Medication Summary
As previously stated, short-term management of supraventricular tachycardia (SVT) involves intravenous adenosine or calcium channel blockers.
In cases of wide-complex tachycardia, hemodynamically stable patients can be treated with intravenous procainamide, propafenone, or flecainide. Amiodarone is preferred in patients with impaired left ventricular function or in patients with heart failure or structural heart disease. [57]
Treatment for atrial fibrillation and atrial flutter includes medications that control the ventricular rate (calcium channel blockers, digoxin, amiodarone, beta-blockers), restore the sinus rhythm (such as ibutilide, flecainide, amiodarone, propafenone), and prevent embolic complications.
Long-term pharmacologic therapy for patients with SVT depends on the type of tachyarrhythmia that is occurring and the frequency and duration of episodes, as well as the symptoms and the risks associated with the arrhythmia (eg, heart failure, sudden death).
Cardiovascular, Other
Class Summary
These medications are used to treat or prevent arrhythmia.
Flecainide (Tambocor)
Flecainide blocks sodium channels, producing a dose-related decrease in intracardiac conduction in all parts of heart. The drug increases electrical stimulation of threshold of ventricle, HIS-Purkinje system. Flecainide shortens phase 2 and 3 repolarization, resulting in a decreased action potential duration and effective refractory period.
This agent is indicated for the treatment of paroxysmal atrial fibrillation/flutter (PAF) associated with disabling symptoms. It is also indicated for paroxysmal SVTs, including atrioventricular nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT), and other SVTs of unspecified mechanism associated with disabling symptoms in patients without structural heart disease.
In addition, Flecainide is indicated for the prevention of documented, life-threatening ventricular arrhythmias, such as sustained ventricular tachycardia. It is not recommended for less severe ventricular arrhythmias, even if patients are symptomatic.
Propafenone (Rythmol)
Propafenone shortens the upstroke velocity (phase 0) of monophasic action potentials. It reduces the fast inward current carried by sodium ions in Purkinje fibers and, to a lesser extent, myocardial fibers. Propafenone may increase the diastolic excitability threshold and prolong the effective refractory period. It also reduces spontaneous automaticity and depresses triggered activity.
Propafenone is indicated for the treatment of documented, life-threatening ventricular arrhythmias, such as sustained ventricular tachycardia. It appears to be effective in the treatment of SVTs, including atrial fibrillation and flutter. The drug is not recommended for patients with less severe ventricular arrhythmias, even if the patients are symptomatic.
Adenosine (Adenocard)
Adenosine is the first-line medical treatment for the termination of paroxysmal SVT. It is a short-acting agent that alters potassium conductance into cells and results in hyperpolarization of nodal cells. This increases the threshold to trigger an action potential and results in sinus slowing and the blockage of AV conduction.
Adenosine is effective in terminating AVNRT and AVRT. More than 90% of patients convert to sinus rhythm with adenosine at 12mg. As a result of its short half-life, adenosine is best administered in an antecubital vein as an intravenous bolus, followed by rapid saline infusion.
Digoxin (Lanoxin)
Digoxin indirectly increases vagal activity, thereby decreasing conduction velocity through the AV node. This can result in termination of paroxysmal SVT.
Calcium Channel Blockers
Class Summary
Class IV calcium channel blockers decrease the conduction velocity and prolong the refractory period.
Verapamil (Isoptin, Calan, Verelan, Covera-HS)
Calcium channel blockers prevent calcium influx into the slow channels of the AV node, decrease the conduction velocity, and prolong the refractory period, which effectively terminates reentrant conduction.
Diltiazem (Cardizem, Tiazac, Dilacor XR)
Diltiazem is similar to verapamil. This agent decreases the conduction velocity in the AV node and increases the refractory period via a blockade of calcium influx. This, in turn, stops the reentrant phenomenon.
Beta-Blockers, Beta-1 Selective
Class Summary
These agents slow the sinus rate and decrease AV nodal conduction. Beta-blockers now have more of a secondary role in AF rate control. Carefully monitor blood pressure.
Atenolol (Tenormin)
Atenolol selectively blocks beta-1 receptors, with little or no effect on beta-2 types. Atenolol is excellent for use in patients at risk for experiencing complications from beta-blockade, particularly those with reactive airway disease, mild-to-moderate LV dysfunction, and/or peripheral vascular disease.
Esmolol (Brevibloc)
Esmolol is a short-acting beta-blocker that abolishes reentry-induced paroxysmal SVT by increasing the refractory period of the AV node.
It selectively blocks beta-1 receptors, with little or no effect on beta-2 receptor types. It is particularly useful in patients with elevated arterial pressure, especially if surgery is planned. It has been shown to reduce episodes of chest pain and clinical cardiac events compared with placebo. It can be discontinued abruptly if necessary. It is useful in patients at risk for experiencing complications from beta-blockade, particularly those with reactive airway disease, mild-to-moderate LV dysfunction, and/or peripheral vascular disease. A short half-life of 8 min allows for titration to the desired effect and quick discontinuation if needed.
Metoprolol (Lopressor, Toprol XL)
Metoprolol is a selective beta-1 adrenergic receptor blocker that decreases the automaticity of contractions. During intravenous administration, carefully monitor blood pressure, heart rate, and ECG.
Beta-blockers, Nonselective
Class Summary
These agents increase the refractory period of the AV node. Beta-blockers that are effective in treating paroxysmal SVT include propranolol, esmolol, metoprolol, atenolol, and nadolol.
Propranolol (Inderal LA, InnoPran XL)
Beta-blockers abolish reentry-induced paroxysmal SVT by increasing the refractory period of the AV node.
Nadolol (Corgard)
Nadolol is frequently prescribed because of its long-term effect. It reduces the effect of sympathetic stimulation on the heart. Nadolol decreases conduction through the AV node and has negative chronotropic and inotropic effects. Patients with asthma should use cardioselective beta-blockers.
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Sinus tachycardia. Note that the QRS complexes are narrow and regular. The patient's heart rate is approximately 135 bpm. P waves are normal in morphology.
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Atrial tachycardia. The patient's heart rate is 151 bpm. P waves are upright in lead V1.
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Multifocal atrial tachycardia. Note the different P-wave morphologies and irregularly irregular ventricular response.
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Atrial flutter. The patient's heart rate is approximately 135 bpm with 2:1 conduction. Note the sawtooth pattern formed by the flutter waves.
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Atrial fibrillation. The patient's ventricular rate varies from 130-168 bpm. The rhythm is irregularly irregular. P waves are not discernible.
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Atrioventricular nodal reentrant tachycardia. The patient's heart rate is approximately 146 bpm with a normal axis. Note the pseudo S waves in leads II, III, and aVF. Also note the pseudo R' waves in V1 and aVR. These deflections represent retrograde atrial activation.
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Same patient as in the previous image. The patient is in sinus rhythm following atrioventricular nodal reentrant tachycardia.
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Image A displays the slow pathway and the fast pathway, with a regular impulse being conducted through the atrioventricular node. Image B displays a premature impulse that is conducted in an anterograde manner through the slow pathway and in a retrograde manner through the fast pathway, as is seen in typical atrioventricular nodal tachycardia. Image C displays the premature impulse conducting in a retrograde manner through the pathway and the impulse reentering the pathway with anterograde conduction, which is seen commonly in patients with atypical atrioventricular nodal tachycardia.
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Wolff-Parkinson-White pattern. Note the short PR interval and slurred upstroke (delta wave) to the QRS complexes.
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The left image displays the atrioventricular node with the accessory pathway. The impulse is conducted in an anterograde manner in the atrioventricular node and in a retrograde manner in the accessory pathway. This circuit is known as orthodromic atrioventricular reentrant tachycardia and can occur in patients with concealed accessory tracts or Wolff-Parkinson-White syndrome. The right image displays the impulse being conducted in an anterograde manner through the accessory pathway and in a retrograde manner via the atrioventricular node. This type of circuit is known as antidromic atrioventricular reentrant tachycardia and occurs only in patients with Wolff-Parkinson-White syndrome. Both patterns may display retrograde P waves after the QRS complexes.
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Orthodromic atrioventricular reentrant tachycardia. This patient has Wolff-Parkinson-White syndrome.
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The left panel depicts antidromic atrioventricular reentrant tachycardia. The right panel depicts sinus rhythm in a patient with antidromic atrioventricular reentrant tachycardia. Note that the QRS complex is an exaggeration of the delta wave during sinus rhythm.
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Atrial fibrillation in a patient with Wolff-Parkinson-White syndrome. Note the extremely rapid ventricular rate and variability in QRS morphology. Several minutes later, the patient developed ventricular fibrillation.
