Utilising a refractory ventricular fibrillation bundle to improve outcome in out of hospital cardiac arrest: A case report

Abstract

Cardiac arrest secondary to persistent ventricular fibrillation or ventricular tachycardia (pVF/VT) is challenging to manage, particularly in the prehospital setting. This report, prepared in keeping with CARE guidelines, discusses a 70-year-old male who survived to discharge with pre-morbid neurological function after a prolonged cardiac arrest with pVF. Clinical interventions included mechanical CPR, vector change defibrillation, de-emphasised adrenaline and intravenous esmolol. We believe this may be the first reported case of a paramedic-led team providing this care bundle in the UK outside of a research setting.

In this case a refractory pVF/VT bundle appeared to be associated with terminating pVF. This report may be of use to other pre-hospital services considering introducing specialised care bundles for this case type, as well as adding to the body of evidence for the complex pharmacological relationship between adrenergic agonists, antagonists and persistent shockable rhythms.

Introduction

Outcomes from an out-of-hospital cardiac arrest (OHCA) with an initial rhythm of ventricular fibrillation/tachycardia (VF/VT) are often better than non-shockable rhythms. However, persistent VF/VT, defined as a shockable rhythm refractory to ≥3 defibrillation attempts, carries a poorer prognosis.¹ The terms “refractory” and “recurrent” VF/VT are used somewhat interchangeably, where “recurrent” refers to VF/VT that only temporarily terminates after defibrillation, while “refractory” refers to VF/VT that persists through and despite defibrillation. Recurrent VF/VT is often mistaken for refractory VF/VT due to the lack of access to ‘see-through’ defibrillator technology allowing for ECG interpretation not impeded by chest compression artefact. We therefore prefer to use the term “persistent VF/VT (pVF/VT)”, as this encompasses both possibilities. These terms have been discussed by the authors of REVIVE, a collaborative research group examining esmolol and de-emphasised adrenaline for OHCA with pVF/VT.¹

We present the case of a 70-year-old male with pVF who survived neurologically intact after a prolonged OHCA treated with esmolol, de-emphasized adrenaline, and revised defibrillation pad placement, in addition to standard ALS including 21 shocks. Emerging evidence supports β-blockade in refractory VF showing improved survival with sympathetic blockade.¹ This report adheres to CARE guidelines.²

The Isle of Wight is a small island off the south-coast of mainland England of which transport options are limited to ferries, hovercrafts and helicopters, sometimes restricted by weather conditions and time of day. This relative geographic isolation limits access to tertiary care as the island’s hospital lacks on-site specialty services, such as interventional cardiology.

Isle of Wight NHS Trust Ambulance Service frontline emergency ambulances are typically staffed by one paramedic and one emergency care assistant. Isle of Wight NHS Trust Ambulance Service has three Critical Care Paramedics and one Specialist Paramedic Researcher who practices with the same scope of practice, covering the island with a single response car. They are supported by the Isle of Wight NHS Trust Ambulance Service Medical Lead who is an ED consultant and air ambulance doctor. Critical Care Paramedics attend 80 % of cardiac arrests on the island and can provide an enhanced layer of pre-hospital care with advanced training and access to medications and equipment that are not available on standard front-line ambulances. Their clinical practice is supported by standard operating procedures (SOPs) that sit on top of national UK paramedic guidelines produced by the Joint Royal Colleges Ambulance Liaison Committee (known as ‘JRCALC’). In 2024 Isle of Wight NHS Trust Ambulance Service introduced a SOP for the management of refractory VF/VT, adapted from Hampshire & Isle of Wight Air Ambulance, a physician led pre-hospital critical care service (Table 1). The SOP was written by consultants in emergency medicine, pre-hospital care and cardiac anaesthesia.

Table 1.

A section of the IOWAS* Shock refractory ventricular fibrillation/ventricular tachycardia SOP. *Adapted from Hampshire & Isle of Wight Air Ambulance.

Immediate actions •Confirm cardiac arrest. •Follow ALS guidelines. •Ensure pads applied in the traditional sternal-apical (SA) placement are correctly positioned (in particular, the axillary pad should be placed appropriately proximally in the axilla). •If the first shock has been delivered, review the energy being delivered and increase from 150 joules to 200 joules. •Use a LUCAS device if patient habitus allows. Actions following the third shock •Declare refractory VF/VT. •Administer adrenaline 1:10,000 and amiodarone 300 mg Intravenous (IV)/Intraosseous (IO) after the 3rd shock. •Consider applying a new set of defibrillator pads in the antero-posterior (AP) position and continue ALS. •For A-P positions ensure that the anterior pad on the left anterior chest wall is placed beside the sternum, overlying the V2 and V3 ECG electrode positions. The posterior pad should be placed between the lower part of the left scapula and the spine, at the same horizontal level as the anterior pad. •Due to pad degradation, a nuanced approach should be taken in regards to when pad replacement should occur but no more than 5 shocks should be delivered through the same set of pads. Actions following the fifth shock •Check the rhythm every 2 min and deliver biphasic shocks at 200 joules if indicated. •If still in VF/VT give a second dose of amiodarone 150 mg IV/IO after the 5th shock, in line with ALS and IOWAS protocols •Consider ‘de-emphasising’ adrenaline as per the Intensive Care Society (ICS) recommendations and give every 8–10 minutes rather than every 3-4 minutes. •Esmolol at 0.5 mg/kg following 5th shock (one repeat dose can be given after 5 min). •Consider intubation if ETT not already in place •If remains in refractory VF/VT intubate and transport to a centre capable of PPCI*

PPCI = Primary Percutaneous Coronary Intervention.

^*On the IOW transport times to PPCI may be significant and, in this situation it may be necessary to consider other options for treatment and transfer. In some cases, if there is strong evidence of a thrombotic cause of the refractory VF/VT and there is no rapid option for PPCI transfer, a rapid transfer to the nearest ED should be undertaken.

Overview of case

The patient presented in this case study is a 70-year-old male living independently at home who had a past medical history of prostate and bowel cancer, for which he was not on active treatment due to remission. A 999 call was made after he had a witnessed collapse in front of family whilst at the dinner table. Two frontline ambulances and a Critical Care Paramedic were dispatched. All neighbouring Helicopter Emergency Service (HEMS) units were unavailable.

The first ambulance arrived within one minute of the 999-call and found the patient laid on his back in the kitchen. Cardiac arrest was confirmed, and the first rhythm analysis showed ventricular fibrillation. A timeline of the patient's treatment from time of 999 call to arrival at ED can be found in Fig. 1.

Fig. 1.

Timeline of pre-hospital care.

Prior to the arrival of the Critical Care Paramedic the patient had a supraglottic airway and intravenous access inserted, nine defibrillation shocks, active mechanical CPR and had two boluses of amiodarone and adrenaline administered as per JRCALC and ALS guidelines.⁴

On arrival of the Critical Care Paramedic, the refractory VF SOP was commenced which included replacing defibrillation pads and changing to an anterior posterior position, de-emphasis of adrenaline by doubling the interval time, endotracheal intubation, and two boluses of esmolol 40 mg with an interval time of five minutes if the first dose had been unsuccessful. The dosage of esmolol administered was calculated according to the patient’s weight of approximately 80 kg (0.5 mg/kg).

After the 16th shock and second bolus dose of esmolol, the patient’s rhythm changed to PEA (Fig. 2). Resuscitation continued, including the next administration of adrenaline 1 mg (as per the de-emphasised adrenaline timing of 8–10 min between doses). However, given the morphology of this PEA was nearly exactly that in the later post-ROSC rhythm, it is possible that this was a pseudo-PEA (low-flow state).³ Point-of-care ultrasound was prepared to check for cardiac contractility, however before obtaining a view the patient returned into VF shortly after the administration of adrenaline.

Fig. 2.

ECG and waveform capnography during rhythm analysis post-16th shock.

JRCALC dictates that, in cases of VF/VT, frontline paramedics are unable to terminate resuscitation and are required to transport the patient to hospital. Critical Care Paramedics are not bound by this and are unlikely to transport the patient to the local hospital, due to its limited services. The nearest ECMO facility is 90 miles away.

The patient’s EtCO2 varied from an initial 3.1 kPa (23 mmHg) to 5.9 kPa (44 mmHg) prior to ROSC. Upon achieving ROSC at shock 21, the Critical Care Paramedic post-ROSC care bundle commenced, comprising adrenaline infusion via syringe driver for hypotension and boluses of ketamine for endotracheal tube tolerance, followed by a ketamine infusion and a targeted mechanical ventilation strategy.

The Critical Care Paramedic decided to transport the patient to the local hospital rather than directly to Primary Percutaneous Coronary Intervention (PPCI) located off island. This would have required a long ferry transfer, and no ST elevation was observed on the post-ROSC ECG (Fig. 3). It was deemed the most likely cause of arrest was an arrythmia and a secondary transfer could be undertaken, if required.

Fig. 3.

Post-ROSC 12-lead ECG by ambulance.

At ED, the patient’s high-sensitivity troponin I was 155.5 ng/L (2.3–19.8), potassium was 4.3 mmol/L (3.5–5.3), pH 7.0 (7.35–7.45) and pO2 18 kPa. The patient was transferred to ICU, extubated within 24 h and transferred a few days later to the nearest PPCI unit where a CT coronary angiogram showed no flow-limiting disease. Troponin I peaked at 1166.5 ng/L and ejection fraction improved from 19 % to 35 % with medical therapy, supporting the arrhythmogenic aetiology of cardiac arrest. The patient was discharged home with a Modified Rankin Scale (mRS) of 0, the same level of functioning before his cardiac arrest.

Discussion

The Isle of Wight NHS Trust Ambulance Service Critical Care Paramedic refractory VF SOP is designed to improve the successful termination of pVF/VT despite standard ALS. Pad misplacement may be a factor of unsuccessful defibrillation. The SOP’s emphasis on pad placement aligns with DOSE-VF data showing improved survival with vector change defibrillation (21.7 %) than those who remained in standard anterolateral pad placement (13.3 %).⁵

The more novel aspects of this SOP are de-emphasised adrenaline and introduction of esmolol. Adrenaline has been a mainstay of advanced life support for decades due to its α-1 adrenergic vasoconstrictive and β-1 adrenergic properties, theoretically shunting blood flow to the heart while also causing positive chronotropy and inotropy.⁶ However, during resuscitation, coronary artery blood flow is significantly impaired while VF causes myocardial oxygen demand to dramatically increase.⁶ The β-1 adrenergic effects of adrenaline further increase this oxygen demand, while also potentially decreasing the efficacy of defibrillation.6, 7 The suspected deleterious effects of adrenaline are an area of increasing interest for OHCA researchers. For example, PARAMEDIC2 showed an increase in survival rate at 30 days with adrenaline administration, but no difference in neurological outcome.¹⁰ More recently Watson et al. described their retrospective observational findings of increased frequency of sustained ROSC in patients who received de-emphasised adrenaline (defined as extended dosing interval of 8-10 mins).⁷ Of 124 patients, 44 had sustained ROSC, of which 25 % were associated with de-emphasised adrenaline (P = 0.004).⁷

Esmolol is a rapidly acting cardio-selective β-1 adrenoreceptor antagonist; its antiarrhythmic properties are due to direct adrenergic blockade (Vaughn-Williams class II).⁸ With a steady state reached in five minutes, esmolol is quickly absorbed, has a distribution half-life of two minutes and an elimination half-life of nine minutes.⁸ The drug is extensively metabolised in the blood with no known active metabolites.⁸ As a result of its pharmacological profile, it is thought that it’s β-1 blockade may help reduce myocardial oxygen demand, block intrinsic and extrinsic catecholamine adrenoreceptor agonism and therefore improve the heart’s responsiveness to defibrillation.¹ Esmolol’s role in pVF/VT is a growing area of interest. Whilst some studies support its benefit in achieving ROSC others do not.11, 12, 13, 14, 15, 16 Gelbenegger et al found the addition of a β-blocker in pVF did not lead to a shorter time to ROSC and could be associated with bradycardia and asystole.¹⁷ Stupca et al., found there was no improved ROSC rate with esmolol and de-emphasised adrenaline versus standard care.⁹ This was a small study with only 126 patients and emphasises the need for a randomised control trial (RCT) to assess its efficacy in pVF/VT in OHCA.¹

In this case, the timing of de-emphasised adrenaline corresponded with the administration of esmolol, potentially causing a conflicting and competing pharmacological environment. There is no clear evidence around the implications of high-dose adrenaline being given for PEA immediately following the successful termination of pVF/VT using an esmolol and de-emphasized adrenaline strategy. ALS guidance requires adrenaline 1 mg to be given when PEA is first noted but it is interesting to note that in this case the administration of adrenaline 1 mg was immediately followed by a return of VF, which would appear to support the concern of its pro-arrhythmogenic properties. An extension of high-dose bolus adrenaline de-emphasis into the period immediately following the termination of VF via a β-blocker and adrenaline de-emphasis strategy may be a consideration.

Conclusion

This case report describes the use of a pVF/VT care bundle in a 70-year-old male with a witnessed OHCA who survived neurologically intact. It demonstrates the value of having access to Critical Care Paramedics in areas of geographical complexity where HEMS are not always available.

Informed consent statement

The authors confirm that the patient about whom this case report is written has reviewed a draft of this report and provided signed informed consent, an anonymised copy of which has been provided to the journal. The patient did not have any comment to add.

CRediT authorship contribution statement

Isabel Horne: Writing – review & editing, Writing – original draft. Thomas Gleeson-Hammerton: Writing – review & editing, Writing – original draft. James Plumb: Writing – review & editing. John Pike: Writing – review & editing.

Funding

The authors received no funding for this manuscript.

Declaration of competing interest

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.