Unit 2: Ep Prinicples

Front 1

True or False- SA nodal disease is the most common cause of bradycardic arrhythmias

Back 1

True ; such as susstained bradycardia , sinus arrest/ sinus block , brady-tachy syndrome (sick sinus syndrome)

Front 2

How is SA nodal disease primarly assessed and treated?

Back 2

Assessed thorugh Sinus Node recovery time ( Can also assess "Sino-Atrio Conduction Time"- SACT) and treated with pacemaker placement

Front 3

Sinus nodal disease is usually a benign condition except for what rhythm ?

Back 3

Inappropriate Sinus Tach (IST)

Front 4

What is inappropriate Sinus Tach?

Back 4

HIgh resting HR; rate which greatly increases with minimal exertion ; usually affects young women , unknown cause

Front 5

What are additional symproms that may be present with Inappropriate Sinus Tach?

Back 5

GI, neurologic, visual , fainting shortness of breath .. ect

Front 6

What is the primary treatment of Inappropriate Sinus Tach?

Back 6

Beta Blockers ; also catheter ablation od the SA Node with permanent pacemaker insertion is possible

Front 7

How does one get a Sinus Node Recovery Time ?

Back 7

Pace SA Node for about 30 seconds , turn off and measure the interval from the last paced beat to the first spontaneous sinus beat ; repeat at progressivly faster cycle length untill longest recovery interval is seen

Front 8

Excessive slowing during SA node pacing indicates what ?

Back 8

Poor SA Nodal function

Front 9

Recovery interval =

Back 9

Time from last paced beat to onset of spontaneous SA stimuli ( SNRT)

Front 10

Upper limit of SNRT value is usually what?

Back 10

1500 ms (Slower HR commonly have longer SNRT times)

Front 11

Corrected SNRT upper limit is usually what?

Back 11

525 ms

Front 12

Why is C-SNRT used?

Back 12

used to factor out the SNRT and BCL relationship ; subtract the (un-paced) BCL from the SNRT

Front 13

Describe the Sino-Artial Condiction Time (SACT)

Back 13

Less frequently used and more complicated to determine than measuring SNRT; Measurment of how well sinus node conducts impuse to surrounding tissues (Cause of SA Blocks )

Front 14

Normal Range of Sino-Atrial Conduction Time (SACT)=

Back 14

50-115 ms

Front 15

SA Nodal reentry tachycardia is initated where? Resembles what? And can be induced by (BLANK) and teminated by (BLANK)

Back 15

SA Nodal reentry tachycardia is initited in the SA Node, resembles Sinus Tach, induced by rapid atrial pacing and terminated by rapid atrial pacing

Front 16

How is SA Nodal Reentry Tach treated?

Back 16

Treated with digitalis (dijoxin), BB, CCB

Front 17

What is the second leading cause of brady arrythmias ?

Back 17

AV Blocks

Front 18

Which type of AV Blocks are usually benign ?

Back 18

Proximal Blocks like first degree, second degree type 1

Front 19

Distal AV blocks are usually what?

Back 19

Lethal with ventricular rates in the 20-40 bpm

Front 20

For an AV Block, if the patient is sympromatic and block is transient what is the treatment?

Back 20

Perform a vagal manuver or give atropine

Front 21

For an AV Block if it is persistant or it is a distal block what is the treatment?

Back 21

Implant pacemaker and will potentially ablate the AV Node after pacemaker is implanted

Front 22

Name the two causes of SVTs-

Back 22

Enhanced automaticity and Re-entry - often seen in patients free of cardiac disease

Front 23

Re-entry can cause what rhythms?

Back 23

Atrial Flutter/ A Fib/ Paroxysmal A- tach , Atrio-ventricualr Nodal Re-entry Tachycardia (AVNRT), Atrio- Ventricular Re-entry Tachycardia (AVNRT), intra-atrial re-entry tachycardia

Front 24

To label Atrial Fib as SVT what is the criteria?

Back 24

Stiumualtion originates in the pulmonary veins and results in a ventricular rate under 100 bpm

Front 25

To label Atrial Fib as a AVRT, what is the criteria?

Back 25

stimulation of accessory pathway resulting in rapid ventricualr rate over 100 bpm

Front 26

How does A Fib present at first and how is it treated ?

Back 26

Paroxysmal at first , then becomes chronic- tx= medical management vs ablation therapy

Front 27

What causes AVRT (AV Reentrant tach)?

Back 27

Caused by accessory pathway creating a macro-reentrant circuit ; includes normal conduction pathway connecting ventricle to the atrium

Front 28

True/ False - most AVRT's are WPW

Back 28

Flase

Front 29

How are AVRTs treated?

Back 29

BB, CCB, Ablation therapy (RF or Cryoablation)

Front 30

Wolf-Parkinson White is a genetic condition characterized by what?

Back 30

Short PRI, Long QRS, "Delta Wave" at beginning of QRS

Front 31

Name the symptoms / risk associated with Wolf-Parkinson White

Back 31

Syncope, palpatations, dizziness, at risk of developling rapid ventircualr response A-Fib , can cause sudden cardic death

Front 32

Treatment of WPW=

Back 32

Class III Anti-Arrhythmics (potasisum channel blockers) - Amiodarone

Avoid BB and CCB (why??)

Front 33

AV Nodal Re-entrant tachycardia results from what?

Back 33

Results from dual AV Nodal pathways , ( very difficult to distinguish form other narrow complex tachycardias outside of EP lab)

Front 34

How are AV Nodal Re-entrant Tachycardias treated ?

Back 34

Vagal maneuvers, digitalis , BB, and CCB

Front 35

Descirbe Intra- Atrial Re-entrant Tachycardia

Back 35

Circuit is entirly within the atrium and differs form SVT by paroxysmal nature and that it can be induced and terminated by pacing

Front 36

Treatment for Intra-Atrial Re-entrant Tachycardia

Back 36

Class 1a anti-arrthymic (procanimide )

Front 37

The leading cause of SCD is what?

Back 37

V-tach/ V-fib caused by re-entrant mechinism , not heart attack , may demonstrate as syncope or palpatations

Front 38

Treatment options for SCD had shifted from what to what?

Back 38

From phamacologic therpy to correcting the cause based on how it is iniated

Front 39

VT will usually present with what symptoms?

Back 39

lightheadedness , palpatations, dizziness that does not cause loss of consciousness , monomorphic V-tach usually under 200 bpm

Front 40

How can one determine if rhythm is VT or SVT?

Back 40

If SVT adenosine will often reveal transient AV block or either junctional escape or IVR after breaking tachycardic rhythm , if VT adenosine will have no effect: But if wide-complex is seen always tx as V-tach

Front 41

If syncope is seen in a patient with past history of MI or cardiomyopathy what should you consider as cause?

Back 41

Non-sustained VT/VF as cause ; around 50% chance of inducible VT in EP study

Front 42

If sncyope is seen in patient with no history of MI or cardiomyopathy , what steps are taken?

Back 42

First rule out patients ability to regulate BP as cause then consier EP

Front 43

How does reentrant tachycardia often begin ?

Back 43

Often begins as a PVC inducing monomorphic tachycardia (200 + bbm) and if not corrected will progress to v-fib

Front 44

Stable V-tach usually has a lower what when compared to unstable v-tach?

Back 44

Lower chance of reoccurance

Front 45

What are the steps to induce ventricular tachycardia ?

Back 45

1. perform atrial and nodal EP study first

2. Catheter is placed in RV apex and programmed stimulation performed with simgle, double and tripple extra-stimulus tech and if not successful , incrimental pacing

3. If unsuccessful then move catheter to RVOT and repeat

4. If still unsuccsessful admin isoproterenol (Isuprel) to increase inducibility and repeat above

Front 46

What is the goal of inducing V-tach?

Back 46

Goal is to induce sustained, monomorphic VT (Unsustained , monoporphic VT is usually acceptable to call a "postive exam " but only if VT is suddiciently long -10 beats or more )

Front 47

What may produce a "flase positive" study when indicuing VT?

Back 47

Sustained polymorphic VT is a common finiding when using extra-stimuli

Front 48

If extra-stimuli protocol is not done what may happen?

Back 48

Some extra-stimuli techniques also lead to sustained VT so if extra stimuli protocol is not done, positive results may be missed

Front 49

How are ventiruclar arrhtymias terminated?

Back 49

Same methods used that resulted in VT are used to terminate VT like incremental pacing / extra-stimuli techniques

Front 50

Name the genetic caused of VT

Back 50

1. Idopathic left venticular tachycardia

2.Outflow tract ventiuclar tachycardia

3. Right ventricular dysplasia

Front 51

What are the triggers for idopathic left ventricular tachycardia and how is it treated?

Back 51

Both reentry and triggered activity as mechanism and treated with BB and CCB

Front 52

What triggers outflow tract ventricular tachycardia and how can it be treated?

Back 52

Provoked by exercise and treated with ablation but can use beta blockers and CCB

Front 53

What causes right ventricular dysplasia tachycardia and how it is treated ?

Back 53

Rare and genetic due to abnomal growth , treat with ICD

Front 54

Additonal genetic causes of VT are:

Back 54

1. Bundle branch reentry

2. Brugada syndrome/ sudden unexpected nocturnal death sybdrome ( SUNDS)

3. VT associated with MVP

Front 55

Describe bundle branch reentry and how its treated

Back 55

Very-rare; treated with ablation of RBB

Front 56

What is Brugada Syndrome/ sudden unexpected Nocturnal Death Syndrome (SUNDS) and hwo is it treated?

Back 56

Sodium channel abnormality that affects males more than females ; asians in particular and treated with ICD implant

Front 57

True/ Flase- VT associated with MVP is commonly seen

Back 57

FLASE; descibed by many , proven by none

Front 58

Name the types of arrhythmia therapy:

Back 58

1. Tx reversible causes

2. Anti-arrhythmic medications

3. Surgical therapy (CABG if caused by ischemia or surgical disruption of accessory pathways)

4. Trans-cathter ablation therapy (mapping electircal system)

5. device therapy (PPM, ICD)

Front 59

Why is cardiac mapping performed ?

Back 59

1. to determine activation patterns of arrythmias

2. Locate sites of arrhythmia origin

3. ID areas of abnormal conduction

Front 60

Primary methods of cardiac mapping include :

Back 60

1. sequential mapping (CARTO)

2. Continuous Mapping (LASSO)

3. Non-contact mapping (Ensite)

4. Non-invasive Mapping (MRI, still investigational)

Front 61

CARTO =

Back 61

Sequential mapping, 3D CT/ MRI electroanatomical reconstuction; simuntaneous recording of catheter location and EGM activation

Front 62

What are the parts invloved with CARTO?

Back 62

Ablation catheter with magnetic sensor at tip, external ulta -low magbetic emitter placed under patient and processor unit

Front 63

What doe the colors (red, yellow, green and purple) represnet on the EGM activation on CARTO ?

Back 63

red= earliest depolarizations

yellow and green= intermediae depolarzations

purple= latest depolarizations

Front 64

Describe the cathters used for continuous mapping

Back 64

Electrodes are 1mm diameter and 1-2mm long, electrode distance between 3-10 mm

Front 65

The accuracy of continuous mapping depends on what ?

Back 65

1. Number of splines per basket

2. Number of electrodes on each spline

3. Percentage of electrodes in contact with endocardial surface

Front 66

What are the limitations of continuous mapping ?

Back 66

-too small or large array results in poor quality

- movement between beating heart and array detrimental to reconstruction process

- provides minimal specific anatomic infromation

-does not map atrial appendage area or pulmonary veins

Front 67

Noncontact Mapping=

Back 67

(EnSite) - Balloon with embedded electrical array and "roving" catheter introduced into same chamber with tip in contact with wall

Front 68

With noncontact mapping, the "roving" catheter demonstates what and when are signals captured ?

Back 68

demonstrates spatial replationship to array and signals are captured during diastole (when points are most distant from array)

Front 69

What are the advantages of noncontact mapping?

Back 69

1. very fast mapping time (seconds)

2. global and local cardiac electrical events`

Front 70

What are the disadvatages of noncontact mapping?

Back 70

1. background noise degrades image

2. too great of distance between rover and array

results in decreased accuracy

3. Complex and very expensive systems

Front 71

Name the three principles of success for ablation therapy

Back 71

1. complete understanding of the arrthymia

2.complete understanding of the anatomy and accessory pathways

3. correct technology

Front 72

The technology for ablations include what?

Back 72

DC ablation , RF ablation and Cryogenic therapy

Front 73

When was DC abalation mostly used and why has its use slowed?

Back 73

Used mostly in the 1980s and its used is less frequently bc its high volatge (2000-4000 V) produces gas that increase pressure within vessel, it creates transmural lesions that are potentialy arrhymogenic. Also its use was limted to AV junction and there was limted catheter selection

Front 74

Describe RF Ablation therapy-

Back 74

AC combined with relativly low radio frequency , untilzes much lower voltage than DC (40-60V), produces less heat (< 100 degrees C), no gas production or pressures within

Front 75

True/ False- similar to DC ablation, there is also a limted cathter selection with RF ablation

Back 75

False - theres a variety of catheter shapes and sizes available , flexible tip for custom postioning and electrode tip is longer than Dx Cathters to increase surface area

Front 76

Name the advantages of RF Ablation-

Back 76

1. Less voltage, less heat , no gas

2. Larger surface area

3. Does not create transmural lesions as easily

4. Can be used on thin walled structures like coronary sinus or cardiac veins

5. Can be used on small sturctures (Av node vs. AV junction)

6. Little stimulation of muscle or nerve ; less need for anesthesia

Front 77

What are the disadvantages of RF Ablation?

Back 77

1. Percise mapping of circuit is required

2. Very wide or very deep target tissue may not be easily resovlved with RF ablation

3. Delivery of RF energy is not quick; requires stable electrode placement for possibly several minutes

Front 78

What are the complicaations of RF Ablation?

Back 78

1. Creation of high- grade heart blocks

2. Cardiac perforation and cardiac tamponade

3. Production of mitral or tricuspid regrigitation

4. Embolization

5. Pulmonary Vein stenosis

6. Potenial for disruption of coronary artery media and creation of coronary artery lesion

Front 79

What is Cryogenic ablation?

Back 79

It utilizes extreme cold to allow for "stunning" of tissue at cellular level; not genrarlly used at first line ablative therapy

Front 80

True/ False- Cryogenic therapy requires mapping of conduction system

Back 80

True !

Front 81

For ablation of AV Node / Junction what device must be inserted ?

Back 81

temporary pacemaker must be in place prior to start of procedure

Front 82

Why is it safer to ablate the AV node than the bundle of his?

Back 82

Bc the bundle of his is in deeper tissue and is the only connection between the atrium and ventricles

Front 83

Development of accelerated junctional tach while ablating AV node/ junction indicates what?

Back 83

successful outcome

Front 84

For AVNRT ablation, what landmark is important?

Back 84

Koch's triangle - fast pathway follows "tendon of tendaro", slow pathway defined by tricuspid annulus (slow pathway usually ablated after mapping bc it posses fewer compliations )

Front 85

What is involved in a typical atrial fib ablation?

Back 85

Ablate between the tricuspid annulus and the IVC; linear ablations around PVs to block or direct stimuli

Front 86

Atypical atrial flutter caused by?

Back 86

Scar tissue

Front 87

What problems are associated with ventricular arrhymias ?

Back 87

1. stimuli will go around scar tissue

2. ablating point just outside exit does not eliminate circuit

3. stimuli travels slowly through scar tissue creating reenty loop

4. ablating at exit point results in stimuli taking a different pathway

Front 88

When is septal alcohol ablation often used?

Back 88

Tx for HOCM with refractory med therapy

Front 89

How is seotal alcholor ablation performed?

Back 89

Pure alcohol is injected into proximal 1st septal artery to create ischemia

Front 90

Septal Alcohol ablation has high potenital for what?

Back 90

High mortality rate (2%), high potential for AV Blocks and BBB requiring pacemaker ( >50%), high potential for reentry VT post-procedre and chance for VF (2.6%)