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Cardiology - Arrhythmias - Fast Facts | NEJM Resident 360

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 reentrant circuit and the latter caused by blockage in the normal cardiac conduction system. A complete discussion of the diagnosis and management of all arrythmias is beyond the scope of this guide. In this section, we cover the most common arrhythmias (listed below) 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

• Pacemaker and implanted cardioverter-defibrillator (ICD)

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. AF can 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

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, treatment with 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 to restore sinus rhythm. Treatment options include flecainide and propafenone (in patients without structural heart disease), sotalol (in patients without heart failure), 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 (e.g., 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 for adverse cardiovascular outcomes. The results of this trial may influence future guidelines in favor of more frequent use of early rhythm control. In patients with AF and heart failure, 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.

Anticoagulation: 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 CHA₂DS₂VASc 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 CHA₂DS₂VASc score ≥2). For anticoagulation management in patients taking concurrent antiplatelet agents, please see the section on coronary artery disease in this rotation guide.

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

The CHA₂-DS₂-VASc Score

Criteria	Points
C: Congestive heart failure (or left ventricular systolic dysfunction)	1
H: Hypertension (blood pressure persistently >140/90 mm Hg or current antihypertensive therapy)	1
A2: Age ≥75 years	2
D: Diabetes mellitus	1
S2: Stroke or transient ischemic attack (TIA) or thromboembolism history	2
V: Vascular disease (e.g., peripheral artery disease, myocardial infarction, aortic plaque)	1
A: Age 65—74 years	1
Sc: Sex category (male=0, female=1)**	1

(Adapted from 2014 AHA/ACC/HRS Guideline for the Management of Patients with Atrial Fibrillation. Circulation 2014.)

Choice of anticoagulant: 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).

Studies of AF Treatment with Direct Oral Anticoagulants 

Study	Primary Endpoint	Statistically Significant?	Adverse Events
RE-LY
Dabigatran(110 mg and 150 mg BD) vs. warfarin	Stroke or systemic embolism noninferiority	Yes, the annual rate of the primary outcome was 1.69% with warfarin vs. 1.53% with 110 mg dabigatran (P<0.001 for noninferiority) and 1.11% with 150 mg dabigatran (P<0.001 for superiority vs. warfarin).	The annual rate of hemorrhagic stroke was 0.38% with warfarin vs. 0.12% with 110 mg dabigratran and 0.10% with 150 mg dabigratran.
ARISTOTLE
Apixaban 5 mg BD) vs. warfarin	Ischemic/hemorrhagic stroke	Yes, after 1.8 years, the rate of the primary outcome was 1.27% with apixaban and 1.6% with warfarin.	The annual rate of hemorrhagic stroke was 0.24% with apixaban vs. 0.47% with warfarin.
ROCKET AF
Rivaroxaban (20 mg OD) vs. warfarin	Stroke or systemic embolism noninferiority	Yes, the annual rate of the primary endpoint was 1.7% with rivaroxaban and 2.2% with warfarin.	The rate of major and nonmajor clinically relevant bleeding was similar with rivaroxaban and warfarin (14.9% vs. 14.5%
per year), but the rate of fatal bleeding was lower with rivaroxaban (0.5% vs. 0.2%).
ENGAGE-AF-TIMI 48
Edoxaban (60 mg/30 mg OD) vs. warfarin	Stroke or systemic embolism noninferiority	Yes, the annualized rate of the primary endpoint was 1.5% with warfarin vs. 1.18% with high-dose edoxaban and 1.61% with low-dose edoxaban.	The annualized rate of major bleeding was 3.43% with warfarin vs. 2.75% with high-dose edoxaban and 1.61% with low-dose edoxaban.

Bleeding risk in patients on DOACs: 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 (referred to as “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. Typical atrial flutter has a characteristic appearance on electrocardiogram (ECG) with a “saw-tooth” 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 history of cardiac surgery or ablation and may arise from either the right or left atrium.

Management: The management of atrial flutter is the same as that of AF 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.

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, which allows a closed loop of electrical activity that continuously activates itself as well as the atria and ventricles.

• Atrioventricular reciprocating (reentrant) tachycardia (AVRT): AVRT is similar to 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 back to the AV node again; or it may proceed in the opposite direction of atria, through the bypass tract, to the ventricles, 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 children.

The different SVTs can be distinguished by the regularity of the rhythm, heart rate, and response after an AV nodal blocking drug is administered. 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 from the arrhythmias. The following table describes more distinguishing features of SVTs.

Differential Diagnosis of the Supraventricular Tachycardias (SVTs), According to Regularity of Rhythm

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 caused by 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 complexes appear wide on ECG, but not all wide complex tachycardias are caused by VT. Therefore, it is important to distinguish SVTs that mimic VT because management may be very different.

The most common cause of VT is scar formation after myocardial infarction. 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 implanted cardioverter-defibrillator (ICD). (See indications for ICD below).

Diagnosis

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

Differential Diagnosis and Treatment of Wide-Complex Tachycardias

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, myocardial infarction, 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 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., 1^st degree or 2^nd degree Mobitz type I AV block) or below and within the His-Purkinje system (i.e., 2^nd degree Mobitz type II or high-grade AV block), the latter of which tends to progress to complete (or 3^rd degree) AV block and portends poorer prognosis. (See figure below for ECG findings associated with each type of AV block).

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

  • Indications for pacemakers in asymptomatic patients include:

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

    • 2^nd degree Mobitz II, high grade, and 3^rd degree AV block not due to reversible causes

    • 2^nd or 3^rd degree AV block associated with cardiac sarcoidosis

    • alternating bundle branch block

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

Electrocardiographic Findings Associated with Atrioventricular-Conduction Disturbances

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

Pacemakers and Implantable Cardiac 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 have a fourth letter, R, which denotes 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: 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 to 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 fracture and left bundle branch block have dyssynchronous contraction of the LV, where the septum and 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 with normal conduction limited by medications.

• Indications: Specifically, CRT is indicated for ambulatory patients with NYHA II or greater symptoms, LVEF ≤35%, and ECG findings of:

  • LBBB with QRS duration ≥150 ms

  • LBBB with QRS duration 120 to 149 ms

  • non-LBBB QRS morphology with duration ≥150 ms

  • high-grade AV block and need for pacemaker

Implantable cardioverter-defibrillator (ICD): 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

  • also 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 myocardial infarction

• Specifically, the following patients 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 who experienced myocardial infarction (MI) must wait at least 40 days after MI and 90 days after revascularization before ICD implantation to see if LVEF improves with guideline-directed medical therapy. Similarly, patients with other types of cardiomyopathies should receive a trial of medical therapy first to see if LVEF improves before placing an ICD. In general, ICD has a greater benefit for patients with heart failure after MI.

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