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Arrhythmia Conference Sandeep Gautam James McKinnie 08/24/07
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46 WF presented to Lakeview Hospital with several days of palpitations. Baseline dyspnea on exertion NYHA II-III. PMH: Marfan’s Syndrome, TOF s/p complete repair ‘72, Pulmonic porcine valve replacement ‘90, CAD s/p PCI, Atrial fibrillationBulimia nervosa, palpitations of lower frequency, OA, FM, Scoliosis, osteoporosis. F&SH: No alcohol or tobacco abuse.
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Allergies: Sulfa, Celebrex, Vioxx, Vicodin, tape. Meds at home: Coumadin, metoprolol 25 mg bid, Lisinopril 2.5 mg daily, Digoxin 0.125 daily, Spironolactone 25 mg daily, Percodan prn, Trazodone 100 mg daily.
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Labs: Na 124 K 4.3 TSH 4.4 Dig 1.35 CxR – Large right perihilar mass with bilateral pleural effusions.
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WQRS tachycardia algorithm
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VT Cluster (VTC) A VTC is defined as ≥ 3 sustained VTs/24 h. Ventricular tachycardia that repeatedly recurs and persists for more than half of a 24-h period despite repeated attempts to terminate the arrhythmia is designated “incessant.” Irrespective of the number of VTs, only 30.2% of patients survived and 15.5% survived without heart transplantation four years after the first cluster. Incessant VT typically takes one of two forms. The most common situation is for VT to be sustained, terminated by external cardioversions, but recurrent. The time between cardioversion and recurrence may be seconds, minutes or more. A second form, common with the idiopathic VTs, manifests as repeated bursts, with runs of VT that spontaneously terminate for a few intervening sinus beats, followed by the next tachycardia burst. Cardioversion is futile, but may be periodically required if bursts of VT occasionally degenerate to ventricular fibrillation.
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VT Cluster (VTC) When incessant VT is polymorphic, drug induced torsade de pointes associated with QT prolongation, or myocardial ischemia are the major concerns. Runs of polymorphic VT may even repeatedly initiate monomorphic VT in patients with reentry circuits in regions of scar. Suppression of torsade de pointes with intravenous administration of magnesium sulfate and/or overdrive pacing may restore stability.
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VT Cluster (VTC) Treatment Options: Antiarrythmic drugs Beta Blockade General anesthesia (to reduce sympathetic tone) Intra aortic balloon counterpulsation Catheter ablation – percutaneous/ epicardial LVAD Inside or out? Another option for incessant ventricular tachycardia J. Am. Coll. Cardiol., June 4, 2003; 41(11): 2044 - 2045.
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Dosage Amiodarone — Amiodarone is given as a 150 mg (or 5 mg/kg) IV bolus over 10 minutes; additional boluses of 150 mg over 10 minutes are given every 10 to 15 minutes as needed. Alternatively, an infusion of 360 mg (1 mg/min) over six hours followed by 540 mg (0.5 mg/min) over the remaining 18 hours can be used. The maximum total dose (including doses given during resuscitation) is 2.2 grams in 24 hours. Lidocaine — Lidocaine is given by IV push in a dose of 0.5 to 0.75 mg/kg; repeated every 5 to 10 minutes as needed. At the same time, a continuous IV infusion of 1 to 4 mg/min is begun. The maximum total dose is 3 mg/kg over one hour.
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Dosage Procainamide: Loading dose: 15-18 mg/kg administered as slow infusion over 25-30 minutes or 100-200 mg/dose repeated every 5 minutes as needed to a total dose of 1 g. Reduce loading dose to 12 mg/kg in severe renal or cardiac impairment. Maintenance dose: 1-4 mg/minute by continuous infusion. Maintenance infusions should be reduced by one-third in patients with moderate renal or cardiac impairment and by two-thirds in patients with severe renal or cardiac impairment. ACLS guidelines: Infuse 20 mg/minute until arrhythmia is controlled, hypotension occurs, QRS complex widens by 50% of its original width, or total of 17 mg/kg is given.
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SHock Inhibition Evaluation with AzimiLiDe (SHIELD) Investigators A randomized trial of azimilide for suppression of ventricular tachycardia/fibrillation (VT/VF) leading to implanted cardioverter defibrillator (ICD) therapies. Of 633 ICD recipients, 148 (23%) experienced at least one ES (electrical storm) over 1-year follow-up. Compared with placebo, azimilide reduced the risk of recurrent ES by 37% (p=0.11) nonsignificantly. CONCLUSION: ES is common and unpredictable in ICD recipients and it is a strong predictor of hospitalization. Eur Heart J. 2006 Dec;27(24):2921-2.
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Left stellate ganglionic blockade Forty-nine patients (36 men, 13 women, mean age 57 years) who had ES associated with a recent MI were separated into 2 groups. Patients in group 1 (n=27) received sympathetic blockade treatment: 6 left stellate ganglionic blockade, 7 esmolol, and 14 propranolol. Patients in group 2 (n=22) received antiarrhythmic medication as recommended by the ACLS guidelines. Patient characteristics were similar in the 2 groups. The 1-week mortality rate was higher in group 2: 18 (82%) of the 22 patients died, all of refractory VF; 6 (22%) of the 27 group 1 patients died, 3 of refractory VF (P<0.0001). Patients who survived the initial ES event did well over the 1- ear follow-up period: Overall survival in group 1 was 67%, compared with 5% in group 2 (P<0.0001). Conclusions—Sympathetic blockade is superior to the antiarrhythmic therapy recommended by the ACLS guidelines in treating ES patients. Our study emphasizes the role of increased sympathetic activity in the genesis of ES. Sympathetic blockade2not class 1 antiarrhythmic drugs2should be the treatment of choice for ES. (Circulation. 2000;102:742-747.)
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Therapies for VT ABLATION Ablation is indicated in patients who are otherwise at low risk for SCD and have sustained predominantly monomorphic VT that is drug resistant, who are drug intolerant, or who do not wish long-term drug therapy. Ablation is indicated in patients with bundle-branch reentrant VT. Ablation is indicated as adjunctive therapy in patients with an ICD who are receiving multiple shocks as a result of sustained VT that is not manageable by reprogramming or changing drug therapy or who do not wish long-term drug therapy. Ablation is indicated in patients with WPW syndrome resuscitated from sudden cardiac arrest due to AF and rapid conduction over the accessory pathway causing VF.
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Therapies for VT Ablation Ablation can be useful therapy in patients who are otherwise at low risk for SCD and have symptomatic nonsustained monomorphic VT that is drug resistant, who are drug intolerant or who do not wish long-term drug therapy. Ablation can be useful therapy in patients who are otherwise at low risk for SCD and have frequent symptomatic predominantly monomorphic PVCs that are drug resistant or who are drug intolerant or who do not wish long-term drug therapy. Ablation can be useful in symptomatic patients with WPW syndrome who have accessory pathways with refractory periods less than 240 ms in duration.
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Incessant VT Revascularization and beta blockade followed by intravenous antiarrythmic drugs such as procainamide or amiodarone are recommended for patients with recurrent or incessant polymorphic VT due to acute MI. Intravenous amiodarone or procainamide followed by VT ablation can be effective in the management of patients with frequently recurring or incessant monomorphic VT. Acute Management of Specific Arrhythmias
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Incessant VT Intravenous amiodarone and intravenous beta blockers separately or together may be reasonable in patients with VT storm. Overdrive pacing or general anesthesia may be considered for patients with frequently recurring or incessant VT. Spinal cord modulation may be considered for some patients with frequently recurring or incessant VT. Acute Management of Specific Arrhythmias
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Digitalis Toxicity An antidigitalis antibody is recommended for patients who present with sustained ventricular arrhythmias, advanced AV block, and/or asystole that are considered due to digitalis toxicity. Patients taking digitalis who present with mild cardiac toxicity (e.g., isolated ectopic beats only) can be managed effectively with recognition, continuous monitoring of cardiac rhythm, withdrawal of digitalis, restoration of normal electrolyte levels (including serum potassium greater than 4 mM/L), and oxygenation. Magnesium or pacing is reasonable for patients who take digitalis and present with severe toxicity (sustained ventricular arrhythmias, advanced AV block, and/or asystole). VA & SCD Related to Specific Populations
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Digitalis Toxicity Dialysis for the management of hyperkalemia may be considered for patients who take digitalis and present with severe toxicity (sustained ventricular arrhythmias; advanced AV block, and/or asystole). Management by lidocaine or phenytoin is not recommended for patients taking digitalis and who present with severe toxicity (sustained ventricular arrhythmias, advanced AV block, and/or asystole). VA & SCD Related to Specific Populations
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DrugInteracting DrugEffect QT-prolonging antiarrhythmics DiureticsIncreased T de P risk due to diuretic-induced hypokalemia Beta blockersAmiodarone, clonidine, digoxin, dilitiazem, verapamil Bradycardia when used in combination DigoxinAmiodarone, beta blockers, clonidine, dilitiazem, verapamil VerapamilAmiodarone, beta blockers, clonidine, digoxin, dilitiazem DiltiazemAmiodarone, beta blockers, clonidine, digoxin, verapamil SildenafilNitratesIncreased and persistent vasodilation; risk of myocardial ischemia ClonidineAmiodarone, beta blockers, digoxin, dilitiazem, verapamil AmiodaroneBeta blockers, clonidine, digoxin, dilitiazem, verapamil Drug Interactions Causing Arrhythmias
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Hospital course Was loaded with IV amiodarone and lidocaine prior to transfer. Initially transferred to Tulane for possible VT ablation. Ablation procedure cancelled due to respiratory distress. She had multiple episodes of monomorphic and polymorphic VT and was emergently intubated after seizures during one of the codes.
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Antiarrythmic therapy included reloading with amiodarone and lidocaine followed by prcainamide loading and infusion. She continued to suffer from VT clusters and intermittent asystole. IABP and LVAD were considered.
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Family decided to stop all aggressive treatement. She died following a terminal VT.
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