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Bradycardia – pathophysiology

Bradyarrhythmias and conduction blocks are common electrocardiographic findings. These arrhythmias can result from a wide variety of disorders of the cardiac conduction system. Bradycardias are generally divided into disorders involving either the sinus node or atrioventricular conduction or as neurally mediated arrhythmias. Bradyarrhythmias may be discovered as incidental electrocardiographic abnormalities or may be found after investigation for symptoms suggestive of their presence. A wide variety of symptoms may be caused by the different etiologies of bradycardia, often times adding diagnostic difficulty to patients with coexisting medical problems.

Disorders of the sinus node

Sinus node dysfunction includes any abnormality involving the sinus node, including sinus bradycardia, sinoatrial arrest, sinoatrial exit block and tachycardia-bradycardia syndrome. The clinical presentation may include fatigue, dyspnea, and syncope. Palpitations may be the primary complaint in patients with tachycardia-bradycardia syndrome. The most common etiology of sinus node dysfunction includes idiopathic degenerative disease with the incidence increasing with age. Other intrinsic factors include coronary disease, hypertension, and infiltrative disorders. Extrinsic factors include drug effects, autonomic influences and electrolyte imbalances. Sinus bradycardia exists in an adult when the sinus node discharges less than 60 beats/min. This occurs normally in young adults from vagal tone or in older individuals from medications or underlying sinus node dysfunction. During sleep, the normal heart rate can decrease to 35-40 beats/min with marked sinus arrhythmia and asymptomatic pauses. Inappropriate sinus bradycardia, or chronotropic incompetence, refers to a failure to increase the sinus rate with exercise. Sinus arrest, or sinus pause, is a disorder of automaticity in which no impulses are generated within the sinus node and may last from seconds to several minutes. The length of the pause is not an exact multiple of the P-P interval, suggesting that the mechanism is due to slowing or interruption of sinus node automaticity and not conduction block. Sinoatrial exit block is recognized electrocardiographically as a sudden pause in atrial depolarization with the length of the pause an exact multiple of the P-P interval. Unlike sinus arrest, this arrhythmia is not due to a disorder of impulse formation, but rather conduction block. Sinoatrial exit block can be divided into type I (SA Wenkebach), type II (SA Mobitz II) and high-degree SA block (Figure 1). Type I SA block can be recognized electrocardiographically as group beating of P waves with shortening of the P-P intervals and pauses that amount to less than twice the shortest P-P cycle. In contrast, type II SA block demonstrates intermittent failure of conduction to the atrium as manifested by fixed P-P intervals with pauses that equal twice the P-P interval. Sick sinus syndrome (SSS) is characterized by episodes of bradycardia with sinus pauses, arrest or exit block associated with poor atrial and junction escape rhythms. Alternating atrial tachyarrhythmias, mainly atrial fibrillation, is seen in many cases and termed tachycardia-bradycardia syndrome. Atrial fibrillation is likely associated with SSS due to the increased dispersion of refractoriness or early after depolarizations (EADs) occurring in the setting of bradycardia. Pauses are often observed after cessation of tachycardia posing difficulty in pharmacologically managing the tachyarrhythmia. AV conduction disturbances occur in approximately half of patients with SSS. Most commonly, atrial fibrillation with a slow ventricular response in the absence of AV nodal blocking medications indicates AV node dysfunction. Etiologies for SSS include sinus node fibrosis, coronary disease (involving the SA nodal artery), drugs, and infiltrative diseases such as amyloidosis and sarcoidosis.

Disorders of atrioventricular and His-Purkinje conduction

The most common etiologies of AV conduction disturbances include fibrosis, degeneration of the conduction system, ischemia and drugs. In the young, the most common etiology is congenital AV block or AV block from surgery for congenital heart disease. Among the elderly, idiopathic fibrosis and calcification of the conduction system is a frequent cause. Ischemic heart disease accounts for approximately one third of cases of AV block, either the result of chronic coronary disease or myocardial ischemia. AV nodal conduction disturbances are seen frequently in acute coronary syndromes (described below). Lev’s disease refers to the sclerotic process that is seen in older individuals involving the fibrous ring. Associated echocardiographic findings include calcification of the mitral and aortic valves. Lenegre’s disease refers to a fibrotic process specifically involving the conduction system and is felt to be hereditary, most often observed in younger individuals. A comprehensive list of causes of atrioventricular conduction disorders are listed in Figure 2. First degree AV block is a misnomer in that every P wave is conducted to the ventricles, however, with a PR interval exceeding 200 msec. Prolonged PR conduction, a more appropriate classification for this conduction disturbance, may be the result of conduction delay within the atrium, AV node, bundle of His or bundle branches. Prolongation of the PR interval most often indicates AV nodal conduction delay. Second degree AV block is characterized by a failure of one or more atrial impulses to reach the ventricles. Block can be either at the level of the AV node or infranodal structures. Type I second degree AV block, or Wenkebach, requires prolongation of the PR interval prior to the blocked impulse with subsequent shortening of the PR interval with the next conducted impulse. On the ECG, the R-R interval progressively shortens up to the point of the blocked ventricular impulse. This occurs because the largest increment in the PR interval occurs between the first and second cycle. The site of block in Type I second degree AV block is the AV node. This conduction disturbance most often is physiologic and seen with high vagal tone and during sleep. Pacing is rarely indicated. Type II second degree AV block, or Mobitz II, is instead characterized by a constant PR interval prior to and following a blocked impulse. Mobitz II second degree block originates from an intra or infra-Hisian location and often is associated with a bundle branch block pattern. On electrophysiologic evaluation, constant H-V intervals are typically seen with spontaneous block within or below the His. Type II second degree AV block often progresses to complete AV block and can manifest as syncope. When development of this type of block or new bundle branch block is seen in association with anterior myocardial infarction, it implies a proximal LAD occlusion. Two-to-one AV block can represent benign block within the AV node or disease of the His-Purkinje system. Certain electrocardiographic features and maneuvers can help in distinguishing where the location of block exists. A long PR interval with a narrow QRS suggests an intranodal block. A short PR interval with intraventricular conduction delay or bundle branch block suggests disease below the node. Responses to atropine, exercise and carotid sinus massage can be helpful in diagnosis. Atropine will improve AV nodal conduction but will worsen block within diseased His-Purkinje fibers. Exercise has a similar effect, improving conduction in cases where block exists only in the node, but worsening when block is subnodal. Alternatively, carotid sinus massage will slow conduction when block occurs in the AV node, but will improve conduction in diseased His-Purkinje tissue by allowing for refractoriness to recover (Figure 3). Not all atrial impulses that fail to conduct to the ventricles are necessarily second degree AV block. If an atrial impulse reaches the AV junction early enough in the cycle while the node is refractory, the impulse is not conducted. This is a common scenario seen with early premature atrial complexes (PACs). Block, which infers pathology of conduction, is an incorrect description on this phenomenon. Likewise, 2:1 conduction, rather than block, is a more apt description of atrial flutter that conducts to the ventricles in this pattern. Third degree heart block results in no conduction of atrial impulses to the ventricles and may be acquired or congenital. Block can occur in either the AV node or His-Purkinje system. The site of block can be somewhat inferred by the nature of the escape rhythm, with narrow QRS escape complexes and rates greater than 40 bpm suggestive of block in the AV node or proximal His. Conversely, block within the distal His or the branching structures will manifest as a wide QRS escape complexes with slower rates. Use of atropine will accelerate the escape rate in instances of AV nodal block and fail to do so otherwise. Congenital third degree AV block occurs in approximately 1 in 20,000 children. In over half, AV block is discovered as a result of bradycardia in utero or neonatally and is secondary to maternal lupus in over 90 percent of cases. Mortality in AV block from neonatal lupus tends to be high. When AV block is diagnosed later in childhood, maternal lupus is rarely responsible and etiologies include structural heart defects and myocarditis. Initially, AV block may be transient but most often progresses to permanent AV block with junctional escape. Intraventricular conduction disturbances (IVCD) occur below the AV node and do not in themselves result in bradyarrhythmias. Conduction delay can occur anywhere along the His-Purkinje system and etiologies are similar to those causing AV block. The most common etiologies include idiopathic fibrosis and ischemia. IVCDs are more commonly seen in structurally abnormal hearts. These are generally classified by the number of fascicles affected. The His-Purkinje system is a trifascicular system, with bifascicular block referring to conduction delay within either both the right bundle and left anterior or posterior fascicle or the left bundle branch in itself. Chronic bifascicular block in asymptomatic patients has a low risk of progression to AV block, however, in the setting of an anterior infarction and new bifascicular block, the risk is substantial. Trifascicular block is a confusing description that is most often applied to those with bifascicular block and prolonged PR intervals. Like bifascicular block, the risk for progression to AV block is less than 1 percent per year. Paroxysmal AV block, an unusual but formidable form of conduction block, occurs when one-to-one conduction abruptly changes to complete AV block. As shown in Figure 4, following carotid sinus massage, the subsequent P-P intervals are prolonged secondary to sinus node suppression. Complete AV block is seen following the lengthening in sinus cycle length. This is secondary to phase 4 block. Phase 4 block occurs in the setting of bradycardia secondary to reduction of transmembrane potential during a prolonged electrical diastole. This type of block is not physiologic and indicates diseased His-Purkinje tissue. Bradycardia-dependent bundle branch block is a similar, but less extreme phenomena related to phase 4 block. In this case, bundle branch block (almost always LBBB) is seen after the end of a longer diastolic cycle (Figure 5). This, as well, indicates organic heart disease and results from diastolic depolarization of the membrane potential with a deterioration of membrane responsiveness so that conduction is impaired through the affected bundle branch.

Conduction abnormalities after myocardial infarction

Both bradyarrhythmias and conduction disturbances can be seen with myocardial infarctions and are generally related to ischemia or autonomic disturbance. The clinical features and management of bradyarrhythmias and conduction block depends on the location of the infarction. The right coronary artery supplies the SA node in 60 percent of people and the left circumflex the remaining. In over 90 percent of people, the RCA feeds the AV node and proximal His. The terminal portion of the His and main left bundle and right bundle branch are supplied by septal perforators of the LAD. Sinus bradycardia, prolonged PR conduction with Wenkebach and complete heart block are common in inferior myocardial infarctions (IMI). Complete AV block occurs in approximately 10 percent of patients with IMI. This rarely occurs suddenly, most often seen with prolonged PR conduction gradually progressing to complete AV block. AV block occurs within the node in over 90 percent of cases and typically results in a transient block. The escape complex is usually narrow and infrequently requires pacing. Bradyarrhythmias occurring in the setting of inferior infarctions are generally responsive to atropine. With anterior infarctions, conduction disturbances are not as benign and are related to the size of the infarction. The development of fascicular or bundle branch block is correlated to the size of infarct. Complete AV block in anterior MI can occur abruptly in the first 24 hours, developing without warning. AV block may also be preceded by the development of an intraventricular conduction delay or by type II second degree block. Escape complexes are unstable and usually wide complex requiring pacing. Complete heart block occurs secondary to necrosis of the distal His and bundle branches within the septum. When AV block occurs with anterior infarctions, mortality is greater increased.

Neurally mediated bradycardia

Autonomic stimulation can lead to sinus node slowing or AV nodal blockade in the absence of sinus or AV node dysfunction. Neurocardiogenic syncope and carotid sinus hypersensitivity are the most common etiologies of autonomically mediated bradycardia. Both occur in the setting of excess vagal tone and have similar clinical manifestations which include a cardioinhibitory response. This results from an increase in parasympathetic tone which can lead to sinus bradycardia, prolonged PR conduction and second and third degree AV block. The pathophysiology involving the cardioinhibitory response in neurocardiogenic syncope is felt to result from an exaggerated response to a physiologic reflex. The syndrome begins with relative hypovolemia that triggers a sympathetic reflex with an increase in heart rate, myocardial contractility and peripheral vasoconstriction. Increased contractility results in ventricular cavity obliteration which, in turn, generates pressure sensed by mechano C fibers. In predisposed individuals, this results in vasodepression and cardioinhibition manifested as hypotension and slowing of the sinus rate or AV nodal block, respectively.

Post-surgical bradyarrhythmias

Bradyarrhythmias following open heart surgery are common. Most commonly, AV block is seen following aortic and mitral valve surgery. Septal myectomy invariably leads to resection of the left bundle and can often require permanent pacing secondary to subsequent AV block. Permanent pacing is required in 2-3% of surgeries involving valve replacement and in approximately 10% of cardiac transplant recipients. In cardiac transplant recipients, resting sinus rates are usually elevated due to denervation of vagal input. Sinus node dysfunction occurs in 50% of patients postoperatively resulting from prolonged donor ischemic or injury to the SA artery. Injury to the SA node or artery can be avoided by performing bicaval, rather than atrial anastomosis. AV block is infrequently seen postoperatively in cardiac transplants. The most frequent intraventricular conduction disturbance is RBBB, likely secondary to repeated biopsies required in these patients.

Bradyarrhythmias secondary to medications

Multiple cardiac medications are known to cause bradycardia. Beta-blockers, calcium-channel blockers, digoxin and antiarrhythmic medications include the most common agents. Through blockade of beta receptors, beta blockers result in sinus bradycardia and prolong AV conduction. Similarly, calcium channels, specifically the non-dihydropyridines, verapamil and diltiazem, slow sinus depolarization and AV conduction. Digoxin, through altering vagal tone and increasing intracellular calcium concentrations, is well known to cause sinus bradycardia, block and arrest as well as junctional bradycardia and AV block.

Diagnostic testing

Diagnostic testing for suspected bradyarrhythmias is generally limited to non-invasive methods. The initial work-up includes a 12-lead ECG followed by 24-48 hour holter monitoring. For patients with infrequent symptoms, an event monitor may be used to monitor the cardiac rhythm for up to 4 weeks. Implantable loop recorders are also available for prolonged continuous diagnostic monitoring. In instances where inappropriate sinus bradycardia is suspected, stress testing can be performed to assess chronotropic competence. Assessment of autonomic tone includes carotid sinus massage and tilt table testing. Carotid sinus pressure with concomitant ECG monitoring can be helpful in identifying patients with carotid sinus hypersensitivity. Pauses exceeding 3 seconds in response to carotid pressure are abnormal. Carotid sinus pressure should not precipitate sinus pauses, although slowing in the sinus rate or AV block can be normal responses. Tilt table testing can be helpful in differentiating bradycardia from sinus node disease and autonomic dysfunction. Bradycardic responses to tilt testing are the result of autonomic dysfunction. Pharmacologic testing can also be useful in differentiating sinus node dysfunction from autonomic dysfunction. Autonomic blockade with atropine (0.4 mg/kg) and propanolol (0.2 mg/kg) can be used to determine the intrinsic heart rate (IHR), which represents the sinus node rate without autonomic influences. IHR can be calculated from the formula: 118 – (0.57 x age). Intrinsic sinus rates lower than the calculated value suggests sinus node dysfunction while sinus rates closer to this value represent autonomic dysfunction. Electrophysiologic evaluation of bradyarrhythmias includes assessment of sinus node function and AV conduction. Sinus node function cannot be measured directly. The 2 most common tests indirectly measure sinoatrial function. Sinus node recovery time (SNRT) is the time taken for sinus rhythm to resume after 30 seconds of overdrive atrial pacing. This interval is measured in the high right atrium from the last paced beat to the first spontaneous sinus beat. A delay of longer than 1500 msec is abnormal. The corrected value (CSNRT) can be determined by subtracting the intrinsic sinus cycle length from the SNRT value. Values of CSNRT longer than 550 msec suggest sinus node dysfunction. The second indirect measurement of sinus node function is the sino-atrial conduction time (SACT). This technique is used for detecting delayed conduction between the sinus node and surrounding atrial tissue. This involves resetting the sinus node with atrial extrastimuli delivered in the high right atrium. After measurement of the intrinsic sinus rate, atrial extrastimuli are delivered during sinus rhythm over a range of coupling intervals (A1A2). Earlier coupled atrial extrastimuli invade and reset the sinus node. The interval of the returning sinus impulse following the atrial extrastimulus is measured and SACT is calculated as: (A2A3 – A1A1)/2. SACT values greater than 115 msec are considered abnormal.

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