10-30: Paroxysmal Supraventricular Tachycardia (PSVT)

PSVT is an intermittent arrhythmia that is characterized by a sudden onset and offset and a regular ventricular response. Episodes may last from a few seconds to several hours or longer. PSVT often occurs in patients without structural heart disease. The most common mechanism for PSVT is reentry, which may be initiated or terminated by a fortuitously timed atrial or ventricular premature beat. The reentrant circuit usually involves dual pathways (a slow and a fast pathway) within the AV node; this is referred to as AV nodal reentrant tachycardia (AVNRT) and accounts for 60% of cases of PSVT. Less commonly (30% of cases), reentry is due to an accessory pathway between the atria and ventricles, referred to as atrioventricular reciprocating tachycardia (AVRT). The pathophysiology and management of arrhythmias due to accessory pathways differ in important ways and are discussed separately below.

A. Symptoms and Signs

Symptoms of PSVT can be quite variable depending on the degree of heart rate elevation, resultant hypotension or the presence of other comorbidities. Symptoms may include palpitations, diaphoresis, dyspnea, dizziness, and mild chest pain (even in the absence of associated CHD). Syncope is rare.

B. ECG

Obtaining a 12-lead ECG when feasible is important to help determine the tachycardia mechanism. The QRS duration will be narrow (less than 120 ms) except in cases of PSVT with aberrant conduction (left bundle branch block, right bundle branch block, or antegrade conducting accessory pathway). The heart rate is regular and is usually 160–220 beats/min but may be greater than 250 beats/min. The P wave usually differs in contour from sinus beats and is often simultaneous with or just after the QRS complex.

In the absence of structural heart disease, serious effects are rare, and most episodes resolve spontaneously. Particular effort should be made to terminate the episode quickly if cardiac failure, syncope, or anginal pain develops or if there is underlying cardiac or (particularly) coronary disease. Because reentry is the most common mechanism for PSVT, effective therapy requires that conduction be interrupted at some point in the reentry circuit and the vast majority of these circuits involve the AV node.

A. Mechanical Measures

A variety of maneuvers have been used to interrupt episodes, and patients may learn to perform these themselves. These maneuvers result in an acute increase in vagal tone and include the Valsalva maneuver, lowering the head between the knees, coughing, splashing cold water on the face, and breath holding. The Valsalva maneuver is performed with the patient semirecumbent (45 degrees), exerting around 40 mm Hg of intrathoracic pressure (by blowing through a 10 mL syringe) for at least 15 seconds. Moving the patient supine immediately following the strain maneuver and passively raising their legs for an additional 15 seconds may increase effectiveness of the maneuver. Carotid sinus massage is an additional technique often performed by clinicians but should be avoided if the patient has a carotid bruit. Firm but gentle pressure and massage are applied first over the right carotid sinus for 10–20 seconds and, if unsuccessful, then over the left carotid sinus. Pressure should not be exerted on both sides at the same time. Continuous ECG or auscultatory monitoring of the heart rate is essential so that pressure can be relieved as soon as the rhythm is broken or if excessive bradycardia occurs. Facial contact with cold water may cause transient bradycardia and termination of PSVT, a phenomenon known as the diving reflex. When performed properly, these maneuvers result in abrupt termination of the arrhythmia in 20–50% of cases.

B. Medication Therapy

If mechanical measures fail to terminate the arrhythmia, pharmacologic agents should be tried. Intravenous adenosine is recommended as the first-line agent due to its brief duration of action and minimal negative inotropic activity (Table 10–11). Because the half-life of adenosine is less than 10 seconds, the medication is given rapidly (in 1–2 seconds) as a 6 mg bolus followed by 20 mL of fluid. If this regimen is unsuccessful at terminating the arrhythmia, a second higher dose (12 mg) may be given. Adenosine causes block of electrical conduction through the AV node and results in termination of PSVT in approximately 90% of cases. Minor side effects are common and include transient flushing, chest discomfort, nausea, and headache. Adenosine may excite both atrial and ventricular tissue causing atrial fibrillation (in up to 12% of patients) or rarely ventricular arrhythmias and therefore administration should be performed with continuous cardiac monitoring and availability of an external defibrillator. Adenosine must also be used with caution in patients with reactive airways disease because it can promote bronchospasm.

When adenosine fails to terminate the arrhythmia or if a contraindication to its use is present, intravenous calcium channel blockers, including verapamil and diltiazem, may be used (Table 10–11). Verapamil in particular has been shown to be as effective at terminating PSVT in the acute setting (approximately 90%) as adenosine. Calcium channel blockers should be used with caution in patients with heart failure due to their negative inotropic effects. Their longer half-life compared to adenosine may result in prolonged hypotension despite restoration of normal rhythm.

Intravenous beta-blockers include esmolol (a very short-acting beta-blocker), propranolol, and metoprolol. While beta-blockers cause less myocardial depression than calcium channel blockers, the evidence of their effectiveness to terminate PSVT is limited. Although intravenous amiodarone is safe, it is usually not required and often ineffective for treatment of these arrhythmias.

C. Cardioversion

If the patient is hemodynamically unstable or if adenosine, beta-blockers, and calcium channel blockers are contraindicated or ineffective, synchronized electrical cardioversion (beginning at 100 J) should be performed. If digitalis toxicity is present or strongly suspected, as in the case of paroxysmal tachycardia with block, electrical cardioversion should be avoided.

A. Catheter Ablation

Because of concerns about the safety and the intolerability of antiarrhythmic medications, radiofrequency ablation is the preferred approach to patients with recurrent symptomatic reentrant PSVT, whether it is due to dual pathways within the AV node or to accessory pathways.

B. Medications

AV nodal blocking agents are the medications of choice as first-line medical therapy (Table 10–11). Beta-blockers or nondihydropyridine calcium channel blockers, such as diltiazem and verapamil, are typically used first. Patients who do not respond to agents that increase refractoriness of the AV node may be treated with antiarrhythmics. The class Ic agents (flecainide, propafenone) can be used in patients without underlying structural heart disease. In patients with evidence of structural heart disease, class III agents, such as sotalol or amiodarone, should be used because of the lower incidence of ventricular proarrhythmia during long-term therapy.

All patients with sustained or symptomatic PSVT should be referred to a cardiologist or cardiac electrophysiologist for long-term treatment options (including observation, pharmacotherapy, or ablation).