303. CCC: Management of Ventricular Tachycardia and Electrical Storm in the CICU with Dr. Janice Chyou

CardioNerds Co-Founder, Dr. Amit Goyal, along with Series Co-Chairs, Dr. Yoav Karpenshif and Dr. Eunice Dugan, and episode Lead, Dr. Sean Dikdan, had the opportunity to expand their knowledge on the topic of ventricular tachycardia and electrical storm from esteemed faculty expert, Dr. Janice Chyou. Audio editing by CardioNerds Academy Intern, Dr. Maryam Barkhordarian. Electrical storm (ES) is a life-threatening arrhythmia syndrome. It is characterized by frequently occurring bouts of unstable cardiac arrythmias. It typically occurs in patients with susceptible substrate, either myocardial scar or a genetic predisposition. The adrenergic input of the sympathetic nervous system can perpetuate arrythmia. In the acute setting, identifying reversible triggers, such as ischemia, electrolyte imbalances, and heart failure, is important. Treatment is complex and varies based on previous treatments received and the presence of intra-cardiac devices. Many options are available to treat ES, including medications, intubation and sedation, procedures and surgeries targeting the autonomic nervous system, and catheter ablation to modulate the myocardial substrate. A multidisciplinary team of cardiologists, intensivists, electrophysiologists, surgeons, and more are necessary to manage this complex disease. The CardioNerds Cardiac Critical Care Series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif. Pearls • Notes • References • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Management of Ventricular Tachycardia and Electrical Storm Electrical storm is defined as 3 or more episodes of VF, sustained VT, or appropriate ICD shocks within 24 hours. It occurs more commonly in ischemic compared to non-ischemic cardiomyopathy, and it is associated with a poor prognosis and high cardiovascular mortality. The classic triad of electrical storm is a trigger, a myocardial susceptible substrate, and autonomic input perpetuating the storm. Triggers for electrical storm include ischemia, heart failure, electrolyte abnormalities, hypoxia, drug-related arrhythmogenicity, and thyrotoxicosis. A thorough evaluation of possible triggers is necessary for each patient, but it is uncommonly found. The evaluation may include laboratory studies, genetic testing, advanced imaging, or invasive testing. Acute treatment options involve acute resuscitation, pharmacotherapy with antiarrhythmics and beta-blockers, device interrogation and possible reprogramming, and sedation. Subacute treatment involves autonomic modulation and catheter ablation. Surgical treatments include sympathectomies and, ultimately, heart transplant. Catheter ablation is safe and effective for the treatment of electrical storm. In select patients, hemodynamic peri-procedural hemodynamic support should be considered. Show notes - Management of Ventricular Tachycardia and Electrical Storm Simple diagram of the classic “triad” of ES (see reference 10). Treatment algorithm provided by the 2017 AHA/ACC/HRS guidelines (see reference 1). 1. Define electrical storm. Electrical storm (ES), also called “arrhythmic storm” or “VT storm” refers to a state of cardiac instability associated with 3 or more episodes of VF, sustained VT, or appropriate ICD shocks within 24 hours. Sustained VT refers to 30 seconds of VT or hemodynamically unstable VT requiring termination in < 30 seconds. Incessant VT refers to continued, sustained hemodynamically stable VT that lasts longer than one hour. VT is incessant or recurrent when it recurs promptly despite repeated intervention for termination.1,2 In patients with ICDs for secondary prevention, ES is estimated to occur in 10-28% of patients.3–5 This incidence is much lower in patients who have ICDs implanted for primary prevention in whom the incidence has been estimated as low as 4% at 20 months of follow up.6 ES occurs at similar rates in patients with ischemic or non-ischemic cardiomyopathy.7 ES is associated with a poor prognosis and high cardiovascular mortality. The three-month mortality in patients with an episode of ES has been estimated at up to 18 times higher than in patients without any VT.6 Risk factors for the development of ES include male sex, advanced age, low left ventricular ejection fraction, use of class 1A antiarrhythmic drugs, and the presence of cardiovascular comorbidities.8,9 2. Evaluate the cause of VT storm (e.g., evaluation for ischemia, sarcoidosis , etc) The classic triad of ES is a trigger, a substrate susceptible to ES, and autonomic input perpetuating the storm.10 Potential triggers are varied and typically include myocardial ischemia, decompensated heart failure, electrolyte abnormalities, hypoxia, drug-related arrhythmogenicity, and thyrotoxicosis.4,11 A clear trigger is often not found (only 13% of the time by some estimates).12 Searching for a trigger should not delay management decisions in the acute setting. Structural heart disease unrelated to ischemia such as congenital heart disease and infiltrative cardiomyopathies can serve as the substrate for ES. Conditions related to genetic causes such as long QT syndrome or catecholaminergic polymorphic VT may be a rare etiology. These conditions represent an electrophysiologic substrate as opposed to a structural substrate.13 3. Choose an initial management strategy for patients with electrical storm in the CCU. Treatment of ES is complex. The initial steps in management involve resuscitation, pharmacotherapy, device interrogation and reprogramming, and sedation. ACLS should be used in patients with pulseless VT or VF. Patients with and without cardioverter-defibrillators may be treated differently. Defibrillations from an implanted device accentuate sympathetic tone and may perpetuate further arrhythmia. Once a patient is stabilized, more advanced therapies involving autonomic modulation or catheter ablation (CA) can be utilized. In the patient with ischemia, emergent revascularization should be pursued. The need for mechanical circulatory support (MCS) should be determined. Inotropes and many vasopressors are sympathetic agonists and may worsen the arrhythmia by accentuating adrenergic tone, and so the benefits of improved hemodynamics need to be weighed against the risk of worsening electrical instability. Initial pharmacotherapy in ES includes an antiarrhythmic drug and a beta blocker. Typically loading the patient with IV amiodarone and administering a non-selective beta blocker like propranolol is done. This combination has been shown in ES patients to have superior freedom of arrhythmia compared to using metoprolol.14 Propranolol’s superiority may also be due to its ability to cross the blood-brain barrier. Lidocaine has improved efficacy in ischemic VT.15,16 Procainamide has been shown to be useful in patients with hemodynamically stable VT.17 4. Identify predisposing conditions that should be managed to help treat electrical storm such as ischemia and AHF. Identifying and managing specific triggers is an important initial step in the management of ES. Hypoxia on vital signs or evidence of decompensated HF on exam (with JVD, edema, crackles on auscultation) can implicate volume overload; this can be managed with diuresis. Ischemic ECG changes on the 12-lead ECG when the patient’s ventricular arrhythmia is broken, can suggest myocardial ischemia. If ischemia is believed to be the trigger, urgent revascularization should be pursued while resuscitation is underway. Blood work should include screening for electrolyte abnormalities and thyroid disease. Carefully screening the patient’s medication list and checking a digoxin level (when appropriate) can help detect drug-induced arrhythmia. Once out of the acute setting, genetic testing may be important in patients without structural disease for determining an etiology. Idiopathic VT, Brugada syndrome, long QT syndrome, short QT syndrome, early repolarization syndrome, catecholaminergic polymorphic VT, arrhythmogenic right ventricular cardiomyopathy, and cardiac sarcoidosis are potential etiologies that may be related to ES.10 5. Recognize when to use general anesthesia to aid in the stabilization of electrical storm and incessant VT. Intubation and deep sedation are immediate next steps to minimize the sympathetic drive contributing to the arrhythmia. This treatment is very effective at terminating arrythmia and preventing immediate recurrence.18,19 This step is used in the acute setting for ES that persists despite pharmacotherapy. Note that propofol is a negative inotrope with the potential to worsen heart failure in decompensated patients and precipitate shock. In addition to breaking the sympathetic cycle that drives this pathophysiology, sedation mitigates some of the psychological stress that repeated ICD shocks can cause in patients.20 6. Describe considerations specific to patients with implanted ICDs. If a patient with an ICD presents with ES, the device should be interrogated. It is important to confirm the shocks are appropriate. Inappropriate shocks can occur in up to 40% of patients with an ICD; causes may include atrial arrythmia, oversensing, and lead fracture.21,22 Inappropriate ICD shocks are associated with a worse outcome. Overdrive pacing is a possible therapy to prevent ES. If the ES is hemodynamically stable, then the ICD therapies may be disabled manually or with the use of a magnet. If anti-tachycardia pacing (ATP) treats the ventricular arrythmia effectively,