Abstract
Circulatory failure in sepsis is common and places a considerable burden on healthcare systems. It is associated with an increased likelihood of mortality, and timely recognition is a prerequisite to ensure optimum results. While there is consensus that aggressive source control, adequate antimicrobial therapy and hemodynamic management constitute crucial determinants of outcome, discussion remains about the best way to achieve each of these core principles. Sound cardiovascular support rests on tailored fluid resuscitation and vasopressor therapy. To this end, an overarching framework to improve cardiovascular dynamics has been a recurring theme in modern critical care. The object of this review is to examine the nature of one such framework that acknowledges the growing importance of adaptive hemodynamic support combining macro- and microhemodynamic variables to produce adequate tissue perfusion.
Highlights
The key pillars of sepsis management are source control, antimicrobial therapy, and circulatory resuscitation [1]
Macro- and microcirculatory disturbances are meaningful and can be lumped pragmatically into two categories: peripheral vascular dysfunction and myocardial dysfunction. The former includes venous and arterial vasodilation, compromised microcirculatory flow distribution [4], and ubiquitous shock-induced endotheliopathy (SHINE) with damaged glycocalyx and increased capillary permeability [5]. The latter has been traditionally attributed to left ventricular (LV) systolic dysfunction
Diastolic dysfunction assumes more credit as it is increasingly evident that it can deleteriously affect outcomes by itself [7]. These circulatory derangements constitute the basis for an altered hemodynamic state mechanistically characterized by potentially disrupted ventricular interdependence, right and left ventricular–arterial (VA) uncoupling [8], inactivation of vascular waterfalls (i.e., precapillary Starling resistor that generates a pressure gradient between Permutt and Riley’s arterial critical closing pressure (CCP) and Guyton’s mean systemic filling pressure (MSFP) meant to stabilize tissue perfusion should low blood flow ensue) [9,10,11], and loss of hemodynamic coherence [12]. In accord with this precept, protocolized care has shifted from a “one size fits all” paradigm to an individualized framework that endorses specific hemodynamic targets, adaptive multi-parametric monitoring, and functional assessment of the cardiovascular reserve to ensure the adequacy of end-organ blood flow [13]
Summary
The key pillars of sepsis management are source control, antimicrobial therapy, and circulatory resuscitation [1]. Diastolic dysfunction assumes more credit as it is increasingly evident that it can deleteriously affect outcomes by itself [7] These circulatory derangements constitute the basis for an altered hemodynamic state mechanistically characterized by potentially disrupted ventricular interdependence, right and left ventricular–arterial (VA) uncoupling [8], inactivation of vascular waterfalls (i.e., precapillary Starling resistor that generates a pressure gradient between Permutt and Riley’s arterial critical closing pressure (CCP) and Guyton’s mean systemic filling pressure (MSFP) meant to stabilize tissue perfusion should low blood flow ensue) [9,10,11], and loss of hemodynamic coherence [12]. Emphasis is placed on discriminating macro- and microcirculatory endpoints and how both components could be reconciled and combined to optimize tissue perfusion
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