TACHYCARDIAS

TACHYCARDIAS

  1. 1
    Current Diagnosis

    • A hemodynamic assessment and a 12-lead ECG should be obtained on every patient presenting with tachycardia.

    • Tachycardia is defined as a cardiac rhythm greater than 100 beats/min.

    •   Tachycardias may be supraventricular or ventricular in origin.

    • SVTs may be narrow complex (QRS duration less than 120 ms) or wide complex (QRS duration greater than 120 ms). VTs are always wide complex.

    • History taking is useful in aiding in the diagnosis and definition of tachycardia.

    • Patients with tachycardias might complain of palpitations, fatigue, lightheadedness, chest discomfort, dyspnea, presyncope, or syncope.

    • A history of syncope is a red flag and should prompt immediate referral to an electrophysiologist.

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  2. 2
    Current Therapy

    • All wide-complex tachycardias should be treated as ventricular in origin unless proved otherwise. The misdiagnosis of SVT when VT is present is associated with worse prognosis.

    • Radiofrequency ablation is often successful in curing SVTs and some VTs.

    • Wide-QRS complex tachycardias are commonly secondary to VT in the setting of structural heart disease, and effective therapy is accomplished with cardioverter-defibrillator implantation.

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  3. 3
    Tachycardia

    Tachycardia is any cardiac rhythm with a rate greater than 100 beats/min. It may be supraventricular or ventricular in origin. Supraventricular tachycardias (SVTs) almost always manifest as narrow-complex (less than 120 msec) tachycardias on an electrocardiogram (ECG). However, wide-complex (greater than 120 msec) tachycardias occur if there is aberrant conduction or a bundle branch block. Ventricular tachycardias (VTs) occur when there are more than three consecutive ventricular beats at a rate greater than 100 beats per minute. VTs always manifest as wide-complex tachycardias.

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  4. 4
    Epidemiology

    Supraventricular Tachycardias

    Though rarely life threatening, SVTs are common, may be persistent, and often reoccur throughout one’s lifetime. The etiology of SVTs varies with age, sex, and comorbid conditions. Paroxysmal SVTs (PSVTs) are estimated to have a prevalence of 2.25 per 1000 and an incidence of 35 per 100,000 person-years, according to the Marshfield Epidemiologic Study Area (MESA) conducted in Wisconsin. In this study, the mean age of onset of PSVT was 57 years, and age of onset ranged from infancy to more than 90 years. Female patients were shown to have a twofold risk compared with their male counterparts in the MESA study.

    Ventricular Tachycardias

    VTs have a prevalence of about 20 per 100,000 persons in the general population and occur more commonly in men. An appreciable percentage (3.5%) of VTs occur after myocardial infarction (MI), and the incidence of post-MI VT increases with age.

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  5. 5
    Pathophysiology

    All tachycardias are produced by one or more mechanisms that include disorders of impulse initiation (automaticity) and abnormalities of impulse conduction (reentrance). Tissues exhibiting abnormal automaticity that underlie SVT can reside in the atria, the AV junction, or vessels that communicate directly with the atria, such as the vena cava or pulmonary veins. Normally, the sinus node contains the dominant pacemaking function and is made of cells with faster rates of phase 4 diastolic depolarization (Figure 1). Cells with abnormal automaticity (enhanced diastolic phase 4 depolarization) can arise in other locations (ectopic foci), and if their firing rate exceeds that of the sinus node, then the ectopic focus becomes the predominant pacemaker of the heart.

    FIGURE 1    A, Diagram of reentry. The impulse is initiated at Π. I and  II represent two distinct pathways. a represents unidirectional block, b represents slow conduction, and c shows the propagation of  the wavefront reentering the circuit. B, A cardiac action potential. The different phases of the action potential are 0–4. Phase 4 demonstrates automaticity, which, when it reaches threshold, will initiate the next cardiac action potential. C, A cardiac action potential demonstrating early afterdepolarization (EAD) at the end of phase 2. D, A cardiac action potential demonstrating a delayed afterdepolarization (DAD) during phase 4.

    Reentry is the most common mechanism by which SVT occurs. It is also the mechanism for atrial flutter, atrioventricular (AV) node reentry tachycardia (AVNRT), some atrial tachycardias, AV reciprocating tachycardia (AVRT), some VTs, and ventricular fibrillation (VF). Initiation and maintenance of a reentrant tachycardia requires a unidirectional block in one limb of the circuit and slow conduction in the other. A unidirectional block can result from acceleration of the heart rate or from a premature impulse that is blocked during the refractory period of the pathway.

    As shown in Figure 1A, a normal impulse arriving at Π is propagated down both a and b. Conduction through pathway a is initially faster and unimpeded, while conduction through b is slow. A normal sinus beat is produced. A second impulse attempts to go down a and b; however, this time finds a refractory, and thus no conduction occurs (unidirectional block). Pathway b, which is slow conducting and has a shorter refractory period, conducts the impulse.

    This results in a premature supraventricular beat with a prolonged PR interval. The impulse through b may continue in a retrograde pathway (c) to a, and if a is past its refractory period a circuit is created through which the impulse can continue to circle, producing a persistent reentrant tachycardia.

     

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  6. 6
    Clinical Manifestations

    Patients with paroxysmal arrhythmias are often asymptomatic on presentation. When symptoms are present, they can include palpitations, fatigue, lightheadedness, chest discomfort, dyspnea, presyncope, and syncope. Syncope is observed in about 15% of patients with SVT. Patients with ventricular arrhythmias more often present with presyncope, syncope, or even cardiac arrest. A history of syncope should warrant immediate referral to an electrophysiologist.

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  7. 7
    Diagnosis

    History taking is useful in aiding in the diagnosis and definition of tachycardia. It is important for the clinician to assess whether or not the palpitations are regular or irregular, the number of episodes, possible triggers, and the nature of onset and termination (whether abrupt or gradual). Recurrent episodes with abrupt onset and termination are designated paroxysmal. Episodes with a gradual onset and termination are nonparoxysmal (e.g., sinus tachycardia). Irregular palpitations likely are due to premature depolarizations, suggesting atrial fibrillation or multifocal atrial tachycardia. Multifocal atrial tachycardia is often encountered in patients with pulmonary disease. Premature beats are often described by the patient as pauses followed by a sensation of a strong heart beat or as irregularities in heart rhythm.

    On physical examination, if irregular cannon A waves are observed in the jugular vein or variation in the intensity of the S1 heart sound is heard, then a ventricular origin is strongly suggested. Termination of the tachycardia with vagal maneuvers strongly suggests a reentrant tachycardia involving AV nodal tissue such as AVNRT or AVRT.

    A resting echocardiogram should be recorded. In the absence of symptoms this may be of low diagnostic yield. However, the presence of preexcitation (Figure 2) on the ECG suggests AVRT and is enough to make a presumptive diagnosis. Baseline ECG with preexcitation in combination with a history consistent with paroxysmal palpitations strongly suggests episodic atrial fibrillation and is concerning. These patients are at risk for sudden cardiac death and require immediate electrophysiologic evaluation. Patients without concerning symptoms such as syncope or persistent regular tachycardia may be sent home with an event monitor, with follow-up at a later date. A 24-hour Holter monitor can be used in patients who report daily transient tachycardia. In patients with infrequent arrhythmias, a loop recorder is more useful. An implantable loop recorder may be used in patients who have rare episodes associated with hemodynamic instability.

    FIGURE 2    A 12-lead electrocardiogram depicting typical AV  node reentry tachycardia. Note the absence of obvious atrial activity or P wave.

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  8. 8
    Differential Diagnosis

    Narrow QRS-Complex Tachycardia

    Narrow QRS-complex (less than 120 msec) SVTs are differentiated according to their mechanism and include sinus tachyarrhythmias, AVNRT, focal and nonparoxysmal junctional tachycardias, AVRT, focal atrial tachycardias, and macro-reentrant atrial tachycardia.

    Wide QRS-Complex Tachycardia

    Wide QRS-complex tachycardias may be supraventricular or ventricular in origin. Examples of wide QRS-complex SVTs include SVT with AV conduction via an accessory pathway, such as in Wolff– Parkinson–White (WPW) syndrome, or any SVT with aberrant conduction or ventricular pacing.

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  9. 9
    Specific Tachycardias

    Supraventricular Tachycardias Sinus Tachyarrhythmias

    Sinus tachycardia can result from physiologic stimulation of the sinus node or sinus node reentry (sinus node reentry tachycardia). The latter results in paroxysmal nonsustained episodes of tachycardia.

    Normally, sinus tachycardia occurs as an appropriate response to physiologic stimulus such as exercise. Pathologic causes that can induce sinus tachycardia include hyperthyroidism, pyrexia, hypovolemia, infections, or anemia. Drugs that can cause sinus tachycardia include atropine, aminophylline, catecholamines, and anticancer treatments (such as doxorubicin [Adriamycin]). Stimulants such as caffeine, alcohol, and nicotine and recreational drugs such as cocaine, amphetamines, and ecstasy can induce sinus tachycardia. It can also result from an excessive stimulus such as hyperthyroidism.

    On ECG, a normal axis with upright P waves in I, II, and aVF and a negative P wave in aVR is revealed.

    In addition to eliminating the underlying offensive agent such as excessive caffeine use or hyperthyroidism, β-blockers are very effective for terminating and suppressing sinus tachycardia.

    Nondihyhdropyridine calcium-channel blockers, such as diltiazem (Cardizem) or verapamil (Istopin) may also be used. Vagal maneuvers, adenosine (Adenocard), β-blockers, and nondihydropyridine calcium-channel blockers are effective in treating reentry sinus tachycardia. In rare cases where inappropriate sinus tachycardia is refractory, catheter ablation may be performed.

    Atrioventricular Nodal Reciprocating Tachycardia

    AVNRT is the most common form of PSVT, and it produces rates of tachycardia between 140 and 250 beats per minute. It is more prevalent in female patients. Patients typically report associated palpitations, dizziness, and neck pulsations.

    The mechanism of AVNRT is a reentry circuit that is now known to involve perinodal atrial tissue as well, and it is not always confined to the compact AV node as previously believed. In AVNRT, reciprocation occurs between two distinct pathways: The first, fast pathway, is located near the apex of Koch’s triangle; the second is a slow pathway that extends from the compact AV-node tissue and stretches along the septal margin of the tricuspid annulus at the level of, or slightly superior to, the coronary sinus. The fast pathway conducts rapidly with a slow recovery time and a longer refractory period, and the second pathway conducts slowly with a short refractory period. AVNRT is initiated when a premature impulse finds the fast pathway refractory and is thus conducted anterogradely through the slow pathway. The impulse continues past the AV node, down the His–Purkinje system, activates the ventricles, and approaches the His bundle. Here, the impulse finds the fast pathway in recovery. The fast pathway then serves as a retrograde pathway for conduction back to the atria (Figure 3). This produces a P wave during or very close to the QRS complex, often with a pseudo-R′ in V1.

    FIGURE 3    A, Normal conduction system. Abbreviations: AVN  = atrioventricular node; LA = left atrium; LBB = left bundle branch; LV = left ventricle; RA = right atrium; RBB, right bundle branch; RV = right ventricle; SN, sinus node. B, Diagram of heart depicting typical atrioventricular node reentry tachycardia (AVNRT) with antegrade conduction via the slow AVN and retrograde conduction via the fast AVN. C, Diagram of the heart depicting orthodromic atrioventricular reciprocating tachycardia (o-AVRT), with antegrade conduction via  the AVN and retrograde conduction via the accessory pathway  (AP).

    Rarely, an atypical AVNRT occurs in which there is anterograde conduction through the fast pathway and retrograde conduction through the slow pathway, producing a long R-P tachycardia. The P wave, negative in III and aVF, is inscribed prior to the QRS. Sometimes, though infrequently, the circuit is composed of slowly conducting tissues in both limbs of the circuit, resulting in a P wave inscribed after the QRS (a retrograde P wave) (Figure 4).

    FIGURE 4    Electrocardiogram lead V1 recorded during  administration of adenosine. Termination of atrioventricular node reentry tachycardia occurs in the antegrade slow pathway. The arrow points to retrograde atrial activity at the terminal portion of the QRS that is sometimes apparent during tachycardia.

    Adenosine 6 mg IV push is administered to terminate the rhythm, and if the initial dose is unsuccessful, two more doses of 12 mg of adenosine may be administered. Adenosine has a half-life of only 9 seconds, and it terminates the circuit by causing transient block in AVN conduction. Long-term therapy with a β-blocker or calcium channel blocker can prevent recurrence. If AVN is recurrent, radiofrequency ablation is the treatment of choice and has a low risk of complication.

    Atrioventricular Reciprocating Tachycardia (Extranodal Accessory Pathways)

    An accessory pathway is a pathway outside the AV node that connects the myocardium of the atrium and the ventricle. Accessory pathways may be located across the mitral or tricuspid annulus and may be capable of anterograde or retrograde conduction, or both.

    Accessory pathways that conduct in a retrograde function are referred to as “concealed” because they do not reveal preexcitation on ECG.

    Those capable of anterograde conduction are referred to as “manifest.” WPW syndrome is diagnosed if the patient has both preexcitation on ECG and tachyarrhythmias (Figure 5). AVRT may be orthodromic or antidromic. Orthodromic AVRT occurs when there is anterograde conduction down the AV node and retrograde conduction up the accessory pathway (Figure 6). In antidromic AVRT the reverse occurs.

    FIGURE 5    Electrocardiogram lead III recording of a  QRS demonstrating ventricular preexcitation (arrow), also called Wolff– Parkinson–White pattern.

    FIGURE 6    A 12-lead electrocardiogram depicting  orthodromic atrioventricular reciprocating tachycardia. The arrow highlights the atrial activity, which is occurring well after the QRS  complex.

    Atrial fibrillation is considered life-threatening in patients with WPW syndrome. This is because rapid repetitive conduction can occur via the accessory pathway (which has a short refractory period), resulting in a rapid ventricular rate that can degenerate into VF.

    Administration of adenosine can precipitate atrial fibrillation in 10% to 15% of patients with an extranodal accessory pathway. Therefore, if it is unknown whether or not the patient has an anterogradely conducting accessory pathway, it is good practice to have a defibrillator present at the bedside during administration of adenosine. For patients with known WPW syndrome (or delta wave on baseline ECG), procainamide (Pronestyl)1 or ibutilide (Corvert), drugs that slow conduction over the accessory pathway, can be administered instead of adenosine.

    Focal and Nonparoxysmal Junctional Tachycardia

    Focal Junctional Tachycardia

    Focal junctional tachycardia is a generally rare phenomenon that can occur by automaticity or reentry mechanisms. By definition, focal junctional tachycardia originates from the AV node or His bundle. On ECG, focal junctional tachycardia may be varied in its features. It often has a rate of 110 to 250 beats/min, with narrow QRS complexes or a bundle branch block (BBB) conduction pattern. AV dissociation often occurs. However, one-to-one retrograde conduction can also occur.

    Focal junctional tachycardia often occurs in young adulthood and is precipitated by exercise or stress. Patients might respond to β-blockers or flecainide (Tambocor) (which may be administered IV initially to terminate the tachycardia, followed by an oral dose), but drug therapy is not always effective. Catheter ablation is most effective and can be curative, though there is a 5% to 10% risk of AV block.

    Nonparoxysmal Junctional Tachycardia

    Nonparoxysmal junctional tachycardia is a benign arrythmia that is characterized by narrow QRS complexes at a rate of 70 to 120 beats/min. It occurs via automaticity and can indicate serious underlying pathology such as digitalis toxicity, hypokalemia, hypoxia, or myocardial ischemia. It is treated by correcting the underlying abnormality.

    Focal Atrial Tachycardias

    Focal atrial tachycardias are usually benign unless they are persistent, when they can cause tachycardia-induced cardiomyopathy. They usually manifest with rates between 100 and 250 beats/min, rarely getting up to 300 beats/min. The mechanism is thought to be via automaticity, and the majority originate along the crista terminalis from the SA node to the AV node. Recommended initial therapy is with calcium channel blockers or β-blockers. If these are unsuccessful, flecainide or propafenone (Rythmol) may be added. If the tachycardia is refractory to drug therapy, catheter ablation may be performed; it had a success rate of up to 86% in one study. Though inadvertent, AV node blockage is of concern.

    Multifocal Atrial Tachycardia

    Multifocal atrial tachycardia is exemplified by ECG findings of an irregular tachycardia with three or more different P-wave morphologies at different rates. It is commonly associated with underlying pulmonary disease or electrolyte abnormalities. Calcium channel blockers are a highly successful form of treatment. There is no role for direct-current cardioversion, antiarrythmic drugs, or ablation.

    Macro-Reentrant Atrial Tachycardia (Atrial Flutter)

    Atrial flutter, also known as macro-reentrant atrial tachycardia, is characterized by an organized atrial rhythm at a rate between 250 and 350 beats/min and occurs via a reentry mechanism. Typical atrial flutter is sometimes called isthmus-dependent flutter (Figure 7), so named because it involves the cavotricuspid isthmus. Patients typically present with a 2:1 AV conduction block producing a ventricular rate of about 150 beats/min. Patients can also present with a variable AV block producing an irregular rhythm. Acute management focuses on ventricular rate control using AVN blocking agents such as β-blockers or calcium channel blockers. Rapid atrial overdrive pacing can also terminate the arrhythmia. Direct current cardioversion is also a very effective mode of therapy for patients who present with hemodynamic collapse. An energy level of 50 J is typically effective. In patients with atrial flutter for more than 48 hours, anticoagulant therapy should be started and an echocardiogram should be obtained to rule out the presence of a intracardiac clot before cardioversion. Anticoagulation is usually achieved with warfarin (Coumadin), with an international normalized ratio (INR) goal of 2 to 3.

    FIGURE 7    Electrocardiogram of leads II and III depicting typical  atrial flutter. Note the sawtooth atrial activity.

    Cure of atrial flutter can be achieved with radiofrequency ablation in more than 98% of patients. The macroreentrant circuit in atrial flutter uses the atrial tissue between the tricuspid valve annulus and the inferior vena cava, and radiofrequency energy delivered across the cavotricuspid isthmus prevents atrial flutter from recurring.

    Radiofrequency ablation is the treatment of choice for patients with recurrent atrial flutter.

    Ventricular Tachycardias

    Three broad categories of pathologies contribute to the development of VT: structural heart disease, prolonged QT syndrome, and accelerated idioventricular rhythm.

    Structural Heart Disease

    VT in patients with structural heart disease is secondary to reentry and is a result of fibrotic tissue or infiltrative disease causing areas of slow conduction. Common causes of structural heart disease include ischemia, congestive heart failure, and infiltrative heart disease (e.g., sarcoidosis, amyloidosis, and Chagas’ disease). The mainstay of treatment is implantation of an implantable cardioverter-defibrillator (ICD) to prevent sudden death from VT or VF. An ICD is indicated in congestive heart failure patients with an ejection fraction less than 35% that is refractory to medical treatment. The administration of a class III antiarrhythmic drug or β-blocker can also reduce episodes of VT.

    Long-QT Syndrome

    A long QT interval may be congenital or drug induced. Patients with a long QT interval are prone to a specific form of polymorphic VT called torsades de pointes. This is characterized by rapid, irregular QRS complexes, which follow a twisting pattern around the baseline of the ECG. Torsades de pointes can degenerate into VF, causing significant hemodynamic compromise and death.

    Congenital long QT syndrome results from genetic defects in cardiac ion channels that enhance sodium or calcium inward currents or inhibit outward potassium currents during the plateau phase of the action potential. This results in prolongation of the action potential and causes the observed long QT. A common scenario for long QT syndrome on board questions is a young patient in whom sudden cardiac death is precipitated by exercising, especially swimming.

    Common drugs that can cause a prolonged QT include class Ia, Ic, or III anthiarrythmic agents, tricyclic antidepressants, phenothiazines, and certain antivirals and antifungals. Torsades de pointes is usually treated with unsynchronized direct-current cardioversion and sometimes defibrillation.

    Accelerated Idioventricular Rhythm

    Accelerated idioventricular rhythm usually has a heart rate that ranges from 60 to 120 beats per minute. It is characterized by gradual onset and offset. It is typically self-limiting and brief in duration. It is often encountered in the setting of cocaine intoxication, acute myocarditis, and digoxin intoxication and following cardiac surgery.

     

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    Vereckei A., Duray G., Szénási G., et al. Application of a new algorithm in the differential diagnosis of a wide QRS complex tachycardia. Eur Heart J. 2007;28:589–600.

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    1  Not FDA approved for this  indication.

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