Medical expert of the article
New publications
ECG analysis and interpretation
Last reviewed: 19.10.2021
All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
ECG displays the processes of occurrence of arousal and its conduct. The teeth are recorded when there is a potential difference between the areas of the excitable system, i.e. One part of the system is agitated, and the other is not. The isopotential line appears in the absence of a potential difference, i.e. When the whole system is not excited or, conversely, is covered by the excitation. From the standpoint of electrocardiology, the heart consists of two excitable systems: the atria and ventricles. The transmission of excitation between them is carried out by the conducting system of the heart. Due to the fact that the mass of the conducting system is small, the potentials arising in it during normal amplifications are not caught by the standard electrocardiograph, so the ECG reflects the consistent coverage of the contractile atrial and ventricular myocardium.
In the atria, excitation extends from the sinoatrial node to the atrioventricular node. Normally, the propagation speed of the excitation of the atria conductive beams approximately equal to the velocity of propagation of atrial myocardium contractile therefore reach its excitation displayed monofaznsh tooth R. The spread of excitation in the myocardium of the ventricles occurs through excitation transfer from the conductive elements on the contractile system of the myocardium that causes complicated complex QRS. At the same time, the Q wave corresponds to the excitation of the apex of the heart, the right papillary muscle and the inner surface of the ventricles, the R wave - to the excitation of the base of the heart and the outer surface of the ventricles. The process of propagation of excitation in the basal divisions of the interventricular septum, right and left ventricles forms an SP wave on the ECG. The ST segment reflects the state of complete excitation of both ventricles, is normally on the isopotential line, since there is no potential difference in the excitable ventricular system. The T wave reflects the process of repolarization, i.e. Restore membrane resting potential of myocardial cells. This process in different cells occurs asynchronously, so there is a potential difference between the still depolarized myocardial regions, which have a negative charge, and the myocardial regions, which have restored their positive charge. The indicated potential difference is recorded as a T wave . This tooth is the most variable part of the ECG. An isopotential line is recorded between the T wave and the subsequent P wave, since at this time there is no potential difference in the ventricular and atrial myocardium.
The total duration of electrical ventricular systole (QRST) is almost the same as the duration of mechanical systole (mechanical systole begins a little later than electrical).
ECG makes it possible to evaluate the nature of disturbances in the excitation in the heart
Thus, in terms of the magnitude of the PQ interval (from the origin of the P wave and to the onset of the Q wave), it can be judged that excitation is performed from the myocardium to the myocardium of the ventricles. Normally this time is 0.12-0.2 s. The total duration of the QRS complex reflects the rate of coverage by excitation of the contractile ventricle myocardium and is 0.06-0.1 s.
Depolarization and repolarization processes occur in different parts of the myocardium non-simultaneously, so the potential difference between the different parts of the cardiac muscle changes throughout the cardiac cycle. The conditional line connecting at each moment two points with the greatest potential difference is usually called the electric axis of the heart. At each time, the electrical axis of the heart is characterized by its length and direction, i.e. Is a vector quantity. Changing the direction of the electrical axis of the heart can be important for diagnosis.
The ECG makes it possible to analyze in detail the changes in the heart rate. Normally, the heart rate is 60-80 per minute, with a more rare rhythm - bradycardia - 40-50, and with more frequent - tachycardia - exceeds 90-100 and reaches 150 per minute or more.
In some pathological conditions of the heart, the correct rhythm is occasionally or regularly disturbed by an extraordinary contraction - the extrasystole. If an extraordinary excitation occurs in the sinoatrial node at the moment when the refractory period is over, but another automatic impulse has not yet appeared, there is an early contraction of the heart - a sinus extrasystole. The pause following such extrasystole lasts the same time as usual.
Extraordinary excitation, which has arisen in the myocardium of the ventricles, does not affect the automatics of the atrioventricular node. This node timely sends another impulse reaching the ventricles at a time when they are in a refractory state after extrasystoles and therefore do not respond to another impulse. At the end of the refractory period, the ventricles can again respond to irritation, but it takes some time until the next impulse comes from the sinoatrial node. Thus, the extrasystole caused by the impulse that appeared in one of the ventricles (ventricular extrasystole) leads to a long-term so-called compensatory pause of the ventricles with an unchanged rhythm of atrial work.
Extrasystoles may appear in the presence of foci of irritation in the myocardium, in the region of atrial or ventricular pacemakers. Extrasystolia can also cause impulses coming into the heart from the central nervous system.
The ECG reflects changes in the magnitude and direction of action potentials, but does not allow one to evaluate the features of the cardiac delivery function. The potentials of the action of the membrane of myocardial cells are only a trigger mechanism of myocardial contraction, which includes a certain sequence of intracellular processes terminating with shortening of myofibrils. These successive processes are called conjugation of excitation and contraction.
Defeat of the myocardium to some extent can be observed with any generalized infection and affect the severity of the course and the outcome of the disease. At the same time, it is assumed that persistent infectious agents, and especially viruses, can lead to the development of chronic cardiac damage. The most clinically important causes of myocardial damage are enteroviruses, Epstein-Barr virus (EBV), cytomegalovirus (CMV), HIV, meningococcal, b-hemolytic group A streptococcus, Yersinia, botulinum toxin Corynebacterium diphtheriae (diphtheria), Borrelia burgdorferi (Lyme borreliosis ), Toxoplasma gondii (toxoplasmosis), etc.
Despite the fact that each infectious disease has its own etiology, pathogenesis and clinical manifestations, there are general patterns of myocardial damage and the corresponding ECG changes in acute and distant periods.
The most frequent infectious diseases on the ECG are changes in the final part of the ventricular complex in the form of depression or elevation of the ST segment and a decrease in the amplitude of the T wave . The severity of myocardial damage may indicate conduction abnormalities in the form of various atrioventricular blockades (AV blockade), left bundle branch blockade and disturbances of excitability in the form of ventricular tachycardia or ventricular extrasystole of high gradations.
ECG signs of blockade of the right bundle of the bundle, His polytropic atrial extrasystole, ST segment elevation usually accompany pericardial damage and / or increased pressure in the small circulation.
The conduction system of the heart in infectious diseases is less often affected than the contractile myocardium, which is manifested on the ECG by a more rare finding of ECG signs of conduction disturbance compared with the change in the ST segment . In the case of infectious pathology, the sensitivity of the ECG is higher than that of the clinical examination method.
ECG allows you to assess the nature of the disorders of the excitation in the heart
Thus, by the size of the PQ interval (from the beginning of the P wave to the beginning of the Q wave), it is possible to judge the conduction of arousal from atrial myocardium to ventricular myocardium. Normally, this time is 0.12-0.2 s. The total duration of the QRS complex reflects the rate of coverage of the excitation of the contractile ventricular myocardium and is 0.06-0.1 s.
The processes of depolarization and repolarization occur in different parts of the myocardium at the same time, so the potential difference between different parts of the heart muscle during the cardiac cycle changes. The conditional line connecting at each moment two points with the greatest potential difference is called the electrical axis of the heart. At each moment of time, the electrical axis of the heart is characterized by length and direction, i.e. Is a vector quantity. Changing the direction of the electrical axis of the heart may be important for diagnosis.
ECG allows you to analyze in detail the changes in heart rhythm. Normally, the heart rate is 60-80 per minute, with a rarer rhythm - bradycardia - 40-50, and with more frequent - tachycardia - it exceeds 90-100 and reaches 150 per minute or more.
See also: ECG in pathology
In some pathological conditions of the heart, the correct rhythm is episodically or regularly broken by an extraordinary contraction - an extrasystole. If an extraordinary excitation occurs in the sinoatrial node at the moment when the refractory period is over, but the next automatic impulse has not yet appeared, an early contraction of the heart occurs - sinus beats. The pause following such an extrasystole lasts the same time as an ordinary one.
Extraordinary excitement that has arisen in the ventricular myocardium does not affect the automaticity of the atrioventricular node. This node sends another pulse in time, reaching the ventricles at the moment when they are in a refractory state after extrasystoles and therefore do not respond to the next pulse. At the end of the refractory period, the ventricles can again respond to irritation, but some time elapses until the next impulse comes from the sinoatrial node. Thus, an extrasystole caused by a pulse arising in one of the ventricles ( ventricular extrasystole ) leads to a prolonged so-called compensatory pause of the ventricles with an unchanged atrial rhythm.
Extrasystoles may appear in the presence of foci of irritation in the myocardium, in the region of the atrial or ventricular pacemakers. Extrasystoles can also cause impulses coming into the heart from the central nervous system.
The ECG reflects changes in the magnitude and direction of action potentials, but does not allow to evaluate the features of the cardiac pressure function. The action potentials of the myocardial cell membrane are only the trigger mechanism for myocardial contraction, including a specific sequence of intracellular processes, resulting in the shortening of myofibrils. These sequential processes are called conjugation excitation and contraction.
Myocardial damage in one degree or another can be observed with any generalized infection and affect the severity and outcome of the disease. At the same time, it is assumed that persistent infectious agents, and above all viruses, can lead to the development of chronic heart damage. The most clinically important causes of myocardial damage are enteroviruses, virus is Epstein-Barr virus (EBV),, cytomegalovirus (CMV),, HIV, meningococcus, b-hemolytic group A streptococcus, Yersinia, botulinum toxin Corynebacterium diphtheriae (diphtheria), Borrelia burgdorferi (Lyme borreliosis) Toxoplasma gondii (toxoplasmosis) and others.
Despite the fact that each infectious disease has its etiology, pathogenesis and clinical manifestations, there are general patterns of myocardial damage and their corresponding changes on the ECG in acute and distant periods.
Most often, in case of infectious diseases, changes in the end part of the ventricular complex in the form of depression or elevation of the ST segment and a decrease in the amplitude of the T wave are determined on the ECG. Conduction disturbances in the form of various atrioventricular blockades (AV blockades) and blockade of the left bundle of His branch can indicate and disturbances of excitability in the form of ventricular tachycardia or ventricular extrasystoles of high gradations.
ECG signs of blockade of the right bundle of His's bundle, polytopic atrial extrasystole, ST- segment elevation are usually associated with pericardial damage and / or an increase in pressure in the pulmonary circulation.
The conduction system of the heart in infectious diseases is less frequently affected than the contractile myocardium, which is manifested on the ECG by the rarer detection of ECG signs of conduction disturbance as compared to the change in the ST segment . In the case of an infectious pathology, ECG sensitivity is higher than that of a clinical examination method.
ECG criteria for clinically significant myocardial damage
- depression of the ST segment more than 2 mm from the contour in three leads and more;
- any conduction disturbances detected for the first time;
- ventricular extrasystole high gradations.
[8], [9], [10], [11], [12], [13], [14], [15], [16], [17], [18]
ECG criteria for severe myocardial damage
- conduction disorders in the form of AV-dissociation with idioventricular rhythm, AV-blockade of the II degree of Mobitz II type, identified for the first time;
- ventricular tachycardia.