Abstract

Abstract The three main pathophysiologic contributors to septic shock include varying combinations of hypovolemia (relative > absolute), vasoplegia, and myocardial dysfunction. The three pillars of hemodynamic support include fluid boluses (FBs), vasopressors ± inotropic agents. The three goals of hemodynamic resuscitation include an adequate cardiac output (CO)/clinical perfusion markers, pressure parameters (adequate mean arterial pressure [MAP] and diastolic blood pressure [DBP]) for organ perfusion, and avoiding congestion (worse filling) parameters. Fluid bolus-induced CO improvements are variable (33%–50%) and ill-sustained on account of sepsis-mediated glycocalyx injury. A pragmatic approach is to administer a small bolus (10 mL/kg over 20–30 min) as a test and judge the response based on clinical perfusion markers, pressure parameters, and congestive features. Vasoplegia is characterized by low DBP, which is a major contributor to hypotension in septic shock; furthermore, FBs may exacerbate vasoplegia. A strategy of restricted FB with early low-dose norepinephrine (NE) (0.05–0.1 µg/kg/min) can be helpful. NE has press or effects and also mild inotropy and can be a useful first-line vasoactive even in patients with mild-moderate septic myocardial dysfunction (SMD) to maintain adequate coronary perfusion and DBP while minimizing tachycardia. Severe SMD may benefit from additional inotropy (epinephrine/dobutamine). Except vasopressin, most vasoactive drugs may safely be administered via a peripheral route. The lowest MAP (5th centile for age) may be an acceptable target, provided that end-organ perfusion and organ function (mentation and urine output) are satisfactory. An individualized rather than protocolized approach combining the history, physical examination, laboratory analyses, available monitoring tools, and re-assessments can improve outcomes.

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