Ventricular Arrhythmias

Eric J Milie, DO

Goals and Objectives

Heart Anatomy

1. Sinoatrial Node (SA Node) 2. Atrioventricular Node (AV Node) 3. Common AV Bundle 4. Right and Left Bundle Branches

Sinoatrial Node

The

Sinoatrial Node

serves as the natural pacemaker for the heart Nestled in the upper area of the right atrium Sends the electrical impulse that triggers each heartbeat Impulse spreads through the atria, prompting the cardiac muscle tissue to contract in a coordinated, wave-like manner Without any neural stimulation, the sinoatrial node rhythmically initiates impulses 70 to 80 times per minute

Atrioventricular Node

The impulse that originates from the sinoatrial node strikes the

Atrioventricular node

Situated in the lower portion of the right atrium In turn sends an impulse through the nerve network to the ventricles, initiating the same wave-like contraction of the ventricles

His-Purkinje System

Located in the walls of the ventricles Parts include Bundle of His, Right and Left Bundle Branches, and Purkinje Fibers Responsible for ventricular contraction

Ventricular Arrhythmias

Depolarization wave spreads through the ventricles by an irregular and therefore slower pathway QRS complex is wide and abnormal Repolarization pathways are also different, causing the T wave to have an unusual morphology Below 120bpm rhythm is termed ventricular, above this rate it is said to be Ventricular Tachycardia.

Causes of Ventricular Arrhythmias

Cardiac causes

Acute and chronic ischemic heart disease Cardiomyopathy Valvular heart disease Mitral valve prolapse

Noncardiac causes

Stimulants: caffeine, cocaine, alcohol Metabolic abnormalities: acidosis, hypoxemia, hyperkalemia, hypokalemia, hypomagnesemia Drugs: digoxin (Lanoxin), theophylline, antipsychotics, tricyclic antidepressants, antiarrhythmics with proarrhythmic potential (e.g., flecainide [Tambocor], dofetilide [Tikosyn], sotalol [Betapace], quinidine)

Ventricular Arrhythmias

Ventricular Extrasystole (PVCs) Ventricular Excape Beats (Idioventricular Rhythm) Ventricular Parasystole Ventricular Tachycardia Torsade de Pointes Ventricular Fibrillation

Premature Ventricular Contraction

Premature impulse of ventricular origin occurring before the next sinus beat May be unifocal (identical or nearly identical QRS morphology with a fixed coupling interval) or multifocal (various QRS morphologies or coupling intervals)

PVCs

Ventricular repolarization and depolarization are abnormal Wide QRS (greater than 0.12 seconds) ST segment and T wave oriented opposite the QRS complex SA node not depolarized, SA nodal rhythm not disturbed, usually accompanied by a full compensatory pause

PVCs

continued

One of the most common arrhythmias, occurring in people with and without heart disease Prevalence ranges from less than 3% in young healthy women to grater than 20% for older African Americans with hypertension Risk factors include male sex, advanced age, African American descent, hypertension, underlying ischemic heart disease, bundle branch block pattern on 12 lead EKG, hypomagnasemia, and hypokalemia

PVC- EKG Findings

PVC Compensatory Pause

Low Grading System for Premature Beats

Grade 0: No premature beats Grade 1: Occasional (<30/hour) Grade 2: Frequent (>30/hour) Grade 3: Multifocal Grade 4: Repetitive (A:couplets; B: salvos of 3 or more) Grade 5: R on T phenomena

R on T Phenomena

Several “R on T” beats

Bi- and Trigeminy

Ventricular bigeminy refers to alternating normal sinus and premature ventricular complexes Ventricular trigeminy refers to two successive sinus beats followed by a premature ventricular complex

Ventricular Bigeminy

Ventricular Trigeminy

Treatment for PVCs

In a patient without structural heart disease, PVCs are associated with little to no risk of malignant arrhythmias, and the risk to benefit ratio of anti-arrhythmic treatment does not support its use Treatment consists of limiting stimulant usage, correcting electrolyte abnormalities, and review medications

CAST and CAST II

Cardiac Arrhythmia Suppression Trials CAST (1989)showed increased mortality in patients post-MI whose PVCs were successfully suppressed with antiarrhythmics CAST II (1992)showed no impact on long term survival from drug treatment that successfully suppressed PVCs

Treatment

continued

If PVCs are debilitating or intolerable, trial with low dose beta blocker warranted Cardiology referral for patients refractory to beta blocker Class I antiarrhythmics (flecainide) or amniodarone sometimes used,but lack good supportive evidence

Structural Heart Disease

Patients with an underlying structural heart disease (ie cardiomyopathy, infarction, valvular heart disease) and complex ectopy (>10 PVCs/hr) have a significantly increased rate of mortality CAST and CAST II show no benefit for treatment of PVCs Left ventricular dysfunction has a stronger association with increased mortality rate than do PVCs EPS has a primary role in risk stratification of patients with frequent or complex PVCs. Patients with PVCs that are noninducible (ie, unable to trigger ventricular tachycardia during stimulation) have a low risk of sudden death

Idioventricular Rhythm

Impulse originating from pacemaker within His-Purkinje network Intrinsic rate of 30-40bpm Idioventricular beats have wide QRS complexes, abnormal ST segments, and secondary T wave changes similar to PVCs If the rate is greater than 40bpm but less than 100bpm, accelerated idioventricular rhythm is present

Idioventricular Rhythm

Accelerated Idioventricular Rhythm

IVR: Demographics

Frequency: No frequency can be determined. In the U.S., most common in the setting of digitalis toxicity or myocardial reperfusion following acute myocardial infarction Morbidity’Mortality: IVR does not affect the clinical course of the patient Race: No racial differences observed Sex: No sexual predilection observed Age: More common in elderly, secondary to increased incidence of MI and coronary disease

IVR: Therapy

No specific antiarrhythmic therapy indicated Generally self-limited in patients with ischemia If digitalis toxicity or electrolyte abnormality the cause, generally corrects rapidly following underlying correction Suppressant drugs such as lidocaine should be avoided, as they may knock out the only reliable pacemaker Atropine sulfate given in 0.5mg increments every 3 to 5 minutes may augment SA node and allow “capture” of ventricles Artificial pacing may be used to support the hart rate if it is insufficient for hemodynamic stability, but is rarely needed

Ventricular Parasystole

Rhythm governed by two pacemakers: one in the SA node and another in the ventricle Variable coupling intervals between sinus and ventricular ectopic rhythm Interectopic intervals are multiples of a common divisor Presence of fusion beats

1. Interval between ectopic beat and preceding sinus beat varies 2. The interectopic intervals all have a common denominator of 0.90 to 0.95s 3. There are occasional fusion beats (third beat in top strip; fourth beat in second strip;last beat in bottom strip).

Ventricular Parasystole

continued

Occurs in the presence of severe underlying heart disease Can precipitate V-Tach or V-Fib, particularly with associated ischemia In absence of ischemia, may remain stable for years

Ventricular Tachycardia

Tachydysrhythmia originating from a ventricular ectopic focus, characterized by a rate typically greater than 120 beats per minute and wide QRS complexes may be monomorphic (typically regular rhythm originating from a single focus with identical QRS complexes) or polymorphic (may be irregular rhythm, with varying QRS complexes) Nonsustained VT is defined as a run of tachycardia of less than 30 seconds duration

Ventricular Tachycardia: EKG Findings

Rate greater than 100 beats per minute (usually 150-200) Wide QRS complexes (>120 ms) Presence of atrioventricular (AV) dissociation Fusion beats

V Tach: EKG

Ventricular Tachycardia

continued

May develop without hemodynamic deterioration Often causes severe hemodynamic compromise and may deteriorate rapidly into ventricular fibrillation

Ventricular Tachycardia: Pathophysiology

Consequence of structural heart disease, with breakdown of normal conduction patterns, increased automaticity (which tends to favor ectopic foci), and activation of re-entrant pathways in the ventricular conduction system Electrolyte disturbances and sympathomimetics may increase the likelihood of VT in the susceptible heart AV dissociation usually is present Retrograde ventriculoatrial conduction may occur, which can generate an ECG complex similar to paroxysmal supraventricular tachycardia (PSVT) with aberrant conduction

Ventricular Tachycardia: Epidemiology

Frequency

: One of the most commonly diagnosed dysrhythmias. Incidence of 0.1 2.0% per year

Morbidity/ Mortality

: Can produce decompensated CHF and hemodynamic instability, but most mortality associated with degeneration into V. Fib

Sex

: Men > Women

Age

: Peaks in the middle decads of life

Ventricular Tachycardia: Management

Acute management strategy depends upon the immediate hemodynamic consequences of the arrhythmia VT associated with loss of consciousness or hypotension is a medical emergency requiring immediate cardioversion When the hemodynamic status is stable, the patient is well perfused, and no evidence for coronary ischemia or infarction is present, then a trial of intravenous medication may be considered Chronic management strategies may include medications, ICD implantation, and catheter-based ablation

Ventricular Tachycardia: Management

continued

In patients with structurally normal hearts, there is little risk of sudden death Antiarrhythmics favored over ICDs in these patients ESVEM (Electrophysiologic Study Versus Electrocardiographic Monitoring) study of VT/VF patients demonstrated the superiority of sotalol over several type I antiarrhythmic drugs, but the trial did not include a placebo control group Cardiac Arrest in Seattle: Conventional versus Amiodarone Drug Evaluation (CASCADE) trial suggested that amiodarone was superior to conventional antiarrhythmics (a mix of class I drugs) for secondary arrhythmia prophylaxis (ie, prior VT/VF) Unlike class I antiarrhythmics, amiodarone appears to be safe in patients with left ventricular dysfunction

Class I Class IA Class 1B

Little effect on phase 0 of action potential in normal tissues; depress phase 0 in abnormal tissues; shorten repolarization or little effect; lidocaine, tocainide, mexilitene, diphenylhydantion

Class IC Class II Class III Class IV Others Vaughn-Williams Classification for Antiarrhythmic Medications

Sodium-channel blockers Depress phase 0 of action potential; delay conduction, prolong repolarization (phase III, IV); quinidine, procainamide, disopyramide Depress phase 0 of the action potential; markedly slow conduction in normal tissues; flecainide, propafenone, moricizine Beta-adrenergic blocking agents; acebutalol, atenolol, bisoprolol, carvedilol, metoprolol, nadolol, pindolol, propranolol and others Prolong action potential duration by increasing repolarization and refractoriness; amiodarone, sotalol, bretylium, dofetilide, azimilide, ibutilide.

Calcium-channel blockers; diltiazem, verapamil Digoxin, adenosine

Ventricular Tachycardia: ICDs

Antiarrhythmics Versus Implantable Defibrillators (AVID) study Canadian Implantable Defibrillator Study (CIDS) Cardiac Arrest Study, Hamburg (CASH) Showed benefit of ICDs compared to antiarrhythmic drugs. Diffeence significant in AVID, borderline significant in CIDS (p=0.06), and of no statistical significance in CASH A meta-analysis of the 3 trials suggested a 28% reduction in the relative risk of death related to ICD implantation in the clinical setting

Ventricular Tachycardia: ICDs

continued

Multicenter UnSustained Tachycardia Trial (MUSTT) and Multicenter Autonomic Defibrillator Implantation Trial (MADIT) studied high-risk patients who had never had VF or sustained VT Patients with ischemic cardiomyopathy, ejection fractions greater than 35-40%, and nonsustained VT were taken to EPS Patients with inducible sustained VT were randomized between conventional antiarrhythmic therapy and prophylactic ICD implantation In each study, ICD patients had better survival than patients receiving antiarrhythmic drugs

ICD

Differentiating Wide Complex Tachycardias: Brugada Diagnostic Algorhythm

Ventricular Tachycardia versus SVT with Aberrancy

Factors favoring SVT with aberrancy Typical right bundle-branch block with normal axis Typical left bundle-branch block with normal axis Delta wave Factors favoring ventricular tachycardia Atrioventricular dissociation Left bundle-branch block with right-axis deviation Left-axis or extreme right-axis deviation QRS complex >140 milliseconds Fusion complexes Capture beats Concordant R wave progression patterns (all leads V 1 -V 6 have predominately positive or negative defections). Note, absence of concordance does not rule out VT, and Antidromic reciprocating tachycardia using a bypass tract may be indistinguishable from VT.

Torsades De Pointes

Literally means “twisting of the points” Term coined in 1966 by Dessertenne to describe a new ventricular arrhythmia with unusual characteristics EKG in limb leads shows a sinusoidal increase and decrease in QRS voltage, resembling rotation about the isoelectric baseline Differentiating between Torsades and V Tach is important, as treatment vastly different

Torsades de Pointes: Epidemiology

Frequency

: Unknown

Morbidity/ Mortality

: Accounts for less than 5% of the 300,000 annual sudden cardiac deaths in the U.S.

Sex

: Women 2-3 times more likely to develop than men

Age

: Most frequently seen between 35-50 years of age

Torsades de Pointes: Causes

Congenital prolonged QT syndromes (Jervell and Lange-Nielson syndrome and the Romano Ward syndrome) Drug induced QT prolongation Complete heart block Hypokalemia Hypomagnesemia Intrinsic heart disease Central nervous system disease

Drug Induced Prolongation

Antiarrhythmic drugs reported to be etiologic include class IA agents (eg, quinidine, procainamide, disopyramide), class IC agents (eg, encainide, flecainide), and class III agents (eg, sotalol, amiodarone) Drug interactions with the antihistamines astemizole

(recalled from US market)

and terfenadine

(recalled from US market)

can precipitate torsade; these drugs should never be used with class IA, IC, or III agents Astemizole and terfenadine, in high dosages or when used in combination with the azole antifungal drugs or the macrolide antibiotics, have been reported to precipitate torsade and sudden death Grapefruit juice has been shown to slow the hepatic metabolism of these antihistamines as well as other drugs and to prolong the QT interval in patients taking astemizole or terfenadine (recently taken off the market by the US Food and Drug Administration)

Drug Induced QT Prolongation:

continued

Phenothiazines (Thorazine, Mellaril, etc) Tricyclic antidepressants (amitryptiline, nortriptyline, etc.) Lithium Cisapride HAART Methadone Chemotherapeutic agents (Doxarubicin, Daunomycin) Other meds affecting CYP3A pathway

Torsades de Pointes: Risk Factors

Female sex Congenital deafness (though prolonged QT found in only 0.25-0.3% of deaf-mute children) Family history of sudden death Cardiac arrest or prolonged syncope

Torsades de Pointes: Therapy

IV magnesium sulfate (effective dose usually 2g): use even in face of normal serum magnesium level Isoproterenol infusion (rate 210 μg/minute) for acute control Temporary overdrive pacing: rate >140bpm Class IA antiarrhythmics should not be used; may worsen QT prolongationan and propagate ventricular fibrillation Propranolol orally may be used in patients with congenital long-QT

Torsades de Pointes: EKG

Brugada Syndrome

First described as a new clinical entity by Drs. Pedro and Josep Brugada in 1992 Cause of sudden cardiac death in young adults Inherited syndrome (arrhythmia) that can lead to life threatening ventricular fibrillation Also known as Sudden Unexpected Death Syndrome (SUDS)

Brugada Syndrome

continued

Due to a mutation in the gene that encodes for the sodium ion channel in the myocytes The gene, named SCN5A, is located on the short arm of the third chromosome (3p21) Inherited in an autosomal dominant pattern Affects mostly males in southeast Asia, and is the leading cause of natural death in young men of Thailand

Brugada Syndrome: EKG

No specific diagnostic criteria set V1-v3 with ST segment elevation Right bundle branch or incomplete right bundle branch

Brugada Syndrome: Clinical Manifestation

Syncopal episodes of unknown cause or of vaso-vagal cause Diagnosis of idiopathic ventricular fibrillation Sudden cardiac death Symptoms typically at night May be link to hyperthermia

Brugada Syndrome: Treatment

Symptomatic individuals: implantable cardio-defibrillator Asymptomatic individuals more controversial If spontaneously abnormal EKG, at risk of sudden cardiac death If EKG findings only after pharmacological elicitation (with procainamide or felcainide), not at increased risk for sudden death

Ventricular Fibrillation

Chaotic ventricular rhythm caused by multiple ectopic foci within the ventricle No organized electrical activity present No ventricular contraction Not a life sustaining rhythm

Ventricular Fibrillation

Ventricular Fibrillation

Ventricular Fibrillation: Causes

Myocardial ischemia

Increased catecholamine levels Improper sympathetic stimulation Electrolyte imbalances Hypoxia or acid-base disturbances Toxic responses due to proarrhythmic drugs Hyperthermia/hypothermia Proarrhythmic conditions, such as prolonged QT syndromes

Ventricular Fibrillation: Epidemiology

Frequency

: VF has been described as the initial rhythm in almost 70% of out-of-hospital arrests

Morbidity/ Mortality

: Although VF seldom is listed as the cause of death, it is thought to be responsible for more than 400,000 SCD cases in the United States annually

Race

: Black males most affected

Sex

: SCD is more common among males than females, although the rates become similar for patients older than 70 years

Age

: Incidence initially peaks during the first 6 months of life, then rapidly declines until a second peak in those aged 45-75 years

Ventricular Fibrillation: Prehospital Care

Early defibrillation critically important Automated external defibrillators (AEDs) have revolutionized prehospital VF management because they have eliminated the need for rhythm-recognition training AEDs identify VF more rapidly than manual defibrillation techniques, are 92-100% specific for VF, and require less time to achieve defibrillation Bystander CPR reportedly plays a significant role in prolonging the period (up to 12 min) in which VF may respond to a defibrillator CPR may increase the number of patients in VF who benefit from defibrillation by response personnel

Data from Olmsted County cardiac arrest data (November 1990 December 2000).

Ventricular Fibrillation: Emergency Department Care

Electrical external defibrillation remains the most successful treatment of VF Successful defibrillation largely depends on the following 2 key factors: duration between onset of VF and defibrillation, and metabolic condition of the myocardium Defibrillation success rates decrease 5 10% for each minute after onset of VF Artificial pacemakers or implantable defibrillators mandate use of anterior posterior paddle placement

A

irway

B

reathing

C

irculation

D

efibrillate: 200J, 300J, 360J Persistent or recurrent VF/ VT Secondary ABC Survey

Vasopressin

40 IU IVP 1-2 q3minutes,

followed by Epinephrine

1mg IV q3-5 minutes

Vasopressin before Epinephrine not yet recommended by AHA

Resume attempts to defibrillate

1x360J within 30-60 seconds

Consider Antiarrhythmics Amiodarone

(IIb):300 mg IVP (may repeat 150mg doses)

Lidocaine

(indeterminate recommendation):1 1.5mg/kg IVP (my repeat 0.5-0.75mg/kg boluses q5 minutes, to max of 3mg/kg)

Magnesium

(IIb if hypomagnesemic or polymorphic V Tach): 1-2g IV

Procainamide

(IIb for recurrent/ intermittent VF)20 50 mg/min to total of 17mg/kg Consider

Bicarb Resume attempts to defibrillate

360J for each minute of CPR or each med given

Ventricular Fibrillation: Further Inpatient Care

Resuscitated patients must be admitted to an intensive care unit and monitored because of high risk of a recurrence Evaluation of ischemic injury to the CNS, myocardium, and other organs is essential Survivors should have thorough diagnostic testing to establish underlying etiology of VF episode Perform indicated interventions if available to improve long-term prognosis Automated implantable defibrillators (AICDs) are used for patients at high risk for recurrent VF indicate patients with VF arrest who receive AICDs have improved long-term survival rates compared to those receiving only medications

Ventricular Fibrillation: Prognosis

Strongest prediction of prognosis is time to defibrillation Postresuscitation morbidity and mortality related to degree of underlying CNS and multiorgan damage caused by hypoperfusion during VF Survival rates following defibrillation vary AICDs show greatest benefit in promoting long term survival

Ventricular Arrhythmias in Selected Populations: Pregnant Women

Incidence and severity of atrial and ventricular ectopy are reported to increase during pregnancy Isolated atrial and ventricular ectopic beats in pregnant women without existing heart disease are usually benign Important to inquire about the use of over the-counter medication in pregnant women who complain about palpitations or extra heartbeats (pseudoephedrine)

Pregnant Women

continued

Amiodarone is the only antiarrhythmic drug that has been associated with significant fetal abnormalities In addition to cardiac disturbances, amiodarone can cause fetal goiter, neonatal hypothyroidism, and fetal growth retardation When used for hypertension management during pregnancy, propranolol (Inderal) and atenolol (Tenormin) have been associated with intrauterine growth restriction Amiodarone and acebutalol should not be given in lactating women (concentrated in breast milk)

Ventricular Arrhythmias in Selected Populations: Athletes

Malignant ventricular tachycardia, the arrhythmia of most concern in athletes, is usually associated with idiopathic hypertrophic cardiomyopathy Shirani et al,

Sudden death in young competitive athletes. Clinical, demographic, and pathological profiles (

JAMA, 1996) 48 of 131 athletes who experienced sudden cardiac death were found to have this disease, and another 14 probably had it

Athletes

continued

Symptoms of syncope or near-syncope with exercise or a family history of sudden cardiac death in a close relative are red flags for the presence of idiopathic hypertrophic cardiomyopathy Hallmark physical exam finding is a murmur that increases with Valsalva's maneuver When hypertrophic cardiomyopathy is identified, treatment with a beta blocker or calcium channel blocker can reduce cardiac contractility and limit heart rate during exertion AICD alternative Expert panels have recommended that athletes with identified hypertrophic cardiomyopathy be barred from participation in strenuous sports

Ventricular Arrhythmias in Selected Populations: Children

Supraventricular tachycardias are the most common sustained pathologic arrhythmias in children younger than 12 Usually caused by an accessory atrioventricular pathway or Wolff-Parkinson-White syndrome Ventricular extra beats are also common in children Not cause for concern if they resolve with exercise in otherwise healthy children Ventricular extra beats are associated with a higher risk of death in children who have existing structural heart disease or cardiomyopathies

Question 1

A 38 year old white female presents to the office because of recurrent episodes of dizziness and a “funny feeling in her chest.” During one of these episodes, she states she almost passed out. She is on a host of antipsychotic medications for her depression. She had a family member die suddenly at a young age. An EKG is obtained.

Question 1

continued

Which of the following put her at an increased risk of this condition?

A. Female sex B. Medications C. Family history of sudden death D. Age group E. All of the above

Question 2

An otherwise healthy 26 year old male presents to your office because he feels his heart “skipping beats.” He has no history of heart disease. He is an endurance runner, and runs in excess of 40 miles weekly with no associated chest pain or syncope. He drinks 3-4 cups of coffee daily, but denies any alcohol or tobacco usage. Physical exam is benign. An EKG is obtained.

Question 2

continued

Based on the EKG and exam, which of the following is most appropriate to tell this patient?

A.

As shown in the CAST trials, he would benefit from a class IA antiarrhythmic for this malignant rhythm B.

C.

D.

He needs urgent referral to a cardiologist for possible ICD Cutting down on caffeine intake should reduce his symptoms He should stop running, as most cardiologists recommend someone with his condition refrain from strenuous exercise

Question 3

While working in the ER one night, a formerly stable patient complaining of nausea suddenly becomes unresponsive. Telemetry alarms are ringing. The following rhythm is observed.

Question 3

continued

• • • • • What is the first step in the management of this patient?

Perform a precordial thump Defibrillate at 200J, followed by repeated attempts at 30J and 360J Check responsiveness, call a code, and survey ABCDs Vasopressin 40U IVP Carotid massage

Works Cited