ventricular tachycardia. (Reprinted with permission. Web-based integrated American Heart
Association Guidelines for CPR and ECC-Part 12: Pediatric Advanced Life Support. © 2018
American Heart Association, Inc.)

FIGURE 9.16 Pediatric Tachycardia With a Pulse and Poor Perfusion Algorithm. ABCs—A,
airway, B, breathing, C, circulation; CBC, complete blood count; CR, cardiorespiratory; ECG,
electrocardiogram; ETCO2 , end-tidal CO2 ; ETI, endotracheal intubation; Hgb, hemoglobin;
HR, heart rate; IV/IO, intravenous/intraosseous; RR, respiratory rate; SVT, supraventricular
tachycardia; VT, ventricular tachycardia; WOB, work of breathing. (Reprinted with permission.
Web-based integrated American Heart Association Guidelines for CPR and ECC-Part 12:
Pediatric Advanced Life Support. © 2015 American Heart Association, Inc.)

VT is characterized by wide complex (QRS >0.08 seconds) and typically has a
rate ranging from 120 to 200 bpm. Etiologies of VT include prolonged QT


syndrome, structural heart disease, myocarditis, cardiomyopathy, and poisonings.
In children presenting with stable VT, close monitoring and immediate
consultation with a pediatric cardiologist to determine etiology and definitive
treatment is the best management. For children with VT with signs of poor
perfusion (altered mental status, delayed capillary refill, hypotension), begin with
synchronized cardioversion. It is important to recognize that SVT, while typically
narrow complex, can also present with wide-complex tachycardia in some
instances; therefore, in the stable patient with either wide- or narrow-complex
tachycardia, adenosine can be given. For hemodynamically stable patients with
VT, chemical conversion using amiodarone or procainamide could be considered
in conjunction with consultation with an expert.

EXTRACORPOREAL CARDIOPULMONARY RESUSCITATION
There is now some information regarding the use of extracorporeal CPR (E-CPR)
through the use of extracorporeal membrane oxygenation (ECMO) or

cardiopulmonary bypass following CPR to treat refractory cardiac arrest in
children presenting to an ED setting. Currently, it is an option available primarily
in large, tertiary care children’s hospitals. The majority of the literature to date
comes from the treatment of inpatients with primary cardiac disease, and
available studies on use for pediatric IHCA favor the use of E-CPR. The 2010
Guidelines state “There is insufficient evidence to recommend the routine use of
ECPR for patients in cardiac arrest. However, in settings where ECPR is readily
available, it may be considered when the time without blood flow is brief and the
condition leading to the cardiac arrest is reversible or amenable to heart
transplantation or revascularization.” The 2015 Guidelines were changed to state
that “E-CRP may be considered for children with underlying cardiac conditions
who have IHCA” given no clear difference in survival found for ECPR versus
standard CPR for IHCA in noncardiac patients. While the patient and disease
factors which make E-CPR least likely to be effective are still not fully known,
the use of E-CPR may be considered for children who have had a short downtime
and have received high-quality CPR, especially among patients where a cardiac
etiology is suspected, when the resources and personnel are available.

NEWLY BORN INFANT RESUSCITATION
Guidelines for CPR in the newly born infants transitioning from intrauterine to
extrauterine life and for neonates who have completed the transition and require
resuscitation during the first few weeks after birth differ from guidelines for CPR
of older infants and children who present to the ED ( Fig. 9.16 ). For non-newly
born young infants presenting in cardiac arrest, either newly born (NRP)


guidelines or infant (PALS) guidelines can be appropriate and there is currently
no evidence for a specific age to transition from one to the other. Hospital or
agency policy should be established which leans on the expertise of the unit to
ensure high-quality CPR is delivered regardless of algorithm followed.

Though rare, the ED team must be prepared for the resuscitation of the newly
born infant. Fortunately, 90% of neonates transition from intrauterine to
extrauterine life without resuscitative needs beyond simple warming and
stimulation. However, the remaining 10% requires some assistance, and 1% will
require extensive resuscitative measures, such as cardiac compressions and
medications. Resuscitative needs vary greatly by gestational age and birth weight.
Approximately 6% of term newborns will require resuscitation at birth, as will
nearly 80% of infants who weigh less than 1,500 g. Given that anticipation of a
high-risk birth in the ED setting is not always feasible, successful newborn
resuscitation for the ED team hinges on readiness of staff and equipment.

EMERGENCY DEPARTMENT READINESS
Education of staff, necessary equipment, and specific policies and procedures are
critical for ED readiness. Early notification, when feasible, allows time to
assemble key personnel. Each institution should have a procedure in place for
rapidly mobilizing a team with complete newborn resuscitation skills for any
birth. In addition to a standard obstetric tray, every ED should have a newborn
resuscitation kit that is readily accessible, maintained, and rapidly restocked after
use. Necessary equipment and medications are listed in Table 9.8 . A radiant
warmer and medication dosing chart are critical. A standardized checklist is
recommended to ensure that all necessary equipment and supplies are present and
functional. Because neonatal resuscitations in the ED are uncommon, simulation
scenarios at regular intervals allow staff to remain familiar with neonatal
resuscitation skills and supplies. Most births that occur outside of the delivery
room have high-risk components such as trauma-induced labor and unexpected
pregnancy. Important historical factors include prematurity, multiple gestation,
meconium-stained amniotic fluid, and maternal drug use. The team can then
anticipate the need for assisted ventilation, simultaneous resuscitations, tracheal
suctioning, or pharmacologic interventions.


PATHOPHYSIOLOGY
The fetal heart has two large right-to-left shunts: from the right atrium to the left
atrium through the foramen ovale, and from the pulmonary artery to the aorta
across the ductus arteriosus. At birth, two major changes occur that eliminate
these shunts: the umbilical cord is clamped, and spontaneous respirations are


initiated. Expansion of the lungs increases the neonate’s PaO2 and pH, which
causes pulmonary vasodilation and a subsequent fall in pulmonary vascular
resistance. The initial breaths taken by the infant must inflate the lungs and effect
a change in vascular pressures so that the lung water is absorbed into the
pulmonary arterial system and cleared from the lung. This inflation pressure is a
powerful mechanism for the release of pulmonary surfactant, which increases
compliance of the lung and establishes functional residual capacity.
Full alveolar development and sufficient surfactant production is not complete
until 34 weeks’ gestation. Prior to 23 to 24 weeks’ gestation, there is a lack of
surfactant and terminal airways have not developed, therefore resuscitation prior
to 23 to 24 weeks is rarely successful outside of a controlled neonatal intensive
care environment.