Arrhythmias

Arrhythmias can manifest as disorders of abnormally fast or slow heart rates, the former typically caused by foci of enhanced electrical activity or a rapidly conducting re-entrant circuit and the latter caused by block in the normal cardiac conduction system. A complete discussion of the diagnosis and management of all arrythmias is outside the scope of this guide. In this section, we will cover the most common arrhythmias and briefly discuss the recognition of uncommon arrhythmias and the use of devices to manage bradyarrhythmia.

• Atrial Fibrillation

• Atrial Flutter

• Supraventricular Tachycardia

• Ventricular Tachycardia

• Bradycardia and Atrioventricular Block

• Pacemakers and Implantable Cardioverter-Defibrillators

Atrial Fibrillation

Atrial fibrillation (AF) is the most common arrhythmia and occurs with increased frequency in patients with hypertension, valvular heart disease, or heart failure (HF). AF may also develop in patients with heavy alcohol use (especially binge drinking), hyperthyroidism, pulmonary embolus, sepsis, fluid overload, or volume depletion, and in those who have undergone surgery (particularly cardiothoracic surgery).

Management

Rhythm control versus rate control: AF is managed with either a rate-control or rhythm-control strategy:

• Rate control: Guidelines recommend a target resting heart rate of <80 beats per minute (bpm). For acute presentation of rapid AF, intravenous beta-blockers or non-dihydropyridine calcium-channel blockers (e.g., diltiazem or verapamil) may be appropriate. In the less acute setting, oral agents (e.g., metoprolol, atenolol, or diltiazem) may be effective.

• Rhythm control: The goal is restoring sinus rhythm. Options include flecainide and propafenone (in patients without structural heart disease), sotalol (in patients without HF), dofetilide, and amiodarone, as well as AF ablation.

Guidelines in the last two decades generally recommended rate control as the preferred treatment choice, with rhythm control reserved for patients in whom the ventricular rate cannot be effectively controlled or in those who remain symptomatic (palpitations, dyspnea, angina, or presyncopal symptoms). However, the EAST-AFNET 4 (Early Treatment of Atrial Fibrillation for Stroke Prevention) trial, published in 2020, demonstrated that early rhythm control lowered the risk of adverse cardiovascular outcomes. The results of this trial may influence the guidelines in favor of more-frequent use of early rhythm control. In patients with AF and HF, a rhythm-control strategy is typically preferred.

Cardioversion: Urgent cardioversion may be appropriate if a patient has newly diagnosed AF, is symptomatic (i.e., has palpitations or presyncopal symptoms), or is hemodynamically unstable. Elective cardioversion is often used in patients with stable AF for whom a rhythm-control strategy is chosen.

Anticoagulants: Patients with AF are at increased risk for stroke, regardless of whether a rate-control or rhythm-control strategy is chosen. Anticoagulation therapy can lower stroke risk. The CHA₂DS₂-VASc score (better risk prediction and preferred over the CHADS₂ score) is usually used to determine risk for stroke and need for anticoagulation therapy (typically indicated in patients with a CHA₂DS₂-VASc score ≥2).

The CHA₂DS₂-VASc calculator calculates stroke risk for patients with AF:

Anticoagulation: Warfarin was historically the anticoagulant of choice. However, direct oral anticoagulant (DOAC) drugs have replaced warfarin for most indications (the most important exceptions are moderate-to-severe mitral stenosis or a mechanical heart valve). See the section on coronary artery disease in this rotation guide for information on anticoagulation management in patients taking concurrent antiplatelet agents.

Bleeding risk and reversal agents: For patients who develop serious bleeding while using a DOAC:

• Idarucizumab is available as a reversal agent for dabigatran.

• Andexanet is available as a reversal agent for patients treated with the factor Xa inhibitors rivaroxaban, apixaban, edoxaban, and betrixaban.

Atrial Flutter

Atrial flutter is a common supraventricular tachycardia that usually results from a macro-reentrant circuit around the tricuspid valve in the right atrium (termed “typical atrial flutter”).

• Typical atrial flutter is characterized by a regular organized atrial rhythm of around 280 to 300 beats per minute with 2:1 atrial-to-ventricular conduction, leading to a heart rate of 140 to 150 beats per minute. It has a characteristic appearance on electrocardiogram (ECG) with a sawtooth pattern most notable in the inferior leads and V1.

• Atypical flutter, in which the course of the reentrant circuit differs from that of typical flutter, can occur in patients with a prior history of cardiac surgery or ablation and may arise from either the right atrium or the left atrium.

Management: The management of atrial flutter is the same as that of atrial fibrillation with regard to anticoagulation, rate control, and rhythm control. The one distinction is that catheter-based ablation is more successful in the treatment of typical atrial flutter than of atrial fibrillation.

Supraventricular Tachycardias

By definition, supraventricular tachycardias (SVTs) include all tachyarrhythmias originating above the ventricles, including the atria and the atrioventricular (AV) node. In addition to AF and atrial flutter, other common SVTs include the following:

• Atrial tachycardia (AT): AT results from a small focus in the atria that has either a micro-reentrant circuit or enhanced automaticity, causing rapid heart rate that mimics sinus tachycardia.

• Multifocal atrial tachycardia (MAT): MAT is similar to AT but with multiple foci of atrial activity.

• Atrioventricular nodal reentrant tachycardia (AVNRT): AVNRT is caused by a small circuit involving some atrial tissue and the AV node that allows a loop of electrical activity to continuously activate itself as well as the atria and ventricles.

• Atrioventricular reciprocating (reentrant) tachycardia (AVRT): AVRT is like AVNRT in that a circuit is necessary to sustain the tachycardia, but the circuit in AVRT includes the normal cardiac conduction system and cardiac tissue that bypasses the insulation between the atria and ventricles. This circuit may proceed from the atria to the AV node, to the bundle of His, to the ventricles, through the bypass tract, back up to the atria, and to the AV node again; or it may proceed in the opposite direction of atria, through the bypass tract, to the ventricles, to the bundle of His, to the AV node, and then atria. AVRT is more common in children and has become less common in adults because of increasing recognition and successful treatment in childhood.

(Source: Evaluation and Initial Treatment of Supraventricular Tachycardia. N Engl J Med 2012.)

Differential diagnosis: SVTs can be distinguished based on the regularity of the rhythm, heart rate, and response after an AV nodal-blocking drug is administered.

Treatment: Once a diagnosis is made, treatment includes medications, catheter ablations, or both, which can cure some SVTs with high rates of success. Cardioversion should be considered for patients with hemodynamic compromise resulting from the arrhythmias.

The following table describes more features of SVTs.

AV denotes atrioventricular, AVRT atrioventricular reciprocating tachycardia, and WPW the Wolff-Parkinson-White syndrome. (Source: Evaluation and Initial Treatment of Supraventricular Tachycardia. N Engl J Med 2012.)

Ventricular Tachycardia

Ventricular tachycardia (VT) results from a wide range of underlying disorders that lead to tachyarrhythmias arising from the ventricles due to micro-reentrant circuits, enhanced automaticity of the ventricular tissue, or less commonly, triggered activity. Because VT does not involve the normal cardiac conduction system, the QRS complex appear wide on ECG, but not all tachycardias with a wide QRS complex are caused by VT. Therefore, it is important to distinguish SVTs that mimic VT because management may be quite different.

The most common cause of VT is scar formation after myocardial infarction (MI). The diseased ventricular tissue predisposes to formation of abnormal micro-reentrant circuits that sustain the tachycardia. The management of VT in this setting typically involves a combination of medications (e.g., sotalol and amiodarone), catheter ablation, and implantable cardioverter-defibrillator (see indications for ICD below).

The following figure details an approach to the differential diagnosis of VTs, which can be complicated and should involve a cardiologist.

(Source: Evaluation and Initial Treatment of Supraventricular Tachycardia. N Engl J Med 2012.)

Bradycardia and Atrioventricular Block

Bradycardia and atrioventricular (AV) block can occur physiologically from heightened vagal tone or pathologically from a variety of etiologies, including infection (e.g., Lyme disease), metabolic derangement (e.g., hyperkalemia), drug effect (e.g., beta-blockers), system disorders (e.g., hypothyroidism, systemic lupus erythematosus), sleep apnea, MI, infiltrative heart disease (e.g., sarcoidosis, amyloidosis), or simply degeneration with aging.

Management: The management of bradycardia starts with identifying and treating underlying causes, particularly in patients younger than 60 years (note, prompt advanced cardiovascular life support (ACLS)-guided management should be provided for unstable patients).

• If AV block is present, it is crucial to determine whether block is occurring above or within the AV node (i.e., first-degree or second-degree Mobitz type I AV block) or below and within the His-Purkinje system (i.e., second-degree Mobitz type II or high-grade AV block), the latter of which tends to progress to complete (or third-degree) AV block and portends poorer prognosis. (See figure below for ECG findings of each type of AV block.)

• In certain scenarios, a pacemaker can improve survival, but in many scenarios a pacemaker serves to improve quality of life. Thus, it is important to correlate bradycardia with symptoms. Additional tests, such as ambulatory cardiac monitoring, exercise stress testing, or invasive electrophysiological study, can help make this connection.

• Some indications for pacemaker in asymptomatic patients include:

  • bradycardia caused by medications necessary for the management of other conditions without an alternative

  • second-degree Mobitz II, high-grade, and third-degree AV block not due to reversible causes

  • second- or third-degree AV block associated with cardiac sarcoidosis

  • alternating bundle branch block

  • syncope with documented sinus pause or AV block >6 seconds

(Source: The Evaluation and Management of Bradycardia. N Engl J Med 2000.)

Pacemakers and Implantable Cardioverter-Defibrillators

Pacemakers

A pacemaker is typically placed subcutaneously in the upper left chest wall with venous leads that are fixated via screws into the right atrium, right ventricle, or both. In general, patients receive leads in both chambers to preserve AV synchrony; exceptions include patients in permanent AF.

• Pacemaker settings are denotated by a three-letter system:

  • The first letter indicates the chamber that is paced.

  • The second letter indicates the chamber that is sensed.

  • The third letter indicates the pacemaker’s response to what is sensed (O for no action, I for inhibit, T for trigger, and D for both inhibit and trigger).

  • Some settings include a fourth letter (R), which indicates that the heart rate set by the pacemaker varies based on a patient’s physical activity level.

• Common pacemaker settings include:

  • VVI: The ventricle is paced and sensed, and when ventricular activity is detected, the pacemaker will inhibit itself and not pace. This setting is used for patients in permanent AF, and the pacemaker provides a minimum heart rate; it will only pace if a normally conducted beat is not detected after a period.

  • AAI: This is similar to VVI, except the atrium is paced and sensed. This setting is used for patients with sick sinus syndrome and normal AV conduction to maintain a minimum heart rate.

  • DDD: In this setting, both the atrium and ventricle are sensed and paced. The dual activity of inhibiting and triggering allows a sensed normal atrial activity to trigger ventricular pacing when ventricular activity is not sensed or inhibit ventricular pacing when ventricular activity is sensed. This setting is commonly used for patients with AV block.

Cardiac resynchronization therapy or biventricular pacing: Patients who have heart failure with reduced ejection fraction and left bundle branch block (LBBB) have dyssynchronous contraction of the left ventricle (LV), where the septum and right ventricle (RV) contracts before the LV free wall, resulting in ineffective contraction and reduced cardiac output. In this situation, cardiac resynchronization therapy (CRT) or biventricular pacing can improve survival and cardiac function.

• For CRT, a third lead is placed, typically via the coronary sinus, against the lateral LV wall and programmed to pace synchronously with the RV lead. Therefore, for CRT to work effectively, patients need to be predominantly paced and normal conduction limited by medications.

• Indications: Specifically, CRT is indicated for ambulatory patients with New York Heart Association (NYHA) class II or greater symptoms, left ventricular ejection fraction (LVEF) ≤35% and the following ECG findings:

  • LBBB with QRS duration ≥150 msec

  • LBBB with QRS duration 120 to 149 msec

  • non-LBBB QRS morphology with duration ≥150 msec

  • high-grade AV block and need for pacemaker

Implantable Cardioverter-Defibrillators

Implantable cardioverter-defibrillators (ICDs) have the combined ability to pace and defibrillate the heart when VT or ventricular fibrillation (VF) is detected.

• Indications:

  • strongly indicated for secondary prevention in patients who have suffered a cardiac arrest due to VT/VF

  • indicated as primary prevention in certain cardiomyopathies and genetic disorders where the patient is at elevated risk for VT/VF

  • most frequently used in patients with reduced LVEF after MI

• Specifically, patients with the following conditions have been shown to benefit from an ICD:

  • structural heart disease with spontaneous, sustained VT

  • LVEF ≤30% with no symptoms

  • LVEF ≤35% with symptomatic heart failure

  • LVEF ≤40% with inducible VF or sustained VT at electrophysiological study

Note: Patients must wait at least 40 days after MI and 90 days after revascularization before ICD implantation to determine if LVEF improves with guideline-directed medical therapy. Similarly, patients with other types of cardiomyopathies should receive a trial of medical therapy first to determine if LVEF improves before placing an ICD. In general, ICD has a greater benefit for patients with heart failure after MI.