Torsades de Pointes. Torsades de pointes (TdP) is a rapid form of polymorphic VT that is characterized by beat-to-beat variability in the QRS complexes, which vary in both ampli-tude and polarity. The resultant QRS complexes appear to
“twist” around the isoelectric line. A prerequisite for the rhythm is baseline prolongation of the QT interval, which may be congenital or acquired, such as can occur with med-ications (type Ia antidysrhythmics) and electrolyte imbalances (hypokalemia, hypomagnesemia). TdP is initiated by a series of ectopic beats that begin with a premature ventricular beat
or salvo of ventricular beats, followed by a pause, and then a supraventricular beat. Another premature ventricular beat arrives at a relatively short coupling interval and falls on the preceding T wave, precipitating the rhythm.
TdP is usually paroxysmal in nature and the underlying rhythm and intervals can be identified during “breaks” in the rhythm. Typically, 5 to 20 complexes are seen in each cycle;
the rhythm may either self-terminate or degenerate into ven-tricular fibrillation. The venven-tricular rate is usually between 200 and 250 bpm, and the amplitude of the QRS complexes varies in a sinusoidal pattern (Fig. 26-13). The baseline ECG usually provides important clues to diagnosis, including corrected QT interval prolongation and ST segment and T wave changes related to the underlying metabolic abnormality (Fig. 26-14).
Polymorphic Ventricular Tachycardia (Normal QRS). This form of VT often appears similar to TdP, with the important dif-ference being the absence of QT prolongation. Patients with CHAPTER26: Ventricular Tachycardia and Ventricular Fibrillation 125
FIGURE 26-13 • Torsades des pointes. This rhythm strip demonstrates the initiation of torsades des pointes by a series of ectopic beats that begin with a premature ventricular beat or salvo of ventricular beats, followed by a pause, and then a supraventricular beat. Another premature ventricular beat arrives at a relatively short coupling interval and falls on the preceding T wave, precipitating the rhythm. The baseline corrected QT interval was 0.64 sec.
this rhythm are often found to have unstable coronary artery disease, and acute coronary ischemia is thought to be an impor-tant prerequisite for this dysrhythmia1,19(see Fig. 26-14).
Ventricular Flutter/Fibrillation. Both ventricular flutter and fibrillation are fatal unless terminated abruptly. The ECG in flutter appears as a continuous sine wave, with no distinc-tion between the QRS complex, ST segment, and T waves (see Fig. 26-5). Ventricular fibrillation is unmistakable—the complexes are chaotic and irregular, without discrete QRS complexes (Fig. 26-15). The patient is always unconscious because this rhythm is unable to generate synchronous ventric-ular contractions.
Digoxin-Toxic Fascicular Tachycardia. This unusual form of ventricular tachycardia is usually a monomorphic VT that has a relatively narrow QRS and can be mistaken for SVT. It can also present as a bidirectional tachycardia, where the QRS usually has a baseline RBBB morphology and alternates its electrical axis with alternating beats. This VT subtype is thought to be due to alternating block in anterior and posterior fascicles of the left bundle branch.
Brugada Syndrome. Brugada and Brugada described a syndrome that was associated with sudden death in individuals with a structurally normal heart and no evidence of athero-sclerotic coronary disease.20 Patients with this syndrome, 126 SECTIONIII: ELECTROCARDIOGRAPHIC MANIFESTATIONS OF DISEASE
FIGURE 26-14• Polymorphic ventricular tachycardias with hypokalemia. Paroxysms of multifocal ventricular ectopy are seen in this ECG from a patient with a serum potassium of 1.9 mEq/dL. Note the ST segment depression and “giant” U waves (arrows).
FIGURE 26-15• Ventricular fibrillation. Ventricular fibrillation is characterized by chaotic, irregular complexes without discrete QRS complex morphology.
known as the Brugada syndrome, were noted to have a distinct set of ECG abnormalities, characterized by an incomplete or complete RBBB pattern with ST segment elevation in the right precordial leads21(Fig. 26-16A and B). Patients with the Brugada syndrome have unpredictable episodes of ventricular tachycardia (most commonly polymorphic).21These patients may present with self-terminating episodes of ventricular tachy-cardia manifested as syncope or near-syncope. Alternatively, patients with persistent dysrhythmia present with ventricular fibrillation. Untreated, the natural history of the syndrome is ominous, with an associated mortality rate of 20% at 2 years.21 ECG abnormalities that suggest the diagnosis were first described by Brugada and Brugada,21when it was noted that patients with sudden death or aborted sudden death had ECGs with RBBB and ST segment elevation in leads V1 to V3.20The RBBB pattern may be complete or incomplete.22–24Two types of ST segment elevation morphologies have been described in the right precordial leads: convex (see Fig. 26-16A) and concave22,23,25(saddle type; see Fig. 26-16B).
Differentiating Ventricular Tachycardia from Other Causes of Wide QRS Complex Tachycardia
Distinguishing the cause of a wide QRS complex tachycardia may be problematic. Potential causes include:
• Supraventricular tachycardia with preexisting bundle branch block
• Supraventricular tachycardia with aberrant ventricular conduction
• Preexcited (Wolff-Parkinson-White syndrome–related) supraven-tricular tachycardia
• Metabolic derangement–related wide QRS complex tachycardia
• Toxin-related wide QRS complex tachycardia
• Pacemaker-mediated tachycardia
Clues to the presence of an SVT with preexisting BBB are the “typical” appearance of the QRS complex with dura-tion less than 0.14 sec and an axis within the normal range.
Triphasic complexes in lead V1–positive rhythms are highly suggestive of SVT with aberrancy, although reversal of the rSR′ (left “rabbit ear” greater than right “rabbit ear,” i.e., RSr′) is seen only in VT. SVTs with LBBB patterns are more likely to have a rapid downstroke from the onset of the QRS complex to the nadir of the S wave (<0.06 sec). The most use-ful finding is the presence of a BBB with identical appearance on an old ECG.
The likelihood that a beat will be conducted aberrantly depends on the proceeding cycle length and underlying rhythm. SVT with aberrant ventricular conduction is often seen in irregular rhythms such as atrial fibrillation, where a beat with a short R-R interval is aberrantly conducted if it follows a beat with a longer R-R interval (Ashman’s phenomenon). This finding is due to the fact that the ventric-ular refractory period is set on a beat-to-beat basis, with longer cycle lengths having longer refractory periods. Most aberrantly conducted beats have an RBBB appearance because the right bundle is both longer and more slowly con-ducting.5,26The appearance of the aberrantly conducted beat CHAPTER26: Ventricular Tachycardia and Ventricular Fibrillation 127
V2
A B
FIGURE 26-16 • Brugada syndrome. A, The convex-type ST segment elevation. B, The saddle-type ST segment elevation with concave morphology.
• In wide-complex tachycardia, assume the rhythm is ventricu-lar tachycardia (VT), particuventricu-larly in the older patients with underlying coronary artery disease; the default diagnosis should not be supraventricular tachycardia with aberrancy.
• Comparison of QRS complex morphology with an old ECG is invaluable.
• Look for breaks or pauses in the rhythm, which often reveal capture or fusion beats.
• Do not rely on finding independent atrial activity to confirm the diagnosis of VT.
• VT may present with a narrow QRS complex.
• After the first few (<20) beats, VT is most often regular.
• A lack of hemodynamic instability does not rule out VT.
ELECTROCARDIOGRAPHIC PEARLS
FIGURE 26-17• Hyperkalemia. In this rhythm strip, hyperkalemia is causing marked prolongation of the QRS complex greater than 0.14 sec. The relatively
“slow” ventricular rates and peaked T waves in leads V4to V6are clues to the correct diagnosis.
is similar to a fixed BBB, the axis is within normal range, and the rate is determined by the underlying supraventricular rhythm. Rate-related aberrancy depends on demonstration of the “widest” beat occurring at the shortest cycle length.
The ECG appearance of tachycardias conducting antero-grade down a bypass track can be readily confused with VT.
These tachycardias are often rapid and wide and may demon-strate concordance, which is almost always positive because of the basal-to-apical direction of ventricular conduction.
Monophasic and biphasic QRS complexes are common in both RBBB and LBBB patterns, making differentiation from VT based on QRS morphology alone difficult. Prior history of tachyarrhythmias in a younger patient, response to vagal maneuvers, and an old ECG showing shortened PR intervals and delta waves are all helpful. Bypass tracts in the setting of atrial fibrillation can be readily identified by the irregular rhythm, extremely rapid ventricular rate, varying beat-to-beat QRS complex appearance, and often the narrowest QRS com-plex at the shortest R-R interval.
Electrolyte abnormalities that prolong conduction in the ventricles can give rise to rhythms that can be mistaken for VT. Hyperkalemia, in particular, can create significant prolongations in the QRS complex, which give the appear-ance of a ventricular origin of the rhythm. Clues to the diag-nosis include a slower ventricular rate because the rhythm is still sinus, diffuse QRS complex widening, and prominent S waves in lead I and the left precordial leads16(Fig. 26-17).
References
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2. Munger TM: Ventricular tachycardia electrocardiographic diagnosis (including aberration) and management. In Murphy JG (ed): Mayo Clinic Cardiology Review. Armonk, NY, Futura, 1997, pp 457–466.
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Reappraisal of a common clinical problem. Ann Intern Med 1988;109:905.
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Practical aspects for the immediate care setting. Pacing Clin Electrophysiol 1995;18:2194.
6. Herbert ME, Votey SR, Mortan MT, et al: Failure to agree on the electro-cardiographic diagnosis of ventricular tachycardia. Ann Emerg Med 1996;27:35.
7. Stewart RB, Bardy GH, Greene HL: Wide complex tachycardia:
Misdiagnosis and outcome after emergent therapy. Ann Intern Med 1986;104:766.
8. Wellens HJJ, Bar FWHM, Lie KI: The value of the electrocardiogram in the differential diagnosis of a tachycardia with a widened QRS complex.
Am J Med 1978;64:27.
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10. Kindwall KE, Brown J, Josephson ME: Electrocardiographic criteria for ventricular tachycardia in wide complex left bundle branch block morphology tachycardias. Am J Cardiol 1988;61:1279.
11. Volosin KJ, Beauregard LM, Fabiszewski R, et al: Spontaneous changes in ventricular cycle length. J Am Coll Cardiol 1991;17:409.
12. Wellens HJJ, Brugada P: Diagnosis of ventricular tachycardia from the 12-lead electrocardiogram. Cardiol Clin 1987;5:511.
13. Coumel P, Leclercq JF, Attuel P, et al: The QRS morphology in post-myocardial infarction ventricular tachycardia: A study of 100 tracings compared with 70 cases of idiopathic ventricular. Eur Heart J 1984;5:792.
14. Morady F, Baerman JM, DiCarlo LA, et al: A prevalent misconception regarding wide complex tachycardias. JAMA 1985;254:2790.
15. Mattu A, Brady WJ, Perron AD, et al: Prominent R wave in lead V1:
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16. Chou T, Knilans TK: Electrolyte imbalance. In Chou T, Knilans TK (eds):
Electrocardiography in Clinical Practice: Adult and Pediatric, 4th ed.
Philadelphia, WB Saunders, 1996, p 532.
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18. Alberca T, Almendral J, Sanz P, et al: Evaluation of the specificity of morphological electrocardiographic criteria for the differential diagnosis of wide QRS complex tachycardia in patients with intraventricular con-duction defects. Circulation 1997;96:3257.
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20. Brugada P, Brugada J: Right bundle branch block, persistent ST segment elevation and sudden cardiac death: A distinct clinical and electrocardio-graphic syndrome. J Am Coll Cardiol 1992;20:1391.
21. Brugada P, Brugada R, Brugada J: The Brugada syndrome. Curr Cardiol Rep 2000;2:507.
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128 SECTIONIII: ELECTROCARDIOGRAPHIC MANIFESTATIONS OF DISEASE
129 27-1 • THE NASPE/BPEG GENERIC (NBG) PACEMAKER CODE
Position
I II III IV V
Chamber(s) paced Chamber(s) sensed Response to sensing Programmability, rate Antitachydysrhythmia
modulation functions
O = none O = none O = none O = none O = none
A = atrium A = atrium T = triggered P = simple P = pacing
programmable (antitachydysrhythmia)
V = ventricle V = ventricle I = inhibited M = multiprogrammable S = shock
D = dual (atrium and D = dual (atrium and D = dual (atrial triggered C = communicating D = dual (pacing + shock)
ventricle) ventricle) and atrial and ventricular
inhibited)
R = rate modulation NASPE/BPEG, North American Society of Pacing and Electrophysiology/British Pacing and Electrophysiology Group.