Rhythms That Go Bump in the Night

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Rhythms That Go Bump in the Night

• Teresa Menendez Hood, M.D.

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FLBs

• Creepy VF
• Eerie VT
• Scary AF
• Ghostly Torsade

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Sudden Cardiac Death

• 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 EPS54 will have inducible VT and 30 will
  have inducible PMVT

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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 262105-112.
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VF

• The primary arrhythmia responsible for SCD
• Acute treatment is with external defibrillation

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VT or SVT with Aberrancy?
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VF (or the EKG of JELLO)
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Ben Franklin would say electricity is a good
thing!
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ICD shock
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Eerie VT in patients with CAD

• Usually seen in patients with a prior
  MIextensive, 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(gt120ms) in NORMAL SINUS RHYTHM.

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VT with CAD
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VT with CAD
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Wide complex tachycardia

• 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), RS interval
  gt100ms 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

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LBBB
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SVT with Aberrancy
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VT or SVT?
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VT or SVT?
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Always err on side that is is VT because

• 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

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VT with CAD

• Mechanism is reentry which means that is can be
  induced by EP study using PES and can be
  entrained and reset
• Do not worry, only EPs 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)

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VT with CAD

• 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)

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VT with Idiopathic Dilated Cardiomyopathy

• IDCCan 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.

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VT with IDCM

• 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!

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IDCM

• 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

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VT with Arrhythmogenic Right Ventricular Dysplasia

• 17 cause of SCD in the young in the US
• Familial in 30
• More common in men and with exercise
• VTs 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

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EPSILON WAVE-can you see it?
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VT in Hypertrophic Cardiomyopathy

• 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

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VT with HCM

• 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.

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EKG in HCM

•     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.

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Other causes of scd

• 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 examiners office. DMN
  10/17/03

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Intracerebral Hemorrhage
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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.
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Normal Heart VTIdiopathic

• Yesit 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!

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RVOT VT
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Long QT
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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
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WPW
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WPW
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WPW with AFIB
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Brugada
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Brugada
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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
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TdP
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Treatment would beremove the culprit drug,
temporary pace at 100 and give magnesium!
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The End