Bradycardia

Paul C. Riggle and Richard W. Harper

Bradycardia, which is defined as a heart rate below 60 beats/minute, results from abnormalities in impulse formation or failure of atrioventricular (AV) conduction. As with all arrhythmias, the physician managing bradycardia must simultaneously address resuscitation and other management issues while identifying the specific cause.

Approach

 In the evaluation of bradycardia, focus on the clinical status of the patient and not on the absolute heart rate. The important tasks in managing bradycardia are to treat life-threatening symptoms, identify the specific bradyarrhythmia, and determine the underlying cause.

 A. Symptomatic bradycardia. Manifestations include hypotension, pulmonary edema, altered mentation, myocardial ischemia, or acute myocardial infarction (MI) (1).

 B. Bradycardia can be classified as primary or secondary. Primary bradycardia, which is seen 15% of the time, is caused by an intrinsic defect in the generation or conduction of an impulse. Secondary causes, which are seen 85% of the time, result from to factors extrinsic to the conduction system (2).

 1. Primary bradycardia is encountered more often in elderly patients and may be a manifestation of sick sinus syndrome.

2. Secondary bradycardia can be caused by the following:

a. Acute coronary ischemia

b. Nonischemic cardiovascular disease (e.g., dilated cardiomyopathies and cardiac tamponade)

c. Metabolic derangements (e.g., hypothyroidism, hypoadrenalism, hyperkalemia, hypercalcemia, hypermagnesemia)

 d. Pharmacologic effects (β-adrenergic blockers, calcium channel blockers, digoxin, α-adrenergic agonist, and cholinergic agents)

History

 A. Symptoms. Bradyarrhythmias may or may not cause symptoms. When symptoms do occur, they are caused by either an awareness of the irregular rhythm (palpitations) or a reduced cardiac output (lightheadedness, syncope, fatigue, shortness of breath, or chest pain) (3) (Chapter 7.9).

 B. Exercise tolerance. Ask patients about their level of physical fitness. In the well-conditioned patient, impulse generation in the sinus node is often slowed.

C. Underlying conditions. It is important to determine any underlying medical conditions that can cause bradycardia [e.g., ischemic heart disease (IHD), cardiomyopathies, previous arrhythmias, rheumatic heart disease, or thyroid disease].

D. Medications. Typical medications associated with bradycardia include digoxin, phenothiazines, quinidine, procainamide, beta-blockers, calcium channel blockers, clonidine, reserpine, methyldopa, flecainide, encainide, propafenone, and lithium.

E. Cardiac risk factors. Elicit risk factors for coronary heart disease (family history, tobacco use, hypercholesterolemia, diabetes, or hypertension).

Physical examination

A. Vital signs. Heart rate and blood pressure determine the immediacy of treatment.

 B. Inspection, palpation, and auscultation. Bradycardia is best revealed on physical examination by inspection of the jugular pulses, palpation of the arterial pulse, and auscultation of the heart. Inspection of the jugular pulses is vital in the evaluation of bradycardia, and they often reveal atrial activity. For example, cannon waves are seen intermittently in complete heart block as the atrium contracts against a closed tricuspid valve. Palpation of the arterial pulse establishes the conducted ventricular rate. Auscultation establishes ventricular rate and rhythm. The intensity of S ₁ is an important heart sound in the evaluation of bradycardia. A soft S₁ suggests a first-degree AV block. A variation in S₁ intensity suggests second- or third-degree AV block. In third-degree AV block, the intensity of heart sounds is augmented when an atrial systole immediately precedes ventricular contraction.

 C. Associated conditions. The physical examination should include an assessment for evidence of cardiac decompensation (e.g., jugular venous distension, pulmonary crackles, lower extremity edema, gallops, murmurs), and thyroid disease.

Testing

A. Electrocardiogram (ECG). It is essential to obtain an ECG when evaluating a patient with bradycardia. Usually, a resting ECG is sufficient, but occasionally an ambulatory (Holter) monitor or exercise ECG is indicated. Atrial activity is best assessed in leads II, III, aVf, and V₁. The presence of P waves, their configuration, and their relationship to QRS complexes must be established. Normally, the PR interval is between 0.12 and 0.20 seconds and each QRS complex is preceded by a P wave (5).

B. Laboratory. The following tests should be considered when appropriate:

1. Electrolytes: potassium, calcium, and magnesium

2. Drug levels: digoxin, quinidine, and procainamide

3. Thyroid function tests

Diagnostic assessment

The key to the diagnosis of bradycardia is a focused history, physical examination, and an ECG. No specific symptoms will separate the various causes of bradycardia.

A. Sinus bradycardia

1. Etiology. Normal (well-conditioned athletes), sleep, carotid sinus massage, glaucoma, increased intracranial pressure, and an acute inferior wall myocardial infarction.

 2. ECG. Normal P-QRS-T sequence at a rate less than 60 beats/minute (5).

 B. Sinus node exit block (sinoatrial node block, SA block).

 1. Etiology. Medications (digitalis, quinidine, procainamide, salicylates), hyperkalemia, cardiomyopathy, IHD, and vagal stimulation or increased vagal tone.

 2. ECG. A missing P wave is the hallmark of SA block. The prolonged PP interval must be a multiple of the baseline PP interval; otherwise it is called a sinus pause.

a. Incomplete SA block: occasional absence of P-QRS-T sequence.

 b. Complete SA block: P waves absent, QRS-T sequence present but at a slow rate, QRS interval varies depending on the origin of the escape pacemaker (5).

 C. Sick-sinus syndrome is a generalized abnormality of cardiac impulse formation and intraatrial and AV conduction abnormalities that can be manifested by various combinations of brady- and tachyarrhythmias (4).

1. Etiology. Idiopathic fibrosis or degeneration of sinoatrial and AV conduction system, IHD, amyloidosis, surgical injury, and hypertension. More prevalent in the geriatric population (4).

2. ECG. The hallmark is sinus nodal depression, including sinus bradycardia, sinus arrest, and sinoatrial exit block. Also seen are AV node dysfunction, and atrial fibrillation or atrial tachyarrhythmias with slow ventricular response (5).

 D. First-degree AV block is defined as a prolonged PR interval. The block may be caused by a prolongation of conduction in any of the structures between the SA node and His bundle.

 1. Etiology. Found in well-conditioned people (long distance runners, heavy laborers), elderly patients; other causes include increased vagal tone (pain, vomiting, vasovagal syncope), medications (digitalis, quinidine, procainamide, propranolol, verapamil), acute rheumatic fever, myocarditis, and congenital heart disease (4).

 2. ECG. PR interval greater than 0.20 seconds. Each P wave followed by a QRS complex (5).

 E. Second-degree AV Block, Mobitz I (Wenckebach), is characterized
by intermittent failure of conduction from atria to ventricles with progressive lengthening of the PR interval, eventually leading to a nonconducted P wave.

 1. Etiology. Normal variant occurs in well-conditioned people; causes include medications (digitalis, beta-blockers, calcium blockers, clonidine, methyldopa, flecainide, encainide, propafenone, lithium), MI (especially inferior MI), acute rheumatic fever, and myocarditis (4).

 2. ECG. PR interval progressively increases and the RR interval shortens until a nonconducted P wave occurs. Typically, small groups of beats occur, such as pairs and trios (5).

 F. Second-degree AV Block, Mobitz II, is characterized by intermittent
failure of conduction from atria to ventricles where appropriately timed
P waves fail to conduct and no pattern is seen of progressive PR lengthening.

 1. Etiology. Almost always secondary to organic heart disease (4).

 2. ECG. PR interval is fixed with intermittent, nonconducted P waves. Conducted P waves with the same PR interval. Often it is associated with a bundle branch block (5).

 G. Third degree block is defined as no atrial impulses reaching the ventricle through the AV conduction system.

 1. Etiology. Causes include congenital heart block (maternal anti-Ro antibodies), cardiomyopathy, IHD, aortic valve disease, endocarditis, Lyme disease, infiltrative processes (amyloid, sarcoid), medications (digitalis, quinidine, procainamide), hyperkalemia, connective tissue disease, trauma, and acute rheumatic fever (4).

 2. ECG. No AV conduction occurs. The atrial rate is faster than the ventricular rate. PP and RR intervals are constant: numerous P waves are seen, which occur at all phases of the ventricular cycle (5).

References

1. Emergency Cardiac Care Committee and Subcommittee, American Heart Association. Guidelines for cardiopulmonary resuscitation and emergency cardiac care. JAMA 1992;268:2171–2302.

2. Brady Jr WJ, Harrigan RA. Evaluation and management of bradyarrhythmias in the emergency department. Emerg Med Clin North Am 1998;16:361–388.

3. Alexander RW, Schlant RC, Fuster V. Bradydysrhythmias in the heart. New York: McGraw-Hill 1998:927–941.

4. DiMarco JP. Cardiac arrhythmias and conduction disorders. In: Freed M, Grimes C, ed. Essentials of cardiovascular medicine. New York: Physician’s Press 1994:137–138, 168, 181–185.

5. Marriott HJL. Practical electrocardiography, 8th ed. Baltimore: Williams & Wilkins, 1988:371, 353–376.

Book Source Details

• Book Title: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter
• Author(s): Robert B. Taylor (editor)
• Year of Publication: 2000
• Copyright Details: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, Copyright © 2000 Lippincott Williams & Wilkins.

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Copyright Details: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, Copyright © 2008 Williams & Wilkins.

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More About This Book: Title: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter Authors: Robert B. Taylor (editor) Publisher: Lippincott Williams & Wilkins Copyright: 2000 ISBN: 0-78172-094-X

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