-arterial coupling