Bradycardia and Cardiac Conduction Delay Guideline Update

The American College of Cardiology, American Heart Association, and Heart Rhythm Society collectively publish guidelines related to the management of cardiac arrhythmias. This column highlights key recommendations from the Guideline on the Evaluation and Management of Patients with Bradycardia and Cardiac Conduction Delay1 and discusses implications for nurses in acute care settings. The guideline is comprehensive and includes recommendations for evaluating and monitoring patients and for pharmacological and device-based treatments. This column describes only select class I recommendations (those that are indicated, beneficial, and effective, and should be done) and class III recommendations (those that are associated with potential harm and should not be performed).1Twelve-lead electrocardiography (ECG) performed when symptoms appear or during bradycardia or a conduction delay may provide a definitive diagnosis of the condition causing the bradycardia or conduction delay. Electrocardiography can also provide valuable information about the etiology of bradycardia or a conduction delay by revealing previous myocardial infarction, ventricular hypertrophy, electrolyte abnormalities, or QT prolongation. For patients presenting with syncope or near syncope, an initial abnormal ECG is associated with adverse events.1Cardiac rhythm monitoring allows bradycardia or a conduction delay to be correlated with symptoms. An ambulatory monitor that continuously evaluates heart activity for 24 to 48 hours (eg, a Holter monitor) is appropriate for patients who have symptoms daily; patients with less frequent symptoms require a device that records and stores information for a longer period of time. The results of cardiac monitoring exclude cardiac arrhythmia or a conduction abnormality as the reason for symptoms more frequently than they confirm the presence of a cardiac rhythm disturbance. Ambulatory monitors, however, can diagnose chronotropic incompetence in persons who are active. For all outpatient monitors, systems need to be in place to notify health care providers and patients of abnormal findings that place the patient at risk for an adverse event.1 The Table describes various outpatient monitors used to diagnose patients with suspected bradycardia or conduction system disease.The presence of structural heart disease impacts prognosis in patients with documented bradyarrhythmia.1 Echocardiography is indicated for certain ECG findings including newly identified left bundle-branch block (LBBB), second-degree type 2 atrioventricular (AV) block, high-grade AV block, and third-degree AV block.1 An echocardiogram allows clinicians to assess left ventricular ejection fraction. New LBBB is associated with markers of structural heart disease, including ECG evidence of left ventricular hypertrophy and ST-T wave changes, and is a predictor of heart failure– related mortality.2 Patients who have an LBBB and heart failure with a reduced ejection fraction may be candidates for cardiac resynchronization therapy, a treatment that has improved symptoms and functional class and reduced mortality and morbidity.3Sinus bradycardia is common during sleep and can occur in healthy people.1 More serious bradyarrhythmia and conduction delays, however, including extreme sinus bradycardia, second-degree AV block, and sinus arrest, can occur during sleep-disordered breathing, specifically obstructive sleep apnea.4 Patients with suspected or documented bradycardia or conduction delay during sleep should be screened for sleep apnea, and they should subsequently be tested as clinically indicated.1 Sleep-related bradycardia and conduction disorders should be treated with continuous positive airway pressure, which decreases the number of episodes of bradyarrhythmia5 and reduces the need for a pacemaker.1 The patient also should lose weight.1Sinus node dysfunction, a cause of bradycardia, is usually irreversible and associated with chronic concerns that do not require acute treatment.1 Potentially reversible causes of sinus node dysfunction exist, however; these include medications, electrolyte abnormalities, infection, myocardial infarction, hypothyroidism, and metabolic abnormalities.1Stable patients with minimal symptoms who require no acute treatment should undergo a diagnostic evaluation as an outpatient. In acute care, however, nurses frequently care for patients with potentially reversible or treatable causes of sinus node dysfunction. In cardiac care, myocardial infarction caused by a right coronary artery occlusion proximal to the sinus node artery may produce sinus node dysfunction,6 and therapeutic hypothermia after cardiac arrest reduces diastolic depolarization of sinoatrial node cells.7 Sick sinus syndrome is common after cardiac surgical procedures (eg, coronary artery bypass surgery, valve surgery, and surgery for atrial fibrillation) and after orthotopic heart transplantation. In these cases, temporary atrial and ventricular epicardial pacing wires are placed during the procedure so they can be used postoperatively if needed. The sinus node often recovers, even in patients who require a permanent pacemaker; only 30% to 40% of patients remain dependent on a pacemaker during long-term follow-up.8No class I recommendations exist for medications in the management of bradycardia. Atropine, however, is reasonable and is a common first-line medication for treating symptomatic bradycardia secondary to sinus node dysfunction.1 Atropine is a parasympatholytic medication that increases sinus node automaticity and conduction through the sinoatrial node. It shortens the sinus cycle, the atrial refractory period, and the time required for the sinus node to recover.9 The typical dose of atropine for the treatment of bradycardia is 0.5 to 2.0 mg. Lower doses of atropine can cause the heart rate to decrease.10 Sympathomimetic drugs such as dopamine or epinephrine can be used as an alternative to atropine in patients who are at low risk for coronary ischemia.1 Atropine is not recommended for treating bradycardia in patients who have received a heart transplant unless evidence shows reinnervation of the autonomic nervous system,1 because in such patients atropine may cause a paradoxical high-grade AV block or sinus arrest, leading to asystole.11, 12 Reinnervation of the autonomic nervous system is possible after transplantation but may occur at different rates between the sympathetic and parasympathetic systems and may be affected by surgical technique.13Temporary or permanent pacing is not recommended in all patients with sinus node dysfunction or bradycardia. Patients who have no or infrequent symptoms, who are hemodynamically stable, or whose bradyarrhythmia occurs only during sleep do not meet the criteria for pacing therapy.1 Pacing is indicated when a patient’s symptoms are directly attributable to sinus node dysfunction, and symptomatic sinus node dysfunction is the most frequent reason for the implantation of a permanent pacemaker. Symptoms of sinus node dysfunction, such as lightheadedness or near syncope, are related to cerebral hypoperfusion.1 The primary outcome of pacing is improved quality of life, and thus it is important to ensure that symptoms are directly related to the bradycardia. Pacing is also indicated for sinus node dysfunction that does not resolve after coronary artery bypass surgery, valve surgery, or surgery for atrial fibrillation. Permanent pacing is indicated when bradycardia is secondary to the use of a guideline-recommended medication that is necessary and for which there is no alternative (eg, a β-blocker).1 In patients with sinus node dysfunction and intact AV conduction, atrial-based pacing is the preferred strategy.1Degenerative changes are a common reason for AV block and are associated with older age, diabetes, and hypertension.1 Infection, particularly Lyme carditis, a rare manifestation of Lyme disease, can cause varying degrees of AV block but can be reversed with appropriate antibiotic therapy.14 Digoxin toxicity and myocardial ischemia are other potential reversible causes of AV block that occur in patients in acute care. High-grade AV block is a complication most often associated with a right coronary artery occlusion, and when present it is associated with a higher 30-day mortality risk compared with patients with right coronary artery occlusion and no high-grade AV block.15Left anterior descending artery occlusions, however, are more associated with the development of a right bundle-branch block—which is associated with a high risker for ventricular arrhythmias, cardiogenic shock, and mortality.16 Temporary (rather than permanent) pacing should be used if indicated in asymptomatic AV block caused by a potentially reversible condition.1 A waiting period is required before a permanent pacemaker is implanted in patients with AV block after myocardial infarction to determine whether the condition can be reversed.1 Atrioventricular block is often not reversible when it occurs with cardiac sarcoidosis and thyroid disease.17, 18Atrioventricular block can be classified according to anatomical location: level of the AV node, within the bundle of His, or below the bundle of His. A block at the level of the AV node typically progresses more slowly, has a junctional escape rhythm, and responds to parasympatholytic and sympathomimetic medications. A block within or below the bundle of His can occur without warning and deteriorate quickly, has unpredictable ventricular escape, and does not respond to atropine, a parasympatholytic drug, but may improve with a sympathomimetic drug.1 Nurses must accurately differentiate between second-degree heart block Mobitz type I and Mobitz type II, because Mobitz type II is more likely to progress to complete heart block.19Atropine improves conduction through the AV node and is reasonable for treating symptomatic second- or third-degree AV block that is thought to be at the level of the AV node. Because of its short half-life, atropine is a bridge to more definitive treatment. Atropine is less effective in a block at the level of or below the bundle of His. Adverse effects are possible in patients with such blocks, and atropine should be used with caution when an AV block with a ventricular escape indicates His bundle disease.1 In a patient with an AV block believed to be at the level of the AV node, such as second-degree AV block Mobitz type I, permanent pacing is not indicated if that patient is asymptomatic or has symptoms that do not clearly correlate to the arrhythmia, or if the AV block is due to a reversible cause or is vagally mediated.1The location of the block plays a role in pacemaker indications. Patients with a block at the level of or below the bundle of His are at risk for an unreliable escape rhythm. Permanent pacing is indicated for (1) patients with second-degree AV block Mobitz type II, high-grade AV block, or third-degree AV block that is not reversible regardless of symptoms; (2) select patients with neuromuscular disorders and associated AV block; (3) patients with permanent atrial fibrillation and symptomatic bradycardia; (4) patients who develop AV block secondary to guideline-directed medical therapy, when therapy is necessary and no alternative exists; and (5) patients with persistent symptomatic AV block that does not resolve after coronary artery bypass surgery, valve surgery, or surgery for atrial fibrillation.1 Although most decisions regarding pacing are made on the basis of symptoms, a block below the level of the AV node requires pacing, regardless of symptoms, because of the high risk for complete heart block, syncope, and harm.1, 19 Unlike patients who receive a pacemaker for sinus node dysfunction, patients with AV block are not candidates for atrial pacing only. Dual-chamber pacing is indicated in most patients. Single-chamber ventricular pacing may be indicated in select patients in whom frequent ventricular pacing is not anticipated.1Although LBBB is associated with the presence of structural heart disease, it is typically asymptomatic. Patients may, however, be symptomatic when LBBB occurs with a reduced ejection fraction, because LBBB creates ventricular dyssynchrony that adversely affects stroke volume.Patients with LBBB may also present with syncope. If the syncope is unexplained, patients may require an electrophysiology study to assess for conduction abnormalities that warrant the insertion of a permanent pacemaker.1, 20 Patients who alternate between a right bundle-branch block and an LBBB have severe disease of the conduction system below the level of the AV node. These patients are at very high risk for developing a complete heart block, and permanent pacing is recommended.1, 21 While a pulmonary artery catheter is being inserted, patients could develop a temporary right bundle-branch block, because the right bundle runs close to the endocardial surface of the right ventricle. Preexisting LBBB increases the patient’s risk for developing a complete heart block. Guidelines do not, however, recommend a prophylactic temporary pacemaker in patients with LBBB who require intraoperative pulmonary artery catheterization.1, 22, 23The Guideline on the Evaluation and Management of Patients with Bradycardia and Cardiac Conduction Delay1 provides comprehensive recommendations for evaluating and managing patients with bradyarrhythmia and conduction delays. Sinus node dysfunction, AV block, and conduction delays occur frequently in patients receiving acute and critical care because of chronic conditions and complications of acute conditions and illnesses. Nurses who are skilled in recognizing ECG findings and rhythms, and in applying guideline-based recommendations, can improve the safety of and clinical outcomes among this high-risk patient population. This column synthesizes key recommendations and provides nurses with information that can be applied at the point of care.