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ASRA Pain Medicine Update

Stellate Ganglion Block for Ventricular Tachycardia

Jun 29, 2026, 09:23 by Dylan Banks, MD, Daniel Wang, DO, Abenezer Amare, MD, Cameron Thiele, MD, and Rosalynn Conic, MD, PhD, MPH

 

 

Case Presentation: 

A 62-year-old male with a history of ischemic cardiomyopathy, coronary artery disease with prior left anterior descending artery stent placement, and prior implantable defibrillator placement was admitted to the intensive care unit (ICU) following multiple shocks at home.

Over the last day, he has been noted to have recurrent episodes of sustained monomorphic ventricular tachycardia (VT). Despite treatment with intravenous (IV) amiodarone, lidocaine infusions, and beta blockade, he continues to have recurrent episodes of VT.

Electrophysiology (EP) recommends a cardiac ablation; however, the patient remains hemodynamically unstable with escalating vasopressor requirements and is considered high risk for transfer to the EP lab. The ICU team contacts the acute pain/regional anesthesia service to evaluate for possible sympathetic blockade.

 

Questions: 

This patient has recurrent/refractory VT.  What are the patient selection criteria for stellate ganglion block (SGB) in recurrent/refractory VT? What therapies are typically attempted before considering sympathetic blockade?

SGB is typically considered for patients with electrical storm or recurrent ventricular arrhythmias (VAs) that remain refractory to conventional therapies. These conventional treatments can include beta-blockers, at least two antiarrhythmic drugs, and catheter ablation.1,2 The procedure serves as a temporary bridge therapy in hemodynamically unstable patients who cannot tolerate or have failed standard treatments.1,3

Patient Selection Criteria

The ideal candidates for SGB include patients with:

  • Electrical storming (≥ 3 VA episodes requiring intervention within 24 hours) or recurrent VT or ventricular fibrillation (VF) despite optimal medical management.1,4
  • Failure of, or intolerance to, beta-blockers and multiple antiarrhythmic agents.2,5
  • Hemodynamic instability precluding immediate catheter ablation or surgical intervention.2,3
  • Both ischemic and nonischemic cardiomyopathy etiologies (SGB is effective regardless of underlying substrate).5

Therapies Attempted Before Sympathetic Blockade Can Include:

  • Antiarrhythmic drugs: Amiodarone (particularly IV) is first line. It is often combined with sotalol for patients without severe ventricular dysfunction. Lidocaine may be added for polymorphic VT/VF.1,6,7
  • Beta-blockers: Nonselective beta-1/2 blockers (e.g., propranolol) are preferred over beta-1 selective agents (e.g., metoprolol). Propranolol typically has superior efficacy in preventing recurrent VT (47% vs 10% freedom from VA at 24 hours).1
  • Device optimization: Reprogramming of implantable cardioverter-defibrillator settings and anti-tachycardia pacing.7
  • Catheter ablation: This is increasingly considered during early intervention. Specifically, it can be used for sustained monomorphic VT in ischemic heart disease.6,7
  • Ultrashort-acting IV beta-blockers: Esmolol or landiolol as second-tier therapy when oral agents are insufficient.1

 

What is the pathophysiologic rationale for SGB in VT? How does sympathetic blockade alter myocardial EP?

Pathophysiologic Rationale

Sympathetic overactivity is a primary driver of VAs in electrical storms. Specifically, the stellate ganglion provides efferent sympathetic innervation to the myocardium.8,9 Myocardial infarction and cardiomyopathy cause adverse adaptations throughout the cardiac neuroaxis. This results in excessive sympatho-neurohumoral responses and reduced parasympathetic input.8 The stellate ganglion (specifically the left) supplies sympathetic fibers to the ventricles. Blocking this ganglion temporarily interrupts sympathetic outflow, reducing cardiac sympathetic tone without the systemic effects of pharmacologic beta-blockade.10,11

Electrophysiologic Effects of Sympathetic Blockade

SGB alters myocardial EP through several mechanisms:

  • Reduction in dispersion of repolarization: Sympathetic stimulation increases heterogeneity of action potential duration from endocardium to epicardium. Thus, blocking this input reduces dispersion and arrhythmogenic substrate.8,12
  • Prevention of triggered activity: Sympathetic blockade prevents spontaneous diastolic calcium increases and calcium handling abnormalities that trigger VAs.12
  • Modulation of autonomic balance: By reducing sympathetic tone while preserving parasympathetic input, SGB shifts the autonomic balance away from the pro-arrhythmic state.8,11
  • Regional denervation effects: Following sympathetic nerve loss, hypo-innervated regions develop supersensitivity to circulating catecholamines while having blunted responses to direct nerve stimulation. This ultimately creates electrophysiologic heterogeneity.12

 

What contraindications or precautions should you assess before performing SGB?

Several contraindications and precautions are noted in the literature prior to performing SGB. The literature does not clarify or expand on absolute versus relative contraindications.2,13

  • Patient refusal (absolute contraindication to performing SGB)
  • Localized or systemic bacterial infection, which has been associated with an increased risk of cervical infection, epidural abscess, or discitis
  • Allergy to an anesthetic
  • Recent myocardial infarction or severe cardiopulmonary disease due to the potential for SGB to alter cardiac conduction and hemodynamics
  • Cardiac conduction block due to SGB can affect cardiac sympathetic tone and potentially worsen conduction blocks
  • Anticoagulated patients or patients with coagulopathy (the risks and benefits of stopping or continuing certain anticoagulation medications must be discussed prior to SGB)
  • Glaucoma due to the potential for sympathetic chain blockade to alter the autonomic function of the eye and worsen glaucoma
  • Preexisting contralateral nerve palsy due to the potential for an ipsilateral laryngeal nerve block to compromise airway safety
  • Severe emphysema due to an increased risk of respiratory compromise and pneumothorax

 

What are the potential complications of SGB, and how would you manage them?

SGB is considered a relatively safe procedure overall. A systematic review comprising 67 clinical studies identified 260 adverse effects.14,15 Of these, the most common complications noted were hoarseness due to recurrent laryngeal nerve blockade (n = 73), hematoma (n = 41), light-headedness (n = 20), blood aspiration (n = 12), hypertension (n = 23), brachial plexus blockade (n = 12), and dysphagia (n = 11).14,15 Less common and minor side effects include headache, somnolence, or xerostomia, dependent on the injectate.14,15

Wulf et al. reported the incidence of serious side effects to be 1.7 per 1000 procedures, with seizures being the most common. Potential other serious complications include retropharyngeal hematoma, neuraxial block, bilateral Horner’s syndrome, transient locked-in syndrome, persistent ptosis, visual hallucinations, myoclonus, pneumothorax, dural puncture, infection, bilateral sympathetic blockade, and local anesthetic toxicity.14,15

The literature does not specifically provide an algorithm for the management of all potential side effects. Rather than managing all potential side effects, the literature focuses on appropriate techniques and safety measures used to prevent and minimize them. Most of these potential complications are transient, usually lasting 8-12 hours, and are managed with supportive care. Rarely, benign side effects can last longer than 12 hours if the volume of local anesthetic used is higher due to spread into adjacent structures.

In the case of a retropharyngeal hematoma, this would require emergent airway management with intubation, as patients can develop airway obstruction.16 Higa et al. found 27 patients with retropharyngeal hematoma after SGB over the past 40 years; 21 of 27 patients required emergent orotracheal intubation, which was unsuccessful in 5. These 5 patients underwent tracheostomy due to anatomical distortion caused by an edematous pharyngolarynx.16 Fujiwara et al. reported one case of convulsive seizure that occurred during SGB, which was managed with midazolam and ventilatory support, with subsequent regaining of consciousness and discharge home post procedure.15 The remaining 4 seizures noted in the literature reported that the patient was treated appropriately, without further information.15

 

What are the steps in fluoroscopically guided SGB? What are the steps for ultrasound-guided SGB?

Ultrasound-Guided TechniqueFluoroscopic-Guided Technique
1.)     Position the patient supine with the head turned slightly to the contralateral side.
2.)     Place the transducer perpendicular to the trachea at the level of the cricoid cartilage.
3.)     Ensure cross-sectional visualization of all relevant anatomic structures including the lateral aspect of the thyroid, carotid artery, internal jugular vein, longus colli, and longus capitis muscles.
4.)     An in-plane needle approach is utilized from lateral to medial.
5.)     The tip of the needle is directed anterior to the prevertebral fascia at the ventral aspect of the longus colli muscle, medial to Chassaignac’s tubercle.
6.)     Local anesthetic is injected under real time visualization.		1.)     The patient is positioned supine and an anteroposterior view is obtained to identify C6 by counting up from T1.
2.)     Oblique the c-arm ipsilaterally to obtain a foraminal oblique view.
3.)     From this view, count down from the most cephalad C3 neural foramen to verify the correct C6 level.
4.)     The targeted structure, which is the junction of the vertebral body and the uncinate process (at or slightly medial to the uncinate line) can be visualized in this view.
5.)     After contrast confirmation, a small (i.e., 0.5 cc) test dose of local anesthetic (e.g., 1% lidocaine) is injected, and the patient is observed for 60-90 seconds to further minimize the risk of intravascular injection.
6.)     The remainder of local anesthetic is then injected.

Table 1: Steps in fluoroscopically guided and ultrasound guided SGB.17,18

 

When would you choose to use fluoroscopy versus ultrasound guidance for a SGB?

Ultrasound guidance is typically favored over fluoroscopic guidance due to the ability to visualize vascular and soft tissue structures, thus allowing for precise needle placement. Use of ultrasound is associated with a 0.7% risk of major adverse events compared to 6.5% when fluoroscopy is used, and it enables shorter procedure time and decreased use of anesthetic.19 However, it is important to note that the stellate ganglion may not be visualized in 20%–25% of patients.20 In patients where ultrasound imaging is limited due to patient habitus, scarring, or anatomical distortion or in those where bony landmarks are needed, fluoroscopy offers an advantage.21,22

 

How do you confirm an effective block?

Effective SGB can be confirmed through a few physiologic changes, most commonly ipsilateral Horner's syndrome and upper extremity temperature change, although both markers have limitations.

  • Horner's Syndrome: The presence of ipsilateral Horner's syndrome (ptosis, miosis, and anhidrosis) can indicate successful sympatholysis following an SGB. However, assessment can be subjective without clear objective criteria.23,24
  • Ipsilateral hand temperature increase: The classic criteria defining achievement of sympathetic blockade is a change in ipsilateral hand temperature (Di) compared to the change in contralateral hand temperature (Dc) of > 1.5 degrees Celsius (Di-Dc = > 1.5). However, this temperature difference may not reliably predict complete sympathetic block in all patients.25,26
  • Additionally, objective markers of successful sympathetic blockade following SGB have been studied. Pulsed transit time can be an objective measure of increased blood flow following SGB, indicating successful sympathetic blockade.24

 

Discuss the role of continuous catheter vs single-shot techniques and when each is preferred.

Single-shot SGB is typically used in emergencies and lasts 3–12 hours depending on the anesthetic used.27 In up to 44% of patients, the arrhythmia recurs unless bridged with definitive therapy, often necessitating repeat procedures.27 This approach is preferred for short-term rescue or if there are contraindications to catheter placement.

In continuous catheter for SGB (C-SGB), a perineural catheter is placed adjacent to the stellate ganglion and allows for prolonged arrhythmia suppression while waiting for definitive therapy. Ropivacaine starting at 12 mg/h and lidocaine starting at 100 mg/h are typically used. Furthermore, C-SGB results in improved arrhythmia suppression, with 59%–63% of patients having complete suppression, for a median of 3 days.28 Ultimately neither technique results in definitive arrhythmia management and other therapies may be needed such as catheter ablation or surgical sympathetic denervation.27

 

What does the current literature show regarding efficacy and duration of benefit of SGB for VT?

SGB has been found to result in a consistent reduction of VT episodes with favorable outcomes regardless of type of VA (VT/VF, monomorphic and polymorphic) or underlying etiology (ischemic and nonischemic). In a multicenter cohort of 117 patients undergoing unilateral or bilateral SGB by Chouairi et al., the largest to date of its type, the median number of VT/VF episodes decreased from 7.5 pre-intervention to 1.0 at 24 hours following SGB (P < 0.001). Moreover, in the 24 hours preceding SGB, the median number of defibrillation events was 2.0, which decreased to 0.0 in the 24 hours following the intervention (P < 0.001). Notably, unilateral SGB is generally preferred, while bilateral interventions are typically reserved for intubated patients given the theoretical risk of laryngeal nerve palsy.3 Additionally, a left-sided SGB is often preferred over a right SGB as it has been suggested to offer more sympathetic tone to the myocardium.29

Based on a meta-analysis including 542 patients across 15 observational studies, most studies report follow-up of 48–72 hours, with the longest extending to 96 hours. This review reported complete resolution of VA events in 70% of patients, while 19% experienced partial improvement.30 To the authors' knowledge, there are no studies assessing long-duration outcomes. These findings suggest that SGB primarily serves as a short-term sympatholytic bridge therapy rather than a definitive treatment strategy. Therefore, early coordination with cardiology and EP teams to define a destination therapy, such as ablation, mechanical circulatory support, surgical sympathectomy, or transplantation, is essential, as durable arrhythmia control is unlikely with SGB alone.31

While SGB has demonstrated a clinically meaningful impact on VA events, especially as it pertains to medically refractory patients who are not suitable for further intervention, it is important to note that there is a lack of control groups or randomized controlled trials, thus limiting the ability to establish causality.

 

References

  1. Jentzer JC, Noseworthy PA, Kashou AH, et al. Multidisciplinary critical care management of electrical storm: JACC state-of-the-art review. J Am Coll Cardiol. 2023;81(22):2189-206. doi:10.1016/j.jacc.2023.03.424 
  2. Fudim M, Qadri YJ, Waldron NH, et al. Stellate ganglion blockade for the treatment of refractory ventricular arrhythmias. JACC Clin Electrophysiol. 2020;6(5):562-71. doi:10.1016/j.jacep.2019.12.017 
  3. Chouairi F, Rajkumar K, Benak A, et al. A multicenter study of stellate ganglion block as a temporizing treatment for refractory ventricular arrhythmias. JACC Clin Electrophysiol. 2024;10(4):750-8. doi:10.1016/j.jacep.2023.12.012 
  4. Savastano S, Baldi E, Compagnoni S, et al. Electrical storm treatment by percutaneous stellate ganglion block: the STAR study. Eur Heart J. 2024;45(10):823-33. doi:10.1093/eurheartj/ehae021 
  5. Fudim M, Boortz-Marx R, Ganesh A, et al. Stellate ganglion blockade for the treatment of refractory ventricular arrhythmias: A systematic review and meta-analysis. J Cardiovasc Electrophysiol. 2017;28(12):1460-7. doi:10.1111/jce.13324 
  6. Sapp JL, Tang ASL, Parkash R, et al. Catheter ablation or antiarrhythmic drugs for ventricular tachycardia. N Engl J Med. 2025;392(8):737-47. doi:10.1056/NEJMoa2409501 
  7. Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS Guideline for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2018;72(14):1677-749. doi:10.1016/j.jacc.2017.10.053
  8. Goldberger JJ, Arora R, Buckley U, Shivkumar K. Autonomic nervous system dysfunction: JACC focus seminar. J Am Coll Cardiol. 2019;73(10):1189-206. doi:10.1016/j.jacc.2018.12.064 
  9. Huang C, Shu S, Zhou M, Sun Z, Li S. Stellate ganglion block therapy in management of ventricular electrical storm: A case report. Heliyon. 2024;10(19):e37724. doi:10.1016/j.heliyon.2024.e37724 
  10. Daswani M, Aggarwal A, Guragain R. Regional anesthesia for arrhythmias: a review of current literature. Curr Opin Anaesthesiol. 2025;38(3):310-5. doi:10.1097/ACO.0000000000001479 
  11. Patel RA, Condrey JM, George RM, Wolf BJ, Wilson SH. Stellate ganglion block catheters for refractory electrical storm: a retrospective cohort and care pathway. Reg Anesth Pain Med. 2023;48(5):224-8. doi:10.1136/rapm-2022-104172 https://rapm.bmj.com/content/48/5/224
  12. Tapa S, Wang L, Francis Stuart SD, et al. Adrenergic supersensitivity and impaired neural control of cardiac electrophysiology following regional cardiac sympathetic nerve loss. Sci Rep. 2020;10(1):18801. doi:10.1038/s41598-020-75903-y
  13. Elias M. Cervical sympathetic and stellate ganglion blocks. Pain Physician. 2000;3(3):294-304.
  14. Tsai EH, Nunez-Rodriguez E, Cata JP. Stellate ganglion block in perioperative practice: a narrative review. Br J Anaesth. 2026;136(1):179-96. doi:10.1016/j.bja.2025.07.095 
  15. Goel V, Patwardhan AM, Ibrahim M, Howe CL, Schultz DM, Shankar H. Complications associated with stellate ganglion nerve block: a systematic review. Reg Anesth Pain Med. Published online April 16, 2019:rapm-2018-100127. doi:10.1136/rapm-2018-100127 https://rapm.bmj.com/content/44/6/669
  16. Higa K, Hirata K, Hirota K, Nitahara K, Shono S. Retropharyngeal hematoma after stellate ganglion block: Analysis of 27 patients reported in the literature. Anesthesiology. 2006;105(6):1238-45; discussion 5A-6A. doi:10.1097/00000542-200612000-00024 
  17. Berkwits L, Furman MB, eds. Atlas of Image-Guided Spinal Procedures. Second edition. Elsevier, Inc; 2017.
  18. Piraccini E, Munakomi S, Chang KV. Stellate Ganglion Blocks. StatPearls. Published online August 13, 2023. Available at: https://www.ncbi.nlm.nih.gov/books/NBK507798/. Accessed June 23, 2026.
  19. Kimura R, Yamamoto N, Watanabe J, Ono Y, Hongo M, Miyakoshi N. Comparative efficacy of ultrasound guidance and fluoroscopy or computed tomography guidance in spinal nerve injections: a systematic review and meta-analysis. Eur Spine J. 2023;32(12):4101-10. doi:10.1007/s00586-023-07968-y 
  20. Li J, Pu S, Liu Z, Jiang L, Zheng Y. Visualizing stellate ganglion with US imaging for guided SGB treatment: A feasibility study with healthy adults. Front Neurosci. 2022;16:998937. doi:10.3389/fnins.2022.998937 
  21. Narouze S. Ultrasound-guided stellate ganglion block: safety and efficacy. Curr Pain Headache Rep. 2014;18(6):424. doi:10.1007/s11916-014-0424-5 
  22. Hughey S, Schafer J, Cole J, Booth G, Tuttle R, Stedje-Larsen E. Ultrasound versus fluoroscopy for stellate ganglion block: a cadaveric study. Pain Med. 2021;22(10):2307-10. doi:10.1093/pm/pnab182 
  23. Harden RN, McCabe CS, Goebel A, et al. Complex regional pain syndrome: practical diagnostic and treatment guidelines, 5th Edition. Pain Med. 2022;23(Suppl 1):S1-S53. doi:10.1093/pm/pnac046 
  24. Kim YU, Cheong Y, Kong YG, et al. The prolongation of pulse transit time after a stellate ganglion block: An objective indicator of successful block. Pain Res Manag. 2015;20(6):305-8. doi:10.1155/2015/324514 
  25. Schürmann M, Gradl G, Wizgal I, et al. Clinical and physiologic evaluation of stellate ganglion blockade for complex regional pain syndrome type I. Clin J Pain. 2001;17(1):94-100. doi:10.1097/00002508-200103000-00012 
  26. Stevens RA, Stotz A, Kao TC, Powar M, Burgess S, Kleinman B. The relative increase in skin temperature after stellate ganglion block is predictive of a complete sympathectomy of the hand. Reg Anesth Pain Med. 1998;23(3):266-70. doi:10.1016/s1098-7339(98)90053-0 
  27. Sanghai S, Abbott NJ, Dewland TA, et al. Stellate ganglion blockade with continuous infusion versus single injection for treatment of ventricular arrhythmia storm. JACC Clin Electrophysiol. 2021;7(4):452-60. doi:10.1016/j.jacep.2020.09.032 
  28. Dusi V, Angelini F, Baldi E, et al. Continuous stellate ganglion block for ventricular arrhythmias: case series, systematic review, and differences from thoracic epidural anaesthesia. Europace. 2024;26(4):euae074. doi:10.1093/europace/euae074 
  29. Ganesh A, Qadri YJ, Boortz-Marx RL, et al. Stellate ganglion blockade: an intervention for the management of ventricular arrhythmias. Curr Hypertens Rep. 2020;22(12):100. doi:10.1007/s11906-020-01111-8 
  30. Motazedian P, Quinn N, Wells GA, et al. Efficacy of stellate ganglion block in treatment of electrical storm: a systematic review and meta-analysis. Sci Rep. 2024;14(1):24719. doi:10.1038/s41598-024-76663-9 
  31. Mircea AA, Rusu M, Liehn EA, Bucur O. Promising therapies for atrial fibrillation and ventricular tachycardia. Int J Mol Sci. 2022;23(20):12612. doi:10.3390/ijms232012612
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