Download Bidirectional ventricular tachycardia associated with digoxin toxicity

Bidirectional ventricular tachycardia associated with
digoxin toxicity and with normal digoxin levels
Michael Chapman, MBChB, MRCP,* Mark Hargreaves, MD, MRCP, CCDS,†
Heiko Schneider, MBChB, MRCP,† Martin Royle, MBChB, MRCP, CCDS‡
From the *North Tyneside Hospital, Newcastle-upon-Tyne, United Kingdom, †Rochdale Infirmary, Rochdale,
United Kingdom, and ‡Whiston Hospital, St Helen’s, Merseyside, United Kingdom.
Introduction
Bidirectional ventricular tachycardia (VT) is a regular
tachyarrhythmia of ventricular focus with 2 different QRS
morphologies alternating on a beat-to-beat basis.1 The rate
typically is between 140 and 180 bpm, with a frontal plane
axis varying between –201 to –301 and 1101.
Causes of this rare arrhythmia are limited and include
catecholaminergic polymorphic VT, digitalis toxicity, myocarditis, left ventricular hypertrophy, myocardial infarction,
herbal aconite poisoning, familial hypokalemic periodic
paralysis, and Andersen-Tawil syndrome.1–7 Recently, pulmonary embolism8 and pheochromocytoma9 have also been
implicated in causing this arrhythmia.
We present 2 cases of bidirectional VT attributable to
digoxin, one of which had a significantly raised serum
digoxin level and 1 within laboratory normal limits.
Case reports
Case 1
A 58-year-old woman presented with severe sepsis secondary to community-acquired pneumonia and acute kidney
injury approximately 1 year after mechanical aortic and
mitral valve replacement for rheumatic heart disease. She
previously had been diagnosed with severe mixed mitral
valve disease, moderate to severe aortic regurgitation, and
pulmonary hypertension with predominantly right-sided
heart failure. Coronary angiography was normal, and computed tomography of the chest showed no evidence of
thromboembolism.
Other past medical history of note was permanent atrial
fibrillation and rheumatoid arthritis. Medication on
KEYWORDS Bidirectional ventricular tachycardia; Digoxin toxicity; Ventricular tachycardia; Digoxin; Arrhythmia
ABBREVIATIONS AVN ¼ atrioventricular node; ECG ¼ electrocardiogram;
LBBB ¼ left bundle branch block; RBBB ¼ right bundle branch block; VT
¼ ventricular tachycardia (Heart Rhythm 2014;11:1222–1225)
Address reprint requests and correspondence: Dr. Martin Royle,
Department of Cardiology, Whiston Hospital, Warrington Rd, Prescot,
Merseyside L35 5DR, United Kingdom. E-mail address: [email protected].
1547-5271/$-see front matter B 2014 Heart Rhythm Society. All rights reserved.
admission included digoxin, warfarin, ramipril, furosemide,
spironolactone, and terbutaline.
Biochemistry tests on admission revealed a urea level of
106 mg/dL (reference range 7–22.4 mg/dL), creatinine 4.41
mg/dL (0.56–1.0 mg/dL), potassium 5.7 mEq/L (3.5–5.0
mEq/L), magnesium 2.16 mg/dL (1.82–2.31 mg/dL), and
adjusted calcium 8.08 mg/dL (8.7–10.3 mg/dL). Routine
hematology tests showed a white cell count of 10.0 109/L
and prothrombin time of 314.9 seconds (international
normalized ratio 28.9).
Twelve-lead ECG revealed bidirectional VT with right
bundle branch block (RBBB) morphology and alternating
frontal plane axis (Figure 1). Serum digoxin level, measured at
8 hours, was significantly elevated at 5.87 ng/mL (0–2.0 ng/mL).
Treatment consisted of intravenous fluids, antibiotics, and
administration of digoxin-specific antibody fragments. Interestingly, this resulted in cardioversion to sinus bradycardia
(Figure 2). The patient’s renal function normalized, and
digoxin was discontinued because of the occurrence of this
arrhythmia and restoration of normal sinus rhythm.
Case 2
An 86-year-old man presented with acute onset of palpitations and dyspnea. He had multiple comorbidities including
previous lung carcinoma with lobectomy in 1975, chronic
obstructive pulmonary disease, permanent atrial fibrillation,
congestive cardiac failure with severe left ventricular systolic
dysfunction, previous cerebrovascular accident, type 2
diabetes mellitus, peripheral vascular disease with previous
femoral–popliteal bypass, and prostate carcinoma.
His regular medications were digoxin, perindopril, warfarin, furosemide, amiloride, gliclazide, beclomethasone
inhaler, and salbutamol inhaler. There was no family history
of arrhythmia or sudden cardiac death, and there had been no
recent change to his medication doses.
Routine biochemistry testing on admission showed
potassium 4.6 mEq/L, urea 16.8 mg/dL, creatinine 0.89
mg/dL, and corrected calcium 9.76 mg/dL. Hematology
testing on admission was unremarkable. Serum digoxin
level, measured at just over 6 hours, was within normal
limits at 0.58 ng/mL.
http://dx.doi.org/10.1016/j.hrthm.2014.03.050
Chapman et al
Figure 1
Bidirectional Ventricular Tachycardia with Digoxin
1223
Twelve-lead ECG showing bidirectional ventricular tachycardia in a patient with acute kidney injury and elevated serum digoxin
The patient was noted to be hypotensive with a blood
pressure of 85/62 mmHg and tachycardic. His admission
ECG (Figure 3) confirmed bidirectional VT that, as in case 1,
had an RBBB morphology and alternating frontal plane axis.
Immediate direct current cardioversion resulted in atrial
fibrillation with partial left bundle branch block (LBBB) and
left-axis deviation (Figure 4). Digoxin was discontinued
because it was the only recognized trigger of bidirectional VT
in this patient. Diltiazem was later commenced for rate control.
Figure 2
Discussion
Digitalis toxicity can produce a diverse set of arrhythmias
because of its effect on intracellular calcium leading to
delayed afterdepolarizations and enhancement of vagal tone
on the atrioventricular node (AVN). These arrhythmias can
include premature atrial or ventricular contractions, varying
degrees of AVN block, accelerated junctional rhythms,
paroxysmal atrial tachycardia with block, and bidirectional
VT. When digitalis toxicity is suspected, the serum glycoside
Twelve-lead ECG post-treatment with digoxin-specific antibody fragments.
1224
Heart Rhythm, Vol 11, No 7, July 2014
Figure 3
Twelve-lead ECG showing bidirectional ventricular tachycardia in a patient receiving digoxin treatment.
level is of considerable value, especially when it is assayed 6
hours post dose. Levels 42 ng/mL are generally considered
toxic; however, there is considerable overlap. Toxic manifestations can seen with levels o2.0 ng/mL but can be absent
in others cases with levels 43 ng/mL.10 Observational
studies have evaluated the clinical characteristics of patients
with arrhythmias attributable to digoxin.10–12 Other than
serum digoxin level, statistically significant differences have
been found with regard to age, elevated blood urea nitrogen
Figure 4
level, presence of coronary artery disease, and acute or
chronic pulmonary disease.10,11 Retrospective analysis of 73
patients presenting with arrhythmias attributable to digoxin
also found serum digoxin levels to be significantly lower in
those patients who were hypokalemic compared to those
who were normokalemic.12
During bidirectional VT, the surface ECG most often
shows a tachycardia with RBBB morphology and alternating
QRS axis best seen in the inferior limb leads. However, there
Twelve-lead ECG after direct current cardioversion.
Chapman et al
Bidirectional Ventricular Tachycardia with Digoxin
are cases of LBBB morphology bidirectional VT8 as well as
alternating LBBB and RBBB morphology,2 leading to some
debate regarding the exact mechanism.
Current understanding is thought to be related to elevated
intracellular calcium causing delayed afterdepolarization in
anatomically separate parts of the conducting system.13 In
2011, a model by Baher et al13 based on rabbit ventricles was
able to produce the ECG characteristics of bidirectional VT.
They proposed that for this arrhythmia to initiate, 2 separate
foci with different rate thresholds for delayed afterdepolarization–induced ventricular bigeminy needed to be present.
Because the ventricular rate exceeded the lower threshold,
ventricular bigeminy would develop. This would effectively
double the heart rate, taking the overall ventricular rate above
the second threshold. Once this had developed, the 2
competing sites would simply alternate on a beat-to-beat
basis. The authors proposed that this mechanism would
explain why the rhythm is often of RBBB morphology with
alternating frontal axis (where the 2 foci are in the anterior
and posterior fascicles of the left bundle branch). It also
explains why cases have been reported with alternating
LBBB and RBBB morphology (with foci in the left and
right bundles) and why this arrhythmia may progress to
polymorphic VT (where Z3 foci develop).
Both of our cases were attributable to digoxin and
remarkably were admitted within 2 weeks of each other.
The finding of this arrhythmia in the presence of a
therapeutic serum digoxin level serves to further highlight
the arrhythmic properties of digoxin within normal laboratory limits. Patient 2 was elderly with severe left ventricular
systolic dysfunction, both of which have been shown to lead
1225
to increased risk of digoxin toxicity.10,11 This may explain
the occurrence of this arrhythmia with a normal digoxin
level.
References
1. Grimard C, De Labroille A, Charbonnier B, Babuty D. Bidirectional ventricular
tachycardia resulting from digoxin toxicity. J Cardiovasc Electrophysiol 2005;16:
807–808.
2. Tai YT, Lau CP, But PP, Fong PC, Li JP. Bidirectional tachycardia induced by
herbal aconite poisoning. Pacing Clin Electrophysiol 1992;15:831–839.
3. Chin A, Nair V, Healey JS. Bidirectional ventricular tachycardia secondary to
subacute myocarditis. Can J Cardiol 2013;29:254.
4. Stubbs WA. Bidirectional ventricular tachycardia in familial hypokalaemic
periodic paralysis. Proc R Soc Med 1976;69:223–224.
5. Sonmez O, Gul EE, Duman C, Düzenli MA, Tokaç M, Cooper J. Type II
bidirectional ventricular tachycardia in a patient with myocardial infarction.
J Electrocardiol 2009;42:631–632.
6. Bonnemeier H, Barantke M. It is not always digitalis: bidirectional ventricular
tachycardia in left ventricular hypertrophy. Ann Noninvasive Electrocardiol
2008;13:208–210.
7. Sumitomo N, Shimizu W, Taniguchi K, Hiraoka M. Calcium channel blocker and
adenosine triphosphate terminate bidirectional ventricular tachycardia in a patient
with Andersen-Tawil syndrome. Heart Rhythm 2008;5:498–499.
8. Tatli E, Aktoz M, Barutcu A, Altun A. Bidirectional tachycardia in a patient with
pulmonary embolism. Cardiol J 2010;17:194–195.
9. Traykov VB, Kotirkov KI, Petrov IS. Pheochromocytoma presenting with
bidirectional ventricular tachycardia. Heart 2013;99:509.
10. Smith TW, Haber E. Digoxin intoxication: the relationship of clinical presentation to serum digoxin concentration. J Clin Invest 1970;49:2377.
11. Beller GA, Smith TW, Abelmann WH, Haber E, Hood WB Jr. Digitalis
intoxication: a prospective clinical study with serum level correlations. N Engl
J Med 1971;284:989–997.
12. Shapiro W. Correlative studies of serum digitalis levels and the arrhythmias of
digitalis intoxication. Am J Cardiol 1978;41:852–859.
13. Baher AA, Uy M, Xie F, Garfinkel A, Qu Z, Weiss JN. Bidirectional ventricular
tachycardia: ping pong in the His-Purkinje system. Heart Rhythm 2011;8:
599–605.