Transcript Ventricular Arrhythmias

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 0.12.0% 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
Vaughn-Williams Classification for Antiarrhythmic Medications
Class I
Sodium-channel blockers
Class IA
Depress phase 0 of action potential; delay conduction, prolong repolarization (phase
III, IV); quinidine, procainamide, disopyramide
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
Depress phase 0 of the action potential; markedly slow conduction in normal tissues;
flecainide, propafenone, moricizine
Class II
Beta-adrenergic blocking agents; acebutalol, atenolol, bisoprolol, carvedilol,
metoprolol, nadolol, pindolol, propranolol and others
Class III
Prolong 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 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
Factors favoring ventricular tachycardia
Typical right bundle-branch
block with normal axis
Typical left bundle-branch
block with normal axis
Delta wave
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 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 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 1990December 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 510% for each minute after onset of VF
Artificial pacemakers or implantable
defibrillators mandate use of anteriorposterior 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):11.5mg/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)2050 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 overthe-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. 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