You are on page 1of 34

Ischemic Heart Disease

MD Cristian Furu

25.02.2014

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 Anterior MI V1-V6 ST elevation Reciprocal ST depression None LAD coronary artery

Septal MI

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

none

LAD-septal branches

Lateral MI Inferior MI

I, aVL, V5, V6 II, III, aVF

II,III, aVF I, aVL

LCX or MO 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 III shows depression in a RCX infarction. Apparently the inferior part is not much affected by this infarction

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 depression in AVF), a sign of proximal LAD occlusion.

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

ST elevation in D2,D3,aVF,V5,V6,maybe V7-9 Bradycardia AMI of the inferioposterior 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 of severe 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) Conclusion? Sinustachycardia] in a patient with a WPW pattern

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 with left bundle branch block pattern. ST morphology ST elevation in V1-V3, AVR. ST depression in I, II, III, AVF, V4-6. 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 ECG is mandatory to evaluate whether the LBBB is new (a sign of myocardial infarction) or 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 origin in 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.

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?
Typical Brugada syndrome ST 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 this patient there is atrial and AV conduction delay. Brugada syndrome is associated with

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. The question now is whether further evaluation is needed

A.A.M. Wilde, T.A. Simmers NHJ edition: 2004; 8, 355 These Rhythm Puzzles have been published in theNetherlands Heart Journal and 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 Author(s)

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 age with a QTc interval <500 msec seem to be at low risk. Molecular genetic screening is mandatory; LQT1 is caused by mutations in the KCNQ1 gene encoding one of the main repolarising potassium currents.

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 dimensions were at the upper limit of normal. What is your diagnosis and what would A.A.M. Wilde, your Y.M. next step be? Author(s) Pinto NHJ edition: 2005:10,373

These Rhythm Puzzles have been published in theNetherlands Heart Journal and 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 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 time pacemaker therapy was considered sufficient, but in recent years it has become