Hemodynamic Management Strategies in Pediatric Septic Shock: Ten Concepts for the Bedside Practitioner

The three pathophysiologic contributors to septic shock include varying combinations of hypovolemia (relative > absolute), decreased vascular tone or vasoplegia, and myocardial dysfunction. The three pillars of hemodynamic support include fluid boluses, vasopressors with or without inotrope infusions. The three end-points of hemodynamic resuscitation include an adequate cardiac output (CO), adequate mean arterial pressure (MAP) and diastolic blood pressure (DBP) for organ perfusion, and avoiding congestion (worse filling) parameters. Only 33-50% of septic patients show post-fluid bolus CO improvements; this may be sustained in ≥10% on account of sepsis-mediated glycocalyx injury. A pragmatic approach is to administer a small bolus (10 mL/kg over 20-30 min) and judge the response based on clinical perfusion markers, pressure elements, and congestive features. Vasoplegia marked by low DBP is a major contributor to hypotension in septic shock. Hence, a strategy of restricted fluid bolus with early low-dose norepinephrine (NE) (0.05-0.1 µg/kg/min) can be helpful. NE may also be useful in septic myocardial dysfunction (SMD) as an initial agent to maintain adequate coronary perfusion and DBP while minimizing tachycardia and providing inotropy. 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 end-organ perfusion is satisfactory. A clinical individualized approach combining the history, serial physical examination, laboratory analyses, available monitoring tools, and repeated assessment to individualize circulatory support may to lead to better outcomes than one-size-fits-all algorithms.