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Introduction   

Torsades de Pointes (TdP) “twisting of the points or twisting of QRS complex on electrocardiogram” is a type of polymorphic ventricular tachycardia characterized on an electrocardiogram by oscillatory changes in the amplitude of the QRS complexes around the isoelectric line [1]. Torsades de Pointes relates to QTc prolongation, which involves the lengthening of the QT interval adjusted for heart rate [1]. QT prolongation measures delayed ventricular repolarization [2]. Excessive QT prolongation can predispose the myocardium to early after-depolarizations, which can trigger re-entrant tachycardias including TdP [2]. Torsades de Pointes (TdP) may either terminate without intervention or degenerate into ventricular fibrillation, leading to sudden death [1]. 

TdP is a rare but fatal arrhythmia if not diagnosed and treated with prompt interventions [3]. Patients may present with a range of symptoms, but the ECG is diagnostic. Conscious patients may experience palpitations and 50% of patients present as asymptomatic [1]. The most common symptoms reported are syncope, palpitations, and dizziness; however, in up to 10% of cases, cardiac death is the initial symptom [1]. Patients with Jervell and Lange-Nielsen syndrome may also have a history of deafness [1]. 

While physicians manage the arrhythmia, it is fundamental for all nurses to recognize it and consult with a cardiologist. Advise patients with congenital prolonged QT intervals to refrain from strenuous exercise [4][5]. Long QT syndrome (LQTS) can be congenital (cLQTS), acquired (aLQTS), or both [6]. TdP runs are often self-terminating but recurrent [1].  

Several pathological conditions and drug toxicities can induce prolonged or abnormal repolarization (QT interval prolongation and/or twisted T or T/U wave morphology), resulting in TdP development, which can lead to ventricular fibrillation and sudden cardiac death [7]. QT intervals represent the duration of the total action potential during ventricular polarization and depolarization events [8].  

Several non-cardiac drugs that modulate cardiac repolarization can prolong QT intervals and trigger TdP onset [34]. Both aLQTS and cLQTS may share similar genetic variants in their pathogenesis [9]. An individual’s genetic background is a critical factor, as even minor prolongation of the QT interval can result in life-threatening manifestations of aLQTS when appropriate pathogenic triggers are present [9]. 

Case Study  

A 78-year-old male, recovering from a C. difficile infection, schedules a colonoscopy under sedation. His medical history is notable for hypertension and a history of paroxysmal supraventricular tachycardia (PSVT). The patient described self-resolving syncopal episodes which led to a suspected diagnosis of PSVT. His pertinent medications include diltiazem, amlodipine, and omeprazole. His social and family histories are non-contributory. He completed a bowel prep before the procedure as instructed and had minimal oral intake in the preceding days due to persistent nausea. 

Diagnostic Assessment 

A pre-procedure EKG displayed inverted T waves, prominent U waves, and a prolonged QTc exceeding 600 milliseconds. The team evaluated the rhythm strip which indicated polymorphic ventricular tachycardia (Torsades de Pointes). Over 15 minutes, the providers administered 2 grams of IV magnesium. Laboratory evaluation showed a potassium level of 2.9 mmol/L (normal range 3.5–4.5), a sodium level of 132 mmol/L (normal range 135–145), glucose at 153 mg/dL (normal fasting level 60–100), normal magnesium at 2.1 mg/dL (normal range 1.6–2.4), low ionized calcium at 1.14 mmol/L (normal range 1.2–1.32), and a low phosphorus level of 0.98 mg/dL (normal range 0.97–1.45) [10]. 

Figure 1. [40] 

Therapeutic Intervention 

After diagnosing Torsades de Pointes, the healthcare team administered 2 grams of magnesium and initiated aggressive repletion of potassium and phosphorus using both intravenous and oral routes, as the patient remained awake, oriented, and following commands. The medical team admitted the patient to the ICU for ongoing electrolyte repletion and continued evaluation. 

Follow-up and Outcomes 

During the patient’s hospital stay, he exhibited long QT syndrome and experienced several episodes of Torsades de Pointes and pulseless ventricular fibrillation, all of which required defibrillation. These episodes occurred in the intensive care unit despite the discontinuation of all QT-prolonging medications and the normalization of his normalization electrolytes. Each episode responded to defibrillation, resulting in a return to normal sinus rhythm. The team consulted interventional cardiology for further evaluation and treatment. Medical management failed, and persistent prolonged QT syndrome led to the diagnosis of congenital long QT syndrome exacerbated by significant diarrhea, electrolyte abnormalities, and QT-prolonging medications. The team implanted a cardioverter-defibrillator (ICD) on day 2 of his hospital stay and discharged him home on day 4. 

Differential Diagnosis  

The differential diagnosis for Torsades de Pointes includes a variety of conditions that can present similar symptoms. Ventricular tachycardia and ventricular fibrillation are primary considerations, as they can also manifest with rapid, irregular heart rhythms [11]. Evaluate dialysis-related complications in patients undergoing renal replacement therapy, as electrolyte imbalances associated with dialysis can precipitate arrhythmias [12]. Syncope, or sudden loss of consciousness, can be both a symptom and a differential diagnosis, necessitating a thorough assessment to distinguish it from arrhythmia-induced syncope [13].  

Drug toxicity from medications such as antihistamines and antiarrhythmics is another crucial consideration [14]. These drugs can prolong the QT interval and lead to arrhythmogenic events [14]. Therefore, a detailed medication history and review of potential drug interactions are essential in the differential diagnosis of Torsades de Pointes [1].  

Assessment & Evaluation 

Providers can diagnose Torsades de Pointes (TdP) through ECG, which shows an undulating QRS axis with the polarity of complexes shifting around the baseline [6]. Between episodes, the ECG can reveal a prolonged QT interval corrected for heart rate (QTc). Consider QTc values normal at 0.40 seconds for men and 0.41 seconds for women, and prolonged when exceeding 0.47 seconds for men or 0.48 seconds for women [6]. Family history may suggest congenital syndrome.  

ECG warning signs of impending TdP VT, besides QT interval prolongation, include fusion of T-wave and U-wave (sometimes with giant TU waves), post-extra systolic changes in repolarization patterns, macroscopic T-wave alternans (visible alternation between two different T-wave appearances), frequent polymorphic ventricular premature beats representing single beats of TdP, often in bigeminy, and repetitive short runs of polymorphic ventricular tachycardia [15].  

Although patients may have a normal QTc, it prolongs around the time of TdP VT. Just before TdP VT, the QT interval is often long and shows a giant TU wave. [16]. Abnormal, giant T-U waves distinguish TdP initiation in LQTS patients from PVCs in other heart diseases and other PVCs in LQTS patients [15]. These ECG analyses suggest that early after-depolarizations initiate TdP and, if present, may help identify an imminent risk for TdP [15][16]. 

Epidemiology 

The prevalence of congenital prolonged QT syndrome suggests that between 1 in 2,000 and 1 in 20,000 people have the genetic mutation for QT prolongation [17]. Torsades de Pointes is 2-3 times more common in women than in males, with women tending to have longer QT intervals and experiencing more QT prolongation as a result of drug therapy [17]. Several European centers estimate the annual reporting rate of drug-induced Torsades de Pointes to range from 0.8 to 1.2 cases per million person-years [3].  

Pathophysiology  

The suspected mechanism for Torsades de Pointes involves inhibiting the delayed rectifier potassium current, leading to an accumulation of positive ions within the cellular membrane and causing a prolonged repolarization phase [1]. If an ectopic beat occurs during this phase, known as an R on T phenomenon, it can trigger Torsades de Pointes [1] [24]. Both congenital and drug-induced QT prolongation affect the cellular membrane by blocking the potassium channel [1]. Unlike ventricular fibrillation, Torsades de Pointes can resolve, but if left untreated, it can progress into ventricular fibrillation. The risk of TdP increases when the QTc prolongation exceeds 0.50 seconds [6].  

The most common factor in acquired TdP is a QT interval–prolonging Class Ia, Ic, or Class III antiarrhythmic drugs [6]. Other drugs that can induce TdP include tricyclic antidepressants, phenothiazines, and certain antivirals and antifungals [18]. Other predisposing causes often coexist, such as female sex, older age, hypokalemia, hypomagnesemia, hypothyroidism, slow or irregular ventricular rates, acute intracranial events (e.g., bleeding, stroke, traumatic brain injury), eating disorders, organophosphate poisoning, and structural heart disease (especially acute ischemia, myocarditis, and ventricular hypertrophy) [1] [6] [19]. 

Treatment & Management 

The initial step in managing Torsades de Pointes (TdP) involves preventing its onset by addressing modifiable risk factors [20]. This includes discontinuing any QT-prolonging medications and optimizing the patient’s electrolyte levels. Correcting hypokalemia, hypomagnesemia, and hypocalcemia can help prevent TdP. Some studies suggest a potential prophylactic benefit of oral or IV magnesium for patients with drug-induced prolonged QT, though its overall benefit is not well established, and there is little evidence that magnesium affects the QT interval [1] [20]. 

Assessment and Immediate Management 

Management of Torsades begins with assessing the patient’s hemodynamic stability. While most episodes are self-limiting, the risk is higher in patients who may develop ventricular fibrillation. Perform electrical cardioversion in cases of hypotension or cardiac arrest due to TdP [21]. Recommend synchronized cardioversion for unstable patients with a pulse (100J monophasic, 50J biphasic), and defibrillate pulseless TdP [1] [21]. 

First-Line Therapy 

Intravenous magnesium is the first-line pharmacologic therapy for TdP [22]. Magnesium stabilizes the cardiac membrane, though the exact mechanism is unknown. The recommended initial dose is a slow 2 g IV push, followed by an infusion of 1 g to 4 g per hour to maintain magnesium levels above 2 mmol/L [1] [23]. Stop the infusion once levels exceed 3 mmol/L. Severe magnesium toxicity, characterized by confusion, respiratory depression, coma, and cardiac arrest, occurs at levels above 3.5 mmol/L [1]. It is also important to correct any hypokalemia, maintaining serum potassium between 4.5 mmol/L and 5 mmol/L.  

Correcting electrolyte hypokalemia is crucial as these imbalances can increase the risk of ventricular arrhythmias [29]. Use lidocaine, a class Ib antiarrhythmic drug, to shorten the QT interval in cases of drug-induced TdP, and avoid class Ia, Ic, and III antiarrhythmics [30]. 

For Intermittent Runs 

For patients experiencing intermittent runs of TdP despite magnesium treatment, increasing the heart rate may help. Providers can achieve this through pharmacological interventions with isoproterenol, a non-selective beta-agonist that increases heart rate and shortens the QT interval, reducing the likelihood of an R-on-T phenomenon leading to TdP [24]. Administer isoproterenol as a 10 mcg to 20 mcg IV push or titrate an infusion to maintain a heart rate of 100 bpm [26]. However, it is contraindicated in patients with congenital prolonged QT, as it can lengthen the QT interval [25] [26]. 

Overdrive Pacing 

Use overdrive pacing as another option for terminating TdP, effective for both frequent runs of TdP and TdP refractory to magnesium [27]. Recommend overdrive pacing for drug-induced TdP, as it terminates drug-induced prolonged QT intervals and consequent TdP by shortening the QT interval [27] [28]. Temporary transvenous overdrive pacing at rates of around 100 bpm has proven effective in terminating TdP [28]. 

Addressing Precipitating Factors 

• Hypokalemia: Treat and target a high-normal potassium level (>4.5 mEq/L). 
• Hypocalcemia: Treat if present, as it may promote TdP.  
• Hypothermia: Reverse. 

Common Medications Linked to TdP 

Antiarrhythmics 

• Class IA: Quinidine, disopyramide, procainamide [30]. 
• Class IC: Flecainide [30]. 
• Class III: Dofetilide, ibutilide, sotalol, dronedarone [30]. 

Psychotropics 

• Haloperidol, droperidol, chlorpromazine, pimozide [31]. 
• Citalopram, escitalopram [31]. 
• Tricyclic antidepressants [31]. 

Antibiotics 

• Clarithromycin, erythromycin [32]. 
• Fluoroquinolones [32]. 
• Fluconazole, itraconazole, voriconazole, posaconazole [32]. 
• Pentamidine [32]. 

Other 

• Methadone [35]. 
• Cocaine, loperamide (when abused in massive doses) [33] [34]. 
• Ondansetron (via rapid administration) [36]. 
• Propofol [37]. 
• Arsenic trioxide, sunitinib, vandetanib [38]. 

Long-Term Management 

For long-term management, avoiding conditions and medications that prolong the QT interval is essential. Some patients with an acquired long QT-interval syndrome may have an underlying subclinical congenital long QT-interval syndrome, as suggested by persistent QTc interval prolongation even after removing exogenous QTc-prolonging factors. 

Conclusion

Torsades de Pointes (TdP), characterized by oscillatory changes in the QRS complex amplitude on an electrocardiogram, is a type of polymorphic ventricular tachycardia associated with QTc prolongation [1]. This prolonged QT interval reflects delayed ventricular repolarization, predisposing the myocardium to early after-depolarizations and triggers re-entrant tachycardias such as TdP [2]. While TdP can sometimes resolve without intervention, it poses a significant risk of degenerating into ventricular fibrillation, leading to sudden death if not promptly recognized and treated [1][24]. The ECG is diagnostic, revealing key warning signs such as giant T-U waves and a prolonged QT interval [15][16].  

Management of TdP involves addressing modifiable risk factors, discontinuing QT-prolonging medications, and correcting electrolyte imbalances [1]. Intravenous magnesium is the first-line treatment, stabilizing the cardiac membrane to prevent further episodes [20][22]. For patients experiencing recurrent TdP despite magnesium therapy, increasing the heart rate through isoproterenol or overdrive pacing can be effective [27]. Healthcare providers must train to recognize ECG signs of TdP and use temporary pacing modalities. 

Long-term management includes avoiding conditions and medications that prolong the QT interval and considering underlying congenital long QT syndrome in persistent cases. Vigilant monitoring and rapid interventions can mitigate the risks associated with TdP. 

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