The Sa Node, Av Node, And His-Purkinje System - Ch 5

Front 1

SA node size

Back 1

3 mm in width, 10 mm in length

Front 2

Crista terminalis

Back 2

Endocardial ridge extending from the SVC to IVC along the lateral right atrium

Front 3

SA Node comma tail

Back 3

Extends downward along the crista terminalis toward the IVC

Front 4

Increased sympathetic tone effects on SA node

Back 4

Trigger the head

Front 5

Increased parasympathetic tone effects on SA node

Back 5

Trigger the tail

Front 6

Most common cause of bradycardia

Back 6

Sick Sinus Syndrome. Degenerative disease of the SA node. Fibrosis and fatty infiltration of nodal cells.

Front 7

SA Nodal Dysfunction Arrhythmia List

Back 7

Sinus bradycardia, arrest, exit block, brady-tachy

Front 8

Symptomatic Sinus Bradycardia

Back 8

Sick Sinus Syndrome (PPM is indicated)

Front 9

Healthy resting sinus rate

Back 9

40 bpm

Front 10

Resting heart rates in upper 80s or 90s

Back 10

Anemia or cardiopulmonary or thyroid disorders

Front 11

Most common cause of SA nodal disease

Back 11

Fibrosis of the SA node

Front 12

Brady-tachy result of exaggerated overdrive suppression

Back 12

Prolonged asystolic pauses

Front 13

Sinus Node Recovery Time

Back 13

Slope of phase 4 automaticity is reduced in the SA node, resulting in a bradycardia

Front 14

SNRT Test

Back 14

30 second drive train and overdrive suppression measurement of the SA node. In SA nodal disease, the recovery time tends to be exaggerated

Front 15

SNRT Test - SA nodal disease results

Back 15

The recovery interval can be longer than normal OR the gradual return to the baseline rate (over 5 or 6 beats) can be interrupted during recovery intervals

Front 16

Recovery times after slower pacing rates

Back 16

Longer recovery times

Front 17

Recovery times after faster pacing rates

Back 17

Shorter recovery times

Front 18

SNRT measurement considered that SA nodal dysfunction is present

Back 18

> 1500 msec

Front 19

Corrected Sinus Node Recovery Time Formula

Back 19

CSNRT = SNRT - BCL (Basic Cycle Length)

Front 20

Positive CSNRT measurement (considered that SA nodal dysfunction is present)

Back 20

> 525 msec

Front 21

SNRT to BCL ratio

Back 21

SNRT/BCL x 100%

Front 22

SNRT Ratio measurement considered that SA nodal dysfunction is present

Back 22

> 160%

Front 23

Sinoatrial Conduction Time (SACT)

Back 23

How well the SA node is able to conduct the electrical impulses it produces out to surrounding atrial tissue

Front 24

SA Nodal Exit Block

Back 24

The sinus node's generated impulses do not pass through the perinodal tissue to the atria

Front 25

SACT Formula

Back 25

1/2 the difference between the Return Cycle length and the Basic Cycle Length

Front 26

Normal SACT interval length

Back 26

50-125 msec

Front 27

Narula Method

Back 27

Drive train given barely faster than the base rate, to minimize any overdrive suppression

Front 28

Strauss Method

Back 28

A series of single premature atrial impulses are used, to guarantee that no overdrive suppression will occur

Front 29

Autonomic Blockade

Back 29

Giving propranolol (0.2 mg/kg) and atropine (0.04 mg/kg)

Front 30

Intrinsic Heart Rate Formula

Back 30

IHR = 118.1 - (0.57 x age)

Front 31

Exercise Test

Back 31

Parasympathetic withdrawal in a patient with sinus bradycardia, diagnosing SA nodal dysfuction

Front 32

Study of choice in assessing SA nodal dysfunction

Back 32

Ambulatory cardiac monitoring

Front 33

EP studies are applied ___% of the time for SA nodal disorders

Back 33

70

Front 34

Symptoms with SA and AV nodal diseases

Back 34

Lightheadedness, dizziness, presyncope, and syncope

Front 35

Ischemia or infarction involving the right coronary artery can cause...

Back 35

His-Purkinje Block

Front 36

Heart block following an inferior myocardial infarction is usually localized where?

Back 36

AV Node - an normal conduction usually recovers (sometimes after a few days or weeks)

Front 37

Drugs that may cause 1 degree heart block

Back 37

Digoxin, B-blockers, calcium blockers

Front 38

High Junctional Escape Rhythm heart rate

Back 38

40-55 bpm

Front 39

Ventricular Escape Rhythm rate

Back 39

20-40 bpm

Front 40

Distal AV block following myocardial infarction is associated with

Back 40

Occlusion of the left anterior descending artery

Front 41

1 degree AV block PR interval prolongation

Back 41

20-40 msec

Front 42

Type of third-degree AV block more likely to produce symptoms

Back 42

Distal

Front 43

AV Dissociation

Back 43

Ventricular rate is higher than the atrial rate (looks like CHB). Some P waves conduct to the Ventricles

Front 44

PPM implanted in which types of AV blocks?

Back 44

Distal 2nd degree and Distal 3rd degree

Front 45

First degree AV block indicated for PPM

Back 45

HV interval > 100 msec

Front 46

Second or third degree AV nodal (proximal) block indicated for PPM

Back 46

Symptomatic bradycardia is present

Front 47

Maneuvers that decrease vagal tone or increase sympathetic tone

Back 47

Improve AV nodal block, but no change in distal block

Front 48

Maneuvers that increase vagal tone or decrease sympathetic tone

Back 48

Worsen AV nodal block, but no change in distal block

Front 49

Exercise or atropine administration with 2:1 second degree AV nodal block

Back 49

Improve or resolve the block; conduction ratio will worsen with distal block

Front 50

Vagal Maneuvers and beta blockers - 2nd degree AV block

Back 50

Worsens AV nodal block, No change in distal block

Front 51

Normal conduction time through His bundle

Back 51

< 25 msec

Front 52

His bundle conduction delay

Back 52

> 25 msec

Front 53

Split His present - indication for PPM?

Back 53

Yes

Front 54

Third degree AV block within AV node

Back 54

H spikes procede V spikes on His EGM

Front 55

Third degree AV block in His-Purkinje system

Back 55

H spikes after A spikes on His EGM

Front 56

FRP

Back 56

Shortest H1-H2 interval attained

Front 57

Drugs used to improve AV nodal function

Back 57

Atropine or isoproterenol

Front 58

H1-H2 interval indicating distal conducting disease with block in the His-Purkinje system

Back 58

> 400 msec

Front 59

Wenckebach cycle length

Back 59

Atrial pacing rate at which Mobitz I block occurs; usually less than or equal to 450 msec

Front 60

RBBB incidence percentage in 50-year-olds

Back 60

1%

Front 61

RBBB incidence percentage in 80-year-olds

Back 61

10%

Front 62

RBBB is common in conditions causing

Back 62

Pulmonary hypertension or right ventricular hypertrophy, inflammation, or infarction

Front 63

The presence of RBBB alone - indication for PPM?

Back 63

No

Front 64

LBBB incidence percentage in 50-year-olds

Back 64

0.5%

Front 65

LBBB incidence percentage in 80-year-olds

Back 65

5-6%

Front 66

LBBB in older patients most often indicates

Back 66

Progressive heart disease (coronary artery disease, cardiomyopathy, valvular heart disease)

Front 67

LBBB and heart failure can be treated with

Back 67

CRT devices

Front 68

Chance of causing a RBBB in a heart catheterization

Back 68

5%

Front 69

LBBB alone - indication for PPM?

Back 69

No

Front 70

AAI used when

Back 70

Patients with SA nodal disease, and likely to have blunted heart rate response to exercise. More likely to see AAIR

Front 71

VVIR used when

Back 71

Chronic atrial fibrillation

Front 72

Pacemaker Syndrome

Back 72

Intrinsic atrial impulses occur during or just after ventricular pacing, thus causing the atria to contract against closed AV valves producing reflux of atrial blood through the SVC and pulmonary veins

Front 73

Percent of patients who require VVI pacing that display some degree of pacemaker syndrome

Back 73

20%

Front 74

Are patients with chronic A fib subject to pacemaker syndrome?

Back 74

No

Front 75

Mode switching

Back 75

When a PPM senses an atrial tachyarrhythmia, the PPM switches to a non-atrial tracking mode

Front 76

Pacemaker Tachycardia

Back 76

A PVC causes a retrograde P wave, and the PPM triggers a V pace, causing a PPM mediated reentrant tachycardia. This occurs at the maximum programmed pacing rate

Front 77

Methods to control pacemaker tachycardia

Back 77

Lengthen PVARP, decrease atrial sensing as to not sense retrograde P waves, algorithm to extend PVARP after a PVC, algorithm to automatically withhold a single ventricular impulse after a certain number of beats

Front 78

Biventricular pacing

Back 78

Improve left ventricular hemodynamic function for patients with systolic heart failure and intraventricular conduction delays (IVCD)

Front 79

A Fib development is reduced with what kind of pacing?

Back 79

Dual chamber

Front 80

Mode used for Sinus Node Dysfunction

Back 80

DDDR

Front 81

Amount of people with SA Nodal disease that have AV conduction disease

Back 81

1/3

Front 82

CSNRT Sensitivity and Specificity Percentage

Back 82

70%

Front 83

Increase Sympathetic Tone

Back 83

Increase catecholomines, Increase heart rate

Front 84

Increase Parasympathetic Tone

Back 84

Decrease Heart rate, Primarily through the vagus nerve

Front 85

Athletes

Back 85

High vagal states

Front 86

Vasovagal Syncope and Hypersensitive Carotid Sinus

Back 86

Parasympathetic response often secondary to sympathetic influence

Front 87

Assessing sinus node dysfunction

Back 87

May induce parasympathetic block with atropine, rates >100 or 30-50% increase

Front 88

Ischemia may cause AV nodal block

Back 88

90% of time blood is supplied from RCA

Front 89

Congenital

Back 89

HB usually occurs at AV nodal level

Front 90

Acute Rheumatic Fever

Back 90

May cause AV block

Front 91

Inflammatory or infectious disease of the myocardium

Back 91

His Purkinje Block, Lenegre & Lev's disease

Front 92

CHB Intranodal

Back 92

H associated with V waves

Front 93

CHB Infranodal

Back 93

H associated with A waves