Bradyarrhythmias is a topic covered in the Washington Manual of Medical Therapeutics.

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General Principles

  • Bradyarrhythmias are commonly encountered rhythms in the inpatient setting that result in a ventricular rate of <60 bpm.
  • Anatomy of the conduction system
    • The sinoatrial (SA) node is a collection of specialized pacemaker cells located in the high right atrium. Under normal conditions, it initiates a wave of depolarization that spreads inferiorly and leftward via atrial myocardium and intranodal tracts, producing atrial systole.
    • The wave of depolarization then reaches another grouping of specialized cells, the atrioventricular (AV) node, located in the lower right atrial side of the interatrial septum. Normally, the AV node should serve as the lone electrical connection between the atria and ventricles.
    • From the AV node, the wave of depolarization travels down the His bundle, located in the membranous septum, and into the right and left bundle branches before reaching the Purkinje fibers that depolarize the remaining ventricular myocardium.


Common causes of bradycardia are listed in Table 7-6.

Table 7-6: Causes of Bradycardia
Congenital disease (may present later in life)
Idiopathic degeneration (aging)
Infarction or ischemia
Infiltrative disease: sarcoidosis, amyloidosis, hemochromatosis
Collagen vascular diseases: systemic lupus erythematosus, rheumatoid arthritis, scleroderma
Surgical trauma: valve surgery, transplantation
Infectious disease: endocarditis, Lyme disease, Chagas disease
Autonomically mediated
Neurocardiogenic syncope
Carotid sinus hypersensitivity
Increased vagal tone: coughing, vomiting, micturition, defecation, intubation
Drugs: β-blockers, calcium channel blockers, digoxin, antiarrhythmic agents
Neurologic disorders: increased intracranial pressure
Electrolyte imbalances: hyperkalemia, hypermagnesemia
Hypercarbia/obstructive sleep apnea


Clinical Presentation

  • When evaluating a suspected bradyarrhythmia, one should efficiently use the history, physical examination, and available data to address stability, symptoms, reversibility, site of dysfunction, and need for temporary as well as permanent pacing.
  • If the patient is demonstrating signs of poor perfusion (hypotension, confusion, decreased consciousness, cyanosis, etc.), immediate management per ACLS protocol should be initiated. The clinical manifestations of bradyarrhythmias are variable, ranging from asymptomatic to nonspecific (lightheadedness, fatigue, weakness, exercise intolerance) to overt (syncope).
  • Emphasis should be placed on delineating whether the presenting symptoms have a direct temporal relationship to underlying bradycardia. Other historical points of emphasis include the following:
    • Ischemic heart disease, particularly involving the right-sided circulation, can precipitate a number of bradyarrhythmias. Therefore, signs and symptoms of acute coronary syndrome should always be thoroughly investigated.
    • Precipitating circumstances (micturition, coughing, defecation, noxious smells) surrounding episodes may help identify a neurocardiogenic etiology of bradycardia.
    • Tachyarrhythmias, particularly in patients with underlying sinus node dysfunction, can be followed by long pauses because of sinus node suppression during tachycardia. These are commonly referred to as conversion pauses.
    • History of structural heart disease, hypothyroidism, obstructive sleep apnea, collagen vascular disease, infections (bacteremia, endocarditis, Lyme, Chagas), infiltrative diseases (amyloid, hemochromatosis, and sarcoid), neuromuscular diseases, and prior cardiac surgery (valve replacement, congenital repair) should be elicited.
    • Medications should be reviewed with emphasis on those that affect the SA and AV nodes (i.e., calcium channel blockers, β-adrenergic blockers, digoxin).
  • After hemodynamic stability is confirmed, a more thorough examination with particular emphasis on the cardiovascular examination and any findings consistent with the above comorbidities is appropriate (Figure 7-3).
    Figure 7-3 Approach to bradyarrhythmias.
    Descriptive text is not available for this image

    ABG, arterial blood gas; ACLS, advanced cardiac life support; ↓BP, hypotension; CAD, coronary artery disease; CCB, calcium channel blocker; CHF, congestive heart failure; CP, chest pain; CVD, cerebrovascular disease; DOE, dyspnea on exertion; dz, disease; EPS, electrophysiologic study; HD, hemodynamic; HPI, history of present illness; ↓HR, bradycardia; Hx, history; ↑K, hyperkalemia; LH, lightheadedness; ↑Mg, hypermagnesemia; OSA, obstructive sleep apnea; PPM, permanent pacemaker; ↓SaO2, hypoxia; SND, sinus node dysfunction; SOB, shortness of breath; TSH, thyroid-stimulating hormone; VS, vital signs; VT, ventricular tachycardia.

    (Reprinted from Fansler D, Chen J. Bradyarrhythmias and permanent pacemakers. In: CuculichPS, KatesAM, eds. The Washington Manual Cardiology Subspecialty Consult. 3rd ed. Philadelphia, PA: Lippincott, Williams and Wilkins; 2014. with permission.)

Diagnostic Testing


Laboratory studies should include serum electrolytes and thyroid function tests in most patients. Digoxin levels and serial troponins should be drawn when clinically appropriate.


  • The 12-lead ECG is the cornerstone for diagnosis in any workup where arrhythmia is suspected.
  • Rhythm strips from leads that provide the best view of atrial activity (II, III, aVF, or V1) should be examined closely.
  • Emphasis should be placed on identifying evidence of SA node dysfunction (P-wave intervals) or AV conduction abnormalities (PR interval).

Special Considerations

  • Often, episodes of bradycardia are transient and episodic; therefore, a baseline ECG may not be sufficient to capture the bradycardia. Some form of continuous monitoring is often required.
    • In the inpatient setting, continuous central telemetry monitoring can be used.
    • If further workup is done as an outpatient, 24- to 72-hour Holter monitoring can be used if the episodes occur somewhat frequently. If infrequent, an event recorder or ILR should be considered.
    • It is vital to correlate symptoms with the rhythm disturbances discovered via continuous monitoring. Therefore, the importance of accurate symptom diaries in the ambulatory setting should be emphasized to patients.
  • To evaluate the sinus node’s response to exertion (chronotropic competence), walking the patient in the hallway or up a flight of stairs under appropriate supervision is easy and inexpensive. A formal exercise ECG can be ordered if necessary.
  • An EPS can also be used to assess sinus node function and AV conduction, but it is rarely necessary if the rhythm is already discovered via noninvasive modalities.

Differential Diagnosis

  • Sinus node dysfunction, or sick sinus syndrome, represents the most common reason for pacemaker implantation in the United States. Manifestations of sick sinus syndrome include the following (Figure 7-4):
    • Sinus bradycardia defined as a regular rhythm with QRS complexes preceded by “­sinus” P waves (upright in II, III, aVF) at a rate <60 bpm. Young patients and athletes often have resting sinus bradycardia that is well tolerated. Nocturnal heart rates are lower in all patients, but the elderly tend to have higher resting heart rates and sinus bradycardia is a far less common normal variant.
      Figure 7-4 Examples of sinus node dysfunction.
      Descriptive text is not available for this image

      A, Sinus bradycardia. The sinus rate is approximately 45 bpm. B, Sinoatrial node exit block. Note that the PP interval in which the pause occurs is exactly twice that of the nonpaused PP interval. C, Blocked premature atrial complexes. This rhythm is often confused for sinus node dysfunction or atrioventricular block. Note the premature, nonconducted P waves inscribed in the T wave that resets the sinus node leading to the observed pauses. D, Tachy-brady syndrome. Note the termination of the irregular tachyarrhythmia followed by a prolonged 4.5-second pause prior to the first sinus beat.

      (Reprinted from Fansler D, Chen J. Bradyarrhythmias and permanent pacemakers. In: CuculichPS, KatesAM, eds. The Washington Manual Cardiology Subspecialty Consult. 3rd ed. Philadelphia, PA: Lippincott, Williams and Wilkins; 2014 with permission.)

    • Sinus arrest and sinus pauses refer to failure of the sinus node to depolarize, which manifest as periods of atrial asystole (no P waves). This may be accompanied by ventricular asystole or escape beats from junctional tissue or ventricular myocardium. Pauses of 2–3 seconds can be found in healthy, asymptomatic people, especially during sleep. Pauses >3 seconds, particularly during daytime hours, raise concern for significant sinus node dysfunction.
    • Sinus exit block represents the appropriate firing of the sinus node, but the wave of depolarization fails to traverse past the perinodal tissue. It is indistinguishable from sinus arrest on surface ECGs except that the R-R interval will be a multiple of the R-R preceding the bradycardia.
    • Tachy-brady syndrome occurs when tachyarrhythmias alternate with bradyarrhythmias. This can be seen in conjunction with a number of types of SVT but is most commonly noted in patients with paroxysmal AF
    • Chronotropic incompetence is the inability to increase the heart rate appropriately in response to metabolic need. This is usually determined by exercising the patient.
  • AV conduction disturbances
    • AV conduction can be diverted (fascicular or bundle branch blocks); delayed (first-degree AV block); occasionally interrupted (second-degree AV block); frequently, but not always, interrupted (advanced or high-degree AV block); or completely absent (third-degree AV block). Assignment of the bradyarrhythmia under investigation to one of these categories allows one to better determine prognosis and, therefore, guide therapy.
    • First-degree AV block describes a conduction delay that results in a PR interval >200 ms on the surface ECG.
    • Second-degree AV block is present when there are periodic interruptions (i.e., “dropped beats”) in AV conduction. Distinction between Mobitz I and II is important because the entities possess differing natural rates of progression to complete heart block.
      • Mobitz type I block (Wenckebach) is represented by a progressive delay in AV conduction with successive atrial impulses until an impulse fails to conduct. On surface ECG, classic Wenckebach block manifests as the following:
        • Progressive prolongation of the PR interval of each successive beat before the dropped beat.
        • Shortening of each subsequent RR interval before the dropped beat.
        • A regularly irregular grouping of QRS complexes (group beating).
        • Type I block is usually within the AV node and portends a more benign natural history with progression to complete heart block unlikely.
      • Mobitz type II block carries a less favorable long-term prognosis and is characterized by abrupt AV conduction block without evidence of progressive conduction delay.
        • On ECG, the PR intervals remained unchanged preceding the nonconducted P wave.
        • The presence of type II block, particularly if a bundle branch block is present, often antedates progression to complete heart block.
      • The presence of AV 2:1 block makes the differentiation between Mobitz type I or II mechanisms difficult. Diagnostic clues to the site of block include the following:
        • Concomitant first-degree AV block, periodic AV Wenckebach, or improved conduction (1:1) with enhanced sinus rates or sympathetic input suggests a more proximal interruption of conduction (i.e., Mobitz type I mechanism).
        • Concomitant bundle branch block, fascicular block, or worsened conduction (3:1, 4:1, etc.) with enhanced sympathetic input localizes the site of block more distally (Mobitz type II mechanism).
  • Third-degree (complete) AV block is present when all atrial impulses fail to conduct to the ventricles. There is complete dissociation between the atria and ventricles (“A > V” rates). This should be distinguished from dissociation with competition at the AV node (“V > A” rates).
  • Advanced or high-degree AV block is present when more than one consecutive atrial depolarization fails to conduct to the ventricles (i.e., 3:1 block or greater). On ECG, consecutive P waves will be seen without associated QRS complexes. However, there will be demonstrable P:QRS conduction somewhere on the record to avoid a “third-degree” designation (Figure 7-5).
    Figure 7-5 Examples of atrioventricular block (AVB).
    Descriptive text is not available for this image

    A, First-degree AVB. There are no dropped beats, and the PR interval is >200 ms. B, 3:2 Second-degree AVB-Mobitz I. Note the “group beating” and the prolonging PR interval prior to the dropped beat. The third P wave in the sequence is subtly inscribed in the T wave of the preceding beat.C, Second-degree AVB-Mobitz II. Note the abrupt atrioventricular conduction block without evidence of progressive conduction delay. D, 2:1 AVB. This pattern makes it difficult to distinguish between Mobitz I versus II type mechanisms of block. Note the narrow QRS complex, which supports a more proximal origin of block (type I mechanism). A wider QRS (concomitant bundle branch or fascicular block) would suggest a type II mechanism. E, Complete heart block. Note the independent regularity of both the atrial and ventricular rhythms (junctional escape) with no clear association with each other throughout the rhythm strip.

    (Reprinted from Fansler D, Chen J. Bradyarrhythmias and permanent pacemakers. In: CuculichPS, KatesAM, eds. The Washington Manual Cardiology Subspecialty Consult. 3rd ed. Philadelphia, PA: Lippincott, Williams and Wilkins; 2014 with permission.)


  • The presence or absence of structural heart disease should be initially evaluated by TTE.
  • Further imaging should be obtained based on suspected etiology.


Pharmacologic Therapy

  • Bradyarrhythmias that lead to significant symptoms and hemodynamic instability should be managed emergently as outlined in ACLS guidelines (see Appendix C).
  • Atropine, an anticholinergic agent given in doses of 0.5–2.0 mg IV, is the cornerstone pharmacologic agent for emergent bradycardia treatment.
    • Dysfunction localized more proximally in the conduction system (i.e., symptomatic sinus bradycardia, first-degree AV block, Mobitz I second-degree AV block) tends to be responsive to atropine.
    • Distal disease is not responsive and can be worsened by atropine.
    • Reversible causes of bradyarrhythmias should be identified, and any agents (digoxin, calcium channel blockers, β-adrenergic blockers) that caused or exacerbated the underlying dysrhythmia should be withheld.

Nonpharmacologic Therapies

  • For bradyarrhythmias that have irreversible etiologies or that are secondary to medically necessary pharmacologic therapy, pacemaker therapy should be considered.
    • Temporary pacing is indicated for symptomatic second-degree or third-degree heart block caused by transient drug intoxication or electrolyte imbalance and complete heart block or Mobitz II second-degree AV block in the setting of an acute MI.
    • Sinus bradycardia, AF with a slow ventricular response, or Mobitz I second-degree AV block should be treated with temporary pacing only if significant symptoms or hemodynamic instability is present.
    • Temporary pacing is achieved preferably via insertion of a transvenous pacemaker. Transthoracic external pacing can be used, although the lack of reliability of capture and patient discomfort make this a second-line modality.
  • Once hemodynamic stability has been established, attention turns to the indications for PPM placement.
    • In symptomatic patients, the key determinants include potential reversibility of causative factors and temporal correlation of symptoms to the arrhythmia.
    • In asymptomatic patients, the key determinant is based on whether the discovered conduction abnormality has a natural history of progression to higher degrees of heart block that portends a poor prognosis.
  • Permanent pacing
    • Permanent pacing involves the placement of anchored, intracardiac pacing leads for the purpose of maintaining a heart rate sufficient to avoid symptoms and hemodynamic instability. Current devices, through maintenance of AV synchrony and rate-adaptive programming, more closely mimic normal physiologic heart rate behavior.
      • Class I and IIa indications for permanent pacing are listed in Figure 7-3.
      • Pacemakers are designed to provide an electrical stimulus to the heart whenever the rate drops below a preprogrammed lower rate limit. Therefore, the ECG appearance of a PPM varies depending on the heart rate and state of AV conduction.
      • The pacing spikes produced by modern pacemakers are low amplitude, sharp, and immediately preceding the generated P wave or QRS complex indicating capture of the chamber. Figure 7-6 illustrates some common ECG appearances of normally and abnormally functioning pacemakers.
        Figure 7-6 Pacemaker rhythms.
        Descriptive text is not available for this image

        A, Normal dual-chamber (DDD) pacing. First two complexes are atrioventricular (AV) sequential pacing, followed by sinus with atrial sensing and ventricular pacing. B, Normal single-chamber (VVI) pacing. The underlying rhythm is atrial fibrillation (no distinct P waves), with ventricular pacing at 60 bpm. C, Pacemaker malfunction. The underlying rhythm is sinus (P) at 80 bpm with 2:1 heart block and first-degree AV block (long PR). Ventricular pacing spikes are seen (V) after each P wave, demonstrating appropriate sensing and tracking of the P waves; however, there is failure to capture. D, Pacemaker-mediated tachycardia. A, paced atrial events; V, paced ventricular events; P, sensed atrial events; R, sensed ventricular events.

        (Reprinted from Fansler D, Chen J. Bradyarrhythmias and permanent pacemakers. In: CuculichPS, KatesAM, eds. The Washington Manual Cardiology Subspecialty Consult. 3rd ed. Philadelphia, PA: Lippincott, Williams and Wilkins; 2014 with permission.)

    • The pacemaker generator is commonly placed subcutaneously in the pectoral region on the side of the nondominant arm. The electronic lead(s) is/are placed in the cardiac chamber(s) via central veins. Complications of placement include pneumothorax, device infection, bleeding, and, rarely, cardiac perforation with tamponade.
      • Before implantation, the patient must be free of any active infections, and anticoagulation issues must be carefully considered. Hematomas in the pacemaker pocket develop most commonly in patients who are receiving IV heparin or subcutaneous low-molecular-weight heparin. In severe cases, surgical evacuation is required.
      • Following implantation, posteroanterior (PA) and lateral CXR are obtained to confirm appropriate lead placement. The pacemaker is interrogated at appropriate intervals—typically, before discharge, 2–6 weeks following implantation, and every 6–12 months thereafter.
    • Pacing modes are classified by a sequence of three to five letters. Most pacemakers are referred to by the three-letter code alone.
      • Position I denotes the chamber that is paced: A for atria, V for ventricle, or D for dual (A + V).
      • Position II refers to the chamber that is sensed: A for atria, V for ventricle, D for dual (A + V), or O for none.
      • Position III denotes the type of response the pacemaker will have to a sensed signal: I for inhibition, T for triggering, D for dual (I + T), or O for none.
      • Position IV is used to signify the presence of rate-adaptive pacing (R) in response to increased metabolic need.
    • The most common pacing systems used today include VVI, DDD, or AAI.
      • AAI systems should be used only for sinus node dysfunction in the absence of any AV conduction abnormalities.
      • The presence of AV nodal or His-Purkinje disease makes a dual-chamber device (i.e., DDD) more appropriate.
      • Patients in permanent AF warrant a single ventricular lead with VVI programming.
    • Modern-day pacemakers also have the capability of mode switching. This is useful in patients with DDD pacers who have concurrent paroxysmal tachyarrhythmias. When these patients develop an atrial arrhythmia faster than a programmed mode switch rate, the device will change to a mode (i.e., VVI) that does not track atrial signals. It will return to DDD when the tachyarrhythmia resolves.
    • Although infrequent, pacemaker malfunction is a potentially life-threatening situation, particularly for patients who are pacemaker dependent. The workup of suspected malfunction should begin with a 12-lead ECG.
      • If no pacing activity is seen, one can place a magnet over the pacemaker to assess for output failure and ability to capture. Application of the magnet switches the pacemaker to an asynchronous pacing mode. For example, VVI mode becomes VOO (ventricular asynchronous pacing) and DDD mode becomes DOO (asynchronous AV pacing).
      • If malfunction is obvious or if the ECG is unrevealing and malfunction is still suspected, then a formal interrogation of the device should be performed. Patients are given a card to carry on implantation that will identify the make and model of the device to facilitate this evaluation.
      • Two view CXR should also be obtained to assess for evidence of overt lead abnormalities (dislodgement, fracture, migration, etc.).
    • General categories of pacemaker malfunction include failure to pace (output failure), failure to capture, failure to sense (undersensing), and pacemaker-mediated dysrhythmias.

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