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As mentioned above, there are several instances in which the provider should
be very cautious about using aggressive fluid resuscitation, as it may worsen the
shock state. If signs of hepatomegaly or pulmonary edema develop, ongoing fluid
resuscitation should be reevaluated. It is also important to perform ongoing
clinical assessment of the patient response to fluid administration. One option is
to monitor the hemodynamic changes as fluid is rapidly administered, as a
decrease in heart rate and increase in blood pressure suggest that the patient is
appropriately responding to fluid administration. Bedside dynamic maneuvers can
approximate this therapeutic effect to predict if a patient is likely to respond
positively to a fluid bolus. For example, a transient decrease in heart and/or
increase in blood pressure in response to a passive leg raise or gentle palpation
over the liver that augments cardiac preload have been shown to predict which
patients are likely to benefit from additional fluid administration. For patients
with an arterial catheter in place, pulse pressure variation ≥15% has also been
associated with fluid responsiveness. POCUS can also be helpful for serial
assessments of volume status. If there is underlying congenital heart disease,
severe malnutrition, or critical level of anemia, fluid administration could
precipitate or worsen congestive heart failure. Similarly, if myocarditis is
suspected, fluid administration should proceed cautiously, with initial volumes of
5 to 10 mL/kg rather than 20 mL/kg. Finally, in patients with pre-existing oliguric
or anuric renal failure, judicious fluid administration is important as the child may
not be able to mobilize the administered fluid after shock reversal.

Vasoactive Agents
Two randomized trials in pediatric septic shock have provided evidence that
epinephrine as first-line vasoactive therapy is more effective at reducing mortality
than dopamine. As such, epinephrine, rather than dopamine, is considered a firstline vasoactive therapy for fluid-refractory shock. However, in children with a
low SVR state in septic, distributive, or neurogenic shock, norepinephrine may be
preferentially used as the first-line vasoactive therapy. Table 10.4 describes the
mechanism of action and considerations for use of vasoactive agents. They may
be run initially via peripheral IV or an IO in dilute concentrations, but should be

transitioned to a central vein once central venous access is obtained.
The decision to add a second vasoactive agent in the ED setting should be
considered for patients in whom hypotension persists despite titration of the
initial vasoactive therapy. For patients with “warm” shock, if initially receiving
norepinephrine, addition of vasopressin or epinephrine may be considered. Case
reports, case series, and one trial indicate that administration of vasopressin is
associated with an increase in mean arterial blood pressure and urine output in