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Arrhythmias Flashcards

1
Q

3 mechanisms of arrhythmia

A

reentry

autmaticity

triggered

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2
Q

reentry arrhythmia

A
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3
Q

Reentry termination

A
  1. stop conduction (Na channel block - IC, IA, IB)
  2. prolong refractoriness (K channel block - III)
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4
Q

Enhanced automaticity

A

Decreased I(K1) - which maintains RMP

increased I(f) current - enhanced diastolic depolarization (phase 4)

Looks like nodal activity (up and down)

responsive to increased sympathetic tone (CHF, post-MI)

More responsive to CCBs than Na

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5
Q

how to decrease automaticity

A
  1. decrease slope of phase 4 (reduced If)
  2. decrease deepness of phase 4
  3. increase threshold potential (decrease Ca channel open probability
  4. prolong RP
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6
Q

Triggered

A

Oscillations in membrane potential after depolarization

may trigger premature deoplarizations

if phase 2, 3 - early after depolarizations (EAD)

if phase 4 - delayed after de polarizations (DAD)

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7
Q

EAD mechanism and inciters

A

net increased inward plateau current

incited by QT prolongation drugs or mutations

long QT states triggering TdP

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8
Q

DAD mechanisms and inciter

A

intracellular Ca overload

incited by Dig, catecholamines

assoc w dig toxicitiy, ischemia, outflow tract VTs, CPVT

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9
Q

First degree AV Block

A

prolongation of normal delay between atrial and ventricle depolarization

PR interval is lengthened (still 1:1)

usually benign

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10
Q

Second degree AV block

A

-intermittent failure of AV conduction - some waves not followed by QRS

Mobitz I (Wenckeback) - degree of AV delay gradually increases with each beat until a QRS is skipped (progressive intervals) - impaired AV node conduction

Mobitz II - sudden intermittent loss of AV conduction without preceeding lengthening - QRS is often widened

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11
Q

Mobitz I

A

Mobitz I (Wenckeback) - degree of AV delay gradually increases with each beat until a QRS is skipped (progressive intervals) - impaired AV node conduction

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12
Q

Mobitz II

A

Mobitz II - sudden intermittent loss of AV conduction without preceeding lengthening - QRS is often widened

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13
Q

Third degree AV block

A

complete heart block - failure of conduction between A and V!

no relationship between P and QRS

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14
Q

supraventricular tach - irregular rhythms

A

A fib - no distinct P waves

multifocal atrial tachycardia - greater than 3 diff P wave shapes

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15
Q

supraventricular tach - regular rhythms

A

constant P-P interval

sinus tach - normal P

reentrant SVTs (AVNRT, AVRT) - hidden/retrograde P

Focal atrial tach - differs from normal P

atrial flutter - saw toothed

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16
Q

Sinus tachycardia mechanism

A

SA node discharge >100 bpm

increased sympathetic or decreased vagal tone

response to exercise or patholgoic

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17
Q

sinus tachycardia treatment

A

treat underlying disease

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18
Q

atrial premature beats

A

automaticity or reentry in an atrial focus outside SA node

often exacerbated by sympathetic stimulation

usually asyptomatic bt can cause palpitations

earlier P wave with abnormal shape

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19
Q

Atrial flutter mechanism

A

rapid regular atrial activity (180-350 bpm)

AV filter (2:1, 3:1, 4:1)

reentry over a fixed circuit (usually tricuspid valve)

often with preexisting heart disease

sawtooth ECG

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20
Q

atrial flutter treatment

A

vagal maneuvers increase AV block

electroconversion pacemaker

increase AV block (Dig, BB, CCBs)

catheter ablation

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21
Q

Atrial fibrilation Mechanism

A

chaotic rhythm with atrial rate 350-600

AV filter

Multiple wandering reentrant circuits

foci around pulmonary veins

usually AE

low CO and atrial stasis (hypotension and pulmonary congestion)

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22
Q

atrial fibrilation treatment

A

ventricular rate control (BB, CCB)

restore sinus rhythm (cardioversion)

anticoagulation

catheter ablation

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23
Q

AVNRT mechanism

A

type of PSVT

2+ potential conduction pathways in the AV node (slow with a fast RP and fast with a slow RP)

impulse usually only travels down fast pathway

unidirectional block in fast pathway - AFB travels down slow pathway and reenters backways

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24
Q

AVNRT ECG

A

regular tachycardia

normal width QRS

P may not be apparent (retrograde atrial depolarization typically occurs at same time as ventricular depolarization so P is hidden in QRS)

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25
AVNRT Treatment
increase vagal tone (carotid massage, Valsalva) IV adenosine to terminate CCB, BB (acutely or chronically) Catheter ablation IA, IC drugs
26
AVRT mechanis
similar to AVNRT but includes AV bypass loop! WPW is an example - no delay in bypass leads to ventricles excited early or PSVT from pathway
27
WPW ECG
short PR (early excitation of the ventriles - earlier than normal through the accessory pathway) QRS is slurred rather than shapr (delta wave) QRS is windened because fusing of 2 impulses
28
Atrial tachycardia mechanism
focal - automaticity or reentry of an ectopic site, more common, looks like sinus tachycardia with different P wave morphology caused by dig toxicity or elevated sym tone multifocal - irregular rhythm with at least 3 p wave morphologyies , abnormal automaticity of several foci
29
ventricular premature beats
ectopic ventricular focus fires an AP widened QRS - takes longer to get through slow cell to cell conductions BB or nothing
30
ventricular tachycardia mechanism
usually in patients with structural heart disese (MI, VH, HF) monomorphic - reentry circuit - MI or CM polymorphic - ectopic foci or reentry low CO, syncope, PE, CA
31
monomorphic VT
sustained - structural abnormality that supports a reentry circuit - scar from MI or cardiomyopathy
32
polymorphic VT
multiple ectopic foci or changing reentry circuit tDP, Brugada,
33
VT treatment
cardioversion amiodarone or other IV drugs ICD BB, CCB catheter ablation
34
Amoidarone Mechanism
Class III Blocks sodium, potassium, calcium channels activity of class IB, II, IV slows phase 4 depolarization prolongs repolarization (blocks outward K in phase III)
35
Amiodarone Indications
SVT AF/AFL VT VF really any rhythm
36
Amiodarone side effects
thyroid,pulmonary inflammation proarrhytmia (TdP rare) drug drug (warfarin!!)
37
Amiodarone EKG changes
May increase PR May increase QRS Increase QT (NO TdP)
38
Adenosine Indications
SVT (AVRT, AVNRT, AT) involve AV node involveent
39
Adenosine Mechanism
total block of Ca influx in AV node 5 seconds - rapid termination of SVT block circuit
40
Adenosine Side Effects
Flusing Chest discomfort Dyspnea
41
Class IA Drugs Mechanism
decrease fast sodium influx (slow conduction) slow potassium efflux (prolong QT, APD)
42
Class IA drug Indications
AF/AFL SVT VT
43
Class IA drug side effects
prolong QT - proarrhythmia lupus-like don't really use anymore!
44
Class IB Mechanism
decrease in late sodium channels (shortens APD, QT) mild decrease in fast sodium channels (mild conduction slowing) preferentially acts on diseased/ischemic tissue
45
Indications of IB
no atrial arrhythmias! slowing VT good in MI
46
Side effects of IB
VT PVC
47
Class IC mechanism
huge decrease in Na influx (conduction slowing) min effect on APD
48
Indications for IC drugs
AF/AFL SVT
49
Side effects of IC
VT
50
EKG changes in IC
Increase PR Increase QRS Increase QT (No TdP)
51
Use Dependency - Class I
IC\>IA IC = pill in pocket
52
Different indications for Class I drugs
IB - only ventricular IC - only SVT IA - everything IB - preferentially diseased heart
53
Class II Drugs
Beta Blockers reduces cAMP --\> reduces PKA --\> reduces cytosolic Ca decrase phase 4 slope prolongs conduction time prolongs RP of nodal tissue
54
Indications for class II drugs
SVT AF/AFL rate VT Long QT
55
ECG changes in Class II drugs
may increase PR
56
Side effects of class II
bradycardia bronchospasm
57
Class III drugs
K blocker with beta blocking activity | (Amiodarone)
58
Indications for Class III drugs
SVT AF/AFL VT VF
59
ECG changes in Class III
May increase PR, QRS Increases QT!
60
Side effects of Class III
proarrhythmia inflammation of thyroid/pulm
61
Class IV drugs
CCBs block L type calcium channel slow rise of AP prolonged repolarization (at AV node) decrease HR decrease reentry decrease AV node conduction
62
Indications for CLass IV
AF/AFL AVNRT AVRT (SVTs - involve AV node)
63
Class V drugs
Digoxin increase intracellular Ca and vagal effects
64
Indications for Class V
SVT AF (rate control)
65
Rhythms that dep on AV node
AVNRT AVRT
66
Rhythms without organized atrial activity
A fib
67
Regular rhythms
ST AT VT AFL (block) AVNRT/AVRT
68
gradual onset rhythms
ST (that's it!)
69
automaticity or triggered activity
abnormal impulse initation
70
reentry
abnomalities in impulse conduction
71
conditions for reentry
1. loop circuit 2. unidirectional block 3. zone of slow conduction
72
characteristics of reentrant arrhythmias
uniform morphology stable rate abrupt onset and termination initated and terminated by premature beats encountering unidirectional block most common mechanism of SVT and VT
73
QTc
long QT interval prolonged depolarization dysfunctional channels normalize to RR interval!
74
normal QT length
400 msec
75
LQTS1
most common long QT problem with K current, decrease K channels AP is long and all cells in heart take a long time to reset triggered by exercise, emotional stress
76
Long QT ion channel issues
can be decrease in K current or increase in NA?
77
Long QT Syndrome
delayed repolarization of the heart can cause TdP VF reduce amt of K channels for repolarization
78
HERG Channel
problem with delayed rectifier K channel leads to increased prolongation also effect of spme meds!
79
Treatment for long QT
BB - don't change QT but decrease amt of arrhythmias ICD
80
Brugada syndrome
channel problems - AP collapses really early increased risk of ventricular arrhythmias phase 2 reentry, which generates a phase 2 reentrant extrasystole that captures the vulnerable window to precipitate ventricular tachycardia and/or ventricular fibrillation that often results in sudden cardiac death many different mutations, but often fast Na in phase 0
81
SCN5A
often mutated in Brugada Syndrome Na channel in cardiac cells responsible for upstroke oss of the action potential dome of some epicardial areas of the right ventricle. This results in transmural and epicardial dispersion of repolarization. The transmural dispersion underlies ST-segment elevation and the development of a vulnerable window across the ventricular wall, whereas the epicardial dispersion of repolarization facilitates the development of phase 2 reentry, which generates a phase 2 reentrant extrasystole that captures the vulnerable window to precipitate ventricular tachycardia and/or ventricular fibrillation that often results in sudden cardiac death.
82
Action Potential in Brugada
The Notch Since Na is dyfnctional - gradient and ready to fire again sooner than region next to it
83
Brugada ECG pattern
84
Brugada arrhytmia
phase 2 reentry epicardial and transmural dispersion of repolarization
85
HOCM therapy
ICD helps! myectomy
86
name the reentry arrhythmias
AVNRT AVRT AFL monomorphic VT (around scar in ventricle) A fib (due to micro reentrant circuits)
87
Name the automaticity arrhythmias
AT AF (focal ectopic firing) VT (due to automatic focus)
88
Name the triggered arrhythmias
long QT Dig overdose

CV Final (6 decks)

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