Atrial Fibrillation

Discussions of drug therapy in atrial fibrillation (Afib) are often centered on the ongoing debate of rate versus rhythm control strategy.[1,2] From the numerous publications including the AFFIRM, RACE, and corresponding meta-analyses, neither strategy has been proven clearly beneficial when compared to the other.[3-6] While the nuances of these studies, and the interventions in question, are hotly debated topics, their discussion revolves around outpatient Afib management. Any attempt at extrapolation of these data to acute management of Afib is flawed since these studies did not include patients in the extremes of acute Afib. Rather, these data examined the chronic treatment strategies of Afib. It’s not that this isn’t a valid discussion, it is simply the wrong context for the ED.

The debate of rate versus rhythm control in the emergency department shares some similarities, but also, important differences to the aforementioned clinical context. When considering rate or rhythm control in acute Afib in the ED, the patient’s clinical status generally guides, if not dictates, the treatment pathway. Patients who are hemodynamically unstable (further defined below) self select into the rhythm control pathway with electrical cardioversion. Whereas patients who are stable, generally receive a ventricular rate control strategy while the underlying cause of Afib is identified. While this is simply a generalization, it roughly accounts for the vast majority of patients presenting to EDs.

But the debate persists with each camp promoting their respective risks versus benefits.[1,2] In the rhythm control proponents, the argument centers on the need to convert Afib to normal sinus since Afib is an abnormal rhythm, which lowers quality of life further worsened by rate control drugs (beta-blockers and calcium channel blockers), causes structural and electrical cardiac remodeling, and anticoagulation carries a 4-9% risk of bleeding.[7] The rate control camp contends that electrical or pharmacological cardioversion itself carries a risk of thromboembolic event and should not be performed since a TEE is often not feasible to rule out the presence of a clot in the left atrium and/or therapeutic anticoagulation has not been achieved. Furthermore, the options for pharmacologic rhythm control are fraught with serious adverse events that patients rarely tolerate and will end up on rate control anyways. Ultimately, the debate rages on, but does it necessarily apply to the management of Afib with RVR in the ED?

In this chapter, we will examine the drug therapies for patients with Afib presenting to the emergency department. Rather than centering the discussion on rate versus rhythm and which is superior, we will examine patient cases that are most common in the ED and tie in the most common clinical scenarios encountered as a result of Afib.

66 year old male presents via EMS for palpitations that have been coming and going for a week (history of hypertension, diabetes, COPD). On the monitor, the patient appears to be in atrial fibrillation with a rate of 155 bpm, blood pressure of 110/80 mmHg, normal temp, 100% on room air. After an EKG confirms Afib with rapid ventricular response (RVR), the physician orders an initial bolus of diltiazem followed by an infusion. What’s the best dose for this patient?

Acute rate control

There are three main strategies for acute rate control of Afib with RVR in the ED: non-dihydropyridine calcium channel blockers (CCB), beta-blockers (BB), and digoxin.[8-12] Despite Afib with RVR being one of the most commonly encountered arrhythmias in the ED, there is very little high quality evidence guiding pharmacotherapy. Our treatment strategies are guided by the current understanding of Afib with RVR and clinical experience. In Afib with RVR, the atrial conduction sends overwhelming depolarizations to the AV node with anywhere from three hundred to six hundred impulses every minute. The inherent refractory period of the AV node limits the number of depolarizations to the ventricle, however, given the sheer number of atrial depolarizations, the ventricular response becomes irregular. When this irregular ventricular rate increases to 150-170 beats per minute, an already compromised cardiac output from poor ventricular filling is exacerbated by the even shorter filling time and poor stroke volume. Hypoperfusion can occur, if the ventricular rate is not addressed in short order.

Before discussing the ideal agent to control ventricular rate, we must first understand the goal of therapy. With rate control strategies of Afib with RVR in the ED, the goal is to lower the ventricular rate to a sufficient degree such that adequate diastole takes place. While there is limited evidence specifically addressing patients in the ED for goal HR, a lenient strategy of a target ventricular rate of less than than 110 beats per minute versus a more strict control (between 80-110) seems reasonable.[13]

When considering the available drug therapy options, an ideal agent would work rapidly to slow the ventricular rate, be easily titratable and short duration of action, but without causing untoward adverse events with concomitant comorbid diseases. While some references discuss the left ventricular ejection fraction (LVEF) as an element to guide therapy, this information is rarely available in the ED.[12] If patients have a documented LVEF on record, it may help, however, it may not be representative of the current hemodynamics. Similarly, comorbid disease states such as asthma, or existing CHF, are considerations in drug selection, not relative contraindications.[8] This nuance of nomenclature should come with the understanding there has been a conscious discussion of the risks of treatment with the potential benefits. Nevertheless, an ideal agent is nothing but a fantasy, and we must select the best of the agents we have: CCBs, BBs, and digoxin.[8]

Non-dihydropyridine calcium channel blockers

Diltiazem and verapamil are the CCBs that are options for ventricular rate control of Afib in the ED. Categorized as class IV antiarrhythmic drugs in the Vaughan Williams classification, these agents increased refractoriness of nodal tissues.[9-11] If you recall the cardiac conduction cycles, and the flow of electrolytes during depolarization, you’ll notice that there are different patterns depending on the type of cardiac tissue in question. While muscle tissue electrical pathways follow the common “side profile of batman” pattern, nodal tissue has a different pattern.

Cardiac nodal tissue (SA and AV nodes) electrical conduction tissues are less negative at rest than non-pacemaker cells and they can also spontaneously depolarize due to slow calcium and sodium influx during phase 4. By blocking these L-type calcium channels, phase 4 is prolonged, thereby increasing the time between depolarizations. This improvement of refractoriness in the AV nodal tissue, decreases the number of depolarizations that make it through to the ventricles. There is also some slowing of the conduction of the depolarization through the ventricles. The end result is a prolonged diastole and improved cardiac output, despite the atrial still in fibrillation.

Controlling of this ventricular rate can be accomplished using CCBs including diltiazem and verapamil. These CCBs have primarily cardiac effects, and do not produce significant vasodilation at normal doses. With escalating doses, however, vasodilation can occur. The AHA support the use of CCBs in patients with Afib and heart failure with preserved ejection fraction (HFpEF), but recommend beta-blockers or digoxin in patients with heart failure with reduced ejection fraction (HFrEF).[8] It’s a common misconception that the guidelines do not recommend CCBs in HFrEF. This is not the case, the guidelines do not make any such statement. In patients with Afib with HFrEf, beta-blockers may be used with caution, or digoxin or amiodarone be selected. These recommendations come with the same level of evidence and strength of recommendation.

Diltiazem is commonly used in EDs for rate control give its extensive history in clinical experience. Traditional dosing is 0.25 mg/kg followed by 0.35 mg/kg, and a subsequent infusion rate between 5-15 mg/hr. More recent evidence suggests that lower bolus doses of 0.1 mg/kg or fixed 10 mg doses may achieve the same lenient rate control goals, without excessive adverse events.[14] Despite it’s relatively long half-life of approximately 4 hours, the onset of IV administration of diltiazem is 3 minutes. Diltiazem is metabolized hepatically by CYP-3A4 to numerous metabolites.

Verapamil is not commonly used in the ED as a result of concerns for more pronounced decreases in blood pressure compared to diltiazem. However, this is a misconception. This belief is held from a prospective, randomized, double-blind, crossover study in 17 men with Afib or atrial flutter.[15] Patients received either diltiazem or verapamil bolus (20 mg then 25 mg vs 5 mg then 10 mg, respectively) followed by infusions for 8 hours, with appropriate wash out and crossover procedures. There was no significant difference between systolic blood pressures after bolus dosing and during infusions with a mean change SBP of -9.7 +/- 11.5% for diltiazem and -2.9 +/- 7.7% for verapamil. Three (n=15) patients who received verapamil, and zero in the diltiazem (n=10) arm had hypotension. One patient in the verapamil group experienced clinically significant hypotension, seizures and EKG changes after the second verapamil bolus, but was discharged with no long term sequelae. It was noted this patient had an LVEF of 20%. Therefore, in this small, limited study, verapamil may cause more hypotension than diltiazem, but this is based on 3 adverse events.

Verapamil for Afib is dosed at 0.1 mg/kg (or 5 to 10 mg) over at least 2 minutes; if no response, an additional 10 mg bolus after 15 to 30 minutes may be given.[12] A continuous infusion of 5 mg/hour is the initial starting rate. Similar to diltiazem, verapamil has a rapid onset when given IV (~3-5 minutes) and a half-life of ~5 hours, with metabolites after hepatic CYP metabolism.

The threshold systolic blood pressure that is clinically defined as ‘unstable’ to hypotensive, necessitating a rhythm control strategy is poorly defined. Taking a single metric alone, without considering the complete clinical picture is a fundamentally flawed approach. Therefore, in patients with SBP in the 90-100’s, it may be reasonable to attempt to use CCB as a rate control strategy before electing for cardioversion. One complementary intervention is the use of push-dose pressors, namely phenylephrine, in this scenario. Bedside titration of intermittent phenylephrine boluses, may allow for adequate vascular support while the ventricular rate is controlled. Consistent with the paucity of evidence guiding therapies for Afib with RVR in the ED, this approach is reasonable under close supervision of experts.

As for which agent is preferred is a matter of uncertainty. The only head to head literature is the aforementioned study in 17 men.[15] Similarly, it is unclear from the available evidence whether CCBs or BBs are the preferred agents for rate control.


Beta-blockers slow cardiac conduction by binding to beta-1 receptors in cardiac nodal tissue, and cardiac muscle tissue.[9,10] In nodal tissue, BBs prevent the activation of a depolarization through the sympathetic nervous system. But in the event of a lack of sympathetic stimulation, BBs can decrease phosphorylation of L-type calcium channels through inhibition of cAMP activated protein kinase A. While the predominant mechanism in acute Afib depends on nodal tissue inhibition, decreasing intracellular calcium may also play a role.

The most commonly used BB for Afib in the ED is metoprolol. Metoprolol should be given in a dose of 2.5 to 5 mg every 5 minutes to a maximum of 15 mg.[9,10] Unlike diltiazem, there is no conversion to a continuous infusion. In such cases, either immediate release oral metoprolol could be used, or an infusion of esmolol. Similar to CCBs, caution should be taken in patients with HFrEF, but also patients with reactive airway disease (aka asthma). Esmolol and propranolol may be used in certain circumstances: propranolol in thyrotoxicosis or thyroid storm, and esmolol in circumstances where a 9 minute half-life is desired.[9,10]

In terms of clinical evidence comparing BBs to CCBs, there is limited head to head data. Two small studies have compared metoprolol to diltiazem in acute management of Afib. In one study, there was no difference in patient-oriented outcomes between the two agents.[16] The most recent comparison randomized patients in a double-blinded manner to metoprolol or diltiazem for Afib in the ED. This study demonstrated more rapid rate control with diltiazem than with metoprolol at 30 min (95.8% vs. 46.4%).[17] While these data support the common clinical practice of diltiazem use, more data is needed to confirm it’s role.


Digoxin is known to inhibit the sodium-potassium ATPase channel in cardiac myocytes, thereby leading to an increased calcium concentration in the cell, ultimately augmenting contractility as well as increasing the slope of phase 4 and increasing automaticity.[9,10] These effects, however, are not the intended mechanism by which digoxin is useful in Afib with RVR. Digoxin in this role inhibits calcium currents in AV nodal tissue and activation of acetylcholine-mediated potassium currents in the atrium causing a hyperpolarization, shortening of atrial action potential, and increases in AV nodal refractoriness.[9,10] This ultimately will permit ventricular diastole and promote improved perfusion.

Loading doses of digoxin are necessary for this effect to take place. The ‘loading dose’ is administered over numerous hours.[9,10] The typical dosing regimen for patients with normal renal function is a IV bolus of 0.5 mg followed by 0.25 mg IV every 6 hours until a total of 1 mg or 1.5 mg is achieved. This prolonged administration comes with a delayed onset of action and time to maximum efficacy. While the onset of some observed benefit is somewhere around 30 minutes, the maximal effect on rate control may not be seen for up to 24 hours. This, coupled with the low therapeutic index of digoxin, its renal dose adjustments, and drug interactions limit the use of digoxin for Afib in the ED.


Another interesting contrasting element of the discussion of rate versus rhythm control between outpatient and ED management is anticoagulation. In the outpatient/less acute realm, a limitation of rate control strategy is the need for systemic anticoagulation for the duration of the arrhythmia.[8] With this potential reduction in the risk of ischemic stroke, there to is an increase in risk of hemorrhage, which varies depending on the particular drug used, and patient specific factors. In acute Afib management, however, rhythm control strategies require immediate anticoagulation followed by a 4 month course. Although rate control strategies require anticoagulation, the timeline in which to initiate this therapy is not as urgent as establishing control of the ventricular rate. Most often, anticoagulant strategies are not determined until after the ED stay in patients receiving rate control.

Bottom line:

Diltiazem is commonly used in the ED for rate control, but verapamil, metoprolol and esmolol are all reasonable choices

Digoxin works, but tomorrow.

Anticoagulation is important, but also tomorrow.

Expanded rate control

Magnesium sulfate

Calcium gluconate for CCBs with low SBP

Rhythm control

Hemodynamically unstable patients are getting shocked. Hemodynamically unstable patients are those in whom there is the presence of end organ hypoperfusion i.e. presence of ischemic cardiac symptoms, altered mental status). [12] These unstable patients are candidates for electrical cardioversion with synchronized cardioversion irrespective of duration of dysrhythmia. Here the best drug therapy is sedation and analgesia, followed by anticoagulation.

44 year old male presents to the ED for palpitations that started today. He has no history of palpitations, and is otherwise healthy. His vital signs are all within normal limits, except for heart rate which is 168 bpm and an EKG shows Afib with RVR. Is flecainide a useful drug for this patient?

The discussion of rhythm control requires appropriate establishment of context. As briefly outlined previously, patients who are hemodynamically unstable presenting with Afib with RVR most often require rhythm control via electrical cardioversion.[9] Elective cardioversion, where patients are hemodynamically stable is a more complex discussion. If this rhythm control strategy is selected, patients undergoing electrical or antiarrhythmic drug therapy for Afib lasting at least 48 hours or for an unknown duration, they require anticoagulation with oral anticoagulation (warfarin or a DOAC) should be given for at least 3 weeks before cardioversion is performed.[9] This scenario is not one that would be managed by the ED. Nor would patients undergo a transesophageal echocardiogram (TEE) prior to cardioversion in the ED. Aggressive rhythm control protocols such as the Ottawa Aggressive protocol, rely on the relative low risk of thromboembolic risks and elect for rhythm strategies with oral propafenone or flecainide.[18,19] Recent evidence suggests supports this low risk of complications and that the risk of thromboembolic complications is 0.7% when cardioversion is performed without anticoagulation within 48 hours of Afib onset, which is consistent with previous evidence.[20,21]

Pharmacologic rate control

Although electrical cardioversion generally has a higher rate of successful restoration of sinus rhythm (~90%), pharmacologic strategies are often attempted first. While the rate of successful cardioversion is closer to 60% with drug therapy, successful cardioversion may be more likely if conducted within 7 days of onset of Afib.[9] Of the available antiarrhythmic agents, the Vaughn Williams class III agents (amiodarone, ibutilide and dofetilide), the class ICs (flecainide and propafenone), may be used for cardioversion of Afib.

In general, the IC agents should only be used for rhythm control in patients with ‘lone’ Afib. The concern, based on the CAST study, is that underlying ‘structural heart disease,’ hypertension, ischemia or heart failure may have an increased risk of mortality.[22] In patients with these risk factors, amiodarone or ibutilide are reasonable, and some resources suggest procainamide is an option as well.[12] However, the warnings generated from CAST extend to all Class I antiarrhythmics, including procainamide.[23] If procainamide is selected, CCBs or BBs may be given to prevent paradoxical increases in the ventricular rate (vagolytic response), with a target of 100 to 120 beats per minute.[12] However, this recommendation is inconsistent in the literature.[11]

Sodium channel blockers


As a Class Ia antiarrhythmic, procainamide blocks open sodium channels, slowing the velocity conduction. In addition to sodium channel blockade, procainamide also inhibits outward potassium flow and prolongs the action potential. Through decreased automaticity in nodal tissues, refractory periods are prolonged. These mechanisms are reflected on the EKG by prolonging the QRS and the QT intervals.

Procainamide has numerous complications with its use. It can cause peripheral vasodilation from it’s ganglion-blocking effects and based on the rate of IV administration. The dosing recommendations for procainamide must be viewed with the knowledge that this drug was once a component of ACLS. The loading dose of procainamide should be given at a rate between 20 to 50 mg/minute until one of the following criteria are met: a total of 17 mg/kg is given, the QRS increases by 50%, hypotension occurs, or the arrhythmia is controlled (ie sinus). At which point an infusion of 1-4 mg/hour may be initiated.

While procainamide itself is a potent sodium channel blocker, its metabolite, NAPA (N-acetyl procainamide), is a potassium channel blocker, with a longer half-life and can induce a Lupus-like syndrome. While these effects are more likely with long term use of procainamide is associated with one of the highest rates of successful cardioversion (~60%) among drug therapy options.[24]

Flecainide and Propafenone

Flecainide and propafenone belong to the class IC agents and are known as sodium channels antagonists with slow unblocking properties. The effects of flecainide are primarily attributed to these slow recovery times from blockade. In the atria, the desired location for action in Afib, flecainide performs better and prolongs potentials at fast rates better than at slower rates of conduction. Flecainide can also block open ryanodine (RyR2) receptors on the sarcoplasmic reticulum, thus preventing calcium dependent calcium release. The effects seen on the EKG are PR, QRS and QT prolongation.

The role of flecainide in Afib is as an oral loading dose protocol, known as ‘pill in the pocket.’ In selected patients, who are maintained on a CCB or BB, if they feel palpitations or other symptoms of Afib, they can take one 300mg dose of flecainide (200mg if they’re less than 70 Kg) and follow up with their cardiologist.[25] Similar protocols have been adapted for use in the ED, where after diagnosis of new onset Afib and initiation of a CCB or BB, an oral loading dose of flecainide (or propafenone, see below) can be given with a first dose of DOAC. After which, patients may be discharged with close follow up, rather than hospital admission.

Flecainide, as with all Class I antiarrhythmics, carries the warning of increased mortality in patients with structural heart disease. Thus, outside of expert consultation, should only be used in patients with ‘lone’ Afib.


Propafenone shares many mechanistic similarities with flecainide: they are Class IC agents, and both are known as sodium channels antagonists with slow unblocking properties and potassium channel blocking properties. While flecainide is a racemic mixture with no significant difference, the enantiomers of propafenone share similarities in sodium channel properties, but differ in that S-propafenone has beta-blocking activity (it shares some similarities with propranolol), and R-propafenone blocks RyR2 channels.

Propafenone can induce a paradoxical increase in ventricular response in some Afib patients, which is why some recommend patients should be taking a CCB or BB prior to initiation. As a substrate of CYP2D6 and subject to significant first pass metabolism, there are numerous drug interactions possible with propafenone.

For pill in the pocket oral loading doses, propafenone should be given as the immediate release product at a dose of 600 mg (450 mg if the patient is less than 70 kg).[26] Consistent with flecainide, and as with all Class I antiarrhythmics, propafenone carries the warning of increased mortality in patients with structural heart disease. Thus, outside of expert consultation, should only be used in patients with ‘lone’ Afib.


Amiodarone is commonly thought of as a Class III antiarrhythmic pertaining to its potassium channel blocking activity. However, it actually possesses therapeutically relevant properties of all classes: sodium channel blocking, calcium channel blocking, and adrenergic blocking effects. This ‘broad spectrum’ antiarrhythmic, so to speak, can be used for a wide range of arrhythmias. For Afib, the recommended dose is different from what is commonly (possibly erroneously) given: 3-5 mg/kg IV over 15-20 minutes.[12] That equates to a dose of roughly 250-400 mg for the average 80 Kg adult (much higher than the 150 mg IV for ventricular arrhythmias for patients with a pulse). The reason for therapeutic failures of amiodarone in this setting is often a result of the incorrect dose being administered.

While amiodarone can be used in every case where Class I agents are ‘contraindicated’ (despite it too having sodium channel blocking properties), amiodarone comes with significant adverse events, drug interactions and therapeutic considerations. Since amiodarone is insoluble in water, it is suspended in polysorbate 80 which itself can cause hypotension and hypersensitivity reactions. Furthermore, since it is insoluble in water, further dilution in dextrose may cause precipitation, and an in-line filter is recommended for administration.

Amiodarone is roughly 37% iodine by weight. Thus, it can have significant impact on thyroid function, can cause corneal deposits, discoloration of soft tissues, but also affords amiodarone a huge volume of distribution. The numerous adverse events of amiodarone impact every organ system to some degree. Similar to the list of adverse events, amiodarone is a potent CYP inhibitor, PGP inhibitor, yielding many drug interactions. Yet, it has a long history of clinical experience and still commonly used today.

Dofetilide and Ibutilide

Dofetilide and ibutilide are class III antiarrhythmics.[27,28] Each agent exerts a dose-dependent block on the rapid component of the delayed rectifier potassium current, prolonging repolarization. The role of these agents is limited in the ED setting due to complications with the initiation of the drugs. With dofetilide, the QTc must be less than 440 msec and renal impairment with GFR less than 60 mL/min requires dose adjustments. Furthermore, serum electrolytes should be followed (particularly potassium and magnesium) and replaced as needed – ideally prior to initiation of dofetilide. The risks of not following these recommendations is torsades de pointe. As for ibutilide, similar considerations should be made prior to initiation.

Dofetilide is only available as an oral agent, where ase ibutilide only available as a parenteral agent. The role of either agent in the ED is limited, if not entirely absent.

Bottom line:

Rhythm control in the ED is not rhythm control for chronic management of Afib

For unstable patients, drugs are not the answer – DC cardioversion

For otherwise stable patients, oral loading dose of Ic agents, procainamide infusion or amiodarone loading are reasonable options.

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  2. Decker WW et al. Selecting Rate Control for Recent-Onset Atrial Fibrillation. Ann Emerg Med 2011; 57(1): 32 – 3.
  3. The Atrial Fibrillation Follow-Up Investigation of Rhythm Management (AFFIRM) Investigators. A comparison of rate control and rhythm control in patients with atrial fibrillation. N Engl J Med 2002;347:1825–1833.
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  12. Yealy D, Kosowsky JM: Dysrhythmias, in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 8. St. Louis, Mosby, Inc., 2010, (Ch) 79: p 1034-63.
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  19. Stiell IG, et al. Association of the Ottawa Aggressive Protocol with rapid discharge of emergency department patients with recent-onset atrial fibrillation or flutter. CJEM. 2010 May;12(3):181-91
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  21. Weigner MJ, Caulfield TA, Danias PG, Silverman DI, Manning WJ. Risk for clinical thromboembolism associated with conversion to sinus rhythm in patients with atrial fibrillation lasting less than 48 hours.Ann Intern Med. 1997 Apr 15;126(8):615-20.
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