Cardiovascular Emergencies in the Pediatric Patient
Pediatric cardiovascular collapse is usually the end-stage of respiratory or hypovolemic failure, so the exam repeatedly tests recognition of compensated shock before hypotension appears. A child maintains blood pressure by increasing heart rate and systemic vascular resistance; hypotension is a late, pre-arrest finding. Know the compensation clues: tachycardia, narrow pulse pressure, cool mottled extremities, delayed capillary refill, weak peripheral pulses, irritability followed by lethargy, and decreased urine output.
Structural disease
Distinguish ductal-dependent lesions (coarctation, critical aortic stenosis, hypoplastic left heart, pulmonary atresia, transposition) that present in the first 2 weeks as shock or cyanosis when the ductus closes. Prostaglandin E1 (0.01–0.05 mcg/kg/min) is started empirically and causes apnea, so anticipate intubation. Tetralogy of Fallot spells are treated by calming the child, knee-chest position, 100% oxygen, a crystalloid bolus, morphine, and vasopressor or beta-blocker therapy - never by leaving the child to cry.
Arrhythmias
SVT in infants typically exceeds 220 beats/min (180 in older children), is abrupt in onset, and produces a fixed rate with no visible P waves. Vagal maneuvers come first, then adenosine 0.1 mg/kg IV/IO (max 6 mg), then 0.2 mg/kg (max 12 mg). Sinus tachycardia has variable rates and identifiable P waves. Pulseless arrest: 2 J/kg defibrillation for VF/VT, epinephrine 0.01 mg/kg of the 0.1 mg/mL concentration.
Trap: Kawasaki disease is missed in infants under 6 months who have incomplete criteria; persistent fever plus any suggestive findings warrants echocardiography and IVIG with aspirin.
Rule of thumb: 10–20 mL/kg isotonic crystalloid per bolus, reassessing after each - do not stack boluses in a child with suspected cardiac dysfunction without reassessment.