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Latest revision as of 05:08, 16 September 2022

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Sara Zand, M.D.[2] Cafer Zorkun, M.D., Ph.D. [3], Avirup Guha, M.B.B.S.[4]

Overview

The mainstay of medical therapy in hemodynamic stable VT is suppression of tachyarrhythmia with antiarrhythmic medications such as amiodarone, sotalol, lidocaine, betablocker alongside with correction of hypokalemia, hypomagnesemia and hypocalcemia. In addition, treating the underlying causes of VT including ischemic heart disease or decompensated heart failure are warranted.

Medical Therapy

Common medications for treatment of VT include:^[1]

Antiarrhythmic medications

^[2]

Sodium channel blocker

In patients with ischemic heart disease, chronic use of sodium channel blocker increased risk of mortality.
Some sodium channel blockers with benefit in special setting include the following:

Lidocaine (class1) for patients with refractory VT, cardiac arrest (especially witnessed) ^[3]
Oral mexiletine for congenital long QT syndrome^[4]
Quinidine for patients with Brugada syndrome
Flecainide for patients with catecholaminergic polymorphic ventricular tachycardia^[5]

Theses medications are useful in ICD patients with drug and ablation refractory VT.

Ranolazine

A new antiangina drug approved by FDA with antiarrhythmic efficacy.
Mechanism of action is late sodium channel current blockade , blockade of the phase 3 repolarizing potassium current.
Reducion ICD shocks in drug resistant VT, VF^[1]

Reducion VT in the first days after NSTEMI according to MERLIN TIMI-36.^[6]

NO efficacy in reduction the fist VT, VF in high risk patients, but significant reduction of recurrent VT, VF requiring ICD implantation.^[7]

Beta blocker

First line therapy for the most of ventricular arrhythmia such as PVC, VT because of safety and efficacy^[8]

Supression of ventricular arrhythmia in structurally normal heart.
Reducing all-cause mortality and SCD in patients with heart failure with reduced EF^[9]
Reducing mortality after MI
Increased mortality and risk of cardiogenic shock after MI in the presence of >70 years of age, symptoms <12 hours ST-elevation MI patients, systolic blood pressure <120 mm Hg, heart rate >110 beat/min ^[10]
Increased antiarrhythmic effect of membrane stabilizing drug in malignant VT.^[11]
Nadolol, propranolol: first-line therapy for some cardiac channelopathies such as long QT syndrome, catecholaminergic polymorphic ventricular tachycardia

Amiodarone, sotalol

Amiodarone is a multichannel blocker by blockade of beta receptors, sodium, calcium, potassium currents
NO survival benefit from amiodarone compared with placebo in patients with LV dysfunction due to prior MI and non ischemic cardiomyopathy according to SCD-HeFT^[12]
Use of amiodarone after MI in patients with NYHA 3 symptoms was associated with increased risk of mortality.^[13]
In patients with nonischemic cardiomyopathy (LVEF<40%), use of amiodarone reduced the risk of SCD (with low quality of support of article), but there was NO benefit of using amiodarone for secondary prevention.^[14]

Infused amiodarone during cardiopulmonary resuscitation prevents recurrent VT, VF.^[15]
Amiodarone decreased risk of SCD and all-cause mortality compared with betablocker or sotalol.^[14]
Chronic use of amiodarone has adverse effect on lung, liver, thyroid, skin, and nervous system.^[14]
ECG, liver function tests, thyroid function tests, chest x-ray, and pulmonary function tests (including diffusing capacity of the lungs for carbon monoxide) is needed before administration of amiodarone. In case of pulmonary toxicity, chest CT scan should be done.^[16]
Although sotalol suppressed ventricular arrhythmia, it was associated with increased risk of mortality in heart failure patients.^[17]
Sotalol may decrease defibrillation threshold and should be avoided in patients with LVEF< 20% due to decompensation of heart failure.^[18]

Calcium channel blocker

Non-dihydropyridines calcium channel blockers have no role in the treatment of most ventricular arrhythmias.
In patients with prior MI, administration of intravenous verapamil for sustained VT has been associated with hemodynamic collapse .^[19]
Verapamil and diltiazem can be used for suppression of some VT originated outflow tract.^[20]
Oral and intravenous verapamil is effective for the treatment of idiopathic interfascicular reentrant left VT in patients with normal structurally heart.^[21]
Non-dihydropyridines Calcium channel blockers should be avoided for converting VT in heart failure reduced EF.

Arrhythmiac medication, class, dose	Indication	Receptor target	Electrophysiologic effect	Pharmacological characteristics	Common advers effects
Acebutolol PO 200–1200 mg daily, up to 600 mg bid	VT, PVC	B1, mild internistic sympathetic activity	Slowing sinus rate, increasing AV nodal refractoriness	Prolonged haft life in renal impairment, metabolism: hepatic	Bradycardia, hypotension, HF, AV block, Dizziness, fatigue, anxiety, impotence, hyperesthesia,hypoesthesia
Amiodarone (III) IV:VF/pulseless VT arrest: 300 mg bolus, stable VT: 150-mg bolus then 1 mg/min x 6 h, then 0.5 mg/min x 18 h PO: 400 mg q 8 to 12 h for 1–2 wk, then 300–400 mg daily; reduce dose to 200 mg daily if possible	VT, VF, PVC	INa, ICa, IKr, IK1, IKs, Ito, Beta receptor, Alpha receptor, nuclear T3 recepto	Slowed sinus rate, QRS prolongation, QTc prolongation, increased AV nodal refractoriness ,increased defibrilation threshold	Metabolism: hepatic, half life: 26-107 days	Hypotension, bradycardia, AV block, TdP, slowing VT below programmed ICD detection rate, increased defibrillation threshold, corneal microdeposits, thyroid abnormalities, ataxia, nausea, emesis, constipation, photosensitivity, skin discoloration, ataxia, dizziness, peripheral neuropathy, tremor, hepatitis, cirrhosis, pulmonary fibrosis, pneumonitis
Atenolol (II) PO: 25–100 mg qd or bid	VT, PVC, ARVC, LQTS	Beta 1	Slowed sinus rate , increased AV nodal refractoriness	Metabolism: hepatic	Bradycardia, hypotension, heart failure, AV block, dizziness, fatigue, depression, impotence
Bisoprolol (II) PO: 2.5–10 mg once daily	VT, PVC	Beta 1 receptor	Slowed sinus rate, increased AV nodal refractoriness	Metabolism: hepatic	Chest pain, bradycardia, AV block, Fatigue, insomnia, diarrhea
Carvedilol (II) PO: 3.125–25 mg q 12 h	VT, PVC	Beta 1, Beta 2, Alpha	Slowed sinus rate, increased AV nodal refractoriness	Metabolism: hepatic	Bradycardia, hypotension, AV block, edema, syncope, Hyperglycemia, dizziness, fatigue, diarrhea
Carvedilol (II) PO: 3.125–25 mg q 12 h	VT, PVC	Beta 1, Beta 2, Alpha	Slowed sinus rate, increased AV nodal refractoriness	Metabolism: hepatic	Bradycardia, hypotension, AV block, edema, syncope, Hyperglycemia, dizziness, fatigue, diarrhea
Diltiazem (IV) IV: 5–10 mg,qd: 15–30 min, Extended release: PO: 120–360 mg/da, PO: 3.125–25 mg q 12 h	RVOT VT, ideopathic left VT	ICa-L	Slowed sinus rate, slowed AV node conduction, PR prolongation	Metabolism: hepatic	Bradycardia, hypotension, AV block, edema, exacerbation of HF reduced EF, Headache, rash, constipation
Esmolol (II) IV: 0.5 mg/kg bolus, 0.05 mg/kg/min	VT	B1	Slowed sinus rate, increased AV node refractoriness	Metabolism: RBC	Bradycardia, hypotension, AV block, HF, dizziness, neusea
Flecainide (IC) PO: 50–200 mg q 12 h	VT, PVC (in the absence of structural heart disease), CPVT	INa, IKr, IKur	Prolonged PR interval, prolonged QRS duration, increased defibrillation threshold	Metabolism: RBC	Sinus node dysfunction, AV block, drug-induced Brugada syndrome, monomorphic VT in patients with a myocardial scar, exacerbation of HFrEF
Lidocaine (IB) IV: 1 mg/kg bolus, 1–3 mg/min, 1–1.5 mg/kg. Repeat 0.5–0.75 mg/kg bolus every 5–10 min (max cumulative dose 3 mg/kg), maintenance infusion: 1–4 mg/min or starting 0.5 mg/min	VT, VF	INa	Slightly shortening of QTc interval	Metabolism: hepatic, prolonged half life in HF, liver disease, shock, severe renal disease	Bradycardia, hemodynamic collapse, AV block, sinus arrest, delirium, psychosis, seizure, nausea, tinnitus, dyspnea, bronchospasm
Metoprolol (II) IV: 5 mg q 5 min up to 3 doses, PO: 25–100 mg Extended release qd or q 12 h	VT, PVC	B1	Slowed sinus rate, increased AV nodal refractoriness	Metabolism: None, Excretion: urine	Bradycardia, hypotension, AV block, dizziness, fatigue, diarrhea, depression, dyspnea
Metoprolol (II) IV: 5 mg q 5 min up to 3 doses, PO: 25–100 mg Extended release qd or q 12 h	VT, PVC	B1	Slowed sinus rate, increased AV nodal refractoriness	Metabolism: None, Excretion: urine	Bradycardia, hypotension, AV block, dizziness, fatigue, diarrhea, depression, dyspnea
Mexiletine (IB), PO: 150–300 mg q 8 h or q 12 h	VT, PVC, VF, Long QT3	INa	Slightly shortening of QTc interval	Metabolism: hepatic	HF, AV block, lightheaded, tremor, ataxia, paresthesias, nausea, blood dyscrasias
Nadolol (II) PO: 40–320 mg daily	VT, PVC, LQTS, CPVT	B1, B2	Slowed sinus rate, increased AV nodal refractoriness	Metabolism: none, excretion: urine	Bradycardia, hypotension, HF, AV block, edema, dizziness, cold extremities, bronchospasm
Procainamide (IA), IV: loading dose 10–17 mg/kg at 20–50 mg/min, maintenance dose: 1–4 mg/min, PO (SR preparation): 500–1250 mg q 6 h	VT, PVC, LQTS, CPVT	B1, B2	Slowed sinus rate, increased AV nodal refractoriness	Metabolism: none, excretion: urine	Bradycardia, hypotension, HF, AV block, edema, dizziness, cold extremities, bronchospasm
Propafenone (IC), PO: Immediate release 150–300 mg q 8 h, Extended release 225–425 mg q 12 h	VT, PVC (in the absence of structural heart disease)	INa, IKr, IKur, Beta receptor, Alpha recept	Prolonged PR interval, prolonged QRS duration, increased defibrillation threshold	Metabolism: hepatic	HF, AV block, drug-induced Brugada syndrome, dizziness, fatigue, nausea, diarrhea, xerostomia, tremor, blurred vision
Propranolol (II), IV: 1–3 mg q 5 min to a total of 5 mg, PO: Immediate release 10–40 mg q 6 h; Extended release 60–160 mg q 12 h	VT, PVC, Long QT syndrome	Beta 1 , B2 , INa	Slowed sinus rate, increased AV nodal refractoriness	Metabolism: hepatic	Bradycardia, hypotension, HF, AV block, sleep disorder, dizziness, nightmares, hyperglycemia, diarrhea, bronchospasm
Quinidine (IA), PO: sulfate salt 200–600 mg q 6 h to q 12 h, gluconate salt 324–648 mg q 8 h to q 12 h, IV: loading dose: 800 mg in 50 mL infused at 50 mg/min	VT, VF, short QT syndrome, brugada	INa, Ito, IKr, M, Alpha receptor	QRS prolongation, QTc prolongation, increased defibrillation threshold	Metabolism: hepatic	Syncope, torsades de pointes, AV block, dizziness, diarrhea, nausea, esophagitis, emesis, tinnitus, blurred vision, rash, weakness, tremor, blood dyscrasias
Ranolazine (not classified), PO: 500–1000 mg q 12 h	VT	INa, IKr	Slowed sinus rate, QTc prolongation	Metabolism: hepatic	Bradycardia, hypotension, headache, dizziness, syncope, nausea, dyspnea
Sotalol (III), IV: 75 mg q 12 h, PO: 80–120 mg q 12 h, may increase dose every 3 d; max 320 mg/d	VT, VF, PVC	B1, B2 IKr	Slowed sinus rate, QTc prolongation, increased AV nodal refractoriness, decreased defibrillation threshold	Metabolism: none	Bradycardia, hypotension, HF, syncope, TdP, fatigue, dizziness, weakness, dyspnea, bronchitis, depression, nausea, diarrhea
Verapamil, IV: 2.5–5 mg q 15–30 min, sustained release PO: 240–480 mg/d	RVOT VT, verapamil-sensitive idiopathic Left VT	ICa-L	Slowed sinus rate,PR prolongation, slowed AV nodal conduction	Metabolism: hepatic	Hypotension, edema, HF, AV block, bradycardia, exacerbation of HF reduced EF, headache, rash, gingival hyperplasia, constipation, dyspepsia

Electrolytes

Correction of hypokalemia and hypomagnesemia is helpful for preventing of ventricular arrhythmia in the setting of myocardial infarction or diuretic therapy in heart failure patients.^[22]
Diuretic therapy in heart failure patients may lead to hypokalemia or hypomagnesemia.^[22]

Hypokalemia and hypomagnesemia may cause ventricular arrhythmia during acute myocardial infarction .
Hypokalemia and hypomagnesemia may increase the risk of torsades de pointes in patients with use of some medications with QTc prolongation effect or long QT syndrome.^[23]
Administration of intravenous magnesium in the setting of torsades de pointes as the first line therapy is recommended.^[24]

Potassium level should be kept 4.5 mmol/L and 5 mmol/L to prevent ventricular arrhythmia or sudden cardiac death.^[25]

In patients with acute MI maintaining potassium level between 3.5 mmol/L and 4.5 mmol/L was associated with lower rate of death ^[26]
Early administration of intravenous magnesium in patients with acute STEMI has not effect on short term mortality.^[27]

Fatty acids, Lipids

The role of N-3 poly-unsaturated fatty acids and statin therapies for preventing of SCD has been proposed by stabilizing bilipid myocyte membrane for maintaining electrolyte gradients. ^[28]
Among patients with recent MI using fish oil 1 g/d reduced SCD and mortality.^[29]
Another clinical trial showed using n–3 Fatty Acids was not effective in the reduction of the cardiovascular event in high risk patients.^[30]
Statin clearly reduced mortality and SCD associated ischemic heart disease.^[31]
Supressing plaque rupture or direct cardiovascular effect are two mechanisms of decrease ventricular arrhythmia by statin.
Statin is effective in prevention of ventricular arrhythmia in ischemic heart disease, however, the role of statine in reducing SCD in heart failure ICD patients is not clearly explained.^[32]

Specific recommendation

The mainstay of therapy in heart failure reduced EF for prevention of SCD and ventricular arrhythmia is the following:
Beta blockers with benefit for preventing of SCD by reducing sympathetic activity and myocardial oxygen demand or countering electrical excitability.
Angiotensin-converting enzyme inhibitors, or angiotensin-receptor blockers is effective by reducing myocardial oxygen demand, preload, afterload, prevention the formation of angiotensin II, and slowing the process of ventricular remodeling and fibrosis.^[33]
Mineralocorticoid receptor antagonists decrease potassium loss, decrease fibrosis, and increase the myocardial uptake of norepinephrine.
Chronic Beta blockers therapy in heart failure reduced EF was associated with reduced SCD, ventricular arrhythmia and all cause mortality.
Bisoprolol, carvedilol, sustained-release metoprolol succinate decrease mortality in patients with heart failure reduced EF.^[34]^[35]^[36]
ACEI and mineralocorticoid-receptor antagonists (spironolactone, eplerenone) reduce mortality and SCD in patients with severe heart failure. ^[37]

Management of patients with Polymorphic Ventricular arrhythmia

Polymorphic Ventricular arrhythmia

Underlying etiology

Acute ischemia

External precipitating factors

Polymorphic Ventricular Arrhythmia triggered by unifocal PVC

Acquired long QT

Primary electrical disease

Approach to STEMI

Treatment of underlying condition (Class I)

Catheter ablation (Class IIa)

Quinidine (Class IIb)

Remove precipitating factors (Class I)

Mg++/K+ i.v.(Class I)

Isoproterenol (Class I)

Pacing (Class I)

Brugada, Early repolarization syndrome

Idiopathic VF

Long QT, CPVT

Recurrent Ventricular arrhythmia

Isoproterenol (Class IIa)

Quinidine (Class IIa)
Catheter ablation (Class IIa)

Isoproterenol (Class IIa)

Quinidine (Class IIa)

Verapamil (Class IIa

Catheter ablation of PVC triggers (Class IIa)

Beta-blocker (Class I)

Pacing (Class I)

Mg++/K+ i.v (Class I)

Antiarrhythmic drugs according to underlying disease (Class 2a)

Autonomic modulation (Class 2a)

Deep sedation/ intubation (Class IIa)

Mechanical circulatory support (Class IIb)

Deep sedation/ intubation (Class IIa)

Mechanical circulatory support (Class IIb)

Deep sedation/ intubation (Class IIa)

Mechanical circulatory support (Class IIb)

Recurrent ventricular arrhythmia

Deep sedation/ intubation (Class IIa)

Mechanical circulatory support (Class IIb)

Deep sedation/ intubation (Class IIa)

Mechanical circulatory support (Class IIb)

Deep sedation/ intubation (Class IIa)

Mechanical circulatory support (Class IIb)

The above algorithm adopted from 2022 ESC Guideline^[38]

Management of sustained monomorphic ventricular tachycardia

Recommendations for acute management of sustained VT

DC cardiovertion (Class I, Level of Evidence B):

❑ DC cardioversion is recommended as the first-line therapy for hemodynamically not-tolerated sustained monomorphic ventricular tachycardia

DC cardiovertion (Class I, Level of Evidence C) :

❑ DC cardioversion is recommended as the first-line treatment for patients presenting with tolerated sustained monomorphic VT when anesthetic/sedation risk is low

Supraventricular tachycardia (Class IIa, Level of Evidence C)

❑ In patients presenting with a regular hemodynamically tolerated wide QRS complex tachycardia suspected for supraventricular tachycardia, administration of adenosine or vagal maneuvers should be considered

Procainamide (Class IIa, Level of Evidence B)

❑In patients presenting with a hemodynamically tolerated sustained monomorphic VT and presence of structural heart disease, intravenous procainamide should be considered

Flecainide, ajmaline, sotalol (Class IIb, Level of Evidence B)

❑In patients presenting with a hemodynamically tolerated sustained monomorphic VT in the absence of significant structural heart disease, flecainide, ajmaline, or sotalol may be considered

Verapamil (Class III, Level of Evidence B)

❑Intravenous verapamil is not recommended in wide QRS complex tachycardia of unknown mechanism

The above table adopted from 2022 ESC Guideline^[38]

Management of electrical storm

Recommendations for management of electrical storm

Sedation (Class I, Level of Evidence C):

❑ Mild to moderate sedation is recommended in patients with the electrical storm to reduce psychological distress and reduce sympathetic tone

Strucrural heart disease (Class I, Level of Evidence B) :

❑ Antiarrhythmic therapy with beta-blockers (non-selective preferred) in combination with intravenous amiodarone is recommended in patients with structural heart disease and electrical storm unless contraindicated
❑Catheter ablation is recommended in patients presenting with incessant VT or electrical storm due to sustained monomorphic VT refractory to antiarrhythmic drugs

Torsades depointes (Class I, Level of Evidence C)

❑ Intravenous magnesium with supplementation of potassium is recommended in patients with TdP
❑Isoproterenol or transvenous pacing to increase heart rate is recommended in patients with acquired LQT syndrome and recurrent TdP despite correction of precipitating conditions and magnesium

Procainamide (Class IIa, Level of Evidence B)

❑In patients presenting with a hemodynamically tolerated sustained monomorphic VT and presence of structural heart disease, intravenous procainamide should be considered

Intubation (Class IIa, Level of Evidence C)

❑Deep sedation/intubation should be considered in patients with an intractable electrical storm non-responsive drug treatment

❑Catheter ablation should be considered in patients with recurrent episodes of VT/VF triggered by a similar PVC, refractory to medical treatment or coronary revascularization

Quinidine (Class IIb, Level of Evidence C)

❑Quinidine may be considered in patients with coronary artery disease and electrical storm due to recurrent VT refractory to other antiarrhythmic drugs

Refractory electerical storm (Class IIb, Level of Evidence C)

❑Autonomic modulation may be considered in patients with electrical storm refractory to medical therapy and in whom catheter ablation is ineffective or not possible
❑ Mechanical circulatory support may be considered in the management of drug-refractory electrical storm and [[cardiogenic shock]]

The above table adopted from 2022 ESC Guideline^[38]

Recommendations for treatment with heart failure medication

Class I
"Optimal medical treatment including ACE-I/ARB/ ARNIs, mineralocorticoid receptor antagonist, beta-blockers, and SGLT2 inhibitors is indicated in all heart failure patients with reduced EF' (Level of Evidence A)"

The above table adopted from 2022 ESC Guideline^[38]

Notes

The most common cause of cardiac arrest is VF, pulseless VT, severe bradycardia, and asystole.
Survival in the presence of VF, VT is better than bradycardia, asystole manifestation.^[39]
Factors associated with better survival include rapid defibrillation and initiation of CPR for a witnessed cardiac arrest.
Survival in patients with cardiac arrest decreases rapidly after the initial 2 minutes from the onset of cardiac arrest, by 4 to 5 minutes, survival may be ≤25%, and by 10 minutes it is 0%.^[40]
Among patients with witnessed cardiac arrest due to initial shock-refractory VF or pulseless VT, administration of amiodarone improved survival to hospital discharge compared with placebo in the setting of out-of-hospital cardiac arrest.
Administration of procainamide in out-of-hospital cardiac arrest due to VF or pulseless VT was correlated with more shocks, more pharmacologic interventions, longer resuscitation times, and lower survival.^[41]
If left untreated, VF and pulseless monomorphic or polymorphic VT, causes loss of consciousness and leads to death.
A short time to direct current cardioversion is the major determinant of survival, and defibrillation should be performed as quickly as possible.
CPR should be continued until restoration a perusing rhythm.
If defibrillation failed to returning spontaneous circulation, advanced cardiovascular life support should be followed.
In unstable patients suspected coronary artery occlusion led to cardiac arrest, emergency coronary angiography should be considered rather than later in the hospital regardless the patient is comatose or awake.^[42]^[43]
Coronary lesion requiring percutaneous coronary intervention was found in one-third of patients with out-of-hospital cardiac arrest without ST elevation in ECG. The outcome was reasonable. ^[44]

In the presence of incessant VT, amiodarone was more effective than lidocaine and improved survival at 24 hours.^[45]

Procainamide is superior to lidocaine in the setting of recurrent stable hemodynamic VT, and also preferred in the absent evidence of acuteMI, or Long QTC on ECG.^[46]

lidocaine was less effective than amiodarone to improve hospital admission after out-of-hospital cardiac arrest due to shock-refractory VF or polymorphic VT, but there were no differences between the two medications in survival to hospital discharge.
Lidocaine improved survival to hospital discharge in witnessed SCA due to initial shock-refractory VF or pulseless VT.
Administration of beta blocker in patients with recent MI was associated with reduced VF and better survival.
If VT, VF storm is refractory to amiodarone, lidocaine, or frequent cardioversion, administration of betablocker has been shown improved survival and finally reducing sympathetic tone by sedation and general anesthesia are recommended.
Administration of high-dose epinephrine ( 0.1 to 0.2 mg/kg IV) in out-of-hospital cardiac arrest unresponsive to defibrillation, improved survival to hospital admission, but there was no difference compared to standard-dose epinephrine in survival to hospital discharge or long term survival compared with standard-dose epinephrine (1 mg given intravenously or intraosseously every 3 to 5 minutes).^[47]
Administration of vasopressin is no longer recommended in the most recent advanced cardiovascular life support guideline.^[48]

Intravenous magnesium is advised in the presence of hypokalemia or medication-induced torsades de pointed by suppression of early and late after depolarization, and inhibition of calcium flux into cardiomyocytes.
Using intravenous magnesium during in-hospital or out-of-hospital cardiac arrest or refractory VF was not associated with restoration of circulation or survival benefit.^[49]

Administration The lidocaine and procainamide routinely after MI for suppression of ventricular arrhythmia was associated with increased mortality, however,

use of beta blockers lessened mortality rate.^[50]

Prophylactic use of Higher dose amiodarone after MI increase mortality, whereas moderate dose amiodarone was not superior to placebo.^[51]

Every wide QRS tachycardia in the presence of structural heart disease should be presumed VT until proven otherwise such as SVT with aberrancy.
Administration of verapamil in wide QRS tachycardia may lead to severe hypotension and syncope and should be avoided.
The specific type of VT is verapamil-sensitive VT (interfascicular reentry) with structurally normal heart, but it is important to notify that the recognition of this rhythm is difficult at initial presentation.^[19]

Sustained monomorphic VT

Hemodynamic stability

Stable

Unstable

12-Lead ECG, history, physical exam

Dirrect current cardioversion,ACLS

Notifying disease causing VT

Cardioversion(class1)

VT termination

Structural heart disease

Intravenous procainamide (class2a)

Yes, therapy of underlying heart disease

NO, cardioversion (class1)

NO, Ideopathic VT

Intravenous amiodarone or sotalole (class2b)

VT termination

Verapamil sensitive VT: Verapamil outflow tract VT: betablocker (class2a)

Effective

Non effective: cardioversion

Yes,therapy of underlying heart disease

NO, Sedation ,anesthesia, reassessing antiarrhythmic therapy, repeating cardioversion

Therapy to prevent recurrence of VT

No VT termination

Catheter ablation (class1)

Verapamil , betablocker (class2a)

The above algorithm adopted from 2017 AHA/ACC/HRS Guideline

Comments

Common antiarrhythmic medications for supression of ventricular arrhythmia include amiodarone, sotalol, and occasionally mexilletine, quinidine,ranolazine.^[1]^[52]
Amiodarone is more effective than sotalol but discontinuation may happen during 12-24 months of use due to adverse effects.^[53]
Contraindication of sotalol may include severely reduced LVEF <20% due to its negative inotropic effects and the risk of torsades de pointed.
In patients with prior MI and recurrent sustained monomorphic VT despite receiving amiodarone , catheter ablation was related to better outcome.^[54]
Recurrent VT after catheter ablation is associated with increased mortality.
Administration of encainide or flecainide for suppression of PVCs and non sustained VT in post MI period was associated with increased mortality and non fatal cardiac arrest.^[55]

In survivors of SCA use of Propafenone increased mortality in comparison with beta-blockers, amiodarone, and the ICD.
In patients with prior MI, Sustained monomorphic VT can be due to scar-related reentry, but not acute ischemia.
Antiarrhythmic medications or ablation may be needed to prevent recurrence of VT in scar-related settings.^[56]

Revascularization is recommended in the setting of ischemia for prevention of VF, polymorphic VT. ^[57]

Recommendations for treatment of recurrent ventricular tachycardia in ischemic heart disease

Medications (Class I, Level of Evidence B):

❑ In patients with IHD and recurrent symptomatic ventricular tachycardia and frequent ICD shocks despite programming, betablocker, sotalol, amiodarone is recommended for supression of arrhythmia
❑ In patients with period MI and presence of VT storm refractory to amiodarone or other antiarrhythmic drugs, catheter ablation is recommended

Catheter ablation (Class IIb, Level of Evidence C) :

❑ Catheter ablation can be the first line therapy for recurrent sustained monomorphic VT in IHD

(Class III, Level of Evidence C)

❑ Class IC antiarrhythmic drugs (flecainide, propafenone ) is harmful for supression of ventricular tachycardia in patients with perior MI
❑ In patients with incessant VT/VF, after controlling tachyarrhythmia ICD should be implanted due to avoiding of repeated ICD shocks
❑ In patients with recurrent monomorphic VT , only revascularization is ineffective for preventing of tachyarrhythmia

The above table adopted from 2017 AHA/ACC/HRS Guideline^[2]

Message

Although ICD reduced mortality, painful ICD shocks can affect on the quality of life and increases morbidity.
The frequent of ICD shocks lessened by amiodarone plus beta blocker compared with sotalol but at the expense of increased risk of amiodarone-related adverse effects.^[53]
All types of non-ischemic cardiomyopathy can produce scar-related VT especially cardiac sarcoidosis.^[58]

Catheter ablation can be used for treatment of scar related VT in non-ischemic cardiomyopathy.^[59]

Recommendations for treatment of recurrent ventricular tachycardia in non-ischemic heart disease

Amiodarone, sotalol (Class IIa, Level of Evidence B):

❑ Amiodarone or sotalol is recommended in the presensence of recurrent ventricular arrhythmia and frequent ICD shocks despite optimal programming or beta blocker therapy

Catheter ablation (Class IIa, Level of Evidence B) :

❑ In the setting of frequent ventricular arrhythmia despite optimal ICD programming or failed antiarrhythmic medications, catheter ablation is recommended

The above table adopted from 2017 AHA/ACC/HRS Guideline^[2]

References

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@@ Line 3: / Line 3: @@
 {{CMG}}; '''Associate Editor-In-Chief:''' {{Sara.Zand}} {{CZ}}, [[User:Avirupguha|Avirup Guha, M.B.B.S.]][mailto:avirup.guha@gmail.com]
 ==Overview==
+The  mainstay of medical therapy in hemodynamic stable [[VT]] is suppression of [[tachyarrhythmia]] with [[antiarrhythmic]] [[medications]] such as [[amiodarone]], [[sotalol]], [[lidocaine]], [[betablocker]] alongside with correction of [[hypokalemia]], [[hypomagnesemia]] and [[hypocalcemia]]. In addition, treating the underlying causes of [[VT]] including
+[[ischemic heart disease]] or [[decompensated heart failure]]
+are warranted.
 ==Medical Therapy==
@@ Line 10: / Line 13: @@
 ===[[Sodium channel blocker]]===
-* In [[patients]] with [[ischemic heart disease]] chronic use of [[sodium channel blocker]] increased risk of [[mortality]].
+* In [[patients]] with [[ischemic heart disease]], chronic use of [[sodium channel blocker]] increased risk of [[mortality]].
-* Some [[sodium channel blockers]] that are benefit in special setting include the following:
+* Some [[sodium channel blockers]] with benefit in special setting include the following:
 :* [[Lidocaine]] (class1) for [[patients]] with refractory [[VT]], [[cardiac arrest]] (especially [[witnessed]]) <ref name="KudenchukBrown2016">{{cite journal|last1=Kudenchuk|first1=Peter J.|last2=Brown|first2=Siobhan P.|last3=Daya|first3=Mohamud|last4=Rea|first4=Thomas|last5=Nichol|first5=Graham|last6=Morrison|first6=Laurie J.|last7=Leroux|first7=Brian|last8=Vaillancourt|first8=Christian|last9=Wittwer|first9=Lynn|last10=Callaway|first10=Clifton W.|last11=Christenson|first11=James|last12=Egan|first12=Debra|last13=Ornato|first13=Joseph P.|last14=Weisfeldt|first14=Myron L.|last15=Stiell|first15=Ian G.|last16=Idris|first16=Ahamed H.|last17=Aufderheide|first17=Tom P.|last18=Dunford|first18=James V.|last19=Colella|first19=M. Riccardo|last20=Vilke|first20=Gary M.|last21=Brienza|first21=Ashley M.|last22=Desvigne-Nickens|first22=Patrice|last23=Gray|first23=Pamela C.|last24=Gray|first24=Randal|last25=Seals|first25=Norman|last26=Straight|first26=Ron|last27=Dorian|first27=Paul|title=Amiodarone, Lidocaine, or Placebo in Out-of-Hospital Cardiac Arrest|journal=New England Journal of Medicine|volume=374|issue=18|year=2016|pages=1711–1722|issn=0028-4793|doi=10.1056/NEJMoa1514204}}</ref>
 :*Oral [[mexiletine]] for [[congenital long QT syndrome]]<ref name="MazzantiMaragna2016">{{cite journal|last1=Mazzanti|first1=Andrea|last2=Maragna|first2=Riccardo|last3=Faragli|first3=Alessandro|last4=Monteforte|first4=Nicola|last5=Bloise|first5=Raffaella|last6=Memmi|first6=Mirella|last7=Novelli|first7=Valeria|last8=Baiardi|first8=Paola|last9=Bagnardi|first9=Vincenzo|last10=Etheridge|first10=Susan P.|last11=Napolitano|first11=Carlo|last12=Priori|first12=Silvia G.|title=Gene-Specific Therapy With Mexiletine Reduces Arrhythmic Events in Patients With Long QT Syndrome Type 3|journal=Journal of the American College of Cardiology|volume=67|issue=9|year=2016|pages=1053–1058|issn=07351097|doi=10.1016/j.jacc.2015.12.033}}</ref>
@@ Line 21: / Line 24: @@
 :* A new [[antiangina]] drug approved by [[FDA]] with [[antiarrhythmic]] efficacy.
 :*Mechanism of action is late [[sodium]] channel current blockade , blockade of the phase 3 [[repolarizing]] [[potassium]] current.
-:* Reducing [[ICD]] shocks in drug resistant [[VT]], [[VF]]<ref name="BunchMahapatra2011">{{cite journal|last1=Bunch|first1=T. Jared|last2=Mahapatra|first2=Srijoy|last3=Murdock|first3=David|last4=Molden|first4=Jamie|last5=Weiss|first5=J. Peter|last6=May|first6=Heidi T.|last7=Bair|first7=Tami L.|last8=Mader|first8=Katy M.|last9=Crandall|first9=Brian G.|last10=Day|first10=John D.|last11=Osborn|first11=Jeffrey S.|last12=Muhlestein|first12=Joseph B.|last13=Lappe|first13=Donald L.|last14=Anderson|first14=Jeffrey L.|title=Ranolazine Reduces Ventricular Tachycardia Burden and ICD Shocks in Patients with Drug-Refractory ICD Shocks|journal=Pacing and Clinical Electrophysiology|volume=34|issue=12|year=2011|pages=1600–1606|issn=01478389|doi=10.1111/j.1540-8159.2011.03208.x}}</ref>
+:* Reducion [[ICD]] shocks in drug resistant [[VT]], [[VF]]<ref name="BunchMahapatra2011">{{cite journal|last1=Bunch|first1=T. Jared|last2=Mahapatra|first2=Srijoy|last3=Murdock|first3=David|last4=Molden|first4=Jamie|last5=Weiss|first5=J. Peter|last6=May|first6=Heidi T.|last7=Bair|first7=Tami L.|last8=Mader|first8=Katy M.|last9=Crandall|first9=Brian G.|last10=Day|first10=John D.|last11=Osborn|first11=Jeffrey S.|last12=Muhlestein|first12=Joseph B.|last13=Lappe|first13=Donald L.|last14=Anderson|first14=Jeffrey L.|title=Ranolazine Reduces Ventricular Tachycardia Burden and ICD Shocks in Patients with Drug-Refractory ICD Shocks|journal=Pacing and Clinical Electrophysiology|volume=34|issue=12|year=2011|pages=1600–1606|issn=01478389|doi=10.1111/j.1540-8159.2011.03208.x}}</ref>
-:* Reducing [[VT]]  in the first days after [[NSTMI]]  according to [[MERLIN TIMI-36]].<ref name="SciricaBraunwald2010">{{cite journal|last1=Scirica|first1=Benjamin M.|last2=Braunwald|first2=Eugene|last3=Belardinelli|first3=Luiz|last4=Hedgepeth|first4=Chester M.|last5=Spinar|first5=Jindrich|last6=Wang|first6=Whedy|last7=Qin|first7=Jie|last8=Karwatowska-Prokopczuk|first8=Ewa|last9=Verheugt|first9=Freek W.A.|last10=Morrow|first10=David A.|title=Relationship Between Nonsustained Ventricular Tachycardia After Non–ST-Elevation Acute Coronary Syndrome and Sudden Cardiac Death|journal=Circulation|volume=122|issue=5|year=2010|pages=455–462|issn=0009-7322|doi=10.1161/CIRCULATIONAHA.110.937136}}</ref>
+:* Reducion [[VT]]  in the first days after [[NSTEMI]]  according to [[MERLIN TIMI-36]].<ref name="SciricaBraunwald2010">{{cite journal|last1=Scirica|first1=Benjamin M.|last2=Braunwald|first2=Eugene|last3=Belardinelli|first3=Luiz|last4=Hedgepeth|first4=Chester M.|last5=Spinar|first5=Jindrich|last6=Wang|first6=Whedy|last7=Qin|first7=Jie|last8=Karwatowska-Prokopczuk|first8=Ewa|last9=Verheugt|first9=Freek W.A.|last10=Morrow|first10=David A.|title=Relationship Between Nonsustained Ventricular Tachycardia After Non–ST-Elevation Acute Coronary Syndrome and Sudden Cardiac Death|journal=Circulation|volume=122|issue=5|year=2010|pages=455–462|issn=0009-7322|doi=10.1161/CIRCULATIONAHA.110.937136}}</ref>
 :* NO efficacy in reduction the fist [[VT]], [[VF]] in high risk [[patients]], but significant reduction of recurrent [[VT]], [[VF]] requiring [[ICD]] implantation.<ref name="ZarebaDaubert2018">{{cite journal|last1=Zareba|first1=Wojciech|last2=Daubert|first2=James P.|last3=Beck|first3=Christopher A.|last4=Huang|first4=David T.|last5=Alexis|first5=Jeffrey D.|last6=Brown|first6=Mary W.|last7=Pyykkonen|first7=Kathryn|last8=McNitt|first8=Scott|last9=Oakes|first9=David|last10=Feng|first10=Changyong|last11=Aktas|first11=Mehmet K.|last12=Ayala-Parades|first12=Felix|last13=Baranchuk|first13=Adrian|last14=Dubuc|first14=Marc|last15=Haigney|first15=Mark|last16=Mazur|first16=Alexander|last17=McPherson|first17=Craig A.|last18=Mitchell|first18=L. 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 ===[[Beta blocker]]===
-:* First line therapy for the most of [[ventricular arrhythmia]] such as [[PVC]], [[VT]] due to safety and efficacy<ref name="ReiterReiffel1998">{{cite journal|last1=Reiter|first1=Michael J.|last2=Reiffel|first2=James A.|title=Importance of beta blockade in the therapy of serious ventricular arrhythmias|journal=The American Journal of Cardiology|volume=82|issue=4|year=1998|pages=9I–19I|issn=00029149|doi=10.1016/S0002-9149(98)00468-8}}</ref>
+:* First line therapy for the most of [[ventricular arrhythmia]] such as [[PVC]], [[VT]] because of safety and efficacy<ref name="ReiterReiffel1998">{{cite journal|last1=Reiter|first1=Michael J.|last2=Reiffel|first2=James A.|title=Importance of beta blockade in the therapy of serious ventricular arrhythmias|journal=The American Journal of Cardiology|volume=82|issue=4|year=1998|pages=9I–19I|issn=00029149|doi=10.1016/S0002-9149(98)00468-8}}</ref>
 :* Supression of [[ventricular arrhythmia]] in [[structurally normal heart]].
-:* Reduction of all-cause mortality and [[SCD]] in [[patients]] with [[heart failure]] with reduced [[EF]]<ref name="pmid10376614">{{cite journal |vauthors= |title=Effect of metoprolol CR/XL in chronic heart failure: Metoprolol CR/XL Randomised Intervention Trial in Congestive Heart Failure (MERIT-HF) |journal=Lancet |volume=353 |issue=9169 |pages=2001–7 |date=June 1999 |pmid=10376614 |doi= |url=}}</ref>
+:* Reducing all-cause mortality and [[SCD]] in [[patients]] with [[heart failure]] with reduced [[EF]]<ref name="pmid10376614">{{cite journal |vauthors= |title=Effect of metoprolol CR/XL in chronic heart failure: Metoprolol CR/XL Randomised Intervention Trial in Congestive Heart Failure (MERIT-HF) |journal=Lancet |volume=353 |issue=9169 |pages=2001–7 |date=June 1999 |pmid=10376614 |doi= |url=}}</ref>
-:* Reduction of [[mortality]] after [[MI]]
+:* Reducing [[mortality]] after [[MI]]
 :* Increased [[mortality]] and risk of [[cardiogenic shock]] after [[MI]] in the presence of >70 years of age, symptoms <12 hours [[ST-elevation MI]] [[patients]], [[systolic blood pressure ]]<120 mm Hg, [[heart rate ]]>110 beat/min <ref name="KontosDiercks2011">{{cite journal|last1=Kontos|first1=Michael C.|last2=Diercks|first2=Debra B.|last3=Ho|first3=P. Michael|last4=Wang|first4=Tracy Y.|last5=Chen|first5=Anita Y.|last6=Roe|first6=Matthew T.|title=Treatment and outcomes in patients with myocardial infarction treated with acute β-blocker therapy: Results from the American College of Cardiology’s NCDR®|journal=American Heart Journal|volume=161|issue=5|year=2011|pages=864–870|issn=00028703|doi=10.1016/j.ahj.2011.01.006}}</ref>
-:*Increased [[antiarrhythmic]] effect of membrane stabilizing drug in [[malignant]] [[VT]]<ref name="HirsowitzPodrid1986">{{cite journal|last1=Hirsowitz|first1=Geoffrey|last2=Podrid|first2=Philip J.|last3=Lampert|first3=Steven|last4=Stein|first4=Joseph|last5=Lown|first5=Bernard|title=The role of beta blocking agents as adjunct therapy to membrane stabilizing drugs in malignant ventricular arrhythmia|journal=American Heart Journal|volume=111|issue=5|year=1986|pages=852–860|issn=00028703|doi=10.1016/0002-8703(86)90633-2}}</ref>
+:*Increased [[antiarrhythmic]] effect of membrane stabilizing drug in [[malignant]] [[VT]].<ref name="HirsowitzPodrid1986">{{cite journal|last1=Hirsowitz|first1=Geoffrey|last2=Podrid|first2=Philip J.|last3=Lampert|first3=Steven|last4=Stein|first4=Joseph|last5=Lown|first5=Bernard|title=The role of beta blocking agents as adjunct therapy to membrane stabilizing drugs in malignant ventricular arrhythmia|journal=American Heart Journal|volume=111|issue=5|year=1986|pages=852–860|issn=00028703|doi=10.1016/0002-8703(86)90633-2}}</ref>
 :*[[Nadolol]], [[propranolol]]: first-line therapy for some [[cardiac]] channelopathies such as [[long QT syndrome]], [[catecholaminergic polymorphic ventricular tachycardia]]
@@ Line 43: / Line 46: @@
 * In [[patients]] with [[nonischemic cardiomyopathy]] ([[LVEF]]<40%), use of  [[amiodarone]] reduced the risk of [[SCD]] (with low quality of support of article), but there was NO benefit of using  [[amiodarone]] for [[secondary prevention]].<ref name="ClaroCandia2015">{{cite journal|last1=Claro|first1=Juan Carlos|last2=Candia|first2=Roberto|last3=Rada|first3=Gabriel|last4=Baraona|first4=Fernando|last5=Larrondo|first5=Francisco|last6=Letelier|first6=Luz M|title=Amiodarone versus other pharmacological interventions for prevention of sudden cardiac death|journal=Cochrane Database of Systematic Reviews|year=2015|issn=14651858|doi=10.1002/14651858.CD008093.pub2}}</ref>
-* Infused [[amiodarone]] during [[cardiopulmonary resucitation]] prevents recurrent [[VT]], [[VF]].<ref name="KudenchukCobb1999">{{cite journal|last1=Kudenchuk|first1=Peter J.|last2=Cobb|first2=Leonard A.|last3=Copass|first3=Michael K.|last4=Cummins|first4=Richard O.|last5=Doherty|first5=Alidene M.|last6=Fahrenbruch|first6=Carol E.|last7=Hallstrom|first7=Alfred P.|last8=Murray|first8=William A.|last9=Olsufka|first9=Michele|last10=Walsh|first10=Thomas|title=Amiodarone for Resuscitation after Out-of-Hospital Cardiac Arrest Due to Ventricular Fibrillation|journal=New England Journal of Medicine|volume=341|issue=12|year=1999|pages=871–878|issn=0028-4793|doi=10.1056/NEJM199909163411203}}</ref>
+* Infused [[amiodarone]] during [[cardiopulmonary resuscitation]] prevents recurrent [[VT]], [[VF]].<ref name="KudenchukCobb1999">{{cite journal|last1=Kudenchuk|first1=Peter J.|last2=Cobb|first2=Leonard A.|last3=Copass|first3=Michael K.|last4=Cummins|first4=Richard O.|last5=Doherty|first5=Alidene M.|last6=Fahrenbruch|first6=Carol E.|last7=Hallstrom|first7=Alfred P.|last8=Murray|first8=William A.|last9=Olsufka|first9=Michele|last10=Walsh|first10=Thomas|title=Amiodarone for Resuscitation after Out-of-Hospital Cardiac Arrest Due to Ventricular Fibrillation|journal=New England Journal of Medicine|volume=341|issue=12|year=1999|pages=871–878|issn=0028-4793|doi=10.1056/NEJM199909163411203}}</ref>
 * [[Amiodarone]] decreased risk of [[SCD]] and all-cause [[mortality ]] compared with [[betablocker]] or [[sotalol]].<ref name="ClaroCandia2015">{{cite journal|last1=Claro|first1=Juan Carlos|last2=Candia|first2=Roberto|last3=Rada|first3=Gabriel|last4=Baraona|first4=Fernando|last5=Larrondo|first5=Francisco|last6=Letelier|first6=Luz M|title=Amiodarone versus other pharmacological interventions for prevention of sudden cardiac death|journal=Cochrane Database of Systematic Reviews|year=2015|issn=14651858|doi=10.1002/14651858.CD008093.pub2}}</ref>
 *Chronic use of [[amiodarone]] has adverse effect on [[lung]], [[liver]], [[thyroid]], [[skin]], and [[nervous system]].<ref name="ClaroCandia2015">{{cite journal|last1=Claro|first1=Juan Carlos|last2=Candia|first2=Roberto|last3=Rada|first3=Gabriel|last4=Baraona|first4=Fernando|last5=Larrondo|first5=Francisco|last6=Letelier|first6=Luz M|title=Amiodarone versus other pharmacological interventions for prevention of sudden cardiac death|journal=Cochrane Database of Systematic Reviews|year=2015|issn=14651858|doi=10.1002/14651858.CD008093.pub2}}</ref>
@@ Line 50: / Line 53: @@
 * [[Sotalol]] may decrease [[defibrillation threshold]]  and should be avoided in patients with [[LVEF]]< 20% due to decompensation of [[heart failure]].<ref name="Page2000">{{cite journal|last1=Page|first1=Richard L|title=Effects of antiarrhythmic medication on implantable cardioverter-defibrillator function|journal=The American Journal of Cardiology|volume=85|issue=12|year=2000|pages=1481–1485|issn=00029149|doi=10.1016/S0002-9149(00)00799-2}}</ref>
-==[[ Calcium channel blocker]]==
+===[[ Calcium channel blocker]]===
 * [[Non-dihydropyridines calcium channel blockers]] have no role in the treatment of most [[ventricular arrhythmia]]s.
-* In [[patients]] with prior [[MI]] administration of intravenous [[verapamil]] for sustained [[VT]] has been associated with [[hemodynamic collapse ]].<ref name="BuxtonMarchlinski1987">{{cite journal|last1=Buxton|first1=Alfred E.|last2=Marchlinski|first2=Francis E.|last3=Doherty|first3=John U.|last4=Flores|first4=Belinda|last5=Josephson|first5=Mark E.|title=Hazards of intravenous verapamil for sustained ventricular tachycardia|journal=The American Journal of Cardiology|volume=59|issue=12|year=1987|pages=1107–1110|issn=00029149|doi=10.1016/0002-9149(87)90857-5}}</ref>
+* In [[patients]] with prior [[MI]], administration of intravenous [[verapamil]] for sustained [[VT]] has been associated with [[hemodynamic collapse ]].<ref name="BuxtonMarchlinski1987">{{cite journal|last1=Buxton|first1=Alfred E.|last2=Marchlinski|first2=Francis E.|last3=Doherty|first3=John U.|last4=Flores|first4=Belinda|last5=Josephson|first5=Mark E.|title=Hazards of intravenous verapamil for sustained ventricular tachycardia|journal=The American Journal of Cardiology|volume=59|issue=12|year=1987|pages=1107–1110|issn=00029149|doi=10.1016/0002-9149(87)90857-5}}</ref>
 * [[Verapamil]] and [[diltiazem]] can be used for suppression of some [[VT]] originated outflow tract.<ref name="GillWard1992">{{cite journal|last1=Gill|first1=Jaswinder S.|last2=Ward|first2=David E.|last3=Camm|first3=A. John|title=Comparison of Verapamil and Diltiazem in the Suppression of Idiopathic Ventricular Tachycardia|journal=Pacing and Clinical Electrophysiology|volume=15|issue=11|year=1992|pages=2122–2126|issn=0147-8389|doi=10.1111/j.1540-8159.1992.tb03033.x}}</ref>
 * Oral and intravenous [[verapamil ]] is effective for the treatment of idiopathic interfascicular reentrant left [[VT]] in [[patients]] with normal structurally [[heart]].<ref name="BadhwarScheinman2007">{{cite journal|last1=Badhwar|first1=Nitish|last2=Scheinman|first2=Melvin M.|title=Idiopathic Ventricular Tachycardia: Diagnosis and Management|journal=Current Problems in Cardiology|volume=32|issue=1|year=2007|pages=7–43|issn=01462806|doi=10.1016/j.cpcardiol.2006.10.002}}</ref>
-* [[Calcium channel blockers]]  should be avoided in [[heart failure]] reduced [[EF]].
+*[[Non-dihydropyridines]]  [[Calcium channel blockers]]  should be avoided for converting [[VT]] in [[heart failure]] reduced [[EF]].
-==[[Electrolytes]]==
-* Correction of [[hypokalemia]] and [[hypomagnesemia]] is helpful for preventing of [[ventricular arrhythmia]] in the setting of [[myocardial infarction]] or [[ diuretic]] therapy in [[heart failure]] [[patients]].<ref name="CooperDries1999">{{cite journal|last1=Cooper|first1=Howard A.|last2=Dries|first2=Daniel L.|last3=Davis|first3=C. E.|last4=Shen|first4=Yuan Li|last5=Domanski|first5=Michael J.|title=Diuretics and Risk of Arrhythmic Death in Patients With Left Ventricular Dysfunction|journal=Circulation|volume=100|issue=12|year=1999|pages=1311–1315|issn=0009-7322|doi=10.1161/01.CIR.100.12.1311}}</ref>
-* [[Duiretic therapy]] in [[heart failure]] [[patients]] may lead to [[hypokalemia]] or [[hypomagnesemia]].<ref name="CooperDries1999">{{cite journal|last1=Cooper|first1=Howard A.|last2=Dries|first2=Daniel L.|last3=Davis|first3=C. E.|last4=Shen|first4=Yuan Li|last5=Domanski|first5=Michael J.|title=Diuretics and Risk of Arrhythmic Death in Patients With Left Ventricular Dysfunction|journal=Circulation|volume=100|issue=12|year=1999|pages=1311–1315|issn=0009-7322|doi=10.1161/01.CIR.100.12.1311}}</ref>
-* [[Hypokalemia]] and [[hypomagnesemia]] may cause [[ventricular arrhythmia]] during acute [[myocardial infarction]] .
-* [[Hypokalemia]] and [[hypomagnesemia]] may increase the risk of [[torsades de pointes]] in the setting of some [[medications]] or [[long QT syndrome]].<ref name="YanAntzelevitch1998">{{cite journal|last1=Yan|first1=Gan-Xin|last2=Antzelevitch|first2=Charles|title=Cellular Basis for the Normal T Wave and the Electrocardiographic Manifestations of the Long-QT Syndrome|journal=Circulation|volume=98|issue=18|year=1998|pages=1928–1936|issn=0009-7322|doi=10.1161/01.CIR.98.18.1928}}</ref>
-* Administration of intravenous [[magnesium]] in the setting of [[torsades de pointes]] as the first line therapy is recommended.<ref name="TzivoniBanai1988">{{cite journal|last1=Tzivoni|first1=D|last2=Banai|first2=S|last3=Schuger|first3=C|last4=Benhorin|first4=J|last5=Keren|first5=A|last6=Gottlieb|first6=S|last7=Stern|first7=S|title=Treatment of torsade de pointes with magnesium sulfate.|journal=Circulation|volume=77|issue=2|year=1988|pages=392–397|issn=0009-7322|doi=10.1161/01.CIR.77.2.392}}</ref>
-* [[Potassium]] level should be kept 4.5 mmol/L and 5 mmol/L to prevent [[ventricular arrhythmia]] or [[sudden cardiac death]].<ref name="CohnKowey2000">{{cite journal|last1=Cohn|first1=Jay N.|last2=Kowey|first2=Peter R.|last3=Whelton|first3=Paul K.|last4=Prisant|first4=L. Michael|title=New Guidelines for Potassium Replacement in Clinical Practice|journal=Archives of Internal Medicine|volume=160|issue=16|year=2000|pages=2429|issn=0003-9926|doi=10.1001/archinte.160.16.2429}}</ref>
-* In [[patients]] with acute [[MI]] maintaining [[potassium]] level between 3.5 mmol/L and 4.5 mmol/L was associated with lower rate of [[death]] <ref name="GoyalSpertus2012">{{cite journal|last1=Goyal|first1=Abhinav|last2=Spertus|first2=John A.|last3=Gosch|first3=Kensey|last4=Venkitachalam|first4=Lakshmi|last5=Jones|first5=Philip G.|last6=Van den Berghe|first6=Greet|last7=Kosiborod|first7=Mikhail|title=Serum Potassium Levels and Mortality in Acute Myocardial Infarction|journal=JAMA|volume=307|issue=2|year=2012|pages=157|issn=0098-7484|doi=10.1001/jama.2011.1967}}</ref>
-*Early administration of  intravenous [[magnesium]] in  [[patients]] with acute [[STEMI]] has not effect on short term [[mortality]].<ref name="Antman2002">{{cite journal|last1=Antman|first1=Elliott M|title=Early administration of intravenous magnesium to high-risk patients with acute myocardial infarction in the Magnesium in Coronaries (MAGIC) Trial: a randomised controlled trial|journal=The Lancet|volume=360|issue=9341|year=2002|pages=1189–1196|issn=01406736|doi=10.1016/S0140-6736(02)11278-5}}</ref>
-==[[Fatty acids]], [[Lipids]]==
-* The role of  [[N-3 poly-unsaturated fatty acids]] and [[statin]] therapies for preventing of [[SCD]] has been proposed by stabilizing  bilipid [[myocyte membrane]] for maintaining [[electrolyte]] gradients. <ref name="LeafKang2003">{{cite journal|last1=Leaf|first1=Alexander|last2=Kang|first2=Jing X.|last3=Xiao|first3=Yong-Fu|last4=Billman|first4=George E.|title=Clinical Prevention of Sudden Cardiac Death by n-3 Polyunsaturated Fatty Acids and Mechanism of Prevention of Arrhythmias by n-3 Fish Oils|journal=Circulation|volume=107|issue=21|year=2003|pages=2646–2652|issn=0009-7322|doi=10.1161/01.CIR.0000069566.78305.33}}</ref>
-* Among [[patients]] with recent [[MI]] using  [[fish oil]] 1 g/d reduced [[SCD]] and [[mortality]].<ref name="MarchioliBarzi2002">{{cite journal|last1=Marchioli|first1=Roberto|last2=Barzi|first2=Federica|last3=Bomba|first3=Elena|last4=Chieffo|first4=Carmine|last5=Di Gregorio|first5=Domenico|last6=Di Mascio|first6=Rocco|last7=Franzosi|first7=Maria Grazia|last8=Geraci|first8=Enrico|last9=Levantesi|first9=Giacomo|last10=Maggioni|first10=Aldo Pietro|last11=Mantini|first11=Loredana|last12=Marfisi|first12=Rosa Maria|last13=Mastrogiuseppe|first13=G.|last14=Mininni|first14=Nicola|last15=Nicolosi|first15=Gian Luigi|last16=Santini|first16=Massimo|last17=Schweiger|first17=Carlo|last18=Tavazzi|first18=Luigi|last19=Tognoni|first19=Gianni|last20=Tucci|first20=Corrado|last21=Valagussa|first21=Franco|title=Early Protection Against Sudden Death by n-3 Polyunsaturated Fatty Acids After Myocardial Infarction|journal=Circulation|volume=105|issue=16|year=2002|pages=1897–1903|issn=0009-7322|doi=10.1161/01.CIR.0000014682.14181.F2}}</ref>
-* Another clinical trial showed using [[n–3 Fatty Acids]] was not effective in the reduction of the [[cardiovascular ]] event in high risk [[patients]].<ref>{{cite journal|title=n–3 Fatty Acids and Cardiovascular Outcomes in Patients with Dysglycemia|journal=New England Journal of Medicine|volume=367|issue=4|year=2012|pages=309–318|issn=0028-4793|doi=10.1056/NEJMoa1203859}}</ref>
-* [[Statin]] clearly reduced [[mortality]] and [[SCD]] associated [[ischemic heart disease]].<ref name="LaRosaHe1999">{{cite journal|last1=LaRosa|first1=John C.|last2=He|first2=Jiang|last3=Vupputuri|first3=Suma|title=Effect of Statins on Risk of Coronary Disease|journal=JAMA|volume=282|issue=24|year=1999|pages=2340|issn=0098-7484|doi=10.1001/jama.282.24.2340}}</ref>
-* Supressing [[plaque rupture]] or direct [[cardiovascular]] effect are two mechanisms of decrease [[ventricular arrhythmia]] by [[statin]].
-* [[Statin]]  is effective in prevention of  [[ventricular arrhythmia]] in [[ischemic heart disease]], however, the role of [[statine]] in reducing [[SCD]] in [[heart failure]] [[ICD]] [[patients]] is not clearly explained.<ref name="pmid18757089">{{cite journal |vauthors=Tavazzi L, Maggioni AP, Marchioli R, Barlera S, Franzosi MG, Latini R, Lucci D, Nicolosi GL, Porcu M, Tognoni G |title=Effect of rosuvastatin in patients with chronic heart failure (the GISSI-HF trial): a randomised, double-blind, placebo-controlled trial |journal=Lancet |volume=372 |issue=9645 |pages=1231–9 |date=October 2008 |pmid=18757089 |doi=10.1016/S0140-6736(08)61240-4 |url=}}</ref>
@@ Line 207: / Line 190: @@
 |-
 | style="padding: 0 5px; background: #F5F5F5; text-align: left;" | [[Propafenone]] (IC), PO: Immediate release 150–300 mg q 8 h, Extended release 225–425 mg q 12 h
-| style="padding: 0 5px; background: #F5F5F5; text-align: left;" | [[VT]], [[PVC]] (in the absence of structural heart disease]]
+| style="padding: 0 5px; background: #F5F5F5; text-align: left;" | [[VT]], [[PVC]] (in the absence of [[structural heart disease]])
 | style="padding: 0 5px; background: #F5F5F5; text-align: left;" |[[INa]], [[IKr]], [[IKur]], [[ Beta receptor]], [[Alpha recept]]
 | style="padding: 0 5px; background: #F5F5F5; text-align: left;" | Prolonged [[PR]] interval, prolonged [[QRS]] duration, increased [[defibrillation threshold]]
@@ Line 225: / Line 208: @@
 | style="padding: 0 5px; background: #F5F5F5; text-align: left;" | [[QRS prolongation]], [[QTc prolongation]], increased [[defibrillation threshold]]
 | style="padding: 0 5px; background: #F5F5F5; text-align: left;" | Metabolism: [[hepatic]]
-| style="padding: 0 5px; background: #F5F5F5; text-align: left;" | [[Syncope], [[ torsades de pointes]], [[AV]] block, [[dizziness]], [[diarrhea]], [[nausea]], [[esophagitis]], [[emesis]], [[tinnitus]], [[blurred vision]], [[rash]], [[weakness]], [[tremor]], [[blood dyscrasias]]
+| style="padding: 0 5px; background: #F5F5F5; text-align: left;" | [[Syncope]], [[ torsades de pointes]], [[AV]] block, [[dizziness]], [[diarrhea]], [[nausea]], [[esophagitis]], [[emesis]], [[tinnitus]], [[blurred vision]], [[rash]], [[weakness]], [[tremor]], [[blood dyscrasias]]
 |-
 | style="padding: 0 5px; background: #F5F5F5; text-align: left;" | [[Ranolazine]] (not classified), PO: 500–1000 mg q 12 h
@@ Line 249: / Line 232: @@
 |}
 {{clear}}
+==[[Electrolytes]]==
+* Correction of [[hypokalemia]] and [[hypomagnesemia]] is helpful for preventing of [[ventricular arrhythmia]] in the setting of [[myocardial infarction]] or [[ diuretic]] therapy in [[heart failure]] [[patients]].<ref name="CooperDries1999">{{cite journal|last1=Cooper|first1=Howard A.|last2=Dries|first2=Daniel L.|last3=Davis|first3=C. E.|last4=Shen|first4=Yuan Li|last5=Domanski|first5=Michael J.|title=Diuretics and Risk of Arrhythmic Death in Patients With Left Ventricular Dysfunction|journal=Circulation|volume=100|issue=12|year=1999|pages=1311–1315|issn=0009-7322|doi=10.1161/01.CIR.100.12.1311}}</ref>
+* [[Diuretic therapy]] in [[heart failure]] [[patients]] may lead to [[hypokalemia]] or [[hypomagnesemia]].<ref name="CooperDries1999">{{cite journal|last1=Cooper|first1=Howard A.|last2=Dries|first2=Daniel L.|last3=Davis|first3=C. E.|last4=Shen|first4=Yuan Li|last5=Domanski|first5=Michael J.|title=Diuretics and Risk of Arrhythmic Death in Patients With Left Ventricular Dysfunction|journal=Circulation|volume=100|issue=12|year=1999|pages=1311–1315|issn=0009-7322|doi=10.1161/01.CIR.100.12.1311}}</ref>
+* [[Hypokalemia]] and [[hypomagnesemia]] may cause [[ventricular arrhythmia]] during acute [[myocardial infarction]] .
+* [[Hypokalemia]] and [[hypomagnesemia]] may increase the risk of [[torsades de pointes]] in patients with use of some  [[medications]] with [[QTc prolongation ]] effect or [[long QT syndrome]].<ref name="YanAntzelevitch1998">{{cite journal|last1=Yan|first1=Gan-Xin|last2=Antzelevitch|first2=Charles|title=Cellular Basis for the Normal T Wave and the Electrocardiographic Manifestations of the Long-QT Syndrome|journal=Circulation|volume=98|issue=18|year=1998|pages=1928–1936|issn=0009-7322|doi=10.1161/01.CIR.98.18.1928}}</ref>
+* Administration of intravenous [[magnesium]] in the setting of [[torsades de pointes]] as the first line therapy is recommended.<ref name="TzivoniBanai1988">{{cite journal|last1=Tzivoni|first1=D|last2=Banai|first2=S|last3=Schuger|first3=C|last4=Benhorin|first4=J|last5=Keren|first5=A|last6=Gottlieb|first6=S|last7=Stern|first7=S|title=Treatment of torsade de pointes with magnesium sulfate.|journal=Circulation|volume=77|issue=2|year=1988|pages=392–397|issn=0009-7322|doi=10.1161/01.CIR.77.2.392}}</ref>
+* [[Potassium]] level should be kept 4.5 mmol/L and 5 mmol/L to prevent [[ventricular arrhythmia]] or [[sudden cardiac death]].<ref name="CohnKowey2000">{{cite journal|last1=Cohn|first1=Jay N.|last2=Kowey|first2=Peter R.|last3=Whelton|first3=Paul K.|last4=Prisant|first4=L. Michael|title=New Guidelines for Potassium Replacement in Clinical Practice|journal=Archives of Internal Medicine|volume=160|issue=16|year=2000|pages=2429|issn=0003-9926|doi=10.1001/archinte.160.16.2429}}</ref>
+* In [[patients]] with acute [[MI]] maintaining [[potassium]] level between 3.5 mmol/L and 4.5 mmol/L was associated with lower rate of [[death]] <ref name="GoyalSpertus2012">{{cite journal|last1=Goyal|first1=Abhinav|last2=Spertus|first2=John A.|last3=Gosch|first3=Kensey|last4=Venkitachalam|first4=Lakshmi|last5=Jones|first5=Philip G.|last6=Van den Berghe|first6=Greet|last7=Kosiborod|first7=Mikhail|title=Serum Potassium Levels and Mortality in Acute Myocardial Infarction|journal=JAMA|volume=307|issue=2|year=2012|pages=157|issn=0098-7484|doi=10.1001/jama.2011.1967}}</ref>
+*Early administration of  intravenous [[magnesium]] in  [[patients]] with acute [[STEMI]] has not effect on short term [[mortality]].<ref name="Antman2002">{{cite journal|last1=Antman|first1=Elliott M|title=Early administration of intravenous magnesium to high-risk patients with acute myocardial infarction in the Magnesium in Coronaries (MAGIC) Trial: a randomised controlled trial|journal=The Lancet|volume=360|issue=9341|year=2002|pages=1189–1196|issn=01406736|doi=10.1016/S0140-6736(02)11278-5}}</ref>
+==[[Fatty acids]], [[Lipids]]==
+* The role of  [[N-3 poly-unsaturated fatty acids]] and [[statin]] therapies for preventing of [[SCD]] has been proposed by stabilizing  bilipid [[myocyte membrane]] for maintaining [[electrolyte]] gradients. <ref name="LeafKang2003">{{cite journal|last1=Leaf|first1=Alexander|last2=Kang|first2=Jing X.|last3=Xiao|first3=Yong-Fu|last4=Billman|first4=George E.|title=Clinical Prevention of Sudden Cardiac Death by n-3 Polyunsaturated Fatty Acids and Mechanism of Prevention of Arrhythmias by n-3 Fish Oils|journal=Circulation|volume=107|issue=21|year=2003|pages=2646–2652|issn=0009-7322|doi=10.1161/01.CIR.0000069566.78305.33}}</ref>
+* Among [[patients]] with recent [[MI]] using  [[fish oil]] 1 g/d reduced [[SCD]] and [[mortality]].<ref name="MarchioliBarzi2002">{{cite journal|last1=Marchioli|first1=Roberto|last2=Barzi|first2=Federica|last3=Bomba|first3=Elena|last4=Chieffo|first4=Carmine|last5=Di Gregorio|first5=Domenico|last6=Di Mascio|first6=Rocco|last7=Franzosi|first7=Maria Grazia|last8=Geraci|first8=Enrico|last9=Levantesi|first9=Giacomo|last10=Maggioni|first10=Aldo Pietro|last11=Mantini|first11=Loredana|last12=Marfisi|first12=Rosa Maria|last13=Mastrogiuseppe|first13=G.|last14=Mininni|first14=Nicola|last15=Nicolosi|first15=Gian Luigi|last16=Santini|first16=Massimo|last17=Schweiger|first17=Carlo|last18=Tavazzi|first18=Luigi|last19=Tognoni|first19=Gianni|last20=Tucci|first20=Corrado|last21=Valagussa|first21=Franco|title=Early Protection Against Sudden Death by n-3 Polyunsaturated Fatty Acids After Myocardial Infarction|journal=Circulation|volume=105|issue=16|year=2002|pages=1897–1903|issn=0009-7322|doi=10.1161/01.CIR.0000014682.14181.F2}}</ref>
+* Another clinical trial showed using [[n–3 Fatty Acids]] was not effective in the reduction of the [[cardiovascular ]] event in high risk [[patients]].<ref>{{cite journal|title=n–3 Fatty Acids and Cardiovascular Outcomes in Patients with Dysglycemia|journal=New England Journal of Medicine|volume=367|issue=4|year=2012|pages=309–318|issn=0028-4793|doi=10.1056/NEJMoa1203859}}</ref>
+* [[Statin]] clearly reduced [[mortality]] and [[SCD]] associated [[ischemic heart disease]].<ref name="LaRosaHe1999">{{cite journal|last1=LaRosa|first1=John C.|last2=He|first2=Jiang|last3=Vupputuri|first3=Suma|title=Effect of Statins on Risk of Coronary Disease|journal=JAMA|volume=282|issue=24|year=1999|pages=2340|issn=0098-7484|doi=10.1001/jama.282.24.2340}}</ref>
+* Supressing [[plaque rupture]] or direct [[cardiovascular]] effect are two mechanisms of decrease [[ventricular arrhythmia]] by [[statin]].
+* [[Statin]]  is effective in prevention of  [[ventricular arrhythmia]] in [[ischemic heart disease]], however, the role of [[statine]] in reducing [[SCD]] in [[heart failure]] [[ICD]] [[patients]] is not clearly explained.<ref name="pmid18757089">{{cite journal |vauthors=Tavazzi L, Maggioni AP, Marchioli R, Barlera S, Franzosi MG, Latini R, Lucci D, Nicolosi GL, Porcu M, Tognoni G |title=Effect of rosuvastatin in patients with chronic heart failure (the GISSI-HF trial): a randomised, double-blind, placebo-controlled trial |journal=Lancet |volume=372 |issue=9645 |pages=1231–9 |date=October 2008 |pmid=18757089 |doi=10.1016/S0140-6736(08)61240-4 |url=}}</ref>
 ==Specific recommendation==
 * The mainstay of therapy in [[heart failure]] reduced  [[EF]] for prevention of [[SCD]] and [[ventricular arrhythmia]] is the following:
-* [[Beta blocker]]s are benefit for preventing of [[SCD]] by reducing [[sympathetic activity]] and [[ myocardial]] [[oxygen]] demand or countering [[electrical excitability]].
+* [[Beta blocker]]s with benefit for preventing of [[SCD]] by reducing [[sympathetic activity]] and [[ myocardial]] [[oxygen]] demand or countering [[electrical excitability]].
-* [[Angiotensin-converting enzyme inhibitors]], [[angiotensin-receptor blockers]] decreasing [[myocardial oxygen demand]], [[preload]], [[afterload]], prevention  the formation of [[angiotensin II]], and slowing the process of [[ventricular remodeling]] and [[fibrosis]].<ref name="pmid2057035">{{cite journal |vauthors=Cohn JN, Johnson G, Ziesche S, Cobb F, Francis G, Tristani F, Smith R, Dunkman WB, Loeb H, Wong M |title=A comparison of enalapril with hydralazine-isosorbide dinitrate in the treatment of chronic congestive heart failure |journal=N Engl J Med |volume=325 |issue=5 |pages=303–10 |date=August 1991 |pmid=2057035 |doi=10.1056/NEJM199108013250502 |url=}}</ref>
+* [[Angiotensin-converting enzyme inhibitors]], or [[angiotensin-receptor blockers]]  is effective by reducing  [[myocardial oxygen demand]], [[preload]], [[afterload]], prevention  the formation of [[angiotensin II]], and slowing the process of [[ventricular remodeling]] and [[fibrosis]].<ref name="pmid2057035">{{cite journal |vauthors=Cohn JN, Johnson G, Ziesche S, Cobb F, Francis G, Tristani F, Smith R, Dunkman WB, Loeb H, Wong M |title=A comparison of enalapril with hydralazine-isosorbide dinitrate in the treatment of chronic congestive heart failure |journal=N Engl J Med |volume=325 |issue=5 |pages=303–10 |date=August 1991 |pmid=2057035 |doi=10.1056/NEJM199108013250502 |url=}}</ref>
 * [[Mineralocorticoid receptor antagonists]] decrease [[potassium loss]], [[decrease fibrosis]], and increase the [[myocardial]] uptake of [[norepinephrine]].
 *  Chronic [[Beta blocker]]s therapy in [[heart failure]] reduced [[EF]] was associated with reduced [[SCD]], [[ventricular arrhythmia]] and all cause [[mortality]].
 *[[Bisoprolol]], [[carvedilol]], [[sustained-release metoprolol succinate]] decrease [[mortality]] in [[patients]] with [[heart failure]] reduced [[EF]].<ref name="pmid10023943">{{cite journal |vauthors= |title=The Cardiac Insufficiency Bisoprolol Study II (CIBIS-II): a randomised trial |journal=Lancet |volume=353 |issue=9146 |pages=9–13 |date=January 1999 |pmid=10023943 |doi= |url=}}</ref><ref name="pmid11356434">{{cite journal |vauthors=Dargie HJ |title=Effect of carvedilol on outcome after myocardial infarction in patients with left-ventricular dysfunction: the CAPRICORN randomised trial |journal=Lancet |volume=357 |issue=9266 |pages=1385–90 |date=May 2001 |pmid=11356434 |doi=10.1016/s0140-6736(00)04560-8 |url=}}</ref><ref name="pmid10714728">{{cite journal |vauthors=Hjalmarson A, Goldstein S, Fagerberg B, Wedel H, Waagstein F, Kjekshus J, Wikstrand J, El Allaf D, Vítovec J, Aldershvile J, Halinen M, Dietz R, Neuhaus KL, Jánosi A, Thorgeirsson G, Dunselman PH, Gullestad L, Kuch J, Herlitz J, Rickenbacher P, Ball S, Gottlieb S, Deedwania P |title=Effects of controlled-release metoprolol on total mortality, hospitalizations, and well-being in patients with heart failure: the Metoprolol CR/XL Randomized Intervention Trial in congestive heart failure (MERIT-HF). MERIT-HF Study Group |journal=JAMA |volume=283 |issue=10 |pages=1295–302 |date=March 2000 |pmid=10714728 |doi=10.1001/jama.283.10.1295 |url=}}</ref>
 * [[ACEI]] and [[mineralocorticoid-receptor antagonists]] ([[spironolactone]], [[eplerenone]]) reduce [[mortality]] and [[SCD]] in [[patients]] with severe [[heart failure]]. <ref name="pmid10471456">{{cite journal |vauthors=Pitt B, Zannad F, Remme WJ, Cody R, Castaigne A, Perez A, Palensky J, Wittes J |title=The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators |journal=N Engl J Med |volume=341 |issue=10 |pages=709–17 |date=September 1999 |pmid=10471456 |doi=10.1056/NEJM199909023411001 |url=}}</ref>
+==Management of  [[patients]] with Polymorphic [[Ventricular arrhythmia]]==
-===2017 ACC/AHA/HRS Guideline for management of [[ventricular tachycardia]]===
+{{Family tree/start}}
-<ref name="Al-KhatibStevenson2018">{{cite journal|last1=Al-Khatib|first1=Sana M.|last2=Stevenson|first2=William G.|last3=Ackerman|first3=Michael J.|last4=Bryant|first4=William J.|last5=Callans|first5=David J.|last6=Curtis|first6=Anne B.|last7=Deal|first7=Barbara J.|last8=Dickfeld|first8=Timm|last9=Field|first9=Michael E.|last10=Fonarow|first10=Gregg C.|last11=Gillis|first11=Anne M.|last12=Granger|first12=Christopher B.|last13=Hammill|first13=Stephen C.|last14=Hlatky|first14=Mark A.|last15=Joglar|first15=José A.|last16=Kay|first16=G. Neal|last17=Matlock|first17=Daniel D.|last18=Myerburg|first18=Robert J.|last19=Page|first19=Richard L.|title=2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death|journal=Circulation|volume=138|issue=13|year=2018|issn=0009-7322|doi=10.1161/CIR.0000000000000549}}</ref>
+{{Family tree | | | | A01 | | | |A01= Polymorphic [[Ventricular arrhythmia]]}}
+{{Family tree | | | | |!| | | | | }}
+{{Family tree | | | | B01 | | | |B01= [[Underlying etiology]]}}
+{{Family tree | |,|-|-|+|-|-|-|v|-|-|-|v|-|-|-|-|-|-|-|-|-|-|.| | | | | | | |}}
+{{Family tree | C0| | C3| | C02 | |C4 | | | | | | | |C5 | | | | | | | | | C3=External precipitating factors| C0=Acute [[ischemia]]| C02= Polymorphic [[Ventricular Arrhythmia]] triggered by unifocal [[PVC]]|C4=[[Acquired long QT]]|C5=Primary [[electrical disease]]}}
+{{Family tree |!| | | | | |!| | | |!| | |!| | | | | |,|-|-|-|+|-|-|-|.| | | | |}}
+{{Family tree | b1| | b2| |b3 | | |b4 | | | | h1| |h2 | |h3 | | | | |b1= Approach to [[STEMI]] | |b3=
+[[Catheter ablation]] (Class IIa)
+*[[Quinidine]] (Class IIb)|b4=Remove [[precipitating]] factors (Class I)
+*[[Mg]]++/[[K]]+ i.v.(Class I)
+*[[Isoproterenol]] (Class I)
+*[[Pacing]] (Class I)|h1=[[Brugada]], [[Early repolarization syndrome]]|h2=Idiopathic [[VF]]|h3=[[Long QT]], [[CPVT]]|b2=Treatment of underlying [[condition]] (Class I)}}
+{{Family tree | | | | | | |:| | | |:| | | |!| | | | |!| | | |!| | | |!| | | |}}
+{{Family tree | | | | | j1| | | |j1 | | j1| | |m1 | |m2 | |m3 | | | | | | | | |j1=[[Recurrent]] [[Ventricular arrhythmia]] | m1=[[Isoproterenol]] (Class IIa)
+*[[Quinidine]] (Class IIa)
+*[[Catheter ablation]] (Class IIa)|m2=[[Isoproterenol]] (Class IIa)
+*[[Quinidine]] (Class IIa)
+*[[Verapamil]] (Class IIa
+*[[Catheter ablation]] of [[PVC]] triggers (Class IIa)|m3=[[Beta-blocker]] (Class I)
+*[[Pacing]] (Class I)
+*[[Mg]]++/[[K]]+ i.v (Class I)
+*[[Antiarrhythmic]] drugs according to underlying [[disease]] (Class 2a)
+*[[Autonomic modulation]] (Class 2a)}}
+{{Family tree | | | | | | |!| | | |!| | | |!| | | | |!| | | |!| | | |!| | | |}}
+{{Family tree | | | | | | |n1 | |n1 | |n1 | | |n2 | |n2 | | n2| | | | | | | | | | | | n1=Deep [[sedation]]/ [[intubation]] (Class IIa)
+*[[Mechanical circulatory support]] (Class IIb)|n2= Recurrent [[ventricular arrhythmia]]}}
+{{Family tree | | | | | | | | | | | | | | | | | | | |!| | | |!| | | |!| | | |}}
+{{Family tree | | | | | | | | | | | | | | | | | | |m1 | |m1 | | m1| | | | | | | | | | | | m1=Deep [[sedation]]/ [[intubation]] (Class IIa)
+*[[Mechanical circulatory support]] (Class IIb)}}
+{{Family tree | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | }}
+{{Family tree | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | |}}
+{{Family tree/end}}
+{|
+! colspan="2" style="background: PapayaWhip;" align="center" + |The above algorithm adopted from 2022 ESC Guideline<ref name="pmid36017572">{{cite journal |vauthors=Zeppenfeld K, Tfelt-Hansen J, de Riva M, Winkel BG, Behr ER, Blom NA, Charron P, Corrado D, Dagres N, de Chillou C, Eckardt L, Friede T, Haugaa KH, Hocini M, Lambiase PD, Marijon E, Merino JL, Peichl P, Priori SG, Reichlin T, Schulz-Menger J, Sticherling C, Tzeis S, Verstrael A, Volterrani M |title=2022 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death |journal=Eur Heart J |volume= |issue= |pages= |date=August 2022 |pmid=36017572 |doi=10.1093/eurheartj/ehac262 |url=}}</ref>
+|-
+|}
+==Management of sustained monomorphic [[ventricular tachycardia]]==
+{| style="cellpadding=0; cellspacing= 0; width: 600px;"
+|-
+| style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF;" align=center |'''Recommendations for acute management of sustained VT'''
+|-
+|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left | ''' DC cardiovertion ([[ESC guidelines classification scheme|Class I, Level of Evidence B]]):'''
+|-
+|style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align=left|
+❑ [[DC cardioversion]] is recommended as the first-line therapy for [[hemodynamically]] not-tolerated [[sustained monomorphic ventricular tachycardia]]
+|-
+|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |'''DC cardiovertion ([[ESC guidelines classification scheme|Class I, Level of Evidence C]]) :'''
+|-
+|style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align=left|
+❑ [[DC cardioversion]] is recommended as the first-line treatment for [[patients]] presenting with tolerated [[sustained monomorphic VT]] when  [[anesthetic]]/[[sedation]] risk is low
+|-
+|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |'''Supraventricular tachycardia  ([[ESC guidelines classification scheme|Class IIa, Level of Evidence C]])'''
+|-
+|style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align=left|
+❑ In [[patients]] presenting with a regular hemodynamically tolerated wide [[QRS]] complex tachycardia suspected for [[supraventricular tachycardia]], administration of [[adenosine]] or [[vagal maneuvers]] should be considered<br>
+|-
+|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |'''Procainamide  ([[ESC guidelines classification scheme|Class IIa, Level of Evidence B]])'''
+|-
+|style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align=left|
+❑In [[patients]] presenting with a hemodynamically tolerated [[sustained monomorphic VT]] and presence of [[structural heart disease]], intravenous [[procainamide]] should be considered
+|-
+|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |'''Flecainide, ajmaline, sotalol ([[ESC guidelines classification scheme|Class IIb, Level of Evidence B]])'''
+|-
+|style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align=left|
+❑In [[patients]] presenting with a hemodynamically tolerated sustained [[monomorphic VT]] in the absence of significant [[structural heart disease]], [[flecainide]], [[ajmaline]], or [[sotalol]] may be considered
+|-
+|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |'''Verapamil ([[ESC guidelines classification scheme|Class III, Level of Evidence B]])'''
+|-
+|style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align=left|
+❑Intravenous [[verapamil]] is not recommended in wide [[QRS]] complex tachycardia of unknown mechanism
+|-
+|}
+{|
+! colspan="2" style="background: PapayaWhip;" align="center" + |The above table adopted from 2022 ESC Guideline<ref name="pmid36017572">{{cite journal |vauthors=Zeppenfeld K, Tfelt-Hansen J, de Riva M, Winkel BG, Behr ER, Blom NA, Charron P, Corrado D, Dagres N, de Chillou C, Eckardt L, Friede T, Haugaa KH, Hocini M, Lambiase PD, Marijon E, Merino JL, Peichl P, Priori SG, Reichlin T, Schulz-Menger J, Sticherling C, Tzeis S, Verstrael A, Volterrani M |title=2022 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death |journal=Eur Heart J |volume= |issue= |pages= |date=August 2022 |pmid=36017572 |doi=10.1093/eurheartj/ehac262 |url=}}</ref>
+|-
+|}
+==Management of electrical storm==
+{| style="cellpadding=0; cellspacing= 0; width: 800px;"
+|-
+| style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF;" align=center |'''Recommendations for management of electrical storm'''
+|-
+|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left | '''Sedation  ([[ESC guidelines classification scheme|Class I, Level of Evidence C]]):'''
+|-
+|style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align=left|
+❑ Mild to moderate [[sedation]] is recommended in [[patients]] with the [[electrical storm]] to reduce [[psychological]] distress and reduce [[sympathetic]] tone
+|-
+|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |'''Strucrural heart disease ([[ESC guidelines classification scheme|Class I, Level of Evidence B]]) :'''
+|-
+|style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align=left|
+❑ [[Antiarrhythmic]] therapy with [[beta-blockers]] (non-selective preferred) in combination with intravenous [[amiodarone]] is recommended in [[patients]] with [[structural heart disease]] and [[electrical storm]] unless contraindicated<br>
+❑[[Catheter ablation]] is recommended in [[patients]] presenting with incessant [[VT]] or [[electrical storm]] due to sustained monomorphic [[VT]] refractory to [[antiarrhythmic]] drugs<br>
+|-
+|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |'''Torsades depointes  ([[ESC guidelines classification scheme|Class I, Level of Evidence C]])'''
+|-
+|style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align=left|
+❑ Intravenous [[magnesium]] with supplementation of [[potassium]] is recommended in [[patients]] with [[TdP]]<br>
+❑[[Isoproterenol]] or [[transvenous pacing]] to increase heart rate is recommended in patients with acquired [[LQT]] syndrome and recurrent [[TdP]] despite correction of precipitating [[conditions]] and [[magnesium]]<br>
+|-
+|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |'''Procainamide  ([[ESC guidelines classification scheme|Class IIa, Level of Evidence B]])'''
+|-
+|style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align=left|
+❑In [[patients]] presenting with a hemodynamically tolerated [[sustained monomorphic VT]] and presence of [[structural heart disease]], intravenous [[procainamide]] should be considered
+|-
+|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |'''Intubation ([[ESC guidelines classification scheme|Class IIa, Level of Evidence C]])'''
+|-
+|style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align=left|
+❑Deep [[sedation]]/[[intubation]] should be considered in [[patients]] with an intractable [[electrical storm]] non-responsive [[drug]] treatment<br>
+❑[[Catheter ablation]] should be considered in [[patients]] with recurrent episodes of [[VT]]/[[VF]] triggered by a similar [[PVC]], refractory to medical treatment
+or [[coronary revascularization]]<br>
+|-
+|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |''' [[Quinidine]] ([[ESC guidelines classification scheme|Class IIb, Level of Evidence C]])'''
+|-
+|style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align=left|
+❑[[Quinidine]] may be considered in [[patients]] with [[coronary artery disease]] and [[electrical storm]] due to recurrent [[VT]] refractory to other [[antiarrhythmic drugs]]
+|-
+|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |'''Refractory electerical storm ([[ESC guidelines classification scheme|Class IIb, Level of Evidence C]])'''
+|-
+|style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align=left|
+❑[[Autonomic modulation]] may be considered in [[patients]] with [[electrical storm]] refractory to medical therapy and in whom [[catheter ablation]] is
+ineffective or not possible <br>
+❑ [[Mechanical circulatory support]] may be considered in the management of drug-refractory [[electrical storm]] and [[cardiogenic
+shock]]<br>
+|-
+|}
+{|
+! colspan="2" style="background: PapayaWhip;" align="center" + |The above table adopted from 2022 ESC Guideline<ref name="pmid36017572">{{cite journal |vauthors=Zeppenfeld K, Tfelt-Hansen J, de Riva M, Winkel BG, Behr ER, Blom NA, Charron P, Corrado D, Dagres N, de Chillou C, Eckardt L, Friede T, Haugaa KH, Hocini M, Lambiase PD, Marijon E, Merino JL, Peichl P, Priori SG, Reichlin T, Schulz-Menger J, Sticherling C, Tzeis S, Verstrael A, Volterrani M |title=2022 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death |journal=Eur Heart J |volume= |issue= |pages= |date=August 2022 |pmid=36017572 |doi=10.1093/eurheartj/ehac262 |url=}}</ref>
+|-
+|}
+== Recommendations for treatment with [[heart failure]] medication ==
 {| class="wikitable"
 |-
-| Colspan="1" style="text-align:center; background:LightGreen"|[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class I]]
+| Colspan="1" style="text-align:center; background:LightGreen"|[[ESC guidelines classification scheme#Classification of Recommendations|Class I]]
 |-
-| Bgcolor="LightGreen"|<nowiki>"</nowiki>'''1.''' In [[heart failure reduced EF]] (LVEF< 40%) for reducing the risk of [[SCD]] and all cause [[mortality]], use of [[betablocker]], a [[mineralocontocoid receptor antagonist]], and either an [[angiotensin converting enzyme inhibitor]], an [[angiotensin receptor blocker]], or an [[angiotensin receptor neprilysin inhibitor]] is recommended. ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence A]])<nowiki>"</nowiki>''
+| Bgcolor="LightGreen"|<nowiki>"</nowiki>[[Optimal medical treatment]] including [[ACE-I]]/[[ARB]]/ [[ARNIs]], [[mineralocorticoid receptor antagonist]], [[beta-blockers]], and [[SGLT2]] inhibitors is indicated in all [[heart failure]] [[patients]] with reduced [[EF]]''' ([[ESC guidelines classification scheme#Level of Evidence|Level of Evidence A]])<nowiki>"</nowiki>''
 |-
 |}
-==Specific notes==
+{|
+! colspan="2" style="background: PapayaWhip;" align="center" + |The above table adopted from 2022 ESC Guideline<ref name="pmid36017572">{{cite journal |vauthors=Zeppenfeld K, Tfelt-Hansen J, de Riva M, Winkel BG, Behr ER, Blom NA, Charron P, Corrado D, Dagres N, de Chillou C, Eckardt L, Friede T, Haugaa KH, Hocini M, Lambiase PD, Marijon E, Merino JL, Peichl P, Priori SG, Reichlin T, Schulz-Menger J, Sticherling C, Tzeis S, Verstrael A, Volterrani M |title=2022 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death |journal=Eur Heart J |volume= |issue= |pages= |date=August 2022 |pmid=36017572 |doi=10.1093/eurheartj/ehac262 |url=}}</ref>
+|-
+|}
+== Notes==
 * The most common cause of cardiac arrest is [[VF]], [[pulseless VT]], severe [[bradycardia]],  and [[asystole]].
 *  Survival in the presence of [[VF]], [[VT]] is better than [[bradycardia]], [[asystole]] manifestation.<ref name="ZipesCamm2006">{{cite journal|last1=Zipes|first1=Douglas P.|last2=Camm|first2=A. John|last3=Borggrefe|first3=Martin|last4=Buxton|first4=Alfred E.|last5=Chaitman|first5=Bernard|last6=Fromer|first6=Martin|last7=Gregoratos|first7=Gabriel|last8=Klein|first8=George|last9=Moss|first9=Arthur J.|last10=Myerburg|first10=Robert J.|last11=Priori|first11=Silvia G.|last12=Quinones|first12=Miguel A.|last13=Roden|first13=Dan M.|last14=Silka|first14=Michael J.|last15=Tracy|first15=Cynthia|title=ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death|journal=Circulation|volume=114|issue=10|year=2006|issn=0009-7322|doi=10.1161/CIRCULATIONAHA.106.178233}}</ref>
@@ Line 281: / Line 422: @@
 * If [[defibrillation ]] failed to returning spontaneous [[circulation]], [[advanced cardiovascular life support]] should be followed.
 * In unstable [[patients]] suspected [[coronary artery occlusion]] led to [[cardiac arrest]], emergency [[coronary angiography ]] should be considered rather than later in the [[hospital]] regardless the [[patient]] is  [[comatose]] or [[awake]].<ref name="SpauldingJoly1997">{{cite journal|last1=Spaulding|first1=Christian M.|last2=Joly|first2=Luc-Marie|last3=Rosenberg|first3=Alain|last4=Monchi|first4=Mehran|last5=Weber|first5=Simon N.|last6=Dhainaut|first6=Jean-François A.|last7=Carli|first7=Pierre|title=Immediate Coronary Angiography in Survivors of Out-of-Hospital Cardiac Arrest|journal=New England Journal of Medicine|volume=336|issue=23|year=1997|pages=1629–1633|issn=0028-4793|doi=10.1056/NEJM199706053362302}}</ref><ref name="ZanuttiniArmellini2012">{{cite journal|last1=Zanuttini|first1=Davide|last2=Armellini|first2=Ilaria|last3=Nucifora|first3=Gaetano|last4=Carchietti|first4=Elio|last5=Trillò|first5=Giulio|last6=Spedicato|first6=Leonardo|last7=Bernardi|first7=Guglielmo|last8=Proclemer|first8=Alessandro|title=Impact of Emergency Coronary Angiography on In-Hospital Outcome of Unconscious Survivors After Out-of-Hospital Cardiac Arrest|journal=The American Journal of Cardiology|volume=110|issue=12|year=2012|pages=1723–1728|issn=00029149|doi=10.1016/j.amjcard.2012.08.006}}</ref>
-* Coronary lesion requiring [[percutaneous coronary intervention]] was found in one-third of [[patients]] with [[out-of-hospital cardiac arrest]] without ST elevation in [[ECG]]. The outcome was reasonable. <ref name="DumasBougouin2016">{{cite journal|last1=Dumas|first1=Florence|last2=Bougouin|first2=Wulfran|last3=Geri|first3=Guillaume|last4=Lamhaut|first4=Lionel|last5=Rosencher|first5=Julien|last6=Pène|first6=Frédéric|last7=Chiche|first7=Jean-Daniel|last8=Varenne|first8=Olivier|last9=Carli|first9=Pierre|last10=Jouven|first10=Xavier|last11=Mira|first11=Jean-Paul|last12=Spaulding|first12=Christian|last13=Cariou|first13=Alain|title=Emergency Percutaneous Coronary Intervention in Post–Cardiac Arrest Patients Without ST-Segment Elevation Pattern|journal=JACC: Cardiovascular Interventions|volume=9|issue=10|year=2016|pages=1011–1018|issn=19368798|doi=10.1016/j.jcin.2016.02.001}}</ref>
+* [[Coronary]] lesion requiring [[percutaneous coronary intervention]] was found in one-third of [[patients]] with [[out-of-hospital cardiac arrest]] without ST elevation in [[ECG]]. The outcome was reasonable. <ref name="DumasBougouin2016">{{cite journal|last1=Dumas|first1=Florence|last2=Bougouin|first2=Wulfran|last3=Geri|first3=Guillaume|last4=Lamhaut|first4=Lionel|last5=Rosencher|first5=Julien|last6=Pène|first6=Frédéric|last7=Chiche|first7=Jean-Daniel|last8=Varenne|first8=Olivier|last9=Carli|first9=Pierre|last10=Jouven|first10=Xavier|last11=Mira|first11=Jean-Paul|last12=Spaulding|first12=Christian|last13=Cariou|first13=Alain|title=Emergency Percutaneous Coronary Intervention in Post–Cardiac Arrest Patients Without ST-Segment Elevation Pattern|journal=JACC: Cardiovascular Interventions|volume=9|issue=10|year=2016|pages=1011–1018|issn=19368798|doi=10.1016/j.jcin.2016.02.001}}</ref>
 * In the presence of incessant [[VT]], [[amiodarone]] was more effective than [[lidocaine]] and improved survival at 24 hours.<ref name="SombergBailin2002">{{cite journal|last1=Somberg|first1=John C|last2=Bailin|first2=Steven J|last3=Haffajee|first3=Charles I|last4=Paladino|first4=Walter P|last5=Kerin|first5=Nicholas Z|last6=Bridges|first6=Duane|last7=Timar|first7=Sandor|last8=Molnar|first8=Janos|title=Intravenous lidocaine versus intravenous amiodarone (in a new aqueous formulation) for incessant ventricular tachycardia|journal=The American Journal of Cardiology|volume=90|issue=8|year=2002|pages=853–859|issn=00029149|doi=10.1016/S0002-9149(02)02707-8}}</ref>
@@ Line 288: / Line 429: @@
 * [[lidocaine]] was less effective than [[amiodarone]] to improve [[hospital]] admission after [[out-of-hospital cardiac arrest]] due to shock-refractory [[VF]] or polymorphic [[VT]], but there were no differences between the two [[medications]] in [[survival]] to [[hospital]] discharge.
-*[[Lidociane]]  improved [[survival]] to [[hospital]] discharge in witnessed [[SCA]] due to initial shock-refractory [[VF]] or pulseless [[VT]].
+*[[Lidocaine]]  improved [[survival]] to [[hospital]] discharge in witnessed [[SCA]] due to initial shock-refractory [[VF]] or pulseless [[VT]].
-* Administration of [[betablocker]] in [[patients]] with recent [[MI]] was associated with reduced [[VF]] and better [[survival]].
+* Administration of [[beta blocker]] in [[patients]] with recent [[MI]] was associated with reduced [[VF]] and better [[survival]].
 * If [[VT]], [[VF]] storm is refractory to [[amiodarone]], [[lidocaine]], or frequent [[cardioversion]], administration of [[betablocker]] has been shown improved [[survival]] and finally reducing [[sympathetic]] tone by [[sedation]] and [[general anesthesia]] are recommended.
 * Administration of high-dose [[epinephrine]] ( 0.1 to 0.2 mg/kg IV) in [[out-of-hospital cardiac arrest]] unresponsive to [[defibrillation]], improved survival to [[hospital]] admission, but there was no difference compared to standard-dose [[epinephrine]] in survival to hospital discharge or long term survival compared with standard-dose [[epinephrine]] (1 mg given [[intravenously]] or intraosseously every 3 to 5 minutes).<ref name="pmid1433686">{{cite journal |vauthors=Callaham M, Madsen CD, Barton CW, Saunders CE, Pointer J |title=A randomized clinical trial of high-dose epinephrine and norepinephrine vs standard-dose epinephrine in prehospital cardiac arrest |journal=JAMA |volume=268 |issue=19 |pages=2667–72 |date=November 1992 |pmid=1433686 |doi= |url=}}</ref>
-*The administration of [[vasopressin]] is no longer recommended in the most recent [[advanced cardiovascular life support]] guideline.<ref name="LinkBerkow2015">{{cite journal|last1=Link|first1=Mark S.|last2=Berkow|first2=Lauren C.|last3=Kudenchuk|first3=Peter J.|last4=Halperin|first4=Henry R.|last5=Hess|first5=Erik P.|last6=Moitra|first6=Vivek K.|last7=Neumar|first7=Robert W.|last8=O’Neil|first8=Brian J.|last9=Paxton|first9=James H.|last10=Silvers|first10=Scott M.|last11=White|first11=Roger D.|last12=Yannopoulos|first12=Demetris|last13=Donnino|first13=Michael W.|title=Part 7: Adult Advanced Cardiovascular Life Support|journal=Circulation|volume=132|issue=18 suppl 2|year=2015|pages=S444–S464|issn=0009-7322|doi=10.1161/CIR.0000000000000261}}</ref>
+* Administration of [[vasopressin]] is no longer recommended in the most recent [[advanced cardiovascular life support]] guideline.<ref name="LinkBerkow2015">{{cite journal|last1=Link|first1=Mark S.|last2=Berkow|first2=Lauren C.|last3=Kudenchuk|first3=Peter J.|last4=Halperin|first4=Henry R.|last5=Hess|first5=Erik P.|last6=Moitra|first6=Vivek K.|last7=Neumar|first7=Robert W.|last8=O’Neil|first8=Brian J.|last9=Paxton|first9=James H.|last10=Silvers|first10=Scott M.|last11=White|first11=Roger D.|last12=Yannopoulos|first12=Demetris|last13=Donnino|first13=Michael W.|title=Part 7: Adult Advanced Cardiovascular Life Support|journal=Circulation|volume=132|issue=18 suppl 2|year=2015|pages=S444–S464|issn=0009-7322|doi=10.1161/CIR.0000000000000261}}</ref>
 * Intravenous [[magnesium]] is advised in the presence of [[hypokalemia]] or [[medication]]-induced [[torsades de pointed]] by suppression of early and [[late after depolarization]], and inhibition of [[calcium]] flux into [[cardiomyocytes]].
 * Using intravenous [[magnesium]] during in-hospital or [[out-of-hospital cardiac arrest]] or refractory [[VF]] was not associated with restoration of [[circulation]] or [[survival]] benefit.<ref name="Hassan2002">{{cite journal|last1=Hassan|first1=T B|title=A randomised trial to investigate the efficacy of magnesium sulphate for refractory ventricular fibrillation|journal=Emergency Medicine Journal|volume=19|issue=1|year=2002|pages=57–62|issn=14720205|doi=10.1136/emj.19.1.57}}</ref>
-* Administration The [[lidocaine]] and [[procainamide]] routinely after [[MI]] for suppression of [[ventricular arrhythmia]] was associated with increased [[mortality]], however [[beta blockers]] lessened [[mortality]] rate.<ref name="pmid8371471">{{cite journal |vauthors=Teo KK, Yusuf S, Furberg CD |title=Effects of prophylactic antiarrhythmic drug therapy in acute myocardial infarction. An overview of results from randomized controlled trials |journal=JAMA |volume=270 |issue=13 |pages=1589–95 |date=October 1993 |pmid=8371471 |doi= |url=}}</ref>
+* Administration The [[lidocaine]] and [[procainamide]] routinely after [[MI]] for suppression of [[ventricular arrhythmia]] was associated with increased [[mortality]], however,
-* Prophylactic use of Higher dose [[amiodaron]] after [[MI]] increase mortality, whereas moderate dose [[amiodarone]] was not superior to placebo.<ref name="Elizari2000">{{cite journal|last1=Elizari|first1=M|title=Morbidity and mortality following early administration of amiodarone in acute myocardial infarction|journal=European Heart Journal|volume=21|issue=3|year=2000|pages=198–205|issn=0195668X|doi=10.1053/euhj.1999.1687}}</ref>
+use of [[beta blockers]] lessened [[mortality]] rate.<ref name="pmid8371471">{{cite journal |vauthors=Teo KK, Yusuf S, Furberg CD |title=Effects of prophylactic antiarrhythmic drug therapy in acute myocardial infarction. An overview of results from randomized controlled trials |journal=JAMA |volume=270 |issue=13 |pages=1589–95 |date=October 1993 |pmid=8371471 |doi= |url=}}</ref>
+* Prophylactic use of Higher dose [[amiodarone]] after [[MI]] increase mortality, whereas moderate dose [[amiodarone]] was not superior to placebo.<ref name="Elizari2000">{{cite journal|last1=Elizari|first1=M|title=Morbidity and mortality following early administration of amiodarone in acute myocardial infarction|journal=European Heart Journal|volume=21|issue=3|year=2000|pages=198–205|issn=0195668X|doi=10.1053/euhj.1999.1687}}</ref>
-* Every [[wide QRS tachycardia]] in the presence of structural heart disease should be presumed [[VT]] untile proven otherwise such as [[SVT]] with aberrancy.
+* Every [[wide QRS tachycardia]] in the presence of [[structural heart disease]] should be presumed [[VT]] until proven otherwise such as [[SVT]] with aberrancy.
-* Administration of [[verapamil]] in [[wide QRS tachycardia]] may lead to  sever [[hypotension]] and [[syncope]] and should be avoided.
+* Administration of [[verapamil]] in [[wide QRS tachycardia]] may lead to  severe [[hypotension]] and [[syncope]] and should be avoided.
 * The specific type of [[VT]] is [[verapamil]]-[[sensitive VT]] ([[interfascicular reentry]]) with [[structurally normal heart]], but it is important to notify that the recognition of this [[rhythm]] is difficult at initial presentation.<ref name="BuxtonMarchlinski1987">{{cite journal|last1=Buxton|first1=Alfred E.|last2=Marchlinski|first2=Francis E.|last3=Doherty|first3=John U.|last4=Flores|first4=Belinda|last5=Josephson|first5=Mark E.|title=Hazards of intravenous verapamil for sustained ventricular tachycardia|journal=The American Journal of Cardiology|volume=59|issue=12|year=1987|pages=1107–1110|issn=00029149|doi=10.1016/0002-9149(87)90857-5}}</ref>
@@ Line 337: / Line 479: @@
 ==Comments==
 *Common [[antiarrhythmic]] medications for supression of [[ventricular arrhythmia]] include [[amiodarone]], [[sotalol]],  and occasionally [[mexilletine]], [[quinidine]],[[ranolazine]].<ref name="BunchMahapatra2011">{{cite journal|last1=Bunch|first1=T. Jared|last2=Mahapatra|first2=Srijoy|last3=Murdock|first3=David|last4=Molden|first4=Jamie|last5=Weiss|first5=J. Peter|last6=May|first6=Heidi T.|last7=Bair|first7=Tami L.|last8=Mader|first8=Katy M.|last9=Crandall|first9=Brian G.|last10=Day|first10=John D.|last11=Osborn|first11=Jeffrey S.|last12=Muhlestein|first12=Joseph B.|last13=Lappe|first13=Donald L.|last14=Anderson|first14=Jeffrey L.|title=Ranolazine Reduces Ventricular Tachycardia Burden and ICD Shocks in Patients with Drug-Refractory ICD Shocks|journal=Pacing and Clinical Electrophysiology|volume=34|issue=12|year=2011|pages=1600–1606|issn=01478389|doi=10.1111/j.1540-8159.2011.03208.x}}</ref><ref name="KetteringMewis2002">{{cite journal|last1=Kettering|first1=Klaus|last2=Mewis|first2=Christian|last3=Dornberger|first3=Volker|last4=Vonthein|first4=Reinhard|last5=Bosch|first5=Ralph F.|last6=Kuhlkamp|first6=Volker|title=Efficacy of Metoprolol and Sotalol in the Prevention of Recurrences of Sustained Ventricular Tachyarrhythmias in Patients with an Implantable Cardioverter Defibrillator|journal=Pacing and Clinical Electrophysiology|volume=25|issue=11|year=2002|pages=1571–1576|issn=0147-8389|doi=10.1046/j.1460-9592.2002.01571.x}}</ref>
 * [[Amiodarone]] is more effective than [[sotalol]] but discontinuation may happen during 12-24 months of use due to adverse effects.<ref name="Connolly2006">{{cite journal|last1=Connolly|first1=Stuart J.|title=Comparison of β-Blockers, Amiodarone Plus β-Blockers, or Sotalol for Prevention of Shocks From Implantable Cardioverter Defibrillators<SUBTITLE>The OPTIC Study: A Randomized Trial</SUBTITLE>|journal=JAMA|volume=295|issue=2|year=2006|pages=165|issn=0098-7484|doi=10.1001/jama.295.2.165}}</ref>
@@ Line 345: / Line 488: @@
 * In survivors of [[SCA]] use of [[Propafenone]] increased [[mortality]] in comparison  with [[beta-blockers]], [[amiodarone]], and the [[ICD]].
-*  In [[patients]] with prior [[ MI]]  Sustained [[monomorphic VT ]] is due to scar-related reentry and is not due to acute [[ischemia]].
+*  In [[patients]] with prior [[ MI]], Sustained [[monomorphic VT ]] can be due to scar-related reentry,  but not acute [[ischemia]].
 * [[Antiarrhythmic]] medications or [[ablation]] may be needed to prevent recurrence of [[VT]] in scar-related settings.<ref name="BrugadaAguinaga2001">{{cite journal|last1=Brugada|first1=Josep|last2=Aguinaga|first2=Luis|last3=Mont|first3=Lluı́s|last4=Betriu|first4=Amadeu|last5=Mulet|first5=Jaume|last6=Sanz|first6=Ginés|title=Coronary artery revascularization in patients with sustained ventricular arrhythmias in the chronic phase of a myocardial infarction: effects on the electrophysiologic substrate and outcome|journal=Journal of the American College of Cardiology|volume=37|issue=2|year=2001|pages=529–533|issn=07351097|doi=10.1016/S0735-1097(00)01133-5}}</ref>
 * Revascularization is recommended in the setting of [[ischemia]] for prevention of [[VF]], [[polymorphic VT]]. <ref name="BerntsenGunnes1993">{{cite journal|last1=Berntsen|first1=R. F.|last2=Gunnes|first2=P.|last3=Lie|first3=M.|last4=Rasmussen|first4=K.|title=Surgical revascularization in the treatment of ventricular tachycardia and fibrillation exposed by exercise-induced ischaemia|journal=European Heart Journal|volume=14|issue=10|year=1993|pages=1297–1303|issn=0195-668X|doi=10.1093/eurheartj/14.10.1297}}</ref>
@@ Line 382: / Line 523: @@
 |}
 {|
-! colspan="2" style="background: PapayaWhip;" align="center" + |The above table adopted from 2017 AHA/ACC/HRS Guideline
+! colspan="2" style="background: PapayaWhip;" align="center" + |The above table adopted from 2017 AHA/ACC/HRS Guideline<ref name="Al-KhatibStevenson2018">{{cite journal|last1=Al-Khatib|first1=Sana M.|last2=Stevenson|first2=William G.|last3=Ackerman|first3=Michael J.|last4=Bryant|first4=William J.|last5=Callans|first5=David J.|last6=Curtis|first6=Anne B.|last7=Deal|first7=Barbara J.|last8=Dickfeld|first8=Timm|last9=Field|first9=Michael E.|last10=Fonarow|first10=Gregg C.|last11=Gillis|first11=Anne M.|last12=Granger|first12=Christopher B.|last13=Hammill|first13=Stephen C.|last14=Hlatky|first14=Mark A.|last15=Joglar|first15=José A.|last16=Kay|first16=G. Neal|last17=Matlock|first17=Daniel D.|last18=Myerburg|first18=Robert J.|last19=Page|first19=Richard L.|title=2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death|journal=Circulation|volume=138|issue=13|year=2018|issn=0009-7322|doi=10.1161/CIR.0000000000000549}}</ref>
 |-
 |}
@@ Line 389: / Line 530: @@
-*Although [[ICD]] reduced [[mortality]],  painful [[ICD]] shocks  can affect on the [[quality of life]] and increased morbidity.
+*Although [[ICD]] reduced [[mortality]],  painful [[ICD]] shocks  can affect on the [[quality of life]] and increases [[morbidity]].
 *The frequent of [[ICD]] shocks lessened by [[amiodarone]] plus [[beta blocker]]  compared with [[sotalol]]  but at the expense of increased risk of [[amiodarone]]-related adverse effects.<ref name="Connolly2006">{{cite journal|last1=Connolly|first1=Stuart J.|title=Comparison of β-Blockers, Amiodarone Plus β-Blockers, or Sotalol for Prevention of Shocks From Implantable Cardioverter Defibrillators<SUBTITLE>The OPTIC Study: A Randomized Trial</SUBTITLE>|journal=JAMA|volume=295|issue=2|year=2006|pages=165|issn=0098-7484|doi=10.1001/jama.295.2.165}}</ref>
 * All types of non-ischemic [[cardiomyopathy]] can produce scar-related [[VT]] especially [[cardiac]] [[sarcoidosis]].<ref name="NaruseSekiguchi2014">{{cite journal|last1=Naruse|first1=Yoshihisa|last2=Sekiguchi|first2=Yukio|last3=Nogami|first3=Akihiko|last4=Okada|first4=Hiroyuki|last5=Yamauchi|first5=Yasuteru|last6=Machino|first6=Takeshi|last7=Kuroki|first7=Kenji|last8=Ito|first8=Yoko|last9=Yamasaki|first9=Hiro|last10=Igarashi|first10=Miyako|last11=Tada|first11=Hiroshi|last12=Nitta|first12=Junichi|last13=Xu|first13=Dongzhu|last14=Sato|first14=Akira|last15=Aonuma|first15=Kazutaka|title=Systematic Treatment Approach to Ventricular Tachycardia in Cardiac Sarcoidosis|journal=Circulation: Arrhythmia and Electrophysiology|volume=7|issue=3|year=2014|pages=407–413|issn=1941-3149|doi=10.1161/CIRCEP.113.000734}}</ref>
-* [[Cather ablation]] can be used for treatment of [[scar related]] [[VT]] in [[non-ischemic cardiomyopathy]].<ref name="DinovFiedler2014">{{cite journal|last1=Dinov|first1=Borislav|last2=Fiedler|first2=Lukas|last3=Schönbauer|first3=Robert|last4=Bollmann|first4=Andreas|last5=Rolf|first5=Sascha|last6=Piorkowski|first6=Christopher|last7=Hindricks|first7=Gerhard|last8=Arya|first8=Arash|title=Outcomes in Catheter Ablation of Ventricular Tachycardia in Dilated Nonischemic Cardiomyopathy Compared With Ischemic Cardiomyopathy|journal=Circulation|volume=129|issue=7|year=2014|pages=728–736|issn=0009-7322|doi=10.1161/CIRCULATIONAHA.113.003063}}</ref>
+* [[Catheter ablation]] can be used for treatment of [[scar related]] [[VT]] in [[non-ischemic cardiomyopathy]].<ref name="DinovFiedler2014">{{cite journal|last1=Dinov|first1=Borislav|last2=Fiedler|first2=Lukas|last3=Schönbauer|first3=Robert|last4=Bollmann|first4=Andreas|last5=Rolf|first5=Sascha|last6=Piorkowski|first6=Christopher|last7=Hindricks|first7=Gerhard|last8=Arya|first8=Arash|title=Outcomes in Catheter Ablation of Ventricular Tachycardia in Dilated Nonischemic Cardiomyopathy Compared With Ischemic Cardiomyopathy|journal=Circulation|volume=129|issue=7|year=2014|pages=728–736|issn=0009-7322|doi=10.1161/CIRCULATIONAHA.113.003063}}</ref>
 {| style="cellpadding=0; cellspacing= 0; width: 600px;"
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@@ Line 401: / Line 542: @@
 |-
 |style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align=left|
-❑ [[Amiodarone]] or [[sotalol]] is recommended in the presensence of recurrent [[ventricular arrhythmia]] and  frequent [[ICD]] shocks despite optimal programming or [[betablocker]] therapy<br>
+❑ [[Amiodarone]] or [[sotalol]] is recommended in the presensence of recurrent [[ventricular arrhythmia]] and  frequent [[ICD]] shocks despite optimal programming or [[beta blocker]] therapy<br>
 |-
 |style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |'''[[Catheter ablation]] ([[ACC AHA guidelines classification scheme|Class IIa, Level of Evidence B]]) :'''
@@ Line 410: / Line 551: @@
 |}
 {|
-! colspan="2" style="background: PapayaWhip;" align="center" + |The above table adopted from 2017 AHA/ACC/HRS Guideline
+! colspan="2" style="background: PapayaWhip;" align="center" + |The above table adopted from 2017 AHA/ACC/HRS Guideline<ref name="Al-KhatibStevenson2018">{{cite journal|last1=Al-Khatib|first1=Sana M.|last2=Stevenson|first2=William G.|last3=Ackerman|first3=Michael J.|last4=Bryant|first4=William J.|last5=Callans|first5=David J.|last6=Curtis|first6=Anne B.|last7=Deal|first7=Barbara J.|last8=Dickfeld|first8=Timm|last9=Field|first9=Michael E.|last10=Fonarow|first10=Gregg C.|last11=Gillis|first11=Anne M.|last12=Granger|first12=Christopher B.|last13=Hammill|first13=Stephen C.|last14=Hlatky|first14=Mark A.|last15=Joglar|first15=José A.|last16=Kay|first16=G. Neal|last17=Matlock|first17=Daniel D.|last18=Myerburg|first18=Robert J.|last19=Page|first19=Richard L.|title=2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death|journal=Circulation|volume=138|issue=13|year=2018|issn=0009-7322|doi=10.1161/CIR.0000000000000549}}</ref>
 |-
 |}

Ventricular tachycardia medical therapy: Difference between revisions

Latest revision as of 05:08, 16 September 2022

Overview

Medical Therapy

Antiarrhythmic medications

Sodium channel blocker

Ranolazine

Beta blocker

Amiodarone, sotalol

Calcium channel blocker

Electrolytes

Fatty acids, Lipids

Specific recommendation

Management of patients with Polymorphic Ventricular arrhythmia

Management of sustained monomorphic ventricular tachycardia

Management of electrical storm

Recommendations for treatment with heart failure medication

Notes

Comments

Message

References

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