AUTHORS

Sreeja Natesan, MD, FACEP, Assistant Program Director, Division of Emergency Medicine, Duke University Medical Center, Durham, NC

Carmen Hoffman, MD, Department of Emergency Medicine, Duke University, Durham, NC

Sarah K. Kennedy, MD, FACEP, Assistant Professor of Clinical Emergency Medicine, Department of Emergency Medicine, Indiana University School of Medicine

PEER REVIEWER

Catherine A. Marco, MD, Professor, Departments of Emergency Medicine and Surgery, Boonshoft School of Medicine, Wright State University, Dayton, OH


Introduction

The American Heart Association (AHA) defines arrhythmias as “any change from the normal sequence of electrical impulses”; this includes bradyarrhythmias, atrioventricular (AV) nodal pathology, and tachyarrhythmias.1,2 The terms arrhythmia and dysrhythmia will be used interchangeably in this article. In 2011, cardiac dysrhythmias were the fifth leading cause of ED visits.3 According to the Healthcare Cost and Utilization Project (HCUP), in 2016, more than 475,000 adult patients visited the ED for dysrhythmias, and more than 155,000 of these patients were admitted.4 Of these, approximately 280,000 visits were for tachycardias, while 115,000 were for bradycardias. More than 67,000 and 58,000 patients required admission for tachycardia and bradycardia, respectively.5

Clinical Features

Bradycardias

The underlying mechanism of bradycardia is the dysfunction of either the generation or conduction of the atrial impulse, from intrinsic or extrinsic factors.6 Extrinsic causes, such as increased vagal tone, medications, and electrolyte abnormalities, are responsible for most bradyarrhythmias. Common causes of increased vagal tone can include urination or defecation, increased intracranial pressure, intubation, suctioning, or vomiting. Medications, such as beta-blockers, calcium channel blockers, digoxin, clonidine, and class IA, IC, and III antiarrhythmics, are prescribed commonly and frequently are culprits for the presentation of bradyarrhythmias. Electrolyte imbalances, especially of potassium, calcium, and magnesium, also are frequent causes of arrhythmias. Other extrinsic causes include hypoxia, hypothyroidism, hypothermia, sepsis, and Lyme disease.7,8

Some important intrinsic causes include myocarditis, trauma, cardiomyopathy, infiltrative cardiac diseases such as amyloid or sarcoid, and collagen vascular diseases.6 Acute myocardial infarction (MI), particularly an inferior infarction, also can cause bradycardia either from a direct effect on the blood supply to the sinoatrial (SA) node (most supplied by the right coronary artery) or by stimulating receptors in the left ventricle, which increases vagal tone.7,9 MI associated with an AV block may be transient, but is associated with increased in-hospital mortality.6,10

Tachycardia

Sinus tachycardia should be considered a symptom of an underlying condition, with inappropriate sinus tachycardia or normal variant as a diagnosis of exclusion.11 Risk factors that may predispose to tachycardias include congestive heart failure, electrolyte abnormalities, MIs, accessory pathways, congenital heart disease, pulmonary hypertension, pulmonary embolism, and valvular dysfunction.9,12,13

Atrial fibrillation (AF) was the most common arrhythmia treated by emergency physicians found in 1-2% of the adult population.14-17 AF can affect up to 9% of the elderly population.14 If untreated, it can progress to heart failure, hypotension, ventricular ectopy, and the potential for cardiovascular collapse.15 AF is associated with a fivefold increased risk of stroke, threefold increase of heart failure, and twofold increase in dementia and mortality when not treated.18 Common etiologies are listed in Table 1.9,11-13

Table 1. Common Causes of Dysrhythmias

Sinus Tachycardia

  • Infection
  • Vital sign abnormalities (hypoxia, hypotension, fever)
  • Sympathomimetic medications (amphetamines, cocaine, pseudoephedrine, albuterol, PCP)
  • Withdrawal (alcohol, beta-blockers, calcium channel blockers)
  • Stimulants (caffeine, nicotine, energy drinks)
  • Metabolic derangement (hyperthyroidism)
  • Psychological strain (pain, anxiety)

Atrial Fibrillation

  • Electrolyte disturbances
  • Atrial enlargement
  • Pulmonary embolism
  • Hyperthyroidism
  • Alcohol abuse
  • Fever
  • Myocardial infarction
  • Valvular dysfunction
  • Stimulants

Polymorphic Ventricular Tachycardia

  • Myocardial infarction
  • QT prolongation
  • Hypocalcemia
  • Hypokalemia
  • Congenital long QT syndrome

Ventricular Fibrillation

  • Toxins
  • Electrolyte disturbances
  • Myocardial infarction
  • Cardiomyopathy
  • Respiratory pathology, including pulmonary embolism or tension pneumothorax

Symptoms/Chief Complaints

The most common chief complaints include palpitations, chest pain, shortness of breath, dyspnea on exertion, lightheadedness, fatigue, generalized weakness, altered mental status, and presyncope or syncope. However, in patients with structurally normal hearts, syncope is less common.11,13 If the atrial kick is lost, as seen in atrial flutter (AFlutter) or AF, the patient may experience symptoms such as fatigue, shortness of breath, exertional symptoms, lightheadedness, or syncope.11

Physical Exam

The patient’s exam may be completely normal or in cardiovascular collapse. Although athletes may have very low resting heart rates, that same level of bradycardia can cause hemodynamic instability in another patient. Similarly, some degree of tachycardia can be tolerated by a patient with minimal symptoms, but others may experience severe effects of a minimally elevated heart rate. Cardiac output is directly proportional to the heart rate and stroke volume; arrhythmias, both slow and fast, can result in a reduced cardiac output by slowing the rate or decreasing filling time and, thus, decrease stroke volume. This can cause hypotension and diminished end organ perfusion. End organ hypoperfusion can be manifested by diaphoresis, syncope, decreased level of consciousness, tachypnea, or chest pain. Pallor, poor capillary refill, and neurologic manifestations may be seen. Sudden death may occur if the patient has a pathological arrhythmia that inhibits cardiac output, such as ventricular tachycardia (VT) or ventricular fibrillation (VF).

Review of Pharmacology

In addition to the internal pacemaker function of the SA node, AV node, and the Purkinje fibers, serum electrolytes and ion channels can affect conduction and are influenced by antiarrhythmic medications. Table 2 shows a summary of the five distinct phases of the cardiac action potential phases and the corresponding electrolyte channel that help facilitate contraction in the heart.19

Table 2. Cardiac Action Potential Phase

Phase

Cardiac Action
Potential Phase

Electrolyte Channel
Physiology

0

Rapid Upstroke

Primarily Na+ channel opening

1

Early Rapid Repolarization

Inactivation of Na+ current, opening of K+ channels

2

Plateau Phase

Balance between K+ and Ca2+ currents

3

Final Rapid Repolarization

Activation of Ca2+ channels

4

Diastolic Depolarization

Balance between Na+ and K+ currents

Supraventricular Tachycardia

Supraventricular tachycardia (SVT) is a comprehensive term that refers to any tachydysrhythmia that originates above the ventricles (sinus nodal, atrial, AV nodal tissue, or some combination).

Sinus Tachycardia (ST). Sinus tachycardia is defined as a heart rate (HR)
> 100 beats per minute (bpm). Typically, the rate falls between 100 bpm and
160 bpm, although it can be higher. ST is a sign rather than a primary disease. ST can be identified on electrocardiogram (ECG) by a regular, narrow QRS complex with associated P waves. The P wave should be negative in aVR and positive in leads I, II, III, and aVF.

Supraventricular wide-complex tachycardias (WCTs) are much less common than narrow-complex arrhythmias. WCTs can be difficult to distinguish and include VF, VT, Wolff-Parkinson-White syndrome (WPW), and SVT with aberrancy or bundle branch block (BBB). It is defined as a rate > 100 bpm with a QRS complex > 100-120 ms.20

Atrial Flutter (AFlutter). Atrial flutter is an SVT that occurs due to a focus in the right atrium. It is less common than AF, but patients with flutter often have coexisting AF.15,18 The ventricular rate is determined by the degree of AV block. The typical atrial rate ranges from 240-300 bpm.18 The most common AV block ratio for atrial flutter is 2:1, which subsequently results in a rate of 150 bpm. Characteristic ECG findings consist of a narrow complex tachycardia with an atrial rate of approximately 300 bpm with “saw tooth” pattern flutter waves, which typically are seen best in leads II, III, and aVF.11,13

Atrial Fibrillation (AF). AF is a rhythm that arises from the atria due to disorganized and uncoordinated electrical activity.18 It subsequently results in an irregularly irregular dysrhythmia that frequently is tachycardic. There is an absence of P waves, irregular R-R intervals, and a chaotic “fibrillation wave” prior to the QRS complex.13,18 Rates can vary from normal to rapid. A rapid ventricular rate in AF is defined as HR > 120 bpm.21 It is the most common cardiac arrhythmia, has an increasing incidence with age, and is seen frequently in the elderly and patients with chronic heart disease.14,20,22

Junctional Tachycardia. Junctional tachycardia, although rare, can carry a high mortality rate. It can be due to congenital heart disease, typically in the first month of life. Classic ECG findings include a rate ranging from 110 to 120 bpm with the P wave buried in the QRS complex (similar to atrioventricular nodal reentry tachycardia [AVNRT]). In adults, it typically is due to inflammation near the AV node from processes such as endocarditis.11

Ectopic (Unifocal) Atrial Tachycardia (UAT). UAT is a atrial that originates from the atrium. The morphology of the P waves depends on the location of the atrial foci, and the QRS complex is narrow. The atrial rate typically is slower than in AF or atrial flutter, usually < 240 bpm.11

Multifocal Atrial Tachycardia (MAT). MAT is defined as a rapid, irregular atrial tachycardia that arises from ectopic foci within the atria. The typical rate may be variable in the 100-150 bpm range, although it may be as high as > 200 bpm. MAT requires at least three P waves of different morphologies in the same lead. The most common underlying conditions are severe chronic obstructive pulmonary disease (COPD) (due to hypoxia or hypercarbia), pulmonary hypertension, or congestive heart failure. Other predisposing conditions are electrolyte abnormalities, such as hypokalemia or hypomagnesemia.11

Atrioventricular Nodal Reentry Tachycardia (AVNRT). AVNRT is the most common form of SVT, accounting for 60% of cases, and typically is not associated with underlying cardiovascular disease.13 It can be identified on ECG by a paroxysmal narrow-complex, regular QRS without preceding P waves.23 In typical AVNRT, retrograde atrial activation results in a retrograde P wave that can be buried in or appear immediately after the QRS complex as a pseudo S wave in leads II, III, and aVF, and as a pseudo R wave in lead V1. Patients can develop ST-segment depression from changes in ventricular repolarization, and it is not necessarily representative of myocardial ischemia.24,25

Atrioventricular Reentrant Tachycardia (AVRT). AVRT is the second most common form of SVT, accounting for 30% of all SVT cases.13 This rhythm occurs because an anatomic accessory pathway exists between the atria and ventricles, bypassing the AV node. WPW is one example of this.11,23

WPW is a preexcitation syndrome that results from an accessory AV pathway.23 Because of this pathway, the atrial impulse reaches the ventricles via both AV node and the accessory AV pathway. However, the accessory pathway is faster, resulting in a short PR interval which is a classic finding in the ECG. Other ECG findings include a delta wave, which is a gentle upsloping prior to the QRS complex. The QRS can be narrow or wide.

Ventricular Rhythms

Monomorphic Ventricular Tachycardia. Wide-complex monomorphic ventricular tachycardia is the most common ventricular tachyarrhythmia. It has a uniform, wide QRS that originates from the ventricles.11,20 VT can lead to impaired cardiac output resulting in hypotension, syncope, and acute cardiac failure, including arrest. Sustained VT has a duration greater than 30 seconds or results in hemodynamic instability or compromise. Nonsustained VT is three or more ventricular wide-complex tachycardia beats that terminate spontaneously before 30 seconds.

Polymorphic Ventricular Tachycardia. Polymorphic VT is when there are multiple foci within the ventricles, resulting in a mix of QRS complexes of varying amplitude, duration, and axis. Torsades de pointes is a form of polymorphic VT that characteristically reveals the QRS complexes “twisting around the isoelectric line.”

Ventricular Fibrillation. VF is from unsynchronized, uncoordinated contractions of the heart. VF leads to cardiovascular collapse.26 ECG findings are notable for a chaotic irregular rhythm with no identifiable P, QRS, or T complexes. The amplitude can be variable, ranging from coarse VF to fine VF.

Bundle Branch Block (BBB/Aberrancy). BBBs can be classified as right or left. In a left BBB (LBBB), there is a block of conduction into the left side, which results in a delayed depolarization and subsequent wide QRS complex (> 120 ms). Other findings on the ECG can include a dominant S wave in V1 and broad monophasic R wave in the lateral leads (I, aVL, and V5-6). For a right BBB (RBBB), there is delayed conduction to the right side, resulting in a secondary R wave known as a R’. This typically is seen in the precordial leads (V1-3). Other ECG findings include broad QRS > 120 ms and atypical RSR’ pattern in the precordial leads described as an “M”-shaped QRS complex.27

Bradyarrhythmias

Sinus Bradycardia. Sinus bradycardia is a ventricular rate < 60 bpm with regular P waves associated with every QRS complex. Typically, the heart rate is < 50 bpm before patients report significant symptoms.11

Sinus Arrest. Sinus arrest occurs when there is no atrial depolarization for a period of time before cardiac conduction restarts, resulting in a pause in rhythm.

Chronotropic Incompetence. This is the inability of the sinus node to regulate the heart rate in response to changes in demand, such as during exercise. Patients may be asymptomatic at rest, but can report exercise intolerance. An underlying cause of this can be medications, such as beta-blockers or calcium channel blockers.

Tachy-Brady Syndrome. This syndrome is defined by periods of sinus bradycardia or sinus arrest alternating with episodes of SVT. AF is a common rhythm for the periods of tachycardia.

Junctional Bradycardia. Junctional bradycardia is the absence of P waves associated with QRS complexes. If a P wave is seen, it typically will be retrograde or have a short PR interval (< 120 ms). The rhythm frequently is narrow-complex with a rate that is bradycardic in the range of 40-60 bpm.

Ventricular Rhythm. This is identified by an extremely profound bradycardia with HR typically of 20-40 bpm with an associated wide complex QRS.

Atrioventricular Blocks

First-Degree AV Block. Patients rarely are symptomatic from a first-degree block. It is identified by a prolonged PR interval > 200 ms with a corresponding QRS complex for every P wave. The overall prevalence is 0.65-1.1%.28 Although traditionally considered a benign finding, these patients are more than twice as likely to develop AF, three times as likely to require pacemaker insertion, and have a moderate increase in risk for all-cause mortality.27,29

Second-Degree AV Block (Mobitz I or Wenckebach and Mobitz II): Second-degree AV blocks are divided into two categories: Type I (Mobitz I/Wenckebach) and Type II (Mobitz II). Mobitz I, or Wenckebach, is identified on ECG by a progressive prolongation of the PR interval followed by a non-conducted QRS beat. Mobitz II has a fixed PR interval with non-conducted QRS beats interspersed throughout rhythm (typically at regular intervals). A second-degree type II AV block is more likely to degenerate into complete heart block.27

Third-Degree AV Block. Third-degree AV block, or complete heart block, is complete dissociation between the atria and ventricles. There is no correlation between the P waves and QRS complexes on the ECG, with varying length of the PR interval. The conduction of P waves and QRS both tend to be at regular rates but independent of each other. P waves may be buried in QRS complexes.27

Medications for Acute Management in the ED 30,31

Pharmacologic Management of Bradyarrhythmias

(For additional information on the medications discussed, view the online supplement at: http://bit.ly/31viCLX .)

Atropine. Atropine is a muscarinic acetylcholine-receptor inhibitor.30,31,32 It increases automaticity of the SA and AV nodes and increases output HR.9,10,.33

Onset: IV. Immediate; maximum effect within three minutes.34

Duration. Half-life is two to four hours in adults, longer in elderly.

Clinical Considerations. The standard first-line treatment for mild-moderate symptomatic bradycardia is atropine. If there is no improvement in heart rate following multiple atropine doses, further administration is unlikely to be effective.10 Although likely ineffective, atropine may be used in symptomatic second-degree or third-degree AV block associated with a narrow QRS complex as a first attempt to improve HR.10,35 Atropine is ineffective in heart transplant patients due to lack of vagal innervation.36 In obese patients, dosing should be calculated using ideal body weight.37 Atropine is used as a premedication before pediatric intubation to avoid reflex bradycardia; 0.02 mg/kg is the standard dose for this indication.38

Adverse Effects and Contraindications. The adverse effects seen with atropine are related to its antimuscarinic properties. (“Hot as a hare, dry as a bone, red as a beet, mad as a hatter, blind as a bat.”) There are no absolute contraindications for atropine use. It should be used with caution in acute ischemia, heart failure, or coronary artery disease. Caution also is advised when atropine is used in patients in whom the anticholinergic effects would be detrimental, such as uropathy, toxic megacolon, myasthenia gravis, or heat exposure.30,335

Dopamine. The effects of dopamine are dose dependent. At lower doses, it acts primarily upon dopaminergic receptors in the renal, mesenteric, and coronary beds, resulting in peripheral vasodilation. At higher doses, it acts primarily on beta-adrenergic receptors, leading to an increase in chronotropy and inotropy.39

Onset. Within 5 minutes.

Duration. Half-life of two minutes; duration < 10 minutes.

Clinical Considerations. Dopamine is a catecholamine that can exhibit alpha-adrenergic, beta-adrenergic, or dopaminergic effects. The effect is dose dependent.35 It is a common second-line agent for the management of bradycardia, after atropine has been unsuccessful. It also can be used for decreased cardiac output, shock, renal failure, or congestive heart failure. At doses > 20 mcg/kg/min, profound vasoconstriction or cardiac arrhythmias can be seen.35

Adverse Effects and Contraindications. Because of its effects as a catecholamine, use of dopamine may cause significant tachycardia and tachyarrhythmias (AF, VT, VF). It should be used with caution in patients with heart transplants, severe cardiomyopathy, or ongoing cardiac ischemia.40 Other side effects include nausea, vomiting, anxiety, and headache. Dopamine is contraindicated in patients with pheochromocytomas and in those patients already in a tachyarrhythmia. Extravasation or infiltration in a peripheral vein can result in extensive tissue damage and necrosis.30

Epinephrine. Epinephrine is a selective vasoconstrictive medication that acts on alpha 2 receptors in the peripheral vasculature. It rapidly improves peripheral and coronary blood flow and pressure.41 Additionally, it is both a beta 1 and 2 agonist, resulting in tachycardia and bronchodilation. However, the activation of the beta 1 receptors may lead to increased myocardial oxygen requirements, resulting in ischemic injury and a lower ventricular fibrillation threshold.41 Epinephrine also increases coronary perfusion pressure with positive inotropic and chronotropic activity.42

Onset. Immediate.

Duration. Half-life < 5 minutes.

Clinical Considerations. Epinephrine is the primary medication used for acute resuscitation in patients who present in cardiac arrest.41 It also is indicated for patients with hypotension and septic shock. Epinephrine is recommended as a second-line medication for bradycardia, after a trial with atropine.9 It is first-line therapy for the management of anaphylaxis.30

Adverse Effects and Contraindications. There are no absolute contraindications to epinephrine use. It can precipitate and potentially worsen ischemia. It should be used with caution in patients with severe cardiac disease. Similar caution should be used in patients with thyroid disease, pheochromocytoma, or other similar sympathomimetic syndromes. Adverse effects include tachycardia and tachyarrhythmia, increased myocardial demand, palpitations, hypertension, dizziness, cerebral hemorrhage, headache, tremors, diaphoresis, nausea, vomiting, dyspnea, pulmonary edema, and anxiety.30

Glucagon. Glucagon increases cAMP production, increasing inotropy and chronotropy in the myocardium.30

Onset: IV. Eight to 18 minutes.

Duration. 60 to 90 minutes.

Clinical Considerations. Glucagon is an option for the management of bradyarrhythmias due to calcium channel blocker and beta-blocker toxicity. It has a short half-life, so an infusion is needed after the initial dose. The dose of glucagon is quite high and may deplete hospital supplies. Therefore, it is important to use adjunct inotropes.43,1

Adverse Effects and Contraindications. A common adverse effect of glucagon administration is nausea and vomiting, making airway protection essential in hemodynamically unstable patients.35 Other effects include hypotension, tachycardia, hypersensitivity reactions, and anaphylaxis. Contraindications include pheochromocytoma, insulinoma, adrenal insufficiency, or chronically malnourished patients.30

AV Nodal Blockers

Adenosine. Adenosine is an AV nodal blocker resulting in a transient cessation of impulse transmission from the atria to the ventricle. It prevents the influx of calcium and forces an efflux of potassium from the cell, creating a temporary AV block.30

Onset. Immediate.

Duration. Half-life of adenosine is
≤ 10 seconds; no risk of accumulation.13

Clinical Considerations. Although it has a short half-life, it is considered first line after failure of vagal maneuvers for SVT. It should be administered in a proximal vein as a rapid push dose, followed by a rapid saline flush. Many patients will report a “sense of impending doom” when given this medication due to the sensation of the cardiac pause from the AV blockade. Adenosine is safe and effective to use during pregnancy and would not be expected to cause harm to the fetus.30

Adverse Effects and Contraindications. Patients should be made aware of potential side effects of adenosine, including facial flushing, chest pain, bronchospasm with dyspnea, hypotension, AV block, cardiac dysrhythmia, and cardiac arrest. Adenosine is contraindicated for patients with a heart transplant because of concern for prolonged asystole.13 It also is contraindicated in patients with WPW because of concern for degeneration into VF.13 Avoid adenosine in patients with asthma, COPD, and tachyarrhythmias with irregularity or a wide QRS complex with suspected accessory tract.13,30 AV nodal-blocking drugs, including adenosine, should be avoided if AVRT or pre-excited AF is suspected.30

Diltiazem. Diltiazem is a calcium channel blocker. It has direct effects on the AV node by blocking L-type calcium channels. This results in a negative inotropic effect, resulting in a slower heart rate.30

Onset. IV bolus: three minutes.

Duration. If given as an IV bolus, duration is 1 to 3 hours; if used as a continuous infusion, its duration after discontinuation can last anywhere from 0.5 to 10 hours.

Clinical Considerations. Diltiazem is used for rate control in patients with rapid ventricular rate associated with atrial fibrillation/flutter or in terminating paroxysmal SVT. Use of a lower dose, or giving calcium before the drug, may prevent hypotension.44,45 AV nodal-blocking drugs, including diltiazem, should be avoided if AVRT or pre-excited AF is suspected.30

Adverse Effects and Contraindications. Diltiazem may result in hypotension or precipitate heart block, or it may cause negative inotropic effects.13 Because of its negative inotropic effects, diltiazem can exacerbate symptoms of acute heart failure from LV systolic dysfunction or decompensated HF.18,21 Additionally, in patients with AF, an accelerated ventricular rate with hypotension or ventricular fibrillation can occur.18 It is generally not recommended to combine calcium channel blockers with beta-blockers (administered in the ED or interactions with home medications) since this could lead to complete heart block.30

Esmolol. Esmolol is a cardioselective beta-blocker and class II antiarrhythmic. It competitively blocks beta-1 receptors with little to no effect on beta-2 receptors. It is effective in terminating narrow QRS complex reentrant tachyarrhythmias involving the AV node. This subsequently reduces ventricular rates, particularly for atrial flutter and fibrillation.30

Onset. IV: Two to 10 minutes.

Duration. 10-30 minutes. May be prolonged following repeated doses resulting in the extended duration of the medication.

Clinical Considerations. Esmolol can be used for SVT as well as atrial fibrillation or flutter. A reduced dose may be needed for the elderly since esmolol may cause significant bradycardia in this population. AV nodal-blocking drugs, including esmolol, should be avoided if AVRT or pre-excited AF is suspected.30

Adverse Effects and Contraindications. Contraindications to use include heart block, sick sinus syndrome, decompensated heart failure, severe bradycardia, or cardiogenic shock. Esmolol should not be used in patients with pulmonary hypertension or in combination with calcium channel blockers. Adverse effects include hypotension, hyperkalemia, nausea, vomiting, dizziness, peripheral ischemia, confusion, agitation, headache, and infusion site reaction.30

Metoprolol. Metoprolol is a beta-blocker and class II antiarrhythmic; it competitively blocks beta-1 receptors with little to no effect on beta-2 receptors. It is effective in terminating narrow QRS complex reentrant tachyarrhythmias involving the AV node. This subsequently reduces ventricular rates, particularly for atrial flutter and fibrillation.30

Onset. 20 minutes (when it is infused over 10 minutes).

Duration. Variable depending on formulation; typically less than six hours.

Clinical Considerations. Metoprolol is a beta-blocker that is beta-1 selective.16 It can be used in SVT, AF, atrial flutter, MI (typically given once admitted), and hypertension. It is indicated in patients with AF with rapid ventricular response (RVR).16 AV nodal-blocking drugs, including metoprolol, should be avoided if AVRT or pre-excited AF is suspected.30

Adverse Effects and Contraindications. Metoprolol can cause central nervous system (CNS) depression resulting in subsequent impairment in mental and physical abilities. Precautions typically are given to patients who are taking this medication chronically. It is contraindicated in patients with heart block. Because of its beta-1 selectivity, patients with pulmonary disorders, including bronchospastic disease, ideally should not receive beta-blockers, although this beta-1 selective medication can be used with close monitoring. Care must be given with patients older than 65 years of age who may require smaller doses. Adverse effects include hypotension, dizziness, fatigue, diarrhea, depression, pruritus, rashes, AV block (most commonly first-degree), and dyspnea.30,31

Propranolol. Propranolol is a nonselective beta adrenergic blocker, class II antiarrhythmic. It blocks both beta-1 and beta-2 receptors, resulting in decreased heart rate and myocardial contractility with decreased myocardial oxygen demand and blood pressure. Because propranolol is nonselective, it also reduces portal pressure by causing splanchnic vasoconstriction. It is effective in terminating narrow QRS complex reentrant tachyarrhythmias involving the AV node. This subsequently reduces ventricular rates, particularly for atrial flutter and fibrillation.30,32

Onset. Oral: One to two hours. IV: Two to 10 minutes. For hypertension, the peak effect of oral medication takes days to weeks.

Duration. Variable based on formulation: Immediate release can last six to 12 hours. Extended release can last 24 to 27 hours.

Clinical Considerations. Propranolol can be used for AF, atrial flutter, AVNRT, or VT (due to catecholamine-induced release or digoxin toxicity).30,31

Adverse Effects and Contraindications. This medication should not be used in patients with hypersensitivity to beta-blockers. Additionally, it should not be used in patients with decompensated heart failure, sick sinus syndrome, bradyarrhythmias, or cardiogenic shock. AV nodal-blocking drugs, including propranolol, should be avoided if AVRT or pre-excited AF is suspected.30 Because it is a non-selective beta-blocker, it should also not be used in patients with bronchospastic disease. Elderly patients may require a reduced dose to prevent bradycardia. Adverse effects include serum glucose abnormalities, hyperkalemia, bradycardia, drowsiness, sleep disorders, cold extremities, and syncope.30,31

Verapamil. Verapamil is a calcium channel blocker. It is effective in terminating narrow QRS complex reentrant tachyarrhythmias involving the AV node.30,31

Onset. IV bolus: Three to five minutes.

Duration. 30 minutes to six hours.

Clinical Considerations. Verapamil has negative inotropic and chronotropic properties, which decreases myocardial oxygen demand, lowers systolic blood pressure, and slows conduction through the AV node. This subsequently reduces ventricular rates, particularly for atrial flutter and fibrillation.30

Adverse Effects and Contraindications. Verapamil can exacerbate heart failure because of its negative inotropic activity. Verapamil’s ability to slow cardiac conduction can exacerbate bradyarrhythmias in patients who have pre-existing sinus or AV nodal dysfunction. It is contraindicated in patients with bradyarrhythmias including sick sinus syndrome or second- or third-degree AV block. AV nodal-blocking drugs, including verapamil, should be avoided if AVRT or pre-excited AF is suspected.30 Verapamil is contraindicated in patients with severe heart failure, severe hypotension, or cardiogenic shock.13,18,21 It should not be used in patients receiving concurrent IV beta-blockers. IV verapamil should not be used in neonates and young infants, especially during SVT, because it can induce severe apnea, hypertension, bradycardia, and potentially cardiac arrest.

Pharmacologic Management to Terminate Tachyarrhythmias

Amiodarone. Amiodarone is a class III antiarrhythmic that prolongs the phase 3 of the cardiac action potential, but has properties of class I, II, and IV medications as well.10 It blocks voltage gated potassium channels, resulting in prolonged recovery time for atrial, Purkinje, and ventricular myocytes. It also slows the conduction time of the sinus and AV nodes.18,30,31,32

Duration. Long half-life of with a large volume of distribution in adipose tissue

Clinical Considerations. Amiodarone is used in new-onset AF and wide complex tachyarrhythmias. It is considered the most effective medication in the maintenance of sinus rhythm in patients with AF (both paroxysmal and persistent). Amiodarone is used in cardiac arrest in patients with VT or VF.18,30

Adverse Effects and Contraindications. In the ED, QT prolongation, hypotension, nausea, vomiting, dizziness, and acute respiratory distress syndrome can be seen. Amiodarone is contraindicated in patients with iodine hypersensitivity, second- or third-degree heart block, cardiogenic shock, and severe bradycardia.30

Digoxin. Digoxin causes increased myocyte contractility with increased cardiac output, and suppression of AV node conduction. Digoxin inhibits the sodium/potassium ATPase pump, which causes calcium influx, leading to increased contractility.19,46 Suppressing conduction through the AV node leads to an increased refractory period and decreased conduction velocity; this decreases heart rate.30

Onset. Oral one to two hours. IV: five to 60 minutes.

Duration. Half-life is 36-48 hours, duration is three to four days.30

Clinical Considerations. Digoxin is used for rate control in rhythms such as atrial fibrillation/flutter and AVNRT. It can be used in patients with heart failure. Hypokalemia, hypomagnesemia, and hypercalcemia can increase risk for digoxin toxicity. Additionally, there are many drug interactions including quinidine, verapamil, amiodarone, and nonsteroidal anti-inflammatory drugs (NSAIDs), which all can increase plasma digoxin levels and lead to toxicity. A disulfiram-like reaction can occur when combined with metronidazole. Finally, digoxin should not be used in patients with accessory pathways because this can lead to ventricular arrhythmias.30,31,47

Adverse Effects and Contraindications. Adverse effects include visual alterations (such as blurred vision or yellow halos), abdominal pain, nausea, vomiting, diarrhea, dizziness, headaches, confusion and delirium, generalized weakness, laryngeal edema, rashes, gynecomastia, and multiple arrhythmias, including junctional tachycardia, atrial tachycardia, heart block, VT/VF, bigeminy or trigeminy, and asystole.30,31,47

Flecainide. Flecainide is a class IC antiarrhythmic that blocks sodium channels located in the heart, slowing the upstroke of the cardiac action potential and the heart rate.48

Onset. Median time to conversion is four hours (one to six hours after oral ingestion).49 Faster conversion seen with IV administration.50

Duration. Half-life is 12-27 hours.49

Clinical Considerations. Flecainide is used for conversion of new-onset atrial flutter or fibrillation in patients with structurally normal hearts, with up to 92% conversion rate.48,50 It should be used with caution in patients with congestive heart failure, coronary artery disease (CAD), renal or liver disease, and certain arrhythmias, such as atrial flutter, infranodal conduction disease, and Brugada syndrome.18 It also is used in preventing and treating ventricular arrhythmias, such as ventricular ectopy and tachycardias. In addition to AF/atrial flutter, flecainide can be used for other AVNRTs, such as WPW.49 It is contraindicated in patients with LV dysfunction.18,30

Adverse Effects and Contraindications. Common adverse effects include palpitations, nausea, dizziness, headache, blurred vision, visual flashes/floaters, dyspnea, and fatigue. More serious adverse effects include cardiac arrest, dysrhythmias such as atrial flutter with 1:1 AV conduction, prolonged QT interval, syncope, torsades de pointes, VT/VF, and new or worsening congestive heart failure. This medication should be avoided in patients with significant structural heart disease, second- or third-degree AV blocks, coronary artery disease, and chronic AF.18,30,31

Ibutilide. Ibutilide is a class IC drug. It acts as a voltage gated potassium channel blocker, which prolongs the recovery of the myocytes of the atrium, Purkinje fibers, and ventricles.32

Onset. Conversion to normal sinus rhythm should be within 90 minutes after starting the infusion. The success rate is 51-58.9% in conversion to sinus rhythm from AF and 76% from atrial flutter.51,52

Duration. Half-life is variable between two to 12 hours, with a mean of approximately six hours.

Clinical Considerations. Ibutilide is used for conversion of new-onset atrial flutter or AF. It is the only FDA-approved IV drug for conversion of AF to sinus.14,18,53 However, it does have an increased risk of ventricular arrhythmias, particularly sustained polymorphic VT.53,54 This risk can be lessened by using high doses of magnesium prophylactically. The median time to conversion is 20-30 minutes.52-55

Adverse Effects and Contraindications. Ibutilide should be avoided in patients with electrolyte abnormalities such as marked hypokalemia, ECG abnormalities such as QT prolongation (defined as initial QTc > 450 ms because of the potential for torsades de pointes), and in those heart failure patients with a very low ejection fraction (EF) of < 30%.14 Its use in these patients can result in the risk of ventricular proarrhythmia.18 There are many potential medication interactions. Adverse effects include hypotension, bradyarrhythmia, heart block, and ventricular arrhythmias.30

Lidocaine. Lidocaine is a class IB antiarrhythmic that blocks the fast voltage gated sodium channels.10

Onset. After bolus dose: 45-90 seconds.

Duration. 10-20 minutes.

Clinical Considerations. Lidocaine is considered third line for VT and VF. It can be used in cardiac arrest patients with shock-refractory VT/VF. It can be proarrhythmic. It should be used cautiously in patients with heart failure, liver disease, respiratory depression/hypoxia, shock, or a history of malignant hyperthermia. Ensure electrolytes are within normal ranges prior to use and during treatment, particularly potassium and magnesium. Elderly patients may be more prone to CNS and cardiovascular adverse effects.30,31

Adverse Effects and Contraindications. Lidocaine is contraindicated in patients with Adam-Stokes syndrome, WPW, high-degree heart block (except in those patients with functioning pacemaker), lidocaine hypersensitivity or allergy, and corn allergy (premixed injection can contain corn-derived dextrose). Adverse effects include methemoglobinemia, headache, agitation, anxiety, bradycardia, metallic taste, hyper-/hypo-esthesia, psychosis, tinnitus, tremors, bronchospasm, respiratory depression, hallucinations, nausea, vomiting, and coronary artery vasospasm.30,31

Magnesium Sulfate. Magnesium decreases the excitability of the cardiac membrane. It also aids in the movement of other electrolytes in and out of cells, including sodium, potassium, and calcium. Additionally, magnesium decreases the sinus node depolarization frequency and prolongs the AV node refractory period.22

Onset. IV is immediate.

Duration. Variable.

Clinical Considerations. Although typically used for hypomagnesemia repletion, asthma exacerbation and eclampsia/preeclampsia, magnesium sulfate also has antiarrhythmic properties. It can be used in torsades de pointes and for a prolonged QT interval. Emerging literature indicates synergy in the use of magnesium sulfate with antiarrhythmic drugs for controlling rapid AF, although the optimal dosage is unclear.22 Use caution with renal dysfunction; patients may need a dose reduction by 50%.30

Adverse Effects and Contraindications. Minor side effects of flushing and lightheadedness may occur during infusion. Some side effects of magnesium sulfate are rate-related; rapid infusion may result in hypotension and cardiovascular collapse. Look for signs of hypermagnesemia by monitoring vital signs, deep tendon reflexes, respiratory status, mental status, potassium and calcium levels, and renal function. It is contraindicated in patients with heart block.30,31

Procainamide. Procainamide is a class IA antiarrhythmic. It rapidly blocks intracellular and extracellular sodium channels.10 This increases the refractory period, reduces excitability in the conduction system by increasing the electrical stimulation threshold of the ventricles, and inhibits ectopic pacemaker activity.10,30,32

Onset. 10-30 minutes, peak concentration 15-60 minutes.

Duration. Has a 52-65% conversion rate of new-onset AF to sinus rhythm, frequently within one hour.48,56,57 The elimination half-life is three to four hours.

Clinical Considerations. Procainamide is used to treat acute wide complex tachyarrhythmias and new-onset AF. In AF, it is used in the conversion to normal sinus rhythm. Careful monitoring of QTc and QRS is important as procainamide can cause an increase in these intervals.30

Adverse Effects and Contraindications. Hypotension is the most common adverse effect of procainamide. Contraindications include second- or third-degree AV block, torsades de pointes, and systemic lupus erythematosus. It should be used cautiously in patients with acute ischemic heart disease, heart failure, liver disease, myasthenia gravis, renal impairment, first-degree AV block, QT prolongation.30,53,56

Propafenone. Propafenone is a class IC antiarrhythmic that stabilizes the myocardial membranes. It acts as an intracellular calcium channel blocker.30,32

Onset. Time to peak concentration is three to eight hours. The median time to conversion is two hours, with 56-83% conversion rate.58

Duration. Half-life two to 10 hours.

Clinical Considerations. Propafenone is used for conversion of new-onset atrial flutter or fibrillation in patients with structurally normal hearts (off-label). It is used to prevent recurrence of AF or paroxysmal supraventricular tachycardia.18 Propafenone also is used for catecholaminergic polymorphic VT.32

Adverse Effects and Contraindications. Common adverse effects of propafenone include chest pain, edema, palpitations, anxiety, dyspnea, fatigue, nausea, vomiting, constipation, dizziness, taste alteration. More serious adverse effects include asystole, dysrhythmias, heart failure, QTc prolongation or torsades de pointes, SLE, thrombosis, renal failure, respiratory failure, cerebrovascular accident (CVA), agranulocytosis, and hepatomegaly.58 Contraindications include bradycardia, severe COPD/asthma, Brugada syndrome, cardiogenic shock, heart failure, severe electrolyte imbalances, liver disease, significant hypotension, and conduction disorders without a pacemaker.18 Propafenone should be avoided with medications that can prolong the QT interval, class IA or III antiarrhythmics. There is a proarrhythmic risk in patients with structural or ischemic heart disease. The Cardiac Arrhythmia Suppression Trial (CAST) showed treatment with class IC antiarrhythmic medications had an increased rate of death in patients with left ventricular dysfunction after myocardial ischemia compared with placebo.30,59

Vernakalant (not approved for use in the United States at the time of publication). Vernakalant is a class III antiarrhythmic medication. It acts as a multi-ion channel blocker. It blocks early-activating potassium channels and the acetylcholine-activated potassium channel, combined with blockage of early-activating sodium channels. It results in a prolonged atrial refractory period and rate-dependently slows atrial conduction, with minimal effect on ventricular repolarization.53,60,61

Onset. Rapid.

Duration. Rapidly and extensively distributed, IV half-life is two to three hours.53,60

Clinical Considerations. Vernakalant is a novel antiarrhythmic agent used for rapid conversion of new-onset atrial flutter or fibrillation, but it is not approved yet in the United States for treatment.62 It has a preferential effect on atrial tissue, making it an ideal medication in the conversion of AF to sinus rhythm.61,62 It was found to be effective in 50-60% of patients following IV administration.32,53,60 Median time to conversion is eight to 14 minutes, with a potential for early hospital discharge.53,60,62 Because of the relative atrial selectivity, vernakalant also has a very low risk of arrhythmias.53

Adverse Effects and Contraindications. Adverse effects of vernakalant include bradycardia, hypotension, sinus arrest, ventricular extrasystoles, urinary retention, troponin elevation, recurrence of AF, dysgeusia, sneezing, paresthesias, nausea, pruritus, and cough.53,60 The most common side effects were sneezing, paresthesias, and dysgeusia during infusion; they were short-lived and resolved spontaneously.60 It should be avoided in patients with hypotension, acute coronary syndrome within 30 days, severe aortic stenosis, and prolonged QT interval.30

Management63

The specific management of the arrhythmia depends on the rhythm identified.

Tachyarrhythmia is defined by Advanced Cardiac Life Support (ACLS) as HR ≥ 150 bpm. If the patient is unstable or has cardiac ischemia, electrical synchronized cardioversion is indicated.

If a narrow complex regular rhythm is seen, the energy level should be set to 50-100 Joules (J). However, if the patient is in a narrow complex irregular rhythm, 120-200 J for biphasic cardioversion (200 J monophasic) should be used. If the patient is in a wide-complex rhythm that is regular, choose 100 J. However, if the patient is in a wide complex irregular rhythm and unresponsive, defibrillation doses should be used, and the rhythm should not be cardioverted but defibrillated. (See Table 3.)

Table 3. ACLS Recommendation of Energy Dosage Based on ECG Characteristics

Characteristics of QRS

Rhythm

Synchronized?

Joule Recommendations

Narrow complex

Regular

Yes

50-100 Joules

Narrow complex

Irregular

Yes

120-200 Joules

Wide complex

Regular

Yes

100 Joules

Wide complex

Irregular

No

Defibrillate at 200 Joules

For stable patients in a regular narrow QRS complex tachycardia, defined as a QRS complex < 120 ms, vagal maneuvers, modified Valsalva maneuver, or isometric contractions can be attempted.11,13,23 If this is unsuccessful, adenosine can be considered.13

For a wide complex tachycardia in a patient, a variety of medications can be used, including procainamide, amiodarone, or sotalol, based on the 2017 AHA guidelines.10

For stable patients who are found in rapid atrial fibrillation or flutter, the initial focus of therapy is rate control.10,15 Traditional teaching in emergency medicine is that early cardioversion within 48 hours of AF onset is acceptable. New literature recommends early cardioversion in patients who present after this 48-hour window but who have been started on anticoagulation (such as an Xa or direct thrombin inhibitor) within 24 hours of AF symptom onset. Patients who have been chronically anticoagulated during the prior four weeks do not need to wait.14

Both metoprolol and diltiazem are used for management of this arrhythmia, with studies showing mixed results.15,64 For use in heart failure patients with reduced EF, the optimal medication is controversial. According to the 2014 American College of Cardiology recommendation, calcium channel antagonists, such as diltiazem, should not be used in patients with decompensated HF because these may lead to further hemodynamic compromise.18 The American College of Emergency Physicians (ACEP) has a new point-of-care AF tool that can be used during clinical shifts to aid in the management of AF or atrial flutter patients (https://www.acep.org/patient-care/afib/).65 For patients who are asymptomatic with bradycardia, treatment is generally not needed.

For patients who shows signs of instability (defined as hypotension, altered mental status, signs of shock, ischemic chest pain, or acute heart failure), immediate intervention is needed. Atropine is the first-line medication used for symptomatic bradycardia. An alternative is transcutaneous/transvenous pacing or starting an antiarrhythmic or vasoactive infusion. For patients in whom transcutaneous pacing or medications are not successful, transvenous pacing should be considered.10

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