While the universal definition of tachycardia considers >100 heartbeats per minute, those presenting with BVT usually have a heart rate of 140-180 beats per minute [1]. Their general condition is often defined by cardiovascular disease and other comorbidities. With regard to cardiac symptoms, the phenotypic spectrum ranges from asymptomatic patients to life-threatening heart failure [1] [2]. Fatigue, chest pain, palpitations, dyspnea, and cough have been reported, and BVT-related circulatory insufficiency may lead to syncopes or prolonged loss of consciousness. These symptoms aren't induced by exercise or stress, which distinguishes classical BVT from catecholaminergic polymorphic ventricular tachycardia [3].

• Recent Upper Respiratory Infection

  A 56-year-old woman with history of hepatitis B presented to the emergency room with 12 hours of intermittent substernal chest pain preceded by a recent upper respiratory infection. [acc.org]

• S3 Gallop

  He had S3 gallop and diminished breath sounds with minimal rales bilaterally. Abdomen was distended and he had 2+ pitting edema. [ncbi.nlm.nih.gov]

• Pulsus Alternans

  Pulsus alternans. Lower tracing is an intra-arterial pressure recording during bidirectional ventricular tachycardia; 4 mm on the vertical axis of the pressure tracing represents 80 mm Hg of systemic arterial pressure. [ahajournals.org]

12-lead electrocardiography is the cornerstone of BVT diagnosis: The electrical heart axis alternates in a regular manner, and this is most easily seen in the lower-limb leads. The heart axis varies on a beat-to-beat basis, usually between -30° and 110°, and BVT may show right or left or alternating bundle branch block morphology, with right bundle branch block morphology being most commonly observed [1]. Atrioventricular dissociation is demonstrated by the appearance of P-waves unrelated to QRS complexes and indicates the arrhythmia to be of ventricular origin [3]. Additional findings may be obtained in those who suffer from further cardiac disorders, which is often the case. Indeed, an underlying cardiac disease may play a crucial role in the pathogenesis of BVT. Patients should, therefore, undergo a thorough cardiological examination. Echocardiography should be performed in all cases; further diagnostic measures should be taken according to anamnestic data and the medical history of the patient and may include additional imaging studies, repeated measurements of blood pressure, laboratory analyses of blood samples, and lung function tests, among others.

With regards to the analyses of blood samples, hemogram, chemistry, and blood gases should be evaluated in all patients. The results of these tests are very helpful in determining the efficiency of circulation and the balance of water and electrolytes. Specific analyses may be required to confirm the trigger of BVT. Because digoxin poisoning is the most common cause of this arrhythmia, serum concentrations of digoxin should be assessed unless another etiology has been identified. Digoxin concentrations >2 ng/ml are regarded as toxic. However, digoxin toxicity has been observed in patients whose serum levels were significantly below that value, so it shouldn't be considered an absolute threshold. Pre-existing heart disease and hypokalemia have been proposed as possible causes of an increased susceptibility to the toxic effects of the cardiac glycoside [1]. Since digoxin may induce renal failure, the confirmation of digoxin toxicity indicates the necessity of an assessment of kidney function.

In hemodynamically unstable patients, cardioversion should be performed immediately. In an emergency setting, electrical cardioversion is preferred over the pharmacological approach. Distinct types of antiarrhythmics may be used to normalize the electrical activity of the heart, such as amiodarone.

Beyond the momentary resolution of arrhythmia, BVT therapy should aim at eliminating its cause. In case of symptomatic digoxin toxicity, digoxin-specific antibody fragments should be administered. There has been much discussion about the dosis to be applied. Digoxin-specific antibody fragments are widely regarded as a safe and effective treatment, but they are very expensive, so their use is generally restricted to life-threatening situations. Evidence of the efficacy of smaller doses may change that approach and has recently been supplied: It has been recommended to administer a bolus of 80 mg to those with acute toxicity, and a bolus of 40 mg to patients suffering from chronic poisoning. Boluses may be repeated if there is no clinical response [4] [5]. Asymptomatic patients who have been diagnosed with digoxin toxicity don't require digoxin-specific antibody fragments, but the cessation of digoxin therapy [1] [4].

Regardless of the underlying disease, water and electrolyte imbalances should be corrected.

Distinct factors should be considered before making a prognosis. Due to the high risk of ventricular fibrillation and sudden death, symptomatic BVT has an unfavorable prognosis [6]. The patient's prognosis largely improves cardioversion is achieved, i.e., if the heart rhythm can be normalized. For a better outcome, recurrence has to be avoided. In the short term, this can be attained by the administration of antidots like digoxin-specific antibody fragments. Indeed, since the introduction of digoxin-specific antibody fragments as a causal treatment option, mortality rates from digoxin toxicity could be reduced to 5-8% [4]. In the long term, the cause of BVT should be eliminated. But while the discontinuation of digoxin treatment is usually feasible, there is no causal therapy of hereditary diseases like catecholaminergic polymorphic ventricular tachycardia, familial hypokalemic periodic paralysis, and Andersen-Tawil syndrome. Affected individuals' life quality and expectancy may be significantly reduced [7] [8] [9] [10].

BVT has long since been considered pathognomonic of digoxin toxicity, and the latter remains the most common cause of BVT. However, BVT may also be a symptom of catecholaminergic polymorphic ventricular tachycardia. As the disease' name suggests, elevated concentrations of catecholamines are the main cause of arrhythmia in affected individuals. Because pheochromocytoma may be associated with an increased release of catecholamines, this type of neoplasm may induce conditions similar to those observed in catecholaminergic polymorphic ventricular tachycardia. Not surprisingly, BVT has been observed in patients diagnosed with pheochromocytoma [11]. Furthermore, BVT has been related to herbal aconite poisoning, myocarditis, myocardial infarction, left ventricular hypertrophy, familial hypokalemic periodic paralysis, and Andersen-Tawil syndrome [1] [12].

BVT is a rare condition, but precise data regarding its incidence and prevalence cannot be provided. It is most frequently diagnosed in patients with pre-existing heart disease and those treated with digitalis glycosides. Accordingly, the majority of BVT patients is of advanced age. Both males and females may be affected.

Under physiological conditions, cardiac activity is coordinated by the electrical conduction system of the heart. Electrical impulses are generated by the sinus node and travel along the atrioventricular node, the bundle of His, the left and right bundle branches, and a complex network of Purkinje fibers. In detail, the left bundle branch splits into the anterior and posterior fascicles before subdividing further. Because each part of the conduction system is capable of generating its own electrical impulses, an ability referred to as automaticity or autorhythmicity, atrioventricular dissociation is followed by impulse formation in the ventricular components. This condition manifests in a ventricular escape beat. According to the hierarchy of ventricular pacemakers, the bundle branches become the dominant pacemakers only if the discharge rate of more proximal structures falls below their own or if the electrical impulses generated by these structures don't reach the bundle branches. Both may occur in BVT patients.

Digoxin is known to induce distinct degrees of atrioventricular block, but the cardiac glycoside may also cause delayed afterdepolarizations, which are related to elevated concentrations of intracellular calcium. The occurrence of delayed afterdepolarizations depends on the heart rate, with faster rates facilitating their onset. If the threshold heart rate for delayed afterdepolarizations is surpassed at a given focus in the bundle branches, ventricular bigeminy develops, and the heart rate is effectively doubled. The higher heart rate exceeds the threshold rate for delayed afterdepolarizations at a second focus in the bundle branches and thus triggers another beat before the formation of the next action potential at the first focus [13]. This way, the ventricular rhythm is faster than the sinus rhythm, regardless of the presence of an atrioventricular block.

According to current knowledge, the two foci of delayed afterdepolarizations are generally located in the anterior and posterior fascicles of the left bundle branch [3]. This hypothesis is consistent with the fact that BVT with right bundle branch block morphology is more frequently seen than BVT with left or alternating bundle branch block morphology. In a scenario where electrical impulses are alternatingly generated in the left and right bundle branches, BVT would be expected to show alternating bundle branch block morphology [13].

The incidence of BVT may and has been reduced by replacing digoxin, which has a complex pharmacokinetic profile and narrow therapeutic index, by compounds that are better tolerated. The majority of patients is now administered β-sympatholytics, angiotensin-converting-enzyme inhibitors, or aldosterone antagonists [14]. If there's no alternative to digoxin, its dose should be kept as low as possible, and the lowest possible dose depends on the patient's sex, age, body weight, renal function, comorbidities, and concomitant medication [15].

Similarly, BVT prevention may consist in avoiding other triggers or alleviating symptoms of primary diseases. For instance, patients suffering from catecholaminergic polymorphic ventricular tachycardia may be treated with β-blockers or may be recommended the implantation of a cardioverter defibrillator to prevent arrhythmias, heart failure, and sudden death [16].

BVT is not a disease but rather a symptom of an impairment of cardiac function. It is generally regarded as pathognomonic of digoxin toxicity, but may rarely be due to hereditary heart disorders, myocardial disease, or poisoning with other non-glycosidic drugs or herbs. Beyond the fact that digoxin is the most common trigger of BVT, it should be considered that digitalis glycosides are mainly administered to the elderly and that comorbidities facilitating the onset of BVT are more frequent in this age group. Thus, BVT is generally diagnosed in the elder, multimorbid individual with pre-existing heart disease, and this is consistent with a very broad phenotypic spectrum. The clinical presentation of BVT patients may be determined by any of their diseases, and BVT itself may go unnoticed until an electrocardiographic examination is done. In other cases, patients may present with signs and symptoms of cardiac insufficiency or heart failure.

Treatment should be provided according to the general and circulatory condition of the patient and should eventually eliminate the cause of BVT. If cardioversion can be achieved and the cause of the disease can be remedied, the patient has a favorable prognosis. However, comorbidities tend to negatively affect the outcome.

The heart consists of four chambers - two atria and two ventricles -, and they contract rhythmically to facilitate the flow of blood through the pulmonary and systemic circulation. If all chambers contracted at the same time, blood flow couldn't be coordinated and directed. Thus, electrical impulses generated by the sinus node, the pacemaker of the heart, are conducted along a complex network of fibers to excite groups of heart muscle cells in a specific order. The conduction of these electrical signals can be observed in an electrocardiogram.

Under pathological conditions, electrical impulses may be generated in so-called ectopic foci, i.e., by groups of heart muscle cells that should be expecting the pacemaker's signal before contracting. The ectopic formation of action potentials may have deleterious consequences: The strictly regulated sequence of contractions may be disturbed, the heart may become unable to fulfill its function of pumping blood through the body, and the patient may develop circulatory insufficiency and life-threatening heart failure. The abnormal generation and conduction of electric signals through the heart reflect in the patient's electrocardiogram. In rare cases, electrical impulses are conducted in opposing directions with every heartbeat, so upward deflections of the electrocardiographic curve alternate with downward deflections. This condition is referred to as bidirectional tachycardia or bidirectional ventricular tachycardia (BVT).

BVT is not a disease but rather a symptom of an impairment of cardiac function. Most frequently, it is caused by the toxic effects of digitalis glycosides like digoxin. Even patients who have tolerated glycosides in the past may develop BVT. Other causes of BVT are the genetic disorders catecholaminergic polymorphic ventricular tachycardia, familial hypokalemic periodic paralysis, and Andersen-Tawil syndrome, or heart conditions like myocarditis, myocardial infarction, and left ventricular hypertrophy. Herbal aconite poisoning may also manifest as BVT.

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