Atrial fibrillation rate control
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2] Anahita Deylamsalehi, M.D.[3]
Overview
Atrial fibrillation with rapid ventricular rate is a common finding in many hospitalized patients. The ventricular rate may be increased up to 150-170. It is essential to bring the ventricular rate down to less than 110 because a rapid ventricular response can cause hemodynamic instabilities and tachycardia mediated cardiomyopathies (heart failure). AF can cause disabling and annoying symptoms. Palpitations, angina, lassitude (weariness), and decreased exercise tolerance are related to rapid heart rate and inefficient cardiac output caused by AF. This can significantly increase mortality and morbidity, which can be prevented by early and adequate treatment of the AF.
Rate Control
Rate control is the first step should be taken in treatment of patients with atrial fibrillation. Based on NICE guideline the exception of this rule is the following conditions:[1]
- If atrial fibrillation is due to a reversible condition
- When heart failure due to atrial fibrillation has developed
- In new onset atrial fibrillation
- In the presence of a atrial flutter that could be restored to sinus rhythm with ablation therapy
- In conditions that clinical judgment prefer rhythm control
Pharmacologic Rate Control
- The ventricular rate in atrial fibrillation is a major determinant of symptoms and hemodynamic consequences.[1]
- The ventricular rate is usually reduced by using atrioventricular nodal-blocking agents. First-line therapies include a standard beta blockers (a beta blocker except sotalol) and nondihydropyridine calcium-channel blockers (verapamil and diltiazem).[1]
- Specific adverse effects of each medication should be taken into consideration when choosing appropriate therapy for each individual patient.
- If monotherapy with the aforementioned drugs are not effective, combination therapy with 2 of the following should be considered in order to achieve appropriate rate:[1]
Mechanism of Action
- Rate control is achieved with medications that work by increasing the degree of the block at the atrioventricular node, effectively decreasing the number of impulses that conduct to the ventricles. This can be accomplished with:
- Calcium channel blockers (diltiazem or verapamil) block the influx of calcium and reduce the upstroke of the action potential.
- Beta blockers (preferably the cardioselective beta blockers such as metoprolol, atenolol, bisoprolol) slow conduction by decreasing sympathetic tone.
- Cardiac glycosides (i.e. digoxin) are vagomimetics and slow conduction by increasing parasympathetic effects on the node.
- Amiodarone is a class III anti-arrhythmic drug which also has atrioventricular node blocking effects. Amiodarone can be used for rate control when other agents are contraindicated or ineffective. The classic situation where amiodarone would be used is when a patient is hypotensive (often septic), but also in atrial fibrillation with rapid ventricular response. Beta blockers and calcium channel blockers are not ideal due to negative inotropic effects. Amiodarone has less negative inotropy and is preferred for this situation.
Beta Blockers
Acute Beta Blocker Therapy
- Intravenous beta blocker like metoprolol and esmolol.
- Useful when atrial fibrillation is secondary to high adrenergic tone like in post operative situations.
Metoprolol
- Dose 2.5-5 mg over 2 minutes.
- Route - Intravenous.
- Maximum dose 15 mg.
- Doses can be repeated over 5 minutes interval.
Esmolol
- Short duration of action (10-20 min).
- Metabolized by RBC esterases.
- Advantage - It can be used in conditions where patients' response and tolerance to beta blocker are uncertain. If there is a concern that beta blocker may cause decompensated heart failure, hypotension, or bradycardia, the short half-life of esmolol permits a therapeutic trial to check the patient's response. Based on that the patient is started on other long-acting beta blocker.
- Doses
- Infusion at a rate of 50 µg/kg per min, with an increase in the rate of administration by 50 µg/kg per min every 30 minutes.
- Some hospitals prefer starting with a bolus of 0.5 mg/kg over one minute, followed by an infusion of 50 µg/kg per min. Monitor for four minutes. Another bolus is given followed by an [Intravenous therapy|infusion]] of 100 µg/kg per min, in case of inadequate response within 4 minutes. In case of inadequate response, a third bolus can be given followed by an [Intravenous therapy|infusion]] at 150 µg/kg per min rate. The maximum [Intravenous therapy|infusion]] that can be given is 200 µg/kg per min.
Chronic Beta Blocker Therapy
- Oral beta blockers are preferred for the treatment of chronic atrial fibrillation.
- Commonly used agents are atenolol or metoprolol
- Atenolol dose - 25 mg per day. The maximum dose permitted is 200 mg per day.
- Metoprolol dose - 25mg to 200mg of short-acting (metoprolol tartrate) twice a day or 50mg to 400mg of long-acting (metoprolol succinate) daily. Metoprolol succinate is the preferred form due to convenience.
- Carvedilol or metoprolol succinate should be used in patients with chronic heart failure with reduced ejection fraction since these agents are also indicated for heart failure with reduced ejection fraction.
Adverse Effects of Beta Blocker Therapy
- Fatigue
- Congestive heart failure: beta blockers are indicated for chronic treatment of heart failure with reduced ejection fraction, but in the short term they risk causing decompensation of tenuous patients due to negative inotropic effects.
- Hypotension
- AV block
- Bradycardia
- Bronchospasm
Calcium Channel Blockers
- Nondihydropyridine calcium channel blockers such as verapamil and diltiazem (Cardizem) are commonly used.
- Calcium-channel blockers may be used in combination with beta-blockers if the beta blockers alone is not sufficient in achieving rate control. However, hypotension may complicate combination therapy in particular in the elderly.
- Diltiazem is common used as a drip for acute rate control when patients present with rapid ventricular response
- Dose 15-20mg once, then start drip at 10mg/minute
- Diltiazem can be transitioned from a drip to a short-acting oral form (given 4x daily), then a long-acting form (given daily)
- Verapamil is less commonly used but is also available as both PO and intravenous therapy formulations.
Digoxin
- Digoxin is a cardiac glycoside with positive inotropic and AV nodal blocking properties (which increases vagal tone at the atrioventricular node).
- Can be useful in patients with heart failure since it is the only positive inotrope that blocks the [[atrioventricular node]. Beta-blockers and calcium channel blockers are negative inotropes.
- Less favored than beta-blockers or calcium channel blockers due to narrow therapeutic index and concerns about increased mortality in atrial fibrillation patients treated with digoxin in the TREAT-AF study [2]
- Digoxin monotherapy could be considered the first line treatment for rate control in non-paroxysmal atrial fibrillation in the presence of the following:[1]
- Patients with no or minimal physical exercise
- Patient preference
- Contraindication or exclusion of other rate control treatments due to other concurrent diseases
2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation (DO NOT EDIT)[3]
Rate Control
| Class I |
| "1. Control of the ventricular rate using a beta blocker or nondihydropyridine calcium channel antagonist is recommended for patients with paroxysmal, persistent, or permanent atrial fibrillation. (Level of Evidence: B) " |
| "2. Intravenous administration of a beta blocker or nondihydropyridine calcium channel blocker is recommended to slow the ventricular rate in the acute setting in patients without pre-excitation. In hemodynamically unstable patients, electrical cardioversion is indicated. (Level of Evidence: B) " |
| "3. In patients who experience atrial fibrillation-related symptoms during activity, the adequacy of heart rate control should be assessed during exertion, adjusting pharmacological treatment as necessary to keep the ventricular rate within the physiological range. (Level of Evidence: C) " |
| Class III: Harm | |
| "1. AV nodal ablation with permanent ventricular pacing should not be performed to improve rate control without prior attempts to achieve rate control with medications. (Level of Evidence: C)" | |
| "2. Nondihydropyridine calcium channel antagonists should not be used in patients with decompensated heart failure as these may lead to further hemodynamic compromise. (Level of Evidence: C)" | |
| "3. In patients with pre-excitation and atrial fibrillation, digoxin, nondihydropyridine calcium channel antagonists, or intravenous amiodarone should not be administered as they may increase the ventricular response and may result in ventricular fibrillation. (Level of Evidence: B)" | |
| "4. Dronedarone should not be used to control the ventricular rate in patients with permanent atrial fibrillation as it increases the risk of the combined endpoint of stroke, [[ST elevation myocardial infarction | MI]], systemic embolism, or cardiovascular death. (Level of Evidence: B)" |
| Class IIa |
| "1. A heart rate control (resting heart rate <80 bpm) strategy is reasonable for symptomatic management of atrial fibrillation. (Level of Evidence: B)" |
| "2. Intravenous amiodarone can be useful for rate control in critically ill patients without pre-excitation. (Level of Evidence: B)" |
| "3. AV nodal ablation with permanent ventricular pacing is reasonable to control the heart rate when pharmacological therapy is inadequate and rhythm control is not achievable. (Level of Evidence: B)" |
| Class IIb |
| "1. A lenient rate-control strategy (resting heart rate <110 bpm) may be reasonable as long as patients remain asymptomatic and left ventricle systolic function is preserved. (Level of Evidence: B)" |
| "2. Oral amiodarone may be useful for ventricular rate control when other measures are unsuccessful or contraindicated. (Level of Evidence: C)" |
Sources
- 2011 ACCF/AHA/HRS Focused Updates Incorporated Into the ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation [4]
- 2011 ACCF/AHA/HRS Focused Update on the Management of Patients With Atrial Fibrillation (Updating the 2006 Guideline) [5]
Rhythm Control
Rate Control versus Rhythm Control
- Rate control treatments seek to reduce the heart rate to normal while allowing the patient to remain in atrial fibrillation. A goal of < 110bpm (lenient rate control) is usually targeted, since patients do not seem to do any better with stricter control[6].
- Rhythm control seeks to restore the normal heart rhythm, called normal sinus rhythm. Options for rhythm control include anti-arrhythmic medications (flecainide, amiodarone, sotalol, and others), catheter-based ablation procedures, and surgical ablation procedures.
- Rate control with anticoagulation was found to be non-inferior to rhythm control in terms of mortality outcomes in the AFFIRM Trial.[7]
- AFFIRM also showed no reduction in risk of stroke with rhythm control strategy compared to rate control with anticoagulation.[7]
- Based on this evidence, a rhythm control strategy is no longer pursued in most atrial fibrillation patients, since the anti-arrhythmic drugs can have serious side effects and catheter or surgical ablation procedures have risks as well.
- Rhythm control may be desired when the patient is significantly symptomatic despite rate control, or if the patients cannot tolerate rate control medications.
References
- ↑ 1.0 1.1 1.2 1.3 1.4 Perry M, Kemmis Betty S, Downes N, Andrews N, Mackenzie S, Guideline Committee (2021). "Atrial fibrillation: diagnosis and management-summary of NICE guidance". BMJ. 373: n1150. doi:10.1136/bmj.n1150. PMID 34020968 Check
|pmid=value (help). - ↑ Mintu P. Turakhia, MD, MAS∗; Pasquale Santangeli, MD†; Wolfgang C. Winkelmayer, MD, MPH, ScD§; Xiangyan Xu, MS∗; Aditya J. Ullal, BA∗; Claire T. Than, MPH∗; Susan Schmitt, PhD∗; Tyson H. Holmes, PhD‖; Susan M. Frayne, MD, MPH∗; Ciaran S. Phibbs, PhD∗; Felix Yang, MD∗∗; Donald D. Hoang, BA∗; P. Michael Ho, MD, PhD††; Paul A. Heidenreich, MD, MS. Increased Mortality Associated With Digoxin in Contemporary Patients With Atrial FibrillationFindings From the TREAT-AF Study. JACC 2014;64(7):660-668.
- ↑ 3.0 3.1 January, C. T.; Wann, L. S.; Alpert, J. S.; Calkins, H.; Cleveland, J. C.; Cigarroa, J. E.; Conti, J. B.; Ellinor, P. T.; Ezekowitz, M. D.; Field, M. E.; Murray, K. T.; Sacco, R. L.; Stevenson, W. G.; Tchou, P. J.; Tracy, C. M.; Yancy, C. W. (2014). "2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society". Circulation. doi:10.1161/CIR.0000000000000041. ISSN 0009-7322.
- ↑ Fuster V, Rydén LE, Cannom DS, Crijns HJ, Curtis AB, Ellenbogen KA et al. (2011) 2011 ACCF/AHA/HRS focused updates incorporated into the ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation: a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. Circulation 123 (10):e269-367. DOI:10.1161/CIR.0b013e318214876d PMID: 21382897
- ↑ Wann LS, Curtis AB, January CT, Ellenbogen KA, Lowe JE, Estes NA; et al. (2011). "2011 ACCF/AHA/HRS focused update on the management of patients with atrial fibrillation (Updating the 2006 Guideline): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines". Heart Rhythm. 8 (1): 157–76. doi:10.1016/j.hrthm.2010.11.047. PMID 21182985.
- ↑ Isabelle C. Van Gelder, M.D., Hessel F. Groenveld, M.D., Harry J.G.M. Crijns, M.D., Ype S. Tuininga, M.D., Jan G.P. Tijssen, Ph.D., A. Marco Alings, M.D., Hans L. Hillege, M.D., Johanna A. Bergsma-Kadijk, M.Sc., Jan H. Cornel, M.D., Otto Kamp, M.D., Raymond Tukkie, M.D., Hans A. Bosker, M.D., Dirk J. Van Veldhuisen, M.D., and Maarten P. Van den Berg, M.D., for the RACE II Investigators* Lenient versus Strict Rate Control in Patients with Atrial Fibrillation. NEJM 2010; 362:1363-1373 April 15, 2010DOI: 10.1056/NEJMoa1001337
- ↑ 7.0 7.1 Wyse DG, Waldo AL, DiMarco JP, Domanski MJ, Rosenberg Y, Schron EB, Kellen JC, Greene HL, Mickel MC, Dalquist JE, Corley SD (2002). "A comparison of rate control and rhythm control in patients with atrial fibrillation". N Engl J Med. 347 (23): 1825–33. PMID 12466506