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CV Final > Arrhythmias > Flashcards

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
Q

AVNRT Treatment

A

increase vagal tone (carotid massage, Valsalva)

IV adenosine to terminate

CCB, BB (acutely or chronically)

Catheter ablation

IA, IC drugs

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26
Q

AVRT mechanis

A

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

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27
Q

WPW ECG

A

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

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28
Q

Atrial tachycardia mechanism

A

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

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29
Q

ventricular premature beats

A

ectopic ventricular focus fires an AP

widened QRS - takes longer to get through slow cell to cell conductions

BB or nothing

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30
Q

ventricular tachycardia mechanism

A

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

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31
Q

monomorphic VT

A

sustained - structural abnormality that supports a reentry circuit - scar from MI or cardiomyopathy

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32
Q

polymorphic VT

A

multiple ectopic foci or changing reentry circuit

tDP, Brugada,

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33
Q

VT treatment

A

cardioversion

amiodarone or other IV drugs

ICD

BB, CCB

catheter ablation

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34
Q

Amoidarone Mechanism

A

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)

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35
Q

Amiodarone Indications

A

SVT

AF/AFL

VT

VF

really any rhythm

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36
Q

Amiodarone side effects

A

thyroid,pulmonary inflammation

proarrhytmia (TdP rare)

drug drug (warfarin!!)

37
Q

Amiodarone EKG changes

A

May increase PR

May increase QRS

Increase QT (NO TdP)

38
Q

Adenosine Indications

A

SVT (AVRT, AVNRT, AT)

involve AV node involveent

39
Q

Adenosine Mechanism

A

total block of Ca influx in AV node

5 seconds - rapid termination of SVT

block circuit

40
Q

Adenosine Side Effects

A

Flusing

Chest discomfort

Dyspnea

41
Q

Class IA Drugs Mechanism

A

decrease fast sodium influx (slow conduction)

slow potassium efflux (prolong QT, APD)

42
Q

Class IA drug Indications

A

AF/AFL

SVT

VT

43
Q

Class IA drug side effects

A

prolong QT - proarrhythmia

lupus-like

don’t really use anymore!

44
Q

Class IB Mechanism

A

decrease in late sodium channels (shortens APD, QT)

mild decrease in fast sodium channels (mild conduction slowing)

preferentially acts on diseased/ischemic tissue

45
Q

Indications of IB

A

no atrial arrhythmias! slowing

VT

good in MI

46
Q

Side effects of IB

A

VT

PVC

47
Q

Class IC mechanism

A

huge decrease in Na influx (conduction slowing)

min effect on APD

48
Q

Indications for IC drugs

A

AF/AFL

SVT

49
Q

Side effects of IC

A

VT

50
Q

EKG changes in IC

A

Increase PR

Increase QRS

Increase QT (No TdP)

51
Q

Use Dependency - Class I

A

IC>IA

IC = pill in pocket

52
Q

Different indications for Class I drugs

A

IB - only ventricular

IC - only SVT

IA - everything

IB - preferentially diseased heart

53
Q

Class II Drugs

A

Beta Blockers

reduces cAMP –> reduces PKA –> reduces cytosolic Ca

decrase phase 4 slope

prolongs conduction time

prolongs RP of nodal tissue

54
Q

Indications for class II drugs

A

SVT

AF/AFL rate

VT

Long QT

55
Q

ECG changes in Class II drugs

A

may increase PR

56
Q

Side effects of class II

A

bradycardia

bronchospasm

57
Q

Class III drugs

A

K blocker with beta blocking activity

(Amiodarone)

58
Q

Indications for Class III drugs

A

SVT

AF/AFL

VT

VF

59
Q

ECG changes in Class III

A

May increase PR, QRS

Increases QT!

60
Q

Side effects of Class III

A

proarrhythmia

inflammation of thyroid/pulm

61
Q

Class IV drugs

A

CCBs

block L type calcium channel

slow rise of AP

prolonged repolarization (at AV node)

decrease HR

decrease reentry

decrease AV node conduction

62
Q

Indications for CLass IV

A

AF/AFL

AVNRT

AVRT

(SVTs - involve AV node)

63
Q

Class V drugs

A

Digoxin

increase intracellular Ca and vagal effects

64
Q

Indications for Class V

A

SVT

AF (rate control)

65
Q

Rhythms that dep on AV node

A

AVNRT

AVRT

66
Q

Rhythms without organized atrial activity

A

A fib

67
Q

Regular rhythms

A

ST

AT

VT

AFL (block)

AVNRT/AVRT

68
Q

gradual onset rhythms

A

ST (that’s it!)

69
Q

automaticity or triggered activity

A

abnormal impulse initation

70
Q

reentry

A

abnomalities in impulse conduction

71
Q

conditions for reentry

A
  1. loop circuit
  2. unidirectional block
  3. zone of slow conduction
72
Q

characteristics of reentrant arrhythmias

A

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
Q

QTc

A

long QT interval

prolonged depolarization

dysfunctional channels

normalize to RR interval!

74
Q

normal QT length

A

400 msec

75
Q

LQTS1

A

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
Q

Long QT ion channel issues

A

can be decrease in K current or increase in NA?

77
Q

Long QT Syndrome

A

delayed repolarization of the heart

can cause TdP

VF

reduce amt of K channels for repolarization

78
Q

HERG Channel

A

problem with delayed rectifier K channel

leads to increased prolongation

also effect of spme meds!

79
Q

Treatment for long QT

A

BB - don’t change QT but decrease amt of arrhythmias

ICD

80
Q

Brugada syndrome

A

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
Q

SCN5A

A

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
Q

Action Potential in Brugada

A

The Notch

Since Na is dyfnctional - gradient and ready to fire again sooner than region next to it

83
Q

Brugada ECG pattern

A
84
Q

Brugada arrhytmia

A

phase 2 reentry

epicardial and transmural dispersion of repolarization

85
Q

HOCM therapy

A

ICD helps!

myectomy

86
Q

name the reentry arrhythmias

A

AVNRT

AVRT

AFL

monomorphic VT (around scar in ventricle)

A fib (due to micro reentrant circuits)

87
Q

Name the automaticity arrhythmias

A

AT

AF (focal ectopic firing)

VT (due to automatic focus)

88
Q

Name the triggered arrhythmias

A

long QT

Dig overdose

CV Final (6 decks)

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