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36 Cards in this Set

  • Front
  • Back
Automatic Mechanisms
PVCs
Myocardial Infarction / Ischemia
Acid based disturbances
electrolyte inbalances
hypoxemia
Drugs and SCD - VT
Beneficial:

a. Beta Blockers are inhibitors - Amiodarone

Harmful:

Flecanide, Sotalol, Proporol

Neutral: Dotefilide
MTWA
Measures T waves to 1 millionth of a volt

Micro T wave Alternans

SCD Heft: ICDs lowered the risk of SCD by 23 %
SAECG
Signal Averaged ECG

let's you see late action potentials
Long QT Syndrome
1. Congenital or
2. Result of drugs
3. Propensity for Syncope or Torsades do Points
Reason for VT Ablation Failure
Isthmus broader than lesion
Intramural or epicardial location is too deep
Mural Thrombos
RVOT
Right Ventricular Outflow Tract

deals with mapping
Endocardial Activation Mapping
Ablation catheter examines area around inside of RVOT. and can possibly determine foci of arrhythmia
Non Contact Mapping
Used for hemodynamic intolerance of VT and is a catheter which is an electrode array from left ventricle
Pace Mapping
pace in area arrhythmia originates. ECG same as during Tachycardia - same morphology
What Causes VT
Premature ventricular depolarization - PVC
What causes VT to move to VF
unknown mechanism
VF Mechanisms
1. Multiple wavelets
2. Mother rotors
SCD in Young
Greater than 1000 die each day in US
HCM - hypertrophic cardiomyopathy is most common
Cardiac Arrest
1. Electrical Phase - first 4 minutes and best treatment is immediate defib

2. Circulatory Phase - 4-10 minutes, delay defib 1-3 minutes and compress chest and ventilate

3. Metabolic Phase 10 minutes + = tissue injury
Commotio Cordis
Blunt force to chest:

1. Hockey, lacrosse, baseball
2. survival following collapse is 15% increasing to 46% when in V-fib when difibrillated
Electrical Storm
Occurrences of 3 or more episodes of VT / VF within 24 hours

6-7 shocks
Precordial Thump
thump to chest if external ICD not available
Seasonal Variation of VT / VF
1. Study show circadian variation patterns and season patterns

2. Wintertime peak with January having highest incidence
Antiarrhythmic therapy
1. Sotalol & Amiodarone - neutral affect on survival

2. Beta Blockers associate with better survival
ICD Indications
Class I - you get the device
a. Spontaneous sustained VT
b. Cardiac arrest due to VF or VT

Class II -
a. Cardiac arrest presumed to be due to VF when electrophysiologic testing precluded by medical conditions

b. Severe symptoms from sustained VT

c. Recurrent Syncope - undetermined origin

Class III

a. Incessant VT / VF because you would shock them all the time
Mechanisms -Automatic
1. PVCs
2. VT and VF associated with acute conditions: MI, Ischemia, Hypoxemia
3. Acid base disturbances

Need to treat the underlying cause and they are not inducible
Mechanisms - Reentry
Pre-entrant Ventricular Arrhythmias
Usually from underlying heart disease
Commonly ischemic heart disease

Can initiate with pacing and can terminate with pacing
Mechanisms - Trigger
1. Pause dependent
2. Catechol dependent
3. Features - both automatic and reentry
4. Both types develop polymorphic VT
Two types of Activation Sequences that maintain fibrillation
1. Wandering wavelets of activation due to multiple reentry

2. Stationary mother rotor - pebble in a pond
ATP limitations for fast VT
1. 70-80 % fast VTs up to 250 bpm
2. may be terminated with a single burst of ATP
3. Medtronic can deliver ATP during charge
Shock delivered after ATP termination
Patient has ATP but gets shocked

Not unusual if it has a type II break
Factors that influence ATP efficacy
1. timing of the stimulus
2. coupling interval
3. rate and number of pulses in the stimulus drive train
4. Proximity of the stimulating site to the circuit
Asterid
Atrial sensing to reduce inappropriate defibrillation:

1. Inappropriate therapy - 20-30 % of patients
Pause Dependent
Pause dependent caused by after potentials in Phase 3 that reach threshold potential

Related to conditions with prolonged action potential
EADs

DADs
1. Early After Depolarization

2. Delayed After Depolarization - occurs in settings DIG toxicity
Factors for EP Study
Factors Increasing Positive Study:
1. Monomorphic VT
2. Sustained
3. Induce single or double stimuli

Factors Decreasing Positive Study

1. Polymorphic
2. Non-sustained
3. Induce triple extrastimuli
VT Mapping
Looking for earliest signal on left side of the line
Upper limit of Vulnerability
Lowest energy given during the vulnerable period of the cardiac cycle that DOES NOT induce VF when other lower energies are successful.

If you do not induce your DFT should be less
Idiopathic VTs - without heart disease such as CAD or MI
1. ARVD - arrhythmogenic RV Displasia - predominately in males - Epsilon waves & family history of arrythmias

2. RVOT - RV Outflow tract - thought to be a harmless condition

3. ILVT - idiopathic LV tachycardia - originates in lower left septum and appears in younger patients. It is usually reentry or triggered

4. BBR - bundle branch reentry tachycardia - reentrant tachycardia found in either right or left bundle branches. May be good to ablate and pace. Patients usually have syncope, palpitations and SCD with rates > 200 bpm
Triggered VTs - 2 types

1. Pause dependent

2. Catechol dependent
Cardiac Action Potentials

1. Pause dependent associated with EAD's or early after depolarizations - Phase 3

2. Catechol dependent associated with DAD's or delayed after depolarizations - phase 4