Troubling Tachycardia

This is an example of bidirectional ventricular tachycardia with

• Regular broad complex tachycardia
• The frontal-plane axis swings 180 degrees from left to right with each alternate beat

• Severe digoxin toxicity
• Familial Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT)

Digoxin toxicity

Clinical features

• GIT: Nausea, vomiting, anorexia, diarrhoea
• Visual: Blurred vision, yellow/green discolouration, haloes
• CVS: Palpitations, syncope, dyspnoea
• CNS: Confusion, dizziness, delirium, fatigue

Electrocardiographic Features

• Digoxin can cause a multitude of dysrhythmias, due to increased automaticity (increased intracellular calcium) and decreased AV conduction (increased vagal effects at the AV node)
• The classic dysrhythmia associated with digoxin toxicity is the combination of a supraventricular tachycardia (due to increased automaticity) with a slow ventricular response (due to decreased AV conduction), e.g.  ‘atrial tachycardia with block’.

Other arrhythmias associated with digoxin toxicity are:

• Frequent VEBs (the most common abnormality), including ventricular bigeminy and trigeminy
• Sinus bradycardia or slow AF
• Any type of AV block (1st degree, 2nd degree & 3rd degree)
• Regularised AF = AF with complete heart block and a junctional or ventricular escape rhythm
• Ventricular tachycardia, including polymorphic and bidirectional VT

Examples of digoxin toxicity:

Clinical features

• An inherited arrhythmogenic disease characterised by episodic palpitations, syncope or cardiac arrest precipitated by exercise or acute emotion (i.e. catecholamine-triggered ventricular dysrhythmias)
• Onset during childhood (mean age: 7-9 years old)
• Family history of sudden cardiac death
• Ventricular arrhythmias reproducible on exercise stress testing

Electrocardiographic Features

• Bidirectional VT
• Polymorphic VT
• Ventricular fibrillation

CPVT Example

• Exercise stress test in a patient with CPVT.
• Progressively worsening ventricular arrhythmias are observed during exercise.
• Typical bidirectional VT develops after 1 minute of exercise with a sinus heart rate of approximately 120 beats per minute.
• Arrhythmias rapidly recede during recovery.

Digoxin

• The antidote for acute or chronic digoxin toxicity is digoxin-specific immune Fab (‘Digibind’)
• Initial empiric dosing of Digibind is 5 ampoules for acute overdose, 2 ampoules for chronic toxicity and up to 20 ampoules for cardiac arrest
• AV block may respond to atropine 0.6 mg IV bolus, repeated to a maxium of 1.8 mg (20 mcg/kg in children)
• Dysrhythmias may be treated with IV lignocaine 1mg/kg (max 100mg) over 2 minutes
• Hyperkalaemia is treated in the usual way with insulin and dextrose, sodium bicarbonate… however, IV calcium is (traditionally) contraindicated!
• DC cardioversion is unlikely to be successful in digoxin poisoning. Patients in cardiac arrest may require continuous CPR until Digibind can be sourced and administered.

Catecholaminergic Polymorphic Ventricular Tachycardia

• Beta blockers (e.g. propranolol) are used for suppression of catecholamine-triggered ventricular tachydysrhythmias.
• Electrical cardioversion / defibrillation may be required for haemodynamically unstable VT/VF, although patients often spontaneously revert to sinus rhythm.
• Implantable cardioverter-defibrillator (ICD) insertion is considered for primary or secondary prevention of cardiac arrest.

• Menduiña MJ, Candel JM, Alaminos P, Gómez FJ, Vílchez J. Taquicardia ventricular bidireccional por intoxicación digitálica [Bidirectional ventricular tachycardia due to digitalis poisoning]. Rev Esp Cardiol. 2005 Aug;58(8):991-3.
• Smith SW, Shah RR, Hunt JL, Herzog CA. Bidirectional ventricular tachycardia resulting from herbal aconite poisoning. Ann Emerg Med. 2005 Jan;45(1):100-1
• Napolitano C, Priori SG, Bloise R. Catecholaminergic Polymorphic Ventricular Tachycardia. Stat Pearls