Fcm Cardiac Arrhythmias

Front 1

What are the two groups of abnormal heart rhythms?

Back 1

- abnormal impulse formation (pacemaker)
- abnormal impusle conduction (movement of depolarizing wavefront through heart)

Front 2

What is the pacemaker hiercharcy?
What is Pacemaker Dominance?
What is "overdrive suppression"?

Back 2

- Hierarchy:
SA Node > Atria > AV Node > His-Purkinje Network > Ventricular Muscle

- Pacemaker Dominance = most rapidly depolarizing tissue controls the hear rhythm (normally the SA Node)

- "Overdrive Suppression" = SA node controls hearth rhythm, and this inhibits the subsidiary cells from dominating

Front 3

Where is the SA Node located?
What is its normal rate of depolarization?

Back 3

- Located in high right artium, at junction with SVC

- Normal Depol Rate: 60-100 bpm

Front 4

What is the normal rate of depolarization of the AV Node?

Back 4

45-60 bpm

Front 5

What is the normal rate of depolarization of the artia and ventricles?

Back 5

<35 bmp

Front 6

What are the two groups of abnormal heart rhythms?

Back 6

- abnormal impulse formation (pacemaker)
- abnormal impusle conduction (movement of depolarizing wavefront through heart)

Front 7

What is the pacemaker hiercharcy?
What is Pacemaker Dominance?
What is "overdrive suppression"?

Back 7

- Hierarchy:
SA Node > Atria > AV Node > His-Purkinje Network > Ventricular Muscle

- Pacemaker Dominance = most rapidly depolarizing tissue controls the hear rhythm (normally the SA Node)

- "Overdrive Suppression" = SA node controls hearth rhythm, and this inhibits the subsidiary cells from dominating

Front 8

Where is the SA Node located?
What is its normal rate of depolarization?

Back 8

- Located in high right artium, at junction with SVC

- Normal Depol Rate: 60-100 bpm

Front 9

What is the normal rate of depolarization of the AV Node?

Back 9

45-60 bpm

Front 10

What is the normal rate of depolarization of the artia and ventricles?

Back 10

<35 bmp

Front 11

What is the sympathetic v. parasympathetic (vagal) effect on heart rate?
- What are the main agonist and antagonist of each?

Back 11

Sympathetic: increases HR
- agonist: Epi, NE
- antag: Beta-Blockers

Parasympathetic/Vagal: slows HR
- agonist: Ach
- antag: Atropine

Front 12

What is sinus arrhythmia?

Back 12

When the HR varies with respiration
= speeds up with inspiration
= slows down with expiration

- common among young people, athletes, and during the relative vagotonia of sleep

Front 13

HR:
What is a normal Sinus Rhythm?
What is Sinus Bradycardia?
What is Sinus Tachycardia

Back 13

- Normal Sinus Rhythm: 60-100 bpm
- Bradycardia: <60 bpm
- Tachycardia: >100 bpm

Front 14

Since the SA and AV Nodes are not visible on the ECG, what is the typical marker used to detect rhythm?

Back 14

P wave - represents atrial depolarization

Front 15

What are the sites of conduction delay?

Back 15

Sites: SA Node, AV Node, Intra-ventricular block (bundle block or fascicular block)

Front 16

What are the degrees of conduction delay?

Back 16

Degrees:

- 1st degree = conduction delay

- 2nd degree = intermittent failure of conduction

--> Type I/Wenckebach Type = progressive slowing prior to block

--> Type II = All or None
(Type II is called Mobitz for AV Blocks only)

3rd degree = complete conduction failure

Front 17

What types of SA Blocks might their be?

Back 17

Only 2nd and 3rd degree SA Blocks are possible

Front 18

What are the features of a Type I SA Block

Back 18

2nd degree, type I SA block:

- P-P interval gradually shortens, then a puase occurs
- Pause duration is < the last 2 P-P intervals
- After the pause, the first new P-P interval is greater than the last one before the pause

Front 19

What are the features of a Type II SA Block?

Back 19

2nd degree, type II SA block:

- P-P interval is constant...
- Pause occurs= 2 x P-P

Front 20

What are the features of a 3rd degree SA Block?
- AKA??

Back 20

Aka: Sinus Arrest/SA Arrest

- No P wave at all bc the impulse fails to depolarize the atrium

Front 21

Sick Sinus Syndrome:
- What are the ECG Findings?
- What are the symptoms?
- What are the cause main causes?
- What is the best treatment?

Back 21

ECG: SA Block, Sinus Arrest, Sinus Bradycardia, (possibly brady-tachy syndrome)

Symptoms: lightheadedness, dizziness, syncope (from the bradycardia). fatigue, angina

*Abnormal foci in the atria might develop --> might lead to bradycardia-tachycardia syndrome

- Causes: idiopathic fibrosis of sinus node region; CAD (rarely)

- Tx: permanent pacing (relieves symptoms, but does not prolong life)

Front 22

Bradycardia-Tachycardia Syndrome

Back 22

In a person with sick sinus syndrome, becase both the impulse formation and conduction are abnormal, abnormal foci in the atria can develop.

--> Tachycardia exaggerates the bradycardia --> long pauses follow each group of tachycardic beats ("post-conversion pause")

Front 23

What does the PR Interval reflect?

Back 23

Reflects the conduction from the sinus node through the atrium, AV node, bundle of His, bundle branches

Front 24

What are the features of a 1st degree AV Block?

Back 24

- PR prolongation >20 s
- slowing in AV nodal conduction
- requires no specific therapy

Front 25

2nd degree AV Block
- aka???
- Type I

Back 25

= Mobitz Type I
- PR interval gradually lengthens in consecutive cycles until a block occurs for one beat (PR intervals lengthen by decreasing amounts)
- First new beat after block has PR Interval shorter than last one prior to block
**PP Intervals remain constant (the PRs lengthen and the RRs shorten)

Front 26

Where in the heart is the source of the delay when AV delay exists?

Back 26

AV Node or His-Purk fibers

Front 27

What clinical conditions are associated with 2nd degree, type I AV block?

Back 27

- drugs that slow AV nodal conduction = beta-blockers, ca-channel blockers, digitalis

- inferior wall MI (due to AV nodal ischemia)

- Increased vagal tone in normal patients - during sleep, trained athletes

Front 28

What is appropriate tx of 2nd degree type I AV block?

Back 28

- if asymptomatic - no tx

- if symptomatic (HR <40 bpm) - remove any meds taht might be slowing AV nodal conduction; pacing required when bradycardia is persisten, symptomatic

Front 29

What are the clinical features of a Type II 2nd degree AV block?
- aka??

Back 29

aka: Mobitz Type II Block

- Sudden absence of QRS despite no change in PP or PR
- RR at the block is a multiple of the one before the block

** Block is generally INFRANODAL (below the level of the AV node)--> suggest disease in His Bundle and Bundle Branches
- Forerunner of complete AV Block

Front 30

What is the tx for Mobitz Type II AV block?

Back 30

Permanent Pacing

Front 31

Second Degree AV Block
Type I v. Type II:
- PR Interval
- QRS Complex
- Site of Block
- Progression
- Permanent Pacing?
- Causes

Back 31

PR Interval:
- I: prolongs
- II: constant

QRS:
- I: narrow
- II: wide

Site of Block:
- I: AV Node
- II: Infranodal

Progression:
- I: rare
- II: common

Permanent Pacemaker?
- I: rarely needed
- II: indicated

Causes:
- I: drugs, vagal tone
- II: conduction system disease

Front 32

What is a 3rd degree AV Block?
- aka?
Where is the underlying block?
What is the physiologic mechanism?

Back 32

= Absence of conduction between atriuma nd ventricles- beat independently
= AV Dissociation
= Ventricular Escape

- Normal P wave; No S Wave


- Block at AV Node or Infranodal
- AV Nodal Block: Junctional Escape (narrow QRS)
- Block Distal to His Bundles: Ventricular Escape (wide QRS)

- Physiologic Mechanism: cardiac pacemaker cells located distal to block become the dominant pacemaker and cause escape rhythm

Front 33

What clinical conditions are associated with 3rd degree AV Block?

Back 33

- congenital

- acquired: primary conduction system disease, cardiomyopathy, infiltrative heart diseases (amyloid, sarcoidosis, metastatic tumor), myocarditis; MI

Front 34

What is the difference between Inferior and Anterior MI in third degree heart block?

Back 34

Inferior MI - due to ischemia; usually reversible

Anterior MI; due to tissue necrosis, usually irreversible

Front 35

Tx of 3rd degree heart block?

Back 35

Inferior MI: pacing only if sx (angina, CHF, hypertension)or rate <40 bpm

Other conditions: permanent pacing, unless reversible (such as lyme disease)

Front 36

What is AV Dissociation?
What are the causes/physiologic mechanisms?

Back 36

When the atria and ventricles have independent rhythms

Physiologic mechanism:

1. slowing of SA node (primary pacemaker) followed by escape rhythm of subsidary pacemaker

2. Acceleration of subsidiary pacemaker faster than SA node, which overtakes sinus rhythm
- New rhythm: Accelerated Idioventricular Rhythm
- Not all AV dissoc is heart block (although 3rd degree AV block is one example)

3. AV Block with escape rhythm from subsidiary focus

Front 37

What are the possible abnormal ventricular conductions?

Back 37

Bundle Branch Blocks

Pre-excitation (Wolff-Parkinson-White Syndrome)

Front 38

What are the characteristics of a Bundle Branch Block?
What types of BB's are there?

Back 38

- Wide QRS - due to slowing within conduction system
- RBBB
- LBBB: Delay in terminal forces; early forces over normal bundle are rapid
- Fascicular Blocks (LAFB, LPFB), non-specific IVDC

Front 39

WPW Syndrome
- what does it stand for?
- what is it?
- what are characteristic ECG findings?

Back 39

Wolff-Parkinson-White Syndrome
- Accessory Pathway from atrial muscle directly into ventricular muscle

- Wide QRS - confuction through ventricular muscle is slower than normal His-Purk conduction

- short PR - accessory fiber enters ventricle faster than normal conduction would (no delay at the AV Node)
--> causes characteristic Delta wave- slurred upstroke of QRS with little space between P and R

- QRS Complex is a fusion complex - both condiction over accessory pathway and AV nodes

Front 40

Premature atrial contraction (PAC):
- cause?
- ECG evidence?

Back 40

- Caused by ectopic foci in the atria (isolated or multiple) causing abnormal depolarization

- ECG: abnormal P wave!
- depending on how premature the contraction is, P wave might be buried in the ST seg or in the T wave
- PR interval prolonged - due to delay at the AV node

Front 41

Where are the different points in the cardiac cycle in which a PAC can occur, and how does thic effect the heart beat?

Back 41

After a cycle (depolarization), the heart needs to repolarize step-wise....

a. if the PAC occurs very early, and the AV node has yet to repolarize, the cycle is blocked from that point on = AV Block

b. if the PAC occurs while one of the bindle branches has yet to repolarize, there is a RBBB or LBBB (aberrant ventricular conduction)

c. If the PAC occurs late enough in the cardiac cycle, after all parts have finished repolarizing, there is a normal, full beat - normal PR interval and QRS complex

Front 42

How do you tell if the premature beat seen on the ECG is atrial (PAC) or ventricular (PVC) in origin?

Back 42

PAC - resets the sinus node, so the next beat occurs very quickly (< 2xP-P away = INCOMPLETE PAUSE)

PVC - allows P-P to propagate bc does not reset sinus node... next beat occurs on time (2xP-P away = COMPLETE PAUSE)

Front 43

What is the current hypothesis for Atrial Fibrillation (AF)?

What is a demographic fact about AF?

Back 43

"Multiple Wavelet Hypothesis" - multiple wavelets wander randomly around atrium --> may combine, divide, vary in size/shape --> atrial rate is thus rapid and irregular (disorganized on ECG)

- AF is most common sustained arrhythmia; >2 million americans (most common in elderly)

Front 44

Atrial Fibrillation ECG:
- At what lead is AF best seen?
- What is the rate of AF?
- What is the ventricular rate and response on ECG?

Back 44

- Lead I: shows irregular heights and spacing
- Rate: 400 +/- 50
- Ventricle: rate depends upon status of AV node; response is irregular; QRS is narrow

Front 45

What are the clinical features of Atrial Fibrillation?

Back 45

- Rapid ventricular response may cause hemodynamic compromise
- Associated with systemic emboli
- Loss of effective atrial contraction may cause fall in cardiac output

Front 46

What clinical heart problems might lead to Atrial Fibrillation?

Back 46

- Valvular heart disease, which causes atrial enlargement
- Atherosclerotic heart disease
- Cardiomyopathy
- Sick Sinus Syndrome
- Pericardial Disease
- Idiopathic

Front 47

What are treatements for Atrial Fibrillation?

Back 47

Prevention of systemic emboli
- Worry of stroke if pt has risk factors:
- valvular heart disease (esp mitral valve)
- other structural heart disease
- age >70
- hypertension
- diabetes
- CHF
- prior TIA/stroke
- L vent dysfunction
- Give anticoagulant (Warfarin)

Conversion to sinus rhythm
- Worried about abnormal ventricular response
- Patients with AF >24 hours
- Give Warfarin for 3 wks before conversion and 1 month after (worried about stroke risk)

Cardioversion - direct defibrillation to restore sinus rhythm
- usually elective
- may be emergent if pt has hemodynamic compromise
- otherwise, use oral drugs and pt can return for elective cardioversion (bc drugs less effective)

Maintain the sinus rhythm:
- Type I or Type II antiarrhythmic drugs to prevent AF

Front 48

What is Atrial Flutter and how is it formed?

Back 48

Current is sent through a single, counterclockwise circuit within the right atrium
--> L atrium is activated passively, not directly part of circuit
- the circuit is located in an area/isthmus of slow conduction btwn the tricuspid annulus, the IVC, and the coronary sinus os

Front 49

Atrial Flutter: ECG
- what is the rate?
- what does the ECG look like?
- in what lead is it best seen?

Back 49

Rate = 300 +/- 50
- Rate depends on conduction time through the circuit and the remainder of the R atrium, as well as the length of the circuit
- Ventricular Rate depends on AV nodal conduction time = some dividend of the atrial rate

- Flutter waves tend to be "saw toothed" with no clear isoelectric period; flutter waves are consistent in timing, size, shape

- Lead II, III, avF are best leads

Front 50

Why is atrial flutter said to be "unstable"?

Back 50

The ventricular response may suddenly become rapid

Front 51

What are the symptoms of atrial flutter and what do they depend on?

Back 51

Symptoms related to ventricular rate
- Rapid ventricular rates may be associated with hemodynamic compromise (decreased BP,low cardiac output)

Front 52

What is the treatment of Atrial Flutter?

Back 52

Want to control heart rate by increasing AV Nodal Block --> slows ventricular response
Then...

- Terminate the arrhythmia by type I or type II antiarrhythmic drugs
- Direct cardioconversion in symptomatic patients
- Prevention with antiarrhythmic drugs
- Catheter Ablation - create linear lesion in IVC/tricuspid annular ishthmus --> prevents reentry from occurring

Front 53

What are the main differences between ATRIAL FIBRILLATION and ATRIAL FLUTTER

Back 53

FIB - f waves irregular
FLU - flutter waves consistent

FIB - best seen in V1, V2
FLU - best seen in II, III, avF

FIB - irregular QRS response (narrom)
FLU - regular QRS response

FIB - atrial rate = 400 +/- 50
FLU - atrial rate = 300 +/- 50

**Both associated with risk of stroke

Front 54

What does AVNRT Stand for?

Back 54

AV Node Reentrant (Supraventricular) Tachycardia

Front 55

What causes 50-60% of atrial tachycardia?

Back 55

AVNRT - problems of reentry within the AV Node

Front 56

What is the mechanism behind AVNRT?

What are the ECG findings?

Back 56

AV node has 2 pathways: slow and fast (Fast is normal)
--> if normal fast pathway is blocked by APD (premature atrial depol), then conduction proceeds down the slow pathway [antegrade] --> once reaches end, can go back up fast pathway [retrograde], then down the slow pathway again [antegrade]
-->continues supraventricular tachycardia

ECG:
- tachycardia
- RP interval is less than PR interval (P wave follows QRS immediately - i.e., atrial contraction immediately follows ventricular contraction)

Front 57

What does AVRT stand for?
Explain...

Back 57

AV Reentrant Supraventricular Tachycardia
= part of the reentrant circuit occurs over tissue that connects the atrium and ventricle, but is outside the AV node region... "accessory pathways" or "bypass tracts"

- Depending on where the pathway crosses the AV groove, they can be:
- L-sided
- R-sided
- septal

For example, WPW Syndrome

**If there is a PAC that blocks the normal WPW Pathway, then the charge goes down the normal AV Node [antegrade] and back up the WPW circuit [retrograde]

Front 58

Summarize the pathways of AVNRT and AVRT

Back 58

AVNRT:
- APC blocks normal fast pathway down AV Node
- Antegrade: down slow pathway
- Retrograde: up fast pathway
- Antegrade: down slow pathway
**P wave immediately follows QRS

AVRT:
- pt has accessory pathway/bypass tract that surpasses the AV node - e.g., WPW Syndrome
- APC blocks the accessory pathway
- antegrade: down normal AV pathway
- retrograde: up accessory pathway
**QRS is narrow

Front 59

What is Ectopic Atrial Tachycardia and what does its ECG reflect?

Back 59

Abnormal impulses arise from cells in atria at rate >100 bpm

- PR interval is shorter than RP (unlike AVNRT)
- abnormal morphology of the ectopic P wave that precedes the QRS Complex

Front 60

What is Multifocal Atrial Tachycardia and what does its ECG reflect?
- What is a common cause?
- What is treatment?

Back 60

Multiple foci in the atrium --> multiple/discrete P wave morphologies

- Often in patients with COPD who suffer from hypoxemia (leads to increased automaticity)
- Tx: reversing factors associated with hypoxia; give supplemental oxygen; treat infections with antibiotics; drugs to slow heartrate (Verapamil) to control symptoms

Front 61

What are the different types of Supraventricular Tachycardias? How common is each?

What is the typical rate?

What are the general ECG findings?

Back 61

*Most are due to reentry
- AVNRT (50-60%)
- AVRT (up to 30%)
- Ectopic Atrial Tachy
- Multifocal Atrial Tachy (both rare)

Rate: 200 +/- 50
Abnormal P wave morphology - may occur before, within, or after QRS
Prologned PR Inverval
Atrial rate regular; QRS narrow

Front 62

Who usually gets the different Supraventricular Tachycardias?

Back 62

AVNRT/AVRT - usually young, healthy people with no structural heart disease
Ectopic Atrial Tachy - pts with and without heart disease
Multifocal Atrial Tachy - pts with pulmonary disease

Front 63

What are the typical symptoms of Supraventricular Tachycardia?

Back 63

depend upon the rate and presence of underlying structural heart disease

Palpitations most frequently; lightheadedness, diaphoresis, chest pain, syncope (rarely)

Front 64

What is treatment of supraventricular tachycardias?

Back 64

Depends upon the mechanism of tachycardia...

- AV Node-Independent: anti-arrhythmic drugs (Class I or III) may control the arrhythmia

- AV Node-Dependent: block the AV Node --> either termination or prevention

- Termination:
- Maneuvers that slow AV nodal conduction (carotid sinus massage, valsalva)
- Drugs that cause AV block - e.g., adenosine, verapamil

- Prevention: These tachys are not life-threatening, so tx the symptoms (only if frequent) -->
- 1st line: AV nodal blocking drugs
- 2nd line: type I and type II antiarrhythmic drugs
- 3rd line: radiofrequency catheter ablation - heat cardiac tissue until cell death, which stops electrical activity (this should be targeted at one limb of the reentrant circuit - e.g., the accessory pathway in pts with WFW)

Front 65

What is AV Node Dependent SVT and what is AV Node Independent SVT?

How can you differentiate?

Back 65

AV Node Dependent - tachycardia occurs with the AV Node in the circuit
- e.g., AVNRT, AVRT

AV Node Independent - the AV node is not required for perpetuation of the circuit

*Differntaite: use Adenosine, which causes an AV Block
- In AV Dependent, production of an AV block will STOP the tachycardia
- In AV Independent, there will be no change in the heart beats

Front 66

What are Premature Ventricular Contractions (PVC)?

Back 66

Beats arising from ectopic foci in the ventricle
- may be unifocal or multifocal
- followed by a full compensatory pause

- Couplet = 2 PVCs in a row
- Nonsustained VT = 3 or more PVCs in a row

Front 67

What is Ventricular Tachycardia (VT)?

What is the rate?

What are the ECG Features of VT?

Back 67

Rapid rhythm that originates in the ventricle
- precipitated by a PVC
- usually due to some form of structural heart disease
** VT post-MI due to reentry of slowly conducting wavefront through area of previous infarction
- can be of RBBB or LBBB morphology

Rate: 150-250

ECG:
- QRS wide and sometimes bizarre, but generally constant
- often AV dissociation (P waves off from QRS)
- sometimes there is a fusion beat - normal beat via AV nodes (narrow QRS) fuses with VT beat (wide QRS)

Front 68

What are the clinical features of Ventricular Tachycardia?

Back 68

- Pts usually have structural heart disease -- often VT of the R ventricle; pts with cardiomyopathy and CAD often have VT of L ventricle

- Sx depend upon ventricular rate, duration, presnce and extent of heart disease and periph vascular disease

- Rapid diagnosis and tx is important!!! can be life-threatening...

***If patient has wide, unstable QRS tachycardia - think VT
***If patient has structural heart disease - think VT

Front 69

What is treatment of Ventricular Tachycardia?

Back 69

Termination:
- (depends on clinical situation -e.g., hypotension, consciousness)
- IV drug tx (amiodarone, lidocaine)
- Direct-current cardioconversion

Prevention:
- ICD implantation = implantable cardioverter/defibrillator
- Drug therapy

Front 70

What is Polymorphic Ventricular Tachycardia?

Back 70

When the QRS intervals are not constant throughout tachycardia
- occurs when there is prolongation of ventricular repolarization - e.g., LONG QT SYNDROME
- acquired or congenital

Front 71

What is Long QT Syndrome?
- aka?
- cause?
- result?

Back 71

aka: Torsades de Pointes - bc QRS complex "twist" around isoelectric baseline
--> the resulting QRS complexes are POLYMORPHIC

Congenital: due to inherited mutation of genes coding for cardiac ion channels; arrhythmias are adrenergic dependent

Acquired: produced by a drug (type IA or III antiarrhythmic, antibiotics (erythromycin, bactrim), haloperidol, tricyclic antidepressants, etc)or metabolic condition (hypokalemia, hypocalcemia, hypomagnesemia); arrhythmias are bradycardia or pause dependent

--> usually short-lived and self-terminating; BUT may degenerate into ventricular fibrillation

Front 72

What is treatment for Torsades de Pointes?

Back 72

Congenital Long QT Syndrome:
- Beta Blockers (since arrhythmias are adrenergic-dependent)
- ICD Implantation (implantable cardioverter-defibrillator) for high-risk pts (e.g., family history)

Acquired Long QT Syndrome:
- Remove offending agents that lengthen QT Interval
- Correct metabolic abnorms
- Increase heart rate (since bradycardia causes lengthening of the interval), via temporary pacing or isoproterenol (Beta-agonist)