Current and investigational therapies for the treatment of refractory ventricular fibrillation

Disclaimer In an effort to expedite the publication of articles related to the COVID-19 pandemic, AJHP is posting these manuscripts online as soon as possible after acceptance. Accepted manuscripts have been peer-reviewed and copyedited, but are posted online before technical formatting and author proofing. These manuscripts are not the final version of record and will be replaced with the final article (formatted per AJHP style and proofed by the authors) at a later time. Purpose Esmolol, dual sequential defibrillation, vector change defibrillation, and left stellate ganglion block are presented and reviewed for the treatment of refractory ventricular fibrillation. Summary Although no formal definition has been established for refractory ventricular fibrillation, the literature describes it as a pulseless ventricular arrhythmia that persists despite 3 standard defibrillation attempts, administration of amiodarone 300 mg intravenously, and provision of three 1-mg intravenous doses of epinephrine. Evolving literature surrounding resuscitation in this particular subset of cardiac arrest challenges the efficacy of traditional therapies, such as epinephrine, and suggests that other treatment modalities may improve outcomes. Case reports, case series, and small retrospective studies have pointed to benefit when utilizing a variety of therapies, namely, esmolol, dual sequential defibrillation, vector change defibrillation, or left stellate ganglion block, in patients with refractory ventricular fibrillation arrest. Conclusion A mounting, although limited, body of evidence suggests that esmolol, dual sequential defibrillation, vector change defibrillation, or left stellate ganglion block may be effective at terminating refractory ventricular fibrillation and improving patient outcomes. Further evidence is required before these therapies can be adopted as standard practice; however, as key members of the code response team, it is imperative for pharmacists to be familiar with the supporting evidence, safety considerations, and logistical challenges of utilizing these treatments during arrest.

Left Stellate Ganglion Block for Refractory Ventricular Tachycardia: A Case Series

Ventricular arrhythmias are usually well controlled with medical management, cardiac implantable electronic devices, or catheter ablation. However, the refractory ventricular tachycardia or fibrillation (VT/VF) is life threatening and challenging. The authors reported a case series of left stellate ganglion blocks (LSGB) in patients with refractory VT/VF, who failed pharmacological treatment and multiple traditional cardiac interventions. Five patients underwent six LSGB. Four patients had significant decreased in ventricular arrhythmia burden. Among the responders, the LSGB suppressed significant VT/VF for three to seven days. Blocks did not only temporary suppress ventricular arrhythmia, but also stabilized the condition and served as a bridge to definitive treatment such as EP ablation or heart transplantation. There was no significant hemodynamic change or devastating side effects. The outcome from the present case series suggested that LSGB could be an effective treatment and a lifesaving intervention frintractable VT/VF. Keywords: Stellate ganglion block, Refractory ventricular tachycardia, Sympathectomy

Anatomical-based percutaneous left stellate ganglion block in patients with drug-refractory electrical storm and structural heart disease: a single-centre case series

Aims The adoption of percutaneous stellate ganglion blockade for the treatment of drug-refractory electrical storm (ES) has been increasingly reported; however, the time of onset of the anti-arrhythmic effects, the safety of a purely anatomical approach in conscious patients and the additional benefit of repeated procedures remain unclear. Methods and results This study included consecutive patients undergoing percutaneous left stellate ganglion blockade (PLSGB) in our centre for drug-refractory ES. Lidocaine, bupivacaine, or a combination of both were injected in the vicinity of the left stellate ganglion. Overall, 18 PLSGBs were performed in 11 patients (age 69 ± 13 years; 63.6% men, left ventricular ejection fraction 31.6 ± 16%). Seven patients received only one PLSGB; three underwent two procedures and one required three PLSGB and two continuous infusions to control ventricular arrhythmias (VAs). All PLSGBs were performed with an anatomical approach; lidocaine, alone, or in combination was used in 77.7% of the procedures. The median burden of VAs 1 h after each block was zero compared with five in the hour before (P < 0.001); 83% of the patients were free from VAs; the efficacy at 24 h increased with repeated blocks. The anti-arrhythmic efficacy of PLSGB was not related to anisocoria. No procedure-related complications were reported. Conclusion Anatomical-based PLSGB is a safe and rapidly effective treatment for refractory ES; repeated blocks provide additional benefits. Percutaneous left stellate ganglion blockade should be considered for stabilizing patients to allow further ES management.

Mechanism of ventricular premature beats elicited by left stellate ganglion stimulation during acute ischaemia of the anterior left ventricle

Aims Enhanced sympathetic activity during acute ischaemia is arrhythmogenic, but the underlying mechanism is unknown. During ischaemia, a diastolic current flows from the ischaemic to the non-ischaemic myocardium. This ‘injury’ current can cause ventricular premature beats (VPBs) originating in the non-ischaemic myocardium, especially during a deeply negative T wave in the ischaemic zone. We reasoned that shortening of repolarization in myocardium adjacent to ischaemic myocardium increases the ‘injury’ current and causes earlier deeply negative T waves in the ischaemic zone, and re-excitation of the normal myocardium. We tested this hypothesis by activation and repolarization mapping during stimulation of the left stellate ganglion (LSG) during left anterior descending coronary artery (LAD) occlusion. Methods and results In nine pigs, five subsequent episodes of acute ischaemia, separated by 20 min of reperfusion, were produced by occlusion of the LAD and 121 epicardial local unipolar electrograms were recorded. During the third occlusion, left stellate ganglion stimulation (LSGS) was initiated after 3 min for a 30-s period, causing a shortening of repolarization in the normal myocardium by about 100 ms. This resulted in more negative T waves in the ischaemic zone and more VPBs than during the second, control, occlusion. Following the decentralization of the LSG (including removal of the right stellate ganglion and bilateral cervical vagotomy), fewer VPBs occurred during ischaemia without LSGS. During LSGS, the number of VPBs was similar to that recorded before decentralization. Conclusion LSGS, by virtue of shortening of repolarization in the non-ischaemic myocardium by about 100 ms, causes deeply negative T waves in the ischaemic tissue and VPBs originating from the normal tissue adjacent to the ischaemic border.