Tachyarrhythmia is defined as a heart rate in excess of 100 bpm in an individual at rest. Tachycardias are classified as supraventricular or ventricular, depending on the mechanism and site of origin. Narrow complex tachycardias are almost exclusively supraventricular in origin; wide complex tachycardias may be either supraventricular or ventricular in origin. Correct identification of the origin and mechanisms of the tachycardia is critical to selecting appropriate treatment. The exact site of the pacing focus may be difficult to determine when the heart rate is very rapid.
The category of supraventricular tachycardias includes paroxysmal atrial tachycardia, AV junctional tachycardia, atrial flutter, and atrial fibrillation. Supraventricular tachycardias may be paroxysmal or chronic, as with chronic atrial fibrillation. Causes include emotional stress; caffeine, alcohol, or drug use; thyrotoxicosis; lung disease; and cardiac disease. A patient with a supraventricular tachycardia often experiences palpitations and, in some cases, syncope. β-Blockers are often useful in the management of these disorders, and catheter-guided radiofrequency ablation may be curative in patients with refractory supraventricular tachycardia. The prognosis for supraventricular tachycardia is usually better than that associated with ventricular tachycardia.
Atrial fibrillation Atrial fibrillation is caused by multiple simultaneous wavelets occurring in both the right and the left atria, leading to a chaotic electrical rhythm with ineffective atrial contraction (Fig 5-5). Cardiac output may be markedly reduced when the ventricular rate is very rapid, possibly resulting in CHF. Atrial thrombi may accumulate from stagnation of blood in the atrial appendages. These thrombi may embolize to the lungs, brain, or other organs. Anticoagulation therapy is indicated for patients with chronic atrial fibrillation and chronic atrial flutter associated with valvular disease, cardiomyopathy, or cardiomegaly and before conversion to sinus rhythm is attempted. Several risk stratification tools (eg, CHADS2) have been devised to weigh the risk of embolism against the risk of bleeding in these patients. Newer classes of oral anticoagulants, including direct thrombin inhibitors (dagibatran) and factor Xa inhibitors (rivaroxaban, apixaban, edoxaban), are superior to warfarin in prevention of stroke, with comparable bleeding risks.
Conversion of atrial fibrillation can be attempted with flecainide, dofetilide, propafenone, ibutilide, or direct-current (DC) cardioversion. In many patients with chronic atrial fibrillation, maintenance therapy is directed toward controlling the ventricular rate, which can usually be accomplished with verapamil, β-blockers, or amiodarone.
Other curative approaches have been developed for both atrial fibrillation and atrial flutter. These treatments include radiofrequency catheter ablation and the surgical maze procedure. The maze procedure interrupts all possible reentry circuits to the atrium with multiple incisions. A single uninterrupted pathway is left intact to allow normal conduction from the SA node to the AV node. This and other ablative procedures can be performed at the time of CABG or valvular surgery to restore sinus rhythm.
January CT, Wann LS, Alpert JS, et al. 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation. Circulation. 2014;130(23):e199–e267. Erratum in: Circulation. 2014;130(23):e272–e274.
Kirchhof P, Benussi S, Kotecha D, et al; ESC Scientific Documentation Group. 2016 ESC guidelines for the management of atrial fibrillation developed in collaboration with EACTS. Eur Heart J. 2016;37(38):2893–2962.
Figure 5-5 Single-lead ECG showing atrial fibrillation. Note the characteristic irregularly irregular rate and rhythm.
(Reproduced with permission from Olshansky B. The electrocardiogram in atrial fibrillation. In: UpToDate, Goldberger AL, Saperia GM [eds]. Available at www.uptodate.com. Accessed August 15, 2018.)
Ventricular tachycardia The ventricular tachyarrhythmias include ventricular tachycardia (VT), torsades de pointes (a variant of VT), ventricular flutter, and ventricular fibrillation. These arrhythmias may present with palpitations, heart failure, or syncope or may progress rapidly to sudden cardiac death. VT occurs infrequently in young patients with no organic heart disease. Brief episodes of VT cause palpitations; prolonged attacks in patients with organic cardiac disease can lead to heart failure or cardiac shock. If the rate is not very high, and there is no significant underlying heart disease, VT may be well tolerated. However, it may degenerate into ventricular fibrillation, resulting in hemodynamic collapse and death.
Treatment with immediate synchronized DC cardioversion is indicated for sustained VT associated with hemodynamic compromise, severe CHF, or ongoing ischemia or infarction. Pharmacologic cardioversion with β-blockers, calcium channel blockers (verapamil, diltiazem), or amiodarone may be attempted in patients with clinically stable VT. Amiodarone is generally the agent of choice for recurrent VT if its adverse effects are tolerated.
Electrophysiologic testing is often performed in patients with suspected or documented ventricular arrhythmias. In this procedure, direct transcatheter electrical stimulation is applied to various sites in the ventricle to induce arrhythmias. Given their efficacy and the low risk associated with implantation, ICDs, in conjunction with antiarrhythmic drugs, have become the treatment of choice for patients with life-threatening ventricular arrhythmias. Radiofrequency catheter ablation can also be performed in patients resistant to medical therapy.
Ventricular fibrillation Ventricular fibrillation (VF) is the most ominous of all the cardiac arrhythmias because it is fatal when untreated or when refractory to treatment. It is a major cause of SCD outside the hospital. The ventricular contractions are rapid and un-coordinated, resulting in ineffective ventricular pumping that soon leads to syncope, convulsions, and death if the VF is not interrupted. The prognosis is generally poor because each episode can be fatal.
Cardiopulmonary resuscitation efforts must be initiated emergently. Immediate unsynchronized DC cardioversion is the primary therapy. After successful cardioversion, continuous intravenous infusion of effective antiarrhythmic therapy should be maintained until any reversible causes have been corrected. The choice of long-term antiarrhythmic therapy depends on the conditions responsible for the initial VF episode. Primary VF occurring within the first few hours of an acute MI is not associated with an elevated risk of recurrence and does not require long-term antiarrhythmic therapy. However, VF without an identifiable and reversible cause requires implantation of an automatic defibrillator. If a patient refuses an ICD, prophylactic antiarrhythmic drug therapy (eg, amiodarone, sotalol) may be used, but multiple studies have demonstrated that an ICD is more effective in preventing SCD.
ICDs monitor heart rhythm and, when a potentially lethal tachyarrhythmia is identified, deliver therapy. Their evolution has been impressive. Initially, a thoracotomy was necessary to implant an epicardial patch or patches. Most patients now receive a transvenous system, which significantly reduces the morbidity and mortality associated with the implantation of these devices. Current-generation ICDs are generally implanted in the prepectoral region (similar to pacemaker implantation). Although first-generation ICDs delivered only high-energy defibrillating shocks, current-generation devices provide tiered therapy, including pacing algorithms for tachycardia, low-energy cardioversion for stable VT, high-energy cardioversion for VT or VF, single-chamber or dual-chamber pacing support for bradycardia, and stored diagnostic information for rhythm discrimination.
ICDs treat arrhythmias when they occur but do not prevent them. Most patients require concomitant antiarrhythmic therapy (β-blockers, amiodarone) to reduce the frequency of device discharges or to facilitate antitachycardia pacing by slowing the ventricular rate. If the device fails to terminate an arrhythmia, cardiopulmonary resuscitation and external defibrillation should proceed normally. Three randomized prospective studies have demonstrated that automatic ICDs are the preferred first-line therapy for patients who have survived a cardiac arrest or an episode of hemodynamically unstable VT, with a 20%–30% relative reduction in the risk of death. The MUSTT and MADIT trials have also proved the benefit of ICDs for primary prevention of sudden death in patients with CHD, reduced EFs, nonsustained VT, or inducible ventricular arrhythmias during electrophysiologic testing. Following an MI, ICDs appear to be the best available therapy for preventing SCD. An ICD should be considered for patients on optimal medical therapy who have left ventricular dysfunction from an MI that occurred at least 40 days previously and an expected survival with good functional status of at least 1 year. Ongoing trials may expand the role of ICDs in the primary prevention of sudden death.
Camm AJ, Lip GY, De Caterina R, et al; ESC Committee for Practice Guidelines. 2012 focused update of the ESC guidelines for the management of atrial fibrillation. Eur Heart J. 2012;33(21):2719–2747.
Russo AM, Stainback RF, Bailey SR, et al. ACCF/HRS/AHA/ASE/HFSA/SCAI/SCCT/SCMR 2013 appropriate use criteria for implantable cardioverter-defibrillators and cardiac resynchronization therapy. J Am Coll Cardiol. 2013;61(12):1318–1368.
Excerpted from BCSC 2020-2021 series: Section 1 - Update on General Medicine. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.