26M with recurrent fast palpitations since 15 years
Title: Refractory Suspected Fascicular Ventricular Tachycardia Complicated by Cardiogenic Shock and Cardiac Arrest in a Non-Compliant Young Adult: A Case Report
Abstract
Fascicular ventricular tachycardia (VT), often an idiopathic left ventricular tachycardia (ILVT), is typically a benign arrhythmia responsive to calcium channel blockers. However, prolonged untreated episodes can lead to severe hemodynamic compromise and tachycardia-induced cardiomyopathy. We present the case of a 26-year-old male with a long-standing, inadequately managed history of suspected fascicular VT who presented with hemodynamic instability. Despite sequential pharmacological and electrical cardioversion attempts, the patient rapidly deteriorated into cardiac arrest requiring cardiopulmonary resuscitation (CPR) before achieving the return of spontaneous circulation (ROSC).
Introduction
Idiopathic left ventricular tachycardia, commonly known as fascicular VT, generally occurs in young, structurally normal hearts. It is classically characterized by a right bundle branch block (RBBB) pattern with axis deviation and is exquisitely sensitive to non-dihydropyridine calcium channel blockers (like verapamil or diltiazem). While often associated with a favorable prognosis, medical non-compliance can lead to frequent recurrences, structural heart changes (tachycardia-induced cardiomyopathy), and, rarely, cardiogenic shock.
Case Presentation
**Patient History**
A 26-year-old male presented to the emergency department with complaints of fast palpitations, giddiness, and shortness of breath (SOB). The patient was previously asymptomatic until 15 years prior (at approximately 11 years of age), when he experienced his first episode of similar symptoms and was diagnosed with suspected fascicular VT. At that time, electrophysiological (EP) studies and radiofrequency ablation were advised but were refused by the patient's family for personal reasons.
Historically, the patient experienced frequent VT episodes that were managed with uptitrated doses of diltiazem (Dilzem). He remained symptom-free for 10 years and eventually discontinued his medications. Symptoms recurred 2 to 3 years ago, prompting the restart of medical therapy. Over the last 7 to 8 months, the frequency of palpitations increased. After a brief period of symptomatic relief upon restarting his regimen, the patient became a medication defaulter, having stopped his therapy completely for the past 2 months. Notably, a coronary angiogram (CAG) performed in 2015 revealed normal coronary arteries.
Previous ECG
Clinical Findings on Admission
Upon arrival, the patient was noticeably restless.
Heart Rate (HR): ~160–180 beats per minute (bpm).
Blood Pressure (BP): Not recordable (NR) indicating profound hemodynamic instability.
Cardiovascular System (CVS): S1 and S2 present with marked tachycardia.
Respiratory System (RS): Bilateral air entry present.
An initial bedside echocardiogram during the tachycardic episode (HR ~160 bpm) revealed global hypokinesia of the left ventricle (LV), severe LV dysfunction, mild mitral regurgitation (MR), and a dilated, collapsing inferior vena cava (IVC).
Emergency Management and Clinical Course
Given the hemodynamic instability and the known history of suspected fascicular VT, an aggressive management protocol was initiated:
1. Pharmacological Intervention: The patient was administered an intravenous (IV) stat dose of Injection Xylocard (Lidocaine) 60 mg, followed by an ongoing infusion. Due to persistent unrecordable blood pressure and lack of reversion, IV Dilzem (5 mg stat) and IV Cordarone (Amiodarone, 150 mg) were sequentially administered. The rhythm did not revert.
2. Electrical Cardioversion: Synchronized direct current (DC) cardioversion was attempted at 100 Joules, followed by an escalation to 150 Joules; however, the rhythm remained refractory.
3. Further Pharmacotherapy and Cardiac Arrest: Injection Betaloc (Metoprolol) was subsequently given. Shortly after, the patient developed sudden seizure-like activity, suspected to be hypoxic seizures, and became severely breathless. The bedside defibrillator monitor displayed a ventricular rate of 160–170 bpm.
4. Resuscitation: The patient rapidly decompensated, necessitating emergency endotracheal intubation. Cardiopulmonary resuscitation (CPR) was initiated. After 2 cycles of CPR, the patient successfully reverted to normal sinus rhythm (NSR).
Post-Resuscitation Care
Following ROSC, central venous and intra-arterial lines were secured. Hemodynamics improved to a HR of ~120 bpm and a BP of 110/50 mmHg, maintained on a Noradrenaline infusion.
A comprehensive formal 2D Echocardiogram performed at 3:00 PM post-arrest revealed:
* Dilated left atrium (LA) and left ventricle (LV internal dimension: 6.0 cm).
* Global LV hypokinesia with severe LV dysfunction (Estimated Ejection Fraction ~30%).
* Mild MR and mild-to-moderate tricuspid regurgitation (TR).
* Right ventricular systolic pressure (RVSP) of 35+15 mmHg.
* Tricuspid annular plane systolic excursion (TAPSE) of 9–10 cm/s.
* Dilated, non-collapsing IVC (2.6 cm).
The ongoing medical regimen post-resuscitation included an IV Xylocard infusion (2 ml/hr), IV Noradrenaline (10 ml/hr to maintain SBP > 110), IV Lasix 20 mg stat, Tab Dilzem 30 mg TID, IV Heparin 5000 IU TID, and IV Levipill 500 mg (likely for seizure prophylaxis following the hypoxic event). Further laboratory diagnostics, including Procalcitonin (PCT) and Thyroid Stimulating Hormone (TSH), were advised.
Final Diagnoses
* Recurrent suspected Fascicular Ventricular Tachycardia.
* Cardiogenic Shock.
* Status post Cardiopulmonary Resuscitation (s/p CPR).
* Status post DC Cardioversion yielding Normal Sinus Rhythm (s/p DCCV -> NSR).
* Severe Left Ventricular Dysfunction (likely Tachycardia-Induced Cardiomyopathy).
Discussion
This case highlights the potentially catastrophic consequences of medication non-adherence in patients with recurrent fascicular VT. While typically hemodynamically tolerated in structurally normal hearts, the prolonged and frequent episodes over 7–8 months, culminating in a 2-month complete cessation of therapy, likely precipitated tachycardia-induced cardiomyopathy (evidenced by global hypokinesia, dilated LV of 6.0 cm, and an EF of ~30%).
The acute presentation was exceptionally refractory. Standard therapy for fascicular VT includes calcium channel blockers, but the profound baseline hypotension (unrecordable BP) severely complicated the pharmacological approach. The sequential failure of lidocaine, diltiazem, amiodarone, metoprolol, and biphasic DC cardioversion underscores the severity of the myocardial irritability and hypoxia, ultimately leading to hypoxic seizures and cardiac arrest.
Definitive therapy for fascicular VT is catheter ablation, which carries a high success rate and is highly recommended for young patients to prevent reliance on lifelong pharmacotherapy and its associated compliance risks.
Conclusion
Recurrent, poorly controlled fascicular VT can progress to severe tachycardia-induced cardiomyopathy and therapy-refractory cardiogenic shock. Early consideration of EP study and catheter ablation is crucial in young individuals to avoid life-threatening complications related to natural disease progression and medication non-compliance. Future management for this patient must prioritize definitive electrophysiological intervention once hemodynamic stability and neurological recovery are ensured.
Comments
Post a Comment