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 diseasePrevalence ranges from less than 3% in young healthy women to grater than 20% for older African Americans with hypertensionRisk 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

PVCCompensatory 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 TrialsCAST (1989)showed increased mortality in patients post-MI whose PVCs were successfully suppressed with antiarrhythmicsCAST 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 mortalityCAST and CAST II show no benefit for treatment of PVCsLeft 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 networkIntrinsic rate of 30-40bpmIdioventricular beats have wide QRS complexes, abnormal ST segments, and secondary T wave changes similar to PVCsIf 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 infarctionMorbidity’Mortality: IVR does not affect the clinical course of the patientRace: No racial differences observedSex: No sexual predilection observedAge: More common in elderly, secondary to increased incidence of MI and coronary disease

IVR: Therapy

No specific antiarrhythmic therapy indicatedGenerally self-limited in patients with ischemiaIf digitalis toxicity or electrolyte abnormality the cause, generally corrects rapidly following underlying correctionSuppressant drugs such as lidocaine should be avoided, as they may knock out the only reliable pacemakerAtropine sulfate given in 0.5mg increments every 3 to 5 minutes may augment SA node and allow “capture” of ventriclesArtificial 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 deathAntiarrhythmics favored over ICDs in these patientsESVEM (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 groupCardiac 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

Vaughn-Williams Classification for Antiarrhythmic Medications

Class I Sodium-channel blockers

Class IADepress phase 0 of action potential; delay conduction, prolong repolarization (phase

III, IV); quinidine, procainamide, disopyramide

Class 1BLittle 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 ICDepress phase 0 of the action potential; markedly slow conduction in normal tissues;

flecainide, propafenone, moricizine

Class IIBeta-adrenergic blocking agents; acebutalol, atenolol, bisoprolol, carvedilol,

metoprolol, nadolol, pindolol, propranolol and others

Class IIIProlong action potential duration by increasing repolarization and refractoriness;

amiodarone, sotalol, bretylium, dofetilide, azimilide, ibutilide.

Class IV Calcium-channel blockers; diltiazem, verapamil

Others 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 CASHA 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 VTPatients 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 AberrancyFactors favoring SVT with

aberrancyFactors favoring ventricular tachycardia

Typical right bundle-branch block with normal axisTypical left bundle-branch block with normal axisDelta wave

Atrioventricular dissociationLeft bundle-branch block with right-axis deviationLeft-axis or extreme right-axis deviationQRS complex >140 millisecondsFusion complexesCapture beatsConcordant R wave progression patterns (all leads V1-V6 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 characteristicsEKG in limb leads shows a sinusoidal increase and decrease in QRS voltage, resembling rotation about the isoelectric baselineDifferentiating 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.)LithiumCisaprideHAARTMethadoneChemotherapeutic 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 levelIsoproterenol infusion (rate 210 μg/minute) for acute controlTemporary overdrive pacing: rate >140bpmClass IA antiarrhythmics should not be used; may worsen QT prolongationan and propagate ventricular fibrillationPropranolol 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 ischemiaIncreased 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 affectedSex: 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 importantAutomated 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

Airway

Breathing

Circulation

Defibrillate: 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 alternativeExpert 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. He needs urgent referral to a cardiologist for possible ICD

C. Cutting down on caffeine intake should reduce his symptoms

D. 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