Beta-blockers in septic shock to optimize hemodynamics? Yes

Abstract

Septic shock represents one of the maximum physical stresses to the organism. The physiological response to stress includes increased release of catecholamines, leading to a stimulation of cardiac β1-adrenergic receptors thereby increasing heart rate and ventricular contractility in order to increase global and microvascular blood flow and oxygen delivery to vital organs. Yet there are adverse effects of adrenergic stimulation including tachyarrhythmias, increased cardiac oxygen consumption with risk of cardiac ischemia, and immune dysregulation. So while it sounds at first contradictory to stabilize the cardiovascular function by giving β-blocking agents to "brake" the system, there could be benefits. However, is beta-blockade in these clinical circumstances really a brake?Dr. Morelli and coworkers present in a recent article in Intensive Care Medicine data on a cohort of 45 patients with the primary diagnosis of septic shock, in whom pulling this brake seems to improve cardiovascular function [1]. After initial hemodynamic stabilization over the first 24 h, patients who were tachycardic (heart rate more than 95 bpm) received a titrated esmolol infusion with the primary goal of reducing heart rate to 80-94 bpm within a time window of 4 h. Indeed, they achieved the intended reduction in heart rate, which could have primarily decreased cardiac output. However, the decreased heart rate was offset by increased ventricular filling time and volume, and decreased left ventricular afterload, ultimately resulting in increased stroke volume, obviously compensating for the decrease in heart rate. Interestingly, left ventricular ejection fraction remained unchanged. This, in combination with a decrease in arterial dP/dt max and a concomitant reduction in the need for norepinephrine, strongly points toward a more economical cardiac function under β-blockade. This mechanism is illustrated in Fig. 1.Similarly, β-blockade seemed paradoxical at first but was ultimately shown to be very effective in chronic heart failure [2]. To follow the automobile metaphor, β-blockade is more a shift to a higher gear, when revolutions per minute are becoming too high. This shift results in the same speed, but with greater fuel efficiency.So the physiological concept of improving cardiac efficiency seems to work as well in selected patients with septic shock. This is a very important message, since a physiological rationale is one indispensable prerequisite for any new treatment concept. With all enthusiasm, we have to keep in mind that this study performed in a selected group of patients without known cardiac comorbidities was not a randomized controlled trial (RCT), nor was any patient-centered clinical outcome assessed. Second, management of preload has an influence on that treatment concept: the automobile metaphor of changing gears works only with adequate engine cubic capacity. The parallel of engine cubic capacity in patients is cardiac preload that must be in the upper range-otherwise diastolic filling would not increase, when slowing ...

Sudden cardiac arrest in hypertrophic cardiomyopathy with dynamic cavity obstruction: The case for a decatecholaminisation strategy

“…27 Sepsis, trauma (especially traumatic brain injury), burns, post-cardiac arrest syndrome, subarachnoid haemorrhage, pheochromocytoma or immoderate beta-2 stimulation are all classic examples of such states and each one of them has already been ascribed an adrenergic storm epitome such as the more specific Takotsubo cardiomyopathy (TCM) or the all-inclusive term stress-cardiomyopathy (SCM). 28,29 TCM is not a mere epiphenomenon but portends a poor risk by itself as shown by Templin et al 30 Within this context, beta-blockade has been advocated in several scenarios: CA resuscitation, 31 traumatic brain injury, 32,33 sepsis 34 and burns. 35 Decatecholaminisation is an 'umbrella' term, 36 encircling much more than beta-blockers.…”

“…28,29 TCM is not a mere epiphenomenon but portends a poor risk by itself as shown by Templin et al. 30 Within this context, beta-blockade has been advocated in several scenarios: CA resuscitation, 31 traumatic brain injury, 32,33 sepsis 34 and burns. 35…”

Comparison of the Protective Effects of Nebivolol and Metoprolol against LPS-Induced Injury in H9c2 Cardiomyoblasts

“…Clinical trials on sepsis-related cardiomyopathy under β-blockade are limited. Nevertheless, a few studies have reported improvements in heart rate, cardia function, and mortality rate during septic shock [19]. Morelli et al, 2013, conducted a randomized controlled trial on patients with severe septic shock, where 77 of them were randomly assigned to receive a continuous infusion of the short-acting β-blocker esmolol titrated to maintain a heart rate between 80 and 94/min.…”

Saturación venosa central: ¿marcador pronóstico en neumonía grave por SARS-CoV-2?

“…Un cúmulo de acontecimientos neuroendocrinos y humorales ocurrirán con la finalidad de mantener el «equilibrio» entre el huésped y el agente infeccioso, es esta respuesta exagerada la causa de la disfunción orgánica aguda que pone en peligro la vida y alcanza una mortalidad hospitalaria de 18 a 35%. 1,2 Diversos estudios a través de los años se han encargado de estudiar y establecer el impacto pronóstico de las alteraciones a nivel de la microcirculación en este grupo de pacientes. 3,4 Existen diferentes métodos disponibles para detectar hipoperfusión tisular y alteración microvascular en el paciente críticamente enfermo que van desde la clínica (hipotensión, piel moteada, acrocianosis, llenado capilar lento o disminución de la temperatura) hasta otros más sofisticados como la tonometría gástrica, capnometría sublingual o espectroscopia.…”