Clinical Problems in Cardiopulmonary Disease |

Wide-Complex Tachycardia*: Management in a Patient With a History of Congenital Heart Disease FREE TO VIEW

Martin N. Wiseman, MD; Morton E. Tavel, MD, FCCP
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*From Case Western Reserve University and University Hospitals of Cleveland, OH.

Correspondence to: Morton E. Tavel, MD, FCCP, 8333 Naab Rd, Suite 200, Indianapolis, IN 46260

Chest. 2000;117(1):268-271. doi:10.1378/chest.117.1.268
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A 33 -year-old man had an abrupt onset of palpitations with rapid heart rate, which persisted for approximately 2 h. Associated with this was transient chest pain radiating into the right jaw lasting for approximately 5 to 10 min. He also noted mild dyspnea but did not manifest syncope. He went to his local hospital emergency department and was found to have a heart rate of 185 beats/min with a BP of 88/44 mm Hg. The ECG displayed the rapid cardiac rhythm (Fig 1 ).

At 6 months of age, he had been treated with a Blalock-Taussig shunt for tetralogy of Fallot (TOF). Subsequently, he underwent complete heart repair at 8 years of age, patching the ventricular septal defect and the opening of the pulmonary outflow tract together with closure of the Blalock-Taussig shunt. Approximately 8 years after this, he underwent repair of an aneurysmal area that had developed in the right ventricular outflow tract at the anastomotic site of the pulmonary artery that was related to the Blalock-Taussig shunt. He had previously had brief episodes of palpitations with tachycardia, which were thought to be supraventricular in origin.

1. What do you believe is the most likely mechanism of the tachycardia? What are your reasons for this assumption?

2. Assuming that you are the first physician to encounter this patient in the emergency department: a. If you are uncertain whether the tachycardia is ventricular or supraventricular, what are the best means at the bedside to make this distinction? What provocative maneuvers or drug interventions do you prefer to use in the effort to make this distinction? b. If you conclude that this is ventricular tachycardia (VT), how would you proceed to treat this condition? c. If you believe that this rhythm disorder is supraventricular in origin, how would you proceed to manage this problem? d. If you cannot reach a conclusion about the origin of this rhythm, how would you then proceed?

3. After the initial rhythm disorder is resolved, how would you proceed in subsequent evaluation and/or management?

Dr. Martin N. Wiseman, Cleveland, OH

  1. The ECG discloses a regular, broad QRS complex (about 200 μs), with a clearly abnormal axis (approximately −80°) and negatively concordant chest leads. The morphology is “left bundle-branch block” (ie, predominantly negative in lead V1). The diagnosis is VT, probably due to a right ventricular reentry mechanism. In patients who have undergone surgical correction of TOF, during supraventricular rhythms, including sinus rhythm, the QRS-complex pattern is nearly always right bundle-branch block in morphology. Ventricular arrhythmias are inducible in ≤ 17% patients; supraventricular arrhythmias are seen in about a third of patients. In any patient who has undergone repair of TOF and tachycardia, VT is always in the differential diagnosis.

In this patient, who is not receiving any antiarrhythmic medications (some of which may cause the widening of rate-dependent QRS complex), the diagnosis of VT should not be in doubt.

  • 2a. In stable patients, carotid sinus massage or administration of IV adenosine (maneuvers that create transient atrioventricular [AV] nodal block), may help differentiate between VT and supraventricular tachycardia (SVT). AV block allows the visualization of the atrial activity in atrial tachyarrhythmias (eg, atrial flutter [AFl] or atrial tachycardia [AT]). In arrhythmias in which the AV node is a part of the circuit (AV nodal reentry tachycardia, or AV reentry tachycardia involving a bypass tract), AV block will terminate the tachycardia. Bolus administration of IV adenosine has been shown to be safe in patients with VT. There are some rather rare adenosine-sensitive VTs, so termination is not proof positive that the arrhythmia was not VT. Moreover, sometimes an inadequate dose reaches the heart, so that SVT will continue unchanged and a larger dose may be needed to terminate the SVT.

  • 2b. Management of VT should begin with consideration of the hemodynamic stability of the rhythm and the hemodynamic consequences of intervention. In this young patient, the BP is 88/44, and he has already tolerated the tachycardia for 2 h. Further spontaneous deterioration of the BP or deterioration into VF are both unlikely. When hemodynamic deterioration does occur in these patients, it is often due to inappropriate medical interventions with negatively inotropic drugs such as verapamil.

All management should be undertaken in a situation in which emergency cardioversion could be undertaken should sudden hemodynamic deterioration occur. IV lidocaine may be tried initially, as it rarely causes the BP to drop. If lidocaine does not induce a response, the patient should be observed until he has been free of oral intake long enough for elective direct current (DC) cardioversion to be performed under general anesthesia. Subsequently, either IV procainamide or amiodarone may be tried, but they may cause a fall in BP to a point at which the patient could become hemodynamically unstable. DC cardioversion under general anesthesia then could be undertaken urgently, but safely. If the first choice of antiarrhythmic drug fails, DC cardioversion should be undertaken. A second drug generally should not be tried. DC cardioversion also would be the course of action for an undiagnosed tachycardia that had failed to respond to simple drug therapy.

The key to management is not to make things worse (multiple or inappropriate drug therapies) and to be prepared to observe a hemodynamically stable patient with tachycardia until DC cardioversion can be undertaken safely.

  • Management of SVT. It should be emphasized that the case presented is clearly not an SVT. The group of rhythms described as SVTs includes any rhythm that is not purely ventricular in origin; thus, atrial fibrillation (AF), AFl, AT, AV nodal tachycardia (AVNRT) and AV reciprocating tachycardia (AVRT) utilizing a bypass tract are all in the differential diagnosis. Diagnostic maneuvers were discussed in response to question 2a.

AF can be managed by rate control through the use of beta-blockers, calcium channel blockers with rate-limiting properties (diltiazem or verapamil), or digoxin. Cardioversion (pharmacologic or by DC shock) also may be considered. In all cases, careful consideration of the patient’s anticoagulation status is needed. The general guidelines are that any patient with a healthy heart and < 48 h of AF can be converted even if that patient has not undergone anticoagulation. However, subsequent anticoagulation is very likely to be required, and in these patients it is our practice to administer both heparin and warfarin, discontinuing the former when they have been adequately anticoagulated with warfarin (international normalized ratio, > 2). Patients who have been in AF > 48 h or who have a structurally abnormal heart may be considered for cardioversion after transesophageal echocardiography is performed, while undergoing anticoagulation with heparin early and with warfarin later.

AFl and AT can be managed similarly to AF. Early cardioversion is advised, as rate control in AFl and AT is more difficult than in AF. Patients with recurrent AFl or AT and failed medical therapy should be referred to an electrophysiologist for consideration of radiofrequency ablation for a permanent cure.

AVNRT and AVRT typically are both terminated by carotid massage or adenosine injection, although they may recur early. A reasonable alternative treatment is to use a bolus of IV verapamil or diltiazem. A subsequent drip is rarely required. Unless there are other problems, it is rarely necessary to admit patients with AVNRT or AVRT to the hospital. If the patient has recurrent episodes, referral for radiofrequency ablation should be considered.

  • Long-term management will be guided by electrophysiologic studies, with ablation and/or implantable cardioverter-defibrillator implantation as most likely definitive therapy.

At the time of presentation to the emergency department, the bedside examination disclosed findings consistent with AV dissociation. These findings consisted of an arterial pulse with variable strength (manifested as irregularly occurring Korotkoff sounds as the sphygmomanometer cuff pressure was lowered to just below systolic pressure), variation in intensity of the first heart sound, and intermittent cannon A waves in the jugular pulse. This evidence of dissociation further supported the diagnosis of VT, as noted above by Dr. Wiseman.

Initially, the patient was given 100 mg lidocaine IV, but the dysrhythmia failed to respond. He then received IV procainamide (500 mg, given over a 30-min period) and again the dysrhythmia failed to respond. Thus, after suitable anesthesia, he was subjected to electrical cardioversion with restoration of normal sinus rhythm. An ECG then showed normal sinus rhythm with first-degree AV block (PR interval, 0.22 s), complete right bundle-branch block, and nonspecific ST-T segment changes. After normal rhythm was restored, the cardiac examination disclosed a prominent right ventricular lift with an intense, narrowly split second heart sound (accentuated pulmonic component), a grade 3/6 pansystolic murmur maximum at the lower left sternal border, and a grade 2/6 early systolic ejection murmur at the upper left sternal border. The patient was admitted to the hospital, and an echocardiogram later demonstrated dilatation of the right ventricle and right atrium, moderate tricuspid regurgitation, together with evidence of moderate pulmonary hypertension. There was no demonstrable pulmonary outflow tract stenosis. He was subsequently subjected to electrophysiologic study, and this demonstrated AT and VT possessing two differing morphologies. The VTs were induced from the right ventricular outflow tract. After a suitable loading period with sotalol, a repeat study showed that VT remained inducible. He was then given loading doses of amiodarone, and on repeat testing 1 week later no sustained VT was initiated. He was, therefore, continued on a maintenance dose amiodarone (gradually reduced to 400 mg daily) and has remained asymptomatic during the following year, manifesting no evidence of cardiac arrhythmias or drug toxicity.

In conclusion, this individual demonstrated a common problem confronting the acute-care physician, that of the “wide-complex” tachycardia. As pointed out by Dr. Wiseman, this case represented VT and was, therefore, treated as such. In addition to the morphologic ECG changes that Dr. Wiseman has pointed out, one can see intermittent“ peaks” between QRS complexes in the bottom rhythm strip of Figure 1 (lead II after complexes 5, 12, 19, and 26), which represent dissociated P waves distorting the baseline at random times. All the findings indicative of AV dissociation are virtually diagnostic of a ventricular origin of the tachycardia. The absence of such dissociation, however, does not exclude this diagnosis, inasmuch as retrograde conduction from the ventricles to the atria occasionally occurs. Thus, in doubtful cases, one may need to resort to the various maneuvers detailed in the case discussion. If the tachycardia causes hemodynamic deterioration or severe symptoms, it is generally safest to proceed promptly to electrical cardioversion as a primary approach. If the patient is conscious and general anesthesia is not readily available, one can minimize the discomfort caused by the electrical shock with the use of an IV sedative such as diazepam, 5 to 10 mg, given shortly prior to the procedure.

Abbreviations: AF = atrial fibrillation; AFl = atrial flutter; AT = atrial tachycardia; AV = atrioventricular; AVNRT = atrioventricular nodal tachycardia; AVRT = atrioventricular reentry tachycardia; DC = direct current; SVT = supraventricular tachycardia; TOF = tetralogy of Fallot; VT = ventricular tachycardia

Figure Jump LinkFigure 1. ECG showing wide-complex tachycardia that was made at the time of presentation to the emergency department.Grahic Jump Location


Figure Jump LinkFigure 1. ECG showing wide-complex tachycardia that was made at the time of presentation to the emergency department.Grahic Jump Location



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