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The normal heart beats in a regular, coordinated way because electrical impulses generated and spread by myocytes with unique electrical properties trigger a sequence of organized myocardial contractions. Arrhythmias and conduction disorders are caused by abnormalities in the generation or conduction of these electrical impulses or both.
Any heart disorder, including congenital abnormalities of structure (eg, accessory atrioventricular connection) or function (eg, hereditary ion channelopathies), can disturb rhythm. Systemic factors that can cause or contribute to a rhythm disturbance include electrolyte abnormalities (particularly low K or Mg), hypoxia, hormonal imbalances (eg, hypothyroidism, hyperthyroidism), and drugs and toxins (eg, alcohol, caffeine).
Anatomy
and Physiology
At the junction of the superior vena cava and high lateral right atrium is a cluster of cells that generates the initial electrical impulse of each normal heart beat, called the sinoatrial (SA) or sinus node. Electrical discharge of these pacemaker cells stimulates adjacent cells, leading to stimulation of successive regions of the heart in an orderly sequence. Impulses are transmitted through the atria to the atrioventricular (AV) node via preferentially conducting internodal tracts and unspecialized atrial myocytes. The AV node is located on the right side of the interatrial septum. It has a slow conduction velocity and thus delays impulse transmission. AV nodal transmission time is heart-rate dependent and is modulated by autonomic tone and circulating catecholamines to maximize cardiac output at any given atrial rate.
The atria are electrically insulated from the ventricles by the annulus fibrosus except in the anteroseptal region. There, the bundle of His, the continuation of the AV node, enters the top of the interventricular septum, where it bifurcates into the left and right bundle branches, which terminate in Purkinje fibers. The right bundle branch conducts impulses to the anterior and apical endocardial regions of the right ventricle. The left bundle branch fans out over the left side of the interventricular septum. Its anterior portion (left anterior hemifascicle) and its posterior portion (left posterior hemifascicle) stimulate the left side of the interventricular septum, which is the first part of the ventricles to be electrically activated. Thus, the interventricular septum depolarizes left to right, followed by near-simultaneous activation of both ventricles from the endocardial surface through the ventricular walls to the epicardial surface.
Electrophysiology:
The passage of ions across the myocyte cell membrane is regulated through specific ion channels that produce cyclical depolarization and repolarization of the cell, called an action potential. The action potential of a working myocyte begins when the cell is depolarized from its diastolic −90 mV transmembrane potential to a potential of about −50 mV. At this threshold potential, voltage-dependent fast Na channels open, causing rapid depolarization mediated by Na influx down its steep concentration gradient. The fast Na channel is rapidly inactivated and Na influx stops, but other time- and voltage-dependent ion channels open, allowing Ca to enter through slow Ca channels (a depolarizing event) and K to leave through K channels (a repolarizing event). At first, these 2 processes are balanced, maintaining a positive transmembrane potential, prolonging the plateau phase of the action potential. During this phase, Ca entering the cell is responsible for electromechanical coupling and myocyte contraction. Eventually, Ca influx ceases, and K efflux increases, causing rapid repolarization of the cell back to the −90 mV resting transmembrane potential. While depolarized, the cell is resistant (refractory) to a subsequent depolarizing event; initially, a subsequent depolarization is not possible (absolute refractory period), and after partial but incomplete repolarization, a subsequent depolarization is possible but occurs slowly (relative refractory period).
There are 2 general types of cardiac tissue. Fast-channel tissues (working atrial and ventricular myocytes, His-Purkinje system) have a high density of fast Na channels and action potentials characterized by little or no spontaneous diastolic depolarization (and thus very slow rates of pacemaker activity), very rapid initial depolarization rates (and thus rapid conduction velocity), and loss of refractoriness coincident with repolarization (and thus short refractory periods and the ability to conduct repetitive impulses at high frequencies). Slow-channel tissues (SA and AV nodes) have a low density of fast Na channels and action potentials characterized by more rapid spontaneous diastolic depolarization (and thus more rapid rates of pacemaker activity), slow initial depolarization rates (and thus slow conduction velocity), and loss of refractoriness that is delayed after repolarization (and thus long refractory periods and the inability to conduct repetitive impulses at high frequencies).
Normally, the SA node has the most rapid rate of spontaneous diastolic depolarization, so its cells produce spontaneous action potentials at a higher frequency than other tissues. Thus, the SA node is the dominant automatic tissue (pacemaker) in a normal heart. If the SA node does not produce impulses, tissue with the next highest automaticity rate, typically the AV node, functions as the pacemaker. Sympathetic stimulation increases the discharge frequency of pacemaker tissue, and parasympathetic stimulation decreases it.
Normal rhythm:
The resting sinus heart rate in adults is usually 60 to 100 beats/min. Slower rates (sinus bradycardia) occur in young people, particularly athletes (see Sports and the Heart: Diagnosis), and during sleep. Faster rates (sinus tachycardia) occur with exercise, illness, or emotion through sympathetic neural and circulating catecholamine drive. Normally, a marked diurnal variation in heart rate occurs, with lowest rates just before early morning awakening. A slight increase in rate during inspiration with a decrease in rate during expiration (respiratory sinus arrhythmia) is also normal; it is mediated by oscillations in vagal tone and is particularly common among healthy young people. The oscillations lessen but do not entirely disappear with age. Absolute regularity of the sinus rhythm rate is pathologic and occurs in patients with autonomic denervation (eg, in advanced diabetes) or with severe heart failure.
Most cardiac electrical activity is represented on the ECG (see Fig. 1: Cardiovascular Tests and Procedures: Diagram of the cardiac cycle, showing pressure curves of the cardiac chambers, heart sounds, jugular pulse wave, and the ECG. ), although SA node, AV node, and His-Purkinje depolarization does not involve enough tissue to be detected. The P wave represents atrial depolarization. The QRS complex represents ventricular depolarization, and the T wave represents ventricular repolarization.
The PR interval (from the beginning of the P wave to the beginning of the QRS complex) is the time from the beginning of atrial activation to the beginning of ventricular activation. Much of this interval reflects slowing of impulse transmission in the AV node. The R-R interval (time between 2 QRS complexes) represents the ventricular rate. The QT interval (from the beginning of the QRS complex to the end of the T wave) represents the duration of ventricular depolarization. Normal values for the QT interval are slightly longer in women; they are also longer with a slower heart rate. The QT interval is corrected (QTc) for influence of heart rate. The most common formula (all intervals in sec) is:
Pathophysiology
Rhythm disturbances result from abnormalities of impulse formation, impulse conduction, or both. Bradyarrhythmias result from decreased intrinsic pacemaker function or blocks in conduction, principally within the AV node or the His-Purkinje system. Most tachyarrhythmias are caused by reentry; some result from enhanced normal automaticity or from abnormal mechanisms of automaticity.
Reentry is the circular propagation of an impulse around 2 interconnected pathways with different conduction characteristics and refractory periods (see Fig. 1: Arrhythmias and Conduction Disorders: Mechanism of typical reentry.).
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Fig. 1
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Mechanism of typical reentry.
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Two pathways connect the same points. Pathway A has slower conduction and a shorter refractory period. Pathway B conducts normally and has a longer refractory period.
I. A normal impulse arriving at 1 goes down both A and B pathways. Conduction through pathway A is slower and finds tissue at 2 already depolarized and thus refractory. A normal sinus beat results.
II. A premature impulse finds pathway B refractory and is blocked, but it can be conducted on pathway A because its refractory period is shorter. On arriving at 2, the impulse continues forward and retrograde up pathway B, where it is blocked by refractory tissue at 3. A premature supraventricular beat with an increased PR interval results.
III. If conduction over pathway A is sufficiently slow, a premature impulse may continue retrograde all the way up pathway B, which is now past its refractory period. If pathway A is also past its refractory period, the impulse may reenter pathway A and continue to circle, sending an impulse each cycle to the ventricle (4) and retrograde to the atrium (5), producing a sustained reentrant tachycardia.
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Fig. 2
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Initiation of an atrioventricular nodal reentry tachycardia.
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There is an abnormal P wave (P′) and atrioventricular nodal delay (long P′R) before onset of the tachycardia.
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Under certain conditions, typically precipitated by a premature beat, reentry can produce continuous circulation of an activation wavefront producing a tachyarrhythmia (see Fig. 2: Arrhythmias and Conduction Disorders: Initiation of an atrioventricular nodal reentry tachycardia.). Normally, reentry is prevented by tissue refractoriness following stimulation. However, 3 conditions favor reentry: shortening of tissue refractoriness (eg, by sympathetic stimulation), lengthening of the conduction pathway (eg, by hypertrophy or abnormal conduction pathways), and slowing of impulse conduction (eg, by ischemia).
Symptoms and Signs
Arrhythmia and conduction disturbances may be asymptomatic or cause palpitations (sensation of skipped beats or rapid or forceful beats—see Approach to the Cardiac Patient: Palpitations), symptoms of hemodynamic compromise (eg, dyspnea, chest discomfort, presyncope, syncope), or cardiac arrest. Occasionally, polyuria results from release of atrial natriuretic peptide during prolonged supraventricular tachycardias (SVTs).
Palpation of pulse and cardiac auscultation can determine ventricular rate and its regularity or irregularity. Examination of the jugular venous pulse waves may help in the diagnosis of AV blocks and atrial tachyarrhythmias. For example, in complete AV block, the atria intermittently contract when the AV valves are closed, producing large a (cannon) waves in the jugular venous pulse (see Approach to the Cardiac Patient: Veins). Other physical findings of arrhythmias are few.
Diagnosis
History and physical examination may detect an arrhythmia and suggest possible causes, but diagnosis requires a 12-lead ECG or, less reliably, a rhythm strip, preferably obtained during symptoms to establish the relationship between symptoms and rhythm.
The ECG is approached systematically; calipers measure intervals and identify subtle irregularities. The key diagnostic features are rate of atrial activation, rate and regularity of ventricular activation, and the relationship between the two. Irregular activation signals are classified as regularly irregular or irregularly irregular (no detectible pattern). Regular irregularity is intermittent irregularity in an otherwise regular rhythm (eg, premature beats) or a predictable pattern of irregularity (eg, recurrent relationships between groups of beats).
A narrow QRS complex (< 0.12 sec) indicates a supraventricular origin (above the His bundle bifurcation). A wide QRS complex (≥ 0.12 sec) indicates a ventricular origin (below the His bundle bifurcation) or a supraventricular rhythm conducted with an intraventricular conduction defect or with ventricular preexcitation in the Wolff-Parkinson-White syndrome.
Bradyarrhythmias:
ECG diagnosis of bradyarrhythmias depends on the presence or absence of P waves, morphology of the P waves, and the relationship between P waves and QRS complexes.
A bradyarrhythmia with no relationship between P waves and QRS complexes indicates AV dissociation; the escape rhythm can be junctional (narrow QRS complex) or ventricular (wide QRS complex).
A regular QRS rhythm with a 1:1 relationship between P waves and QRS complexes indicates absence of AV block. P waves preceding QRS complexes indicate sinus bradycardia (if P waves are normal) or sinus arrest with an escape atrial bradycardia (if P waves are abnormal). P waves after QRS complexes indicate sinus arrest with a junctional or ventricular escape rhythm and retrograde atrial activation. A ventricular escape rhythm results in a wide QRS complex; a junctional escape rhythm usually has a narrow QRS (or a wide QRS with bundle branch block or preexcitation).
When the QRS rhythm is irregular, P waves usually outnumber QRS complexes; some P waves produce QRS complexes, but some do not (indicating 2nd-degree AV block—see Arrhythmias and Conduction Disorders: Second-degree AV block). An irregular QRS rhythm with a 1:1 relationship between P waves and the following QRS complexes usually indicates sinus arrhythmia with gradual acceleration and deceleration of the sinus rate (if P waves are normal).
Pauses in an otherwise regular QRS rhythm may be caused by blocked P waves (an abnormal P wave can usually be discerned just after the preceding T wave or distorting the morphology of the preceding T wave), sinus arrest, or sinus exit block (see Arrhythmias and Conduction Disorders: Sinus Node Dysfunction), as well as by 2nd-degree AV block.
Tachyarrhythmias:
Tachyarrhythmias may be divided into 4 groups, defined by being visibly regular vs irregular and by having a narrow vs wide QRS complex.
Irregular,
narrow QRS complex tachyarrhythmias include atrial fibrillation (AF), atrial flutter or true atrial tachycardia with variable AV conduction, and multifocal atrial tachycardia. Differentiation is based on atrial ECG signals, which are best seen in the longer pauses between QRS complexes. Atrial ECG signals that are continuous, irregular in timing and morphology, and very rapid (> 300/min) without discrete P waves indicate AF. Discrete P waves that vary from beat to beat with at least 3 different morphologies suggest multifocal atrial tachycardia. Regular, discrete, uniform atrial signals without intervening isoelectric periods suggest atrial flutter.
Irregular, wide
QRS complex tachyarrhythmias include the above 4 atrial tachyarrhythmias, conducted with either bundle branch block or ventricular preexcitation, and polymorphic ventricular tachycardia (VT). Differentiation is based on atrial ECG signals and the presence in polymorphic VT of a very rapid rate (> 250/min).
Regular,
narrow QRS complex tachyarrhythmias include sinus tachycardia, atrial flutter or true atrial tachycardia with a consistent AV conduction ratio, and paroxysmal SVTs (AV nodal reentrant SVT, orthodromic reciprocating AV tachycardia in the presence of an accessory AV connection, and SA nodal reentrant SVT). Vagal maneuvers or pharmacologic AV nodal blockade can help distinguish among these tachycardias. With these maneuvers, sinus tachycardia is not terminated, but it slows or AV block develops, disclosing normal P waves. Similarly, atrial flutter and true atrial tachycardia are usually not terminated, but AV block discloses flutter waves or abnormal P waves. The most common forms of paroxysmal SVT (AV nodal reentry and orthodromic reciprocating tachycardia) must terminate if AV block occurs.
Regular, wide QRS
complex tachyarrhythmias include those listed for a regular, narrow QRS complex tachyarrhythmia, each with bundle branch block or ventricular preexcitation, and monomorphic VT. Vagal maneuvers can help distinguish among them. ECG criteria to distinguish between VT and SVT with an intraventricular conduction defect have been proposed (see Table 1: Arrhythmias and Conduction Disorders: Modified Brugada Criteria for Ventricular Tachycardia ). When in doubt, the rhythm is assumed to be VT because some drugs for SVTs can worsen the clinical state if the rhythm is VT; however, the reverse is not true.
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Table 1
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Modified Brugada Criteria
for Ventricular Tachycardia
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Question
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Answer
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1. Is there AV dissociation (independent P/QRS, capture beats, fusion beats)?
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Yes = VT
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2. If no, is there an RS in any precordial lead?
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No = VT
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3. If yes, is QRS onset to nadir of S wave > 100 msec in any precordial lead?
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Yes = VT
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4. If no, are there morphologic criteria* for VT in both V1 and V6?
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Yes = VT
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5. If no.
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Supraventricular tachycardia
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*With RBBB QRS:
In V1, monophasic R, or QR, or RS
In V6, R/S < 1 or monophasic R or QR
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With LBBB QRS:
In V1, R > 30 msec wide or RS > 60 msec wide
In V6, QR or QS
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AV = atrioventricular; LBBB = left bundle branch block; RBBB = right bundle branch block; VT = ventricular tachycardia.
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Treatment
The need for treatment varies; it is guided by symptoms and risks of the arrhythmia. Asymptomatic arrhythmias without serious risks do not require treatment even if they worsen. Symptomatic arrhythmias may require treatment to improve quality of life. Potentially life-threatening arrhythmias require treatment.
Treatment is directed at causes. If necessary, direct antiarrhythmic therapy, including antiarrhythmic drugs, cardioversion-defibrillation, pacemakers, or a combination, is used. Patients with arrhythmias that have caused or are likely to cause symptoms of hemodynamic compromise may have to be restricted from driving until response to treatment has been assessed.
Drugs
for Arrhythmias
Most antiarrhythmic drugs are grouped into 4 main classes (Vaughan Williams classification) based on their dominant cellular electrophysiologic effect (see Table 2: Arrhythmias and Conduction Disorders: Antiarrhythmic Drugs (Vaughan Williams Classification) ). Digoxin and adenosine are not included in the Vaughan Williams classification. Digoxin shortens atrial and ventricular refractory periods and is vagotonic, thereby prolonging AV nodal conduction and AV nodal refractory periods. Adenosine slows or blocks AV nodal conduction and can terminate tachyarrhythmias that rely upon AV nodal conduction for their perpetuation.
Class
I:
Na channel blockers (membrane-stabilizing drugs) block fast Na channels, slowing conduction in fast-channel tissues (working atrial and ventricular myocytes, His-Purkinje system). In the ECG, this effect may be reflected as widening of the P wave, widening of the QRS complex, prolongation of the PR interval, or a combination.
Class I drugs are subdivided based on the kinetics of the Na channel effects. Class Ib drugs have fast kinetics, class Ic drugs have slow kinetics, and class Ia drugs have intermediate kinetics. The kinetics of Na channel blockade determine the heart rates at which their electrophysiologic effects become manifest. Because class Ib drugs have fast kinetics, they express their electrophysiologic effects only at fast heart rates. Thus, an ECG obtained during normal rhythm at normal rates usually shows no evidence of fast-channel tissue conduction slowing. Class Ib drugs are not very potent antiarrhythmics and have minimal effects on atrial tissue. Because class Ic drugs have slow kinetics, they express their electrophysiologic effects at all heart rates. Thus, an ECG obtained during normal rhythm at normal heart rates usually shows fast-channel tissue conduction slowing. Class Ic drugs are more potent antiarrhythmics. Because class Ia drugs have intermediate kinetics, their fast-channel tissue conduction slowing effects may or may not be evident on an ECG obtained during normal rhythm at normal rates. Class Ia drugs also block repolarizing K channels, prolonging the refractory periods of fast-channel tissues. On the ECG, this effect is reflected as QT-interval prolongation even at normal rates. Class Ib drugs and class Ic drugs do not block K channels directly.
The primary indications are SVTs for class Ia and Ic drugs and VTs for all class I drugs. The most worrisome adverse effect is proarrhythmia, a drug-related arrhythmia worse than the arrhythmia being treated. Class Ia drugs may produce torsades de pointes VT; class Ia and class Ic drugs may organize and slow atrial tachyarrhythmias enough to permit 1:1 AV conduction with marked acceleration of the ventricular response rate. All class I drugs may worsen VTs. They also tend to depress ventricular contractility. Because these adverse effects are more likely to occur in patients with a structural heart disorder, class I drugs are not generally recommended for such patients. Thus, these drugs are usually used only in patients who do not have a structural heart disorder or in patients who have a structural heart disorder but who have no other therapeutic alternatives.
Class
II:
Class II drugs are β-blockers, which affect predominantly slow-channel tissues (SA and AV nodes), where they decrease rate of automaticity, slow conduction velocity, and prolong refractoriness. Thus, heart rate is slowed, the PR interval is lengthened, and the AV node transmits rapid atrial depolarizations at a lower frequency. Class II drugs are used primarily to treat SVTs, including sinus tachycardia, AV nodal reentry, AF, and atrial flutter. These drugs are also used to treat VTs to raise the threshold for ventricular fibrillation (VF) and reduce the ventricular proarrhythmic effects of β-adrenoceptor stimulation. β-Blockers are generally well tolerated; adverse effects include lassitude, sleep disturbance, and GI upset. These drugs are contraindicated in patients with asthma.
Class
III:
Class III drugs are primarily K channel blockers, which prolong action potential duration and refractoriness in slow- and fast-channel tissues. Thus, the capacity of all cardiac tissues to transmit impulses at high frequencies is reduced, but conduction velocity is not significantly affected. Because the action potential is prolonged, rate of automaticity is reduced. The predominant effect on the ECG is QT-interval prolongation. These drugs are used to treat SVTs and VTs. Class III drugs have a risk of ventricular proarrhythmia, particularly torsades de pointes VT.
Class
IV:
Class IV drugs are the nondihydropyridine Ca channel blockers, which depress Ca-dependent action potentials in slow channel tissues and thus decrease rate of automaticity, slow conduction velocity, and prolong refractoriness. Heart rate is slowed, the PR interval is lengthened, and the AV node transmits rapid atrial depolarizations at a lower frequency. These drugs are used primarily to treat SVTsv.
Devices
and Procedures
Direct-current
(DC) cardioversion-defibrillation:
A transthoracic DC shock of sufficient magnitude depolarizes the entire myocardium, rendering the entire heart momentarily refractory to repeat depolarization. Thereafter, the most rapid intrinsic pacemaker, usually the SA node, reassumes control of heart rhythm. Thus, DC cardioversion-defibrillation very effectively terminates tachyarrhythmias that result from reentry. However, it is less effective for terminating tachyarrhythmias that result from automaticity because the return rhythm is likely to be the automatic tachyarrhythmia. For tachyarrhythmias other than VF, the DC shock must be synchronized to the QRS complex (called DC cardioversion) because a shock that falls during the vulnerable period (near the peak of the T wave) can induce VF. In VF, synchronization of a shock to the QRS complex is neither necessary nor possible. A DC shock applied without synchronization to a QRS complex is DC defibrillation.
When DC cardioversion is elective, patients should fast for 6 to 8 h to avoid the possibility of aspiration. Because the procedure is frightening and painful, brief general anesthesia or IV analgesia and sedation (eg, fentanyl 1 μg/kg, then midazolam 1 to 2 mg q 2 min to a maximum of 5 mg) is necessary. Equipment and personnel to maintain the airways must be present.
The electrodes (pads or paddles) used for cardioversion may be placed anteroposteriorly (along the left sternal border over the 3rd and 4th intercostal spaces and in the left infrascapular region) or anterolaterally (between the clavicle and the 2nd intercostal space along the right sternal border and over the 5th and 6th intercostal spaces at the apex of the heart). After synchronization to the QRS complex is confirmed on the monitor, a shock is given. The most appropriate energy level varies with the tachyarrhythmia being treated. Cardioversion efficacy increases with use of biphasic shocks, in which the current polarity is reversed part way through the shock waveform. Complications are usually minor and include atrial and ventricular premature beats and muscle soreness. Less commonly, but more likely if patients have marginal left ventricular function or multiple shocks are used, cardioversion precipitates myocyte damage and electromechanical dissociation.
DC cardioversion-defibrillation can also be applied directly to the heart during a thoracotomy or through use of an intracardiac electrode catheter; then, much lower energy levels are required.
Pacemakers:
Pacemakers sense electrical events and respond when necessary by delivering electrical stimuli to the heart. Permanent pacemaker leads are placed via thoracotomy or transvenously, but some temporary emergency pacemaker leads can be placed on the chest wall.
Indications are numerous (see Table 3: Arrhythmias and Conduction Disorders: Indications for Permanent Pacemakers ) but generally involve symptomatic bradycardia or high-grade AV block. Some tachyarrhythmias may be terminated by overdrive pacing with a brief period of pacing at a faster rate; the pacemaker is then slowed to the desired rate. Nevertheless, ventricular tachyarrhythmias are better treated with devices that can cardiovert and defibrillate as well as pace (implantable cardioverter defibrillators).
Types of pacemakers are designated by 3 to 5 letters (see Table 4: Arrhythmias and Conduction Disorders: Pacemaker Codes), representing which cardiac chambers are paced; which chambers are sensed; how the pacemaker responds to a sensed event (inhibits or triggers pacing); whether it can increase heart rate during exercise (rate-modulating); and whether pacing is multisite (in both atria, both ventricles, or more than one pacing lead in a single chamber). For example, a VVIR pacemaker paces (V) and senses (V) events in the ventricle, inhibits pacing in response to sensed event (I), and can increase its rate during exercise (R).
VVI and DDD pacemakers are the devices most commonly used. They offer equivalent survival benefits, but compared with VVI pacemakers, physiologic pacemakers (AAI, DDD, VDD) appear to reduce risk of AF and heart failure and slightly improve quality of life.
Advances in pacemaker design include lower-energy circuitry, new battery designs, and corticosteroid-eluting leads (which reduce pacing threshold), all of which increase pacemaker longevity. Mode switching refers to an automatic change in the mode of pacing in response to sensed events (eg, from DDDR to VVIR during AF).
Pacemakers may malfunction by oversensing or undersensing events, failing to pace or capture, or pacing at an abnormal rate. Tachycardias are an especially common complication. Rate-modulating pacemakers may increase stimuli in response to vibration, muscle activity, or voltage induced by magnetic fields during MRI. In pacemaker-mediated tachycardia, a normally functioning dual-chamber pacemaker senses a ventricular premature or paced beat transmitted to the atrium through the AV node or a retrograde-conducting accessory pathway, which triggers ventricular stimulation in a rapid, repeating cycle. Additional complications associated with normally functioning devices include cross-talk inhibition, in which sensing of the atrial pacing impulse by the ventricular channel of a dual-chamber pacemaker leads to inhibition of ventricular pacing, and pacemaker syndrome, in which AV asynchrony induced by ventricular pacing causes fluctuating, vague cerebral (eg, light-headedness), cervical (eg, neck pulsations), or respiratory (eg, dyspnea) symptoms. Pacemaker syndrome is managed by restoring AV synchrony by atrial pacing (AAI), single lead atrial sensing ventricular pacing (VDD), or dual-chamber pacing (DDD), most commonly the latter.
Environmental interference comes from electromagnetic sources such as surgical electrocautery and MRI, although MRI may be safe when the pacemaker generator and leads are not inside the magnet. Cellular telephones and electronic security devices are a potential source of interference; telephones should not be placed close to the device but are not a problem when used normally for talking. Walking through metal detectors does not cause pacemaker malfunction as long as patients do not linger.
Complications during implantation are uncommon but may include myocardial perforation, bleeding, and pneumothorax. Postoperative complications include infection, lead migration, and impulse generator migration.
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Table 4
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Pacemaker Codes
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I
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II
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III
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IV
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V
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Chamber Paced
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Chamber Sensed
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Response to Sensed Event
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Rate
Modulation
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Multisite Pacing
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A = Atrium
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A = Atrium
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O = None
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O = Not programmable
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O = None
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V = Ventricle
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V = Ventricle
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I = Inhibits pacemaker
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A = Atrium
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D = Dual (both)
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D = Dual (both)
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T = Triggers pacemaker to stimulate ventricles
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R = Rate-modulated
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V = Ventricle
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D = Dual (both): For events sensed in ventricles, inhibits; for events sensed in atria, triggers
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D = Dual (both)
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Implantable
cardioverter-defibrillators (ICDs):
ICDs cardiovert or defibrillate the heart in response to VT or VF. Contemporary tiered-therapy ICDs also provide antibradycardia pacing and antitachycardia pacing (to terminate responsive atrial or ventricular tachycardias) and store intracardiac electrograms. ICDs are implanted subcutaneously or subpectorally, with electrodes inserted transvenously into the right ventricle and sometimes also the right atrium. A biventricular ICD has a left ventricular epicardial lead placed.
ICDs are the preferred treatment for patients who have had an episode of VF or hemodynamically significant VT not due to reversible or transient conditions (eg, electrolyte disturbance, antiarrhythmic drug proarrhythmia, acute MI). ICDs may also be indicated for patients with VT or VF inducible during an electrophysiologic study and for patients with idiopathic or ischemic cardiomyopathy, a left ventricular ejection fraction of < 35%, and a high risk of VT or VF. Other indications are less clear (see Table 5: Arrhythmias and Conduction Disorders: Indications for Implantable Cardioverter-Defibrillators in Ventricular Tachycardia and Ventricular Fibrillation).
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Table 5
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Indications for Implantable
Cardioverter-Defibrillators in Ventricular Tachycardia and Ventricular
Fibrillation
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Level of Evidence
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Specific Indications
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Indicated (established by evidence)
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Hemodynamically-unstable VT or VF when there is no transient or reversible cause
Hemodynamically-stable sustained VT in patients with a structural heart disorder
Patients with CAD, NYHA class II or III heart failure symptoms on optimal medical therapy, and LV ejection fraction ≤ 0.30 measured at least 40 days post-MI and 3 mo after CABG surgery or PCI
Patients with CAD, NYHA class II or III heart failure symptoms on optimal medical therapy, and LV ejection fraction ≤ 0.40 measured at least 40 days post-MI and 3 mo after CABG surgery or PCI, spontaneous nonsustained VT and inducible VT/VF at electrophysiologic study
Patients with idiopathic CCM, NYHA class II or III heart failure symptoms on optimal medical therapy, and LV ejection fraction ≤ 0. 35
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Possibly indicated and supported by bulk of evidence
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Patients with CAD, NYHA class I heart failure symptoms on optimal medical therapy, LVEF ≤ 0.35 measured at least 40 days post-MI and 3 months after CABG surgery or PCI.
Patients with idiopathic CCM, significant LV dysfunction on optimal medical therapy, with unexplained syncope.
Patients with HCM with one or more high risk factors other than sustained VT/VF (family history of premature sudden death, unexplained syncope, LV thickness ≥ 30 mm, abnormal exercise BP response, nonsustained VT).
Patients with ARVC with one or more high risk factors other than sustained VT/VF (extensive RV disease, affected family member with sudden death, undiagnosed syncope)
Long QT syndrome, syncope or VT while receiving beta-blocker.
Brugada syndrome with spontaneous Type 1 Brugada ECG and syncope.
Hemodynamically-stable VT in patients without structural heart disorder in absence of applicability or response to specific therapies for recognized idiopathic VT disorders.
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Possibly indicated but less well supported by evidence
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Patients with idiopathic CCM, NYHA class I on optimal medical therapy, LVEF ≤ 0.35
Patients with long QT syndrome, without syncope or VT with one or more high risk factors (QTc > 0.5 sec, LQT1 with 2 abnormal copies of the abnormal gene and deafness [formerly Jervell and Lange-Neilsen syndrome], LQT2, LQT3)
Patients with Brugada syndrome with spontaneous Type 1 Brugada ECG and inducible sustained VT/VF at electrophysiologic study
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Not indicated
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Syncope of unknown etiology in absence of inducible VT or VF or a structural heart disorder
Incessant VT or VF
VT or VF with mechanisms amenable to catheter or surgical ablation
VT or VF due to transient or reversible disorders when correction is feasible and likely to reduce risk
Psychiatric disorders that may worsen with ICD implantation or that preclude follow-up
Life expectancy < 6 mo
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ARVC = arrhythmogenic right ventricular cardiomyopathy, CABG = coronary artery bypass graft; CAD = coronary artery disease; CCM = congestive cardiomyopathy; HCM = hypertrohpic cardiomyopathy, ICD = implantable cardioverter defibrillator; LQT1 = long QT syndrome type 1; LQT2 = long QT syndrome type 2; LQT3 = long QT syndrome type 3; LV = left ventricular; NYHA = New York Heart Association; PCI = percutaneous coronary intervention; QTc = correct QT interval, VF = ventricular fibrillation; VT = ventricular tachycardia.
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Data modified from Zipes DP et al: ACC/AHA/ESC 2006 Guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. Circulation 114(10):1088-1132, 2006.
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Because ICDs treat rather than prevent VT or VF, patients prone to these arrhythmias may require an ICD and antiarrhythmic drugs to reduce the number of episodes and need for uncomfortable shocks; this approach also prolongs the life of the ICD.
Impulse generators for ICDs typically last about 5 yr. ICDs may malfunction by delivering inappropriate pacing or shocks in response to sinus rhythm or SVTs or by not delivering appropriate pacing or shocks when needed. Causes include lead or impulse generator migration, undersensing and an increase in pacing threshold due to epicardial fibrosis at the site of prior shocks, and battery depletion.
In patients who report that the ICD has discharged but that no associated symptoms of syncope, dyspnea, chest pain or persistent palpitations occurred, follow up with the electrophysiologist within the week is appropriate. The ICD can then be electronically interrogated to determine the reason for discharge. If such associated symptoms were present, or the patient received multiple shocks, emergency department referral is indicated to look for a treatable cause (eg, coronary ischemia, electrolyte abnormality) or device malfunction.
Radiofrequency
(RF) ablation:
If a tachyarrhythmia depends on a specific pathway or ectopic site of automaticity, the site can be ablated by low-voltage, high-frequency (300 to 750 MHz) electrical energy, applied through an electrode catheter. This energy heats and necroses an area < 1 cm in diameter and up to 1 cm deep. Before energy can be applied, the target site or sites must be mapped during an electrophysiologic study (see Cardiovascular Tests and Procedures: Electrophysiologic Studies (EPS)).
Success rate is > 90% for reentrant tachycardias (via the AV node or an accessory pathway), focal atrial tachycardia and flutter, and focal idiopathic VTs (right ventricular outflow tract, left septal, or bundle branch reentrant VT). Because AF often originates or is maintained by an arrhythmogenic site in the pulmonary veins, this site can be ablated directly or, more commonly, electrically isolated by ablations at the pulmonary vein–left atrial junction or in the left atrium. Alternatively, in patients with refractory AF and rapid ventricular rates, the AV node may be ablated after permanent pacemaker implantation. RF ablation is sometimes successful in patients with VT refractory to drugs and with ischemic heart disease.
RF ablation is safe; mortality is < 1/2000. Complications include valvular damage, pulmonary vein stenosis or occlusion (if used to treat atrial fibrillation), stroke or other embolism, cardiac perforation, tamponade (1%), and unintended AV node ablation.
Surgery:
Surgery to remove a focus of a tachyarrhythmia is becoming less necessary as the less invasive RF ablation techniques evolve. But it is still indicated when an arrhythmia is refractory to RF ablation or when another indication requires a cardiac surgical procedure, most commonly when patients with AF require valve replacement or repair or when patients with VT require revascularization or resection of a left ventricular aneurysm.
Last full review/revision January 2008 by L. Brent Mitchell, MD
Content last modified January 2008
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