Verapamil | Medication Reference

Bedside Snapshot

What it does: Non-dihydropyridine calcium channel blocker with strong effects on the AV node—slows conduction, prolongs AV nodal refractoriness, decreases heart rate; also causes coronary and peripheral vasodilation and mild-to-moderate negative inotropy
Key Acute IV Uses: Conversion or rate control of narrow-complex SVT (PSVT/AVNRT/AVRT) and ventricular rate control in atrial fibrillation/flutter in hemodynamically stable patients
Adult IV Dosing: 2.5–5 mg IV over at least 2 minutes (over ~3 minutes in older/frail patients); if tolerated but inadequate, repeat 5–10 mg IV after 15–30 minutes (or 0.075–0.15 mg/kg up to 10 mg); maximum cumulative bolus usually 20–30 mg
Continuous Infusion: After successful bolus for AF/flutter rate control, some protocols start ~0.005 mg/kg/min (around 5–10 mg/hour in adults) for short-term maintenance, titrated to heart rate and blood pressure
Onset & Duration (IV): Onset 3–5 minutes with peak effect by ~5–10 minutes; hemodynamic and rate-control effect after single bolus typically lasts 30–60 minutes
Oral Therapy: Used chronically for rate control in AF/flutter, PSVT prevention, angina, hypertension, and some forms of hypertrophic cardiomyopathy; typical adult total daily dose 240–480 mg/day (immediate release divided TID/QID or once-daily extended-release)
Major Hazards: Hypotension, bradycardia, high-grade AV block, cardiogenic shock, and acute decompensation of systolic heart failure; risk is higher in patients with baseline LV dysfunction, on beta-blockers, or with conduction disease
CRITICAL WARNINGS:
- Absolutely avoid IV verapamil in atrial fibrillation/flutter with pre-excitation (e.g., Wolff–Parkinson–White) and in undifferentiated wide-complex tachycardia—assume VT or pre-excited AF until proven otherwise
- Do NOT give IV verapamil and IV beta-blockers in close succession; combination can precipitate severe bradycardia, AV block, and cardiogenic shock

Brand & Generic Names

Generic Name: Verapamil
Brand Names: Calan, Isoptin, Verelan, Covera-HS, plus multiple generics (availability is institution- and region-specific)

Medication Class

Non-dihydropyridine calcium channel blocker (L-type); Class IV antiarrhythmic

Pharmacology

Mechanism of Action:

Verapamil is a non-dihydropyridine L-type calcium channel blocker (phenylalkylamine) that inhibits voltage-dependent L-type calcium channels in cardiac myocytes, nodal tissue (SA and AV node), and vascular smooth muscle
At SA and AV nodes: Action potentials rely heavily on calcium influx; verapamil decreases phase 0 depolarization slope in nodal cells, slows conduction, and prolongs AV nodal refractoriness, thereby slowing ventricular response in atrial tachyarrhythmias and interrupting re-entrant circuits (AVNRT/AVRT)
In ventricular myocardium: Reduces intracellular calcium, leading to negative inotropic effects (reduced contractility); clinically relevant in patients with reduced ejection fraction, where it can precipitate or worsen heart failure
In vascular smooth muscle: Causes vasodilation (particularly in coronary arteries and peripheral arterioles), which decreases afterload and relieves coronary vasospasm but can also contribute to hypotension and reflex tachycardia at low doses
Overall hemodynamic profile: Decreased heart rate and AV conduction, decreased afterload, and decreased contractility; balance of these effects is highly patient- and dose-dependent; in fragile or volume-depleted patients, hypotension and bradycardia can be profound
Also a moderate inhibitor of CYP3A4 and P-glycoprotein, leading to important drug–drug interactions (e.g., increased levels of digoxin, some statins, and other CYP3A4 substrates)

Pharmacokinetics:

Routes: Oral (immediate- and extended-release) and intravenous injection; in acute care, IV bolus (± infusion) used for arrhythmias; oral forms for chronic rate control, angina, and hypertension
Onset: IV: 3–5 minutes; peak effect usually within ~5–10 minutes; Oral: slower onset, generally 1–2 hours to peak concentration for immediate-release tablets
Bioavailability (oral): Although >90% absorbed from GI tract, high first-pass hepatic metabolism yields systemic bioavailability of only ~10–35%, with substantial interpatient variability
Protein binding: Approximately 90% bound to plasma proteins; volume of distribution large (about 3–5 L/kg), reflecting extensive tissue distribution
Metabolism: Extensively metabolized in liver (CYP3A4) to multiple metabolites, including norverapamil (which has ~20% of the vasodilatory activity of parent drug)
Half-life: Terminal elimination half-life about 2–8 hours after single IV or oral doses; may extend to ~4.5–12 hours with chronic oral therapy; prolonged in hepatic impairment and older adults
Elimination: Primarily hepatic metabolism with ~70% of dose excreted in urine and ~16% in feces as metabolites; only small fraction excreted unchanged in urine; not significantly removed by hemodialysis
Hepatic dysfunction: Clearance predominantly hepatic; patients with significant liver disease require lower initial doses and slower titration with careful monitoring for hypotension and bradycardia

Indications

Acute treatment of hemodynamically stable, narrow-complex paroxysmal supraventricular tachycardia (PSVT), including AV nodal re-entrant tachycardia (AVNRT) and some AV re-entrant tachycardias (AVRT), particularly when adenosine is ineffective or contraindicated
Acute ventricular rate control in atrial fibrillation or atrial flutter with rapid ventricular response (RVR) in hemodynamically stable patients without pre-excitation or decompensated systolic heart failure
Chronic rate control in atrial fibrillation/flutter and prevention of recurrent PSVT (primarily via oral therapy)
Management of stable angina (especially vasospastic/variant angina) and chronic stable angina in patients who cannot tolerate beta-blockers
Treatment of hypertension as part of chronic outpatient therapy (usually extended-release formulations)
Adjunctive therapy for symptomatic hypertrophic cardiomyopathy (HCM) in patients intolerant of or unresponsive to beta-blockers, particularly with preserved systolic function

Diseases & Conditions Treated:

Paroxysmal supraventricular tachycardia (PSVT, including AVNRT and some AVRT forms)
Atrial fibrillation and atrial flutter with rapid ventricular response (rate control)
Multifocal atrial tachycardia (in selected patients)
Stable angina pectoris, including vasospastic (Prinzmetal) angina
Chronic hypertension (usually with extended-release formulations)
Hypertrophic cardiomyopathy with symptomatic outflow obstruction in selected patients (oral)

Dosing & Administration

Available Forms:

IV injection: Verapamil hydrochloride 2.5 mg/mL solution, commonly supplied as 5 mg/2 mL or 10 mg/4 mL vials/ampoules
Immediate-release oral tablets: Commonly 40 mg, 80 mg, and 120 mg strengths
Extended-release oral tablets/capsules: Typical strengths 100 mg, 120 mg, 180 mg, 200 mg, 240 mg, 300 mg, and 360 mg, depending on formulation (e.g., Calan SR, Isoptin SR, Verelan, Covera-HS)

IV Dosing (Always Follow Local Protocols and ACLS/Arrhythmia Guidelines):

Indication / Population	Initial IV Dose	Repeat / Infusion	Typical Maximum
Adult stable narrow-complex SVT or AF/flutter with RVR	2.5–5 mg IV over ≥2 min (over ~3 min if elderly); alternatively 0.075–0.15 mg/kg (max 10 mg) over ≥2 min	If tolerated but inadequate response, give 5–10 mg IV (or 0.15 mg/kg) after 15–30 min; consider infusion 0.005 mg/kg/min (~5–10 mg/hr) for short-term maintenance	Total IV bolus generally limited to 20–30 mg in most adult protocols
Pediatric SVT / AF/flutter (hemodynamically stable, specialist use)	0.1–0.3 mg/kg IV over ≥2 min; usual single dose 2–5 mg; max initial dose 5 mg	May repeat 0.1–0.3 mg/kg (max 10 mg total) after ~30 min if inadequate and well tolerated; continuous infusion rarely used outside specialist care	Maximum single dose 5 mg; maximum repeat dose typically 10 mg total

Oral Dosing (Chronic Therapy):

Indication	Initial Dose	Titration	Typical Range
Rate control, PSVT prophylaxis, angina, hypertension	Immediate-release: 80 mg PO TID Extended-release: 120–180 mg PO once daily	Titrate by 40–80 mg/day increments (IR) or 60–120 mg/day (ER) every 1–2 weeks based on HR/BP and symptom control	240–480 mg/day total (IR divided or ER once daily); do not exceed product-specific maximum

Administration Guidelines:

Give IV boluses through a dedicated line or the most proximal port available, with continuous ECG and noninvasive (or arterial) blood pressure monitoring
Administer IV verapamil over at least 2 minutes (longer in older or frail patients) to reduce risk of abrupt hypotension or AV block
If rhythm converts or ventricular rate is adequately controlled, do not automatically repeat the bolus; instead, monitor for recurrence and hemodynamics
Consider infusion only if frequent recurrence occurs and patient remains hemodynamically stable
In patients with impaired LV function, borderline blood pressure, or on other AV nodal blockers, strongly consider alternative agents (e.g., amiodarone, digoxin, or cautious beta-blockade) and involve cardiology or critical care early
For oral therapy, extended-release formulations generally preferred for hypertension and chronic rate control due to smoother plasma levels and once-daily dosing

Contraindications

Absolute Contraindications (IV and Generally Oral):

Severe hypotension or cardiogenic shock (e.g., systolic BP <90 mmHg or signs of end-organ hypoperfusion)
Severe left ventricular systolic dysfunction (ejection fraction markedly reduced) unless tachyarrhythmia-related and managed in a monitored setting with expert oversight
Sick sinus syndrome, second- or third-degree AV block, or marked bradycardia (unless a functioning pacemaker is present)
Atrial fibrillation or atrial flutter with an accessory pathway (e.g., Wolff–Parkinson–White syndrome) because AV nodal blockade can accelerate conduction via the accessory pathway and precipitate ventricular fibrillation
Wide-complex tachycardia of unknown origin—treat as VT until proven otherwise; do not give verapamil empirically
Concomitant use of IV beta-blockers in close temporal proximity (especially in patients with LV dysfunction or conduction disease)

Major Precautions:

Heart failure with reduced ejection fraction (HFrEF): Verapamil's negative inotropy can acutely worsen cardiac output; beta-blockers and/or digoxin are usually preferred for rate control in decompensated HFrEF
Baseline conduction disease: First-degree AV block, bundle-branch block, or sinus bradycardia—verapamil can unmask or worsen higher-grade block
Hepatic impairment: Verapamil clearance is reduced; start with smaller doses and titrate slowly with close monitoring
Renal impairment: Hemodynamic sensitivity may be increased even though drug is hepatically cleared; monitor BP and heart rate closely
Older adults and frail patients: Start at low end of dosing ranges and consider slower infusion times due to increased susceptibility to hypotension and bradycardia
Concomitant drugs: Use caution with digoxin (verapamil can increase digoxin levels), other AV nodal blockers (beta-blockers, diltiazem, amiodarone), and CYP3A4 substrates such as certain statins (e.g., simvastatin, lovastatin)
Pregnancy and lactation: Generally avoid unless benefits clearly outweigh risks; verapamil crosses the placenta and is excreted in breast milk

Wolff–Parkinson–White Warning: In atrial fibrillation with known or suspected WPW (delta waves, very rapid irregular wide-complex tachycardia), AV nodal blockers such as verapamil, diltiazem, beta-blockers, digoxin, and adenosine are CONTRAINDICATED—use procainamide or electricity instead.

Wide-Complex Tachycardia Warning: In undifferentiated wide-complex tachycardia, treat as VT (or pre-excited AF) and avoid AV nodal blockers like verapamil; this is a classic exam and real-world pitfall.

Adverse Effects

Common:

Hypotension, dizziness, or lightheadedness (especially after IV boluses)
Bradycardia and first-degree AV block
Headache, flushing, and sensation of warmth due to vasodilation
Peripheral edema with chronic oral therapy
Constipation (a classic chronic side effect of verapamil)
Nausea, fatigue, and mild peripheral neuropathic symptoms (paresthesias) in some patients

Serious:

Symptomatic hypotension and cardiogenic shock
High-grade AV block (Mobitz II or third-degree) and sinus arrest
Severe bradycardia with syncope or asystole, especially when combined with beta-blockers or in conduction disease
Acute decompensation of systolic heart failure with pulmonary edema
Ventricular fibrillation or rapid pre-excited tachycardia in patients with AF/flutter and accessory pathways (e.g., WPW)
Rare but serious dermatologic or hematologic reactions (e.g., Stevens–Johnson syndrome, agranulocytosis)
In overdose: profound hypotension, bradycardia, AV block, hyperglycemia, shock, and potentially refractory cardiovascular collapse

Overdose Management: In significant verapamil overdose, early aggressive management (high-dose insulin euglycemia therapy, vasopressors, calcium, lipid emulsion, and mechanical circulatory support where available) can be life-saving. These cases should trigger toxicology and critical care consultation.

Drug Interactions

Beta-blockers: Additive negative inotropic and chronotropic effects; combination can precipitate severe bradycardia, AV block, and heart failure; avoid IV administration of both in close succession
Digoxin: Verapamil inhibits P-glycoprotein, increasing digoxin levels by 50–75%; monitor digoxin levels and reduce digoxin dose as needed
CYP3A4 substrates: Verapamil inhibits CYP3A4; increases levels of simvastatin, lovastatin, atorvastatin (increased myopathy risk), certain immunosuppressants (cyclosporine, tacrolimus), and other substrates
Other AV nodal blockers: Diltiazem, amiodarone—additive effects on heart rate and AV conduction; increased risk of bradycardia and heart block
Antihypertensives: Additive hypotensive effects; monitor blood pressure closely
CYP3A4 inducers: Rifampin, phenytoin, carbamazepine may decrease verapamil levels and efficacy
CYP3A4 inhibitors: Erythromycin, clarithromycin, ketoconazole, grapefruit juice may increase verapamil levels and toxicity risk

Special Populations

Hepatic Impairment:

Clearance significantly reduced in liver disease
Start with 30–40% of normal dose
Titrate slowly with careful monitoring for hypotension and bradycardia
Consider alternative agents in severe hepatic dysfunction

Renal Impairment:

No specific dose adjustment for renal impairment (hepatically cleared)
Monitor hemodynamics closely as sensitivity may be increased
Not removed by hemodialysis

Pregnancy & Lactation:

Pregnancy: Category C; generally avoid unless benefits clearly outweigh risks
Crosses placenta; limited human data
Lactation: Excreted in breast milk; use with caution or consider alternative

Pediatric Considerations:

IV dosing: 0.1–0.3 mg/kg over ≥2 minutes (max 5 mg initial dose)
Repeat dosing: 0.1–0.3 mg/kg after 30 minutes if needed (max 10 mg total)
Use only in hemodynamically stable patients with specialist oversight
Monitor continuously for bradycardia and hypotension

Geriatric Considerations:

Increased sensitivity to hypotensive and bradycardic effects
Prolonged half-life in elderly patients
Administer IV doses over 3 minutes (slower than standard)
Start oral therapy at lower end of dosing range
Higher risk of AV block and falls from orthostatic hypotension

Monitoring

Clinical Monitoring:

Continuous ECG monitoring during IV administration and for a period afterward to detect bradycardia, AV block, or ventricular arrhythmias
Frequent blood pressure monitoring (ideally q1–5 minutes during bolus and early post-bolus period in unstable patients; arterial line if available in ICU)
Heart rate and rhythm assessment, including evaluation of conversion to sinus rhythm or degree of rate control in AF/flutter
Signs of heart failure or low output: dyspnea, crackles, JVD, peripheral edema, mental status changes, urine output, and lactate trends

Laboratory Monitoring:

Serum electrolytes and renal function when verapamil is used in critically ill patients or combined with diuretics or other cardioactive drugs
For chronic oral therapy: periodic assessment of blood pressure, heart rate, symptom control (angina, palpitations), and potential drug–drug interactions or side effects (e.g., edema, constipation)
Digoxin levels if co-administered (verapamil increases digoxin concentration)

Clinical Pearls

Always Confirm the Rhythm: Always confirm the rhythm diagnosis before giving IV verapamil. Narrow-complex, regular SVT in a young, structurally normal heart is one thing; irregular wide-complex tachycardia in a 70-year-old with cardiomyopathy is something else entirely.

Wide-Complex Tachycardia Rule: In undifferentiated wide-complex tachycardia, treat as VT (or pre-excited AF) and avoid AV nodal blockers like verapamil; missteps here are a classic exam and real-world pitfall.

WPW and Verapamil Don't Mix: In atrial fibrillation with known or suspected Wolff–Parkinson–White (delta waves, very rapid irregular wide-complex tachycardia), AV nodal blockers such as verapamil, diltiazem, beta-blockers, digoxin, and adenosine are contraindicated—use procainamide or electricity instead, per local protocols.

Think Globally in AF/Flutter with RVR: When using verapamil for AF/flutter with RVR, think globally: what is the patient's ventricular function? Are they septic, hypovolemic, or post-MI? In tenuous patients, verapamil may convert a fast-but-stable tachycardia into profound bradycardic shock.

Patients Already on Beta-Blockers: For patients already on a beta-blocker, consider increasing that agent or using amiodarone rather than layering IV verapamil on top of existing AV nodal blockade, unless cardiology specifically directs otherwise.

Calcium Pretreatment: Pretreatment with IV calcium (e.g., calcium chloride) has been used in some settings to blunt hypotension from verapamil without abolishing its AV nodal effects; this is a specialist-level maneuver and should follow local protocols.

Chronic Therapy Selection: For chronic therapy, choose between beta-blocker vs. verapamil/diltiazem based on comorbidities (e.g., asthma, HFrEF, vasospastic angina). Non-dihydropyridine CCBs are usually avoided in patients with reduced ejection fraction.

References

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