Calcium Channel Blockers

Name: Calcium Channel Blockers — Cardiovascular pharmacology
Creator: LearnDrugs

Verified · Oct 2026

One channel, two preferences: dihydropyridines bind the inactivated L-type channel and relax arterioles, while verapamil and diltiazem bind the open channel and slow the calcium-driven SA and AV nodes.

Nursing view → administration, monitoring and patient teaching

Compare: Antiarrhythmics by Vaughan-Williams class →

Compare: Antihypertensives compared — mechanism and drug choice →

Drugs

amlodipine Norvasc

nifedipine Procardia XL

clevidipine Cleviprex

nicardipine Cardene IV

diltiazem Cardizem

verapamil Verelan

Mechanism

Block L-type voltage-gated calcium channels. Dihydropyridines (-dipine) act mainly on vascular smooth muscle → peripheral vasodilation; non-dihydropyridines (diltiazem, verapamil) act on the myocardium and SA/AV nodes → ↓ heart rate, conduction, and contractility.

One channel, three tissues

Calcium channel blockers inhibit the L-type (long-lasting) voltage-gated calcium channel, Cav1.2, which lets calcium in during membrane depolarization. All of them bind the pore-forming α1C subunit, but at different sites — which is why the subclasses behave differently. L-type channels are found in the heart, vascular smooth muscle and pancreas.

Cardiac and smooth muscle rely on calcium entering from outside the cell, whereas skeletal muscle relies mainly on intracellular stores. In vascular smooth muscle, the entering calcium binds calmodulin; activated calmodulin switches on myosin light chain kinase (MLCK), which phosphorylates the regulatory light chain on myosin and starts contraction. Less calcium entry means a relaxed arteriole and a lower systemic vascular resistance.

Pancreatic β cells also need calcium influx through L-type channels to release insulin — the reason CCB overdose causes hyperglycemia (see Toxicity).

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In vascular smooth muscle, calcium entry through L-type channels drives contraction via calmodulin and MLCK; blocking the channel relaxes the arteriole.

Channel states: why dihydropyridines pick vessels

The two subclasses prefer different channel states. Dihydropyridines bind preferentially to the inactivated state of the L-type channel — a voltage-dependent block. Vascular smooth muscle operates at a more depolarized membrane potential than cardiac myocytes, which gives dihydropyridines roughly 100-fold selectivity for vessels over the heart. They bind an extracellular region of the channel.

Nondihydropyridines bind preferentially to the activated (open) state in cardiac tissue, producing a frequency-dependent block; the verapamil label describes it slowing AV conduction “in a rate-related manner”. Verapamil (a phenylalkylamine) reaches the channel’s inner pore from inside the cell; diltiazem (a benzothiazepine) binds a site that overlaps both the dihydropyridine and verapamil sites, so its cardiac effects are intermediate.

The selectivity is relative. Verapamil acts strongly on both myocardium and vascular smooth muscle; diltiazem dilates vessels less and has a greater relative effect on heart rate; dihydropyridines are potent vasodilators with comparatively little effect on pacemaker activity or contractility. In a large overdose the selectivity is lost.

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The channel state each subclass prefers explains where it acts.

The nodes run on calcium

Calcium influx drives the spontaneous depolarization of SA-node pacemaker cells and conduction through the AV node. Verapamil and diltiazem therefore suppress SA-node automaticity and slow AV conduction by reducing calcium-dependent phase 0 depolarization in nodal tissue; verapamil prolongs the effective refractory period within the AV node.

Slowing the AV node is the basis for rate control in atrial fibrillation or flutter and for treating PSVT — and it is why verapamil and diltiazem make up the class IV antiarrhythmics. The AV node normally limits how many rapid atrial impulses reach the ventricles, and AV-nodal reentrant tachycardia — the most common regular SVT in adults — circulates through dual pathways in and around the node.

The same action turns dangerous when an accessory pathway bypasses the node. In atrial fibrillation or flutter with an accessory bypass tract (as in Wolff–Parkinson–White), verapamil may shorten the pathway’s antegrade refractory period, and IV verapamil has produced a very rapid ventricular response or ventricular fibrillation; the label contraindicates it. Adding another AV-node suppressant — a β-blocker or digoxin — risks bradycardia and AV block.

The nondihydropyridines’ negative inotropy lowers myocardial oxygen consumption, which helps in stable angina but is hazardous in systolic heart failure.

Reflexes, edema and the gums

A rise in heart rate is a normal response to vasodilation and a falling blood pressure. Short-acting immediate-release nifedipine caused rapid vasodilation followed by reflex sympathetic activation — headache, palpitations and flushing — which led to extended-release forms. Amlodipine has a charged, amphiphilic structure that embeds in the cell membrane as a depot, giving a long half-life (about 30–50 hours in the label) and a gradual onset that minimizes reflex sympathetic activation.

Ankle edema with dihydropyridines is not fluid retention. Preferential dilation of precapillary arterioles raises intracapillary hydrostatic pressure, so more fluid filters into the tissues (Starling forces), and it does not respond to diuretics. Adding an ACE inhibitor or ARB attenuates it by dilating the postcapillary venules and restoring the balance of capillary pressures.

Gingival overgrowth (more common with nifedipine) reflects impaired collagen breakdown by gingival fibroblasts. The inducing drugs inhibit calcium uptake into the fibroblasts and reduce their folate uptake; less intracellular folate means less activation of the matrix metalloproteinases that turn inactive collagenase into active collagenase, so connective tissue builds up. Diltiazem and verapamil cause it less often than nifedipine.

Constipation — up to 25% of patients on verapamil — comes from calcium-channel blockade in gastrointestinal smooth muscle.

Comparing the drugs

Subclass and selectivity

Drug	Subclass	Acts most on	Heart rate	Distinguishing point
Amlodipine	Dihydropyridine	Vascular smooth muscle	Little direct effect	Membrane depot — half-life 30–50 h
Nifedipine	Dihydropyridine	Vascular smooth muscle	Reflex rise (immediate-release)	Gingival overgrowth most often
Clevidipine	Dihydropyridine (IV)	Arterial resistance; no effect on preload	Rises if titrated fast	Esterase-cleared; BP recovers in 5–15 min
Nicardipine	Dihydropyridine (IV or oral)	More vascular than cardiac	Rises (reflex)	Hepatic CYP; inhibits CYP3A4
Diltiazem	Benzothiazepine (non-DHP)	Heart and vessels — intermediate	Slows — greater relative effect on rate	Less vasodilation than verapamil
Verapamil	Phenylalkylamine (non-DHP)	Myocardium, nodes and vessels	Slows; AV block	Constipation; raises digoxin

Dihydropyridines bind the inactivated channel (voltage-dependent); verapamil and diltiazem bind the open channel (frequency-dependent).

Pharmacokinetics at a glance

Drug	Oral bioavailability	Half-life	Clearance	Interaction note
Amlodipine	64–90%	30–50 h (steady state in 7–8 days)	Hepatic	CYP3A inhibitors raise exposure
Nifedipine	Extended-release: 86% of capsules	About 2 h	CYP3A4	Grapefruit doubles exposure; phenytoin cuts it about 70%
Clevidipine	IV only	About 1 min initial; about 15 min terminal	Esterases in blood and tissue	No CYP inhibition or induction
Nicardipine	About 35% (saturable first pass)	IV: 2.7 min, 44.8 min and 14.4 h phases	Hepatic CYP2C8, 2D6, 3A4	Inhibits CYP3A4: ↑ cyclosporine, tacrolimus
Diltiazem	About 40%	3.0–4.5 h	Hepatic; desacetyl diltiazem active	Inhibits CYP3A4 (statins)
Verapamil	20–35%	2.8–7.4 h single dose; 4.5–12 h repeated	Hepatic CYP3A4; norverapamil active	Inhibits CYP3A4 and P-gp; ↑ digoxin

Most oral CCBs are well absorbed but lose much of the dose to hepatic first-pass metabolism, mainly by CYP3A4.

Pharmacokinetics

First-pass metabolism and CYP3A4: CCBs are readily absorbed, but many have low bioavailability because of hepatic first-pass metabolism, mainly by CYP3A4, so CYP3A4 inhibitors and inducers shift their levels. Verapamil and diltiazem also inhibit CYP3A4 and P-glycoprotein themselves, raising statins and cyclosporine, and chronic verapamil can raise digoxin levels by 50–75% in the first week.
Saturation: exposure rises with repeated or large doses: With repeated doses or overdose, the hepatic enzymes saturate and first-pass extraction falls, so more active drug is absorbed. Verapamil’s half-life lengthens with repeated dosing, and oral nicardipine has nonlinear kinetics because its first-pass metabolism is saturable.
Amlodipine: the slow, long-acting depot — amlodipine: Amlodipine peaks 6–12 hours after a dose, has an absolute bioavailability of 64–90% unaffected by food, and a terminal half-life of about 30–50 hours, so steady state takes 7–8 days of daily dosing. Its membrane depot explains the long half-life and gradual onset.
Nifedipine: why extended release — nifedipine: Nifedipine’s elimination half-life is about 2 hours. Extended-release tablets raise plasma levels gradually to a plateau at about 6 hours and hold them for 24 hours, with less fluctuation than immediate-release capsules — avoiding the rapid vasodilation and reflex sympathetic activation of the short-acting form.
Active metabolites of the nondihydropyridines — verapamil, diltiazem: Norverapamil, verapamil’s main active metabolite, can reach steady-state levels about equal to the parent drug. Desacetyl diltiazem circulates at 10–20% of diltiazem’s level and is 25–50% as potent a coronary vasodilator.
The IV dihydropyridines: minutes versus hours — clevidipine, nicardipine: Clevidipine is hydrolyzed by esterases in blood and extravascular tissue, so hepatic or renal dysfunction is unlikely to affect it, and blood pressure recovers 5–15 minutes after the infusion stops. Nicardipine is cleared by hepatic CYP enzymes; its effect falls by half about 30 minutes after stopping, and a slow terminal phase (half-life 14.4 hours) appears only after long infusions.
Why dialysis does not help: CCBs are highly lipophilic, strongly protein-bound and widely distributed (volume of distribution above 2 L/kg), so hemodialysis and hemofiltration remove little drug.

Uses & drug choice

Hypertension
IV clevidipine or nicardipine for short-term blood pressure reduction when oral therapy is not feasible, e.g. hypertensive emergency
Chronic stable & vasospastic (Prinzmetal) angina
Rate control in atrial fibrillation / SVT (non-dihydropyridines: diltiazem, verapamil)

Hypertension → A dihydropyridine (e.g. amlodipine)

Dihydropyridines relax vascular smooth muscle and are the preferred subclass for hypertension; CCBs are first-line antihypertensives that reduce cardiovascular events comparably to thiazides, except heart failure.

Atrial fibrillation with a rapid ventricular rate (no heart failure with reduced EF, no accessory pathway) → Diltiazem or verapamil

Slowing calcium-dependent AV-node conduction controls the ventricular rate; the dihydropyridines lack this nodal effect. Avoid them in heart failure with reduced EF, second- or third-degree AV block and sick sinus syndrome.

Atrial fibrillation with an accessory pathway (Wolff–Parkinson–White) → Avoid verapamil

Verapamil may shorten the accessory pathway’s antegrade refractory period; IV verapamil has caused a very rapid ventricular response or ventricular fibrillation, and the label contraindicates it.

Hypertensive emergency needing IV titration → IV nicardipine or clevidipine

Both are first-line IV agents. Clevidipine is esterase-cleared (not affected by hepatic or renal dysfunction) and wears off in minutes, but is contraindicated with soy or egg allergy, defective lipid metabolism or severe aortic stenosis; nicardipine is hepatically cleared and inhibits CYP3A4.

Ankle edema on a dihydropyridine → Add an ACE inhibitor or ARB rather than a diuretic

The edema comes from precapillary arteriolar dilation, not fluid retention, so it does not respond to diuretics; RAAS inhibitors attenuate it by postcapillary venodilation. It is dose-dependent.

Transplant patient on tacrolimus or cyclosporine who needs IV blood-pressure control → Clevidipine rather than nicardipine (and check trough levels)

Nicardipine inhibits hepatic CYP3A4 and raises tacrolimus and cyclosporine levels; clevidipine is cleared by esterases and neither inhibits nor induces CYP enzymes.

Adverse effects

Common

Dihydropyridines: peripheral edema, headache, flushing, dizziness, reflex tachycardia. Verapamil: constipation.

Serious

Non-dihydropyridines: bradycardia, AV block, severe hypotension, and worsening of heart failure with reduced EF.

IV dihydropyridines (clevidipine, nicardipine)

IV clevidipine or nicardipine: hypotension and reflex tachycardia with rapid upward titration; headache, nausea and vomiting; infusion-site phlebitis (nicardipine); raised triglycerides (clevidipine’s lipid emulsion).

Peripheral (ankle) edema — dihydropyridines: Precapillary arteriolar dilation raises intracapillary hydrostatic pressure, so fluid filters into the tissues. It is dose-dependent, is not fluid retention, and does not respond to diuretics; an ACE inhibitor or ARB attenuates it by dilating postcapillary venules.
Headache, flushing, dizziness: These follow directly from vasodilation.
Reflex tachycardia, palpitations: A falling blood pressure from vasodilation normally raises the heart rate; rapid vasodilation by short-acting formulations triggers reflex sympathetic activation. Amlodipine’s gradual onset minimizes it.
Hypotension and reflex tachycardia on IV titration (clevidipine, nicardipine): Both drugs lower systemic vascular resistance in a dose-dependent way, so too-rapid upward titration overshoots; the heart-rate rise is the normal response to vasodilation. Clevidipine is not a β-blocker and does not slow the heart.
Bradycardia and AV block — verapamil, diltiazem: They reduce calcium-dependent phase 0 depolarization in the SA and AV nodes, suppressing automaticity and conduction. The risk is greatest when combined with β-blockers or digoxin.
Worsening heart failure: Verapamil and diltiazem reduce contractility (negative inotropy), which can precipitate or worsen heart failure with reduced systolic function. The IV dihydropyridine labels also warn of possible negative inotropic effects in heart failure.
Constipation — verapamil: Calcium-channel blockade in gastrointestinal smooth muscle slows the gut; it affects up to 25% of patients on verapamil.
Gingival overgrowth: The drugs reduce calcium and folate uptake by gingival fibroblasts; with less folate, matrix metalloproteinases are not activated to convert inactive collagenase, so collagen accumulates. It is more common with nifedipine.

Toxicity & antidote

CCBs account for the most deaths among cardiovascular drug exposures reported to US poison centers, with amlodipine and diltiazem most often implicated. Hypotension and bradycardia dominate, from peripheral vasodilation plus reduced contractility. Nondihydropyridine overdoses add conduction disturbances (AV block, complete heart block, junctional rhythms); dihydropyridines may first cause reflex tachycardia, but selectivity is lost in a large overdose. Reduced insulin secretion and insulin resistance cause hyperglycemia, a marker of severity. Patients can look well and then deteriorate quickly, so an asymptomatic patient may be observed for up to 24 hours after a sustained-release ingestion.

Treatment works around the blocked channel. IV calcium raises the extracellular calcium concentration to drive more influx through unblocked L-type channels; it helps blood pressure and contractility more than conduction and bradycardia. High-dose insulin (hyperinsulinemic euglycemia) targets the energy failure: the poisoned heart shifts from fatty acids to carbohydrate while insulin secretion falls, and insulin improves contractility and blood pressure, with close monitoring for hypoglycemia and hypokalemia. Vasopressors support the circulation (norepinephrine for vasoplegic shock, epinephrine for contractility and rate); atropine has limited effect in severe poisoning; glucagon raises heart rate and output through adenylate cyclase. Lipid emulsion is reserved for arrest or peri-arrest. Activated charcoal works best within 1–2 hours, and whole-bowel irrigation is considered for sustained-release ingestions.

Interactions

Grapefruit juice (nifedipine, oral verapamil)

Inhibits CYP3A4 → about double the nifedipine exposure and excess hypotension; it also raises oral verapamil bioavailability, risking excessive levels (StatPearls). The amlodipine label reports no effect of grapefruit juice on amlodipine exposure.

Beta-blockers

Additive AV-node suppression with non-dihydropyridines (diltiazem, verapamil) → profound bradycardia or heart block.

Cyclosporine or tacrolimus (nicardipine)

Nicardipine inhibits CYP3A4 → raised cyclosporine and tacrolimus levels; monitor trough levels.

Cimetidine (nicardipine)

Raises oral nicardipine levels (per the label) — monitor the response closely.

Contraindications

Heart failure with reduced EF — diltiazem & verapamil — Their negative inotropic effect further weakens an already-failing pump. (Amlodipine’s label notes it has been used safely in well-compensated heart failure, but StatPearls lists heart failure among its contraindications — it is not a heart-failure drug.)
2nd/3rd-degree AV block or sick sinus syndrome (no pacemaker) — diltiazem & verapamil — Suppressing AV conduction on top of an existing block can cause complete heart block.
Concurrent beta-blocker with a non-dihydropyridine use caution — Additive suppression of the SA and AV nodes can produce profound bradycardia or asystole.
Severe hypotension (SBP < 90 mmHg) — Further vasodilation or negative inotropy would drop cardiac output and perfusion dangerously.
Severe (advanced) aortic stenosis — clevidipine & nicardipine — Part of their effect comes from reducing afterload; with a fixed outflow obstruction, the lower diastolic pressure can worsen rather than improve the heart’s oxygen balance.
Soy or egg allergy, or defective lipid metabolism — clevidipine — Clevidipine comes in a soybean-oil emulsion with egg phospholipids. It is contraindicated with soy or egg allergy and with defective lipid metabolism such as pathologic hyperlipemia, lipoid nephrosis, or acute pancreatitis with hyperlipidemia.

High-yield

Ankle edema on amlodipine that does not improve with furosemide Precapillary arteriolar dilation (not fluid retention) — add an ACE inhibitor or ARB

Gingival overgrowth in a patient taking an antihypertensive Nifedipine (dihydropyridine CCB)

Most common adverse effect of verapamil, from gut smooth-muscle blockade Constipation

CCB that raises serum digoxin levels Verapamil

Overdose with bradycardia, hypotension and hyperglycemia Nondihydropyridine CCB (verapamil, diltiazem) — blocked insulin release

Binds the inactivated L-type channel; voltage-dependent, vessel-selective block Dihydropyridines

Frequency-dependent block that slows AV conduction in a rate-related manner Verapamil (and diltiazem)

IV antihypertensive contraindicated with soy or egg allergy Clevidipine (lipid emulsion)

IV antihypertensive whose effect is gone 5–15 minutes after stopping Clevidipine — esterase hydrolysis

Rate-control drug to avoid in atrial fibrillation with Wolff–Parkinson–White Verapamil

The -dipines Dilate; V and D Delay

-dipines Dilate — dihydropyridines bind the inactivated channel in depolarized vascular smooth muscle: vasodilation, reflex tachycardia, ankle edema
V and D Delay — verapamil and diltiazem bind the open channel in the nodes: slower SA firing and AV conduction, rate control, bradycardia and AV block

Verapamil acts most on the heart (and the gut: constipation); diltiazem sits between verapamil and the dihydropyridines.

Clevidipine is the Cleaved, Creamy -dipine

Cleaved — split by esterases in blood and tissue: blood pressure recovers in 5–15 minutes, unaffected by liver or kidney function
Creamy — a milky lipid emulsion of soybean oil and egg phospholipids: contraindicated in soy or egg allergy and defective lipid metabolism; triglycerides can rise

Nicardipine, the other IV dihydropyridine, is cleared by the liver and inhibits CYP3A4.

Practice questions

Q1A 68-year-old woman with hypertension takes amlodipine. Over two months she develops bilateral ankle swelling. Her clinician added furosemide, but the swelling has not changed. Her jugular venous pressure, lung examination and serum albumin are normal.

Which mechanism best explains her edema?

A.Renal sodium and water retention
B.Hypoalbuminemia from reduced hepatic synthesis
C.Precapillary arteriolar dilation raising capillary hydrostatic pressure
D.Right heart failure from negative inotropy
E.Lymphatic obstruction

Show answer

C. Precapillary arteriolar dilation raising capillary hydrostatic pressure — Dihydropyridines preferentially dilate precapillary arterioles, raising intracapillary hydrostatic pressure and transcapillary filtration. The edema is not fluid retention and does not respond to diuretics, which is why furosemide did not help. An ACE inhibitor or ARB attenuates it by dilating postcapillary venules. Amlodipine has not been associated with a negative inotropic effect in the therapeutic range, and her normal venous pressure and albumin argue against heart failure and hypoalbuminemia.

Q2A 72-year-old man has atrial fibrillation with a ventricular rate of 138/min. His blood pressure is 142/86 mm Hg, his ejection fraction is normal, and there is no pre-excitation on the ECG.

Which drug would best control his ventricular rate, and why?

A.Amlodipine, because it dilates arterioles
B.Nifedipine, because it relaxes vascular smooth muscle
C.Clevidipine, because it is titratable intravenously
D.Nicardipine, because it is more selective for vessels than heart
E.Diltiazem, because it slows calcium-dependent AV-node conduction

Show answer

E. Diltiazem, because it slows calcium-dependent AV-node conduction — AV-node conduction depends on calcium influx, and diltiazem (like verapamil) binds the open channel in nodal tissue, slowing AV conduction and controlling the ventricular rate in atrial fibrillation. The dihydropyridines — amlodipine, nifedipine, clevidipine and nicardipine — are vessel-selective with little effect on pacemaker or nodal tissue; clevidipine does not reduce heart rate, and their vasodilation can even raise it reflexly. Diltiazem would be avoided with heart failure with reduced EF or an accessory pathway.

Q3A 45-year-old woman is brought in 3 hours after taking a large number of extended-release verapamil tablets. Her heart rate is 38/min, blood pressure 72/40 mm Hg, and serum glucose 290 mg/dL. She has no history of diabetes.

Which direct effect of verapamil best explains her hyperglycemia?

A.Blocked L-type channels in pancreatic β cells reduce insulin release
B.A stress-induced cortisol surge from hypotension
C.Opening of ATP-sensitive K⁺ channels in β cells
D.CYP3A4 inhibition increases hepatic gluconeogenesis
E.Blocked calcium entry into skeletal muscle prevents contraction-driven glucose uptake

Show answer

A. Blocked L-type channels in pancreatic β cells reduce insulin release — Pancreatic β cells depend on calcium influx through L-type channels to release insulin, so CCB overdose reduces insulin secretion and promotes insulin resistance; the hyperglycemia is a marker of severity, especially with nondihydropyridines. The verapamil label also lists hyperglycemia among overdose effects secondary to hypoperfusion — an indirect effect, whereas the drug’s own action is on the β cell. The same energy failure in the heart is why high-dose insulin with glucose improves contractility. Verapamil inhibits L-type voltage-gated calcium channels rather than opening β-cell ATP-sensitive K⁺ channels, and skeletal muscle depends mainly on intracellular calcium stores rather than calcium influx; its CYP3A4 and P-glycoprotein inhibition raises levels of other drugs such as statins, cyclosporine and digoxin rather than driving gluconeogenesis. Her bradycardia and hypotension reflect nodal suppression, vasodilation and reduced contractility; IV calcium, vasopressors and high-dose insulin are the mainstays, and whole-bowel irrigation is considered for an extended-release ingestion.

Q4A 58-year-old kidney-transplant recipient taking tacrolimus is admitted with a hypertensive emergency and started on a nicardipine infusion. Two days later his tacrolimus trough level has risen sharply.

What is the most likely mechanism?

A.Nicardipine displaces tacrolimus from plasma proteins
B.Nicardipine reduces tacrolimus renal excretion by lowering GFR
C.Nicardipine induces P-glycoprotein in the gut
D.Nicardipine inhibits hepatic CYP3A4, which metabolizes tacrolimus
E.The infusion fluid dilutes the blood sample

Show answer

D. Nicardipine inhibits hepatic CYP3A4, which metabolizes tacrolimus — Oral or IV nicardipine raises tacrolimus (and cyclosporine) levels by inhibiting hepatic microsomal enzymes, including CYP3A4, so trough levels need close monitoring. Clevidipine, cleared by esterases with no CYP inhibition or induction, is the IV dihydropyridine without this interaction. Protein displacement, a lower GFR or P-glycoprotein induction is not the mechanism the label describes.

Q5A 24-year-old man with known Wolff–Parkinson–White syndrome presents with palpitations. His ECG shows a fast, irregular, wide-complex rhythm consistent with pre-excited atrial fibrillation.

Why is IV verapamil dangerous in this setting?

A.It causes reflex tachycardia through arteriolar dilation
B.It slows the AV node but may shorten the accessory pathway’s refractory period, letting more impulses reach the ventricles
C.It completely blocks the accessory pathway, causing asystole
D.It acts mainly on vascular smooth muscle, like the dihydropyridines
E.It has no effect on AV-node conduction

Show answer

B. It slows the AV node but may shorten the accessory pathway’s refractory period, letting more impulses reach the ventricles — Verapamil prolongs the AV-node refractory period but may shorten the antegrade refractory period of an accessory bypass tract. With the node slowed, impulses run down the accessory pathway, and IV verapamil has produced a very rapid ventricular response or ventricular fibrillation — so the label contraindicates it in atrial fibrillation or flutter with an accessory pathway. Verapamil acts strongly on the heart, not mainly on vessels, and it clearly slows AV conduction; reflex tachycardia is a dihydropyridine effect.

More in the Cardiovascular question bank →

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By LearnDrugs

Educational summary for medical students. Always verify against current prescribing information and guidelines. Not medical advice.