The electrocardiogram in myocardial acute infartion

The healthy myocardium, at rest, is polarized. The intracellular space is negative with respect to the positive extracellular space. In electric activation, this polarity changes suddenly due to the transmembrane ion currents and propagates through the myocardium, from the endocardium to the epicardium in the ventricles and by contiguity in the atria.

This planar surface with opposite electrical charges on one side and the other that travels through the myocardium, very rapidly during depolarization and more slowly in repolarization, is called a dipole. A dipole, when moving, generates an electric field that can be registered with an explorer electrode, such registration will depend on the direction and direction in which the dipole moves and the electric charge intensity it has; it is, therefore, of a vectorial magnitude.

The Electrocardiogram (ECG) results from the spatial and temporal summation of all the generated vectors. After the systolic electrical activation, the myocardium returns to its resting state, in diastole, during which it remains electrically charged in a stable and homogeneous manner. In this phase there are no dipoles that move and an electrocardiograph will record only its baseline.

In myocardial ischemia the properties of the affected tissue are altered, local electrical events tend to be slower and lower in voltage, and the repolarization sequence is usually inverted (going from epicardium to endocardium in normal tissue and vice versa in ischemic tissue). Ischemia mainly affects ventricular repolarization and its most characteristic electrocardiographic expression is the reversal of the T wave.

In the areas of myocardial necrosis there is no electrical activity, the ECG records through this electrical “hole” the activity of the opposite side of the heart (Q waves).

In our subject -the acute phase of the infarction-, the fundamental aspects of the clinic and the ECG revolve around a determining histopathological fact: myocardial injury. When the tissue suffers such a degree of damage, it is unable to recover all of its transmembrane diastolic potential (it is repolarized less); this generates a potential difference between the positive healthy areas, completely repolarized, and the negative ones affected. Such a difference in diastolic potential constitutes a dipole that migrates from negative injurious areas to positive positive ones. We can say then that the electrocardiographic expression characteristic of transmural injury-the ST supra-level-is, to a large extent, an optical illusion. In effect, the substance of this phenomenon occurs in diastole and is the decrease of the baseline between the T wave and the beginning of the QRS following. It is admitted that there are also systolic electric forces that move the ST upwards, but they are of little magnitude and we will not consider them.

The electrocardiographic diagnosis of AMI is based on the presence of an ST segment elevation> 1 mm in two contiguous leads, or> 2 mm in leads V1 to V4, or in the occurrence of a complete left bundle branch block (BCRI) new or presumably new. In a “guideline” on AMI of the American College of Cardiology and the American Heart Association (ACC/AHA) these criteria are maintained with slight modifications, namely: limits to V2 and V3 the requirement of an ST elevation of> 2 mm in men and it drops to> 1.5 mm in women.

Electrocardiography is an academic discipline, the ECG is a clinical instrument. In order to take advantage of this clinical instrument, we must analyze and interpret it from its foundations, that is, from the basic principles of electrocardiography. There is no other way, the practice of visually memorizing some electrocardiographic patterns is not consistent with a good cardiological training and conditions frequent errors and rapid forgetting. It is true that the formidable development of imaging techniques has displaced the ECG as a diagnostic resource in many chapters of cardiology, but not in all. The ECG continues to be the cornerstone in medical decision-making in patients presenting with acute coronary or arrhythmic events.

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