ECG Flashcards
Where is ectopic foci that induces atrial fibrillation?
ectopic foci in the pulmonary vein ostia
How changes refractory period and conductivity due to electrical remodeling induced by atrial fibrillation?
Shortened refractory period and increased conductivity
Effects of shortened refractory period and increased conductivity in atrial fibrillation?
creation and persistence of multiple ectopic foci and reentrant impulses within atria
The most common tachyarrhytmia?
atrial fibrillation
What illnesses precipitate atrial fibrillation?
Systemic ilnesses such: long-standing HTN, HF, hyperthyroidism.
Increased sympathetic tone
What is holiday heart syndrome?
Atrial fibrillation seen in patients after excessive alcohol consumption
atrial fibrillation treatment in symptomatic patients?
catheter ablation of pulmonary vein trigger sites
Atrial fibrillation ecg? P, regularity R-R, QRS?
P - truly absent, because absent organized depolarization
Irregularly-irregular R-R intervals
Narrow QRS
normal QRS duration?
<0,12s (3 mazi langeliai)
Normal PR interval duration?
0,12-0,20s (5 mazi langeliai)
WPW. What is accessory pathway?
Accessory bypass tract=bundle of Kent
What connects bundle of Kent?
Directly connects the atria to the ventricles and allows electrical impulses to bypass the AV node
Young patient has repeated episodes of palpitations. What suspect?
PSVT –> suspect WPW
What causes electrical impulses that goes through the bundle of Kent?
preexcitation of the ventricles
What changes creates the preexcitation of the ventricles in WPW?
characteristic triad on ECG
Triad of WPW?
Delta wave; Shortened PR interval (<0,12s) (normal PR 0,12-0,22s) Wide QRS (>0,12s)
WPW asymptomatic. ECG? How is it called?
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
WPW symptomatic. ECG? How is it called?
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)
WPW pattern. Symptomatic or asymptomatic?
Asymptomatic
WPW syndrome. Symptomatic or asymptomatic?
symptomatic
Symptoms if arrythmia occurs in WPW?
Intermitent palpitations, sensation of racing heart, lightheadness or syncope.
Atrial fibrillation. What is ventricular response? What is average ventricular rate? regularity?
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.
3 factors for thrombus formation in atrial fibrillation?
Left atrial enlargement.
Blood stasis due to ineffective atrial contraction;
Atrial inflammation and fibrosis (exerts a procoagulant effect).
Which part of the heart is the most susceptible for thrombus formation in Afib?
Left atrial appendage.
Afib. There is a thrombus. Where can it embolize?
Stroke, acute limb ischemia, acute mesenteric ischemia
If thrombus in Afib forms in right heart. In which part and where can embolize?
forms in right atrial appendage; Embolize to pulmonary circulation.
In what 2 cases can thrombus develop in LV?
In case of LV aneurysm (eg post-MI) and severe LV systolic dysfunction. NOT ASSOCIATED WITH Afib.
What is the backgroud to develop for thrombus in case patients has prostetic valves?
lack of adequate anticoagulation.
How often thrombus form in pulmonary veins or sinus.of valsalva (aortic sinus)?
Rarely and they are not assoc. with Afib.
What is crista terminalis?
thick band of atrial muscle that separates smooth sinus venosus from the right atrial appendage and atrium proper.
What originates from crista terminalis?
crista terminalis is the sito of origin of the atrial pectinate muscles.
Duration of paroxysmal afib?
resolving spontaneously within 7 days
Duration of persistent afib?
lasting > 7 days.
What primarily drives development of afib?
structural and electrical remodeling.
What are structural remodeling causes for afib?
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.
What are electrical remodeling causes for afib?
Age related changes; Previous exposure to afib. electrical foci (in pulmonary vein ostia) Alcohol intake and increased SNS activity may contribute
Monomorphic VT - causes?
in myocard ischemia or LV systolic dysfunction
Polymorphic VT - causes?
torsades de pointes
Idiopathic VT - causes?
repetitive VT that occurs in the abscence of structural heart disease.
monomorphic VT ECG?
Tachycardia (>100k.min);
P - absent
R-R - rhythmic
QRS - wide (>0,12s)
Why QRS abnormalities in bundle branch block?
due to impaired synchronization of ventricular depolarization
RBBB ECG?
P waves - present;
Wide QRS (>0,12s)
V1-V3: M (RSR’) + T inversion/ST depression
I, aVL, V5-V6: W (qRs) - S wave slurred
LBBB ECG?
P waves - present;
Wide QRS (>0,12s)
V1-V3: W (rS’) + ST elevation
I, aVL, V5-V6: M (R) + T inversion/ST depression
What pathology is equal to LBBB?
STEMI
hlab algoritmas. Bradikardija, abnormal P. What do nexT?
ask if duration of QRS <0,12s
hlab algoritmas. Bradikardija, abnormal P, QRS <0,12s, what diagnosis?
AV jungties ritmas
hlab algoritmas. Bradikardija, abnormal P, QRS >0,12s, what diagnosis?
idioventrikulinis ritmas
What impaired process and of what part of heart can lead to tdp?
Delayed repolarization of ventricular cardiomyocytes.
QT prolongation in otherwise healthy individuals?
congenital
What reflects QT-interval?
starts with Q, ends with the end of T. Reflects cardiomyocyte action potential duration
Delayed repolarization of ventricular cardiomyocytes can lead to ……..
tdp
Unprovoked syncope in othervise healthy individual. What suspect?
long QT syndrome
QT prolongation. autosomal dominant, no deafness. What congenital syndrome?
Romano-Ward syndrome
QT prolongation. autosomal recessive, neurosensory deafness. What congenital syndrome?
Jervell and Lange-Nielsen syndrome
Romano-Ward syndrome?
QT prolongation. autosomal dominant, no deafness.
Jervell and Lange-Nielsen syndrome
QT prolongation. autosomal recessive, neurosensory deafness.
Young age. Syncope + seizures+ sudden death. What probably cause?
Qt prolongation (congenital) –> tdp
what are ventricular tachyarrythmia?
tdp and ventricular fibrillation
what current is impaired in QT prolongation?
outward-rectifying potassium current
mutations in what genes in QT prolongation?
KCNQ1 and KCNQ2 that encode alpha and beta subunits of voltage-gated potassium chanels.
what phase is potassium current?
phase 3
how changes duration of action potential in long-QT?
decreased outward K flow –> prolongation of action potential –> predisposes tdp and ventricullar fibrillation
Long-QT ECG.
P-normal
R-R regular
QRS normal
QTc plonged >440ms
ventricular fibrillation ECG.
rate 150-500bpm, no identifiable P-QRS-T waves. Amplitude decreases with duration
What circuit is in aflut?
reentrant circuit involving cavotricuspid isthmus.
what is cavotricuspid isthmus?
region of right atrial tissue between the inferior vena cava and the tricuspid valve annulus
aflut. what is the target for radiofrequency ablation?
cavotricuspid isthmus
atrial flutter ecg?
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
supraventricular tachycardias? 5
Afib, aflut, atrial tachycardia, AVNodalRT, AVRT(WPW)
polymorphic VT. ECG?
tdp - QRS complexes that oscillate in height and position
What creates signals in III AV block?
P wave - due to SA node signal
QRS - due to pacemaker of the His bundle
AV BLOCK - therefore no signal from it!!
How is called signal that generates bundle of His in case on III AV bock?
ESCAPE RHYTHM
What is rate of P and QRS in III AV?
P - 60-100/min (generated by SA node)
QRS - 40-60/min (generated by Bundle of His)
What structures generate 40-60min rate?
AV node and bundle of His
Slow ventricular rate in III AV leads to what symptoms?
slow ventricular rate –> reduced CO –> dyspnea, fatigue, lightheadeness, syncope
treatment on III AV?
pacemaker
What can cause III AV?
ischemia, infiltrative diseases (eg sarcoidosis), infection (Lyme disease), age-related fibrosis with cellular degeneration.
What is generated by junctional escape rhythm in III AV?
QRS complexes.
P waves - by atrial rhythm, i.e. SA node
I AV ECG?
P- normal (sinus rhythm)
QRS - normal
R-R - normal (regular rhythm)
PQ trukme: >0,2s
What is the main abnormality in ECG in I AV?
PQ trukme > 0,2sec.
II 1 tipo AV. ECG?
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)
II 2 tipo AV. ECG?
P - normal P rysys su QRS? - yra P pries kiekviena QRS?- NE P-Q vienoda? - TAIP QRS - normal
in what conditions (1 and 1) short PR where prolonged PR?
Short - WPW
Prolonged - I AV block
classic scenario for congenital QT?
young patients with reccurent seizures
PR prolonged, lenghtened and shortened in what conditions?
Prolonged in AV block
Lengthens with vagal tone, drugs
Shortens with sympathetic tone
what induces QT prolongation and shortening?
Prolonged with ↓ Ca (tetany; numbness; spasms)
Prolonged by antiarrhythmic drugs
Shortened with ↑ Ca (confusion, constipation)
ST elevation what condition?
transmural ischemia
ST depression what condition?
subendocardial ischemia
T inversion what condition?
ischemia
U wave what condition?
hypokalemia, bradycardia
T peaked what condition?
Early ischemia and hyperkalemia
