Bradyarrhythmia Including Heart Block

Bradyarrhythmia Including Heart Block

Seongwook Han

Mithilesh K. Das

Bradycardia refers to a heart rate of <60 beats per minute (bpm). The term bradyarrhythmia should be reserved for any heart rhythm <60 bpm. Bradyarrhythmias may be associated with symptoms such as dizziness, near-syncope or syncope, congestive heart failure, exercise intolerance, fatigue, or a confusion that improves with resolution of the bradycardia. The mere presence of a slow heart rate of <60 bpm that is not associated with any symptoms almost never justifies aggressive interventions. However, it may be important to determine whether the bradyarrhythmia will not resolve spontaneously or with the alleviation of a condition that is the likely cause of the bradyarrhythmia. Management of bradycardia includes the management of reversible causes such as drugs. Nonreversible symptomatic bradycardia warrants pacemaker implant. However, if a hemodynamically stable patient can be observed safely while being treated for a metabolic or ischemic condition or an adverse drug reaction, then it is not justified to implant a permanent pacemaker, even though a temporary pacemaker may be necessary in the interim.


Sinus rhythm is present when the dominant pacemaker controlling impulse generation is the sinus node. In this setting, activation of the atria is from right to downwards and left as well as from anterior to posterior. The normal P wave in sinus rhythm may appear slightly notched as the activation of the right atrium precedes that of the left atrium. The normal P wave is positive (upright) in leads 1 and 2, negative in aVR, and it may be positive, negative, or biphasic in lead 3. It is of variable polarity in lead aVL. In the precordial (chest) leads, V1 and V2, there is often a terminal negative component of the P wave, reflecting the posterior location (with respect to the right atrium) and later activation of the left atrium. The P wave is typically positive in the remaining precordial leads. In normal sinus rhythm with 1:1 atrioventricular conduction, a P wave with a uniform morphology precedes each QRS complex. The rate is between 60 and 100 bpm and the variation in the heart rates fairly uniform between sequential P waves and QRS complexes. In addition, the P wave morphology and PR intervals appear identical from beat to beat.


Although the sinus node has an intrinsic automaticity and always produces an impulse, the rate of impulse generation is controlled by other factors, particularly the autonomic nervous system. With augmented parasympathetic (vagal) influence or reduced sympathetic stimulation, the sinus rate slows, and the PR interval prolongs owing to a vagal-mediated slowing of conduction through the atrioventricular node. By comparison, increased sympathetic activity and decreased vagal effects increase the sinus nodal rate and enhance atrioventricular nodal conduction, resulting in a shortened PR interval.


Sinus arrhythmia is present when there is a sinus rhythm with variability in the cycle lengths between successive P waves. The physiologic variability observed in sinus arrhythmia is the result of respiratory-related changes in autonomic tone that influence the heart rate. Inspiration and the stretching of lung tissue cause a reflex inhibition of vagal tone, which will increase the heart rate. The reverse occurs during expiration. A continuous electrocardiographic recording of sinus arrhythmia reveals a gradual increase and decrease in the heart rate because the cycle lengths between QRS complexes vary with the respiratory cycle. Although sinus arrhythmia is a normal finding, it may be confused with other arrhythmias if the respiratory changes in the RR intervals are prominent.


Sick sinus syndrome results from intrinsic disease of the sinus node. Some individuals with this syndrome also have underlying disease of other portions of the conduction system, particularly the AV node. Manifestations of the sick sinus syndrome are symptomatic sinus bradycardia, sinus pauses or arrest, chronotropic incompetence, and tachy-bradycardia syndrome.


Sinus bradycardia is defined as a sinus rhythm with a rate <60 bpm. Sinus bradycardia is most frequently caused by an increase in vagal tone or a reduction in sympathetic tone (and thus a physiologic change). Sinus bradycardia occurs in normal children and adults, particularly during sleep when rates of 30 bpm and pauses of up to 2 seconds are not
uncommon. It may also be seen in the absence of heart disease in the following settings:

  • At rest, in 25% to 35% of asymptomatic individuals under 25 years of age

  • In well-conditioned athletes

  • In some elderly patients.

As a result, sinus bradycardia is very common at night. When sinus bradycardia results from increased vagal tone, slowing of impulse conduction through the atrioventricular node also results in PR interval prolongation. There is no prognostic significance to sinus bradycardia in otherwise healthy subjects.


Sinus bradycardia can be the result of pathophysiologic condition including intrinsic disease of the sinus node (“sick sinus”) and several extrinsic causes, manifested as a decrease in spontaneous automaticity and the impulse generation rate (Table 15.1).

  • Exaggerated vagal activity: Vasovagal responses may be associated with a profound bradycardia owing to heightened parasympathetic activity and sympathetic withdrawal on the sinus node. The combination of the slow heart rate and an associated decline in peripheral vascular resistance is often sufficient to produce presyncope or syncope. There are a variety of stimuli for vagal activation: Pressure on the carotid sinus, as may occur with a tight collar or with the impact of the stream of water in a shower, vomiting, or coughing, Valsalva maneuver when straining at stool, sudden exposure of the face to cold water, and prolonged standing through a Bezold-Jarisch reflex. Hypervagotonia can also result in chronic (i.e., nonepisodic) resting sinus bradycardia. This is the primary mechanism of resting bradycardia in well-trained athletes. Junctional bradycardia and Mobitz type I AV block can also be seen in this setting.

  • Increased intracranial pressure: Increased intracranial pressure should be excluded when sinus bradycardia occurs in a patient with neurologic dysfunction.

  • Acute myocardial infarction (AMI): Sinus bradycardia occurs in 15% to 25% of patients with AMI, particularly those affecting the inferior wall as the right coronary artery supplies the sinus node in approximately 60% of people. Increased vagal activity is primarily responsible, and the bradycardia is typically transient.

  • Obstructive sleep apnea: Individuals with obstructive sleep apnea frequently have sinus bradycardia and sinus pauses during apneic episodes. Therapies to improve the apnea frequently alleviate the bradycardia.

  • Drugs: A number of drugs can depress the sinus node and slow the heart rate. These include parasympathomimetic agents, sympatholytic drugs (β-blockers, reserpine, guanethidine, methyldopa, and clonidine), cimetidine, digitalis, calcium channel blockers, amiodarone and other antiarrhythmic drugs, and lithium.

  • Others: Other causes of sinus bradycardia include hypothyroidism, hypothermia, and severe prolonged hypoxia. Infectious agents associated with relative sinus bradycardia include Chagas’ disease, legionella, psittacosis, Q fever, typhoid fever, typhus, babesiosis, malaria, leptospirosis, yellow fever, dengue fever, viral hemorrhagic fevers, trichinosis, and Rocky Mountain Spotted fever.


Sinus pause or sinus arrest is the result of intermittent failure of sinus node impulse generation. Sinus pause or arrest may be owing to intrinsic sinus node disease and dysfunction or from drugs that directly or indirectly (through the autonomic nervous system) depress sinus node activity. On the surface ECG, a sinus pause or arrest is manifest as a long PP cycle length that is longer than the P-P interval of the underlying sinus rhythm but less than two P-P intervals. There is no relationship between the cycle length of the pause and that of the intrinsic sinus rhythm. This occurs in intrinsic sinus node disease or in the setting of vagal stimulation such as respiratory lavage in an intubated patient in intensive care unit.


Sinoatrial (SA) exit block most commonly arises from a change in the electrophysiologic characteristics of the tissue surrounding the sinus node resulting in an inability to respond to or conduct an impulse from the sinus node into the atrium. This can be owing to drugs, disease, or increased vagal activity. SA nodal exit block is classified as the first degree, second degree, and third degree.

TABLE 15.1 Major cause of bradycardia


Idiopathic degeneration (aging)

Infarction or ischemia

Infiltrative diseases




Collagen vascular diseases

Systemic lupus erythematosus

Rheumatoid arthritis


Myotonic muscular dystrophy

Surgical trauma

Valve replacement

Correction of congenital heart disease

Heart transplantation

Familial diseases

Infectious diseases

Chagas’ disease



Autonomically mediated syndromes

Neurocardiac syncope

Carotid-sinus hypersensitivity

Situational disturbances






β-Adrenergic blockers

Calcium-channel blockers



Antiarrhythmic agents



Neurologic disorders

Electrolyte imbalances



  • First degree SA nodal exit block reflects a slowing of impulse exit but there is still 1:1 conduction. This abnormality cannot be recognized on the surface ECG.

  • Second degree SA nodal exit block has two types. Type I (Wenckebach type) is characterized by progressively decreasing P-P intervals prior to a pause caused by a dropped P wave; the pause has a duration that is less than two P-P cycles. The mechanisms of progressive shortening of P-P interval is Wenckebach phenomenon between sinus node to atrium (Figure 15.1). In type II exit block, the P-P output is an arithmetic multiple of the presumed sinus pacemaker input (e.g., 2:1, 3:1, 4:1). Therefore the P-P cycle length surrounding the pause is a multiple of the normal P-P interval (Figure 15.2).

  • Third degree SA nodal exit block prevents pacemaker impulses from reaching the right atrium, giving the appearance of sinus arrest (i.e., no P waves).


This form of the syndrome is most often characterized by bursts of an atrial tachyarrhythmia (usually atrial fibrillation) which terminate spontaneously and are followed by long offset pauses and symptoms (Figure 15.3). The pause is often long, and there may be no junctional escape rhythm because of associated AV nodal disease. The tachy-bradycardia syndrome is the result of overdrive suppression of the sinus node by the atrial arrhythmia. After arrhythmia termination, there is a variable delay before the sinus node recovers and again generates an impulse because of sinus node dysfunction. Catheter ablation of atrial arrhythmia sometimes cures the arrhythmia. Symptomatic patients, who are not a candidate for catheter ablation, receive permanent pacemakers for bradycardia, and tachycardia is treated by calcium or β-blockers.

Figure 15.1. Type I second degree SA block. The rhythm strip shows sinus rhythm with normal AV conduction. There is progressive shortening of P-P interval followed by a dropped P wave suggestive of second degree type 1 (Wenckebach) SA block.

Figure 15.2. Type II second degree SA block. The rhythm strip shows a fixed P-P interval and dropped P waves similar to the rhythm strip of the upper panel.

Figure 15.3. Tachy-bradycardia syndrome. The rhythm strip shows atrial fibrillation that terminates into a prolonged pause followed by a slow junctional rhythm.


Chronotropic incompetence is defined as inability to accelerate sinus rate appropriate to the level of exercise. This definition includes inability to reach 70th to 80th percentile of maximum predicted heart rate, delayed peak of heart rate (heart rate peaks during recovery period after the exercise), early peaking of heart rate (prior to the peak exercise), fluctuations of heart rate during exercise or inability to reach a heart rate of 100 to 120 bpm. The heart rate response to exercise also depends on several factors such as deconditioning, drug therapy, and comorbidities.


AV block can be defined as a delay or interruption in the transmission of an impulse from the atria to the ventricles owing to an anatomical or functional impairment in the conduction system. The conduction disturbance can be transient or permanent, and it can have many causes (Table 15.2). The conduction can be delayed, intermittent, or absent. The commonly used terminology includes first degree (slowed conduction without missed beats), second degree (intermittent conduction, often in a regular pattern, for example, 2:1, 3:2, or higher degrees of block), and third degree or complete AV block.


  • Increased vagal tone: Enhanced vagal tone owing to sleep, athletic training, pain, carotid sinus massage, or hypersensitive carotid sinus syndrome can result in slowing of the sinus rate and/or the development of AV block.

  • Idiopathic progressive cardiac conduction disease: Fibrosis and sclerosis of the conduction system accounts for about one-half of cases of AV block and may be induced by several different conditions that often cannot be distinguished clinically. Progressive cardiac conduction defect, also called Lenegre’s
    or Lev’s disease, is characterized by progressive impairment of the conduction system: The term Lenegre’s disease has been traditionally used to describe a progressive, fibrotic, sclerodegenerative affliction of the conduction system in younger individuals. It is frequently associated with slow progression to complete heart block and may be hereditary. Lev’s disease has referred to “sclerosis of the left side of the cardiac skeleton” in older patients, such as that associated with calcific involvement of the aortic and mitral rings. It is caused by fibrosis or calcification extending from any of the fibrous structures adjacent to the conduction system into the conduction system. Fibrosis of the top of the muscular septum is a common cause of right bundle branch block (RBBB) with left anterior fascicular block in the elderly patient. Involvement of the mitral ring or the central fibrous body, for example, may be the commonest cause of complete heart block with a narrow QRS complex in the elderly. Aortic valve calcification, on the other hand, can invade the bundle of His, the right and/or left bundle branch as well as the left anterior fascicle. Thus, the QRS complex may be prolonged.

    TABLE 15.2 Major Causes of Atrioventricular Block

    Physiologic and Pathophysiologic


    Increased vagal tone


    Fibrosis and sclerosis of the conduction system

    digitalis, calcium channel blockers,

    Ischemic heart disease

    β-blockers, amiodarone

    Cardiomyopathy and myocarditis

    Cardiac surgery

    Congenital heart disease

    Transcatheter closure of VSD

    Familial AV block

    Alcohol septal ablation for HCM


    Hyperkalemia, infiltrative malignancies, neonatal lupus syndrome, severe hypo- or hyperthyroidism, trauma, degenerative neuromuscular diseases

  • Ischemic heart disease: Ischemic disease accounts for about 40% of cases of AV block. Conduction can be disturbed with either chronic ischemic disease or during an AMI. It is estimated that approximately 20% of patients with AMI develop AV block: 8% with first degree 5% with second degree, and 6% with third degree. Intraventricular conduction disturbances (IVCDs), including bundle and fascicular blocks, also occur in 10% to 20% of cases of acute MI. Left bundle branch block (LBBB) and RBBB with left anterior fascicle block are most common, each occurring in about one-third of patients with an IVCD. RBBB with or without left posterior fascicular block and alternating bundle branch block are less frequently seen, whereas isolated left anterior or posterior fascicle block is distinctly unusual.

  • Cardiomyopathy and myocarditis: AV block can be seen in patients with cardiomyopathies, including hypertrophic obstructive cardiomyopathy and infiltrative processes such as amyloidosis and sarcoidosis, and in patients with myocarditis owing to a variety of causes including rheumatic fever, Lyme disease, diphtheria, viruses, systemic lupus erythematosus, toxoplasmosis, bacterial endocarditis, and syphilis. The development of AV block in myocarditis is often a poor prognostic sign.

  • Congenital heart disease: Congenital complete heart block may be an isolated lesion or may be associated with other types of congenital heart disease.

  • Familial disease: Familial AV conduction block, characterized by a progression in the degree of block in association with a variable apparent site of block, may be transmitted as an autosomal dominant trait. Several sodium channel gene (SCN5A) mutations have been associated with sinus node and AV nodal disease. Some of these mutations produce AV block in childhood, whereas others present in middle-age and have been called hereditary Lenegre’s disease. In some families with SCN5A mutations, AV block or other conduction abnormalities are present with or without associated dilated cardiomyopathy. Different SCN5A mutations are associated with other cardiac abnormalities including congenital long QT syndrome type 3, the Brugada syndrome, familial sick sinus syndrome, and familial dilated cardiomyopathy with conduction defects and susceptibility to atrial fibrillation.

  • Other: AV block can also occur in a variety of other disorders:

    • Hyperkalemia, usually when the plasma potassium concentration is above 6.3 mEq per L.

    • Infiltrative malignancies, such as Hodgkin lymphoma and other lymphomas, and multiple myeloma.

    • Hereditary neuromuscular degenerative disease such as myotonic dystrophy, Kearns-Sayre syndrome, and Erb’s dystrophy.

    • Rheumatologic disorders including dermatomyositis and Paget disease.

    • Hyperthyroidism, myxedema, and thyrotoxic periodic paralysis.

    • Neonatal lupus syndrome, which results from transplacental passage of anti-Ro/SSA or anti-La/SSB antibodies from the mother.

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May 27, 2016 | Posted by in CARDIAC SURGERY | Comments Off on Bradyarrhythmia Including Heart Block
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