InternalMed_Harrison

InternalMed_Harrison. Temporary or permanent artificial pacing is the most reliable treatment for patients with symptomatic AV conduction system disease. However, exclusion of reversible causes of AV block and the need for temporary heart rate support based on the hemodynamic condition of the patient are essential considerations in each patient. Correction of electrolyte derangements and ischemia, inhibition of excessive vagal tone, and withholding of drugs with AV nodal blocking properties may increase the heart rate. Adjunctive pharmacologic treatment with atropine or isoproterenol may be useful if the block is in the AV node. Since most pharmacologic treatment may take some time to initiate and become effective, temporary pacing may be necessary. The most expeditious technique is the use of transcutaneous pacing, where pacing patches are placed anteriorly over the cardiac apex (cathode) and posteriorly between the spine and the scapula or above the right nipple (anode). Acutely, transcutaneous pacing is


InternalMed_Harrison

InternalMed_Harrison. where pacing patches are placed anteriorly over the cardiac apex (cathode) and posteriorly between the spine and the scapula or above the right nipple (anode). Acutely, transcutaneous pacing is highly effective, but its duration is limited by patient discomfort and longer-term failure to capture the ventricle owing to changes in lead impedance. If a patient requires more 1. Third-degree or high-grade AV block at any anatomic level associated with: a.


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InternalMed_Harrison. b. c. Periods of asystole >3 s or any escape rate <40 beats/min while awake, or an escape rhythm originating below the AV node d. Postoperative AV block not expected to resolve e. Catheter ablation of the AV junction f. Neuromuscular diseases such as myotonic dystrophy, Kearns-Sayre syndrome, Erb dystrophy, and peroneal muscular atrophy, regardless of the presence of symptoms 2. Second-degree AV block with symptomatic bradycardia 3. Type II second-degree AV block with a wide QRS complex with or without symptoms 4. Exercise-induced second-or third-degree AV block in the absence of ischemia 5. Atrial fibrillation with bradycardia and pauses >5 s 1. Asymptomatic third-degree AV block regardless of level 2. Asymptomatic type II second-degree AV block with a narrow QRS complex 3. Asymptomatic type II second-degree AV block with block within or below the His at electrophysiologic study 4. Firstor second-degree AV block with symptoms similar to pacemaker syndrome 1.


InternalMed_Harrison

InternalMed_Harrison. Asymptomatic type II second-degree AV block with block within or below the His at electrophysiologic study 4. Firstor second-degree AV block with symptoms similar to pacemaker syndrome 1. AV block in the setting of drug use/toxicity, when the block is expected to recur even with drug discontinuation 2. Neuromuscular diseases such as myotonic dystrophy, Kearns-Sayre syndrome, Erb dystrophy, and peroneal muscular atrophy with any degree of AV block regardless of the presence of symptoms 1. 2. Asymptomatic type I second-degree AV block at the AV node level 3. AV block that is expected to resolve or is unlikely to recur (Lyme disease, drug toxicity) Source: Modified from AE Epstein et al: J Am Coll Cardiol 51:e1, 2008.


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InternalMed_Harrison. AV block that is expected to resolve or is unlikely to recur (Lyme disease, drug toxicity) Source: Modified from AE Epstein et al: J Am Coll Cardiol 51:e1, 2008. The Bradyarrhythmias: Disorders of the Atrioventricular Node than a few minutes of pacemaker support, transvenous temporary pacing should be instituted. Temporary pacing leads can be placed from the jugular or subclavian venous system and advanced to the right ventricle, permitting stable temporary pacing for many days, if necessary. In most circumstances, in the absence of prompt resolution, conduction block distal to the AV node requires permanent pacemaking.


InternalMed_Harrison

InternalMed_Harrison. There are no randomized trials that evaluate the efficacy of pacing in patients with AV block, as there are no reliable therapeutic alternatives for AV block and untreated high-grade AV block is potentially lethal. The consensus guidelines for pacing in acquired AV conduction block in adults provide a general outline for situations in which pacing is indicated (Table 275-2). Pacemaker implantation should be performed in any patient with symptomatic bradycardia and irreversible second-or third-degree AV block, regardless of the cause or level of block in the conducting system. Symptoms may include those directly related to bradycardia and low cardiac output or to worsening heart failure, angina, or intolerance to an essential medication. Pacing in patients with asymptomatic AV block should be individualized; situations in which pacing should be considered are patients with acquired CHB, particularly in the setting of cardiac enlargement; left ventricular dysfunction; and waking heart


InternalMed_Harrison

InternalMed_Harrison. be individualized; situations in which pacing should be considered are patients with acquired CHB, particularly in the setting of cardiac enlargement; left ventricular dysfunction; and waking heart rates ≤40 beats/min. Patients who have asymptomatic second-degree AV block of either type should be considered for pacing if the block is demonstrated to be intraor infra-His or is associated with a wide QRS complex. Pacing may be indicated in asymptomatic patients in special circumstances, in patients with profound first-degree AV block and left ventricular dysfunction in whom a shorter AV interval produces hemodynamic improvement, and in the setting of milder forms of AV conduction delay (first-degree AV block, intraventricular conduction delay) in patients with neuromuscular diseases that have a predilection for the conduction system, such as myotonic dystrophy and other muscular dystrophies, and Kearns-Sayre syndrome.


InternalMed_Harrison

InternalMed_Harrison. AV block in acute MI is often transient, particularly in inferior infarction. The circumstances in which pacing is indicated in acute MI are persistent second-or third-degree AV block, particularly if symptomatic, and transient second-or third-degree AV block associated with bundle branch block (Table 275-3). Pacing is generally not indicated in the setting of transient AV block in the absence of intra-ventricular conduction delays or in the presence of fascicular block 1. Persistent second-degree AV block in the His-Purkinje system with bilateral bundle branch block or third-degree block within or below the His after AMI 2. Transient advanced (second-or third-degree) infranodal AV block and associated bundle branch block. If the site of block is uncertain, an electrophysiologic study may be necessary 3. 1. Persistent secondor third-degree AV block at the AV node level 1. Transient AV block in the absence of intraventricular conduction defects 2.


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InternalMed_Harrison. 1. Persistent secondor third-degree AV block at the AV node level 1. Transient AV block in the absence of intraventricular conduction defects 2. Transient AV block in the presence of isolated left anterior fascicular block 3. Acquired left anterior fascicular block in the absence of AV block 4. Persistent first-degree AV block in the presence of bundle branch block that is old or age-indeterminate Source: Modified from AE Epstein et al: J Am Coll Cardiol 51:e1, 2008. 1. 2. 3. 1. Syncope not demonstrated to be due to AV block when other likely causes (e.g., ventricular tachycardia) have been excluded 2. Incidental finding at electrophysiologic study of a markedly prolonged HV interval (>100 ms) in asymptomatic patients 3.


InternalMed_Harrison

InternalMed_Harrison. Incidental finding at electrophysiologic study of a markedly prolonged HV interval (>100 ms) in asymptomatic patients 3. Incidental finding at electrophysiologic study of pacing-induced infra-His block that is not physiologic 1. Neuromuscular diseases such as myotonic dystrophy, Kearns-Sayre syndrome, Erb dystrophy, and peroneal muscular atrophy with any degree of fascicular block regardless of the presence of symptoms, because there may be unpredictable progression of AV conduction disease 1. 2. Fascicular block with first-degree AV block without symptoms Source: Modified from AE Epstein et al: J Am Coll Cardiol 51:e1, 2008. or first-degree AV block that develops in the setting of preexisting bundle branch block. Fascicular blocks that develop in acute MI in the absence of other forms of AV block also do not require pacing (Table 275-3 and Table 275-4).


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InternalMed_Harrison. Distal forms of AV conduction block may require pacemaker implantation in certain clinical settings. Patients with bifascicular or trifascicular block and symptoms, particularly syncope that is not attributable to other causes, should undergo pacemaker implantation. Pacemaking is indicated in asymptomatic patients with bifascicular or trifascicular block who experience intermittent third-degree, type II second-degree AV block or alternating bundle branch block. In patients with fascicular block who are undergoing electro-physiologic study, a markedly prolonged HV interval or block below the His at long cycle lengths also may constitute an indication for permanent pacing. Patients with fascicular block and the neuromuscular diseases previously described should also undergo pacemaker implantation (Table 275-4).


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InternalMed_Harrison. In general, a pacing mode that maintains AV synchrony reduces complications of pacing such as pacemaker syndrome and pacemaker-mediated tachycardia. This is particularly true in younger patients; the importance of dual-chamber pacing in the elderly, however, is not well established. Several studies have failed to demonstrate a difference in mortality rate in older patients with AV block treated with a single-(VVI) compared with a dual-(DDD) chamber pacing mode. In some of the studies that randomized pacing mode, the risk of chronic atrial fibrillation and stroke risk decreased with physiologic pacing. In patients with sinus rhythm and AV block, the very modest increase in risk with dual-chamber pacemaker implantation appears to be justified to avoid the possible complications of single-chamber pacing. Gregory F. Michaud, William G. Stevenson


InternalMed_Harrison

InternalMed_Harrison. Gregory F. Michaud, William G. Stevenson Supraventricular tachyarrhythmias originate from or are dependent on conduction through the atrium or atrioventricular (AV) node to the ventricles. Most produce narrow QRS-complex tachycardia (QRS duration <120 ms) characteristic of ventricular activation over the Purkinje system. Conduction block in the left or right bundle branch or activation of the ventricles from an accessory pathway produces a wide QRS complex during supraventricular tachycardia that must be distinguished from ventricular tachycardia (Chap. 277). Supraventricular tachyarrhythmia may be divided into physiologic sinus tachycardia and pathologic tachycardia (Table 276-1). The prognosis and treatment vary considerably depending on the mechanism and underlying heart disease.


InternalMed_Harrison

InternalMed_Harrison. Supraventricular tachycardia can be of brief duration, termed nonsustained, or can be sustained such that an intervention, such as cardioversion or drug administration, is required for termination. Episodes that occur with sudden onset and termination are referred to as paroxysmal. Paroxysmal supraventricular tachycardia (PSVT) refers to a family of tachycardias including AV node reentry, AV reentry using an accessory pathway, and atrial tachycardia. Symptoms of supraventricular arrhythmia vary depending on the rate, duration, associated heart disease, and comorbidities and include palpitations, chest pain, dyspnea, diminished exertional capacity, and occasionally syncope. Rarely, a supraventricular arrhythmia precipitates cardiac arrest in patients with the Wolff-Parkinson-White syndrome or severe heart disease, such as hypertrophic cardiomyopathy.


InternalMed_Harrison

InternalMed_Harrison. Diagnosis requires obtaining an electrocardiogram (ECG) at the time of symptoms. For transient arrhythmia, ambulatory ECG recording is warranted (see Table 277-1). Exercise testing is useful for assessing exercise-related symptoms. Occasionally an invasive electro-physiology study is warranted to provoke the arrhythmia with pacing, confirm the mechanism, and often, perform catheter ablation.


InternalMed_Harrison

InternalMed_Harrison. Physiologic Sinus Tachycardia The sinus node is comprised of a group of cells dispersed within the superior aspect of the thick ridge of muscle known as the crista terminalis where the posterior smooth atrial wall derived from the sinus venosus meets the trabeculated anterior portion of the right atrium (Fig. 276-1). Sinus p waves are characterized by a frontal plane axis directed inferiorly and leftward, with positive p waves in leads II, III, and aVF; a negative p wave in aVR; and an initially positive biphasic p wave in V1. Normal sinus rhythm has a rate of 60–100 beats/min. Sinus tachycardia (>100 beats/min) typically occurs in response to sympathetic stimulation and vagal withdrawal, whereby the rate of spontaneous depolarization of the sinus node increases and the focus of earliest activation within the node typically shifts more leftward and closer to the superior septal aspect of the crista terminalis, thus producing taller p waves in the inferior limb leads when compared to


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InternalMed_Harrison. activation within the node typically shifts more leftward and closer to the superior septal aspect of the crista terminalis, thus producing taller p waves in the inferior limb leads when compared to normal sinus rhythm.


InternalMed_Harrison

InternalMed_Harrison. Sinus tachycardia is considered physiologic when it is an appropriate response to exercise, stress, or illness. Sinus tachycardia can be difficult to distinguish from focal atrial tachycardia (see below) that originates from a focus near the sinus node. A causative factor (such as exertion) and a gradual increase and decrease in rate favors sinus tachycardia, whereas an abrupt onset and offset favor atrial tachycardia. The distinction can be difficult and occasionally requires extended ECG monitoring or even invasive electrophysiology study. Treatment for physiologic sinus tachycardia is aimed at the underlying condition (Table 276-2). Nonphysiologic Sinus Tachycardia Inappropriate sinus tachycardia is an uncommon condition in which the sinus rate increases spontaneously at rest or out of proportion to physiologic stress or exertion. I. Physiologic sinus tachycardia Defining feature: normal sinus mechanism precipitated by exertion, stress, concurrent illness (Table 276-2) II. A.


InternalMed_Harrison

InternalMed_Harrison. I. Physiologic sinus tachycardia Defining feature: normal sinus mechanism precipitated by exertion, stress, concurrent illness (Table 276-2) II. A. Tachycardia originating from the atrium Defining feature: tachycardia may continue despite beats that fail to conduct to the ventricles, indicating that the AV node is not participating in the tachycardia circuit 1. Inappropriate sinus tachycardia Defining feature: tachycardia from the normal sinus node area that occurs without an identifiable precipitating factor as a result of dysfunctional autonomic regulation 2. Focal atrial tachycardia Defining feature: Regular atrial tachycardia with defined p wave; may be sustained, nonsustained, paroxysmal, or incessant. Frequent sites of origin occur along the valve annuli of left or right atrium, pulmonary veins, coronary sinus musculature, superior vena cava 3. Atrial flutter – macroreentrant atrial tachycardia


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InternalMed_Harrison. Defining feature: organized reentry creates organized atrial activity, commonly seen as sawtooth flutter waves at rates typically faster than 200 beats/min a. i. Right atrial reentry parallel to the tricuspid annulus and dependent on conduction through the isthmus between the inferior vena cava and tricuspid annulus 1. Counterclockwise (as viewed from the ventricular aspect) 2. b. i. Usually due to reentry in left or right atrium associated with scars usually from prior surgery or catheter ablation for atrial fibrillation, but may be idiopathic 4. Atrial fibrillation Defining feature: chaotic rapid atrial electrical activity with variable ventricular rate; the most common sustained cardiac arrhythmia in older adults 5. Multifocal atrial tachycardia Defining feature: multiple discrete p waves often seen in patients with pulmonary disease during acute exacerbations of pulmonary insufficiency B. AV nodal reentry tachycardia


InternalMed_Harrison

InternalMed_Harrison. Defining feature: multiple discrete p waves often seen in patients with pulmonary disease during acute exacerbations of pulmonary insufficiency B. AV nodal reentry tachycardia Defining feature: paroxsymal regular tachycardia with P waves visible at the end of the QRS complex or not visible at all; the most common paroxysmal sustained tachycardia in healthy young adults; more common in women C. Tachycardias associated with accessory atrioventricular pathways a. Orthodromic AV reentry tachycardia Defining feature: paroxysmal sustained tachycardia similar to AV nodal reentry; during sinus rhythm, evidence of ventricular preexcitation may be present (Wolff-Parkinson-White syndrome) or absent (concealed accessory pathway) b. Preexcited tachycardia Defining feature: wide QRS tachycardia with QRS morphology similar to VT 1. 2.


InternalMed_Harrison

InternalMed_Harrison. 2. Atrial fibrillation with preexcitation – irregular wide complex, or intermittently wide complex tachycardia, some with dangerously rapid rates faster than 250/min 3. Atrial tachycardia or flutter with preexcitation Abbreviations: AV, atrioventricular; VT, ventricular tachycardia.


InternalMed_Harrison

InternalMed_Harrison. Affected individuals are often women in the third or fourth decade of life. Fatigue, dizziness, and even syncope may accompany palpitations, which can be disabling. Additional symptoms of chest pain, headaches, and gastrointestinal upset are common. It must be distinguished from appropriate sinus tachycardia and from focal atrial tachycardia, as discussed above. Misdiagnosis of physiologic sinus tachycardia with an anxiety disorder is common. Therapy is often ineffective or poorly tolerated. Careful titration of beta blockers and/ or calcium channel blockers may reduce symptoms. Clonidine and 1477 serotonin reuptake inhibitors have also been used. Ivabradine, a drug that blocks the If current causing sinus node depolarization, is promising but is not approved for use in the United States. Catheter ablation of the sinus node has been used, but long-term control of symptoms is usually poor, and it often leaves young individuals with a permanent pacemaker.


InternalMed_Harrison

InternalMed_Harrison. When symptomatic sinus tachycardia occurs with postural hypo-tension, the syndrome is called postural orthostatic tachycardia syndrome (POTS). Symptoms are often similar to those in patients with inappropriate sinus tachycardia. POTS is sometimes due to autonomic dysfunction following a viral illness and may resolve spontaneously over 3–12 months. Volume expansion with salt supplementation, oral fludrocortisone, compression stockings, and the α-agonist midodrine, often in combination, can be helpful. Exercise training has also been purported to improve symptoms.


InternalMed_Harrison

InternalMed_Harrison. Focal Atrial Tachycardia Focal atrial tachycardia (AT) can be due to abnormal automaticity, triggered automaticity, or a small reentry circuit confined to the atrium or atrial tissue extending into a pulmonary vein, the coronary sinus, or vena cava. It can be sustained, nonsustained, paroxysmal, or incessant. Focal AT accounts for approximately 10% of PSVT referred for catheter ablation. Nonsustained AT is commonly observed on 24-h ambulatory ECG recordings, and the prevalence increases with age. Tachycardia can occur in the absence of structural heart disease or can be associated with any form of heart disease that affects the atrium. Sympathetic stimulation is a promoting factor such that AT can be a sign of underlying illness. AT with AV block can occur in digitalis toxicity. Symptoms are similar to other supraventricular tachycardias (SVTs). Incessant AT can cause tachycardia-induced cardiomyopathy.


InternalMed_Harrison

InternalMed_Harrison. AT typically presents as an SVT either with 1:1 AV conduction or with AV block that can be Wenckebach type conduction or fixed (e.g., 2:1 or 3:1) block. Because it is not dependent on AV nodal conduction, AT will not terminate with AV block, and the atrial rate will not be affected, which distinguishes AT from most AV nodal–dependent SVTs, such as AV nodal reentry and AV reentry using an accessory pathway (see below). An accelerated warm-up phase after initiation or cool-down phase prior to termination also favors AT rather than AV nodal–dependent SVT. P waves are often discrete, with an intervening isoelectric segment, in contrast to atrial flutter and macroreentrant AT (see below). When 1:1 conduction to the ventricles is present, the arrhythmia can resemble sinus tachycardia typically with a P-R interval shorter than the R-P interval (Fig. 276-2). It can be distinguished from sinus tachycardia by the p-wave morphology, which usually differs from sinus p waves depending on the


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InternalMed_Harrison. with a P-R interval shorter than the R-P interval (Fig. 276-2). It can be distinguished from sinus tachycardia by the p-wave morphology, which usually differs from sinus p waves depending on the location of the focus. Focal AT tends to originate in areas of complex atrial anatomy, such as the crista terminalis, valve annuli, atrial septum, and atrial muscle extending along cardiac thoracic veins (superior vena cava, coronary sinus, and pulmonary veins) (Fig. 276-3), and the location can often be estimated by the P-wave morphology. AT from the right atrium has a positive P-wave morphology in lead I and biphasic P-wave morphology in lead V1. AT from the atrial septum will frequently have a narrower P-wave duration than sinus rhythm. AT from the left atrium will usually have a monophasic, positive P wave in lead V1. AT that originates from superior atrial locations, such as the superior vena cava or superior pulmonary veins, will be positive in the inferior limb leads II, III, and aVF,


InternalMed_Harrison

InternalMed_Harrison. P wave in lead V1. AT that originates from superior atrial locations, such as the superior vena cava or superior pulmonary veins, will be positive in the inferior limb leads II, III, and aVF, whereas AT from a more inferior location, such as the ostium of the coronary sinus, will inscribe negative P waves in these same leads. When the focus is in the superior aspect of the crista terminalis, close to the sinus node, however, the p wave will resemble that of sinus tachycardia. Abrupt onset and offset then favor AT rather than sinus tachycardia. Depending on the atrial rate, the P wave may fall on top of the t wave or, during 2:1 conduction, may fall coincident with the QRS. Maneuvers that increase AV block, such as carotid sinus massage, Valsalva maneuver, or administration of AV nodal–blocking agents, such as adenosine, are useful to create AV block that will expose the p wave (Fig. 276-4).


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InternalMed_Harrison. II, III, aVF FIGURE 276-1 Right atrial anatomy pertinent to normal sinus rhythm and supraventricular tachycardia. A. Typical P-wave morphology during normal sinus rhythm based on standard 12-lead electrocardiogram. There is a positive P wave in leads II, III, and aVF; biphasic, initially positive P wave in V1; and negative P wave in aVR. B. Right atrial anatomy seen from a right lateral perspective with the lateral wall opened to view the septum. AVN, atrioventricular node; CS Os, coronary sinus ostium; FO, fossa ovalis; IVC, inferior vena cava; SVC, superior vena cava; TVA, FIGURE 276-3 Location of focal atrial tachycardia focus estimated by P-wave morphology. LAA, left atrial appendage; LIV, left inferior pulmonary vein; LSV, left superior pulmonary vein; RAA, right atrial appendage; RIV, right inferior pulmonary vein; RSV, right superior pulmonary vein; SVC, superior vena cava.


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InternalMed_Harrison. FIGURE 276-2 Common mechanisms underlying paroxysmal supraventricular tachycardia along with typical R-P relationships. A. Schematic showing a four-chamber view of the heart with atrioventricular node in green and an accessory pathway between the left atrium and left ventricle in yellow. Atrial tachycardia (AT; red circuit) is confined completely to atrial tissue. Atrioventricular nodal reentry tachycardia (AVNRT; blue circuit) uses atrioventricular (AV) nodal and perinodal atrial tissue. Atrioventricular reentry tachycardia (AVRT; black circuit) uses atrial and ventricular tissue, accessory pathway, AV node, and specialized conduction fibers (His-Purkinje) as part of the reentry circuit. B. Typical relation of the p wave to QRS, commonly described as the R-P to P-R relationships for the different tachycardia mechanisms. tricuspid valve annulus. 1. 2. Acute illness with fever, infection, pain 3. Hypovolemia, anemia 4. 5. 6.


InternalMed_Harrison

InternalMed_Harrison. tricuspid valve annulus. 1. 2. Acute illness with fever, infection, pain 3. Hypovolemia, anemia 4. 5. 6. Drugs that have sympathomimetic, vagolytic, or vasodilator properties, e.g., albuterol, theophylline, tricyclic antidepressants, nifedipine, hydralazine 7. II, III, aVF FIGURE 276-4 Atrial tachycardia (AT) with 1:1 and 2:1 atrioventricular (AV) conduction. Arrows indicate p waves. A. AT with 1:1 AV relationship and R-P > P-R. B. Same AT with 2:1 AV relationship after AV nodal–blocking agent administered. (Adapted from F Marchlinski: The tachyarrhythmias. In Longo DL et al [eds]: Harrison’s Principles of Internal Medicine, 18th ed. New York, McGraw-Hill, 2012, pp 1878–1900.)


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InternalMed_Harrison. (Adapted from F Marchlinski: The tachyarrhythmias. In Longo DL et al [eds]: Harrison’s Principles of Internal Medicine, 18th ed. New York, McGraw-Hill, 2012, pp 1878–1900.) Acute management of sudden-onset, sustained AT is the same as for PSVT (see below), but the response to pharmacologic therapy is variable, likely depending on the mechanism. For AT due to reentry, administration of adenosine or vagal maneuvers may transiently increase AV block without terminating tachycardia. Some ATs terminate with a sufficient dose of adenosine, consistent with triggered activity as the mechanism. Cardioversion can be effective in some, but fails in others, suggesting automaticity as the mechanism. Beta blockers and calcium channel blockers may slow the ventricular rate by increasing AV block, which can improve tolerance of the arrhythmias. Potential precipitating factors and intercurrent illness should be sought and corrected. Underlying heart disease should be considered and excluded.


InternalMed_Harrison

InternalMed_Harrison. For patients with recurrent episodes, beta blockers, the calcium channel blockers diltiazem or verapamil, and the antiarrhythmic drugs flecainide, propafenone, disopyramide, sotalol, and amiodarone can be effective, but potential toxicities and adverse effects often warrant avoiding these agents (Tables 276-3, 276-4, and 276-5). Catheter ablation targeting the AT focus is effective in more than 80% of patients and is recommended for 1479 recurrent symptomatic AT when drugs fail or are not desired or for incessant AT causing tachycardia-induced cardiomyopathy.


InternalMed_Harrison

InternalMed_Harrison. Atrioventricular Nodal Reentry Tachycardia AV nodal reentry tachycardia (AVNRT) is the most common form of PSVT, representing approximately 60% of cases referred for catheter ablation. It most commonly manifests in the second to fourth decades of life, often in women. It is often well tolerated, but rapid tachycardia, particularly in the elderly, may cause angina, pulmonary edema, hypotension, or syncope. It is not usually associated with structural heart disease.


InternalMed_Harrison

InternalMed_Harrison. The mechanism is reentry involving the AV node and likely the perinodal atrium, made possible by the existence of multiple pathways for conduction from the atrium into the AV node (Fig. 276-5). In the most common form, a slowly conducting AV nodal pathway extends from the compact AV node near the bundle of His, inferiorly along the tricuspid annulus, adjacent to the coronary sinus os. The reentry wavefront propagates up this slow pathway to the compact AV node and then exits from the fast pathway at the top of the AV node. The path back to the slow pathway to complete the circuit is not defined. The conduction time from the compact AV node region to the atrium is similar to that from the compact node to the His bundle and ventricles, such that atrial activation occurs at about the same time as ventricular activation. The p wave is therefore inscribed during, slightly before, or slightly after the QRS and can be difficult to discern. Often the P wave is seen at the end of the QRS


InternalMed_Harrison

InternalMed_Harrison. time as ventricular activation. The p wave is therefore inscribed during, slightly before, or slightly after the QRS and can be difficult to discern. Often the P wave is seen at the end of the QRS complex as a pseudo-r′ in lead V1 and pseudo-S waves in leads II, III, and aVF (Fig. 276-5A). The rate can vary with sympathetic tone. Simultaneous atrial and ventricular contraction results in atrial contraction against a closed tricuspid valve that produces cannon a waves visible in the jugular venous pulse and that the patient often perceives as a fluttering sensation in the neck. Elevated venous pressures may also lead to release of natriuretic peptides that cause posttachycardia diuresis. Less frequently, the AV nodal reentry circuit revolves in the opposite direction and gives rise to a tachycardia with an R-P interval longer than the P-R interval, similar to AT. The p wave will have the morphology noted above, and in contrast to ATs, maneuvers or medications that produce AV block


InternalMed_Harrison

InternalMed_Harrison. a tachycardia with an R-P interval longer than the P-R interval, similar to AT. The p wave will have the morphology noted above, and in contrast to ATs, maneuvers or medications that produce AV block terminate the arrhythmia.


InternalMed_Harrison

InternalMed_Harrison. Acute treatment is the same as for PSVT (discussed below). Whether ongoing therapy is warranted depends on the severity of symptoms and frequency of episodes. Reassurance and instruction as to performance of the Valsalva maneuver to terminate episodes are sufficient for many patients. Administration of an oral beta blocker, verapamil, or diltiazem at the onset of an episode has been used to


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InternalMed_Harrison. Adenosine 6–18 mg (rapid bolus) N/A Terminate reentrant SVT — involving AV node Amiodarone 15 mg/min for 10 min, 1 mg/ 0.5–1 mg/min AF, AFL, SVT, VT/VF III min for 6 h Digoxin 0.25 mg q2h until 1 mg total 0.125–0.25 mg/d AF/AFL rate control — Diltiazem 0.25 mg/kg over 3–5 min 5–15 mg/h SVT, AF/AFL rate control IV (max 20 mg) Esmolol 500 μg/kg over 1 min 50 μg/kg per min AF/AFL rate control II Ibutilide 1 mg over 10 min if over 60 kg N/A Terminate AF/AFL III Lidocaine 1–3 mg/kg at 20–50 mg/min 1–4 mg/min VT IB Metoprolol 5 mg over 3–5 min × 3 doses 1.25–5 mg q6h SVT, AF rate control; exercise-II induced VT; long QT Procainamide 15 mg/kg over 60 min 1–4 mg/min Convert/prevent AF/VT IA Quinidine 6–10 mg/kg at 0.3–0.5 mg/kg N/A Convert/prevent AF/VT IA per min Verapamil 5–10 mg over 3–5 min 2.5–10 mg/h SVT, AF rate control IV aClassification of antiarrhythmic drugs: class I—agents that primarily block inward sodium current; class IA agents also prolong action potential duration; class


InternalMed_Harrison

InternalMed_Harrison. 2.5–10 mg/h SVT, AF rate control IV aClassification of antiarrhythmic drugs: class I—agents that primarily block inward sodium current; class IA agents also prolong action potential duration; class II—antisympathetic agents; class III—agents that primarily prolong action potential duration; class IV—calcium channel–blocking agents.


InternalMed_Harrison

InternalMed_Harrison. Abbreviations: AF, atrial fibrillation; AFL, atrial flutter; AV, atrioventricular; SVT, supraventricular tachycardia; VF, ventricular fibrillation; VT, ventricular tachycardia. Digoxin 0.125–0.25 qd 38–48 Renal AF rate control — Diltiazem 30–60 q6h 3–4.5 Hepatic AF rate control/SVT IV Disopyramide 100–300 q6–8h 4–10 Renal 50%/hepatic AF/SVT prevention Ia Dofetilide 0.125–0.5 q12h 10 Renal AF prevention Nadolol 40–240 per d 10–24 Renal Same as metoprolol II Verapamil 80–120 q6–8h 4.5–12 Hepatic/renal AF rate control/RVOT VT IV Idiopathic LV VT aClassification of antiarrhythmic drugs: class I—agents that primarily block inward sodium current; class II—antisympathetic agents; class III—agents that primarily prolong action potential duration; class IV—calcium channel-blocking agents. bAmiodarone and dronedarone both are grouped in class III, but both also have class I, II, and IV properties.


InternalMed_Harrison

InternalMed_Harrison. Abbreviations: AF, atrial fibrillation; LV, left ventricular; RVOT, right ventricular outflow tract; SVT, supraventricular tachycardia; VT, ventricular tachycardia.


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InternalMed_Harrison. facilitate termination. Chronic therapy with these medications or frequently encountered as an incessant tachycardia in children, often flecainide is an option if prophylactic therapy is needed. Catheter abla-in the perioperative period of surgery for congenital heart disease. tion of the slow AV nodal pathway is recommended for patients with It presents as a narrow QRS tachycardia, often with ventriculoatrial recurrent or severe episodes or when drug therapy is ineffective, not (VA) block, such that AV dissociation is present. JET can occur as tolerated, or not desired by the patient. Catheter ablation is curative in a manifestation of increased adrenergic tone and may be seen after over 95% of patients. The major risk is heart block requiring perma-administration of isoproterenol. It may also occur for a short period of nent pacemaker implantation, which occurs in less than 1% of patients. time after ablation for AVNRT.


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InternalMed_Harrison. Accelerated junctional rhythm is a junctional automatic rhythm Junctional Tachycardia Junctional ectopic tachycardia (JET) is due between 50 and 100 beats/min. Initiation may occur with gradual to automaticity within the AV node. It is rare in adults and more acceleration in rate, suggesting an automatic focus, or after a premature Sotalol Long QT and torsades des pointes Hypotension, bronchospasm from β-blocking effect Abbreviations: AF, atrial fibrillation; AV, atrioventricular; VT, ventricular tachycardia. extension: Compact AV node: Fast pathway FIGURE 276-5 Atrioventricular (AV) node reentry. A. Leads II and V1 are shown. P waves are visible at the end of the QRS complex and are negative in lead II, and may give the impression of S waves in the inferior limb leads II, III, and aVF and an R’ in lead V1. B. Stylized version of the AV nodal reentry circuit within the triangle of Koch (Fig. 276-1) that involves AV node and its extensions along with perinodal atrial tissue.


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InternalMed_Harrison. ventricular contraction, suggesting a focus of triggered automaticity. VA conduction is usually present, with p-wave morphology and timing such that it resembles slow AVNRT. Accessory pathways (APs) occur in 1 in 1500–2000 people and are associated with a variety of arrhythmias including narrow-complex PSVT, wide-complex tachycardias, and, rarely, sudden death. Most patients have structurally normal hearts, but APs are associated with Ebstein’s anomaly of the tricuspid valve and forms of hypertrophic cardiomyopathy including PRKAG2 mutations, Danon’s disease, and Fabry’s disease.


InternalMed_Harrison

InternalMed_Harrison. APs are abnormal connections that allow conduction between the atrium and ventricles across the AV ring (Fig. 276-6). They are present from birth and are due to failure of complete partitioning of atrium and ventricle by the fibrous AV rings. They occur across either an AV valve annulus or the septum, most frequently between the left atrium and free wall of the left ventricle, followed by posteroseptal, right free wall, and anteroseptal locations. If the AP conducts from atrium to ventricle (antegrade) with a shorter conduction time than the AV node and His bundle, then the ventricles are preexcited during sinus rhythm, and the ECG shows a short P-R interval (<0.12 s), slurred initial portion of the QRS (delta wave), and prolonged QRS duration produced by slow conduction through direct activation of ventricular myocardium over the AP (Fig. 276-6A). The morphology of the QRS and delta wave is determined by the AP location (Fig. 276-7) and the degree of fusion between the excitation


InternalMed_Harrison

InternalMed_Harrison. activation of ventricular myocardium over the AP (Fig. 276-6A). The morphology of the QRS and delta wave is determined by the AP location (Fig. 276-7) and the degree of fusion between the excitation wavefronts from conduction over the AV node and conduction over the AP. Right-sided pathways preexcite the right ventricle, producing a left bundle branch block–like configuration in lead V1, and often show marked preexcitation because of relatively close proximity of the AP to the sinus node (Fig. 276-7). Left-sided pathways preexcite the left ventricle and may produce a right bundle branch–like configuration in lead V1 and a negative delta wave in aVL, indicating initial depolarization of the lateral portion of the left ventricle that can mimic q waves of lateral wall infarction (Fig. 276-7). Preexcitation due to an AP at the diaphragmatic surface of the heart, typically in the paraseptal region, produces delta waves that are negative in leads III and aVF, mimicking the q waves of


InternalMed_Harrison

InternalMed_Harrison. 276-7). Preexcitation due to an AP at the diaphragmatic surface of the heart, typically in the paraseptal region, produces delta waves that are negative in leads III and aVF, mimicking the q waves of inferior wall infarction (Fig. 276-7). Preexcitation can be intermittent and disappear during exercise as conduction over the AV node accelerates and takes over ventricular activation completely.


InternalMed_Harrison

InternalMed_Harrison. Wolff-Parkinson-White (WPW) syndrome is defined as a preexcited QRS during sinus rhythm and episodes of PSVT. There are a number of variations of APs, which may not cause preexcitation and/ or arrhythmias. Concealed APs allow only retrograde conduction, from ventricle to atrium, so no preexcitation is present during sinus rhythm, but SVT can occur. Fasciculoventricular connections between the His bundle and ventricular septum produce preexcitation but do not cause arrhythmia, nor do fibers such as atrio-Hisian connections, probably because the circuit is too short to promote reentry. Atriofascicular pathways, also known as Mahaim fibers, probably represent a duplicate AV node and His-Purkinje system that connect the right atrium to fascicles of the right bundle branch and conduct slowly only in the anterograde direction.


InternalMed_Harrison

InternalMed_Harrison. AV Reentry Tachycardia The most common tachycardia caused by an AP is the PSVT designated orthodromic AV reentry. The circulating reentry wavefront propagates from the atrium anterogradely over the AV node and His-Purkinje system to the ventricles and then reenters the atria via retrograde conduction over the AP (Fig. 276-6B). The QRS is narrow or may have typical right or left bundle branch block, but without preexcitation during tachycardia. Because excitation through the normal AV conduction system and AP are necessary, AV or VA block results in tachycardia termination. During sinus rhythm, preexcitation is seen if the pathway also allows anterograde conduction (Fig. 276-6A). Most commonly, during tachycardia the R-P interval is shorter than the P-R interval and can resemble AVNRT (Fig. 276-1). Unlike typical AVNRT, P-wave timing is never simultaneous with a narrow QRS complex because the ventricles must be activated before the reentry wavefront reaches the AP and conducts back to


InternalMed_Harrison

InternalMed_Harrison. 276-1). Unlike typical AVNRT, P-wave timing is never simultaneous with a narrow QRS complex because the ventricles must be activated before the reentry wavefront reaches the AP and conducts back to the atrium. The morphology of the P wave is determined by the pathway location, but can be difficult to assess because it is usually inscribed during the ST segment. The p wave in posteroseptal APs is negative in leads II, III, and aVF, similar to that of AV nodal reentry, but P-wave morphology differs from AV nodal reentry for pathways in other locations (Fig. 276-7).


InternalMed_Harrison

InternalMed_Harrison. Occasionally, an AP conducts extremely slowly in the retrograde direction, which results in tachycardia with a long R-P interval, similar to most ATs. These pathways are usually located in the septal region and have negative p waves in leads II, III, and aVF. Slow conduction facilitates reentry, often leading to nearly incessant tachycardia, known as paroxysmal junctional reciprocating tachycardia (PJRT). Tachycardia-induced cardiomyopathy can occur. Without an invasive electrophysiology study, it may be difficult to distinguish this form of orthodromic AV reentry from atypical AV nodal reentry or AT. FIGURE 276-6 Wolff-Parkinson-White (WPW) syndrome. A. A 12-lead electrocardiogram in sinus rhythm (SR) of a patient with WPW demonstrating short P-R interval, delta waves, and widened QRS complex. This patient had an anteroseptal location of the AP.


InternalMed_Harrison

InternalMed_Harrison. B. Orthodromic AV reentry in a patient with WPW syndrome using a posteroseptal AP. Note the P waves in the ST segment (arrows) seen in lead III and normal appearance of QRS complex. C. Three most common rhythms associated with WPW syndrome: sinus rhythm demonstrating antegrade conduction over the AP and AV node; orthodromic AVRT using retrograde conduction over the AP and antegrade conduction over the AV node; and antidromic AVRT using retrograde conduction over the AV node and antegrade conduction over the AP. AP, accessory pathway; AV, atrioventricular; AVRT, atrioventricular reentry tachycardia; WPW, Wolff-Parkinson-White.


InternalMed_Harrison

InternalMed_Harrison. Preexcited Tachycardias Preexcitated tachycardia occurs when the ventricles are activated by antegrade conduction over the AP (Fig. 276-6C). The most common is antidromic AV reentry in which activation propagates from atrium to ventricle via the AP and then conducts retrogradely to the atria via the His-Purkinje system and the AV node (or rarely a second AP). The wide QRS complex is produced entirely via ventricular excitation over the AP because there is no contribution of ventricular activation over more rapidly conducting specialized His-Purkinje fibers. This tachycardia is often indistinguishable from monomorphic ventricular tachycardia. The presence of preexcitation in sinus rhythm suggests the diagnosis.


InternalMed_Harrison

InternalMed_Harrison. FIGURE 276-7 Potential locations for accessory pathways in patients with Wolff-Parkinson-White Syndrome and typical QRS appearance of delta waves that can mimic underlying structural heart disease such as myocardial infraction of bundle branch block. AV, aor-tic valve; MV, mitral valve; PV, pulmonary valve; TV, tricuspid valve.


InternalMed_Harrison

InternalMed_Harrison. Preexcitated tachycardia also occurs if an AP allows antegrade conduction to the ventricles during AT, atrial flutter, atrial fibrillation (Fig. 276-8), or AV nodal reentry. Atrial fibrillation and atrial flutter are potentially life threatening if the AP allows very rapid repetitive conduction. Approximately 25% of APs causing preexcitation allow minimum R-to-R intervals of less than 250 ms during atrial fibrillation are therefore associated with a risk of inducing ventricular fibrillation and sudden death. Preexcited atrial fibrillation presents as a wide-complex, very irregular rhythm. During atrial fibrillation, the ventricular rate is determined by the conduction properties of the AP and AV node. The QRS complex can appear quite bizarre and change on a beat-to-beat basis due to the variability in the degree of fusion from activation over the AV node and AP, or all beats may be due to conduction over the AP (Fig. 276-8). Ventricular activation from the Purkinje system may


InternalMed_Harrison

InternalMed_Harrison. to the variability in the degree of fusion from activation over the AV node and AP, or all beats may be due to conduction over the AP (Fig. 276-8). Ventricular activation from the Purkinje system may depolarize the ventricular end of the AP and prevent 1:1 atrial wavefront conduction over the AP. Slowing AV nodal conduction can thereby facilitate AP conduction and dangerously accelerate the ventricular rate. Administration of AV nodal–blocking agents including oral or intravenous verapamil, diltiazem, beta blockers, intravenous adenosine, and intravenous amiodarone are contraindicated. Preexcited tachycardias should be treated with electrical cardioversion or intravenous procainamide or ibutilide, which may terminate or slow the ventricular rate.


InternalMed_Harrison

InternalMed_Harrison. Management of Patients with Accessory Pathways Acute management of orthodromic AV reentry is discussed below for PSVT. Patients with WPW syndrome may have wide-complex tachycardia due to antidromic AV reentry, orthodromic AV with bundle branch block, or a preexcited tachycardia, and treatment depends on the underlying rhythm. Initial patient evaluation should include assessment for aggravating factors, including intercurrent illness and factors that increase sympathetic tone. Examination should focus on excluding underlying heart disease. An echocardiogram is reasonable to exclude Ebstein’s anomaly and hypertrophic cardiomyopathy.


InternalMed_Harrison

InternalMed_Harrison. Patients with preexcitation who have symptoms of arrhythmia are at risk for developing atrial fibrillation and sudden death if they have an AP with high-risk properties. The risk of cardiac arrest is in the range of 2 per 1000 patients in adults but is likely greater in children. An invasive electrophysiology study is warranted to determine if the AP is high enough risk to warrant potentially curative catheter ablation. For patients with concealed APs or known low-risk APs causing orthodromic AV reentry, chronic therapy is guided by symptoms and frequency of events. Vagal maneuvers may terminate episodes, as may a dose of beta blocker, verapamil, or diltiazem taken at the onset of an episode. Chronic therapy with these agents or flecainide can reduce the frequency of episodes in some patients. Catheter ablation is warranted for recurrent arrhythmias when drugs are ineffective, not tolerated, or not desired by the patient or if the AP is considered high risk (Fig. 276-8). Efficacy is


InternalMed_Harrison

InternalMed_Harrison. Catheter ablation is warranted for recurrent arrhythmias when drugs are ineffective, not tolerated, or not desired by the patient or if the AP is considered high risk (Fig. 276-8). Efficacy is in the range of 95% depending on the location of the AP. Serious complications occur in fewer than 3% of patients, but can include AV block, cardiac tamponade, thromboemboli, coronary artery injury, and vascular access complications. Mortality occurs in less than 1 in 1000 patients.


InternalMed_Harrison

InternalMed_Harrison. Adults who have preexcitation but no arrhythmia symptoms have a risk of sudden death estimated to be 1 per 1000 patient-years. Electrophysiology study is usually advised for people in occupations for which an arrhythmia occurrence would place them or others at risk, such as police, military, and pilots, or for individuals who desire evaluation for risk. Routine follow-up without therapy is reasonable in others. Children are at greater risk of sudden death, approximately 2 per 1000 patient-years. FIGURE 276-8 Preexcited atrial fibrillation (AF) due to conduction over a left free wall accessory pathway (AP). The electrocardiogram shows rapid irregular QRS complexes that represent fusion between conduction over the atrioventricular node and left free wall AP. Shortest R-R intervals between preexcited QRS complexes of less than 250 ms, as in this case, indicate a risk of sudden death with this arrhythmia.


InternalMed_Harrison

InternalMed_Harrison. Acute management of narrow QRS PSVT is guided by the clinical presentation. Continuous ECG monitoring should be implemented and a 12-lead ECG should always be obtained when possible. In the presence of hypotension with unconsciousness or respiratory distress, QRS-synchronous direct current cardioversion is warranted, but this is rarely needed, because intravenous adenosine works promptly in most situations (see below). For stable individuals, initial therapy takes advantage of the fact that most PSVTs are dependent on AV nodal conduction (AV nodal reentry or orthodromic AV reentry) and therefore likely to respond to sympatholytic and vagotonic maneuvers and drugs (Fig. 276-9). As these are administered, the ECG should be continuously recorded, because the response can Hemodynamically stable regular, Narrow QRS tachyca Hemodynamically stable regular, narrow QRS tachycardia


InternalMed_Harrison

InternalMed_Harrison. Hemodynamically stable regular, Narrow QRS tachyca Hemodynamically stable regular, narrow QRS tachycardia Vagal maneuversi.v. adenosine i.v. verapamil/diltiazemNo terminationVagal maneuvers IV adenosine IV verapamil/diltiazem No termination i.v. Ibutilide + AV nodal blocking agenti.v. procainamide + AV nodal blocking agent cardioversion IV ibutilide + AV nodal–blocking agent IV procainamide + AV nodal–blocking agent Cardioversion FIGURE 276-9 Treatment algorithm for patients presenting with hemodynamically stable paroxysmal supraventricular tachycardia. AV, atrioventricular.


InternalMed_Harrison

InternalMed_Harrison. 1484 establish the diagnosis. AV block with only transient slowing of tachycardia may expose ongoing p waves, indicating AT or atrial flutter as the mechanism. Carotid sinus massage is reasonable provided the risk of carotid vascular disease is low, as indicated by absence of carotid bruits and no prior history of stroke. A Valsalva maneuver should be attempted in cooperative individuals, and if effective, the patient can be taught to perform this maneuver as needed. If vagal maneuvers fail or cannot be performed, intravenous adenosine will terminate the vast majority of PSVT by transiently blocking conduction in the AV node. Adenosine may produce transient chest pain, dyspnea, and anxiety. It is contraindicated in patients with prior cardiac transplantation due to potential hypersensitivity. It can theoretically aggravate bronchospasm. Adenosine precipitates atrial fibrillation, which is usually brief, in up to 15% of patients, so it should be used cautiously in patients with WPW


InternalMed_Harrison

InternalMed_Harrison. It can theoretically aggravate bronchospasm. Adenosine precipitates atrial fibrillation, which is usually brief, in up to 15% of patients, so it should be used cautiously in patients with WPW syndrome in whom AF may produce hemodynamic instability. Intravenous beta blockers and calcium channel blockers (verapamil or diltiazem) are also effective but may cause hypotension before and after arrhythmia termination and have a longer duration of action. These agents can also be given orally and can be taken by the patient on an as-needed basis to slow ventricular rate and facilitate termination by Valsalva maneuver. The differential diagnosis of wide-complex tachycardia includes ventricular tachycardia (Chap. 277), PSVT with bundle branch block aberrancy, and preexcited tachycardia (see above). In general, these should be managed as ventricular tachycardia until proven otherwise. If the tachycardia is regular and the patient is stable, a trial of intravenous adenosine is reasonable. Very


InternalMed_Harrison

InternalMed_Harrison. In general, these should be managed as ventricular tachycardia until proven otherwise. If the tachycardia is regular and the patient is stable, a trial of intravenous adenosine is reasonable. Very irregular wide-complex tachycardia should be managed with cardioversion, intravenous procainamide, or ibutilide, which presumes preexcited atrial fibrillation or flutter (see above). If the diagnosis of PSVT with aberrancy is unequivocal, as may be the case in patients with prior episodes, treatment for PSVT is reasonable. In all cases, continuous ECG monitoring should be implemented, and emergency cardioversion and defibrillation should be available.


InternalMed_Harrison

InternalMed_Harrison. Macrorrentrant atrial tachycardia is due to a large reentry circuit, often associated with areas of scar in the atria. Common or typical right atrial flutter is due to a circuit that revolves around the tricuspid valve annulus, bounded anteriorly by the annulus and posteriorly by functional conduction block in the crista terminalis. The wavefront passes through an isthmus between the inferior vena cava and the tricuspid valve annulus, known as the sub-Eustachian or cavotricuspid isthmus, where it is susceptible to interruption by catheter ablation. Thus, common atrial flutter is cavotricuspid isthmus-dependent atrial flutter. This circuit most commonly revolves in a counterclockwise direction (as viewed looking toward the tricuspid annulus from the ventricular aspect), which produces the characteristic negative sawtooth flutter waves in leads II, III, and aVF and positive P waves in lead V1 (Fig. 276-10). When the direction is reversed, clockwise rotation produces the opposite P-wave


InternalMed_Harrison

InternalMed_Harrison. characteristic negative sawtooth flutter waves in leads II, III, and aVF and positive P waves in lead V1 (Fig. 276-10). When the direction is reversed, clockwise rotation produces the opposite P-wave vector in those leads. The atrial rate is typically 240–300 beats/min but may be slower in the presence of atrial disease or antiarrhythmic drugs. It often conducts to the ventricles with 2:1 AV block, creating a regular tachycardia at 150 beats/min, with p waves that may be difficult to discern. Maneuvers that increase AV nodal block will typically expose flutter waves, allowing diagnosis.


InternalMed_Harrison

InternalMed_Harrison. Common right atrial flutter often occurs in association with atrial fibrillation and with atrial scar from senescence or prior cardiac surgery. Some patients with atrial fibrillation that is treated with an antiarrhythmic drug, particularly flecainide, propafenone, or amiodarone, will present with atrial flutter rather than fibrillation. Macroreentrant ATs that are not dependent on conduction through the cavotricuspid isthmus are referred to as atypical atrial flutters. They can occur in either atrium and are usually associated with areas of scar. Left atrial flutter and perimitral left atrial flutter are commonly seen after extensive left atrial ablation for atrial fibrillation or atrial surgery. The clinical presentation is similar to common atrial flutter, but with different P-wave morphologies. They can be difficult to distinguish from focal AT, and in most cases, the mechanism can only be confirmed by an electrophysiology study.


InternalMed_Harrison

InternalMed_Harrison. FIGURE 276-10 A. Common right atrial flutter, also known as cavotricuspid isthmus flutter, showing positive P waves in lead V1 and negative “sawtooth” pattern in lead II typical of counterclockwise rotation relative to the tricuspid valve annulus. (Adapted from F Marchlinski: The tachyarrhythmias. In Longo DL et al [eds]: Harrison's Principles of Internal Medicine, 18th ed. New York, McGraw-Hill, 2012, pp 1878–1900.) B. A right atrial map of common counterclockwise flutter is shown. Colors indicate activation time, progressing from red to yellow to green, blue, and purple. The reentry path parallels the tricuspid annulus.


InternalMed_Harrison

InternalMed_Harrison. Initial management of atrial flutter is similar to that for atrial fibrillation, discussed in more detail below. Electrical cardioversion is warranted for hemodynamic instability or severe symptoms. Otherwise, rate control can be achieved with administration of AV nodal–blocking agents, but this is often more difficult than for atrial fibrillation. The risk of thromboembolic events is felt to be similar to that associated with atrial fibrillation. Anticoagulation is warranted prior to conversion for episodes more than 48 h in duration and chronically for patients at increased risk of thromboembolic stroke based on the CHA2DS2-VASc scoring system (Table 276-6).


InternalMed_Harrison

InternalMed_Harrison. For a first episode of atrial flutter, conversion to sinus rhythm with no antiarrhythmic drug therapy is reasonable. For recurrent episodes, antiarrhythmic drug therapy with sotalol, dofetilide, disopyramide, and amiodarone may be considered, but more than 70% of patients experience recurrences. For recurrent episodes of common atrial flutter, catheter ablation of the cavotricuspid isthmus abolishes the arrhythmia in over 90% of patients with a low risk of complications that are largely related to vascular access and infrequent heart block. Approximately 50% of patients presenting with atrial flutter develop atrial fibrillation within the next 5 years.


InternalMed_Harrison

InternalMed_Harrison. Multifocal AT (MAT) is characterized by at least three distinct P-wave morphologies with rates typically between 100 and 150 beats/min. Unlike atrial fibrillation, there are clear isoelectric intervals between P waves (Fig. 276-11). The mechanism is likely triggered automaticity from multiple atrial foci. It is usually encountered in patients with chronic pulmonary disease and acute illness. Therapy for MAT is directed at treating the underlying disease and correcting any metabolic abnormalities. Electrical cardioversion has no effect. The calcium channel blockers verapamil or diltiazem may slow the atrial and ventricular rate. Patients with severe pulmonary disease often do not tolerate beta blocker therapy. MAT may respond to amiodarone, but long-term therapy with this agent is usually avoided due to its toxicities, particularly pulmonary fibrosis.


InternalMed_Harrison

InternalMed_Harrison. Atrial fibrillation (AF) is characterized by disorganized, rapid, and irregular atrial activation with loss of atrial contraction and with an irregular ventricular rate that is determined by AV nodal conduction (Fig. 276-12). In an untreated patient, the ventricular rate also tends aModified from GY Lip et al: Lancet 379:648, 2012. bU.S. Food and Drug Administration recommended dosing; other regimens are available outside the United States. Abbreviations: CCr, creatinine clearance; Cr, creatinine; INR, international normalized ratio; TIA, transient ischemic attack. FIGURE 276-11 Multifocal atrial tachycardia. Rhythm strip obtained from a patient with severe pulmonary disease during an acute illness. Arrows note three distinct P-wave morphologies. to be rapid and variable, between 120 and 160 beats/min, but in some patients, it may exceed 200 beats/min. Patients with high vagal tone or AV nodal conduction disease may have slow rates.


InternalMed_Harrison

InternalMed_Harrison. AF is the most common sustained arrhythmia and is a major public health problem. Prevalence increases with age, and more than 95% of AF patients are older than 60 years of age. The prevalence by age 80 is approximately 10%. The lifetime risk of developing AF for individuals 40 years old is approximately 25%. AF is slightly more common in men than women and more common in whites than blacks. Risk factors for developing AF in addition to age include hypertension, diabetes mellitus, cardiac disease, and sleep apnea. AF is a marker for heart disease, the severity of heart disease, and age, and it is therefore difficult to determine the extent to which AF itself contributes to associated increased mortality and morbidity. AF is associated with increased risk of developing heart failure. AF increases the risk of stroke by fivefold and is estimated to be the cause of 25% of strokes. It also increases the risk of dementia.


InternalMed_Harrison

InternalMed_Harrison. AF is occasionally associated with an acute precipitating factor such as hyperthyroidism, acute alcohol intoxication, or an acute illness including myocardial infarction or pulmonary embolism. AF occurs in up to 30% of patients recovering from cardiac surgery, associated with inflammatory pericarditis.


InternalMed_Harrison

InternalMed_Harrison. The clinical type of AF suggests the underlying pathophysiology (Fig. 276-12). Paroxysmal AF is defined as episodes that start and stop spontaneously. It is often initiated by small reentrant or rapidly firing foci in sleeves of atrial muscle along the pulmonary veins. Catheter ablation that isolates these foci usually abolishes the AF. Persistent AF has a longer duration, exceeding 7 days, and, in many cases, will continue unless cardioversion is performed. Cardioversion can be followed by prolonged periods of sinus rhythm. Episodes may be initiated by rapidly firing foci, but persistence of the arrhythmia is likely due to single or multiple areas of reentry facilitated by structural and electrophysiologic atrial abnormalities. In patients with long-standing persistent AF (>1 year), significant structural changes are present in the atrium that support reentry and automaticity, making it difficult to restore and maintain sinus rhythm. Some patients progress over years from paroxysmal


InternalMed_Harrison

InternalMed_Harrison. structural changes are present in the atrium that support reentry and automaticity, making it difficult to restore and maintain sinus rhythm. Some patients progress over years from paroxysmal to persistent AF. Fibrosis that develops with aging and atrial hypertrophy in response to hypertension and other cardiac disease may be an important promoting factor, although electrophysiologic changes to conduction and refractoriness occur as well in response to chronic tachycardia in the atrium.


InternalMed_Harrison

InternalMed_Harrison. Types of AF Paroxysmal AF Persistent AF requires cardioversion Long-standing persistent or permanent AF Ectopic foci Triggers Electrophysiologic remodeling fibrosis Chronic substrate fibrosis FIGURE 276-12 A rhythm strip of atrial fibrillation (AF) showing no distinct P-wave morphology and irregular ventricular response. Diagram depicts atrial fibrillation types. Paroxysmal AF is initiated by premature beats, as shown in the rhythm strip (arrow) after two sinus beats. Triggering foci are often an important cause of this arrhythmia. Persistent AF is associated with atrial structural and electrophysiologic remod-eling, as well as with triggering foci in many patients. Long-standing persistent AF is associated with greater structural remodeling with atrial fibrosis and electrophysiologic remodeling.


InternalMed_Harrison

InternalMed_Harrison. Clinical consequences are related to rapid ventricular rates, loss of atrial contribution to ventricular filling, and predisposition to thrombus formation in the left atrial appendage with potential embolization. Presentations vary with the ventricular rate and underlying heart disease and comorbidities. Many patients are asymptomatic. Rapid rates may cause hemodynamic collapse or heart failure exacerbations particularly in patients with impaired cardiac function, hypertrophic cardiomyopathy, and heart failure with preserved systolic function. Exercise intolerance and easy fatigability are common. Occasionally, dizziness or syncope occurs due to pauses when AF terminates to sinus rhythm (Fig. 276-13).


InternalMed_Harrison

InternalMed_Harrison. Treatment for AF is primarily guided by patients’ symptoms, the hemodynamic effect of AF, the duration of AF if there are persistent risk factors for stroke, and underlying heart disease. Oral anticoagulation in high-risk patients with AF includes vitamin K antagonists or the newer anticoagulants such as thrombin inhibitors (dabigatran) or factor Xa inhibitors (rivaroxaban, apixaban), but not antiplatelet agents (aspirin and clopidogrel), which have substantially less effect.


InternalMed_Harrison

InternalMed_Harrison. New-onset AF that produces severe hypotension, pulmonary edema, or angina should be electrically cardioverted starting with a QRS synchronous shock of 200 J, ideally after sedation or anesthesia is achieved. Greater shock energy and different electrode placements may be tried if the shock fails to terminate AF. If AF terminates and reinitiates, administration of an antiarrhythmic drug, such as ibutilide, and repeat cardioversion may be considered. If the patient is stable, immediate management involves rate control to alleviate or prevent symptoms, anticoagulation if appropriate, and cardioversion to restore 1487 sinus rhythm if AF is persistent. Anticoagulation strategies for new-onset AF are debated. In the absence of contraindications, it is usually appropriate to initiate systemic anticoagulation with heparin immediately, while evaluation and other therapies are implemented.


InternalMed_Harrison

InternalMed_Harrison. Cardioversion within 48 h of the onset of AF is common practice in patients who have not been anticoagulated, provided that they are not at high risk for stroke due to a prior history of embolic events, rheumatic mitral stenosis, or hypertrophic cardiomyopathy with marked left atrial enlargement. These patients are usually at risk of recurrence, such that initiation of anticoagulation is considered based on the patient’s individual risk for stroke, commonly assessed from the CHA2DS2-VASc score.


InternalMed_Harrison

InternalMed_Harrison. If the duration of AF exceeds 48 h or is unknown, there is greater concern for thromboembolism with cardioversion, even in patients considered low risk for stroke. There are two approaches to mitigate the risk related to cardioversion. One option is to anticoagulate continuously for 3 weeks before and a minimum of 4 weeks after cardioversion. A second approach is to start anticoagulation and perform a transesophageal echocardiogram to determine if thrombus is present in the left atrial appendage. If thrombus is absent, cardioversion can be performed and anticoagulation continued for a minimum of 4 weeks because recovery of atrial mechanical function after electrical or pharmacologic cardioversion may be delayed and thrombus can form and embolize days after cardioversion. Some patients may merit ongoing anticoagulation after cardioversion, depending on stroke risk profile.


InternalMed_Harrison

InternalMed_Harrison. Acute rate control can be achieved with beta blockers and/or the calcium channel blockers verapamil and diltiazem administered either intravenously or orally, as warranted by the urgency of the clinical situation. Digoxin may be added, particularly in heart failure Recorded: 02/24/2013 @ 12:44 AM (CT) 25 mm/sec, 32 mm/mV Continues-> Recorded: 02/24/2013 @ 12:44 AM (CT) 25 mm/sec, 32 mm/mV Continues-> Recorded: 02/24/2013 @ 12:44 AM (CT) 25 mm/sec, 32 mm/mV Continues-> Post trigger 7.2 seconds FIGURE 276-13 A continuous rhythm strip is shown. Atrial fibrillation is present at the top and abruptly terminates in the second tracing, with atrial and ventricular standstill for 7.2 s until resumption of sinus rhythm. The patient experienced syncope.


InternalMed_Harrison

InternalMed_Harrison. 1488 patients, because it does not have negative inotropic effects, particularly if use of AV nodal–blocking agents is limited by poor tolerance or is contraindicated. Its effect is modest but synergistic with the other AV nodal–blocking agents, but it is particularly limited when sympathetic tone is elevated. Typically, the goal of acute rate control is to reduce the ventricular rate to less than 100/min, but the goal must be guided by the clinical situation.


InternalMed_Harrison

InternalMed_Harrison. For patients who remain in AF chronically, the goal of rate control is to alleviate and prevent symptoms and prevent deterioration of ventricular function from excessive rates. β-Adrenergic blockers, calcium channel blockers, and digoxin are used, sometimes in combination. Rate should be assessed with exertion and medications adjusted accordingly. Exertion-related symptoms are often an indication of inadequate rate control. The initial goal is a resting heart rate of less than 80 beats/min that increases to less than 100 beats/min with light exertion, such as walking. If it is difficult to slow the ventricular rate to that degree, allowing a resting rate of up to 110 beats/min is acceptable provided it does not cause symptoms and ventricular function remains normal. Periodic assessment of ventricular function is warranted because some patients develop tachycardia-induced cardiomyopathy.


InternalMed_Harrison

InternalMed_Harrison. If adequate rate control in AF is difficult to achieve, further consideration should be given to restoring sinus rhythm. Catheter ablation of the AV junction to create heart block and implantation of a permanent pacemaker reliably achieve rate control without the need for AV nodal agents, but implement life-long permanent pacing. Right ventricular apical pacing induces dyssynchronous ventricular activation that can be symptomatic or depress ventricular function in some patients. Biventricular pacing may be used to minimize the degree of ventricular dyssynchrony.


InternalMed_Harrison

InternalMed_Harrison. The majority of patients warrant chronic anticoagulation, but selection of therapy should be individualized based on patient profile and risks and benefits of individual agents. Anticoagulation with a vitamin K antagonist is warranted for all patients with AF who have rheumatic mitral stenosis or mechanical heart valves for whom the newer anticoagulants have not been tested. Anticoagulation with a vitamin K antagonist (warfarin) or the newer oral anticoagulants is warranted for patients who have had more than 48 h of AF and are undergoing cardioversion, for patients who have a prior history of stroke, or for patients with a CHA2DS2-VASc score of ≥2, but it may be considered in patients with a risk score of 1. The approach to patients with paroxysmal AF is the same as for persistent AF. It is recognized that many patients who appear to have infrequent AF episodes often have asymptomatic episodes that put them at risk. Absence of AF during periodic monitoring is not sufficient to


InternalMed_Harrison

InternalMed_Harrison. AF. It is recognized that many patients who appear to have infrequent AF episodes often have asymptomatic episodes that put them at risk. Absence of AF during periodic monitoring is not sufficient to indicate low risk. The role of continuous monitoring with implanted recorders or pacemakers is not yet clear as a guide for anticoagulation in patients with a borderline risk profile. Bleeding is the major risk of anticoagulation. Major bleeding requiring transfusion or in a critical area (e.g., intracranial) occurs in approximately 1% of patients per year. Risk factors for bleeding include age >65–75 years, heart failure, history of anemia, and excessive alcohol or nonsteroidal anti-inflammatory drug use. Patients with coronary stents who require antiplatelet therapy with aspirin and a thienopyridine are at particularly high risk of bleeding.


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InternalMed_Harrison. Warfarin reduces the annual risk of stroke by 64% compared to placebo and by 37% compared to antiplatelet therapy. The newer anticoagulants, dabigatran, rivaroxaban, and apixaban, have been found to be noninferior to warfarin in individual trials, and analysis of pooled data suggests superiority to warfarin by small absolute margins of 0.4–0.7% in reduction of mortality, stroke, major bleeding, and intracranial hemorrhage. Warfarin is an inconvenient agent that requires several days to achieve a therapeutic effect (prothrombin time [PT]/international normalized ratio [INR] >2), requires monitoring of PT/INR to adjust dose, and has many drug and food interactions, thus limiting patient compliance. The newer agents are easier to use and achieve reliable anticoagulation promptly without requiring dosage adjustment based on blood tests. Dabigatran, rivaroxaban, and apixaban have renal excretion, cannot be used with severe renal insufficiency, and require dose adjustment for modest renal


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InternalMed_Harrison. dosage adjustment based on blood tests. Dabigatran, rivaroxaban, and apixaban have renal excretion, cannot be used with severe renal insufficiency, and require dose adjustment for modest renal impairment, which is of particular concern in the elderly, who are at increased bleeding risk. Excretion can also be influenced by P-glycoprotein inducers and inhibitors. Warfarin anticoagulation can be reversed by administration of fresh frozen plasma and vitamin K. Reversing agents for the newer anticoagulants are lacking (but in development), and bleeding must be managed with supportive care, with the expectation that clotting will improve over 12 h as the anticoagulant is excreted.


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InternalMed_Harrison. The antiplatelet agents aspirin and clopidogrel are inferior to warfarin for stroke prevention in AF and do not reduce the risk of bleeding. Clopidogrel combined with aspirin is better than aspirin alone but inferior to warfarin and has greater bleeding risk than aspirin alone. Chronic anticoagulation is contraindicated in some patients due to bleeding risks. Because most atrial thrombi are felt to originate in the left atrial appendage, surgical removal of the appendage, combined with atrial maze surgery, may be considered for patients undergoing surgery, although removal of the appendage has not been unequivocally shown to reduce the risk of thromboembolism. Percutaneous devices that occlude or ligate the left atrial appendage are being studied for safety and efficacy.


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InternalMed_Harrison. The decision to administer antiarrhythmic drugs or perform catheter ablation to attempt maintenance of sinus rhythm (commonly referred to as the “rhythm control strategy”) is mainly guided by patient symptoms and preferences regarding the benefits and risks of therapies. In general, patients who maintain sinus rhythm have better survival than those who continue to have AF. This is likely because continued AF is a marker of disease severity. In randomized trials, administration of antiarrhythmic medications to maintain sinus rhythm did not improve survival or symptoms compared to a rate control strategy, and the drug therapy group had more hospitalizations. Disappointing efficacy and toxicities of available antiarrhythmic drugs and patient selection bias may be factors that influenced the results of these trials. The impact of catheter ablation on mortality is not known. A rhythm control strategy is usually selected for patients with symptomatic paroxysmal AF, a first episode of


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InternalMed_Harrison. the results of these trials. The impact of catheter ablation on mortality is not known. A rhythm control strategy is usually selected for patients with symptomatic paroxysmal AF, a first episode of symptomatic persistent AF, AF with difficult rate control, and AF that has resulted in depressed ventricular function or that aggravates heart failure. A rhythm control strategy is more likely to be favored in younger patients than in sedentary or elderly patients in whom rate control is usually easily achieved. Even if sinus rhythm is apparently maintained, anticoagulation is recommended according to the CHA2DS2-VASc stroke risk profile because asymptomatic episodes of AF are common. Following a first episode of persistent AF, a strategy using AV nodal–blocking agents, cardioversion, and anticoagulation is reasonable, in addition to addressing possible aggravating factors, including hypertension, heart failure, and sleep apnea. If recurrences are infrequent, periodic cardioversion is


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InternalMed_Harrison. anticoagulation is reasonable, in addition to addressing possible aggravating factors, including hypertension, heart failure, and sleep apnea. If recurrences are infrequent, periodic cardioversion is reasonable.


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InternalMed_Harrison. Pharmacologic Therapy for Maintaining Sinus Rhythm The goal of pharmacologic therapy is to maintain sinus rhythm or reduce episodes of AF. Drug therapy can be instituted once sinus rhythm has been established or in anticipation of cardioversion. β-Adrenergic blockers and calcium channel blockers help control ventricular rate, improve symptoms, and possess a low-risk profile, but have low efficacy for preventing AF episodes. Risks and side effects of antiarrhythmic drugs are a major consideration in selecting therapy. Class I sodium channel–blocking agents (e.g., flecainide, 1489 propafenone, disopyramide) are options for subjects without sig-ventricular Arrhythmias nificant structural heart disease, but they have negative inotropic


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InternalMed_Harrison. Roy M. John, William G. Stevenson and proarrhythmic effects that warrant avoidance in patients with coronary artery disease or heart failure. The class III agents sotalol and dofetilide can be administered to patients with coronary artery disease or structural heart disease but have approximately a 3% risk of inducing excessive QT prolongation and torsades des pointes. Dofetilide should be initiated only in a hospital with ECG monitoring, and many physicians take this approach with sotalol as well. Dronedarone increases mortality in patients with heart failure. All of these agents have modest efficacy in patients with paroxysmal AF, of whom approximately 30–50% will benefit. Amiodarone is more effective, maintaining sinus rhythm in approximately two-thirds of patients. It can be administered to patients with heart failure and coronary artery disease. Over 20% of patients experience toxicities during long-term therapy.


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InternalMed_Harrison. Catheter ablation avoids antiarrhythmic drug toxicities but has procedural risks and requires an experienced center. For patients with previously untreated but recurrent paroxysmal AF, catheter ablation has similar efficacy to antiarrhythmic drug therapy and is superior to antiarrhythmic drugs for patients who have recurrent AF despite drug treatment. The procedure involves cardiac catheterization, transatrial septal puncture, and radiofrequency ablation or cryoablation to electrically isolate the regions around the pulmonary veins, abolishing the effect of triggering foci to interact with the left atrial AF substrate. Extensive areas of ablation are required, and gaps in healed ablation areas necessitate a repeat procedure in 20–50% of patients. Sinus rhythm is maintained for more than 1 year after one procedure in approximately 60% of patients and in 70–80% of patients after multiple procedures. Some patients become more responsive to antiarrhythmic drugs.


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InternalMed_Harrison. There is a 2–7% risk of major complications, including stroke (0.5–1%), cardiac tamponade (1%), phrenic nerve paralysis, bleeding from femoral access sites, and fluid overload with heart failure, that can emerge 1–3 days after the procedure. It is important to recognize the potential for delayed presentation of some complications. Ablation within the pulmonary veins can lead to pulmonary vein stenosis, presenting weeks to months after the procedure with dyspnea or hemoptysis. Esophageal ulcers can form immediately after the procedure and may rarely lead to a fistula between the left atrium and esophagus (estimated incidence of 0.1%) that presents as endocarditis and stroke 10 days to 3 weeks after the procedure.


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InternalMed_Harrison. Catheter ablation is less effective for persistent AF. More extensive ablation is often required, including areas that likely support reentry in regions outside the pulmonary venous antra, but individual strategies are debated. More than one ablation procedure is often required to maintain sinus rhythm. Surgical ablation of AF is typically performed concomitant with cardiac valve or coronary artery surgery and less commonly as a stand-alone procedure; however, for patients with persistent AF, surgical or hybrid procedures may have higher single-procedure efficacy. Risks include sinus node injury requiring pacemaker implantation. Surgical removal of the left atrial appendage may reduce stroke risk, although thrombus can form in the remnant of the appendage or if the appendage is not completely ligated. Portions of this chapter were retained from the work of the previous author, Francis Marchlinski.


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InternalMed_Harrison. Portions of this chapter were retained from the work of the previous author, Francis Marchlinski. Arrhythmias that originate in the ventricular myocardium or His-Purkinje system include premature ventricular beats, ventricular tachycardias that can be sustained or nonsustained, and ventricular fibrillation. Arrhythmia may emerge from a focus of myocardial or Purkinje cells capable of automaticity, or triggered automaticity, or from reentry through areas of scar or a diseased Purkinje system. Ventricular arrhythmias are often associated with structural heart disease and are an important cause of sudden death (Chap. 327). They also occur in some structurally normal hearts, in which case they are usually benign. Evaluation and management are guided by the risk of arrhythmic death, which is assessed based on symptoms, type of arrhythmia, and associated underlying heart disease.


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InternalMed_Harrison. Ventricular arrhythmias are characterized by their electrocardiographic appearance and duration. Conduction away from the ventricular focus through the ventricular myocardium is slower than activation of the ventricles over the Purkinje system. Hence, the QRS complex during ventricular arrhythmias will be wide, typically >0.12 s. Premature ventricular beats (also referred to as premature ventricular contractions [PVCs]) are single ventricular beats that fall earlier than the next anticipated supraventricular beat (Fig. 277-1). PVCs that originate from the same focus will have the same QRS morphology and are referred to as unifocal (Fig. 277-1A). PVCs that originate from different ventricular sites have different QRS morphologies and are referred to as multifocal (Fig. 277-1B). Two consecutive ventricular beats are ventricular couplets.


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InternalMed_Harrison. Ventricular tachycardia (VT) is three or more consecutive beats at a rate faster than 100 beats/min. Three or more consecutive beats at slower rates are designated an idioventricular rhythm (Fig. 277-1C). VT that terminates spontaneously within 30 s is designated nonsustained (Fig. 277-2), whereas sustained VT persists longer than 30 s or is terminated by an active intervention, such as administration of an intravenous medication, external cardioversion, or pacing or a shock from an implanted cardioverter-defibrillator.


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InternalMed_Harrison. Monomorphic VT has the same QRS complex from beat to beat, indicating that the activation sequence is the same from beat to beat and that each beat likely originates from the same source (Fig. 277-3A). The initial site of ventricular activation largely determines the sequence of ventricular activation. Therefore, the QRS morphology of PVCs and monomorphic VT provides an indication of the site of origin within the ventricles (Fig. 277-4). The likely origin often suggests whether an arrhythmia is idiopathic or associated with structural disease. Arrhythmias that originate from the right ventricle or septum result in late activation of much of the left ventricle, thereby producing a prominent S wave in V1 referred to as a left bundle branch block–like configuration. Arrhythmias that originate from the free wall of the left ventricle have a prominent positive deflection in V1, thereby producing a right bundle branch block–like morphology in V1. The frontal plane axis of the QRS is also


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InternalMed_Harrison. from the free wall of the left ventricle have a prominent positive deflection in V1, thereby producing a right bundle branch block–like morphology in V1. The frontal plane axis of the QRS is also useful. An axis that is directed inferiorly, as indicated by dominant R waves in leads II, III, and AVF, suggests initial activation of the cranial portion of the ventricle, whereas a frontal plane axis that is directed superiorly (dominant S waves in II, III, and AVF) suggests initial activation at the inferior wall.


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InternalMed_Harrison. Very rapid monomorphic VT has a sinusoidal appearance, also called ventricular flutter, because it is not possible to distinguish the QRS complex from the T wave (Fig. 277-3B). Relatively slow sinusoidal VTs have a wide QRS indicative of slowed ventricular conduction (Fig. 277-3C). Hyperkalemia, toxicity from excessive effects of drugs that blocks sodium channels (e.g., flecainide, propafenone, or Art. Pr. 1000 ms I


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InternalMed_Harrison. Art. Pr. 1000 ms I FIGURE 277-1 Examples of types of premature ventricular contractions (PVCs). A. Unifocal PVCs follow every sinus beat in a bigeminal frequency. Trace shows electrocardiogram lead 1 and arterial pressure (Art. Pr.). Sinus rhythm beats are followed by normal arterial waveform. The arterial pressure following premature beats is attenuated (arrows) and imperceptible to palpation. The pulse in this patient is registered at half the heart rate. B. Multifocal PVCs. The two PVCs shown have different morphologies. C. Example of accelerated idioventricular rhythm. The second QRS is a normally conducted beat. All other QRS complexes on this rhythm strip are ventricular due to accelerated idioventricular rhythm. tricyclic antidepressants), and severe global myocardial ischemia are causes.


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InternalMed_Harrison. tricyclic antidepressants), and severe global myocardial ischemia are causes. Polymorphic VT has a continually changing QRS morphology indicating a changing ventricular activation sequence. Polymorphic VT that occurs in the context of congenital or acquired prolongation of the QT interval often has a waxing and waning QRS amplitude creating a “twisting about the points” appearance referred to as Torsade de Pointes (Fig. 277-3D). Ventricular fibrillation (VF) has continuous irregular activation with no discrete QRS complexes (Fig. 277-3E). Monomorphic or polymorphic VT may transition to VF in susceptible patients. FIGURE 277-3 Examples of types of ventricular tachycardia (VT). A. Monomorphic VT with dissociated P waves (short arrows). B. Ventricular flutter. C. Sinusoidal VT due to electrolyte disturbance or drug effects. D. Polymorphic VT resulting from prolongation of QT interval (torsade de pointes VT). E. Ventricular fibrillation.


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InternalMed_Harrison. Common symptoms of ventricular arrhythmias include palpitations, dizziness, exercise intolerance, episodes of lightheadedness, syncope, or sudden death. These arrhythmias can be asymptomatic and encountered unexpectedly as an irregular pulse or heart sounds on examination, or seen on a routine electrocardiogram (ECG), exercise test, or cardiac ECG monitoring. Syncope is a concerning symptom that can be due to an episode of VT with hypotension. Syncope due to a ventricular arrhythmia often indicates that there is a significant risk for subsequent cardiac arrest and sudden death with arrhythmia recurrence. Although benign causes of syncope, such as reflex-mediated neurocardiogenic (vasovagal) syncope and orthostatic hypotension, are generally more common, it is important to consider the possibility of heart disease or a genetic syndrome causing VT. When these are suspected, hospitalization for further evaluation and monitoring is often appropriate.


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InternalMed_Harrison. Sustained VT may present with cardiac arrest, often with degeneration of the VT to VF. Occasionally a sustained VT will be hemo dynamically tolerated and present with diminished exercise capacity or exacerbation of heart failure. Many patients who are at risk for VT have known heart disease and may have an implantable cardioverterdefibrillator (ICD). In patients with an ICD, spontaneous episodes of VT may elicit an episode of transient lightheadedness, palpitations, or syncope that may be followed by a shock from the ICD (see below).


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InternalMed_Harrison. The diagnosis of ventricular arrhythmias is established by recording of the arrhythmia on an ECG or, in some cases, initiation of the arrhythmia during an electrophysiologic study (Table 277-1). A 12-lead ECG of the arrhythmia should be obtained when possible and often provides clues to the potential site of origin and possible presence of underlying heart disease (see above). When the arrhythmia is intermittent with days to weeks between symptoms, prolonged ambulatory monitoring to capture the ECG at the time of symptoms is required to make the diagnosis. Continuous ambulatory monitoring or looping event recording monitors are options. Exercise testing should be considered in patients with exercise-induced symptoms. APPROACH TO THE PATIENT:


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InternalMed_Harrison. APPROACH TO THE PATIENT: Initial assessment focuses on hemodynamic stability and evaluation for underlying heart disease. A family history of sudden death or cardiomyopathy suggests the possibility of a genetic basis for the arrhythmia and greater risk. The electrocardiogram can provide important clues. Patients with benign idiopathic arrhythmias usually have a completely normal ECG during sinus rhythm. Cardiac imaging is warranted to assess ventricular function and look for evidence of depressed ventricular function indicative of a cardiomyopathy or ventricular hypertrophy that may indicate hypertrophic cardiomyopathy. Cardiac magnetic resonance imaging (MRI) with late gadolinium enhancement can detect areas of ventricular scar, which are usually present in patients who are at risk for sustained monomorphic VT (Fig. 277-5). Evaluation to exclude atherosclerotic coronary artery disease should be performed in patients at risk, guided by age and other risk factors.


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InternalMed_Harrison. SPECIFIC ARRHYTHMIAS PVCs and Nonsustained VT Ventricular extrasystoles (Fig. 277-1A) can be due to automaticity or reentry (Chap. 278e). PVCs can be a sign of increased sympathetic tone; myocardial ischemia; hypoxia; electrolyte abnormalities, particularly hypokalemia; or underlying heart disease. During myocardial ischemia or in association with other heart disease, PVCs can be a harbinger of sustained VT or II III III II LVRVV1 = LBBB Septal or RV origin V1 = RBBB LV origin V1 II, III AVF = Inferior axis superior origin II, III AVF = Superior axis inferior origin FIGURE 277-4 Site of VT origin based on QRS morphology. LBBB, left bundle branch block; LV, left ventricle; RBBB, right bundle branch block; RV, right ventricle. I. 12-Lead ECG A. Should be obtained for PVCs, nonsustained VT, and monomorphic VT when possible


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InternalMed_Harrison. I. 12-Lead ECG A. Should be obtained for PVCs, nonsustained VT, and monomorphic VT when possible B. QRS morphology suggests ventricular region of origin V1 – dominant S = septum or RV V1 – dominant R = LV Superior axis = inferior wall origin Inferior axis = outflow region or anterior wall II. A. 24to 48-h continuous Holter monitor Useful for evaluation of daily symptoms to quantitate PVCs B. Event recorder: can be used for weeks at a time Useful for evaluation of infrequent symptoms Some require patient activation and will miss asymptomatic III. A. B. QT interval response to exercise may be abnormal in long QT syndrome IV. A. Can establish definitive diagnosis of VT versus supraventricular tachycardia with aberrancy or ventricular preexcitation B. Can provoke some arrhythmias that are otherwise infrequent C. D. Procedural risks determined by vascular access, whether ablation is performed, and the location of the arrhythmia substrate


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InternalMed_Harrison. B. Can provoke some arrhythmias that are otherwise infrequent C. D. Procedural risks determined by vascular access, whether ablation is performed, and the location of the arrhythmia substrate Abbreviation: RV, right ventricle. See text for other abbreviations. VF. In patients with heart disease, a higher frequency of ectopy and complexity (couplets and nonsustained VT) are associated with more severe disease and, in those with heart failure, with increased mortality. However, suppression of these arrhythmias with antiarrhythmic drugs does not improve survival. In the absence of cardiac disease, PVCs and nonsustained VT generally have a benign prognosis. PVCs that occur at a bigeminal frequency may not generate sufficient cardiac output for a radial pulse and hence may register at rates half that of the heart rate (Fig. 277-1A). Very frequent PVCs can depress ventricular function (see below).


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InternalMed_Harrison. Evaluation and managEmEnt When encountered during acute illness or as a new finding, evaluation should focus on detection and correction of potential aggravating factors and causes, specifically myocardial ischemia, ventricular dysfunction, and electrolyte abnormalities, most commonly hypokalemia. Underlying heart disease should be defined.


InternalMed_Harrison

InternalMed_Harrison. The ECG characteristics of the arrhythmia are often suggestive of whether structural heart disease is present. PVCs with smooth uninterrupted contours and sharp QRS deflections suggest an ectopic focus in relatively normal myocardium, whereas broad notching and slurred QRS deflections suggest a diseased myocardial substrate. The most frequent site of origin for idiopathic ventricular arrhythmias is the right ventricular outflow tract, giving rise to PVCs or VT that have a left bundle branch block configuration, with an inferiorly directed frontal plane axis as discussed below (Fig. 277-2). However, QRS morphology alone is not reliable as an indicator of disease or subsequent risk. Nonsustained VT is usually monomorphic with rates less than 200 beats/min and typically lasts less than 8 beats (Fig. 277-2). Nonsustained VT that is very rapid, polymorphic, or with a first beat that occurs prior to the peak of the T wave (“short-coupled”) is uncommon and should prompt careful evaluation


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InternalMed_Harrison. (Fig. 277-2). Nonsustained VT that is very rapid, polymorphic, or with a first beat that occurs prior to the peak of the T wave (“short-coupled”) is uncommon and should prompt careful evaluation for underlying disease or genetic syndromes associated with sudden death.


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InternalMed_Harrison. A family history of sudden death should prompt evaluation for genetic syndromes associated with sudden death, including cardiomyopathy, long QT syndrome, and arrhythmogenic right ventricular cardiomyopathy (see below). Any abnormality on the 12-lead ECG warrants further evaluation (Fig. 277-6). Repolarization abnormalities are seen in a number of genetically determined syndromes associated with sudden death, including the long QT syndrome, Brugada syndrome, arrhythmogenic right ventricular cardiomyopathy (ARVC), and hypertrophic cardiomyopathy. An echocardiogram is often necessary to assess ventricular function, wall motion abnormalities, and valvular heart disease. Cardiac magnetic resonance (CMR) imaging is also useful for this purpose and for the detection of ventricular scarring that is the substrate for sustained VT (Fig. 277-5). Exercise stress testing should be performed in patients with effort-related symptoms and in those at risk for coronary artery disease.


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InternalMed_Harrison. idiopathic pvcs and nonsustainEd vt For PVC and nonsustained VT in the absence of structural heart disease or a genetic sudden death syndrome, no specific therapy is needed unless the patient has significant symptoms or evidence that frequent PVCs are depressing ventricular function (see below). Reassurance that the arrhythmia is benign is often sufficient to allow the patient to cope with the symptoms, which will often wax and wane in frequency over years. Avoiding stimulants, such as caffeine, is helpful in some patients. If symptoms require treatment, β-adrenergic blockers and nondihydropyridine calcium channel blockers (verapamil and diltiazem) are sometimes helpful (see Table 276-3). If these fail, more potent antiarrhythmic drugs or catheter


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InternalMed_Harrison. CHAPTER 2771493 FIGURE 277-5 Imaging studies of the left ventricle (LV) used to assist ablation for ventricle tachycardia (VT). Left panel is a magnetic resonance image of a longitudinal section demonstrating thinning of the anterior wall and late gadolinium enhancement in a subendocardial scar (white arrows). The middle panel shows a two-dimensional image of the LV in long axis corresponding to the sector through the mid LV (arrow, right panel) obtained by an intracardiac echo probe positioned in the right ventricle. An electroanatomic three-dimensional map of the LV in the left anterior oblique projection is displayed in the right panel. The purple color depicts areas of normal voltage (>1.5 mV). Blue, green, and yellow represent progressively lower voltages with the red areas indicating scar (<0.5 mV). Channels of viable myocardium with slow conduction within the scar are identified with the light blue dots. Areas of ablation delivered to regions involved in reentrant VT are


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InternalMed_Harrison. scar (<0.5 mV). Channels of viable myocardium with slow conduction within the scar are identified with the light blue dots. Areas of ablation delivered to regions involved in reentrant VT are indicated by maroon dots.