Ischemic Heart Disease

MD Cristian Furu

25.02.201
4

Interpretation of the normal ECG

according to the 7+2 step plan
7+2 step plan
Step 1:Rhythm
Step 2:Rate
Step 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

Coronary Arteries

Normal ECG

Help with the localisation of a myocardial infarct

localisation

ST elevation

Reciprocal ST depression

coronary artery

Anterior MI

V1-V6

None

LAD

Septal MI

V1-V4, disappearance of
septum Q in leads V5,V6

none

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

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

Sinus rhythm
Around 75 bpm
PQ normal, QRS interval 0.11 seconde, QT not prolonged
Left axis
normal p wave
QRS morphology: widened QRS, but not enough for LBBB diagnosis
ST elevation in AVR, V1, V2, V3. Reciprocal ST depression in II, III, AVF, V6. ST
vector is upright ('pointing to heaven' (where the patient might go soon if not
treated immediately)

sinus rhythm, with 3 ventricular premature beats

about 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

ECG MI 5

sinus rhythm
about 60/min
normal conduction
intermediate axis
normal p wave morphology
No 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

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: 410ms
Heartaxis: 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

ECG MI 12.
11. Click on image for enlargement.

ST elevation in D2,D3,aVF,V5,V6,maybe V7-9 Bradycardia AMI of the

inferio-posterior and basal posterior ==> RCA is blockage

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 ischemia
Tachycardia

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 ofsevere hyperkalemia

The ECG

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=320ms
Heart 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)

The ECG

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 rate
78 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 axis
P wave morphology
The P waves have normal morphology.
QRS morphology
Wide QRS complexes withleft bundle branch blockpattern.
ST morphology
ST elevation in V1-V3, AVR. ST depression in I, II, III, AVF, V46. The Sgarbossa 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

The ECG

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 bpm
Conduction (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.

The ECG

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 waves
preceding the first QRS complexes the rhythm must be of
nodal originin competition withsinusrhythm. 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?

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 80bpm
Conduction (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 waves
QRS 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?
TypicalBrugada syndromeST segments in right precordial ECG leads
(on spot diagnosis) aka 'type-1 Brugada ECG' with 1st degree AV
block and broad P-waves.

Ventricular tachycardia or idioventricular rythm during sinus tachycardia with fusion

beats
This case report is kindly provided by Dr. Alberto
Giniger from the ICBA and is part of the
ICBA case reports

AV block with idionodal escape (the third P wave is inside the QRS)

Complete AV block and left ventricle escape

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. His brothers 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.
A.A.M.
Wilde, is needed
The question now
is whether further
evaluation
Author(s)

T.A. Simmers

NHJ edition:

2004; 8, 355

These Rhythm Puzzles have

been published in the
Netherlands 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

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 history of 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-QT syndrome, 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 are diving 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

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 any peculiarities. Her ECG is shown in figure 1. Her
echocardiogram is normal,
although
cardiac
A.A.M.
Wilde,
Y.M.dimensions were at the
Author(s)
upper
limit of normal.
Pinto
What is your diagnosis and what would your next step be?
NHJ edition:
2005:10,373
These Rhythm Puzzles have been
published in the
Netherlands 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

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 muscle neurologist 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 signs of 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