Amiodarone for Torsades de Pointe

Firstly, let’s look at the definition of polymorphic ventricular tachycardia and torsades de pointe (TdP). Polymorphic ventricular tachycardia (PVT) is a form of ventricular tachycardia in which there are multiple ventricular foci with the resultant QRS complex varying in amplitude, axis, and duration. The most common cause of PVT is myocardial ischemia and/or infarction. Torsades de pointes is a polymorphic ventricular tachycardia that presents on an ECG as a series of QRS complexes that appear to “twist” around the isoelectric line. The twisting pattern is indicative of varying amplitudes and axes of the QRS complexes. TdP is associated with QT prolongation that can be congenital or acquired. TdP is often short lived and self-terminating, however it can be associated with hemodynamic instability and collapse, and it can deteriorate into ventricular fibrillation.

Acquired QT prolongation can be caused by specific medications, disease processes, or a combination of both. Some common QT-prolonging medications include Sotalol, Haloperidol, Erythromycin, Azithromycin, Ciprofloxacin, Citalopram, Amitriptyline, Diphenhydramine, Hydroxyzine, Methadone, and Ondansetron. To note, just because a patient is on these medications does not mean that they will indeed have QT prolongation, but rather, special considerations should be made with these patients for possible increased risk. QT prolongation can also be caused by various clinical conditions such as kidney or liver disease, electrolyte imbalances, thyroid disease, hypothermia, and other arrhythmias.

Clinical management guidelines emphasize that for polymorphic VT with prolonged QT (i.e., TdP), all QT‑prolonging medications should be stopped; amiodarone is one of them. With that, prehospitally, amiodarone should not be considered as first line treatment of TdP. Evidence shows that amiodarone can prolong the QT interval, and although TdP from amiodarone is rare, it can occur. It’s also important to recognize that the diagnosis of TdP and withholding of Amiodarone should not be solely based on morphology (which could be challenging in the out of hospital setting), but a medical history suggestive of QT prolongation.

It’s also essential not to overlook that the administration of any anti-arrhythmic medication has the potential to cause additional arrhythmias that we must also be prepared for.

Prehospital management of this arrythmia includes:

1. Recognizing TdP is vital. The TdP rhythm is known to look like it “twists” around the baseline.
2. If the patient is pulseless, the situation should be treated and managed as a cardiac arrest. Begin CPR and defibrillate immediately.
3. If the patient has a pulse but is unstable (hypotension, syncope, altered LOC, etc.) then cardioversion is indicated. Patching to a base hospital physician (BHP) is required.
4. Correct underlying causes when possible. Consider supporting perfusion and oxygenation as needed and identifying possible overdose or toxin exposure causing QT prolongation.

Evidence-based hospital management of TdP (prolonged QT polymorphic VT) includes:

1. IV magnesium sulfate is the first line therapy for TdP, even if the serum magnesium level is normal. Additionally, termination of all QT‑prolonging medications is advised.
2. Correcting electrolyte imbalances is also really important mainly aggressively correcting potassium levels (goal 4.5–5.0 mEq/L).
3. Increasing and maintenance of the patient’s heart rate might also be required. With that, overdrive pacing may be used.
4. If the patient becomes unstable (hypotension, altered level of awareness, syncope, shock, etc.), cardioversion would then be indicated.