| JOURNAL HOME | CME HOME | THIS MONTH | PAST ISSUES | ETOC | COLLECTIONS |
| AUTHORS | REVIEWERS | EDITORIAL BOARD | FEEDBACK | RSS | HELP |
| ||||||||||||||
| ||||||||||||||
|
|
|
|
||||||||||||
|
||||||||||||||
*Section of Critical Care Medicine, Department of Anesthesiology, and Section of Cardiology, Department of Internal Medicine, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire; and Section of Cardiology, Department of Medicine, The Mercy Hospital of Pittsburgh, Pittsburgh, Pennsylvania
Address correspondence and reprint requests to Ali Al-Khafaji, MD, Dartmouth Medical School, Section of Critical Care Medicine, Dartmouth Hitchcock Medical Center, One Medical Center Dr., Lebanon, NH 03756. Address e-mail to Alkhafaji{at}hotmail.com
 |
Abstract |
|---|
 Top Abstract IntroductionCase 1DiscussionReferences |
|---|
IMPLICATIONS: Bidirectional tachycardia is an uncommon and unique arrhythmia. It typically occurs in patients with digitalis toxicity, but it can also be associated with other causes. There has been controversy regarding the origin and the mechanism of bidirectional tachycardia. Treatment of bidirectional tachycardia involves the correction of reversible factors and the use of some antiarrhythmic medication.
|
Introduction |
|---|
|
TopAbstractIntroductionCase 1DiscussionReferences |
|---|
Bidirectional tachycardia is usually associated with digitalis toxicity (1); however, it can be caused by other conditions, such as hypokalemic and hyperkalemic periodic paralysis (2,3), severe structural heart disease (1), familial sudden death syndrome (4), and aconite poisoning (5).
Our first case represents a classic example of bidirectional tachycardia associated with digitalis toxicity in a patient with a severe ischemic cardiomyopathy, which resolved with the treatment of digitalis toxicity. In the second patient, the bidirectional tachycardia developed soon after the administration of IV digoxin and may have been secondary to a transiently increased serum level of digoxin.
Both patients demonstrated a characteristic morphologic pattern of wide complex tachycardia, with right bundle branch block morphology and beat-to-beat alternation of the morphology of the QRS complexes seen in several EKG leads.
|
Case 1 |
|---|
|
TopAbstractIntroductionCase 1DiscussionReferences |
|---|
There was no clinical evidence of congestive heart failure. Medications included captopril 12.5 mg three times a day, digoxin 0.25 mg every day (qd), allopurinol 300 mg qd, KCl 20 mEq twice daily, warfarin 5 mg qd, imipramine 25 mg at bedtime, and furosemide 40 mg twice daily. Laboratory results showed an Na+ of 133 mmol/L, K+ of 4.0 mmol/L, Cl- of 89 mmol/L, CO2 of 26 mmol/L, Mg2+ of 2.4 mmol/L, and PO4 of 8.3 mg/dL. An ionized Ca level was mildly decreased at 1.05 mmol/L. Blood urea nitrogen and creatinine were 134 and 4.4 mg/dL, respectively. The digoxin level was 7.4 ng/mL. A chest radiograph revealed cardiomegaly but no signs of congestive heart failure. The EKG showed a ventricular paced rhythm at 70 bpm (Fig. 1).
|
The patient was given IV fluid, and digoxin was withheld. Two hours after admission, the patient developed an asymptomatic episode of sustained wide complex tachycardia consistent with ventricular tachycardia that lasted approximately 5 min. This was treated with IV lidocaine. The next 2 days were uneventful, and the patient underwent physical therapy at the bedside for range of motion. On the third hospital day, while still receiving lidocaine 2 mg/min IV, the patient developed an asymptomatic episode of sustained wide complex tachycardia (Fig. 2) at a rate of 130 bpm, during which the arterial blood pressure was 140/90 mm Hg. The diagnosis of bidirectional tachycardia was made. Electrolyte levels were within the normal range. The digoxin level was still markedly increased at 7.1 ng/mL, and three vials (114 mg) of Digibind (digoxin immune Fab; Burroughs Wellcome Co., Research Triangle Park, NC) were administered IV. Soon thereafter, the tachycardia resolved. The lidocaine was subsequently discontinued. No further episodes of bidirectional tachycardia were observed. Frequent runs of nonsustained monomorphic ventricular tachycardia of 7 to 15 beats’ duration were subsequently noted.
|
|
|
|
Discussion |
|---|
|
TopAbstractIntroductionCase 1DiscussionReferences |
|---|
Scherf and Kisch (7), who reported the largest number of cases (n = 18), classified the arrhythmia into three groups. Type 1 demonstrates two alternating QRS configurations with a regular rhythm, i.e., equal diastolic intervals. Type 2 consists of alternating longer and shorter diastolic intervals. Usually the intervals between the similar complexes are equal, whereas those between the dissimilar ones are unequal. Type 3 is a pattern in which the configuration of the ventricular complexes, as well as the length of diastole, varies irregularly.
Bidirectional tachycardia typically occurs in the setting of severe structural heart disease (1). In a review of 72 published cases, Cohen et al. (1) reported that atrial fibrillation was present in 44% of cases and that digitalis was used in 82%. Digitalis was often implicated as causing bidirectional tachycardia in this review. Of 39 patients whose clinical course was reported, only 15% were alive at one year (1). Cases of bidirectional tachycardia have also been described in association with hypokalemic and hyperkalemic periodic paralysis (2,3) and herbal aconite poisoning (5). Familial bidirectional tachycardia, unassociated with structural heart disease, has also been reported (4). Therefore, the natural history of this condition is variable, and it is likely to be determined by the nature of any underlying heart disease. It may have a benign course in the absence of structural heart disease (4).
There has been controversy with regard to the site of origin of bidirectional tachycardia. Rosenbaum et al. (8) hypothesized that bidirectional tachycardia is due to supraventricular tachycardia and associated trifascicular conduction disease. In the cases they studied, they noted that the QRS complex had right bundle branch block with alternating left anterior hemiblock and left posterior hemiblock. They stated that there was permanent aberrant conduction in the right bundle branch alternating with an aberrant conduction in the two divisions of the left bundle branch (8). This mechanism was confirmed with His bundle recordings in a case report (9).
Chevalier (10) studied one case of bidirectional tachycardia and interpreted it as a nodal tachycardia with variable block in the presence of aberrant ventricular conduction or ventricular premature beats (no intracardiac recordings). A more recent case report with His bundle recordings confirmed that bidirectional tachycardia can be the result of ventricular bigeminy in the presence of a junctional tachycardia (11).
Bidirectional tachycardia caused by two separate ventricular foci has been hypothesized (12,13) and was demonstrated by Scherf and Bornemann (14) in a dog by injection of hypertonic saline subepicardially into each ventricle. This mechanism has not been substantiated in humans and has been presumed to be unlikely on the basis of a very regular rhythm in one case (15) and an identical negative HV (VH) interval for each QRS configuration in another case (16). Mihai and Lazar (17) reported a case of bidirectional tachycardia that was thought to be of ventricular origin, after atrial pacing faster than the tachycardia produced a narrow QRS complex (arguing against aberrancy).
Electrophysiologic studies have clearly demonstrated the ventricular origin of some bidirectional tachycardias with classic right bundle branch block and alternating fascicular block morphology (1,12,13,16). The case of Levy et al. (16) suggested a left bundle branch origin for the tachycardia, given a slightly negative HV interval. Presumably, the left anterior and posterior fascicles were activated in an alternate fashion. A His potential was not visible during tachycardia in the cases of Kastor and Goldreyer (12) or Cohen et al. (1).
In summary, biventricular tachycardia can be supraventricular or ventricular in origin. Although relatively few patients have had intracardiac recordings obtained during bidirectional tachycardia, a ventricular site of origin is probably most common (16).
Data on the mechanism of bidirectional tachycardia are limited by the relatively few sustained tachyarrhythmias that have been evaluated with electrophysiology studies and the limitation of programmed electrical stimulation in distinguishing reentry from triggered activity (18). Typically, reentrant tachyarrhythmias and tachyarrhythmias due to triggered activity can be initiated and terminated by pacing techniques (programmed premature beats or burst pacing), whereas automatic tachyarrhythmias can neither be initiated nor terminated by programmed electrical stimulation.
Levy and Aliot (19) reported that either isolated reentry or reentry associated with ectopic foci is the likely mechanism for bidirectional tachycardia of ventricular origin. Through intracardiac recording along with programmed electrical stimulation, Levy and Aliot postulated reentry as the mechanism of one case because of interruption of the tachycardia by programmed atrial and ventricular premature beats. It is interesting to note that burst pacing from the ventricle did not terminate this tachycardia (16).
In contrast, Martini et al. (13) favored automaticity over a reentry mechanism for their case of bidirectional tachycardia. They could briefly overdrive-suppress the tachyarrhythmia with pacing of the atrium and ventricle, but they could not terminate the tachycardia with pacing. Kastor and Goldreyer (12) also reported only transient suppression of bidirectional tachycardia with atrial pacing.
Tai et al. (5) favored automaticity or triggered activity as the mechanism for bidirectional tachycardia in a case of aconite poisoning. Aconites are plant alkaloids present in some Chinese herbal mixtures, and in canine Purkinje fibers they can induce early afterdepolarizations—oscillations in membrane potential that can cause tachyarrhythmias because of triggered activity (5). Bidirectional tachycardia was transiently suppressed by vagotonic maneuvers (vomiting, carotid sinus massage, and edrophonium) and the administration of IV adenosine triphosphate. A single 200-J synchronized direct current cardioversion had no effect on the tachyarrhythmia. The arrhythmia was terminated by the infusion of flecainide acetate (5).
The fact that bidirectional tachycardia classically occurs in patients with a high digoxin level suggests that triggered activity caused by delayed afterdepolarizations might be the likely mechanism (20). However, bidirectional ventricular tachycardia may occur in patients with structurally normal hearts who are not receiving digoxin (4).
In summary, bidirectional tachycardia is not a homogeneous clinical syndrome and therefore may have more than one mechanism. However, automaticity or triggered activity is more often implicated than reentry (5).
As for other tachyarrhythmias, the correction of reversible factors (e.g., decompensated congestive heart failure, digoxin excess, electrolyte abnormalities) is an important part of the treatment of bidirectional tachycardia. For patients with sustained and especially hemodynamically compromising bidirectional tachycardia caused by digoxin toxicity, antidigoxin antibody fragments (digoxin immune Fab) are the treatment of choice (21). As a temporary measure for these patients and for other severely affected patients without digoxin toxicity, antiarrhythmic drugs may be used. Lidocaine is a reasonable drug of first choice, given its rapid onset of action and minimal hemodynamic effects. In addition, most of the published experience is with this drug. Lidocaine was successful in 9 of 10 patients in 1 series at a dose of 3 mg/min IV after two 75-mg boluses (22). Lidocaine has been effective in some (12,15) but not all case reports (13). Quinidine and flecainide have been used effectively in two cases when lidocaine was ineffective (5,13).
Other modalities for treating tachyarrhythmias include antitachycardia pacing and electrical cardioversion. These techniques are most effective for terminating tachyarrhythmias caused by reentry, are variably effective for treating rhythms caused by triggered activity, and are ineffective for tachyarrhythmias caused by automaticity. There is minimal reported experience in using these techniques in bidirectional tachycardia, but they would be expected to be of limited utility because automaticity and triggered activity seem to be the mechanisms most often underlying bidirectional tachycardia (5). Another reason for the limited role of electrical cardioversion in bidirectional tachycardia is that concomitant digoxin toxicity is often present, which increases the risk of ventricular proarrhythmia after electrical cardioversion (23). For relatively slow bidirectional tachycardias with hemodynamic compromise, overdrive atrial pacing might be useful to restore atrioventricular synchrony and improve hemodynamics. This form of pacing does not terminate automatic rhythms but suppresses automaticity by repetitively depolarizing the focus at a faster rate than its intrinsic rate of firing (24).
We concluded that there is not a single site of origin or a definite singular mechanism responsible for producing the EKG findings of bidirectional tachycardia. Therefore, it is prudent to treat each patient on an individual basis and not assume that all EKGs demonstrating bidirectional tachycardia represent the same pathophysiology. In general, though, bidirectional tachycardia is usually ventricular in origin, and digoxin toxicity is a common antecedent.
|
References |
|---|
|
TopAbstractIntroductionCase 1DiscussionReferences |
|---|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
