13.1 Pediatric Resuscitation, Status Epilepticus & PALS Pharmacotherapy

13.1 Pediatric Resuscitation, Status Epilepticus & PALS Pharmacotherapy

Pediatric Emergency Physiology & Airway-Centric Resuscitation

Pediatric cardiopulmonary arrest exhibits fundamental physiological differences from adult cardiac arrest. While sudden cardiac arrest in adults is overwhelmingly arrhythmogenic (primary ventricular fibrillation or pulseless ventricular tachycardia secondary to ischemic coronary artery disease), pediatric cardiac arrest is predominantly hypoxic-asphyxial in etiology. It represents the end-stage consequence of progressive respiratory failure (e.g., severe bronchiolitis, foreign body aspiration, status asthmaticus) or uncompensated shock (e.g., septic shock, severe dehydration).

Cardiovascular Dynamics & Rate Dependence

The immature pediatric myocardium is characterized by non-compliant ventricles, fewer contractile myofibrils, and incomplete sympathetic innervation. Consequently, the pediatric heart cannot substantially augment stroke volume in response to hypoperfusion. Cardiac output is almost entirely heart-rate dependent:

Cardiac Output = Heart Rate × Stroke Volume

In pediatric patients, tissue hypoxia and acidosis rapidly depress sinoatrial node automaticity and atrioventricular conduction. Therefore, progressive bradycardia is the primary clinical herald of impending respiratory arrest and cardiovascular collapse, rather than an isolated primary cardiac conduction pathology.

Weight Estimation & Length-Based Tapes

Accurate weight estimation is essential to avoid fatal under- or overdosing in pediatric resuscitations. When the patient's exact weight is unknown, length-based resuscitation tapes (e.g., Broselow tape) correlate body length to predetermined weight cohorts (color zones ranging from pink [6-7 kg] to green [30-36 kg]).

• Dosing in Obese Pediatric Patients: In obese children, length-based tapes estimate ideal body weight (IBW). Resuscitation medications that are highly water-soluble or distribute primarily into extracellular fluid (e.g., epinephrine, adenosine, succinylcholine, aminoglycosides) must be dosed on length-predicted ideal body weight to avoid life-threatening supratherapeutic peak concentrations. Lipophilic medications (e.g., fentanyl, midazolam) may require dosing based on adjusted or total body weight depending on volume of distribution.

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PALS Cardiac Arrest Resuscitation Algorithm

                     PALS CARDIAC ARREST ALGORITHM
  ┌─────────────────────────────────────────────────────────────────────────────┐
  │ Sudden Collapse / Pulseless Arrest: Initiate CPR (15:2 with 2 rescuers)     │
  │ Attach Monitor / Defibrillator & Establish IV or IO Access                  │
  └──────────────────────────────────────┬──────────────────────────────────────┘
                                         ▼
                               Check Cardiac Rhythm
                                         │
                 ┌───────────────────────┴───────────────────────┐
                 ▼ SHOCKABLE                                     ▼ NON-SHOCKABLE
        [ VF / Pulseless VT ]                                 [ Asystole / PEA ]
                 │                                               │
  ┌──────────────┴──────────────┐                 ┌──────────────┴──────────────┐
  │ • Defibrillate 2 J/kg       │                 │ • CPR immediately (2 min)   │
  │ • CPR 2 min immediately     │                 │ • Epinephrine 0.01 mg/kg    │
  │ • Defibrillate 4 J/kg       │                 │   IV/IO (0.1 mL/kg of       │
  │ • Epinephrine 0.01 mg/kg    │                 │   0.1 mg/mL) q3-5min        │
  │ • Defibrillate ≥4 J/kg      │                 │ • Identify / treat 6 H's    │
  │ • Amiodarone 5 mg/kg bolus  │                 │   and 5 T's                 │
  │   (or Lidocaine 1 mg/kg)    │                 └─────────────────────────────┘
  └─────────────────────────────┘

Cardiac Arrest Pharmacotherapy

• Epinephrine:
  • Mechanism: Alpha-1 mediated vasoconstriction increases systemic vascular resistance, elevating coronary and cerebral perfusion pressure during chest compressions; beta-1 adrenergic stimulation enhances inotropy and chronotropy.
  • IV/IO Dose: 0.01 mg/kg of the 0.1 mg/mL concentration (1:10,000 formulation), equivalent to 0.1 mL/kg (maximum single dose 1 mg / 10 mL). Administer every 3 to 5 minutes.
  • Endotracheal (ET) Dose: IV or IO access is strongly preferred because ET absorption is unreliable, and the 2025 adult guidelines dropped the ET route. If neither IV nor IO access can be obtained, older PALS teaching uses 0.1 mg/kg of the 1 mg/mL concentration (1:1,000 formulation), equivalent to 0.1 mL/kg (maximum 2.5 mg), followed by a 5 mL normal saline flush and 5 rapid positive pressure ventilations.
• Amiodarone:
  • Indication: Shock-refractory ventricular fibrillation (VF) or pulseless ventricular tachycardia (pVT) after at least 2 to 3 defibrillation attempts.
  • Dose: 5 mg/kg IV/IO rapid bolus (maximum single dose 300 mg). May repeat twice up to a maximum cumulative dose of 15 mg/kg (or adult maximum 2.2 g over 24 hours).
• Lidocaine:
  • Indication: Alternative to amiodarone for shock-refractory VF/pVT.
  • Dose: 1 mg/kg IV/IO initial bolus, followed by a continuous maintenance infusion of 20 to 50 mcg/kg/min.

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Pediatric Bradycardia with Poor Perfusion

In children, bradycardia is defined clinically as a heart rate slower than normal for age (typically <60 bpm in infants and young children). When associated with cardiorespiratory compromise, it requires rapid pharmacotherapy:

1. Ventilation & Oxygenation: The initial and most critical intervention is establishing an open airway and delivering 100% oxygen via positive pressure ventilation.
2. Chest Compressions: If HR remains <60 bpm with poor perfusion despite 30 seconds of effective ventilation, start chest compressions immediately.
3. Epinephrine: First-line agent for persistent symptomatic hypoxic bradycardia. Dose: 0.01 mg/kg IV/IO (0.1 mL/kg of 0.1 mg/mL formulation) every 3 to 5 minutes.
4. Atropine:
   • Indications: Specifically indicated for bradycardia caused by increased vagal tone (e.g., post-intubation vagal surge, nasopharyngeal suctioning), primary atrioventricular (AV) block, or organophosphate toxicity.
   • Dose: 0.02 mg/kg IV/IO.
   • Critical Thresholds: Minimum single dose is 0.1 mg (to prevent paradoxical central vagal stimulation and worsening bradycardia caused by subtherapeutic doses); maximum single dose is 0.5 mg in a child and 1.0 mg in an adolescent.

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Pediatric Tachycardias: Supraventricular Tachycardia (SVT)

Narrow-complex tachycardias must be differentiated into Sinus Tachycardia versus Supraventricular Tachycardia (SVT):

Management of Pediatric SVT

• Hemodynamically Stable:
  • Vagal Maneuvers: In infants and toddlers, apply an ice bag to the upper half of the face for 15 to 20 seconds, ensuring no airway obstruction or ocular compression. In older children, perform a modified Valsalva maneuver (blowing into a 10 mL syringe).
  • Adenosine Pharmacotherapy:
    • Mechanism: Slows conduction time through the AV node, interrupting AV nodal re-entry pathways.
    • Initial Dose: 0.1 mg/kg rapid IV/IO push (maximum initial dose 6 mg).
    • Second Dose: If no conversion within 1 to 2 minutes, administer 0.2 mg/kg rapid IV/IO push (maximum second dose 12 mg).
    • Administration Technique: Adenosine has an ultra-short half-life (<10 seconds). It must be administered via a proximal IV site (antecubital or central) using a two-syringe stopcock technique, followed immediately by a rapid flush of 5 to 10 mL normal saline.
• Hemodynamically Unstable (Hypotension, altered mental status, signs of shock):
  • Perform immediate synchronized cardioversion at 0.5 to 1 J/kg.
  • If refractory, escalate subsequent cardioversion energy to 2 J/kg.

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Pediatric Status Epilepticus: Timed Pharmacotherapy Pathways

Pediatric Status Epilepticus (SE) is defined as continuous seizure activity lasting >5 minutes or recurrent seizures without full return to baseline neurological status between episodes. Prolonged seizure activity results in excitotoxic NMDA receptor upregulation, GABA-A receptor internalization, blood-brain barrier disruption, and irreversible neuronal injury.

Phase 1: Emergent Initial Therapy (0 to 10 Minutes)

• Intravenous Access Available:
  • Lorazepam: 0.1 mg/kg IV (maximum single dose 4 mg), administered slowly over 2 minutes. May repeat once at 5 to 10 minutes if seizures persist.
• No Intravenous Access (Prehospital / Rapid Bedside):
  • Midazolam: 0.2 mg/kg intranasally (IN) or intramuscularly (IM) (maximum single dose 10 mg). Intranasal delivery requires the concentrated 5 mg/mL injectable formulation divided equally between both nares using a mucosal atomization device (MAD).
  • Diazepam Rectal Gel: 0.2 to 0.5 mg/kg PR (maximum 20 mg) if midazolam is unavailable.

Phase 2: Urgent Control Therapy (10 to 30 Minutes)

If seizures continue despite adequate first-line benzodiazepine administration (established status epilepticus), non-sedating IV antiepileptic drugs (AEDs) must be initiated immediately. The landmark ESETT trial demonstrated equivalent efficacy (~45-50% seizure cessation at 60 minutes) among three primary agents:

1. Levetiracetam: 60 mg/kg IV (maximum single dose 4,500 mg), infused over 10 to 15 minutes. Preferred in hepatic disease; low drug-interaction profile.
2. Fosphenytoin: 20 mg PE/kg IV (maximum single dose 1,500 mg PE), infused at a rate not to exceed 150 mg PE/min (or 3 mg PE/kg/min). Water-soluble prodrug that avoids the propylene glycol vehicle toxicities of phenytoin (phlebitis, purple glove syndrome, severe hypotension).
3. Valproate Sodium: 40 mg/kg IV (maximum single dose 3,000 mg), infused over 10 minutes. Strictly contraindicated in children with known or suspected mitochondrial disorders (e.g., POLG mutations) or urea cycle disorders due to fatal hepatotoxicity and hyperammonemic encephalopathy.

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Pediatric Fluid Resuscitation & The Hypoglycemia "Rule of 50s"

Fluid Resuscitation in Pediatric Septic Shock

• Initial Volume: Administer 10 to 20 mL/kg of balanced crystalloid (Lactated Ringer's or Plasma-Lyte) as an intravenous push or rapid pressure bag infusion over 10 to 20 minutes.
• Reassessment & Fluid Overload: Following each bolus, rigorously examine the patient for signs of fluid overload: hepatomegaly, new or worsening pulmonary crackles/rales, increased work of breathing, or gallop rhythm. If signs of fluid overload appear, stop fluid boluses immediately and initiate vasoactive infusions (epinephrine for cold shock; norepinephrine for warm vasodilatory shock).

Acute Hypoglycemia Resuscitation: The "Rule of 50s"

Pediatric patients have limited hepatic glycogen stores and elevated basal metabolic rates, predisposing them to profound neuroglycopenia. Hypoglycemia thresholds: neonates <45 mg/dL; infants and children <60 mg/dL.

To prevent osmolar injury, fluid shifts, and chemical phlebitis, dextrose concentrations are selected based on age using the Rule of 50s:

Dextrose Concentration (%) × Volume (mL/kg) = 50