ecg ischemie si infarct

8/12/2019 ECG Ischemie Si Infarct

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MD Cristian Furu

Ischemic Heart Disease

25.02.2014


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Interpretation of the normal ECG

according to the 7+2 step plan

7+2 step plan

Step 1: Rhythm

Step 2: RateStep 3: Conduction(PQ,QRS,QT)

Step 4: Heart axis

Step 5: P wave morphology

Step 6: QRS morphology

Step 7: ST morphology

Step 7+1: Compare the current ECG with a

previous one

Step 7+2: Conclusion
http://en.ecgpedia.org/wiki/Rhythmhttp://en.ecgpedia.org/wiki/Ratehttp://en.ecgpedia.org/wiki/Conductionhttp://en.ecgpedia.org/wiki/Heart_axishttp://en.ecgpedia.org/wiki/P_wave_morphologyhttp://en.ecgpedia.org/wiki/QRS_morphologyhttp://en.ecgpedia.org/wiki/ST_morphologyhttp://en.ecgpedia.org/wiki/Compare_the_old_and_new_ECGhttp://en.ecgpedia.org/wiki/Compare_the_old_and_new_ECGhttp://en.ecgpedia.org/wiki/Conclusionhttp://en.ecgpedia.org/wiki/Conclusionhttp://en.ecgpedia.org/wiki/Compare_the_old_and_new_ECGhttp://en.ecgpedia.org/wiki/Compare_the_old_and_new_ECGhttp://en.ecgpedia.org/wiki/ST_morphologyhttp://en.ecgpedia.org/wiki/QRS_morphologyhttp://en.ecgpedia.org/wiki/P_wave_morphologyhttp://en.ecgpedia.org/wiki/Heart_axishttp://en.ecgpedia.org/wiki/Conductionhttp://en.ecgpedia.org/wiki/Ratehttp://en.ecgpedia.org/wiki/Rhythm


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Coronary Arteries


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Normal ECG


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Help with the localisation of a myocardial infarct

localisation ST elevation Reciprocal ST depression coronary artery

Anterior MI V1-V6 None LAD

Septal MIV1-V4, disappearance of

septum Q in leads V5,V6none LAD-septal branches

Lateral MI I, aVL, V5, V6 II,III, aVF LCX or MO

Inferior MI II, III, aVF I, aVL RCA (80%) or RCX (20%)

Posterior MI V7, V8, V9

high R in V1-V3 with ST

depression V1-V3 > 2mm

(mirror view)

RCX

Right Ventricle MI V1, V4R I, aVL RCA

Atrial MI PTa in I,V5,V6 PTa in I,II, or III RCA
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Where is this myocardial infarction located?

Answer

sinus rythm

normal conduction intervals

normal p-waver morphology

Q in II and AVF. Tall R wave in V2-V3

ST elevation in II, III, AVF & V5, V6. ST depression in V2.

Conclusion: Infero- (II,III,AVF) postero- (depressions in V2-V3) lateral (V5,V6) infarct
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sinus rhythm, with 3 ventricular premature beatsabout 80 /min

normal conduction

horizontal axis

normal p wave morphology

Q in V1. slow anterior R-wave progression.

ST elevation in V1-V4, AVL. ST depression in II,III,AVF. The ST vector is upright.Conclusion: Anterior MI with proximal LAD occlusion
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ECG MI 5

sinus rhythm

about 60/min

normal conduction

intermediate axis

normal p wave morphologyNo pathologic Q or LVH. Tall R in V2, V3.

ST depression in V2, V3. Also depression in III and AVF. Some elevation in I and AVL.

Conclusion: Postero-lateral MI caused by an RCX occlusion.

Note! The high frequency vibration that is most clearly seen in lead AVR (with a

frequency of > 300/min) is an artefact and not a suprvaventricular tachycardia. In SVT,

there would be no P waves. It is quite unusual that lead III shows depression in a RCXinfarction. Apparently the inferior part is not much affected by this infarction
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ECG MI 20. Click on image for enlargement.

Rhythm: The ECG shows a regular rhythm with normal P waves (positive in I, III and AVF, negative in

AVR), followed by QRS complexes. Sinusrhythm

Heart rate: 100 bpm

Conduction (PQ,QRS,QT): PQ: 140ms QRS: 100ms QT: 320ms QTc: 410msHeartaxis: QRS positive in I and AVF: normal heart axis

P wave morphology: The P waves have normal morphology.

QRS morphology: Narrow QRS. No left ventricular hypertrophy. No pathologic Q waves.

ST morphology: ST elevation in V1-V4 and lead I. ST depression in II, III, AVF and V6. Lead V3 shows

V4R which is not elevated

Compare with the old ECG (not available, so skip this step)

Conclusion?

Sinusrhythm with anteroseptal infarction. Ischemic vector is pointing upwards (ST depression inAVF), a sign of proximal LAD occlusion.
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http://en.ecgpedia.org/wiki/File:Ami0013.jpg


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ECG MI 13. Click on image for enlargement.

Culprit lesion: LAD

Sinustachycardia: about 100/min

normal conduction intermediate heart axis

tall p wave in II consistent with right atrial dilatation. (the sawtooth-basline between the 2nd and 3rd

complex in AVR is probably a motion artefact). PTA depression in II

Loss of R waves throughout the anterior wall (V1-V6). QS complexes in V3-V5.

ST elevation in V1-V5 with terminal negative T waves

Conclusion: Large anterior MI due to LAD occlusion.

Characteristics that suggest a large infarct in this case are:

Loss of R waves throughout the anterior wall (V1-V6). QS complexes in V3-V5.

Left and right sided decompensation, resulting in right atrial dilatation and ischemiaTachycardia
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ECG 1

Answer

The ECG shows a rhythm around 60 bpm with severe QRS prolongation and

prominent T waves. This might be sinus rhythm with very small P waves or

atrial fibrillation with a relatively regular rate. These changes are typical

of severe hyperkalemia
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The ECG

A
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Answer

Following the 7+2 steps:

Rhythm

This is a regular rhythm and every QRS complex is preceded by a p

wave. The p wave is positive in II,III, and AVF and thus originates from

the sinus node. Conclusion: sinus rhythm.Heart frequency

Use the 'count the squares' method (a bit less than 3 large squares ~>

300-150-100), thus about 110 bpm and thus sinustachycardia.

Conduction (PQ,QRS,QT)

PQ-interval=0.10sec (2.5 small squares), QRS duration=0.10sec, QT

interval=320msHeart axis

Positive in I, II, negative in III and AVF. Thus a horizontal (normal) heart

axis.

P wave morphology

The p wave is rather large in II, but does not fulfill the criteria for right

atrial dilatation.QRS morphology

The QRS shows a slurred upstroke or delta wave.

ST morphology

Negative T wave in I and AVF. Flat ST in V3-V5.


Conclusion?Sinustach cardia in a atient with a WPW attern
http://en.ecgpedia.org/wiki/Sinustachycardiahttp://en.ecgpedia.org/wiki/WPWhttp://en.ecgpedia.org/wiki/WPWhttp://en.ecgpedia.org/wiki/Sinustachycardia


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The ECG

A
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Answer

Following the 7+2 steps:

Rhythm

The ECG shows a regular rhythm with normal P waves (positive in I, III

and AVF, negative in AVR), followed by QRS complexes. Sinusrhythm

Heart rate78 bpm

Conduction (PQ,QRS,QT)

PQ: 180ms QRS: 160ms QT: 370ms QTc: 420ms

Heartaxis

Negative in III, AVF and AVR, positive QRS complexes in I, II and AVL:

horizontal heart axisP wave morphology

The P waves have normal morphology.

QRS morphology

Wide QRS complexes with left bundle branch blockpattern.

ST morphology

ST elevation in V1-V3, AVR. ST depression in I, II, III, AVF, V4-6. TheSgarbossa criteria for ischemia in LBBB are not met (nog concordant ST

deviation, no ST depression V1-V3, nog discordant ST elevation > 5 mm).


Conclusion?

Sinusrhythm with left bundle branch block, comparison with an old ECG is

mandatory to evaluate whether the LBBB is new (a sign of myocardial infarction)or old.
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The ECG
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Rhythm

The ECG starts with a regular rhythm with normal P waves (positive in I,

III and AVF, negative in AVR), followed by QRS complexes. Sinusrhythm

Heart rate

around 60 bpmConduction (PQ,QRS,QT)

PQ: 240ms QRS: 120ms QT: 440ms QTc: same as QT at this heart rate

Heartaxis

Negative in II, III and AVF: left heart axis

P wave morphology

The P wave duration is somewhat prolonged.

QRS morphology

Wide QRS complexes with [[[RBBB|right bundle branch block]]] pattern.

No LVH or pathologic Q waves.

ST morphology

ST depression in V1. Overall flat ST segments.Compare with the old ECG (not available, so skip this step)

Conclusion?

Trifascicular block with first degree AV block, right bundle branch block and

left anterior fascicular block.


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The ECG
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Rhythm

The ECG shows a regular rhythm, but the last couple of beats are faster.

Between these last beats clear P waves are discernable. De distance

between the P waves and QRS complexes changes and there seems to be

no relation between the two: AV dissociation. As there are no P wavespreceding the first QRS complexes the rhythm must be of nodal originin

competition with sinusrhythm. The 10th, 12th and 13th beats are preced

by a P wave, here the sinusrhythm has taken over from the nodal rhythm.

Heart rate

around 80 bpm

Conduction (PQ,QRS,QT)PQ: not applicable. QRS: 110ms QT: 380ms

Heartaxis

Positive in I and II, negative in III. Slightly positive in AVF. An intermediate

heart axis.

P wave morphology The P waves that are present seem to have a normal

morphology.QRS morphology Slightly broad QRS complexes. QS in V1.

ST morphology Negative T in III oreceded by a negative QRS complex (normal).


Conclusion?

Nodal rhythm in competition with sinusrhythm.
http://en.ecgpedia.org/wiki/AV_dissociationhttp://en.ecgpedia.org/wiki/Nodal_Rhythmhttp://en.ecgpedia.org/index.php?title=Sinusrhythm&action=edit&redlink=1http://en.ecgpedia.org/index.php?title=Sinusrhythm&action=edit&redlink=1http://en.ecgpedia.org/wiki/Nodal_Rhythmhttp://en.ecgpedia.org/wiki/AV_dissociation


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Rhythm

The ECG shows a regular rhythm. Every P wave is followed by a QRS

complex. P waves are positive in I and AVF. Normal sinus rhythm

Heart rate

about 80bpmConduction (PQ,QRS,QT)

In lead II: PQ: 210ms QRS: 90ms QT: 380ms QTc: 450ms

Heartaxis

QRS positive in I and AVF: normal heart axis

P wave morphology

Broad based P wavesQRS morphology

Normal QRS complexes

ST morphology

Typical ST elevation in V1, V2 and V3, with a coved type morphology in

V1.


Conclusion?

Typical Brugada syndromeST segments in right precordial ECG leads (on spot

diagnosis) aka 'type-1 Brugada ECG' with 1st degree AV block and broad P-waves.

Atrial/AV/ventricular conduction delay is commonly seen in Brugada syndrome, in thispatient there is atrial and AV conduction delay. Brugada syndrome is associated with
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This case report is kindly provided by Dr. Alberto Giniger

from the ICBA and is part of the ICBA case reports

Ventricular tachycardia or idioventricular rythm during sinus tachycardia with fusionbeats
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AV block with idionodal escape (the third P wave is inside the QRS)


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A 14-year-old boy died suddenly while playing soccer He was in the middle of a


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A 14-year-old boy died suddenly while playing soccer. He was in the middle of a

sprint when he suddenly succumbed. Resuscitation efforts were unsuccessful.

His family assured us that he had had no previous symptoms and that his family

history was unremarkable. His two-year older brother, however, remembered

that he had also collapsed once while playing an exciting soccer match. This

occurred at the age 10, after which he experienced no further events. Hisbrothers death worried him (and his family) and he visited a cardiologist for

medical advice. Physical examination was unremarkable; his ECG is shown in

figure 1. An echocardiogram was completely normal.

The question now is whether further evaluation is needed

Author(s)A.A.M. Wilde,

T.A. SimmersNHJ edition: 2004; 8, 355

These Rhythm Puzzles have been

published in theNetherlands Heart

Journaland are reproduced here

under the prevailing creativecommons license with permission

from the publisher, Bohn Stafleu Van

Loghum.

The ECG can be enlarged twice by

clicking on the image and it's firstenlargement
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Answer

The ECG shows sinus rhythm (70 beats/min) with a normal QRS axis. PQ interval and

QRS width are normal. Repolarisation is completely normal and the QTc interval is 384

msec, well within normal limits. Hence the ECG is completely normal. From the historyof the patient and from his family history it became clear that both events (his collapse

and the circumstances of his brothers death) were triggered by exercise. An exercise

test should therefore be part of the cardiological work-up. Figure 2 shows the ECG after

six minutes of exercise. There is still sinus rhythm, 130 beats/min, and conduction

intervals remain normal. The QT interval is now markedly prolonged and approaches

530 msec (QTc: 527 msec). This response should raise suspicion of a long-QTsyndrome, type 1 and in conjunction with the symptom(s) -blockade therapy is

warranted. Molecular genetic screening indeed revealed a mutation in the KCNQ1 gene.

Type 1 LQTS is characterised by QT prolongation, in particular during exercise. The QT

interval fails to adapt to an increase in rate and therefore inappropriately prolongs with

an increase in rate. In conjunction, events (dizziness, syncope and sudden death) are

typically triggered by adrenergic stimuli among which exercise. Other typical triggers arediving and swimming; the age of onset of symptoms is usually around five years. A

careful family history should be taken. Treatment of choice is a -blocker, in symptomatic

patients titrated up to the highest possible tolerated dose. Asymptomatic young patients

should receive prophylactic treatment but asymptomatic individuals over 20 years of age

with a QTc interval


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A 33 year old lady visited the cardiologist because of the sudden death of her

brother at age 35. He died while watching TV and had been without symptoms

as far as she was aware. Her father received a pacemaker at the age of 48.

She had no complaints of dizziness, palpitations, dyspnoea or chest pain. Her

only complaint was some weakness in her arms shortly after lifting them to get

something from above her head. Physiological examination did not reveal anypeculiarities. Her ECG is shown in figure 1. Her echocardiogram is normal,

although cardiac dimensions were at the upper limit of normal.

What is your diagnosis and what would your next step be?Author(s)

A.A.M. Wilde, Y.M.

Pinto

NHJ edition: 2005:10,373

These Rhythm Puzzles have been published in

theNetherlands Heart Journaland are

reproduced here under the prevailing creative

commons license with permission from the

publisher, Bohn Stafleu Van Loghum.

The ECG can be enlarged twice by clicking

on the image and it's first enlargement
http://www.pubmedcentral.nih.gov/tocrender.fcgi?action=archive&journal=384http://www.pubmedcentral.nih.gov/tocrender.fcgi?action=archive&journal=384


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Answer

The ECG shows sinus rhythm 60 beats/min. The QRS width is normal (80

msec) and the QRS axis is almost horizontal. Repolarisation is normal. The

primary abnormality is the prolonged PQ interval (300 msec). In addition, the P

wave has a very low amplitude (in all leads). The combination of prolonged PQ

interval, lowvoltage P waves and the patients history of muscle weakness

should raise the suspicion of a myopathy associated with conduction disease.

The family history with one sudden death and a pacemaker in first-degree

relatives narrows this down even more to a laminopathy i.e. a disease linked to

mutations in the lamin A/C gene. In that case referral to a recognised muscleneurologist is mandatory. In our patient the neurologist found clear evidence of

proximal myopathy. The clinical diagnosis limb-girdle disease was made and

molecular diagnostic testing indeed revealed a mutation in the lamin A/C gene.

The ECG findings are typical for Limb-Girdle disease type 1b (the variant linked

to lamin A/C mutations). Conduction abnormalities almost always precede signsof cardiomyopathy, which only progresses to overt dilated cardiomyopathy in

some cases. Particularly the conduction system is sensitive to damage, most

likely increased fibrosis. In our patient the conduction system is affected (long

PQ interval and undoubtedly a prolonged HV interval) and it is also likely that

the atrial tissue is abnormal as well (low-amplitude P waves). For a long timepacemaker therapy was considered sufficient, but in recent years it has become


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