Pharmacology about psvt and treatment

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"paroxysmal supraventricular tachycardia" AND treatment

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Paroxysmal Supraventricular Tachycardia (PSVT) - Pharmacology and Treatment

Definition and Classification

PSVT is a clinical syndrome characterized by a rapid, regular tachycardia with abrupt onset and termination. The term covers all tachyarrhythmias arising from or involving supraventricular tissue. The three main mechanisms are:

Type	Frequency	Mechanism
AV Nodal Reentrant Tachycardia (AVNRT)	~65%	Reentry within dual AV node pathways
AV Reentrant Tachycardia (AVRT) / WPW	~30%	Reentry via accessory pathway
Atrial Tachycardia (AT)	~5%	Ectopic atrial focus

Fuster and Hurst's The Heart, p. 1126

ECG Features

(ECG strip showing PSVT - Tintinalli's Emergency Medicine)

Key ECG features (Table 18-16, Tintinalli's):

Narrow QRS complex (<100 ms) - unless aberrant conduction
Rate: typically 170-300 bpm (usually 170-180 bpm)
No normal sinus P waves - P waves either buried in QRS (~70%) or appear as retrograde P waves immediately adjacent to QRS (in ~30%)
Abrupt onset and termination

Pathophysiology: The Reentry Circuit

Most PSVT depends on AV nodal conduction as part of the reentry loop:

In AVNRT, the AV node has dual pathways - a "fast" pathway (short conduction, long refractory) and a "slow" pathway (long conduction, short refractory). A premature atrial contraction can trigger unidirectional block in the fast pathway, allowing a reentry circuit to form.
In AVRT (WPW), a bypass tract allows antegrade conduction via the AV node and retrograde conduction via the accessory pathway (orthodromic) or vice versa (antidromic).

This AV-node dependence is the key pharmacological target for both termination and prevention.

Treatment Algorithm

FIGURE 256-6 from Harrison's 22E: Treatment algorithm for hemodynamically stable PSVT

Step 1: Vagal Maneuvers (Non-pharmacologic)

If applied early, vagal maneuvers are often effective:

Valsalva maneuver - preferred if the patient is cooperative; can be taught for self-management
Carotid sinus massage - reasonable if no carotid bruits or prior stroke history
Cold water/ice to face - effective especially in children (diving reflex)
Modified Valsalva (semi-recumbent, then leg raise) - increases efficacy

Mechanism: increase vagal tone → increase AV nodal refractoriness → interrupt reentry circuit

Step 2: Pharmacological Termination (Acute)

Drug of Choice: ADENOSINE

Mechanism (Katzung's Pharmacology, 16th Ed.):

Naturally occurring endogenous nucleoside
Activates inward rectifier K+ current → hyperpolarization
Inhibits calcium current → suppresses calcium-dependent action potentials
Directly inhibits AV nodal conduction and increases AV nodal refractory period
Half-life: <10 seconds in blood

Dose:

6 mg IV bolus (rapid push + NS flush) - first dose
If ineffective: 12 mg IV bolus (can repeat once)
Given via a large/proximal vein; very short-acting so must be pushed fast

Efficacy: 90-95% conversion to sinus rhythm

Adverse effects:

Flushing (~20%)
Dyspnea/chest burning/bronchospasm (>10%) - use cautiously in asthmatics
Transient chest pain and anxiety
Brief high-grade AV block (very short-lived due to ultrashort half-life)
Atrial fibrillation in up to 15% (usually brief) - use with caution in WPW

Contraindications:

Cardiac transplant recipients (hypersensitivity due to denervation)
WPW with pre-excited AF (can accelerate conduction via accessory pathway)

Drug interactions:

Theophylline/caffeine - adenosine receptor blockers → reduce efficacy (need higher dose)
Dipyridamole - adenosine uptake inhibitor → potentiates effect (reduce dose)

CLASS IV - Non-Dihydropyridine Calcium Channel Blockers

Verapamil

Mechanism: Blocks L-type Ca2+ channels in AV node → prolongs AV nodal conduction and refractoriness
Dose: IV 5-10 mg over 2 minutes
Use: Adenosine or verapamil is preferred over older treatments (propranolol, digoxin, cardioversion) for PSVT termination
Toxicity: Hypotension (before and after arrhythmia termination), negative inotropy
WARNING: Never give IV verapamil to VT misdiagnosed as PSVT - can cause hypotension and ventricular fibrillation
Longer duration of action than adenosine - useful for prevention

Diltiazem

Similar efficacy to verapamil for SVT management
IV form available - causes hypotension or bradyarrhythmias less frequently than verapamil
Also used for rate control in atrial fibrillation and flutter

CLASS II - Beta-Blockers

IV metoprolol or esmolol can terminate PSVT by blocking sympathetic input to AV node
Less effective acutely than adenosine or verapamil
Useful when adenosine/CCBs fail or are contraindicated
Risk of hypotension (especially combined with CCBs)
Can be given orally for outpatient "pill-in-the-pocket" or prevention

Digoxin (Historical/Special Situations)

Increases vagal tone on AV node
Slow onset - not useful for acute termination
Was used historically; largely replaced by adenosine and CCBs
Still occasionally used in heart failure with SVT for rate control

Special Situation: WPW / Pre-excited Tachycardia

DO NOT USE AV nodal blocking agents (adenosine, verapamil, beta-blockers, digoxin) if pre-excited AF is suspected:

Blocking the AV node forces all conduction through the accessory pathway
Rapid accessory pathway conduction can cause ventricular fibrillation

For WPW with pre-excited AF:

DC cardioversion (if hemodynamically unstable)
Procainamide IV - blocks accessory pathway
Ibutilide IV - alternative

For orthodromic AVRT (narrow-complex) in WPW, adenosine can be used cautiously.

Wide-Complex PSVT

Could be PSVT with bundle branch block aberrancy, pre-excited tachycardia, or VT
Treat as VT until proven otherwise
If regular and patient is stable: a trial of IV adenosine is reasonable
Irregular wide-complex tachycardia: likely pre-excited AF/flutter → cardioversion, IV procainamide, or ibutilide

Step 3: Hemodynamic Instability

Synchronized DC cardioversion is the treatment of choice if the patient is:

Hypotensive with altered consciousness
In respiratory distress
Otherwise hemodynamically compromised

Initial energy for PSVT/atrial flutter: 50-100 J (synchronized)

Long-Term Prevention / Outpatient Management

Option	Details
Oral beta-blockers	First-line for prevention; patient can take on as-needed basis
Oral CCBs (verapamil/diltiazem)	Alternative; can facilitate termination during Valsalva
"Pill-in-the-pocket"	Oral flecainide or diltiazem for episodic self-treatment
Catheter ablation	Definitive cure - preferred for recurrent/refractory PSVT; most patients with recurrent episodes are candidates

Summary Table: Drug Comparison

Drug	Class	Mechanism	Dose	Efficacy	Key Concern
Adenosine	Misc.	K+ activation + Ca2+ inhibition	6 mg → 12 mg IV bolus	90-95%	Brief AF, bronchospasm; avoid in transplant
Verapamil	Class IV	Ca2+ channel block	5-10 mg IV	High	Hypotension; never in suspected VT
Diltiazem	Class IV	Ca2+ channel block	15-20 mg IV	Similar to verapamil	Less hypotension than verapamil
Metoprolol/Esmolol	Class II	Beta blockade	Titrated IV	Moderate	Hypotension, bradycardia
Procainamide	Class IA	Na+ channel block	10-17 mg/kg IV	For WPW/wide-complex	Hypotension, QT prolongation

Sources:

Harrison's Principles of Internal Medicine 22E (2025), Chapter 256
Katzung's Basic and Clinical Pharmacology, 16th Edition, Chapters 14 & 16
Fuster and Hurst's The Heart, 15th Edition, Chapter 35
Tintinalli's Emergency Medicine, Chapter 18
Roberts and Hedges' Clinical Procedures in Emergency Medicine

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