Cardiac Medications Reference

Mechanism: Transiently blocks AV node conduction and slows SA node firing by activating adenosine receptors — interrupts re-entrant circuits that depend on AV node conduction.

Primary indication: First-line drug for stable narrow-complex supraventricular tachycardia (SVT) not responsive to vagal maneuvers.

Dose (ACLS): 6 mg rapid IV push followed immediately by 20 mL NS flush. If no response in 1–2 min: 12 mg rapid IV push (may repeat 12 mg once). Must be administered through a large proximal vein (antecubital or central) — extremely short half-life of < 10 seconds.

Nursing considerations:

• Warn the patient: brief but intense sensations — chest pressure, flushing, shortness of breath, sense of impending doom — typically last 15–30 seconds
• Monitor on continuous cardiac monitor — transient asystole or AV block is expected before conversion
• Ineffective for atrial fibrillation, atrial flutter, or VT — used only for rhythm termination, not rate control
• Use with caution in patients with severe asthma (bronchospasm risk) or WPW syndrome (may accelerate conduction via accessory pathway in Afib)
• Caffeine and theophylline antagonize adenosine — higher doses may be needed
• Dipyridamole potentiates adenosine — lower doses required

Mechanism: Multi-channel blocker (potassium, sodium, calcium channels, and beta-adrenergic receptors) with complex pharmacokinetics. Prolongs action potential duration and effective refractory period in atrial and ventricular tissue.

Indications:

• Cardiac arrest (VF/pVT) refractory to defibrillation — after 3rd shock
• Hemodynamically stable VT or SVT
• Atrial fibrillation — rate control and/or rhythm conversion

Dose (ACLS — cardiac arrest): 300 mg IV/IO bolus; may repeat 150 mg IV/IO once. For stable VT: 150 mg IV over 10 min, then 1 mg/min infusion for 6 hours, then 0.5 mg/min.

Nursing considerations:

• Dilute in D5W for IV infusion (incompatible with NS for infusion); use dedicated line — incompatible with many medications
• Monitor QT interval — amiodarone significantly prolongs QTc; report QTc > 500 ms
• Hypotension is a common side effect of IV loading — have vasopressors available
• Long-term use: pulmonary toxicity, thyroid dysfunction (hypo- or hyperthyroidism), hepatotoxicity, photosensitivity, corneal microdeposits — monitor function tests
• Interacts with warfarin (potentiates anticoagulation), digoxin, and statins

Mechanism: Competitive antagonist of muscarinic acetylcholine receptors — blocks vagal tone at the SA and AV nodes, increasing heart rate and AV conduction velocity.

Indications:

• Symptomatic sinus bradycardia
• First-degree and Mobitz I AV block with symptoms
• PEA and asystole (in conjunction with CPR and epinephrine per older protocols — note: current AHA guidelines de-emphasize atropine in PEA/asystole)

Dose (ACLS): 1 mg IV every 3–5 minutes; maximum cumulative dose 3 mg. Doses < 0.5 mg may paradoxically worsen bradycardia (paradoxical bradycardia due to central vagal stimulation).

Nursing considerations:

• Ineffective for infranodal blocks (Mobitz II, complete heart block) — block is below the AV node where vagal tone has no effect; may worsen conduction
• Side effects: dry mouth, urinary retention, blurred vision, constipation, tachycardia, confusion (especially in elderly)
• Use with caution in patients with glaucoma, BPH, or ischemia (tachycardia increases myocardial oxygen demand)
• Have transcutaneous pacing available if atropine fails

Mechanism: Dose-dependent stimulation of dopaminergic, beta-1, and alpha-1 adrenergic receptors — effects vary significantly by infusion rate.

Indications: Symptomatic bradycardia refractory to atropine (as alternative to transcutaneous pacing); cardiogenic shock with hypotension.

Nursing considerations:

• Administer via central line whenever possible — extravasation causes severe tissue necrosis; if peripheral IV must be used, monitor site vigilantly and discontinue immediately if signs of extravasation occur (phentolamine reversal agent)
• Monitor HR, BP, and rhythm continuously — can cause tachycardia, ectopy, or worsening arrhythmias
• Titrate to desired clinical response; wean gradually — abrupt discontinuation can cause rebound hypotension
• Use D5W or NS for dilution; incompatible with alkaline solutions (sodium bicarbonate)

Mechanism: Stimulates alpha-1 (vasoconstriction — increases aortic diastolic pressure and coronary perfusion pressure during CPR) and beta-1/beta-2 receptors (increases heart rate, contractility, and bronchodilation).

Indications:

• Cardiac arrest (VF, pVT, PEA, asystole) — standard vasopressor in ACLS
• Anaphylaxis (drug of choice)
• Severe bradycardia or hypotension (infusion)

Dose (ACLS — cardiac arrest): 1 mg IV/IO every 3–5 minutes. Administer as soon as IV/IO access is established. For VF/pVT: give after 2nd shock. For PEA/asystole: give as soon as possible.

Nursing considerations:

• Follow each dose with 20 mL IV flush and elevate the limb if administered peripherally
• Post-resuscitation: monitor for tachycardia, hypertension, myocardial ischemia
• Extravasation can cause tissue necrosis — prefer central access when possible during resuscitation if readily available without delaying therapy
• For anaphylaxis: 0.3–0.5 mg IM (anterolateral thigh) is the preferred route — do not delay for IV access

Mechanism: Blocks fast sodium channels in ventricular tissue — suppresses automaticity and re-entrant circuits in ischemic myocardium. Minimal effect on atrial tissue.

Indications:

• Alternative to amiodarone for VF/pVT refractory to defibrillation (ACLS)
• Stable VT when amiodarone is unavailable or contraindicated
• Frequent symptomatic PVCs in the setting of acute MI (less common — use per provider order)

Dose (ACLS — cardiac arrest): 1–1.5 mg/kg IV/IO bolus; may repeat 0.5–0.75 mg/kg every 5–10 min to maximum 3 mg/kg. Maintenance infusion: 1–4 mg/min.

Nursing considerations:

• Toxicity signs: CNS effects appear first — perioral numbness, metallic taste, lightheadedness, confusion, tinnitus; severe toxicity: seizures, respiratory depression, cardiac arrest
• Reduce dose in hepatic failure, heart failure, and elderly patients — lidocaine is hepatically metabolized
• Monitor ECG during infusion — PR prolongation and QRS widening may indicate toxicity
• Do not use for bradycardia or escape rhythms — sodium channel blockade will suppress the escape pacemaker and worsen bradycardia