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Slow Ventricular Tachycardia and Electrical Storm in a CRT-D Patient: A Clinical Case and Diagnostic Pitfalls - Part 1

Introduction

Electrical storm and incessant ventricular tachycardia are among the most challenging conditions in acute cardiology, particularly in patients with structural heart disease and implanted cardiac devices. Rhythm diagnosis and selection of the correct treatment strategy can be difficult, and misclassification of arrhythmia may have serious clinical consequences.

This case report describes the clinical course of a patient with ischemic cardiomyopathy and CRT-D, in whom slow ventricular tachycardia was initially misinterpreted as a supraventricular arrhythmia. The article is written in collaboration with Dr Njord Nordstrand, consultant cardiologist at the cardiac intensive care unit, Oslo University Hospital Rikshospitalet, and is intended as a practical learning tool for healthcare professionals in acute clinical practice.


Background

A man in his 60s with ischemic cardiomyopathy (ejection fraction approximately 30 percent), prior myocardial infarction, and CRT-D implanted for primary prevention had known atrial fibrillation. He had previously undergone an unsuccessful ablation and experienced recurrent episodes despite treatment with beta-blockers and amiodarone. The patient had been electrically cardioverted multiple times and was referred for repeat ablation.

The ECG below shows an atrial arrhythmia with ventricular tracking, at a rate of 123 beats per minute and a QRS duration of 210 ms.

Atrial arrhytmia, tracked by the ventricles (biventricular pacing)
Atrial arrhytmia, where the ventricle is tracking the atrial rhythm with biventricular pacing.

ECG after electrical cardioversion shows a rate of 60 beats per minute, atrial paced and ventricular paced rhythm, with a QRS duration of approximately 210 ms.

Atrial oacing and biventricular pacing
EKG after cardioversion - atrial pacing and biventricular pacing

In-Hospital Clinical Course

The patient was admitted with presumed atrial arrhythmia and planned electrical cardioversion. He had been cardioverted for the same rhythm two days earlier but experienced rapid recurrence. On admission, however, the ECG demonstrated slow monomorphic ventricular tachycardia with a QRS duration of 170 ms and a rate of approximately 120 beats per minute, below the ICD detection threshold.


Ventricular tachycardia - 120 beats/min
Ventricular tachycardia - 120 beats/min. Pay attention to the morphology of lead AVL in this ECG, compared to the previous ones.

Programmed antitachycardia pacing (ATP) was delivered and successfully converted the rhythm to sinus. A few hours later, the arrhythmia recurred. ECG then showed a rate of 105 to 110 beats per minute and a QRS duration of approximately 170 ms, again below the ICD detection threshold.


Slow VT - 107 bpm
Slow VT - 107 beats/min

Manually programmed ATP again restored sinus rhythm, and the VT detection zone was adjusted to capture slower VT episodes. Despite this, the patient continued to have frequent VT recurrences. Flecainide was trialed without effect.


Repeat echocardiography showed unchanged infarct sequelae and moderate to severe secondary mitral regurgitation. During hospitalization, the patient developed increasingly frequent VT episodes, eventually progressing to incessant VT with clinical deterioration.


Hemodynamic Support and Sedation

Nitroprusside did not result in clinical improvement. An intra-aortic balloon pump (IABP) was therefore inserted for hemodynamic unloading, with the aim of improving coronary perfusion and increasing effective inotropy, potentially breaking the vicious cycle between VT and heart failure.


Lidocaine was added to amiodarone and beta-blocker therapy. The patient did not respond adequately to sedation with dexmedetomidine, but intubation and deep sedation led to a marked reduction in VT activity. He subsequently underwent VT ablation with good clinical outcome.


Rhythm Diagnosis and ECG Findings

The patient had two arrhythmias: an atrial arrhythmia tracked by the CRT system, and a ventricular tachycardia. Both produced wide QRS complexes with relatively similar morphology.


Key findings:

  • Paced QRS complexes were very wide (approximately 210 ms), whereas VT complexes were narrower (approximately 170 ms).

  • VT morphology was relatively similar to paced rhythm, but with reproducible differences, particularly in lead aVL.

  • VT was slower than the atrial arrhythmia, which is common in patients treated with amiodarone.

  • Device spikes were visible during paced rhythm but absent during VT.


In patients with CRT, a rhythm with narrower QRS complexes than the paced QRS strongly suggests a ventricular origin rather than atrial tracking. The same principle applies in bundle branch block: a rhythm that is narrower than the patient’s baseline QRS is almost diagnostic of ventricular tachycardia.


Clinical Assessment of Triggering Factors

Electrical storm and incessant VT are often triggered by a combination of:


  1. Established structural heart disease (infarction, fibrosis), creating a vulnerable arrhythmic substrate.


  2. External precipitating factors, such as:

    • Heart failure and increased sympathetic drive

    • Electrolyte disturbances

    • Infection or other systemic stress

    • Thyrotoxicosis during amiodarone therapy

    • Renal failure or dehydration


  3. Autonomic imbalance, with increased sympathetic activity as a key driver.


Evaluation should include a thorough history, electrolytes, hemoglobin, renal function, thyroid function tests, infection workup, and echocardiography.


Key Management Lessons From This Case

  1. Slow VT in patients treated with amiodarone may be hemodynamically tolerated and fall below ICD detection thresholds.

  2. Connection of a programmer in patients with implanted devices is often necessary for accurate rhythm diagnosis.

  3. Differences between paced QRS and VT-QRS provide crucial diagnostic information.

  4. Hemodynamic unloading with IABP can improve coronary perfusion and help interrupt the vicious cycle between VT and heart failure.

  5. Early sedation, and intubation when necessary, can significantly reduce VT burden.

  6. Early consideration of catheter ablation is essential in incessant VT or refractory electrical storm.


Short Summary

This case illustrates how ventricular arrhythmias in patients with CRT-D and structural heart disease can be difficult to recognize, and why slow VT is often underestimated. A combination of accurate device-based rhythm diagnosis, hemodynamic stabilization, sympathetic modulation, and early consideration of ablation is critical.


In Part 2, a structured and practical clinical guide for the management of electrical storm and incessant VT will be presented.

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Legesnakk is an independent and non-commercial knowledge platform in cardiology, developed by Faraz Afzal, MD, PhD. The content is intended for educational purposes only and is not a substitute for medical advice.

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