EP 101: Bradyarrhythmias

Bradyarrhythmia is defined as having a ventricular rate of less than 60 beats per minute (bpm) and is due to dysfunction of the cardiac conduction system at the level of the sinus node, atria or the atrioventricular (AV) node/His-Purkinje system. A wide range of abnormalities may lead to a bradyarrhythmia, including idiopathic fibrosis, infiltrative diseases, drugs, metabolic abnormalities, ischemic heart disease, traumatic injury and congenital heart diseases. The morphology of the P wave, the duration of the PR interval and the relation of the P wave to the QRS complex play key roles in diagnosis of bradyarrhythmias on 12-lead electrocardiography (ECG). In addition to ECG, autonomic testing and electrophysiology study (EPS) may be required to differentiate the type of bradyarrhythmia. Recognition of the type of bradyarrhythmia is necessary, since some of these arrhythmias carry an excellent prognosis and do not need treatment, while others are life-threatening and require immediate intervention. The mainstay of treatment is pacemaker implantation when it is indicated.

Sinus Node Dysfunction Generation and conduction of the impulse in the atria. The sinus node is the main natural pacemaker of the heart and is located near the junction of the right atrium and the superior vena cava. When the generated impulse leaves the sinus node and perinodal tissues, it spreads to the right and then to the left atrium and reaches the AV node. At least three internodal pathways containing Purkinje fibers connect the sinus node to the AV node. Depolarization of the atria is recorded as a P wave on surface ECG and, for practical purposes, the early part of the P wave may be considered to represent right atrium depolarization and the late part, left atrium depolarization.

Pathogenesis and etiology. The most common cause of structural abnormalities of the sinus node is idiopathic degeneration of the node. Inflammatory states (e.g., autoimmune diseases), infections (e.g., myocarditis), chronic ischemia and acute myocardial infarction (e.g., inferior MI), cardiomyopathies, and neuromuscular disorders are other causes of sinus node dysfunction. In addition to structural abnormalities, some extrinsic factors may contribute to sinus node dysfunction, such as autonomic nervous system abnormalities (e.g., carotid sinus hypersensitivity), drugs (e.g., antiarrhythmics, antipsychotics, glycosides), and metabolic derangement (hyperkalemia, hypothermia, hypoxia, and hypothyroidism). Trauma (including heart surgeries), intracranial hypertension, and systemic hypertension are also associated with sinus node dysfunction.

Classification Sinus bradycardia. Sinus bradycardia is defined as sinus rhythm with a rate less than 60 bpm. Similar to normal sinus rhythm, each P wave is followed by a QRS complex, and because all of the P waves originate from the sinus node, they show similar morphologies and the PP interval is equal to the RR interval. Depending on the presence of other conduction abnormalities (e.g., bundle branch block) the QRS complex following the P wave may or may not be normal in morphology and duration. The main difference between sinus bradycardia and normal sinus rhythm is the heart rate (or RR interval). Sinus bradycardia usually does not cause hemodynamic instability and is seen most often in the elderly or athletes.

Sinus pause. When the sinus node fails to generate a pulse, there will be no P wave or its associated QRS and T wave on the ECG. The rhythm that follows such a sinus pause varies greatly. Sometimes when the sinus node is suppressed, the AV node or even lower parts of the conduction system take on the role of principal pacemaker; therefore, the sinus pause will be followed by a junctional rhythm or an idioventricular rhythm (see below). If no part of the conduction system generates the pulse and the pause continues, then it is called asystole. Sinus pauses of less than three seconds may be seen in normal individuals. However, pauses longer than three seconds usually should be investigated further; if it leads to asystole, the patient may need advanced cardiac life support (ACLS).

Junctional rhythm. When the sinus node is suppressed or blocked, the AV node may become the principal pacemaker. The impulse is generated at the AV node and spreads to the atria and ventricles simultaneously at a rate of about 40 to 60 bpm. Because ventricular depolarization creates a much bigger deflection on ECG (i.e., the QRS complex), the P wave, which represents atrial depolarization, may fall within the QRS and not be seen on ECG. Occasionally the P wave may follow the QRS or it may precede the QRS complex if ventricular depolarization happens prior to or after the atrial depolarization. In junctional rhythm when there is a P wave prior to the QRS, the PR interval is always shorter than a sinus beat (less than 110 msec) this criterion is very useful to differentiate an escape junctional rhythm from sinus bradycardia. Since ventricular depolarization occurs in a normal fashion, the morphology and duration of the QRS complexes are usually normal unless other conduction abnormalities coexist. Since the junctional escape rate is usually above 40 bpm, it may not cause hemodynamic instability in an otherwise healthy individual.

Idioventricular rhythm. The mechanism is similar to junctional rhythm, but the principal pacemaker of the heart is now within the ventricles. Therefore, the depolarization of ventricles does not happen in a normal fashion and the QRS complexes are usually wide (more than 120 msec). The heart rate is also lower, between 20 to 40 bpm. Due to this low heart rate, idioventricular rhythm may cause hemodynamic instability.

Sinoatrial exit block. In sinoatrial (SA) block, the sinus node generates the impulse, but there is a conduction abnormality between the sinus node and the surrounding atrial tissue. In first-degree SA exit block, the time for the sinus node impulse to exit the SA node and depolarize the atrial tissue increases. Generation of an impulse in the SA node produces no deflection on surface ECG; therefore, the increased time between impulse generation and its propagation through the atria cannot be measured on surface ECG. Thus, first-degree SA exit block cannot be diagnosed without EPS. Second-degree SA block has two types. In type 1, it takes progressively longer for each SA node impulse to exit the node until an impulse fails to exit the node and depolarize the atria. On surface ECG, there is a shortening of the PP interval until a P-QRS-T complex is dropped. Shortening of the PP interval is helpful to distinguish this condition from a sinus pause. In type 2 second-degree SA block, the impulse generated in the SA node occasionally fails to propagate into the atria, which appears as a dropped P-QRS-T complex on surface ECG. Since the SA node generates the impulses at a regular rate, the PP interval surrounding the dropped complexes is two times (or a multiple) of the baseline PP interval. In third-degree SA exit block , none of the generated impulses exits the SA node. Therefore, on surface ECG there will be a pause or junctional rhythm. However, diagnosis of SA exit block on surface ECG is difficult, so it often requires invasive electrophysiology studies.

Management. As a general principle, any arrhythmia that causes hemodynamic instability requires further investigation and treatment. Except for the use of atropine in selected patients with bradycardia, the mainstay of treatment is pacemaker implantation. In making the clinical decision as to whether pacemaker placement is required, the single most important factor is correlation of the symptoms with the episodes of bradyarrhythmia. The most common symptoms include lightheadedness, dizziness, near-syncope, syncope, and fatigue. To establish the diagnosis and correlate the arrhythmia with the patient s symptoms, an ECG, ambulatory ECG monitoring and EPS may be required. Since syncope can have serious consequences, patients who present with syncope and are found to have sinus node dysfunction may be candidates for pacemaker placement, even if a correlation between the syncope and the sinus node dysfunction has not been documented. There is an association between sinus node dysfunction and atrial fibrillation (i.e., tachycardia-bradycardia syndrome), and it is important to uncover any paroxysmal atrial fibrillation in a patient with sinus node dysfunction since this may change the management. In the presence of reversible causes (e.g., hypothermia, hyperkalemia, or drugs) the patient may need temporary pacing, but permanent pacemaker placement should be postponed until after the reversible cause is treated.

Pacemaker mode. The DDDR mode, which has sensing and pacing capabilities in both the atrium and ventricle, is the most commonly used mode of pacing in patients with sinus node dysfunction. The AAIR mode, in which the atrium is paced and sensed and the pacemaker is inhibited in response to sensed atrial beats, can be used too. Its disadvantage is its lack of protection against an AV conduction abnormality. Although it is appropriate for patients with sinus node dysfunction who have intact AV nodal function, some clinicians believe that the chance of developing an AV conduction problem is significant enough to consider implanting a dual-chamber pacemaker even for sinus node dysfunction. In VVI mode the right ventricle is paced and sensed, and the pacemaker is inhibited in response to a sensed beat. Its advantages include that it requires only one lead and it gives protection against bradycardia of any etiology by pacing the ventricle. The disadvantage of the VVI mode is the lack of AV synchrony, which can result in pacemaker syndrome in the short term and, potentially, heart failure and atrial fibrillation in the long term.

Atrioventricular Blocks

Conduction of the impulse through the atrioventricular junction. In a normal subject, the electrical impulse passes only through the AV node to depolarize the ventricles. The AV node, about 5 mm in size, consists of specialized cells and connects to the AV bundles and His-Purkinje system. It is located beneath the right atrial endocardium at the apex of the triangle of Koch. The triangle of Koch is limited by the base of the septal leaflet of the tricuspid valve inferiorly, tendon of Todaro anterosuperiorly, and anterior margin of the coronary sinus orifice. The speed of conduction within the AV node is slower than the His-Purkinje system (0.03 meters/second versus 2.4 meters/second), and the resultant delay in conduction through the AV node allows atria to contract completely. The His bundle arises from the AV node and divides into left and right bundle branches. The left bundle itself divides into the left anterior fascicle and the left posterior fascicle, and then supplies the left ventricle via Purkinje fibers. The right bundle divides to a network of branches and supplies the right ventricle. The AV node has rich innervations, and its blood supply usually derives from the right coronary artery. The blood supply of the bundle of His arises from the left anterior descending artery.

Pathogenesis and etiology. A wide range of pathologies may cause AV block, including cardiac ischemia, cardiomyopathy, connective tissue diseases, congenital AV block, drugs, Lev s disease (idiopathic fibrosis), Lenegre s disease, infiltrative diseases, infections (endocarditis, myocarditis), metabolic and endocrine disorders (hyperkalemia, hypermagnesemia, hypothyroidism, Addison s disease), neurocardiogenic syncope, trauma (e.g., catheter, surgery), myotonic and muscular dystrophies, and tumors. It is important to differentiate reversible from permanent causes of AV block. In general, for reversible causes such as drugs or metabolic/endocrine abnormalities, permanent pacemaker placement is not indicated. Some of the listed etiologies such as acute MI, trauma, and endocarditis may cause either temporary or permanent AV block.

Classification. In general, the site at which the block occurs determines the type of delay in conduction, ranging from delayed transmission to the ventricles (first-degree AV block), to intermittent failure of impulse transmission (second-degree AV block), to complete conduction failure (third-degree AV block). Each of these abnormalities has characteristics on the surface ECG; however, the most precise way to identify the site of the block is by EPS. First-degree AV block. Delay in conduction of the atrial impulse to the ventricles may be due to abnormal conduction in the atrial tissue or a conduction disturbance at the level of the AV node, the latter being the most common cause of first-degree AV block. The AV nodal conduction disturbance in this case is usually due to an autonomic imbalance (e.g., well-trained athletes, cardiac glycoside excess, transient hypervagotonia) and not due to a structural abnormality of the node. First-degree AV block appears as a prolonged PR interval (> 200 ms) on ECG and a prolonged AH interval at EPS. Although the most common site of the conduction disturbance is the AV node, about 40% of first-degree AV blocks with wide QRS complexes arise from an infra-nodal block. Since the level of the block may change the management of the patient, it is important to pay attention to the width of the QRS complex. Second-degree AV block. The pathogenesis of second-degree AV block Mobitz type 1 is similar to that of first-degree AV block and the conduction disturbance is usually at the level of the AV node. It appears as a progressive prolongation of the PR interval occurring prior to a non-conducted P wave on ECG (Wenckebach phenomenon). Mobitz type 1 usually shows the following characteristics on ECG as well: PR interval prolongation at progressively decreasing increments, the pause after the blocked P wave being less than the sum of the two beats prior to the block, and progressive shortening of RR intervals. Similar to first-degree AV block, wide QRS complexes may indicate that the level of the block is infra-nodal. EPS would show an H electrogram that is not followed by ventricular activity. Mobitz type 2 second-degree AV block appears as an abrupt blocking of a P wave with a fixed PR interval. There is no PR interval prolongation, and the RR interval surrounding the blocked P wave is two times the baseline RR interval. Mobitz type 2 is frequently associated with significant underlying disorders such as bundle branch block and usually progresses to complete heart block. The level of conduction disturbance is at the His-Purkinje system. In EPS, the H electrogram is recorded, but there is no subsequent ventricular activity in the blocked cycle. 2:1 AV block is a second-degree AV block in which every other P wave is not conducted. Since the main electrocardiographic characteristic used to differentiate Mobitz 1 from Mobitz 2 is the variability of PR interval in Mobitz 1, it is impossible to categorize a second-degree AV block as either Mobitz 1 or Mobitz 2 when the conduction ratio is 2:1. Determination of the site of the block in this case is by EPS. However, features that suggest an AV nodal level for conduction disturbance are normal QRS duration, very long PR interval, concomitant type 1 block, and worsening of the degree of the block with vagal maneuvers. The opposite characteristics are seen in infra-nodal block. In high-grade AV block , two or more P waves are not conducted. It may be associated with a junctional or ventricular escape rhythm. Third-degree (complete) AV block. In third-degree AV block, none of the P waves are conducted to the ventricles. If the block is at the AV nodal level, then the escape rhythm may be junctional with a rate of 40 to 60 bpm; if the block is at the level of the His-Purkinje system, then the escape rhythm is idioventricular with a rate of 20 to 40 bpm, with the latter block causing more hemodynamic instability. There is no relation between P waves and QRS complexes (AV dissociation with atrial rate faster than ventricular rate). At EPS, the recorded H electrogram helps to determine the site of the conduction disturbance.

Management. All hemodynamically unstable patients with AV block require pacemaker placement. The decision regarding placing a permanent pacemaker depends on the reversibility of the etiology of the AV block. Asymptomatic patients with first-degree AV block or Mobitz 1 second-degree AV block usually do not need any intervention unless there are features suggesting infra-nodal AV block. In this case, the patient would undergo EPS to determine the location of conduction disturbance; if the block is infra-nodal, pacemaker placement is recommended. There is a high chance of progression from Mobitz 2 to complete AV block, and third-degree AV block is associated with hemodynamic instability; therefore, pacemaker placement is recommended for these two conditions. A stable patient with 2:1 AV block should undergo EPS to determine the site of the block. Those with infra-nodal block need a permanent pacemaker. A patient with high-grade AV block usually needs pacemaker placement unless it is secondary to a reversible cause. A dual-chamber pacemaker with the ability to sense and pace both the right atrium and right ventricle is the most commonly used.

Summary

Bradyarrhythmias are divided into two major groups: sinus node dysfunction and AV blocks. Although a precise determination of the conduction disturbance would require EPS, many bradyarrhythmias can be recognized on ECG. In AV block, the most important prognostic factor is the location of the block (i.e., AV nodal versus infra-nodal). A pitfall would be to assume that all first-degree and Mobitz 1 second-degree AV blocks are low-risk conditions. The mainstay of treatment is pacemaker implantation. A wide range of conditions, including ischemia, infections, inflammatory and infiltrative disorders, may cause bradyarrhythmia. The decision regarding permanent pacemaker implantation depends on the reversibility of the etiology of bradyarrhythmia.