Notes by dr Claudio Italiano
How to interpret the signs of a myocardial infarction by reading an ECG?
The ECG has a fundamental role in the diagnosis and decision-making of acute coronary syndromes. On it is based the distinction between infarction with (STEMI) and without ST segment elevation (NSTEMI) and therefore the subsequent choice of the most appropriate therapeutic strategy. In patients with STEMI, the careful reading of the ECG is able to give information not only on the site of the infarct but also on the guilty coronary and therefore on the share of myocardium at risk. Even after thrombolytic treatment or coronary angioplasty, the behavior of the ECG provides useful indications on the degree of myocardial reperfusion and therefore on the risk of postinfarction ventricular remodeling. In patients with NSTEMI, the size, location, and extent of ST-segment subtraction are useful for stratifying acute risk.
Pericarditis: Generalized overlap in the absence of specularity. The T wave
starts to become negative only after the ST tract has returned to the
isoelectric. Sub-segmentation of the PR section
Myocarditis: Absence of agreement between the location of kinetic changes at the
echocardiogram and coronary anatomy. Atrioventricular conduction disorders. Left
ventricular hypertrophy
Hypervagotonia / repolarization: ST elevation where the T wave is clearly
positive, early / youthful age ST elevation with a higher concavity, especially
in V3-V4, in the absence of specularity. Absence of evolution of alterations
Hyperkalaemia Over-leveling ST "downsloping", normal or slightly reduced QT
interval, extremely widened QRS, reduction in amplitude / absence of P waves
Brugada syndrome: Maximum over-segmentation of point J V1-V2 vs V3 (type 1),
Extremely fast descent, with high slope, of the ST segment, towards the nadir of
the T wave (type 1), elevation ST <1 mm, with concavity upper (type 2 and 3)
In this jungle the doctor must know how to recognize the patient with a heart
attack. In fact, the guidelines always recommend interventions in hemodynamics (coronarography
and angioplasty). Antiplatelet and thrombolytic therapy is not always ideal.
Meanwhile, from the clinic: chest pain, sweating, vomiting, severe lack of
strength, agitation, sense of weight in the chest. In these conditions the ecg
must be monitored, the necrosis enzymes must be requested. In any case, the
practical doctor must be able to immediately recognize the electrocardiographic
signs of a myocardial infarction: check for altered STs, or other signs of
injury, eg Pardee waves. An immediate intervention, in the space of a few hours,
can save the patient's life and avoid dangerous complications (see infarct
treatment). In the infarction of the myocardium the ecg trace appears the waves
of necrosis, lesion and ischemia.
- Stage 1 (acute): the lesion wave typical of transmural ischemia (elevation of the ST segment) is associated with the isolated T-wave changes typical of phase 0. The overlapped ST segment is detached from the QRS indistinctly; the over-leveling is maximum at 1-3 hours after which it progressively reduces. The differential diagnosis in this phase should be performed with acute pericarditis and with vagal hypertonicity. In this phase the Q waves already begin to be sketched.
- Stage 2 (subacute): it is characterized by the progressive
negativization of T waves, the progressive formation of Q waves with ST tract
that remains still overlapped; the persistence of the elevation of the ST
segment is extremely variable, lasting a few days or remaining unchanged for
weeks, months or years. Generally a rapid return to the isoelectric line is
associated with a lower increase in CK.
- Stage 3 (chronic): it is characterized by the return of the ST segment
to the isoelectric and by the progressive positivization of the T wave. The Q of
necrosis remains.
The electrocardiographic evolution is faster in the lower infarct, while it is
slower in the anterior infarct, especially if there are dyskinetic alterations
of the infarct zone. The ecg trace will first show the appearance of a T wave of
ischemia and, subsequently, the upward leveling of the RS-T segment. In the
first phase of the IMA, during the first 3 hours, a large T wave of
subendocardial ischemia appears, very high and positive, as you can see below in
V2-V3, wave with symmetrical branches and pointed like a "camp tent" ";
During the subsequent first 24 hours, a sub-epicardial lesion occurs which
involves the upward leveling of the RS-T segment and can incorporate the T wave,
creating the monophasic wave of Smith-Pardee. This can be seen if you observe
the derivations V2-V3 and V4, besides there is no increase of the waves r from
V1 to V4. In this case the lesion is localized in the antero-septa-apical area.
During the first few days, the Q wave of necrosis appears, but the sub-epicardial lesion wave still remains for several days; sub-epicardial ischemia involves the appearance of a negative, pointed and symmetrical T wave (Pardee's coronary wave)
Before continuing to read, try to understand what a normal ecg looks like; meanwhile there are the P of sinus rhythm? Is P-Q conduction within the limits? Is the electric axis oriented well or is aVF negative, sign of the carrier pointing upwards and not towards the feet? We see a normal ECG and redo our eyes.
And up to here everything is clear!