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HLT-EMT39-05 · Lesson 6 · 30 clock hours · theory

Cardiovascular and Antidysrhythmic Pharmacology

Objective. Students will describe the mechanism of action, indications, contraindications, dosing range, and adverse effects of the primary cardiovascular and antidysrhythmic agents used in prehospital advanced cardiac life support.

⚠ Pending professional review

This lesson, its worked examples and its practice questions has not yet been verified by a licensed clinician in the field or by a certification or approval body. It is a study draft and may contain errors. Do not use it to make decisions about any patient or medication. Always follow your instructor, your supervising professional, and current official references and regulations.

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Cardiovascular and Antidysrhythmic Pharmacology

Cardiovascular emergencies are among the most time-critical situations a paramedic manages. Understanding how the primary cardiac medications work—and when not to use them—is essential to safe, effective advanced cardiac life support (ACLS).

How the Heart's Electrical System Is Targeted by Drugs

Cardiac drugs act on ion channels, receptors, or autonomic pathways to change heart rate, rhythm, conduction, or contractility. The most useful framework is the Vaughan Williams classification for antidysrhythmics, alongside the broader categories of vasopressors and antifibrillatory agents.

Epinephrine

Epinephrine (adrenaline) is the cornerstone drug in cardiac arrest. It stimulates both alpha-1 and beta-1 adrenergic receptors. Alpha-1 stimulation causes peripheral vasoconstriction, raising aortic diastolic pressure and improving coronary perfusion pressure during CPR. Beta-1 stimulation increases myocardial contractility and automaticity.

Indications: Ventricular fibrillation (VF), pulseless ventricular tachycardia (pVT), asystole, pulseless electrical activity (PEA), and severe anaphylaxis.

Contraindications/Cautions: No absolute contraindications in cardiac arrest. Use with caution in patients with hypertension or known coronary artery disease in non-arrest settings.

Adverse effects: Tachycardia, hypertension, increased myocardial oxygen demand, and anxiety in conscious patients.

Amiodarone

Amiodarone is a Class III antidysrhythmic with properties spanning all four Vaughan Williams classes. It primarily blocks potassium channels, prolonging the action potential and refractory period. It also has beta-blocking, sodium-channel blocking, and calcium-channel blocking effects.

Indications: Shock-refractory VF and pVT during cardiac arrest; hemodynamically stable wide-complex tachycardia; rate control in atrial fibrillation or flutter.

Contraindications: Hypersensitivity, cardiogenic shock (in stable patients), and severe sinus-node dysfunction without a pacemaker.

Adverse effects: Hypotension (especially with rapid infusion), bradycardia, QT prolongation, and phlebitis at the IV site. Long-term use causes thyroid, pulmonary, and hepatic toxicity—important background knowledge for patient handoff.

Lidocaine

Lidocaine is a Class IB antidysrhythmic that blocks fast sodium channels, decreasing automaticity and suppressing ventricular ectopy. It is an acceptable alternative to amiodarone for VF/pVT when amiodarone is unavailable.

Indications: VF and pVT (alternative agent); stable wide-complex tachycardia of ventricular origin.

Contraindications: Known hypersensitivity, heart blocks (second or third degree without a pacemaker), and Wolff-Parkinson-White syndrome with rapid conduction.

Adverse effects: CNS toxicity (dizziness, slurred speech, seizures), cardiovascular depression, and cardiac arrest at toxic levels. Always monitor for early neurological signs.

Adenosine

Adenosine is a naturally occurring nucleoside that transiently blocks the AV node by activating potassium channels and inhibiting calcium influx. This briefly interrupts re-entrant circuits dependent on AV-node conduction.

Indications: Stable, narrow-complex supraventricular tachycardia (SVT) that has not responded to vagal maneuvers.

Contraindications: Second- or third-degree heart block, sick sinus syndrome without a pacemaker, and Wolff-Parkinson-White syndrome with pre-excitation (adenosine can accelerate conduction through accessory pathways).

Adverse effects: Transient chest pressure, flushing, dyspnea, and a brief period of asystole (a few seconds)—warn the patient and have the monitor recording. Give as a rapid IV bolus followed immediately by a saline flush.

Atropine

Atropine is an anticholinergic (muscarinic antagonist) that blocks vagal tone on the SA and AV nodes, increasing heart rate and conduction velocity.

Indications: Symptomatic bradycardia with hemodynamic compromise.

Contraindications: There are no absolute contraindications in the symptomatic setting, but atropine is generally not effective for third-degree (complete) heart block at the infranodal (His-Purkinje) level—transcutaneous pacing or dopamine/epinephrine infusion should not be delayed.

Adverse effects: Tachycardia, urinary retention, dry mouth, blurred vision, and paradoxical bradycardia at very low doses.

Dopamine and Norepinephrine

These catecholamines are used as continuous infusions for hemodynamically unstable patients. Dopamine has dose-dependent effects: at lower infusion rates it has predominantly dopaminergic effects; at higher rates it acts mainly on beta-1 and then alpha-1 receptors to raise cardiac output and blood pressure. Norepinephrine is a potent alpha-1 agonist used for vasodilatory shock.

Key Safety Principles

Key terms8

AntidysrhythmicA drug that suppresses, prevents, or converts abnormal cardiac rhythms by acting on ion channels or receptors in the cardiac conduction system.
Vaughan Williams ClassificationA widely used system that groups antidysrhythmic drugs into four classes based on their primary electrophysiological mechanism (e.g., sodium-channel blockade, beta blockade, potassium-channel blockade, calcium-channel blockade).
Action PotentialThe rapid sequence of electrical changes across a cardiac cell membrane that triggers contraction; antidysrhythmic drugs alter its shape, duration, or conduction speed.
ChronotropyThe property of affecting heart rate; a positive chronotrope increases rate, a negative chronotrope decreases it.
InotropyThe property of affecting the force of myocardial contraction; epinephrine and dopamine at cardiac doses are positive inotropes.
Refractory PeriodThe interval after a cardiac action potential during which the cell cannot be re-stimulated; drugs such as amiodarone prolong this period to suppress re-entrant dysrhythmias.
Supraventricular Tachycardia (SVT)A rapid rhythm originating above the bundle of His, typically presenting as a narrow-complex tachycardia; adenosine is the first-line drug for stable AV-node-dependent SVT.
Coronary Perfusion PressureThe pressure gradient that drives blood into the coronary arteries during CPR; epinephrine improves it through vasoconstriction, increasing the likelihood of return of spontaneous circulation.

Worked examples4

1. A 70-kg adult in cardiac arrest (VF) requires an epinephrine dose. The standard adult ACLS dose is 1 mg IV/IO. How many milliliters of a 1:10,000 epinephrine solution (0.1 mg/mL) are needed?
  1. Identify the required dose: 1 mg.
  2. Identify the concentration: 1:10,000 = 0.1 mg per mL.
  3. Divide dose by concentration: 1 mg ÷ 0.1 mg/mL = 10 mL.
  4. Confirm the volume is reasonable for a pre-filled syringe (standard pre-filled syringes of 1:10,000 epinephrine contain 10 mL).
Answer: 10 mL of 1:10,000 epinephrine delivers 1 mg.
2. A pediatric patient weighing 20 kg is in VF. The weight-based epinephrine dose for pediatric cardiac arrest is 0.01 mg/kg IV/IO. Using 1:10,000 solution (0.1 mg/mL), what volume should be drawn up?
  1. Calculate the dose: 0.01 mg/kg × 20 kg = 0.2 mg.
  2. Identify the concentration: 0.1 mg/mL.
  3. Divide dose by concentration: 0.2 mg ÷ 0.1 mg/mL = 2 mL.
  4. Cross-check: 2 mL × 0.1 mg/mL = 0.2 mg. Correct.
Answer: 2 mL of 1:10,000 epinephrine delivers 0.2 mg for a 20-kg child.
3. Amiodarone for shock-refractory VF in an adult is given at 300 mg IV/IO for the first dose. The available concentration is 50 mg/mL. What volume is required?
  1. Identify the required dose: 300 mg.
  2. Identify the concentration: 50 mg/mL.
  3. Divide dose by concentration: 300 mg ÷ 50 mg/mL = 6 mL.
  4. Verify: 6 mL × 50 mg/mL = 300 mg. Correct.
Answer: 6 mL of the 50 mg/mL amiodarone solution delivers 300 mg.
4. A symptomatic bradycardia patient is to receive atropine 0.5 mg IV. The vial contains atropine 1 mg/10 mL (0.1 mg/mL). What volume is drawn up?
  1. Identify the required dose: 0.5 mg.
  2. Identify the concentration: 0.1 mg/mL.
  3. Divide dose by concentration: 0.5 mg ÷ 0.1 mg/mL = 5 mL.
  4. Verify: 5 mL × 0.1 mg/mL = 0.5 mg. Correct.
Answer: 5 mL of the 0.1 mg/mL atropine solution delivers 0.5 mg.
In class: Drug card project: students create a standardized drug reference card for each major cardiovascular agent covered, including mechanism, indication, contraindication, adult and pediatric dosing range, route, and monitoring parameters. · Rhythm-pharmacology matching exercise: given 10 printed ECG rhythm strips, students identify the dysrhythmia and select the appropriate pharmacological intervention from a list, citing the indication and route. · Simulated cardiac arrest scenario (tabletop): small groups receive a running ACLS scenario script and must sequence medication interventions in correct order, calculating each dose for the assigned patient weight.
Materials: EMS pharmacology textbook, ACLS algorithm reference cards, blank drug card templates, printed ECG rhythm strips, tabletop scenario scripts, whiteboard
Check: Written unit exam (30 multiple-choice questions) covering cardiovascular pharmacology; pass mark 80%. Students scoring below 80% complete targeted remediation and a 15-question alternate-form retest before the next lesson.

Practice check8

Answer each question, then check it. Nothing is recorded; this is your own practice.

Pharmacology / ACLS
1. A patient is in pulseless ventricular fibrillation. After a defibrillation attempt and resuming CPR, the team prepares medication. Which drug is the first-line vasopressor in this cardiac arrest?
Pharmacology
2. Which mechanism best explains why adenosine terminates AV-node-dependent supraventricular tachycardia?
Pharmacology / Patient Safety
3. A paramedic prepares to administer adenosine to a patient with a rapid, regular, narrow-complex tachycardia. Which finding would be the strongest reason to withhold adenosine?
Pharmacology
4. Which adverse effect is MOST important to anticipate and explain to a conscious patient immediately before adenosine administration?
Pharmacology
5. Amiodarone is primarily classified as a Class III antidysrhythmic. What is its primary cellular mechanism?
Pharmacology / Cardiology
6. A 55-year-old patient has a heart rate of 36 bpm, is hypotensive, and is diaphoretic. Medical direction orders atropine. Why is atropine potentially ineffective if the block is at the infranodal (His-Purkinje) level?
Pharmacology / Patient Safety
7. A patient develops VF that is refractory after multiple defibrillation attempts and epinephrine. The team administers amiodarone. Shortly after the next defibrillation attempt, return of spontaneous circulation is achieved, but blood pressure is 74/40 mmHg. Which amiodarone-related adverse effect most likely contributes to hypotension in this situation?
Pharmacology
8. When administering adenosine by peripheral IV for SVT, the correct technique is to give the bolus rapidly and follow it immediately with a large saline flush. What is the primary reason for this technique?
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