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 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.
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.
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.