Ventricular Arrhythmia Storms in Acute Myocarditis

Acute myocarditis can turn a short presentation with chest pain and troponin elevation into a critical rhythm emergency. When ventricular tachycardia or fibrillation recurs despite resuscitation, the storm reflects several interacting processes: active inflammation, myocardial oedema, transient electrical injury and, in some patients, scar capable of sustaining re-entry. The immediate task is to prevent death; the longer task is to identify which component drives the circuit.

Treatment decisions sit between supportive intensive care, immunomodulation and catheter ablation. None is a substitute for the others. Immunosuppression is not routine for every case of myocarditis, and ablation performed during the unstable inflammatory phase can be hazardous. A defensible plan therefore depends on timing, ventricular function, evidence of persistent inflammation, the stability of the arrhythmic substrate and the experience of the treating centre.

Recognising the electrical storm

Electrical storm is usually defined clinically by recurrent sustained ventricular tachycardia or ventricular fibrillation, often three or more episodes in 24 hours or repeated shock or cardioversion. In acute myocarditis, the first sign may be syncope, pulseless electrical activity or an arrest rather than an organised rhythm. Continuous monitoring, serial 12-lead electrocardiograms and a focused history for viral prodromes, chest pain, exercise and drug exposure are essential. Recurrent instability should trigger an immediate critical-care response.

Evaluation must distinguish inflammatory myocarditis from acute coronary syndrome and other causes of elevated troponin. Coronary angiography is often required when ST elevation or haemodynamic compromise is present. Echocardiography identifies global or regional dysfunction, while cardiac magnetic resonance can show oedema and late gadolinium enhancement. Endomyocardial biopsy is reserved for selected uncertain cases because of sampling limitations and procedural risk; no single biomarker reliably identifies who will develop a storm.

Australian emergency departments are familiar with a rapid “resus bay” response, but geography changes what happens next. A patient presenting in regional New South Wales or Queensland may need retrieval by ambulance, critical-care flight or the flying doctors, then transfer to a tertiary cardiac centre in Sydney, Melbourne, Brisbane, Perth or Adelaide. For a collapse at home, 000 remains the emergency route; arranging specialist support in parallel can prevent prolonged delay.

Stabilising the patient before treating the substrate

During recurrent ventricular tachycardia or fibrillation, standard resuscitation takes priority over elective immunosuppression or mapping. Defibrillation and cardiopulmonary resuscitation are followed by an antiarrhythmic infusion such as amiodarone or lidocaine, selected according to ischaemia, ventricular function and local protocol. Potassium and magnesium should be corrected, and contributors such as hypoxia, acidosis, catecholamine excess, digoxin toxicity or ongoing ischaemia addressed. Antiarrhythmic therapy is a bridge rather than proof that the underlying inflammation has settled.

Profound cardiogenic shock warrants early discussion of temporary mechanical support. An intra-aortic balloon pump may improve coronary perfusion; venoarterial extracorporeal membrane oxygenation can provide circulation while the heart recovers, and percutaneous assist devices are available in selected centres. Temporary pacing may be needed for bradycardia or high-degree block. These therapies create time for anti-inflammatory treatment and multidisciplinary decision-making, but they do not directly terminate a ventricular re-entry circuit.

Transfer thresholds should be set before collapse rather than after repeated shock. The referring team should send real-time electrocardiograms, echocardiographic images, medication and infusion records, airway access and the chronology of the storm. In a widely dispersed health system, a regional hospital can stabilise and treat while a tertiary electrophysiology and advanced heart-failure team co-ordinates arrival. If no intensive-care or ablation resource is reachable, the immediate plan remains resuscitation, antiarrhythmic therapy and transfer.

Using immunosuppression in selected cases

Myocarditis is an inflammatory injury, but routine corticosteroids are not recommended for uncomplicated acute myocarditis and have not been shown to prevent ventricular arrhythmia storms. In fulminant disease with persistent shock or refractory arrhythmia, some centres consider a short course of intravenous methylprednisolone, often with intravenous immunoglobulin, when active inflammation is strongly suspected and treatable infection has been excluded or controlled. This is a selected specialist strategy rather than an automatic response to ventricular tachycardia.

The evidence remains limited and largely observational, with heterogeneous steroid regimens and differing definitions of recovery. Response is judged over days using haemodynamic trends, ventricular function, arrhythmia burden and inflammatory markers rather than a single troponin result. Infectious disease, rheumatology and cardiology input helps distinguish immune-mediated myocarditis from ongoing viral or bacterial infection. Viral polymerase-chain-reaction results cannot, by themselves, establish that immunosuppression is appropriate.

Potential harms need equal attention: hyperglycaemia, infection, gastrointestinal bleeding, neuropsychiatric effects and prolonged immunosuppression. Drug availability also differs between public hospital formularies and community prescribing. In Australia, the Therapeutic Goods Administration governs approval, while the Pharmaceutical Benefits Scheme may subsidise outpatient use, but neither guarantees immediate access to an inpatient regimen or a paediatric preparation. Decisions should therefore document the intended duration, monitoring plan and stop criteria.

Defining the role of catheter ablation

Catheter ablation is most defensible when recurrent ventricular tachycardia or fibrillation persists despite antiarrhythmic therapy and supportive care, particularly when a fixed re-entry circuit can be targeted. It may be used as rescue treatment, as a bridge while inflammation improves, or as definitive therapy once the substrate has matured. In the first days of myocarditis, oedema and injury can change electrical properties from hour to hour, so a non-inducible circuit is not proof that the risk has passed, and widespread low voltage need not represent permanent scar.

At experienced centres, mapping combines activation, pace mapping and identification of late, fractionated or split electrograms consistent with slow conduction. Scar may be inferred from electrograms and imaging, with cardiac magnetic resonance and computed tomography used cautiously because oedema can mimic fixed fibrosis. Possible targets include re-entry around injured myocardium or Purkinje-related exits. Lesion delivery must balance the need to interrupt a circuit against the risk of further injury, and haemodynamic support may be required throughout.

Acute-phase ablation also carries risks of vascular injury, bleeding, perforation, heart block and worsening ventricular function. If a concurrent atrial procedure requires transseptal access, the review of septal puncture complications is relevant because an iatrogenic atrial septal defect may change discharge planning and follow-up. The immediate endpoint is usually suppression of the clinical arrhythmia, with repeat ablation considered when a stable substrate appears later. Defibrillator implantation is assessed separately because some inflammation resolves while substantial scar does not.

Knowing when ablation should wait

Ablation is least suitable when the rhythm is driven by a reversible systemic disturbance, such as unresolved ischaemia, severe electrolyte disturbance or active toxic myocarditis, and no fixed substrate is demonstrable. It is also difficult when ventricular function is too unstable for prolonged mapping or when recoverable oedema produces widespread abnormal electrograms without a clear circuit. In that setting, resuscitation, mechanical support and correction of the inflammatory process remain central, with planned reassessment rather than repeated lesions.

Experience reported with hybrid convergent ablation illustrates how combining endocardial and epicardial approaches can widen lesion delivery in difficult arrhythmias, but those atrial-fibrillation data do not establish efficacy for inflammatory ventricular storms. Epicardial mapping may have a role in selected ventricular cases, yet access, bleeding risk and the lack of standardised protocols limit routine use. The acute myocarditis literature remains dominated by small series and highly selected patients.

A staged strategy is often practical: stabilise in intensive care, document the rhythm substrate, reassess when inflammation and haemodynamics improve, then perform or repeat ablation at a centre with advanced electrophysiology, imaging and mechanical support. If the storm continues but the patient cannot safely undergo intervention, a temporary antiarrhythmic strategy and communication with the family about goals may be necessary. Reassessment should be active rather than a reason to wait passively.

Coordinating care and taking action

Regional and metropolitan services benefit from a single ventricular-storm protocol identifying when to call an electrophysiologist, heart-failure specialist, infectious-disease physician, radiologist, perfusionist and critical-care team. It should state the roles of the cardiac catheter laboratory and theatre, criteria for extracorporeal support, and how quickly repeated arrhythmia is escalated. Regular case review across referral networks can expose delays that remain hidden when decisions are made one hospital at a time.

Shared records are crucial because patients often arrive with incomplete transfer notes. A concise bundle should include serial electrocardiograms, all defibrillation and cardioversion times, antiarrhythmic doses, coronary angiography, echocardiographic findings, cardiac magnetic resonance images, blood results and trends in lactate, renal function and troponin. Videoconference discussion can let a regional team define the safe transfer window. This is particularly important for communities far from a tertiary centre, where a transfer decision may involve overnight flights, severe weather or a long road journey.

After survival, care should include recurrent electrocardiographic monitoring, repeat ventricular imaging, psychological support and graded activity advice. Decisions about an implantable cardioverter-defibrillator should consider persistent ventricular dysfunction, scar, sustained arrhythmia and the reversible nature of some myocarditis. Return-to-work and driving advice varies with state rules and the individual’s symptoms and device function. Patients also need clear instructions about warning symptoms and when to seek emergency care.

Act before the next storm: agree on a 24-hour contact, transfer thresholds and a shared review process for immunosuppression and ablation; audit recurrent ventricular tachycardia cases; and establish these pathways across regional and metropolitan services, not only inside tertiary cardiac units.