Diltiazem in PSVT

Mechanism of Action

Diltiazem is a non-dihydropyridine calcium channel blocker (Class IV antiarrhythmic, Vaughan Williams classification). It blocks L-type Ca²⁺ channels selectively in cardiac nodal tissue - unlike dihydropyridines (e.g. nifedipine) which act mainly on vascular smooth muscle. Its key electrophysiological effects are:

Slows AV nodal conduction - decreases the velocity of impulse transmission through the AV node, increasing the PR interval
Prolongs AV nodal refractory period - blocks the slow inward calcium current during depolarization
Decremental conduction - both effects together produce AV nodal block

PSVT (most commonly AVNRT or orthodromic AVRT) is a reentrant tachycardia dependent on AV nodal conduction as part of its circuit. By blocking the AV node, diltiazem interrupts the reentrant loop and terminates the arrhythmia.

Its effects on AV nodal tissue are selective - it reduces conduction in the tissue responsible for the tachycardia while sparing normal conduction tissue.

Goodman & Gilman's Pharmacological Basis of Therapeutics, p. 245-247
Roberts and Hedges' Clinical Procedures in Emergency Medicine, p. 3737-3741

Clinical Indications

Setting	Role
Acute PSVT (narrow-complex)	Rapid termination / conversion to sinus rhythm
Rate control in AF/atrial flutter	Ventricular slowing (without accessory bypass conduction)
Chronic PSVT prophylaxis	Oral diltiazem to prevent recurrent episodes
Automaticity-driven SVTs	Ectopic, multifocal, or junctional tachycardia (stable, narrow-complex)

Parenteral diltiazem is approved for temporary control of rapid ventricular rate in atrial flutter/AF and for rapid conversion of PSVT to sinus rhythm - though IV adenosine has largely supplanted it for acute termination due to its shorter onset and action.

Goodman & Gilman, p. 247

Position in the Treatment Algorithm

Treatment algorithm for hemodynamically stable PSVT - Harrison's Principles of Internal Medicine 22E

Harrison's Principles of Internal Medicine 22E - PSVT Treatment Algorithm

Step-wise approach for hemodynamically stable narrow-complex PSVT:

Vagal maneuvers (Valsalva, carotid sinus massage) - first line
IV Adenosine - if vagal maneuvers fail (terminates the vast majority of PSVT)
Non-DHP CCB (diltiazem or verapamil) and/or beta-blocker - if adenosine fails or PSVT is recurrent
Antiarrhythmic therapy - if above ineffective
Catheter ablation - for recurrent/incessant PSVT

Hemodynamically unstable PSVT → immediate DC cardioversion.

Dosing (IV)

Dose	Details
Initial bolus	0.25 mg/kg IV
Repeat bolus	0.35 mg/kg IV (if first dose insufficient)
Maintenance infusion	5-15 mg/hr IV
Pre-treatment	Consider IV calcium (calcium gluconate) if patient is hypotensive

For chronic/prophylactic use: oral diltiazem (various extended-release formulations).

Roberts and Hedges' Clinical Procedures in Emergency Medicine, p. 3747

Contraindications

Sick sinus syndrome, 2nd-degree or 3rd-degree AV block (unless internal pacer present)
Severe hypotension / cardiogenic shock
Hypersensitivity to diltiazem
IV beta-blocker use within a few hours (risk of compounded AV blockade and bradycardia)
WPW / LGL syndrome (AF or atrial flutter with accessory bypass tract) - diltiazem may paradoxically accelerate conduction down the accessory pathway, precipitating VF
Ventricular tachycardia - Ca²⁺ channel blockers are generally ineffective and can be dangerous; this is a key pitfall when VT is misdiagnosed as PSVT
Wide-complex tachycardia of uncertain origin - treat as VT until proven otherwise

Roberts and Hedges', p. 3745

Adverse Effects

Effect	Notes
Hypotension	Most important with bolus IV dosing; mitigated by pre-treating with IV calcium
Severe bradycardia / AV block	Especially in patients also on beta-blockers or with baseline conduction disease
Worsening LV dysfunction	Negative inotropy; avoid in significant systolic heart failure
Drug interaction - Digoxin	Both drugs can increase serum digoxin levels; risk of excess AV slowing in AF
Constipation	With oral (chronic) therapy

The most dangerous scenario historically was IV diltiazem/verapamil given to a patient with VT misdiagnosed as PSVT - causing severe hemodynamic collapse.

Goodman & Gilman, p. 252

Diltiazem vs. Verapamil in PSVT

Feature	Diltiazem	Verapamil
Class	Non-DHP CCB	Non-DHP CCB
Effect on peripheral vasodilation	Intermediate	Least
Negative inotropy	Moderate	Greater
First-pass hepatic metabolism	Extensive	Extensive (stereoselective)
Hypotension risk (IV)	Less than verapamil	Greater
Oral dose for prophylaxis	Yes	Yes
Constipation	Less common	Common

Special Considerations

WPW with PSVT: If the tachycardia is orthodromic AVRT with a concealed or known low-risk accessory pathway, diltiazem/verapamil may be used. However, if there is overt preexcitation (delta waves) with AF/flutter, avoid all AV nodal blockers - use IV procainamide or cardioversion.
Pregnancy: PSVT treatment in pregnancy follows the same algorithm (vagal maneuvers → adenosine → CCB); diltiazem/verapamil are options when adenosine fails.
"Pill-in-the-pocket": For patients with recurrent PSVT and known low-risk APs, a single dose of oral beta-blocker, verapamil, or diltiazem taken at episode onset can terminate the arrhythmia.
Long-term management: Most patients with recurrent PSVT are candidates for catheter ablation, which is curative. Diltiazem oral therapy is an alternative for those who decline ablation.

- Harrison's Principles of Internal Medicine 22E, p. 887-913 - Fuster and Hurst's The Heart, 15th Edition

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