Pharmacotherapy

Epinephrine

• First-line vasopressor used in pulseless arrest to increase coronary and cerebral perfusion.
• Mechanism: Combined alpha and beta adrenergic agonist. Causes peripheral vasoconstriction to increase coronary and cerebral perfusion pressures. Also increases myocardial contractility and heart rate.
• Dosing:
  • IV/IO: 0.01 mg/kg (0.1 mL/kg of 1:10,000 concentration). Max single dose 1 mg. Repeat every 3-5 minutes.
  • ETT: 0.1 mg/kg (0.1 mL/kg of 1:1,000 concentration).
• Side effects: Tachycardia, hypertension, arrhythmias.
• Contraindications: No absolute contraindications in pulseless arrest. Use with caution in patients with hypertension or coronary artery disease when pulse present.
• Monitoring: Continuous rhythm monitoring.
• Clinical pearls:
  • IV/IO route preferred over ETT. ETT dose is 10 times higher than IV/IO dose.
  • Confirm IV/IO dose with flush to ensure medication reaches central circulation.
  • May see transient α effects (hypertension, reflex bradycardia) if epinephrine given with perfusing rhythm.

Atropine

• First-line for symptomatic bradycardia, especially with increased vagal tone. Helps increase heart rate.
• Mechanism: Anticholinergic, blocks parasympathetic effects. Causes increased HR by blocking vagal influences on SA and AV nodes.
• Dosing: 0.02 mg/kg IV/IO. Minimum single dose 0.1 mg. Maximum single dose 0.5 mg child, 1 mg adolescent. May repeat to maximum total dose 1 mg child, 2 mg adolescent.
• Side effects: Tachycardia, delirium, blurred vision, dry mouth.
• Contraindications: Avoid in cardiac transplant patients (denervated heart). Porcine or bovine valve patients (may cause heart block).
• Monitoring: Heart rate and rhythm, mental status.
• Clinical pearls:
  • Often needs repeat dosing for bradycardia.
  • Paradoxical bradycardia can occur if first dose too low. Use minimum 0.1 mg dose.
  • Works within 1-3 minutes IV/IO. Peak effect ~5 minutes. Short duration 30-60 minutes.

Amiodarone

• Antidysrhythmic used for shock-refractory VF, pulseless VT, stable VT, SVT refractory to adenosine.
• Mechanism: Blocks potassium, sodium, and calcium channels. Prolongs action potential and refractory periods. Noncompetitive α and β blocker.
• Dosing:
  • VF/pulseless VT: 5 mg/kg IV/IO bolus. May repeat up to 2 more times (up to 15 mg/kg total).
  • Stable VT: 5 mg/kg IV/IO over 20-60 minutes.
  • SVT: 5 mg/kg IV/IO over 20-60 minutes.
• Side effects: Hypotension, bradycardia, QT prolongation, torsades (rare), phlebitis.
• Contraindications: Severe sinus node dysfunction, second- or third-degree AV block. Avoid other QT prolonging drugs.
• Monitoring: Continuous ECG monitoring, blood pressure. Check QT interval.
• Clinical pearls:
  • Effects persist long after infusion stopped due to long half-life (days).
  • Monitor thyroid function, liver function.
  • Frequently causes hypotension with rapid infusion. Infuse over 20-60 mins.

Lidocaine

• Antidysrhythmic used for pulseless VT/VF, stable VT.
• Mechanism: Stabilizes cardiac membrane by blocking sodium channels. Shortens action potential duration and refractory periods.
• Dosing: VF/pulseless VT: 1 mg/kg IV/IO bolus. Repeat 0.5-0.75 mg/kg every 5-10 minutes to maximum dose of 3 mg/kg.
• Stable VT with pulses: 1 mg/kg IV/IO bolus followed by infusion 20-50 mcg/kg/min.
• Side effects: Seizures, slurred speech, confusion, hypotension, bradycardia, asystole, altered mental status.
• Contraindications: AV blocks, severe sinus node dysfunction, Adams-Stokes syndrome. Use caution in hepatic disease.
• Monitoring: Continuous ECG and blood pressure monitoring. Monitor mental status.
• Clinical pearls:
  • Onset 1-3 min IV/IO. Duration 10-20 minutes after single dose.
  • Less negative inotropy compared to amiodarone but also less effective.
  • Lower doses in hepatic dysfunction.

Magnesium sulfate

• First-line antidysrhythmic for torsades de pointes, suspected hypomagnesemia. Also used as adjunctive treatment in refractory VF.
• Mechanism: Stabilizes cardiac membranes, increases refractory periods. Also replaces magnesium.
• Dosing: 25-50 mg/kg IV/IO push over 1-2 minutes for torsades, pulseless VT. Maximum 2 g.
• Side effects: Flushing, sweating, hypotension, respiratory depression.
• Contraindications: Heart block, renal failure. Use caution with concomitant calcium channel blockers.
• Monitoring: Continuous ECG, blood pressure monitoring, magnesium levels.
• Clinical pearls:
  • Rapid administration can cause hypotension.
  • Monitor calcium levels since magnesium lowers ionized calcium.

Adenosine

• First-line for stable, narrow-complex SVT. Helps interrupt AV nodal reentry pathway to terminate SVT.
• Mechanism: Activates potassium channels resulting in transient AV nodal blockade
• Dosing:
  • First dose: 0.1 mg/kg IV/IO (max 6 mg)
  • Second dose (if needed): 0.2 mg/kg IV/IO (max 12 mg)
• Side effects: Chest pain/discomfort, shortness of breath, flushing, headache, transient AV block, asystole (rare)
• Contraindications: Second- or third-degree AV block, sick sinus syndrome, atrial fibrillation with accessory pathway. Use with caution in asthma – may cause bronchoconstriction.
• Monitoring: Continuous ECG monitoring before and during administration. Have defibrillator available.
• Clinical pearls:
  • Extremely short half-life of 10 seconds. Rapid IV push followed by flush.
  • May transiently slow ventricular rate as it blocks AV node.
  • 6 mg typically used for first dose in adolescent/adult.
  • Effects occur in 1-2 minutes, last for 10-30 seconds once discontinued.

Sodium bicarbonate

• Used for severe metabolic acidosis, hyperkalemia, cyclic antidepressant toxicity
• Mechanism: Increases plasma pH. Helps stabilize cardiac cell membrane in acidosis. Shifts potassium into cells.
• Dosing: 1 mEq/kg IV/IO
• Side effects: Hypokalemia, hyperosmolality, hypernatremia, tetany, alkalosis
• Contraindications: Avoid in hypocalcemia, alkalosis, hypokalemia. Do not administer together with calcium solutions.
• Monitoring: Blood gases, electrolytes, pH, ECG for arrhythmias
• Clinical pearls:
  • Onset within 5 minutes IV. Duration 30-60 minutes.
  • Avoid extravasation. Can cause tissue necrosis.

Calcium chloride

• Used for hyperkalemia, calcium channel blocker toxicity, hypocalcemia, magnesium toxicity
• Mechanism: Increases cardiac contractility, competes with potassium for membrane binding sites
• Dosing: 20 mg/kg (0.2 mL/kg of 10% solution) IV/IO over 30-60 minutes
• Side effects: Bradycardia, heart block, cardiac arrest, tissue necrosis with extravasation
• Contraindications: Avoid in digitalis toxicity, hypercalcemia, sarcoidosis
• Monitoring: Ionized calcium levels, ECG, signs of toxicity
• Clinical pearls:
  • 10% solution (100 mg/mL)
  • Administer slowly – can cause bradycardia
  • Do not administer together with sodium bicarbonate – form insoluble precipitate. Flush line between them.
  • Onset 5-15 minutes IV. Duration 30-60 minutes.

Dextrose

• Indicated for hypoglycemia
• Mechanism: Provides supplemental glucose.
• Dosing: 0.5-1 g/kg IV/IO (D10W 5 mL/kg or D25W 2 mL/kg)
• Side effects: Hyperglycemia, phlebitis, tissue necrosis if extravasation
• Contraindications: None in setting of hypoglycemia
• Monitoring: Bedside glucose meter to assess response
• Clinical pearls:
  • Dilute concentrated dextrose before giving peripheral IV in small children
  • Onset Within 5 minutes. Check glucose 10 minutes after.
  • Duration 1-2 hours. May require additional supplementation.

The pharmacologic agents used in PALS target cardiac output, perfusion, rhythm disturbances, and reversible underlying causes of arrest such as hypoglycemia. Epinephrine is first-line for pulseless arrest to improve coronary and cerebral perfusion. Atropine is first-line for symptomatic bradycardia while amiodarone, lidocaine and magnesium sulfate are antidysrhythmics used for shock-refractory VF, pulseless VT, and stable VT. Adenosine is used for narrow complex SVT. Sodium bicarbonate treats severe acidosis while calcium treats hypocalcemia and hyperkalemia. Dextrose reverses hypoglycemia. The IV/IO route is preferred over ETT administration for all drugs. Providers should be familiar with the mechanisms of action, dosing, side effects, contraindications, and monitoring to safely and effectively administer these agents. Attention to details such as dose, concentration, dilution, administration rate, monitoring, and potential drug interactions are crucial clinical pearls.