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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
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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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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.
Compare with the old ECG (not available, so skip this step)
Conclusion?Sinustach cardia in a atient with a WPW attern
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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).
Compare with the old ECG (not available, so skip this step)
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).
Compare with the old ECG (not available, so skip this step)
Conclusion?
Nodal rhythm in competition with sinusrhythm.
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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.
Compare with the old ECG (not available, so skip this step)
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
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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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