a. Bradyarrhythmias. Bradycardia is defined as a heart rate below 60 beats/min in adults. Bradyarrhythmias are common, are often benign, and usually do not pose a diagnostic dilemma.
i. Bradyarrhythmias include:
1. Sinus node dysfunction: inappropriate sinus bradycardia, sinoatrial node exit block, sinus pauses, sinus arrest.
2. Atrioventricular (AV) conduction disturbances.
3. Junctional/ventricular escape rhythms.
ii. When examining an electrocardiogram (EKG) or rhythm tracing, bradyarrhythmias can be divided into four groups based on regularity and QRS width:
1. Regular with narrow complex QRS: sinus bradycardia, second-degree AV block with 2:1 conduction, atrial flutter with slow ventricular response, junctional escape rhythm, third-degree AV block.
2. Irregular with narrow complex QRS: atrial fibrillation with slow ventricular response, atrial flutter with variable conduction and slow ventricular response, second-degree AV block.
3. Regular with wide complex QRS: regular, narrow complex bradyarrhythmias with aberrancy, idioventricular rhythm.
4. Irregular with wide complex QRS: irregular, narrow complex bradyarrhythmias with aberrancy.
iii. The management of bradyarrhythmias is focused on reversing underlying causes (e.g., medications, ischemia, endocrine disorders). Rarely a permanent pacemaker is indicated. Indications for permanent pacemakers include:
1. Sinus node dysfunction (SND): overtly symptomatic SND, equivocal symptoms with sinus bradycardia to less than 40 beats/min or symptomatic chronotropic incompetence.
2. AV node conduction disturbances:
a. Symptomatic high-grade AV block (third-degree AV block or infranodal second-degree AV block).
b. Asymptomatic high-grade AV block with unreliable escape rhythm (heart rate less than 40 beats/min, asystole greater than 3 seconds, atrial fibrillation with pauses greater than 5 seconds).
c. Persistent high-grade AV block with exercise in the absence of ischemia.
3. Bifascicular/trifascicular block: in the setting of alternating bundle branch block, severe His-Purkinje disease with symptoms or neuromuscular disease.
b. Tachyarrhythmias: defined as a heart rate exceeding 100 beats/min; may pose a diagnostic challenge. They are also often each treated differently; therefore, accurate diagnosis and EKG interpretation is necessary. All tachyarrhythmias can be classified according to whether they are (1) regular (same distance between successive R waves) or irregular, and (2) whether the QRS complex is narrow (<0.12 sec) or wide (>0.12 sec). Making these two determinations and consulting Table 7.1 can narrow the diagnostic possibilities. The presence or absence of P waves and their morphology and relationship to QRS complexes is essential to differentiate between various tachyarrhythmias. Examining the onset and termination of the tachycardia (abrupt vs. gradual, preceded by premature contraction) can also provide valuable information.
c. For all arrhythmias: obtain a 12-lead EKG/rhythm tracing as opposed to the commonly obtained three-channel telemetry tracing. Try to obtain an older EKG for comparison.
Often the most important clue to determining the etiology of a tachyarrhythmia is close inspection of the P waves.
Table 7.1 Classification of Tachyarrhythmias
Atrial flutter with variable conduction
Multifocal atrial tachycardia
Sinus tachycardia with frequent PACs
Atrial fibrillation with aberrancy
SVT with preexisting aberrancy
Irregular SVT with aberrancy*
SVT with conduction abnormalities due to electrolyte or metabolic derangements
Ventricular tachycardia (often polymorphic)
SVT with rate-dependent aberrancy
Paced rhythm (including pacemaker mediated tachycardia)
AVNRT = atrioventricular nodal reentrant tachycardia; AVRT = atrioventricular reentrant tachycardia; PAC = premature atrial contraction; SVT = supraventricular tachycardia.
* Because all arrhythmias characterized by an irregular rhythm and a narrow QRS complex can become irregular with a wide QRS complex in the presence of aberrant conduction, atrial flutter with variable block and multifocal atrial tachycardia must also be considered here, although they are much less common than atrial fibrillation.
B. Narrow, Regular Tachyarrhythmias
a. Mechanism: The basic mechanism of tachyarrhythmias can be explained by one or a combination of these categories: disorders of impulse formation (such as abnormal automaticity or triggered activity) or disorders of impulse conduction (reentrant circuits).
b. Differential diagnosis
1. Etiologies. Sinus tachycardia is usually a physiologic response to stress. Important etiologies include:
a. Low stroke volume states (e.g., from intravascular volume depletion or myocardial dysfunction)
b. Hypoxemia (e.g., from heart failure, pulmonary embolism)
c. Hypercatecholamine states (e.g., from pheochromocytoma, pain, anxiety, drug withdrawal)
d. Drugs (e.g., inhaled β-agonists, theophylline, caffeine)
e. Systemic causes (e.g., fever, sepsis, anemia, hyperthyroidism)
f. Myocarditis and pericarditis
g. Inappropriate sinus tachycardia
2. EKG appearance. Upright P waves in leads I, II, and aVF are always followed by a QRS complex. There is usually a gradual increase in heart rate at onset.
The maximum predicted heart rate in sinus tachycardia equals 220 minus the patient’s age. If the patient’s heart rate is greater than the maximum predicted heart rate, then look for a cause other than sinus tachycardia.
ii. Atrioventricular nodal reentrant tachycardia (AVNRT) accounts for more than 50% of all supraventricular tachyarrhythmias. (By definition, the term supraventricular tachycardia [SVT] refers to any tachycardia of nonventricular origin. However, in clinical practice SVT is classically used for AVNRT, atrioventricular reentrant tachycardia (AVRT), and atrial tachycardia [AT]). AVNRT is common in patients without underlying heart disease.
1. Characteristics include:
a. Heart rate of 150–250 beats/min
b. Inverted P waves with short RP interval and pseudo R' waves on the EKG particularly seen in lead V1.
2. Mechanism. 30% of the population has a dual AV node that contains a fast pathway with a long refractory period and a slow pathway with a short refractory period.
a. Sinus rhythm. During sinus rhythm, the impulse is conducted down the fast pathway to the ventricles. Conduction down the fast pathway is also able to traverse the AV node retrograde and block impulses on the slow pathway (Figure 7.1).
b. Excitation loop. A premature atrial contraction (PAC) may be blocked at the fast pathway secondary to its long refractory period; the impulse is then conducted down the slow pathway, which has a short refractory period (this is manifested as a long PR interval on the EKG immediately before the initiation of tachycardia). The impulse may then enter the fast pathway retrograde, which is no longer refractory, and activate the atria (slow-fast AVNRT or typical AVNRT) (Figure 7.2).
3. EKG appearance
a. In typical AVNRT (accounts for 90% of cases and is also known as slow-fast AVNRT), a PAC begins the loop of excitation. The P wave is inverted and can usually be seen in the terminal portion of the QRS complex (pseudo R′ waves) in lead V1. Typical AVNRT is characterized by short RP interval (long PR interval) due to conduction along the slow pathway.
b. In atypical AVNRT (10% of cases), a premature ventricular contraction (PVC) initiates the conduction of an impulse up the slow pathway and down the fast one (fast-slow) (Figure 7.3). Because the retrograde P waves are formed from the slower pathway, they are inverted and occur after ventricular activation and often seen just before the next QRS complex. This EKG resembles atrial tachycardia and may require an electrophysiologic study to further differentiate the cause of arrhythmia.
iii. Atrioventricular reentrant tachycardia (AVRT) accounts for more than 30% of all supraventricular tachyarrhythmias.
1. Characteristics. AVRT is usually characterized by a short RP interval on the EKG.
2. Mechanism. AVRT involves an accessory pathway (e.g., bundle of Kent in Wolff-Parkinson-White syndrome), an abnormal tract of fast conducting tissue between the atria and ventricles that bypasses the AV node. Accessory pathways often conduct in both an anterograde and retrograde direction. Like AVNRT, AVRT is an AV node–dependent tachycardia.
3. EKG appearance
a. Sinus rhythm
i. During sinus rhythm, anterograde conduction results in ventricular preexcitation, manifested as a short PR interval and a delta wave on the EKG.
ii. If only retrograde conduction is possible (as occurs in approximately 25% of patients), no abnormality is seen during sinus rhythm (concealed accessory pathway).
b. Excitation loop
i. Orthodromic conduction (accounts for 95% AVRT) occurs when an impulse is conducted through the AV node and then up the accessory pathway in a retrograde direction (Figure 7.4). Because the loop is longer than that of AVNRT, the retrograde P wave is easily seen (i.e., it is not buried within the QRS complex). The interval from the R wave to the ensuing retrograde P wave will be less than that from the P wave to the next R wave (short RP or RP < PR tachycardia). This characteristic helps distinguish AVRT from atrial tachycardia and sinus tachycardia. The QRS complex remains narrow because the ventricle is depolarized normally (i.e., via the His-Purkinje system).
ii. Antidromic conduction occurs when the impulse is conducted antegrade down the bypass tract. Antidromic conduction produces a wide QRS complex because the tract terminates on ventricular muscle fibers. (Conduction from fiber to fiber is slow.)
iv. Atrial Tachycardia accounts for 15% of all SVTs.
a. The atrial rate (as reflected by the P waves on the EKG) is usually less than 250 beats/min. (In atrial flutter, the atrial rate is approximately 300 beats/min.)
b. A long RP interval is noted on the EKG.
2. Mechanism. Either enhanced automaticity of atrial tissue (automatic/ectopic atrial tachycardia) or atrial reentry with a focus usually located in the lower right atrium is thought to be the mechanism.
a. Occurs in patients with structural/ischemic heart disease, pulmonary disease, electrolyte imbalances, or drug toxicity.
b. Because digitalis increases atrial and ventricular automaticity and depresses conduction tissue, atrial tachycardia with variable degrees of AV nodal block is a common presentation of digitalis toxicity.
3. EKG appearance. The P wave has an unusual axis due to depolarization of the atria from a focus below the sinus node and is followed by a narrow QRS complex (produced by conduction of the impulse down the AV node). The preceding P wave is linked to the R wave, and the PR interval is shorter than the RP interval (a long RP tachycardia). Atrial tachycardia commonly has an abrupt onset, but due to enhanced automaticity may demonstrate a “warm-up” phenomenon.
The supraventricular tachycardias can be classified according to the RP interval:
Short RP = AVRT and typical AVNRT
Long RP = atrial tachycardia, atypical AVNRT, and sinus tachycardia
No RP = typical AVNRT, junctional tachycardia
v. Atrial flutter. Atrial flutter is the second most common of all atrial tachyarrhythmias.
a. The atrial rate is often 300 beats/min, and the ventricular rate is typically 150 beats/min. (In other words, a 2:1 AV block is commonly seen.) Whenever the ventricular rate is approximately 150 beats/min with little variation, think of atrial flutter.
b. Atrial flutter is typically transient, often degenerating to atrial fibrillation or returning to sinus rhythm. In general, the causes of atrial flutter are similar to those of atrial fibrillation (see Chapter 8).
2. Mechanism. Due to a macro-reentrant loop in the atrium. For typical atrial flutter, the reentrant circuit is located in the right atrium and involves the cavotricuspid isthmus.
3. EKG appearance. In typical atrial flutter, because the waves often move in a superior-inferior direction, “sawtooth” flutter waves are best seen in the inferior leads (i.e., leads II, III, and aVF).
Atrial flutter with 2:1 conduction can often be mistaken for sinus tachycardia. When patients are noted to be tachycardic at a steady rate of about 150 beats/min, atrial flutter with 2:1 conduction should be suspected.
c. Treatment of narrow, regular tachycardia
i. Acute treatment depends on the patient’s hemodynamic stability.
1. Hemodynamically unstable (or ischemic) patient. Determine whether the patient is in sinus rhythm.
a. If the patient is not in sinus rhythm, initiate electrical cardioversion immediately.
b. If the patient is in sinus rhythm, treatment is aimed at the underlying cause.
2. Hemodynamically stable patient
a. Carotid sinus massage or Valsalva maneuvers may increase vagal tone and block impulses at the level of the AV node. Carotid sinus massage is contraindicated in the presence of a carotid bruit and should be performed with continuous EKG monitoring and a crash cart available.
i. AVNRT and AVRT, tachycardias that involve reentrant loops through the AV node, may terminate.
ii. Atrial tachycardia is usually unaffected by carotid sinus massage but may terminate abruptly.
iii. Sinus tachycardia. Carotid sinus massage may slow the atrial rate.
b. Administer adenosine as a rapid intravenous (IV) push in incremental doses of 6 mg and then 12 mg each followed by 20–50 mL saline push if carotid sinus massage or Valsalva maneuvers are ineffective. Adenosine is contraindicated in patients with acute bronchospasm and heart transplant recipients; patients taking dipyridamole may also exhibit increased sensitivity. The effects of adenosine occur within 15–30 seconds of administration and last for 10–20 seconds. Adenosine has effects similar to those of carotid sinus massage, but they are more pronounced because it results in transient complete AV nodal block. Warn the patient that a sense of fear or doom is commonly felt but the sensation will pass within 10–20 seconds.
i. AVNRT and AVRT. More than 90% of these tachycardias will be terminated with a 12-mg dose of adenosine.
ii. Atrial tachycardia rarely terminates. IV administration of verapamil or diltiazem is preferable for arresting atrial tachycardia and may decrease the ventricular response, even if the tachycardia persists.
3. Sinus tachycardia transiently slows. Additional treatment should be directed at the underlying cause.
4. Atrial flutter. AV block increases, and flutter waves are more evident. The heart rate returns to its previous accelerated rate as the effects of adenosine wane. Additional treatment may involve AV nodal blockade with digitalis, β-blockers, or calcium channel blockers, followed by either chemical (e.g., procainamide, ibutilide) or electrical cardioversion. If the atrial flutter has been long-standing, cardioversion should only be considered after anticoagulation for 4 weeks or a transesophageal echocardiogram is done to rule out left atrial thrombus, as with atrial fibrillation (see Chapter 8).
In atrial flutter, type 1a or 1c antiarrhythmics should not be given before the administration of AV nodal blocking agents because these agents may slow atrial conduction sufficiently to permit 1:1 conduction through the AV node, increasing ventricular response.
ii. Chronic treatment
1. AVNRT. If the patient experiences sporadic episodes, control may be possible using vagal maneuvers. For patients who experience frequent or symptomatic episodes, antiarrhythmic drugs, AV nodal blocking agents, or radiofrequency ablation (RFA) may be used (>95% successful). Given the high success and low rates of complications, RFA is considered first line of treatment.
2. AVRT. Symptomatic patients with evidence of preexcitation on a baseline EKG should receive RFA. Patients with symptoms but no evidence of anterograde conduction (i.e., concealed bypass tract) can be treated with RFA or an initial trial of an AV nodal blocking agent.
3. Atrial tachycardia. Calcium channel blockers or β-blockers are often the drugs of first choice. If pharmacologic therapy fails, ablation may be indicated.
4. Atrial flutter. RFA is 95% successful and should be considered in patients with recurrent symptoms. Antiarrhythmic drugs are typically less successful. Because of its high association with atrial fibrillation and independent association with stroke, anticoagulation also should be considered using atrial fibrillation risk assessment tools.
C. Narrow, Irregular Tachyarrhythmias
a. Differential diagnosis. In general, the members of this category can be differentiated easily on the basis of a 12-lead EKG. Sometimes, it can be difficult to distinguish “coarse” atrial fibrillation from atrial flutter with variable block.
i. Atrial fibrillation is discussed in detail in Chapter 8. This arrhythmia is characterized by irregular atrial fibrillatory waves at a rate of 350–600 beats/min and a ventricular rate of usually 120–160 beats/min.
ii. Atrial flutter with variable block. To help differentiate atrial flutter with variable block from atrial fibrillation:
1. Look at the inferior leads (II, III, aVF). With typical atrial flutter, flutter waves can often be “marched out” at a rate of approximately 300 beats/min. These flutter waves must have exactly the same morphology. Variable block will produce a ventricular rate in proportion to the atrial rate (i.e., the ventricular response to 2:1, 3:1, and 4:1 AV block will be 150 beats/min, 100 beats/min, and 75 beats/min, respectively).
2. Increase AV block by massaging the carotid sinus or administering adenosine. Flutter waves that may have been hidden become obvious.
iii. Multifocal atrial tachycardia
1. Mechanism. In approximately 60% of patients, multifocal atrial tachycardia is associated with pulmonary disease. For example, cor pulmonale causes right atrial stretch, producing different foci of atrial depolarization. Multifocal atrial tachycardia may also be caused by hypokalemia or hypomagnesemia.
2. EKG appearance. Diagnosis requires the presence of at least three distinct P wave morphologies in the same lead and three different PR intervals. As a result of multiple atrial foci, the RR interval varies (i.e., it is irregularly irregular). Heart rate is generally in the 100–140 beats/min range.
iv. Sinus tachycardia with frequent PACs. When frequent, PACs may give the appearance of an irregular rhythm.
b. Treatment of narrow, irregular tachyarrhythmias
i. Hemodynamically unstable (or ischemic) patients with tachycardia and atrial fibrillation or atrial flutter with variable block should undergo immediate electrical cardioversion.
ii. Hemodynamically stable
1. Atrial fibrillation. Treatment is discussed in Chapter 8.
2. Atrial flutter with variable block. Treatment is the same as for atrial flutter without variable block (see II. B. 1. b.).
3. Multifocal atrial tachycardia. Treat the underlying condition (usually related to bronchospasm, hypoxemia, or metabolic derangements). Verapamil, magnesium, and β-blockers are often tried, but this is a difficult arrhythmia to treat. Antiarrhythmic medications have a limited role in the treatment of multifocal atrial tachycardia and electrical cardioversion is usually ineffective.
D. Wide, Regular Tachyarrhythmias
a. Mechanism of wide QRS. Normally, the impulse is conducted from the sinoatrial (SA) node to the AV node, through the bundle of His, and through the left and right bundle branches (the Purkinje fibers). The bundles conduct rapidly, and ventricular depolarization is efficient (like traveling down the interstate highway at a fast speed), producing a narrow QRS complex (<0.1 sec in duration).
i. If one bundle is blocked, conduction will spread down the remaining bundle and then from muscle fiber to muscle fiber (like traveling on local roads at a slower speed). This slow process produces a wide QRS complex (>0.12 sec in duration). A QRS complex between 0.1 and 0.12 second in duration represents an incomplete bundle branch block and is often termed an interventricular conduction delay.
ii. The QRS complex will be wide if the impulse starts in the ventricle and spreads fiber to fiber (as is the case with ventricular tachycardia [VT]) or if it starts above the ventricle but eventually spreads fiber to fiber (as is the case with SVT with aberrancy). There are three mechanisms of aberrant conduction:
1. A preexisting underlying bundle branch block.
2. A rate-related bundle branch block. As the heart rate increases, one bundle (usually the right bundle) is unable to keep up with the other because of a longer refractory period. The impulse is conducted down the faster bundle and then from fiber to fiber, producing a wide QRS.
3. An accessory pathway. These tracts terminate on ventricular muscle, necessitating fiber-to-fiber conduction.
b. Differential diagnosis for regular, wide complex tachycardia. As in Table 7.1, the differential includes VT, SVT with aberrancy, antidromic AVRT, pacemaker-mediated tachycardia, or artifact.
Patients with cardiac disease and a wide-complex tachyarrhythmia should be assumed to have VT until proven otherwise.
i. Definitions. VT represents three or more consecutive QRS complexes of ventricular origin occurring at a rate exceeding 110 beats/min. VT is considered sustained if it lasts longer than 30 seconds or has to be terminated with therapy (antitachycardia pacing or shocks). Nonsustained ventricular tachycardia (NSVT) represents three or more consecutive ventricular beats that terminate spontaneously within less than 30 seconds.
ii. Diagnosis. The Brugada criteria can help distinguish between VT and SVT with aberrancy.
1. The precordial leads (V1–V6) are examined on a 12-lead EKG. Each criterion is extremely specific, but not particularly sensitive, for VT. Therefore, if a criterion is met, initiate treatment for VT; if the criterion is not met, continue to the next.
2. Absence of a true RS pattern in all the precordial leads. An S wave is a discrete negative deflection. A broad negative deflection is an inverted T wave (as opposed to an S wave). If there is a monomorphic pattern (no RS) or “concordance,” the arrhythmia is VT.
3. RS interval (from onset of QRS/R wave to nadir of S) is greater than 100 msec in at least one precordial lead. Ventricular depolarization takes more time if it starts in the ventricle, rather than begins supraventricularly and is conducted aberrantly. If the RS interval is greater than 100 msec, then the arrhythmia is VT.
4. Evidence of AV dissociation includes P waves marching through at different points of the wide complexes and fusion or capture beats. Although these clues are difficult to discern, they are diagnostic of VT. If a diagnosis has still not been reached, morphologic criteria (given in several texts) can be used to arrive at a diagnosis.
iii. Other supportive findings of VT:
1. Right superior axis (extreme right axis deviation) or change in axis by more than 40o.
2. Initial R wave in lead aVR.
3. Very wide QRS complex (>160 msec with LBBB morphology or >140 msec with RBBB morphology).
“Quick and dirty” rule for distinguishing VT from SVT with aberrancy: Is there a past medical history of coronary artery disease? If yes, then VT is the diagnosis more than 80% of the time. Hemodynamic stability alone should not be used to distinguish VT from SVT.
i. Pulseless VT: Advanced cardiac life support (ACLS) protocol.
ii. Hemodynamically unstable (or ischemic) patients should undergo electrical cardioversion, starting with at least 200 J.
iii. Hemodynamically stable patients
a. Amiodarone. Usual IV dosage is 150-mg bolus (may be repeated) followed by 1 mg/min for 6 hours and then 0.5 mg/min.
b. Lidocaine. The initial bolus is 0.75–1.5 mg/kg administered intravenously; followed by an infusion of 1–4 mg/min. Lidocaine is more effective for ischemic VT.
c. Procainamide should be considered in patients who do not respond to amiodarone or lidocaine. Procainamide is effective at terminating VT, but hypotension and cardiosuppression may occur.
2. Supraventricular arrhythmias with aberrancy. Carotid sinus massage and adenosine should be employed as described earlier in this chapter.
a. Amiodarone or lidocaine. The patient may be given a trial of either agent.
b. Adenosine. If there is no response, adenosine trials in 6- and 12-mg increments (half doses if administered by a central line) should be tried. If the patient has a history of cardiac disease, VT is likely and needs to be treated immediately.
c. Procainamide. If the patient still fails to respond, a procainamide trial may be indicated.
E. Wide, Irregular Tachyarrhythmias
a. Differential diagnosis. The differential diagnosis is atrial fibrillation with aberrancy versus VT (monomorphic or polymorphic).
All members of the irregular, narrow category will appear irregular and wide in the setting of aberrant conduction.
1. Preexisting underlying bundle branch block. If, upon comparing a previous 12-lead EKG, there is evidence of an old bundle branch block that has the same morphology as the present one, this diagnosis is extremely likely.
2. Rate-related bundle branch block will usually have a right bundle branch block pattern on the EKG because the right bundle is often slower than the left bundle.
3. Accessory pathway. If there is evidence of preexcitation during sinus rhythm (i.e., a short PR interval, delta waves) on a prior 12-lead EKG, this diagnosis is extremely likely. Another clue to an accessory pathway is bizarre conduction (e.g., lead V1 suggests a left bundle but the nearby V2 lead suggests a right bundle). An accessory pathway is a dangerous situation because fibrillatory waves occur at rates of approximately 600 beats/min and the accessory pathway allows much faster conduction than does the AV node. Thus, very fast ventricular rates (i.e., 200–300 beats/min) can be generated, and this arrhythmia can quickly degenerate to ventricular fibrillation. AV nodal agents (e.g., calcium channel blockers, β-blockers, digoxin, and adenosine) should be strictly avoided in all suspected cases.
Whenever you see a patient with a wide, irregular tachyarrhythmia with a rate greater than 200 beats/min, consider atrial fibrillation with an accessory pathway. If atrial fibrillation with accessory pathway is suspected, AV nodal blocking agents should be avoided.
i. Hemodynamically unstable (or ischemic) patients should undergo cardioversion starting at 200 J.
ii. Hemodynamically stable patients
1. Procainamide is the drug of choice.
a. If the rhythm is atrial fibrillation with aberrancy, procainamide may convert the patient to sinus rhythm. If the cause of the patient’s aberrant conduction is an accessory pathway, procainamide will slow conduction through the pathway, decreasing the ventricular rate, even though conversion may not occur.
b. Procainamide also treats VT. However:
i. Procainamide is contraindicated in the setting of torsades de pointes. If a morphology consistent with torsades de pointes is present or there are strong epidemiologic factors suggestive of torsades de pointes (e.g., an increased baseline QT interval, history of heavy alcohol use, use of quinidine or tricyclic antidepressants, or electrolyte disturbances such as hypokalemia or hypomagnesemia), procainamide is contraindicated because it will increase prolongation of the QT interval and promote further torsades. Procainamide frequently leads to hypotension, so patients with borderline blood pressures (i.e., 90–100 mm Hg) and fast heart rates may be better served with cardioversion.
2. AV nodal blocking agents (β-blockers, calcium channel blockers, or digitalis) should only be considered when the patient shows strong evidence of atrial fibrillation with an underlying bundle branch block (i.e., a prior EKG shows the same bundle branch block during sinus rhythm). Otherwise, AV nodal blocking agents should not be administered to patients with wide, irregular tachycardias because if the patient has an accessory pathway, AV nodal blocking agents will promote conduction down the tract, thereby increasing the heart rate to dangerous levels.
F. Ventricular Tachycardia
a. Monomorphic VT. In VT, the rhythm may be irregular for the first 50 beats. A persistently irregular rhythm after 50 beats essentially rules out monomorphic VT.
b. Polymorphic VT. Because the impulse is originating from different foci in the ventricle, the rhythm is irregular. Torsades de pointes is a type of polymorphic VT that is associated with a prolonged QT interval and undulates around the isoelectric baseline.
i. Acute treatment. Therapy for monomorphic VT is as described earlier (see IV. C. 2. a.). For polymorphic VT, emergently treat any reversible metabolic abnormalities (i.e., hypokalemia or hypomagnesemia) and hold potentially dangerous drugs that may be prolonging the QT interval. Additional treatment typically involves IV magnesium or overdrive cardiac pacing with or without β-blockers.
ii. Chronic treatment. Patients with VT, especially without a clear reversible cause, should be considered as candidates for an implantable cardiac defibrillator (ICD). In the setting of a structurally normal heart, medical therapy depends on the underlying etiologies, including right ventricular outflow tract VT (calcium channel blockers are usually effective) or the type of underlying channelopathy.
Suggested Further Readings
Brugada P, Brugada J, Mont L, Smeets J, Andries EW. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation 1991;83:1649–59. (Classic Article.)Find this resource:
Ganz LI, Friedman PL. Supraventricular tachycardia. N Engl J Med 1995;332:162–73. (Classic Article.)Find this resource:
Goldberger ZD, Rho RW, Page RL. Approach to the diagnosis and initial management of the stable adult patient with a wide complex tachycardia. Am J Cardiol 2008;101:1456–66.Find this resource:
Mangrum JM, DiMarco JP. The evaluation and management of bradycardia. N Engl J Med 2000;342:703–9. (Classic Article.)Find this resource:
Page RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS guideline for the management of adult patients with supraventricular tachycardia: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol 2016;67:e27–e115.Find this resource:
Russo RJ, Costa HS, Silva PD, et al. Assessing the risks associated with MRI in patients with a pacemaker or defibrillator. N Engl J Med 2017;376:755–64.Find this resource:
Tracy CM, Epstein AE, Darbar D, et al. 2012 ACCF/AHA/HRS focused update of the 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2012;60:1297–313.Find this resource: