Transcript Rhythms That Go Bump in the Night

Rhythms That Go Bump in
the Night
Teresa Menendez Hood, M.D.
FLB’s
Creepy VF
 Eerie VT
 Scary AF
 Ghostly Torsade
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Sudden Cardiac Death
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Death within one hour of onset with an abrupt
change in clinical status
In the field: VF is present 40%, EMD 20% and
Asystole 40%
 Order of survival: 25%, 6%, 1%
Monomorphic VT is actually not that common
This represents 50% of ALL cardiac deaths
(300,000/year)
It is the initial manifestation of CAD in ½ of all
SCD victims.
20% will have no structural heart disease.
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CAD accounts for 80% of all SCD in
Western societies
Only 20% are due to an acute MI
Risk Factors: coronary artery disease and
its risk factors, LVH, certain
cardiomyopathies and genetic diseases
Transient risk factors include: ischemia,
systemic abnormalities, autonomic factors
and proarrythmic factors
At EPS:54% will have inducible VT and
30% will have inducible PMVT
Creepy VF
Inventor of the
external
defibrillator!
 Paul Zoll, M.D.
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Original article: NEJM 1960
Ventricular Fibrillation: Treatment and Prevention by External Electric
Currents
Ventricular fibrillation, usually a rapidly fatal arrhythmia, occurs most commonly in coronary-artery
disease, in patients with atrioventricular block and in toxic reactions to digitalis, quinidine and procaine
amide. Occasionally, it succeeds ventricular tachycardia. This paper presents additional experiences
confirming the clinical value of external countershock in terminating ventricular tachycardia and
fibrillation and of external electric stimulation in preventing these arrhythmias. Alternating current (60
cycle, 0.15 second, 150 to 450 volts) was applied to the unopened chest with large electrodes. A
cardiac pacemaker providing monophasic rounded impulses of 2 milliseconds duration over wide
ranges of rate and amplitude was used to stimulate the heart externally. Ventricular tachycardia and
fibrillation were terminated by externally applied electric countershock more than five hundred and
thirty-two times in 8 patients; 5 have survived for one month to two and a half years. The technique is
immediately effective, clinically feasible and safe. Prevention of recurrent ventricular tachycardia and
fibrillation in patients with complete heart block remains an unsolved problem. Drugs are largely
ineffective; external electric cardiac stimulation at rates above the basic idioventricular rate has been
effective in preventing these recurrent ventricular arrhythmias, but long-term stimulation is difficult.
Zoll PM, Linenthal AJ, Normal Zarsky LR. Ventricular Fibrillation: Treatment and Prevention by External
Electric Currents. New Eng J Med 1960; 262:105-112.
VF
The primary arrhythmia responsible
for SCD
 Acute treatment is with external
defibrillation
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VT or SVT with Aberrancy?
VF (or the EKG of JELLO)
Ben Franklin would say
electricity is a good thing!
ICD shock
Eerie VT in patients with
CAD
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Usually seen in patients with a prior
MI:extensive, healed, at least 2 weeks old
May result in syncope or SCD
Poor predictors: previous large MI that
involves the septum and with low EF; if
the MI involved CHF/hypotension or VF
that is also not good; if you are left with
an LV aneurysm or a wide QRS(>120ms)
in NORMAL SINUS RHYTHM.
VT with CAD
VT with CAD
Wide complex tachycardia
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If the patient has structural heart disease, then it is VT
It does not matter what the BP is in your decision making
Things that favor VT:
• positive or negative concordance, visible AV
dissociation, NW axis, absence of an RS complex in
all the precordial leads(v1-v6), R:S interval >100ms
in any precordial lead
Things that favor SVT with aberrancy:
• Looks like a classic LBBB/RBBB (know what this is in
V1 and lead 1), has the same QRS as in NSR
LBBB
SVT with Aberrancy
VT or SVT?
A sixty-five-year-old female is POD #1 after
appendectomy for acute appendicitis. She has a history
of prior bypass surgery and hypertension; her
medications include aspirin, atenolol, and lisinopril. The
following asymptomatic arrhythmia is noted on
telemetry:
VT or SVT?
Always err on side that is is
VT because………
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1. VT is more common than SVT with aberrancy
2. In patients with structural heart disease,
particularly prior infarction, VT is much, much
more common than SVT with aberrancy
3. If SVT is misdiagnosed as VT for the
purposes of acute treatment, no harm will
come to the patient
4. If VT is misdiagnosed as SVT for the
purposes of acute treatment, a cardiac arrest
can be precipitated
VT with CAD
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Mechanism is reentry which means that is
can be induced by EP study using PES
and can be entrained and reset
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Do not worry, only EP’s understand this
Among patients with spontaneous VT and
CAD , 95% will have it induced in the lab
22% will need 2 sites used for induction
of VT (RVA and RVOT)
VT with CAD
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The key feature that predicts how well
tolerated it will be is the rate and thus
dictates the initial strategy
If not well tolerated? SYNCH CVN
Little data that Lidocaine does
anything..may be helpful if patient is
having an MI
IV amiodarone is the drug of choice for
acute stable VT or VT recurrences
Long term treatment should be an ICD
with or without AAD therapy(amiodarone
or Class III drugs)
VT with Idiopathic Dilated
Cardiomyopathy
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IDC:Can have multiple etiologies and 1/3
are familial
Arrhythmogenesis may be due to
extensive subendocardial scarring and
patchy fibrosis which can lead to areas of
reentry
Other triggers may be microvascular
ischemia,electrolyte abnormalities,
geometric alterations and changes in
catecholamines.
VT with IDCM
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Bundle Branch Reentry VT-this is a
VT that occurs in up to 30% of
patients and is a reentrant circuit in
the His Purkinje system.This VT
tends to be fast (~300 beats per
minute) and result in syncope and
degenerate to VF. This VT is treated
with ablation on the RBB and not an
ICD!
IDCM
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These patients tend to have EMD or
Bradyarrythmias along with VT/VF as a
mode of SCD (especially in those with
Functional Class 4 CHF)
Syncope should be taken seriously and is
an indication for ICD
EP studies are not as predictive as in
patients with CAD
Amiodarone appears to be more helpful
than in patients with CAD
VT with Arrhythmogenic
Right Ventricular Dysplasia
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17% cause of SCD in the young in the US
Familial in 30%
More common in men and with exercise
VT’s usually come from the RV
Fibrous tissue and fat in the RV (the epicardial
layer) and replaces normal myocardial cells
EKG usually may show an epsilon wave in the RV
leads or t wave inversion and see ST elevation
on stress testing of the RV leads
Positive signal average EKG
Treatment is ICD +/- Ablation
EPSILON WAVE-can you
see it?
This is called an epsilon wave, and reflects delayed
conduction in the right ventricle, a right
ventricular “late potential”. This is a classic ECG
for arrhythmogenic right ventricular
cardiomyopathy.
VT in Hypertrophic
Cardiomyopathy
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HCM is when there is hypertrophy in the absence
of a cardiac or systemic cause
Due to genetic mutations in the cardiac
sarcomere proteins and autosomal dominant in
45%
Can get AFIB which is not tolerated well
VT/VF is often preceded by AFB or ST
Those who are young and male have the worst
prognosis
They tend to also have microvascular ischemia,
autonomic dysfunction and abnormal response
to exercise
VT with HCM
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40% of the SCD occurs during or after
exercise
They also have enhanced AV nodal
conduction which makes their atrial
fibrillation conduct faster and 5% have an
accessory pathway
Those at highest risk are those with
positive FH of SCD, NSVT, Syncope,
Inducible VT/VF at EP study, and
abnormal BP to exercise.
EKG in HCM
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It varies from normal to significantly
abnormal.
Left ventricular hypertrophy is common.
Often has left anterior hemiblock.
Q waves in anterolateral leads which can
simulate recent myocardial infarction is not
unusual.
Many times deep Q in II, III , AVF with ST
segment elevation can be seen.
Other causes of scd
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Valvular
Congenital Heart Disease
MVP
Neurological Disease- “cerebral T waves”
Congenital Long QT
Myocarditis
WPW, Brugada, Short QT
Coronary anomalies-anomalous artery passes
between the aorta and the pulmonary trunk
• “A congenital heart defect caused the death of an Everman High School football player
who collapsed Thursday morning on the school track, according to preliminary findings
released Friday by the Tarrant County medical examiner’s office. “ DMN 10/17/03
Intracerebral Hemorrhage
Short QT Syndrome
A Familial Cause of Sudden Death
The short QT syndrome is characterized by familial sudden death,
short refractory periods, and inducible ventricular fibrillation. It is
important to recognize this ECG pattern because it is related to a
high risk of sudden death in young, otherwise healthy subjects.
Normal Heart VT:Idiopathic
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Yes……it does exist
RVOT VT-catecholamine sensitive
LVOT VT-catecholamine sensitive
Fascicular VT-from left anterior or
posterior fascicle-Belhassen's VT. Due to
microreentry and adenosine sensitive and
can respond to verapamil.
These are treated with ablation and NOT
AN ICD!
RVOT VT
Long QT
Mutations in potassium-channel genes KCNQ1 (LQT1 locus) and
KCNH2 (LQT2 locus) and the sodium-channel gene SCN5A
(LQT3 locus) are the most common causes of the congenital
long-QT syndrome
Long QT
WPW
WPW
WPW with AFIB
Brugada
Brugada
Polymorphic VT
Need to look at the QT interval and
decide whether it is long or normal…
 If it is long? Is it due to acquired or
congenital long QT?
 If it is normal, then must rule out
ischemia and once you have done
that, consider Brugada syndrome or
Short QT syndrome …
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Drug induced Long QT
TdP
Treatment would be…remove the
culprit drug, temporary pace at 100
and give magnesium!
The End