Cardio Part 8

Front 1

in what order do the three heart layers repolarize?

Back 1

epicardium first,

then endocardium

myocardium is *last*

Front 2

3 mechanisms of arrhythmias:

Back 2

1. abnl automaticity

2. abnl trigger

3. reentry
(by far the most common cause of arrhythmias)

Front 3

automaticity occurs as a result of:

Back 3

fibrosis, ischemia, degeneration, hypokalemia, etc.

that damgae the SA/AV nodes

=> other cells (e.g. Perkinje cells) fire on their own to maintain heart beat

Front 4

abnormal triggers =

Back 4

afterdepolarizations = abnl depolarizations of myocytes

Front 5

afterdepol's are either:

Back 5

early or delayed

Front 6

2 basic requirements for reentry:

Back 6

1. 2 pathways

2. heterogeneous electrical activity b/w them

Front 7

remember that conduction blocks can:

Back 7

stop a signal in one direction but allow it in the other

Front 8

refractoriness =

Back 8

insensitivity/Resistance to s/t

Front 9

2 types of reentry:

Back 9

1. anatomic reentry

2. functional reentry

Front 10

in anatomic reentry, the depolarization goes around:

Back 10

a fixed obstacle, e.g. scar or normal part of the heart

Front 11

anatomic reentry implies:

Back 11

excitable gap

Front 12

excitable gap =

Back 12

any area ready to conduct

Front 13

3 types of arrhythmias that occur as a result of anatomic reentry:

Back 13

1. AVNRT

2. AVRT

3. VT

Front 14

2 features of functional reentry:

Back 14

1. NO fixed reentry

2. eddy in a stream - depols in every direction

Front 15

in functional reentry, circuits may be:

(2)

Back 15

variable (like in A-fib)

OR

settle into a specific ruts (~atrial flutter)

Front 16

3 goals of catheter ablation:

Back 16

1. break the reentry circuit

2. create a barrier to conduction

3. *eliminate the source* of abnormal automaticity or triggered activity

Front 17

bradyarrhythmias are the result of:

(2)

Back 17

1. abnl automaticity

2. degeneration of nl conduction system

Front 18

sinus brady =

Back 18

abnormal automaticiity of the SA node

Front 19

(a sinus P is an:

Back 19

upright P)

Front 20

4 causes of sinus bradycardia:

Back 20

high vagal tone, deg. disease, ischemia, drugs, etc.

Front 21

what does a high vagal tone do?

Back 21

decreases HR

Front 22

treatment of sinus brady:

Back 22

nothing.

RARE that it's symptomatic - pacemaker if so

Front 23

sinus pause =

Back 23

NO sinus activity for a bit

- otherwise e/t looks normal

Front 24

cause of sinus pause =

Back 24

degeneration around SA node

Front 25

treat sinus pause with pacemaker, only if symptomatic; main symptom =

Back 25

syncope >= 3 seconds

Front 26

tachy-brady syndrome =

Back 26

pauses at the end of tachyarrhythmias due to A-fib

Front 27

2 features of tachy-brady syndrome:

Back 27

1. *significant* symptoms, usually syncope

2. *req's* pacemaker

Front 28

compared to sinus rhythm of SA node, AV node slowness is a result of:

Back 28

slower phase 4 depolarization (takes longer to get to threshold)

Front 29

to distinguish P waves from T waves:

Back 29

P waves should be much more narrow

Front 30

junctional escape rhythm:

(2)

Back 30

1. due to SA node dysfunction, **AV takes over**

2. e/t normal, just slower (50-60 bpm)

Front 31

3 features of first-degree AV node "block":

Back 31

1. it IS prolonged PR interval (>0.20)

- prolonged PR = first-degree block

2. every P wave gets through

3. no treatment - it's asymp

Front 32

normal PR interval =

Back 32

0.12 - 0.20 sec.

Front 33

causes of first-degree block:

Back 33

AV nodal disease,

high vagal tone,

drugs, etc

Front 34

2 features that Mobitz I and II have in common:

Back 34

1. some P's occur *w/o* QRS

2. regular rhythm

Front 35

in Mobitz type II, the refractioness is fixed =>

Back 35

NO CHANGE in heart beat by inc. vagal tone OR exercising

Front 36

3rd-degree block ~~

Back 36

NO relationship between P and QRS

= complete separation of atria and ventricles

- NO P-wave gets through => different numbers of P and QRS

Front 37

3 features of 3rd-degree block:

Back 37

1. independent atrial and ventricular rates, as ventricles fire on their own

2. ~somewhere below the AV node has taken over (duh)

3. slow HR (also duh - ventricle is in control of its own fate)

Front 38

carotid massage =>

Back 38

inc. vagal tone

=> dec. HR

Front 39

PAC ~~ premature P-waves of:

Back 39

different appearances

Front 40

2 features of PAC:

Back 40

1. **atrial signal might not get to ventricles => pauses**

2. **no treatment, but watch for trigger of other arrhythmias**

Front 41

PVC ~~

Back 41

ventricular cells firing on their own

Front 42

3 features of PVC:

Back 42

1. **wide QRS** of different appearances

2. don't treat unless there's a high burden

3. can trigger other arrythmias

Front 43

tachyarrhythmias and QRS: wide QRS =

Back 43

signal to contract is coming from below the AV node

=> ***conduction is NOT traveling through the normal conduction system***

Front 44

wide QRS/signal not going through normal conduction pathway corresponds to:

(3)

Back 44

1. aberancy (BBB)

2. pre-excitation (accessory pathway)

3. ventricular origin of rate

Front 45

sinus tachy:

(2)

Back 45

1. P is upright in I, II, and aVF

2. treat UC (pain, dehydration, etc)

Front 46

atrial flutter =

Back 46

reentry arrhythmia of RA, involving the cavo-tricuspid isthmus

Front 47

in atrial flutter, the atrial cycle takes:

Back 47

~0.2. sec

~~300 bpm (fast)

=> continual atrial activation with sawtooth pattern

Front 48

with atrial flutter, ventricular rate depends on:

Back 48

how many atrial signals get through to the AV node

Front 49

ventricular rates tend to be dividends of:

Back 49

300

=> 300, 150, 75

Front 50

conduction rate of atrial flutter, wrt atria signals reaching ventricles, comes in 3 forms:

Back 50

2:1,

4:1,

or irregular (variable conduction)

Front 51

irregular conduction from atria to ventricles in atrial flutter is:

Back 51

regularly irregular

Front 52

treatment of atrial flutter =

(3)

Back 52

1. anticoagulants for stroke prevention

2. rate control/AV nodal blockers

3. ablation of cavo-tricuspid isthmus

Front 53

AVNRT = AV Node Reentry Tachy =

Back 53

slow pathway (from SA to AV node) being used over fast pathway

=> self-sustaining circuit

Front 54

(in normal conduction from SA to AV node, the fast pathway "blocks" the slow one; however, in the event of a:

Back 54

*PAC,* the fast pathway is blocked

=> slow pathway used => reaches AV node, but also goes back up fast pathway

=> already repolarized by the time it's back to the beginning of the slow pathway => circuit)

Front 55

AVNRT on EKG:

Back 55

**P and QRS occur at nearly the same time**

=> P is either buried or comes immediately *after*

Front 56

treatment of AVNRT =

(3)

Back 56

1. transiently block AV node with adenosine

2. chronic: AV node blockers (anti-arr's)

3. chronic: ablation of slow pathway

Front 57

AVRT ~~

Back 57

accessory pathways of muscular portions surrounding MV, TV

(these are normal - fuse with AV node signal to provide unified contraction)

Front 58

AVRT occurs when:

Back 58

forward conduction through the accessory pathway is blocked

=> AV node conduction continues

=> travels retrograde through the accessory pathway

=> activates atria prematurely

Front 59

EKG of AVRT:

Back 59

**P wave after QRS** (later than in AVNRT)

(QRS is narrow, regular, like in AVNRT)

Front 60

relationship between WPW and AVRT:

Back 60

WPW is a specific kind of AVRT

- accessory pathway exists in WPW

- normally has a wider QRS

Front 61

WPW is a _________________________ disorder

Back 61

pre-excitation;

if something happens such that AV conduction and accessory conduction don't match anymore, the accessory pathway becomes a part of a circuit

=> pre-excitation of the ventricles

=> delta waves

Front 62

delta waves =

Back 62

QRS *immediately* after P - NO INTERVAL

Front 63

treatment of AVRT:

(2)

Back 63

1. adenosine, vagal maneuvers to transiently block AV node

2. ablation of accessory pathway

Front 64

***for both AVNRT and AVRT:***

Back 64

the AV node is **part of the circuit**

Front 65

significance of the AV node being part of the circuit in AVNRT and AVRT:

Back 65

***interrupting AV nodal transmission for even one beat TERMINATES the tachy***

- of course, need to follow up with chronic treatment to prevent it from happening again

Front 66

adenosine comes in:

mechanism:

Back 66

***rapid*** IV push

- it reverses arousal by increasing efflux of K+ out of AV node cells => dec. concentration of K+ inside AV node =>

=> hyperpolarization => dec. conduction in AV node

(also dec's cAMP in SA node => dec. SA node depol)

Front 67

atrial tachycardia =

Back 67

tachy as a result of **signal originating in muscle,** NOT SA or AV

Front 68

**atrial tachycardia does NOT involve:**

Back 68

the AV node

- *adenosine is useless* in atrial tachycardia

Front 69

EKG of atrial tachy:

(2)

Back 69

1. **inverted P-wave**

2. terminates into sinus rhythm

Front 70

treatment of atrial tachy:

(2)

Back 70

1. if infrequent, leave it alone

2. if incessant, use anti-arr drug or cath ablation

Front 71

what's the most common tachyarrhythmia?

Back 71

A-fib

Front 72

fibrillation =

Back 72

muscular twitching without coordination

Front 73

A-fib is initiated by:

(2)

Back 73

trigger or automaticity

Front 74

**A-fib is maintained by:**

Back 74

**functional reentry**

Front 75

QRS activity of A-fib:

Back 75

**irregularly irregular**

Front 76

2 other features of A-fib:

Back 76

1. no consistent atrial activity = **NO discernible P WAVES**

2. rate varies, depending on refractoriness of AV node

Front 77

3 treatments of A-fib:

Back 77

1. anticoagulants for stroke prevention

2. AV nodal blockers for rate control, as nec.

3. rhythm control if symptomatic

Front 78

3 ways to control rhythm (as in A-fib)

Back 78

1. anti-arr drugs

2. cath ablation

3. DC cardioversion - change herat rate via electricity

Front 79

main feature of VT =

Back 79

WIDE QRS

(b/c signal originates in the ventricles)

Front 80

treatment of VT:

(3)

Back 80

1. ACLS like defib - acute

2. ICD - chronic

3. may require anti-arr, cath ablation

Front 81

Torsades (twisting) is the result of:

Back 81

an EAD like PVC triggering reentry

Front 82

treatment of Torsades =

(2)

Back 82

1. ACLS - acute

2. ICD - chronic

Front 83

a long QT is >

Back 83

450 ms

- congenital or acquired

Front 84

A-fib can cause:

Back 84

pre-excitation of ventricle via accessory

=> can become VF => sudden death

Front 85

acute treatment of A-fib that became VFib:

Back 85

DC cardioversion, then ablation of accessory pathway

Front 86

PR interval begins at:

Back 86

P,

goes to beginning of QRS

Front 87

Normal QRS width =

Back 87

0.1

Front 88

B-blockers lower HTN by;

Back 88

lowering the work of the heart, which lowers BP

Front 89

ventricular myocytes are ectopically faster than:

Back 89

Perkinje fibers

(bundle branches and Perkinje fibers fire at the same rate)

Front 90

***3 types of SVT's:***

Back 90

1. AVNRT

2. AVRT

3. AT

Front 91

anti-arr drugs are VERY:

Back 91

toxic

Front 92

Mobitz type I is a ____________ condition

Back 92

stable;

NO adverse outcomes => no treatment

Front 93

3 biochem ways to decrease abnormal automaticity (of pacemakers or non-pacemakers):

Back 93

1. dec. slope (rate) of phase 4 depol

2. hyperpolarize the troublemaking cells

3. inc. the threshold necessary to cause AP

Front 94

2 ways to stop triggered activity:

Back 94

1. dec. AP duration

2. correct Ca2+ overload (prevents DAD's)

Front 95

3 ways to stop renetry arrhythmia:

Back 95

1. dec. conduction of circuit
(signal can become so slow that it fails)

2. inc. refractory periods within circuit

3. suppress premature beats

Front 96

***4 classes of anti-arr drugs:***

Back 96

Class I = Na+ channel blockers

Class II = B-blockers

Class III = DRK+ channel blockers

Class IV = L-type Ca2+ channel blockers

Front 97

**all 4 classes combat:**

Back 97

automaticity

Front 98

how do all anti-arr drugs combat automaticity?

(2)

Back 98

1. dec. slope/rate of phase 4 depolarization

2. inc. threshold

Front 99

Class IA effects on Reentry =

(2)

Back 99

1. moderate Na+ chan. block (dec's amplitude of AP)

2. inc. AP duration

Front 100

3 Class IA drugs:

Back 100

1. Quinidine

2. Procainamide

3. Disopyramide

Front 101

risk with Quinidine:

Back 101

inc's risk of Torsades

Front 102

A-fib ~~

Back 102

irregularly irregular

(as is atrial flutter of *variable* conduction - not 2:1 or 4:1)

Front 103

Torsades =>

Back 103

QT prolong

=> syncope/sudden death

Front 104

Procainamide ~~

Back 104

less-pronounced QT prolongation

- **best one to use**

Front 105

Disopyramide =>

Back 105

decreased inotropy

=> constipation/urinary retention

Front 106

Class IB effects on Reentry =

(2)

Back 106

1. only mildly blocks Na+ channels

2. *shortens* AP

Front 107

2 Class IB drugs:

Back 107

1. Lidocaine

2. Mexiletine

(both have CNS SE's)

Front 108

**special feature of Lidocaine:**

Back 108

ONLY IV

(Mexiletine is oral)

Front 109

Class IC effects on Reentry =

(2)

Back 109

1. *markedly* inhibit Na+ channels

2. NO effect on AP duration

Front 110

2 Class IC drugs:

Back 110

1. Flecainide

2. Propafenone

(both have CNS effects)

Front 111

Flecainide:

(2)

Back 111

1. oral

2. *increases ventricular arrhythmias - AVOID

Front 112

Propafenone is a:

Back 112

*weak B-blocker*

Front 113

Class II anti-arr's are B-blockers; they are used for:

Back 113

treating all sorts of arr's

Front 114

Class II/B-blockers dec. reentry by:

Back 114

prolonging repolarization of the **AV node**

- also block catecholamine-induced arr's

(catecholamines make arr's worse)

Front 115

names of B-blockers/class II:

Back 115

Propranolol,

other "-olols"

Front 116

2 effects of Class III DRK channel blockers:

Back 116

inc. AP duration by blocking K+ efflux in stages 2 and 3

(cells can't get as negative)

Front 117

blocking DRK's during reentry arr's =>

(2)

Back 117

1. inc. AP duration,

2. => prolonged repolarization

Front 118

worst/best Class III drug =

Back 118

Amiodarone

- a drug of all 4 classes

- decreases SA node firing, dec. automaticity, dec. reentry circuits

- but incredibly toxic

- though first-line treatment for resuscitation

- takes forever to observe, forever to get rid of - monitor closely

Front 119

3 other Class III drugs:

Back 119

1. Dronedarone

2. Dofetilide

3. Sotalol

Front 120

Dronedarone:

(2)

Back 120

1. analogue of Amiodarone

2. GI SE's but no Torsades

Front 121

major SE of Dofetilide =

Back 121

**Torsades**

Front 122

Sotalol:

(2)

Back 122

1. a B-blocker

2. SE's common to all B-blockers - cardiac depression, bronchospasm

Front 123

**Class IV anti-arr's are:**

Back 123

L-type Ca2+ blockers

Front 124

***L-type Ca2+ channels are found mostly in:***

Back 124

**the SA and AV nodes**

Front 125

the 2 Class IV drugs used are:

Back 125

1. Diltiazem

2. Verapamil

Front 126

too much Diltiazem or Varepamil =>

Back 126

cardiac depression

- dec. CO, hypotension

Front 127

Class IV anti-arr's stop reentry by:

(2)

Back 127

1. inc. refractory period

2. dec. conduction velocity

Front 128

***Class lV anti-arr's are the primary treatment for:***

Back 128

AVNRT

Front 129

Class IV drugs cannot be given to pts with B-blockers; result =

Back 129

HF

Front 130

Digoxin can also be an anti-arr; what does it do?

(2)

Back 130

1. enhances vagal tone

2. reduces sympathetic activity

Front 131

Digoxin is used to treat:

(3)

Back 131

1. A-fib

2. a-flutter

3. SVT's

Front 132

SVT's originate:

Back 132

at or above the AV node

Front 133

adenosine is also an:

Back 133

antiarrhythmatic

Front 134

the Left Bundle has two parts:

Back 134

Left Anterior Fascicle,

Left Posterior (Inferior) Fascicle

Front 135

in the event of a Left Anterior Fascicle Block, conduction travels:

Back 135

inferiorly from the septum to the LPF,

then around the bottom of the heart

- from the bottom, conduction goes up and to the left

Front 136

3 EKG results of a LAF Block:

Back 136

1. Left Axis Deviation

2. tall R in lateral leads (I, aVL, v5, v6)

3. deep S in inferior leads (II, III, aVF)

Front 137

in the event of a Left Posterior Fascicle Block, conduction travels:

Back 137

from LAF,

down and to the right

Front 138

3 EKG results of a RPF Block:

Back 138

1. RAD, between 90 and 180

2. deep S in lateral leads (I, aVL, v5, v6)

3. tall R in inferior leads (II, III, aVF)

Front 139

3 EKG features of RBBB:

Back 139

1. rSR' rabbit ears in v1

2. normal qrs in v6

3. S waves in I, aVL

Front 140

3 EKG features of LBBB:

Back 140

1. notched/broad QRS in I, aVL

2. upside-down notch in III

3. qs complex in v1

***in all cases, QRS and T-wave are discordant*** (opposite)

Front 141

diagnosing ST elevation (acute MI) in LBBB: look for:

(2)

Back 141

1. 2mm ST elevation concordant with QRS

2. 2mm ST depression in v1-v3

Front 142

EKG of a pacemaker =

Back 142

EKG of **LBBB**

Front 143

4 EKG features of WPW syndrome:

Back 143

1. decreased PR interval (< 0.12 sec)

2. QRS >0.10 sec (wide)

3. delta wave

4. A-fib with QRS of varying width

Front 144

what do B-blockers and adenosine do in WPW pts?

Back 144

slow conduction

=> bigger delta waves

(HUGE with adenosine)

Front 145

most accessory pathways are in:

Back 145

the left free wall

Front 146

best place to check for long QT =

Back 146

lead II

Front 147

**accessory pathways => **

Back 147

*fused* P and QRS

~~ smaller/no PR interval

Front 148

classic EKG finding of PE:

Back 148

S1Q3T3

Front 149

S1Q3T3 explained:

Back 149

S wave in lead I,

Q in lead III

inverted T in lead III

Front 150

**more common EKG findings in PE** =

(2)

Back 150

1. sinus tachy

2. new A-fib

Front 151

Brugada = inherited syndrome that predisposes to:

Back 151

arrhythmias

- defect in SCN5a sodium channel

=> long slop down on QRS

Front 152

clinical symptoms of LQT's ~~

Back 152

broad spectrum of presentations, including asymp

Front 153

LQT1 is exacerbated by:

Back 153

exercise

Front 154

LQT2 is exacerbated by:

Back 154

emotions/stress

Front 155

LQT3 is exacerbated by:

Back 155

sleep/rest

Front 156

what kind of defects do the LQT's fall under?

Back 156

LQT1 and LQT2 K+ channel defects,

LQT3 = Na+ channel defect

Front 157

B-blockers are protective in:

Back 157

LQT1,

not 2 or 3

Front 158

classic EKG finding of Arrhythmic RC CM:

Back 158

Epsilon wave b/w end of QRS and beginning T

(fatty infiltration => myocyte loss)