Out-of-hospital cardiac arrest without return of spontaneous circulation after more than 2 hours: is termination of resuscitation the only option? A case report

Abstract

Background

Out-of-hospital cardiac arrest (OHCA) remains a major cause of mortality, with survival rates of approximately 8% despite timely cardiopulmonary resuscitation. While indications to initiate resuscitation are well established, decisions regarding termination remain complex, particularly in prolonged arrests with potentially reversible mechanisms. The routine application of termination-of-resuscitation rules may be limited by imperfect prognostic accuracy.

Case summary

We report a previously healthy 20-year-old Caucasian man who suffered a witnessed OHCA with an initial shockable rhythm. Despite prolonged advanced life support and a total cardiac arrest duration of 135 min, venoarterial extracorporeal membrane oxygenation (ECMO) was initiated as a rescue therapy. Return of spontaneous circulation was achieved, followed by gradual haemodynamic stabilization and a complete neurological recovery. Extensive diagnostic evaluation excluded coronary artery disease, myocarditis, and structural cardiomyopathy. A diagnosis of primary ventricular fibrillation syndrome related to short-coupled ventricular premature complexes was established. A subcutaneous implantable cardioverter-defibrillator was implanted for secondary prevention. The patient was discharged without neurological or functional impairment and continued to be asymptomatic at the last visit.

Discussion

This case highlights that meaningful recovery may be possible after prolonged resuscitation in carefully selected patients. It illustrates the potential role of ECMO in refractory OHCA and emphasizes the need for individualized decision-making when considering termination of resuscitative efforts, particularly in young patients with favourable initial characteristics.

Learning points.

• Meaningful recovery may be possible after prolonged resuscitation in carefully selected patients.

• Venoarterial extracorporeal membrane oxygenation might be used in refractory out-of-hospital cardiac arrest, particularly in young patients with favourable initial characteristics.

Introduction

Out-of-hospital cardiac arrest (OHCA) is a leading cause of global mortality, with survival remaining around 8% despite prompt cardiopulmonary resuscitation.¹ A rapid return of spontaneous circulation (ROSC) is essential for neurologically intact survival,² and outcomes are strongly influenced by factors such as bystander-witnessed arrest and an initial shockable rhythm. Guidelines define when to initiate cardiopulmonary resuscitation (CPR), but determining when to terminate it remains uncertain, and the application of termination-of-resuscitation rules in prolonged and complex cases is limited.^3,4 To our knowledge, complete neurological recovery after such an extended low-flow time remains exceptional and rarely reported.

Case Report

A healthy 20-year-old Caucasian with no prior medical history was admitted after an OHCA. On a Saturday afternoon at 03:45 p.m., he was found by relatives with agonal breathing. The family initiated basic CPR and transferred him to our centre in their private vehicle, while trying to apply continuous chest compressions.

He arrived at the emergency department approximately 30 min later with ventricular fibrillation as the initial rhythm. Advanced CPR was started. Despite five defibrillation attempts, the arrhythmia persisted, progressing to asystole. The first venous lactate level was 3.6 mmol/L.

During resuscitation, a total of 35 epinephrine 1 mg doses were administered, along with 300 mg of amiodarone after the third shock and 150 mg after the fifth shock, 150 mg of lidocaine, and volume resuscitation with both crystalloid and colloid solutions. After 30 min, the extracorporeal membrane oxygenation (ECMO) team for the cardiac arrest protocol was activated. The team required 25 min to arrive. Repeated percutaneous cannulation attempts were unsuccessful due to extreme vasoconstriction, and vascular surgery was called to perform open cannulation via dissection of the left femoral vein and artery in the emergency department. ECMO support was successfully initiated 90 min after the patient’s arrival to the emergency department, with a total cardiac arrest duration of 135 min and a venous lactate at ECMO initiation that exceeded 17 mmol/L.

Following ECMO initiation, the patient reverted to ventricular fibrillation. After two additional defibrillations, the patient finally reverted to sinus rhythm (Figure 1). The electrocardiogram revealed sinus rhythm with generalized ST-segment depression and a corrected QT interval of 450 ms, consistent with post-cardiac arrest changes. The patient was transferred to the Cardiac Intensive Care Unit. Bedside echocardiography showed a non-dilated left ventricle with a 15% left ventricular ejection fraction. Despite high-dose norepinephrine infusion (up to 1.5 mcg/kg/min), the patient remained haemodynamically unstable, requiring continuous epinephrine infusion. High-sensitivity troponin exceeded 35 000 ng/L.

Figure 1.

Sequence of events and cardiopulmonary resuscitation (CPR) management after out-of-hospital cardiac arrest (OHCA) in the emergency department (ED). VF, ventricular fibrillation; ECMO, extracorporeal membrane oxygenation.

The patient’s young age and the absence of cardiovascular risk factors suggested a low risk of acute coronary syndrome. Moreover, the ECG, once sinus rhythm was achieved, did not show ST-segment elevation. Since myocarditis was a possibility and the patient presented with a long cardiac arrest, corticosteroids were used.

Blood was collected at hospitalization for genetic testing (cardiomyopathy panel) after obtaining family consent. Drug testing at admission was positive for cannabis.

At admission, the patient remained unresponsive, although no sedatives had been administered. Both the haemodynamic and neurological state improved progressively, and, on Day 5, the patient was successfully weaned from ECMO. Brain computed tomography (CT) scan and coronary angiography were performed on Day 6, showing no abnormalities. Endomyocardial biopsy showed no evidence of acute myocarditis, and viral serology was negative for common respiratory viruses.

On Day 8, the patient developed sustained polymorphic ventricular tachycardia triggered by a short-coupled premature ventricular complex with a normal QT interval (Figure 2), leading to another cardiac arrest that required five defibrillations and reintubation. No electrolyte imbalances or pH disturbances were found to be responsible for the arrhythmic relapse. Due to the fact that all the arrhythmic episodes initiated with the same premature ventricular complex, an overdrive pacing strategy was established, at first with isoprenaline and later with an atrial percutaneous pacemaker. At the same time, treatment with quinidine at doses of 400 mg/8 h per os was initiated. An electrophysiological study was performed (Figure 3) to ablate the premature ventricular complex, which was found to originate on the basal lateral portion of the right ventricle and was successfully ablated. Despite initial success, arrhythmias recurred, prompting implantation of a temporary atrial pacemaker with an active fixation lead for overdrive pacing, which terminated the episodes.

Figure 2.

Non-sustained polymorphic ventricular tachycardia triggered by a short-coupled ventricular premature complex with a normal QT interval.

Figure 3.

Electrophysiological study. Electrophysiological study of premature ventricular complexes (PVC). Clinical PVC with left bundle branch block morphology, transition in V4, and superior axis. Endocardial right ventricular voltage mapping showing no significant substrate (>1 mV). Pulsed field ablation delivery sites (Sphere-9 catheter, Affera electroanatomic navigation system, Medtronic Inc.). (A) Local electrogram preceding the clinical PVC up to −30 ms at the basal lateral right ventricle relative to QRS onset. (B) Pacemapping with 12/12 lead concordance on surface electrocardiogram.

As a complication secondary to high-dose quinidine administration (400 mg/8 h p.o.), the patient developed generalized myoclonus and pyramidal signs on Day 20 of admission; a repeated brain CT scan was normal, and electroencephalography showed no data suggesting structural brain injury.

Cardiac magnetic resonance imaging revealed elevated T1 signals, non-ischaemic scarring, and mild left ventricular systolic dysfunction, with a left ventricular ejection fraction of 46%. Genetic testing was inconclusive, identifying a filamin variant of uncertain significance. A diagnosis of primary ventricular fibrillation syndrome secondary to short-coupled ventricular premature complex was established, and a subcutaneous implantable cardioverter-defibrillator (s-ICD) was used for secondary prevention. The patient was discharged without neurological sequelae on quinidine (200 mg/day). Figure 4 shows a timeline depicting the in-hospital treatment.

Figure 4.

In-hospital treatment course. OHCA, out-of-hospital cardiac arrest; ECMO, extracorporeal membrane oxygenation; CT, computed tomography; VT, ventricular tachycardia; EP, electrophysiological study; RV, right ventricle; EEG, electroencephalogram; S-ICD, subcutaneous implantable cardioverter-defibrillator.

At the last visit in December 2025, the patient presented no neurological deficits. At the interrogation of the s-ICD, no arrhythmias or shocks were recorded.

Discussion

OHCA has an estimated annual incidence of 67–170 cases per 100 000 inhabitants.^5,6 Among young subjects, the predominant aetiologies include inherited cardiac conditions, congenital heart disease, myocarditis, and substance use.⁷ Despite advances in life support, outcomes for refractory OHCA remain poor, particularly in the absence of reversible causes.

ECMO has emerged as a rescue strategy in carefully selected cases of refractory cardiac arrest with potentially reversible causes, provided it can be rapidly implemented by an experienced team. The decision to initiate ECMO was supported by young age, witnessed arrest, initial shockable rhythm, and absence of comorbidities. Current guidelines support ECMO resuscitation with a Class IIa recommendation, although the quality of evidence remains limited.⁸ Optimal candidates typically present with an initial shockable rhythm, witnessed arrest, bystander CPR, minimal comorbidities, and ECMO initiation within 60 min.⁷ Recent randomized data suggest that, in this context, ECMO may improve survival to discharge and 6-month outcomes compared to conventional advanced life support.⁹

For patients presenting with a non-shockable rhythm, prolonged advanced resuscitation is generally considered futile, with survival rates traditionally below 1% when ROSC is not achieved after 20 min of high-quality CPR and no reversible cause is identified.¹⁰ In unwitnessed arrests, the likelihood of meaningful recovery is even lower, and the risks of continued resuscitation may outweigh potential benefits. Conversely, in OHCA with an initial shockable rhythm, there is no universally defined time limit for resuscitation. In fact, resuscitative efforts are often continued if the patient remains in ventricular fibrillation or pulseless ventricular tachycardia, and the potential for a favourable outcome remains. Persistently low end-tidal CO₂ levels (<10 mm Hg) after 20 min of high-quality CPR are strongly predictive of poor outcomes and may justify the termination of resuscitative efforts, even in the continued presence of a shockable rhythm.¹¹

Termination-of-resuscitation rules have been developed to support clinicians in navigating these complex decisions, balancing prognostic accuracy with resource stewardship. While these rules can help standardize practice, concerns remain regarding the potential to exclude viable survivors. A systematic review of 43 non-randomized studies evaluating 29 termination-of-resuscitation rules found that the best-performing rule would miss approximately 1% of potential survivors at a survival rate of 8%. However, as survival rates improve, the proportion of missed survivors could exceed clinically acceptable thresholds (>1%).³ Consequently, the International Liaison Committee on Resuscitation recommends that no termination-of-resuscitation rule be used as the sole determinant for discontinuing resuscitation.¹⁰

It is important to acknowledge that ECMO is a scarce resource. Resource availability and institutional expertise are critical considerations when deciding whether to pursue or terminate resuscitation attempts. Physicians attending arrests far from ECMO-capable centres may be prompted not to continue resuscitation in these complicated cases. This single case does not support systematic prolongation of resuscitation or indiscriminate use of ECMO.

This case underscores that favourable neurological and survival outcomes can be achieved even after prolonged time to ROSC in selected patients. Decision-making in emergency situations is frequently difficult due to time constraints and limited information. Checklists and protocols might be used to determine when to terminate resuscitation. However, exceptions might be justified. In our case, the decision to pursue ongoing resuscitation was supported by prognostic factors associated with improved outcomes in ECMO-treated refractory arrests, including young age, absence of comorbidities, and an initial shockable rhythm.¹² Despite delays in ECMO initiation due to off-hours constraints and technical challenges, coordinated interdepartmental collaboration proved critical to success. These findings highlight the need for streamlined protocols enabling rapid ECMO activation and for refinement of termination-of-resuscitation criteria to prevent premature cessation of resuscitation in patients with reversible causes and a reasonable likelihood of recovery.

Based on the Committee on Publication Ethics guidelines, patient consent for publication was obtained. The consent was informed, written, and included the publication of text and images. The authors confirm that the patient is aware the material will be available online.

Lead author biography

Javier Fernandez-Pereira, MD, is a graduate of the University of Santiago de Compostela School of Medicine. He is currently a fourth-year Cardiology resident at Hospital General Universitario Gregorio Marañón in Madrid, Spain. His clinical and research interests primarily focus on acute cardiovascular care and cardiac imaging.

Author contributions

Javier Fernandez Pereira (Conceptualization, Formal analysis, Investigation, Methodology, Writing—original draft, Writing—review & editing [equal]), Jimmy Alexis Rojas-Rodas (Conceptualization, Data curation, Investigation, Methodology, Writing—original draft, Writing—review & editing [equal]), Roberto Gomez-Sanchez (Data curation, Formal analysis, Investigation, Supervision, Validation, Writing—review & editing [equal]), María Eugenia Vázquez-Álvarez (Conceptualization, Data curation, Formal analysis, Investigation, Methodology, Supervision, Validation, Writing—original draft, Writing—review & editing [equal]), and Manuel Martínez-Sellés (Conceptualization, Data curation, Formal analysis, Investigation, Methodology, Project administration, Supervision, Validation, Visualization, Writing—original draft, Writing—review & editing [lead])

Funding

None declared.

Data availability

All relevant data regarding this case report have been included in the present manuscript. In any case, further information is available from the corresponding author under reasonable request.