Bradycardia medical therapy

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: M.Umer Tariq [2] Ibtisam Ashraf, M.B.B.S.[3] Nehal Eid, M.D.[4]

Overview

Medical treatment of bradycardia is categorized into emergent and permanent. Usually, sinus bradycardia treatment is not recommended for asymptomatic patients. Correcting underlying electrolyte or acid-base deficiencies or hypoxia in symptomatic patients. Intravenous atropine can temporarily help symptomatic patients.

2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society

Procedural / Surgical Therapy

Temporary Pacing

Temporary Pacing for AV Block

Class IIa

1. For patients with second-degree or third-degree atrioventricular block associated with symptoms or hemodynamic compromise that is refractory to medical therapy, temporary transvenous pacing is reasonable to increase heart rate and improve symptoms. (Level of Evidence: B-NR)

2. For patients who require prolonged temporary transvenous pacing, it is reasonable to choose an externalized permanent active fixation lead over a standard passive fixation temporary pacing lead. (Level of Evidence: B-NR)

Class IIb

1. For patients with second-degree or third-degree atrioventricular block and hemodynamic compromise refractory to antibradycardic medical therapy, temporary transcutaneous pacing may be considered until a temporary transvenous or permanent pacemaker is placed or the bradyarrhythmia resolves. (Level of Evidence: B-R)

Temporary pacing is used to acutely treat bradycardia causing hemodynamically significant instability, such as prolonged and symptomatic pauses, life-threatening ventricular arrhythmias mediated by bradycardia, or severe symptomatic bradycardia attributable to a reversible cause with the goal to avoid permanent pacemaker implantation. Reported adverse event rates associated with temporary transvenous pacing range from 14% to 40%, including venous thrombosis, pulmonary emboli, life-threatening arrhythmias, loss of capture (10%–37%), perforation, and death. Temporary transvenous pacing should be used for the minimum duration necessary to provide hemodynamic support or back-up pacing to prevent asystole. If atrioventricular block is felt to be irreversible and the means to place a permanent pacing system is available, it may be best for the patient to avoid temporary pacing and proceed directly to permanent system implantation.

Analgesic and/or anxiolytic agents should be considered in conscious patients undergoing transcutaneous pacing, and effective capture must be assessed by pulse or arterial waveform acquired by noninvasive or invasive means.

Temporary Pacing for SND

Class IIa

1. In patients with persistent hemodynamically unstable SND refractory to medical therapy, temporary transvenous pacing is reasonable to increase heart rate and improve symptoms until a permanent pacemaker is placed or the bradycardia resolves. (Level of Evidence: C-LD)

Class IIb

1. In patients with SND with severe symptoms or hemodynamic compromise, temporary transcutaneous pacing may be considered to increase heart rate and improve symptoms until a temporary transvenous or permanent pacemaker is placed or the bradycardia resolves. (Level of Evidence: C-LD)

Class III (Harm)

1. In patients with SND with minimal and/or infrequent symptoms without hemodynamic compromise, temporary transcutaneous or transvenous pacing should not be performed. (Level of Evidence: C-LD)

Recommendations for Atropine and Beta Agonists for Bradycardia Attributable to SND

Class IIa

1.In patients with SND associated with symptoms or hemodynamic compromise, atropine is reasonable to increase sinus rate.(Level of Evidence: C-LD)

Class IIb

1.In patients with SND associated with symptoms or hemodynamic compromise who are at low likelihood of coronary ischemia, isoproterenol, dopamine, dobutamine, or epinephrine may be considered to increase heart rate and improve symptoms. (Level of Evidence: C-LD)

Recommendations for Atropine and Beta Agonists for Bradycardia Attributable to AV Block

Class IIa

1. In patients with second-degree or third-degree atrioventricular block associated with symptoms or hemodynamic compromise, atropine is reasonable to increase heart rate and improve symptoms. (Level of Evidence: C-LD)

Class IIb

1. In patients with second-degree or third-degree atrioventricular block associated with symptoms or hemodynamic compromise who are at low likelihood of coronary ischemia, isoproterenol, dopamine, dobutamine, or epinephrine may be considered to increase heart rate and improve symptoms. (Level of Evidence: C-LD)

Class III (Harm)

1. In patients who have undergone heart transplant without evidence for autonomic reinnervation, atropine should not be used to treat sinus bradycardia. (Level of Evidence: C-LD)

Recommendations for Therapy of Beta Blocker and Calcium Channel Blocker Mediated Bradycardia

Class IIa

1.In patients with bradycardia associated with symptoms or hemodynamic compromise because of calcium channel blocker overdose, intravenous calcium is reasonable to increase heart rate and improve symptoms. (Level of Evidence: C-LD)

2. In patients with bradycardia associated with symptoms or hemodynamic compromise because of beta- blocker or calcium channel blocker overdose, glucagon is reasonable to increase heart rate and improve symptoms. (Level of Evidence: C-LD)

3. In patients with bradycardia associated with symptoms or hemodynamic compromise because of beta- blocker or calcium channel blocker overdose, high-dose insulin therapy is reasonable to increase heart rate and improve symptoms. (Level of Evidence: C-LD)

Recommendations for Therapy of Digoxin Mediated Bradycardia Attributable to SND or Atrioventricular Block

Class IIa

1.In patients with bradycardia associated with symptoms or hemodynamic compromise in the setting of digoxin toxicity, digoxin Fab antibody fragment is reasonable to increase heart rate and improve symptoms. (Level of Evidence: C-LD)

Recommendations for Theophylline/Aminophylline for Bradycardia Attributable to SND

Class IIa

1.In post-heart transplant patients, aminophylline or theophylline is reasonable to increase heart rate if clinically indicated. (Level of Evidence: C-LD)

2. In patients with SND associated with symptoms or hemodynamic compromise in the setting of acute spinal cord injury, aminophylline or theophylline is reasonable to increase heart rate and improve symptoms. (Level of Evidence: C-LD)

Medical Therapy

Initial Management

The initial management of symptomatic bradycardia focuses on both supporting perfusion and identifying and reversing the underlying cause(s).

Assessment of stability:

Determine whether the patient is hemodynamically stable or unstable

Assess for signs of poor perfusion: hypotension, acutely altered mental status, signs of shock, ischemic chest discomfort, acute heart failure

Evaluate for and treat reversible causes: myocardial ischemia, hypoxemia, hypothermia, electrolyte abnormalities, medications/toxins

Reversible causes:

Patients presenting with symptomatic bradycardia secondary to a reversible cause should first be managed by directing therapy at eliminating or mitigating the offending condition (Class I, LOE: C-EO). When sinus bradycardia is the consequence of nonessential medications, permanent cardiac pacing should not be considered a first-line treatment; withdrawal of the offending drug or dosage reduction can improve the heart rate and symptoms.

Atropine

Atropine is a parasympatholytic drug that enhances atrioventricular nodal conduction and sinus node automaticity.

Dose: 0.5 to 1.0 mg IV, may repeat every 3 to 5 minutes

Maximum dose: 3 mg total

Onset: Rapid (within minutes)

Duration: Approximately 2 hours

Cautions:

Atropine is unlikely to improve atrioventricular block at the His bundle or His-Purkinje level and isolated reports have suggested occasional worsened atrioventricular conduction and/or hemodynamic compromise in such patients; it should be used judiciously in patients with AV block and wide QRS complexes

In patients who have undergone heart transplant without evidence for autonomic reinnervation, atropine should not be used to treat sinus bradycardia (Class III: Harm)

Adverse effects include dry mouth, blurred vision, anhidrosis, urinary retention, and delirium

Excessive increase in heart rate may be problematic in patients with acute MI

Beta-Adrenergic Agonists

For patients with symptomatic bradycardia and hemodynamic compromise who have low likelihood for coronary ischemia, beta-adrenergic agonists may be considered (Class IIb):

Drug	Dose	Notes
Epinephrine	2–10 mcg/min IV infusion, titrated to hemodynamic response	Strong alpha- and beta-adrenergic effects; increases chronotropy, inotropy, blood pressure, and myocardial oxygen consumption
Dopamine	5–20 mcg/kg/min IV infusion	At lower doses (1–2 mcg/kg/min), predominantly vasodilatory; at 5–20 mcg/kg/min, enhanced chronotropy and inotropy predominate; higher doses may cause vasoconstriction and proarrhythmias
Isoproterenol	1–20 mcg/min IV infusion	Nonselective beta-adrenergic agonist; potent chronotropic and inotropic effects; may cause peripheral vasodilation and hypotension; increases myocardial oxygen demand; should be avoided in patients with active coronary ischemia
Dobutamine	5–20 mcg/kg/min IV infusion	Predominantly beta-1 adrenergic agonist; increases inotropy and chronotropy; may cause hypotension at lower doses due to beta-2 mediated vasodilation

Drug-Specific Antidotes

When bradycardia is caused by specific drug toxicity, targeted antidotes should be considered:

Offending Drug	Antidote	Dose
Beta blockers	Glucagon	3–10 mg IV bolus; may follow with infusion of 3–5 mg/h; titrate to clinical response
Calcium channel blockers	Calcium chloride or calcium gluconate	Calcium chloride 10%: 1–2 g IV over 10 minutes; calcium gluconate 10%: 3–6 g IV over 10 minutes; may repeat as needed
Calcium channel blockers / Beta blockers	High-dose insulin euglycemic therapy	Regular insulin 1 unit/kg IV bolus, then 1–10 units/kg/h infusion; concurrent dextrose infusion to maintain euglycemia; monitor serum glucose and potassium closely
Digoxin	Digoxin-specific antibody fragments (Digibind/DigiFab)	Dose based on estimated total body digoxin load; each vial (40 mg) binds approximately 0.5 mg of digoxin; for acute ingestion of known amount: number of vials = (total digitalis body load in mg) × (1.6) / (0.5); for chronic toxicity with known steady-state level: number of vials = (serum digoxin concentration in ng/mL) × (weight in kg) / 100

Chronic Management

There are two main reasons for treating bradycardia:

1. With bradycardia, the first is to address the associated symptoms, such as fatigue, limitations on how much an individual can physically exert, fainting (syncope), dizziness or lightheadedness, or other vague and non-specific symptoms.
2. The other reason to treat bradycardia is if the person's ultimate outcome (prognosis) will be changed or impacted by the bradycardia.

Treatment in this vein depends on whether any symptoms are present, and what the underlying cause is. Primary or idiopathic bradycardia is treated symptomatically if it is significant, and the underlying cause is treated if the bradycardia is secondary.

Symptoms

Yes→ Hemodynamically Stable

Uncertain/no→ No immediate treatment Consider additional diagnostic testing: Ambulatory ECG ETT TSH

No→ IV atropine 0.5mg IV push; Can be repeated every three to five minutes upto 3mg total

Yes→ Signs/Symptoms of acute MI

Do HR and symptoms improve?

Yes→ Treat Accordingly

No→ Check for other causes (TSH, infection)

No→ Temporary Pacemaker

Yes→ Monitor

Contraindicated medications

Persistently severe bradycardia is considered an absolute contraindication to the use of the following medications:

• Acebutolol
• Atenolol
• Carvedilol
• Metoprolol
• Nebivolol
• Pindolol
• Propafenone
• Timolol
• Labetalol

Symptomatic bradycardia (except in patients with a functioning artificial pacemaker) is considered an absolute contraindication to the use of the following medications:

• Adenosine