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1 STEP Uworld cardio > ECG > Flashcards

ECG Flashcards

1
Q

Where is ectopic foci that induces atrial fibrillation?

A

ectopic foci in the pulmonary vein ostia

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2
Q

How changes refractory period and conductivity due to electrical remodeling induced by atrial fibrillation?

A

Shortened refractory period and increased conductivity

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3
Q

Effects of shortened refractory period and increased conductivity in atrial fibrillation?

A

creation and persistence of multiple ectopic foci and reentrant impulses within atria

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4
Q

The most common tachyarrhytmia?

A

atrial fibrillation

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5
Q

What illnesses precipitate atrial fibrillation?

A

Systemic ilnesses such: long-standing HTN, HF, hyperthyroidism.
Increased sympathetic tone

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6
Q

What is holiday heart syndrome?

A

Atrial fibrillation seen in patients after excessive alcohol consumption

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7
Q

atrial fibrillation treatment in symptomatic patients?

A

catheter ablation of pulmonary vein trigger sites

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8
Q

Atrial fibrillation ecg? P, regularity R-R, QRS?

A

P - truly absent, because absent organized depolarization
Irregularly-irregular R-R intervals
Narrow QRS

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9
Q

normal QRS duration?

A

<0,12s (3 mazi langeliai)

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10
Q

Normal PR interval duration?

A

0,12-0,20s (5 mazi langeliai)

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11
Q

WPW. What is accessory pathway?

A

Accessory bypass tract=bundle of Kent

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12
Q

What connects bundle of Kent?

A

Directly connects the atria to the ventricles and allows electrical impulses to bypass the AV node

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13
Q

Young patient has repeated episodes of palpitations. What suspect?

A

PSVT –> suspect WPW

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14
Q

What causes electrical impulses that goes through the bundle of Kent?

A

preexcitation of the ventricles

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15
Q

What changes creates the preexcitation of the ventricles in WPW?

A

characteristic triad on ECG

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16
Q

Triad of WPW?

A 
Delta wave;
Shortened PR interval (<0,12s) (normal PR 0,12-0,22s)
Wide QRS (>0,12s)
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17
Q

WPW asymptomatic. ECG? How is it called?

A

Many WPW patients asymptomatic and only WPW pattern (triad) is seen on ECG.
It is called Ventricular preexcitation.
Impulse just go through the bundle of Kent.

Name: ventricular preexitation
ECG: WPW pattern

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18
Q

WPW symptomatic. ECG? How is it called?

A

Symptomatic can be if WPW pattern + symptomatic arrythmia. ECG: AVRT
It is called WPW syndrome. AVRT is the most common arrythmia that occurs with WPW.
Reentrant circle via bundle of Kent.

Name: WPW syndrome
ECG: reentrant tachycardia (AVRT)

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19
Q

WPW pattern. Symptomatic or asymptomatic?

A

Asymptomatic

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20
Q

WPW syndrome. Symptomatic or asymptomatic?

A

symptomatic

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21
Q

Symptoms if arrythmia occurs in WPW?

A

Intermitent palpitations, sensation of racing heart, lightheadness or syncope.

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22
Q

Atrial fibrillation. What is ventricular response? What is average ventricular rate? regularity?

A

Depends on the transmission via AV node. Once AV is excited, it enters refractory period, so additional impulses cannot be transmited to the ventricles despite there is excitation of atria. Ventricular rate: 90-170k/min. Irregular, because atrial excitation is chaotic.

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23
Q

3 factors for thrombus formation in atrial fibrillation?

A

Left atrial enlargement.
Blood stasis due to ineffective atrial contraction;
Atrial inflammation and fibrosis (exerts a procoagulant effect).

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24
Q

Which part of the heart is the most susceptible for thrombus formation in Afib?

A

Left atrial appendage.

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25
Q

Afib. There is a thrombus. Where can it embolize?

A

Stroke, acute limb ischemia, acute mesenteric ischemia

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26
Q

If thrombus in Afib forms in right heart. In which part and where can embolize?

A

forms in right atrial appendage; Embolize to pulmonary circulation.

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27
Q

In what 2 cases can thrombus develop in LV?

A

In case of LV aneurysm (eg post-MI) and severe LV systolic dysfunction. NOT ASSOCIATED WITH Afib.

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28
Q

What is the backgroud to develop for thrombus in case patients has prostetic valves?

A

lack of adequate anticoagulation.

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29
Q

How often thrombus form in pulmonary veins or sinus.of valsalva (aortic sinus)?

A

Rarely and they are not assoc. with Afib.

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30
Q

What is crista terminalis?

A

thick band of atrial muscle that separates smooth sinus venosus from the right atrial appendage and atrium proper.

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31
Q

What originates from crista terminalis?

A

crista terminalis is the sito of origin of the atrial pectinate muscles.

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32
Q

Duration of paroxysmal afib?

A

resolving spontaneously within 7 days

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33
Q

Duration of persistent afib?

A

lasting > 7 days.

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34
Q

What primarily drives development of afib?

A

structural and electrical remodeling.

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35
Q

What are structural remodeling causes for afib?

A

comorbidities that lead to atrial stretching and dilation: hypertension, HF, mitral valve disease. Physiologic age-related atrial dilation. CAD and its assoc factor (DM, smoking), may induce structucal changes due to ischemia –> ventricular dysfunction –> consequent atrial dilation.

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36
Q

What are electrical remodeling causes for afib?

A 
Age related changes;
Previous exposure to afib.
electrical foci (in pulmonary vein ostia)
Alcohol intake and increased SNS activity may contribute
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37
Q

Monomorphic VT - causes?

A

in myocard ischemia or LV systolic dysfunction

38
Q

Polymorphic VT - causes?

A

torsades de pointes

39
Q

Idiopathic VT - causes?

A

repetitive VT that occurs in the abscence of structural heart disease.

40
Q

monomorphic VT ECG?

A

Tachycardia (>100k.min);
P - absent
R-R - rhythmic
QRS - wide (>0,12s)

41
Q

Why QRS abnormalities in bundle branch block?

A

due to impaired synchronization of ventricular depolarization

42
Q

RBBB ECG?

A

P waves - present;
Wide QRS (>0,12s)
V1-V3: M (RSR’) + T inversion/ST depression
I, aVL, V5-V6: W (qRs) - S wave slurred

43
Q

LBBB ECG?

A

P waves - present;
Wide QRS (>0,12s)
V1-V3: W (rS’) + ST elevation
I, aVL, V5-V6: M (R) + T inversion/ST depression

44
Q

What pathology is equal to LBBB?

A

STEMI

45
Q

hlab algoritmas. Bradikardija, abnormal P. What do nexT?

A

ask if duration of QRS <0,12s

46
Q

hlab algoritmas. Bradikardija, abnormal P, QRS <0,12s, what diagnosis?

A

AV jungties ritmas

47
Q

hlab algoritmas. Bradikardija, abnormal P, QRS >0,12s, what diagnosis?

A

idioventrikulinis ritmas

48
Q

What impaired process and of what part of heart can lead to tdp?

A

Delayed repolarization of ventricular cardiomyocytes.

49
Q

QT prolongation in otherwise healthy individuals?

A

congenital

50
Q

What reflects QT-interval?

A

starts with Q, ends with the end of T. Reflects cardiomyocyte action potential duration

51
Q

Delayed repolarization of ventricular cardiomyocytes can lead to ……..

A

tdp

52
Q

Unprovoked syncope in othervise healthy individual. What suspect?

A

long QT syndrome

53
Q

QT prolongation. autosomal dominant, no deafness. What congenital syndrome?

A

Romano-Ward syndrome

54
Q

QT prolongation. autosomal recessive, neurosensory deafness. What congenital syndrome?

A

Jervell and Lange-Nielsen syndrome

55
Q

Romano-Ward syndrome?

A

QT prolongation. autosomal dominant, no deafness.

56
Q

Jervell and Lange-Nielsen syndrome

A

QT prolongation. autosomal recessive, neurosensory deafness.

57
Q

Young age. Syncope + seizures+ sudden death. What probably cause?

A

Qt prolongation (congenital) –> tdp

58
Q

what are ventricular tachyarrythmia?

A

tdp and ventricular fibrillation

59
Q

what current is impaired in QT prolongation?

A

outward-rectifying potassium current

60
Q

mutations in what genes in QT prolongation?

A

KCNQ1 and KCNQ2 that encode alpha and beta subunits of voltage-gated potassium chanels.

61
Q

what phase is potassium current?

A

phase 3

62
Q

how changes duration of action potential in long-QT?

A

decreased outward K flow –> prolongation of action potential –> predisposes tdp and ventricullar fibrillation

63
Q

Long-QT ECG.

A

P-normal
R-R regular
QRS normal
QTc plonged >440ms

64
Q

ventricular fibrillation ECG.

A

rate 150-500bpm, no identifiable P-QRS-T waves. Amplitude decreases with duration

65
Q

What circuit is in aflut?

A

reentrant circuit involving cavotricuspid isthmus.

66
Q

what is cavotricuspid isthmus?

A

region of right atrial tissue between the inferior vena cava and the tricuspid valve annulus

67
Q

aflut. what is the target for radiofrequency ablation?

A

cavotricuspid isthmus

68
Q

atrial flutter ecg?

A

P- Characteristic saw-toothed flutter (F waves)
R-R - regular or irregular, depending on how consistently flutter waves are conducted through the AV node
QRS-narrow
atrial rate: 300/min
ventricular rate: 2:1, 3:1, 4:1 = 150, 100, 75

69
Q

supraventricular tachycardias? 5

A

Afib, aflut, atrial tachycardia, AVNodalRT, AVRT(WPW)

70
Q

polymorphic VT. ECG?

A

tdp - QRS complexes that oscillate in height and position

71
Q

What creates signals in III AV block?

A

P wave - due to SA node signal
QRS - due to pacemaker of the His bundle

AV BLOCK - therefore no signal from it!!

72
Q

How is called signal that generates bundle of His in case on III AV bock?

A

ESCAPE RHYTHM

73
Q

What is rate of P and QRS in III AV?

A

P - 60-100/min (generated by SA node)

QRS - 40-60/min (generated by Bundle of His)

74
Q

What structures generate 40-60min rate?

A

AV node and bundle of His

75
Q

Slow ventricular rate in III AV leads to what symptoms?

A

slow ventricular rate –> reduced CO –> dyspnea, fatigue, lightheadeness, syncope

76
Q

treatment on III AV?

A

pacemaker

77
Q

What can cause III AV?

A

ischemia, infiltrative diseases (eg sarcoidosis), infection (Lyme disease), age-related fibrosis with cellular degeneration.

78
Q

What is generated by junctional escape rhythm in III AV?

A

QRS complexes.

P waves - by atrial rhythm, i.e. SA node

79
Q

I AV ECG?

A

P- normal (sinus rhythm)
QRS - normal
R-R - normal (regular rhythm)
PQ trukme: >0,2s

80
Q

What is the main abnormality in ECG in I AV?

A

PQ trukme > 0,2sec.

81
Q

II 1 tipo AV. ECG?

A 
P - normal
P rysys su QRS? - yra
P pries kiekviena QRS?- NE
P-Q vienoda? - NE
QRS - normal
R-R regularly irregular (QRS periodically drops)
82
Q

II 2 tipo AV. ECG?

A 
P - normal
P rysys su QRS? - yra
P pries kiekviena QRS?- NE
P-Q vienoda? - TAIP
QRS - normal
83
Q

in what conditions (1 and 1) short PR where prolonged PR?

A

Short - WPW

Prolonged - I AV block

84
Q

classic scenario for congenital QT?

A

young patients with reccurent seizures

85
Q

PR prolonged, lenghtened and shortened in what conditions?

A

Prolonged in AV block
Lengthens with vagal tone, drugs
Shortens with sympathetic tone

86
Q

what induces QT prolongation and shortening?

A

Prolonged with ↓ Ca (tetany; numbness; spasms)
Prolonged by antiarrhythmic drugs
Shortened with ↑ Ca (confusion, constipation)

87
Q

ST elevation what condition?

A

transmural ischemia

88
Q

ST depression what condition?

A

subendocardial ischemia

89
Q

T inversion what condition?

A

ischemia

90
Q

U wave what condition?

A

hypokalemia, bradycardia

91
Q

T peaked what condition?

A

Early ischemia and hyperkalemia

1 STEP Uworld cardio (7 decks)

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