The region of the myocardium in which MI develops depends on the location of the occluded coronary artery and the degree of collateral blood flow. There are two main blood supply systems to the myocardium, one supplies the right half of the heart, the other the left half.
The right coronary artery passes between the right atrium and the right ventricle and then curves onto the posterior surface of the heart. In most people, it has a descending branch that supplies the AV node.
The left coronary artery divides into the left descending and left circumflex arteries. The left descending artery supplies the anterior wall and most of the interventricular septum. The circumflex artery passes between the left atrium and the left ventricle and supplies the lateral wall of the left ventricle. In approximately 10% of the population, it has a branch that supplies blood to the AV node.
Localization of the infarction is important for prognostic and therapeutic purposes to determine the area of necrosis.
The location of the infarction can be grouped into several anatomical groups. These are inferior, lateral, anterior and posterior myocardial infarctions. Combinations of these groups are possible, for example, anterolateral MI, which is very common.
| Four main anatomical sites of MI. |
Almost all myocardial infarctions involve the left ventricle. This is not surprising because the left ventricle is the largest chamber of the heart and experiences the greatest stress. Therefore, it is the most vulnerable area in case of disruption of the coronary blood supply. Some inferior MIs also involve part of the right ventricle.
Characteristic electrocardiographic changes of MI are recorded only in those leads that are located above or near the site of the lesion.
· Inferior MI involves the diaphragmatic surface of the heart. It is often caused by occlusion of the right coronary artery or its descending branch. Characteristic electrocardiographic changes may be seen in inferior leads II, III, and aVF.
· Lateral MI involves the left lateral wall of the heart. It often occurs due to occlusion of the left circumflex artery. Changes will occur in left lateral leads I, aVL, V5 and V6.
· Anterior MI involves the anterior surface of the left ventricle and is usually caused by occlusion of the left anterior descending artery. Any of the chest leads (V1 - V6) may show changes.
· Posterior MI involves the posterior surface of the heart and is usually caused by occlusion of the right coronary artery. Unfortunately, there are no leads that are located above the posterior wall. The diagnosis is therefore based on reciprocal changes in the anterior leads, especially V1. Reciprocal changes will be discussed later.
Note: The anatomy of the coronary arteries can vary markedly among individuals, making it impossible to accurately predict which vessel is affected.
Inferior infarcts
Inferior MI is usually the result of occlusion of the right coronary artery or its descending branch. Changes occur in leads II, III And aVF. Reciprocal changes may be noticeable in the anterior and left lateral leads.
Although most MI lesions retain abnormal Q waves throughout the patient's life, this is not necessarily true for inferior MIs. During the first six months, the criteria for pathological Q waves disappear in 50% of patients. The presence of small Q waves in the inferior leads may therefore suggest scarring after MI. Remember, however, that small inferior Q waves may also be noticeable normally.
Lateral infarctions
Lateral MI results from occlusion of the left circumflex artery. Changes may be noticeable in leads I, aVL, V5 And V6. Reciprocal changes are noted in the inferior leads.
Anterior infarcts
Anterior MI is the result of occlusion of the left anterior descending artery. Changes are noticeable in the chest leads ( V1 - V6). If the entire left coronary artery is affected, anterolateral MI is observed with changes in the precordial leads and in leads I and aVL. Reciprocal changes are noted in the inferior leads.
Anterior MI is not always accompanied by the formation of a Q wave. In some patients, the normal progression of the R wave in the precordial leads may only be disrupted. As you already know, normally the chest leads show a progressive increase in the height of the R waves from V1 to V5. The amplitude of the R waves should increase by at least 1 mV in each lead from V1 to V4 (and often V5). This dynamic may be disrupted by anterior MI, an effect called delayed R wave progression. Even in the absence of abnormal Q waves, delayed R wave progression may indicate anterior MI.
Delayed R wave progression is not specific for the diagnosis of anterior MI. It may also be seen in right ventricular hypertrophy and in patients with chronic lung disease.
Posterior infarctions
Posterior MI is usually the result of right coronary artery occlusion. Since none of the usual leads lies above the posterior wall, the diagnosis is verified by reciprocal changes in the anterior leads. In other words, since we will not be able to find ST segment elevation and Q waves in the posterior leads (which are not there), we must look for ST segment depression and tall R waves in the anterior leads, especially in lead V1. Posterior MI is a mirror image of anterior MI on the ECG.
The normal QRS complex in lead V1 consists of a small R wave and a deep S wave; therefore, the presence of a high R wave, especially with ST segment depression, is easily noticeable. In the presence of clinical signs, an R wave of greater amplitude than the corresponding S wave indicates posterior MI.
Another useful tip. Since the inferior and posterior walls usually share a common blood supply, posterior MI is often accompanied by the formation of an inferior wall infarction.
One reminder: The presence of a large R wave greater than the amplitude of the S wave in lead V1 is also a criterion for the diagnosis of right ventricular hypertrophy. The diagnosis of right ventricular hypertrophy, however, requires the presence of a right axis deviation, which is absent in posterior MI.
What is the location of the infarction? Is it really spicy?
Non-Q myocardial infarction
Not all myocardial infarctions are accompanied by the appearance of a Q wave. Previously, it was believed that Q waves were recorded when the MI penetrated the entire thickness of the myocardial wall, while the absence of Q waves indicated the formation of a heart attack only during inner layer myocardial wall called the subendocardium. These infarctions were called transmural or subendocardial.
However, studies have found that there is no clear correlation between the appearance of Q waves and the depth of myocardial damage. Some transmural MIs do not show Q waves, and some subendocardial MIs do not show Q waves. Therefore, the old terminology has been replaced by the terms “Q-wave infarction” and “non-Q-wave infarction.”
The only ECG changes seen in non-Q wave myocardial infarction are T wave inversion and ST segment depression.
It has been established that with non-Q-MI there is lower mortality and more high risk relapse and mortality in Q-MI.
Angina pectoris
Angina pectoris is a typical chest pain associated with coronary artery disease. A patient with angina may develop a myocardial infarction or angina may persist for many years. An ECG recorded during an attack of angina will show ST segment depression or T wave inversion.
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| Three examples of ECG changes that may accompany angina: (A) T wave inversion; (B) ST segment depression; and (C) ST segment depression with T wave inversion. |
Important differences between ST segment depression in angina and non-Q-MI are the clinical picture and dynamics. In angina, the ST segments usually return to their base soon after the attack subsides. In non-Q MI, ST segments remain depressed for at least 48 hours. It may be useful to determine cardiac enzymes that will be increased during the formation of MI, and do not change with angina.
Prinzmetal's angina
There is one type of angina, which is accompanied by ST segment elevation. Unlike typical angina, which is usually provoked by exercise and is the result of progressive atherosclerotic disease of the coronary arteries, Prinzmetal's angina can occur at any time and in many patients is the result of coronary artery spasm. ST segment elevation appears to reflect reversible transmural damage. The contours of the ST segments will often not have a rounded, dome-shaped different shapes, as in MI, and the ST segments quickly return to the base after the attack stops.
Patients with Prinzmetal's angina are actually divided into two groups: without atherosclerosis of the coronary arteries, the pain is determined solely by spasm of the coronary artery, and with atherosclerotic lesions. ECG does not help distinguish between these two groups.
Summary
ST segment at coronary disease hearts
ST segment elevation
It may be noticeable with the development of transmural myocardial infarction or with Prinzmetal's angina.
ST segment depression
May be noticeable in typical angina or non-Q wave myocardial infarction.
The shape of the ST segment in patients with acute ischemic pain is the main determining factor in the choice of therapy. Patients with acute ST segment elevation on the ECG require immediate reperfusion therapy (thrombolysis or angioplasty). Patients with ST segment depression or no ST segment changes usually receive conservative therapy.
Limitations of ECG in the diagnosis of myocardial infarction
The electrocardiographic picture of developing myocardial infarction usually includes changes in the ST segment and the appearance of new Q waves. Any factors that mask these effects, distorting the ST segment and the QRS complex, have Negative influence for electrocardiographic diagnosis of AMI. Two of these factors are WPW syndrome and left bundle branch block.
Rule: In case of left bundle branch block or Wolff-Parkinson-White syndrome, the diagnosis of myocardial infarction cannot be reliable by ECG. This rule includes patients with left bundle branch block on ECG due to ventricular pacing.
In patients with WPW syndrome, delta waves are often negative in the inferior leads (II, III, and aVF). These changes are often referred to as pseudoinfarcts because delta waves can resemble Q waves. A short PR interval is a major clue to distinguish WPW from AMI.
Exercise testing
Exercise testing is a noninvasive method for assessing the presence of CAD. This method is not perfect (false positives and false negatives are common), but it is one of the best screening methods available.
Exercise testing is usually performed by the patient on a treadmill with steady walking or on an exercise bike. The patient is connected to an ECG monitor and the rhythm strip is continuously recorded during the procedure. A complete 12-lead ECG is recorded at short intervals. Every few minutes, the speed and inclination of the walking belt are increased until the following conditions occur: (1) the patient is unable to continue the procedure for any reason; (2) achieving the patient's maximum heart rate; (3) appearance of cardiac symptoms; (4) the appearance of significant changes on the ECG.
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The physiology of testing assessment is simple. The classified loading protocol causes a safe and gradual increase in the patient's heart rate and systolic blood pressure. The patient's blood pressure multiplied by the heart rate is a good indicator of myocardial oxygen consumption. If the myocardial oxygen demand exceeds the ability to deliver it, changes characteristic of myocardial ischemia may be recorded on the ECG.
Significant atherosclerotic damage to one or more coronary arteries restricts blood supply to the myocardium and limits oxygen consumption. Although the ECG at rest may be normal, subclinical signs of CAD may be recorded during exercise.
At positive test on coronary artery disease, the ECG will show ST segment depression. T wave changes are too vague to be of clinical significance.
If the ST segment is depressed during testing, especially if the changes persist for several minutes during the recovery period, there is a high probability of the presence of CAD and damage to the left coronary artery or several coronary arteries. The appearance of cardiac symptoms and a decrease in blood pressure are particularly important signs at which testing should be stopped immediately.
The rate of false positives and false negatives depends on the population being tested. A positive test in a young, healthy person without symptoms or risk factors for CAD is likely to be a false positive. On the other side positive test in an elderly person with chest pain, post-MI, and hypertension, it is highly likely to be a true positive. A negative test result does not exclude the possibility of CAD.
Indications for exercise testing are as follows:
· Differential diagnosis pain in chest
Evaluating a patient with a recent MI to assess the prognosis of the patient and the need for further invasive testing, such as cardiac catheterization
· General assessment of patients over 40 years of age with risk factors for coronary artery disease.
Contraindications include any acute illness, severe aortic stenosis, decompensated congestive heart failure, severe hypertension, resting angina, and the presence of significant arrhythmia.
Mortality from the procedure is very low, but the equipment for cardiopulmonary resuscitation must always be available.
Joan L. is a 62-year-old executive. She is on an important business trip and spends the night in a hotel. Early in the morning she wakes up with shortness of breath and heaviness in the chest, which radiates to the lower jaw and left hand, moderate dizziness and nausea. She gets out of bed, but the pain does not go away. She calls in emergency department. Her complaints are telephoned to the hotel doctor, who immediately orders an ambulance to take her to the local department. emergency care. She arrives there only 2 hours after the onset of her symptoms, which continue despite taking three nitroglycerin tablets.
In the emergency department, an ECG shows the following:
Does she have a myocardial infarction? If the answer is yes, can you tell if the changes are acute and what area of the heart is affected?
Joan's prompt arrival in the emergency department, ST segment elevation, and absence of Q waves on the ECG mean that she is an excellent candidate for either thrombolytic therapy or acute coronary angioplasty. Unfortunately, she only got sick 1 month ago hemorrhagic stroke, has mild hemiparesis on the left, which prevents thrombolytic therapy. In addition, acute angioplasty surgery is not available in this small hospital, and the closest major medical Center several hours away. Therefore, Joan was hospitalized in the cardiology department.
Late at night, one of the nurses notices specific contractions on her ECG:
Joan's ECG shows that the ventricular ectopies have been suppressed. It also shows the appearance of new Q waves in the anterior leads with sequential full development anterior infarction myocardium.
Later in the day, Joan begins to experience chest pain again. A repeat ECG was taken: What has changed?
Joanna developed third degree AV block. Severe conduction blocks usually occur with anterior MI. Her dizziness is due to inadequate pumping function of the myocardium at a ventricular rate of 35 beats/min. Installation artificial driver rhythm is required.
Finishing touches
There are many medications, disorders electrolyte metabolism and other violations that may significantly change normal structure ECG.
In some of these cases, the ECG may be the most sensitive indicator of impending disaster. In others, even subtle electrocardiographic changes may be an early sign of a growing problem.
We will not dwell on the mechanisms of these changes in this chapter. In many cases, the reasons for ECG changes are simply not known. Topics we will cover include the following:
Electrolyte disturbances
Hypothermia
· Medicines
· Other cardiac disorders
Lung diseases
Diseases of the central nervous system
· The heart of an athlete.
Electrolyte disturbances
Changes in potassium and calcium levels can significantly alter the ECG.
Hyperkalemia
Hyperkalemia is accompanied by progressive ECG changes that can culminate in ventricular fibrillation and death. The presence of electrocardiographic changes is more reliable clinical sign potassium toxicity than the serological potassium level.
As potassium increases, T waves begin to increase in all 12 leads. This effect can easily be confused with peaked T waves when acute heart attack myocardium. One difference is that changes in T waves in AMI are limited to those leads that lie above the infarction area, whereas in hyperkalemia, the changes are diffuse.
With a further increase in potassium, the PR interval lengthens, and the P wave gradually flattens and then disappears.
Subsequently, the QRS complex widens, then it merges with the T wave, forming sinusoidal complexes. Eventually ventricular fibrillation develops.
It is important to note that these changes do not always correspond to blood potassium levels. Progression from hyperkalemia to ventricular fibrillation can occur very quickly. Any ECG change due to hyperkalemia requires close clinical attention.
Hypokalemia
For hypokalemia, ECG may also be a better indicator of potassium toxicity than serum potassium levels. Three changes may be noticed, occurring in no particular order:
ST segment depression
T wave smoothing
· Appearance of a U wave.
The term U wave is given to the wave appearing after the T wave in the cardiac cycle. Its exact physiological significance not completely clear. Although U waves are the most characteristic feature hypokalemia, they are not an accurate diagnostic sign. U waves can sometimes be noticeable in normal conditions and in normal level potassium
Calcium disorders
Changes in serum calcium levels primarily affect the QT interval. Hypocalcemia prolongs it; hypercalcemia reduces it. Do you remember the potentially fatal arrhythmia associated with QT prolongation?
Fusiform ventricular tachycardia, type ventricular tachycardia, observed in patients with prolongation of the QT interval.
Hypothermia
When body temperature drops below 30°C, several changes occur on the ECG:
· Everything slows down. Distributed sinus bradycardia, and all segments and intervals (PR, QRS, QT) may lengthen.
· A distinctive and virtually diagnostic pattern of ST segment elevation may be seen. It consists of a sharp rise right at the J point and then a sudden decline back to the bottom. This configuration is called a J wave or Osborne wave.
· Ultimately, various arrhythmias may occur. Low heart rate atrial fibrillation is the most common, although almost any rhythm disorder can occur.
· Muscle tremors due to shaking may complicate ECG analysis. A similar effect may be seen in patients with Parkinson's disease. Do not confuse this with atrial flutter.
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| Interference from muscle tremors resembles atrial flutter. |
Medicines
Cardiac glycosides
There are two categories of electrocardiographic changes caused by cardiac glycosides: those associated with therapeutic doses of the drug, and changes due to overdose (toxicity) of cardiac glycosides.
ECG changes associated with therapeutic doses of SG
Therapeutic doses of SG are characterized by changes in the ST segment and T wave in most patients. These changes are known as the digitalis effect, and consist of ST segment depression with flattening or inversion of the T wave. The reduction of the ST segments has an oblique downward shape, starting almost immediately from the R wave. This distinguishes the digitalis effect from the more symmetrical ST segment depression of ischemia. It is more difficult to differentiate the digitalis effect from ventricular hypertrophy from repolarization disorders, especially because SGs are often used in patients with congestive heart failure, who often have left ventricular hypertrophy.
The digitalis effect is usually most noticeable in leads with tall R waves. Remember: the digitalis effect is normal, expected, and does not require discontinuation of the drug.
ECG changes associated with overdose (toxicity) of cardiac glycosides
Toxic manifestations of FH may require clinical intervention. SG intoxication can manifest itself as conduction blocks and tachyarrhythmias, alone or in combination.
Suppression (suppression) of the sinus node
Even with therapeutic doses of SG, the sinus node can slow down, especially in patients with sick sinus syndrome. In case of overdose, sinoatrial blockades or complete depression of the sinus node may occur.
Blockades
SGs slow conduction through the AV node and can cause 1st, 2nd, and 3rd degree AV blocks.
The ability of cardiac glycosides to slow down AV conduction is used in the treatment of supraventricular tachycardia. For example, SGs may slow the ventricular rate in patients with atrial fibrillation; however, the ability of SG to slow heart rate is clearly noticeable in patients at rest, but disappears during exercise. Beta blockers such as atenolol or metoprolol also have a similar effect on AV conduction but may better control heart rate during exercise or stress.
Tachyarrhythmias
Since SG increases the automaticity of all cells of the conduction system, causing them to act as pacemakers, there is no tachyarrhythmia that they cannot cause. Paroxysmal atrial tachycardia and atrial premature contractions are the most common; Atrioventricular rhythms, atrial flutter and fibrillation are quite common.
Combinations
The combination of atrial tachycardia with second degree AV block is the most characteristic rhythm disorder in SG intoxication. Conduction block is usually 2:1, but may vary. This is the most common, but not the only, cause of AT with conduction block.
Sotalol and other drugs that prolong the QT interval
Antiarrhythmic drug sotalol increases the QT interval and therefore may, paradoxically, increase the risk of ventricular tachyarrhythmias. The QT interval should be monitored carefully in all patients taking sotalol. The drug should be discontinued if the QT interval increases by more than 25%.
Other drugs that may prolong the QT interval include other antiarrhythmics (eg, quinidine, procainamide, disopyramide, amiodarone, and dofetilide), tricyclic antidepressants, phenothiazines, erythromycin, quinolone antibiotics, and various antifungal medications.
Some patients taking quinidine may experience U waves. This effect does not require any intervention.
Several inherited repolarization disorders with QT prolongation have been identified and associated with specific chromosomal disorders. All individuals in these families should be tested for the presence of the genetic defect by recording resting and exercise ECGs. If the above changes are detected, beta blockers and sometimes implantable defibrillators are recommended, since the risk of sudden death is high. These patients should also be excluded from athletic competition and should never be prescribed medications that may prolong the QT interval.
Because the QT interval typically changes with heart rate, the corrected QT interval, or QTc, is used to assess the absolute length of the QT. QTc adjusts to fluctuations in heart rate, determined by dividing the QT interval by the square root R-R. QTc should not exceed 500 ms during therapy with any medicine which can prolong the QT interval (550 ms if there is interventricular block); Compliance with this rule reduces the risk of ventricular arrhythmias.
Other cardiac disorders
Pericarditis
Acute pericarditis can cause ST segment elevation and T wave flattening or inversion. These changes can easily be confused with developing AMI. Certain ECG features may be helpful in differentiating pericarditis from myocardial infarction:
· ST segment and T wave changes of pericarditis tend to be diffuse (but not always), involving many more leads than the limited changes of MI.
· In pericarditis, T wave inversion usually occurs only after the ST segments have returned to the base. In myocardial infarction, T wave inversion usually precedes ST segment normalization.
· In pericarditis, Q wave formation is not observed.
· Sometimes the PR interval decreases.
The formation of effusion in the pericardial cavity reduces the electrical power of the heart, which is accompanied by a decrease in voltage in all leads. ST segment and T wave changes may not be noticeable.
If the effusion is large enough, the heart actually floats freely within the pericardial cavity. This is accompanied by the phenomenon of electrical alternans, in which the electrical axis of the heart changes with each contraction. Not only the axis of the QRS complex can change, but also the P and T waves. A change in EOS is manifested on the ECG by a change in the amplitude of the waves from contraction to contraction.
Hypertrophic obstructive cardiomyopathy (HOCM)
We have already discussed hypertrophic obstructive cardiomyopathy, formerly known as idiopathic hypertrophic subaortic stenosis, in the case of patient Tom L. Many patients with HOCM have a normal ECG, but left ventricular hypertrophy and left axis deviation are often noted. Occasionally, Q waves may be seen in the lateral and inferior leads, but they do not indicate MI.
Myocarditis
Any diffuse inflammatory process involving the myocardium can cause many changes on the ECG. The most common are conduction blocks, especially interventricular blocks and hemiblocks.
Lung diseases
Chronic obstructive disease lungs (COPD)
The ECG of a patient with long-standing pulmonary emphysema may show low voltage, right axis deviation, and slow progression of the R wave in the precordial leads. Low voltage is caused by the effect of increasing the residual air volume in the lungs. The deviation of the electrical axis to the right is caused by the expansion of the lungs, displacing the heart into a vertical position.
COPD can lead to chronic cor pulmonale and right ventricular congestive heart failure. The ECG in this case may show right atrium dilatation (P-pulmonale) and right ventricular hypertrophy with repolarization disorders.
Acute pulmonary embolism
Sudden massive pulmonary embolism can greatly alter the ECG. Research results may include the following:
Right ventricular hypertrophy with repolarization changes due to acute right ventricular dilatation
Right bundle branch block
Electrocardiography (ECG) is a widely used method for diagnosing cardiovascular diseases. During the survey, the difference is recorded electrical potentials, arising in the cells of the heart during its work.
During myocardial infarction, a series of characteristic features, which can be used to predict the time of onset of the disease, the size and location of the lesion. This knowledge allows you to make a timely diagnosis and begin treatment.
- I, II, III - standard bipolar from the limbs;
- aVR, aVL, aVF - reinforced unipolar from the limbs;
- V1, V2, V3, V4, V5, V6 - six unipolar chest ones.
- 1. Acute - the period from several hours to two weeks after a heart attack.
- 2. Subacute - a period of up to 1.5–2 months from the onset of the disease.
- 3. Cicatricial - stage during which damaged muscle tissue is replaced by connective tissue.
Show all
Cardiogram is normal
The ECG reflects the potential difference that occurs when the parts of the heart are excited during its contraction. Pulses are recorded using electrodes installed on different parts of the body. There are certain leads that differ from each other in the areas from which the measurement takes place.
Chest leads
Typically, a cardiogram is taken in 12 leads:
In some situations, additional leads are used - V7, V8, V9. In the projection of each positive electrode there is certain part muscular wall of the heart. Based on changes in the ECG in any of the leads, it can be assumed in which part of the organ the source of damage is located.
ECG is normal, waves, intervals and segments
When the heart muscle (myocardium) relaxes, a straight line is recorded on the cardiogram - an isoline. The passage of excitation is reflected on the tape in the form of teeth, which form segments and complexes. If the tooth is located above the isoline, it is considered positive, if below it is considered negative. The distance between them is called the interval.
The P wave reflects the process of contraction of the right and left atria, the QRS complex registers the increase and decrease of excitation in the ventricles. The RS-T segment and the T wave show how the myocardium relaxes.
ECG for myocardial infarction
Myocardial infarction is a disease in which death (necrosis) of part of the muscle tissue of the heart occurs. The cause of its occurrence is an acute disturbance of blood flow in the vessels supplying the myocardium. The development of necrosis is preceded by reversible changes - ischemia and ischemic damage. Signs characteristic of these conditions can be recorded on an ECG at the onset of the disease.
ECG fragment with ST segment elevation, coronary T
During ischemia, the structure and shape of the T wave and the position of the RS-T segment change on the cardiogram. The process of restoring the original potential in the cells of the ventricles when their nutrition is disrupted proceeds more slowly. In this regard, the T wave becomes taller and wider. It is called "coronary T". It is possible to register a negative T wave in the chest leads, depending on the depth and location of the lesion in the heart muscle.
A prolonged absence of blood flow in the myocardium leads to ischemic damage. On the ECG this is reflected in the form of a displacement of the RS -T segment, which is normally located on the isoline. With different localizations and volumes of the pathological process, it will either rise or fall.
Heart muscle infarction develops in the walls of the ventricles. If necrosis affects a large area of the myocardium, they speak of a large-focal lesion. If there are many small foci - small focal. Deterioration in performance when interpreting the cardiogram will be detected in leads whose positive electrode is located above the site of cell death. In opposite leads, mirror-reciprocal changes are often recorded.
Large focal infarction
The dead area of the myocardium does not contract. In the leads recorded above the area of necrosis, changes in the QRS complex are detected - an increase in the Q wave and a decrease in the R wave. Depending on the location of the lesion, they will be recorded in different leads.
A large-focal process can cover the entire thickness of the myocardium or its part located under the epicardium or endocardium. Total damage is called transmural. Its main sign is the appearance of the QS complex and the absence of the R wave. With partial necrosis of the muscle wall, pathological Q and low R are detected. The duration of Q exceeds 0.03 seconds, and its amplitude becomes more than 1/4 of the R wave.
During a heart attack, three pathological processes are observed at once, which exist simultaneously - ischemia, ischemic damage and necrosis. Over time, the infarction zone expands due to the death of cells that were in a state of ischemic damage. When blood flow is restored, the ischemic area decreases.
The changes recorded on the ECG film depend on the time of development of the infarction. Stages:
Acute stage
Changes in the ECG during a heart attack by stage
15–30 minutes after the onset of a heart attack, a zone of subendocardial ischemia is detected in the myocardium - a disturbance in the blood supply to the muscle fibers located under the endocardium. High coronary T waves appear on the ECG. The RS-T segment shifts below the isoline. These initial manifestations of the disease are rarely recorded; as a rule, patients do not yet seek medical help.
A few hours later, the damage reaches the epicardium, the RS-T segment moves upward from the isoline and merges with the T, forming a flat curve. Further, in the sections located under the endocardium, a focus of necrosis appears, which quickly increases in size. A pathological Q begins to form. As the infarction zone expands, the Q deepens and lengthens, the RS-T drops to the isoline, and the T wave becomes negative.
Subacute stage
The area of necrosis is stabilized, the area of ischemic damage is reduced due to the death of some cells and the restoration of blood flow in others. The cardiogram shows signs of infarction and ischemia - pathological Q or QS, negative T. RS-T is located on the isoline. Gradually, the ischemic zone decreases and the amplitude of T decreases, it smoothes out or becomes positive.
Scar stage
The connective tissue that replaced the dead muscle tissue does not participate in excitation. Electrodes located above the scar record the Q wave or QS complex. In this form, the ECG is stored for many years or the entire life of the patient. RS-T is on the isoline, T is smoothed or weakly positive. Negative T waves are also often observed over the replaced area.
Small focal infarction
Signs of infarction at different depths of myocardial damage
Small areas of damage in the heart muscle do not disrupt the excitation process. Pathological Q and QS complexes will not be detected on the cardiogram.
In small-focal infarction, changes on the ECG film are caused by ischemia and ischemic damage to the myocardium. A decrease or increase in the RS-T segment is detected, negative T waves are recorded in the leads located next to the necrosis. Biphasic T waves with a pronounced negative component are often recorded. With the death of muscle cells located in the posterior wall, only reciprocal changes are possible - coronary T in V1-V3. Leads V7-V9, onto which this area is projected, are not included in the diagnostic standard.
Widespread necrosis of the anterior part of the left ventricle is evident in all chest leads, I and aVL. Reciprocal changes - a decrease in RS-T and a high positive T, are recorded in aVF and III.
The upper sections of the anterior and lateral walls are located outside the recorded leads. In this case, the diagnosis is difficult; signs of the disease are found in I and aVL or only in aVL.
Damage to the back wall
Posterior phrenic, or infarction of the inferior wall of the left ventricle, is diagnosed by leads III, aVF and II. Reciprocal signs are possible in I, aVL, V1-V3.
Posterobasal necrosis is less common. Ischemic changes are fixed when additional electrodes V7-V9 are applied on the back side. An assumption about a heart attack of this localization can be made in the presence of mirror manifestations in V1-V3 - high T, increased amplitude of the R wave.
Damage to the posterolateral portion of the ventricle is seen in leads V5, V6, II, III, and aVF. In V1-V3 reciprocal signs are possible. In a widespread process, changes affect III, aVF, II, V5, V6, V7 -V9.
It appears on the ECG depending on the stage of development. This procedure is always carried out to determine the location and size of the necrosis focus. This is a reliable study, the decoding of which helps to notice any pathological changes in heart.
What is ECG
An electrocardiogram is a diagnostic technique that detects disruptions in the functioning of the heart. The procedure is performed using an electrocardiograph. The device provides an image in the form of a curve, which indicates the passage of electrical impulses.
This is a safe diagnostic technique and is approved for use during pregnancy and childhood.
Using a cardiogram, the following is determined:
- what is the state of the structure that promotes myocardial contraction;
- heart rate and rhythm;
- work of pathways;
- assess the quality of supply to the heart muscle through the coronary vessels;
- detect the presence of scars;
- heart pathologies.
For more accurate information about the state of the organ, they can use daily monitoring, ECG with stress, transesophageal ECG. Thanks to these procedures, the development of pathological processes can be detected in a timely manner.
This is the last and most difficult part of my ECG cycle. I’ll try to tell you clearly, using as a basis “ Guide to Electrocardiography"V. N. Orlova (2003).
Heart attack(lat. infarcio - stuffing) - necrosis (death) of tissue due to cessation of blood supply. The reasons for stopping blood flow can be different - from blockage (thrombosis, thromboembolism) to a sharp spasm of blood vessels. A heart attack may occur in any organ, for example, there is a cerebral infarction (stroke) or a kidney infarction. In everyday life, the word “heart attack” means exactly “ myocardial infarction", i.e. death of cardiac muscle tissue.
In general, all heart attacks are divided into ischemic(more often) and hemorrhagic. With an ischemic infarction, the flow of blood through the artery stops due to some obstacle, and with a hemorrhagic infarction, the artery bursts (ruptures) with the subsequent release of blood into the surrounding tissues.
Myocardial infarction affects the heart muscle not chaotically, but in certain places. The point is what the heart gets arterial blood from the aorta through several coronary (coronary) arteries and their branches. If using coronary angiography Find out at what level and in which vessel the blood flow has stopped, you can predict which part of the myocardium is suffering from ischemia(lack of oxygen). And vice versa.
Myocardial infarction occurs when the
blood flow through one or more arteries of the heart.
Coronary angiography - study of patency coronary arteries hearts by introducing a contrast agent into them and performing a series x-rays to estimate the speed of contrast propagation.
Even from school we remember that the heart has 2 ventricles and 2 atria, therefore, logically, they should all be affected by a heart attack with the same probability. Nevertheless, It is the left ventricle that always suffers from a heart attack, because its wall is the thickest, is subjected to enormous loads and requires a large blood supply.
Heart chambers in section.
The walls of the left ventricle are much thicker than the right.
Isolated atrial and right ventricular infarctions- a huge rarity. Most often, they are affected simultaneously with the left ventricle, when ischemia moves from the left ventricle to the right or to the atria. According to pathologists, the spread of infarction from the left ventricle to the right is observed in 10-40% all patients with a heart attack (the transition usually occurs along the posterior wall of the heart). Transition occurs to the atrium in 1-17% cases.
Stages of myocardial necrosis on ECG
Between healthy and dead (necrotic) myocardium, intermediate stages are distinguished in electrocardiography: ischemia And damage.
ECG appearance is normal.
Thus, the stages of myocardial damage during a heart attack are as follows:
- ISCHEMIA: this is the initial damage to the myocardium, in which There are no microscopic changes in the heart muscle yet, but the function is already partially impaired.
As you should remember from the first part of the cycle, two opposing processes sequentially occur on the cell membranes of nerve and muscle cells: depolarization(excitement) and repolarization(restoration of potential difference). Depolarization is a simple process, for which you only need to open ion channels in the cell membrane, through which, due to the difference in concentrations, ions will flow outside and inside the cell. Unlike depolarization, repolarization is an energy-intensive process, which requires energy in the form of ATP. Oxygen is necessary for the synthesis of ATP, therefore, during myocardial ischemia, the repolarization process first begins to suffer. Repolarization disorder is manifested by changes in the T wave.
Variants of T wave changes during ischemia:
a - normal, b - negative symmetrical “coronal” T wave(occurs during a heart attack)
V - tall positive symmetrical “coronal” T wave(for heart attack and a number of other pathologies, see below),
d, e - two-phase T wave,
e - reduced T wave (amplitude less than 1/10-1/8 R wave),
g - smoothed T wave,
h - weakly negative T wave.With myocardial ischemia, the QRS complex and ST segments are normal, but the T wave is changed: it is widened, symmetrical, equilateral, increased in amplitude (span) and has a pointed apex. In this case, the T wave can be either positive or negative - this depends on the location of the ischemic focus in the thickness of the heart wall, as well as on the direction of the selected ECG lead. Ischemia - reversible phenomenon, over time, metabolism (metabolism) is restored to normal or continues to deteriorate with the transition to the damage stage.
- DAMAGE: this deeper defeat myocardium, in which determined under a microscope an increase in the number of vacuoles, swelling and degeneration of muscle fibers, disruption of membrane structure, mitochondrial function, acidosis (acidification of the environment), etc. Both depolarization and repolarization suffer. The injury is thought to primarily affect the ST segment. The ST segment may move above or below the baseline, but its arc (this is important!) when damaged convex in the direction of displacement. Thus, when the myocardium is damaged, the arc of the ST segment is directed towards the displacement, which distinguishes it from many other conditions in which the arc is directed towards the isoline (ventricular hypertrophy, bundle branch block, etc.).
Options for ST segment displacement in case of damage.
T wave when damaged, it can be of different shapes and sizes, which depends on the severity of concomitant ischemia. The damage also cannot exist for long and turns into ischemia or necrosis.
- NECROSIS: myocardial death. Dead myocardium is unable to depolarize, so dead cells cannot form an R wave in the ventricular QRS complex. For this reason, when transmural infarction(death of the myocardium in a certain area along the entire thickness of the heart wall) in this ECG lead of the tooth There is no R at all, and is formed ventricular complex type QS. If necrosis affected only part of the myocardial wall, a complex like QrS, in which the R wave is reduced and the Q wave is increased compared to normal.
Variants of the ventricular QRS complex.
Normal teeth Q and R must obey a number of rules, For example:
- the Q wave should always be present in V4-V6.
- The width of the Q wave should not exceed 0.03 s, and its amplitude should NOT exceed 1/4 of the amplitude of the R wave in this lead.
- prong R should increase in amplitude from V1 to V4(i.e., in each subsequent lead from V1 to V4, the R wave should be raised higher than in the previous one).
- in V1, the r wave may normally be absent, then the ventricular complex has the form QS. In people under 30 years of age, the QS complex can normally occasionally be in V1-V2, and in children - even in V1-V3, although this is always suspicious infarction of the anterior part of the interventricular septum.
What does an ECG look like depending on the area of infarction?
So, to put it simply, necrosis affects the Q wave and for the entire ventricular QRS complex. Damage affects ST segment. Ischemia affects T wave.
The formation of waves on the ECG is normal.
Next, let's look at the drawing I improved from V.N. Orlov's "Manual on Electrocardiography", in which in the center of the conditional wall of the heart there is necrosis zone, along its periphery - damage zone, and outside - ischemic zone. Along the wall of the heart are the positive ends of the electrodes (from No. 1 to 7).
To make it easier to understand, I drew conditional lines that clearly show which zones the ECG is recorded from in each of the indicated leads:
Schematic view of the ECG depending on the infarction zone.
- Electrode No. 1: located above the transmural infarction area, so the ventricular complex has a QS appearance.
- No. 2: non-transmural infarction (QR) and transmural injury (ST elevation with upward convexity).
- No. 3: transmural injury (ST elevation with upward convexity).
- No. 4: here in the original drawing it is not very clear, but the explanation indicates that the electrode is located above the zone of transmural damage (ST elevation) and transmural ischemia (negative symmetrical “coronal” T wave).
- No. 5: above the zone of transmural ischemia (negative symmetrical “coronary” T wave).
- No. 6: the periphery of the ischemic zone (biphasic T wave, i.e. in the form of a wave. The first phase of the T wave can be either positive or negative. The second phase is opposite to the first).
- No. 7: away from the ischemic zone (reduced or smoothed T wave).
Here is another picture for you to analyze on your own (“Practical electrocardiography”, V.L. Doshchitsin).
Another diagram of the dependence of the type of ECG changes on the infarction zones.
Stages of infarction development on the ECG
The meaning of the stages of development of a heart attack is very simple. When the blood supply completely stops in any part of the myocardium, then in the center of this area the muscle cells die quickly (within several tens of minutes). At the periphery of the lesion, cells do not die immediately. Many cells gradually manage to “recover”; the rest die irreversibly (remember how I wrote above that the phases of ischemia and damage cannot exist for too long?). All these processes are reflected in the stages of development of myocardial infarction. There are four of them: acute, acute, subacute, cicatricial. Below I present the typical dynamics of these stages on the ECG according to Orlov’s guidance.
1) The most acute stage of a heart attack (stage of damage) has an approximate duration from 3 hours to 3 days. Necrosis and its corresponding Q wave may begin to form, but it may not exist. If the Q wave is formed, then the height of the R wave in this lead decreases, often to the point of complete disappearance (QS complex with transmural infarction). The main ECG feature of the most acute stage of myocardial infarction is the formation of the so-called monophasic curve. The monophasic curve consists of ST segment elevation and tall positive T waves, which merge together.
Displacement of the ST segment above the isoline by 4 mm and above in at least one of the 12 regular leads indicates the severity of heart damage.
Note. The most attentive visitors will say that myocardial infarction cannot begin with stages of damage, because between the norm and the damage phase there should be the one described above ischemic phase! Right. But the ischemic phase lasts only 15-30 minutes, so the ambulance usually does not have time to register it on the ECG. However, if this is possible, the ECG shows tall positive symmetrical “coronal” T waves, characteristic of subendocardial ischemia. It is under the endocardium that the most vulnerable part of the myocardium of the heart wall is located, since in the heart cavity high blood pressure, which interferes with the blood supply to the myocardium (“squeezes” blood out of the heart arteries back).
2) Acute stage lasts up to 2-3 weeks(to make it easier to remember - up to 3 weeks). Areas of ischemia and damage begin to decrease. The zone of necrosis expands, the Q wave also expands and increases in amplitude. If the Q wave does not appear in the acute stage, it is formed in the acute stage (however, there are heart attacks and without Q waves, about them below). ST segment due to limited damage area begins to gradually approach the isoline, A T wave becomes negative symmetrical “coronary” due to the formation of a zone of transmural ischemia around the damaged area.
3) Subacute stage lasts up to 3 months, occasionally longer. The damage zone disappears due to the transition to the ischemic zone (therefore the ST segment comes close to the isoline), the necrosis zone stabilizes(so about true size of infarction judged at this stage). In the first half of the subacute stage, due to the expansion of the ischemic zone, negative the T wave widens and increases in amplitude up to gigantic. In the second half, the ischemia zone gradually disappears, which is accompanied by normalization of the T wave (its amplitude decreases, it tends to become positive). The dynamics of changes in the T wave are especially noticeable on the periphery ischemic zones.
If ST segment elevation does not return to normal after 3 weeks from the moment of heart attack, it is recommended to do echocardiography (EchoCG) to exclude cardiac aneurysms(pouch-like expansion of the wall with slow blood flow).
4) Scar stage myocardial infarction. This is the final stage, in which a durable tissue is formed at the site of necrosis. connective tissue scar. It is not excited and does not contract, therefore it appears on the ECG as a Q wave. Since a scar, like any scar, remains for the rest of life, the scar stage of a heart attack lasts until the last contraction of the heart.
Stages of myocardial infarction.
Which Do ECG changes occur in the scar stage? The scar area (and therefore the Q wave) may, to some extent, decrease due to:
- contractions ( thickening) scar tissue, which brings together intact areas of the myocardium;
- compensatory hypertrophy(increase) adjacent areas of healthy myocardium.
There are no zones of damage and ischemia in the scar stage, therefore the ST segment is on the isoline, and The T wave can be positive, reduced or smoothed. However, in some cases, in the scar stage, it is still recorded small negative T wave, which is associated with constant irritation of adjacent healthy myocardium by scar tissue. In such cases, the amplitude of the T wave should not exceed 5 mm and should not be longer than half of the Q or R wave in the same lead.
To make it easier to remember, the duration of all stages obeys the rule of three and increases incrementally:
- up to 30 minutes (ischemia phase),
- up to 3 days (acute stage),
- up to 3 weeks (acute stage),
- up to 3 months (subacute stage),
- the rest of life (scar stage).
In general, there are other classifications of the stages of infarction.
Differential diagnosis of infarction on ECG
In the third year while studying pathological anatomy and physiology every student of a medical university must learn that all reactions of the body to the same influence in different tissues occur at the microscopic level same type. The sets of these complex sequential reactions are called typical pathological processes . Here are the main ones: inflammation, fever, hypoxia, tumor growth, dystrophy etc. With any necrosis, inflammation develops, resulting in the formation of connective tissue. As I indicated above, the word heart attack comes from lat. infarcio - stuffing, which is caused by the development of inflammation, edema, migration of blood cells into the affected organ and, consequently, its seal. At the microscopic level, inflammation occurs in the same way anywhere in the body. For this reason infarct-like ECG changes there are also for heart injuries and heart tumors(metastases in the heart).
Not every “suspicious” T wave, deviated ST segment or suddenly appearing Q wave is caused by a heart attack.
Normal amplitude T wave ranges from 1/10 to 1/8 of the amplitude of the R wave. A high positive symmetrical “coronary” T wave occurs not only with ischemia, but also with hyperkalemia, increased tone vagus nerve, pericarditis(see ECG below), etc.
(A - normal, B-E - with increasing hyperkalemia).
T waves may also appear abnormal when hormonal imbalances(hyperthyroidism, menopausal myocardial dystrophy) and with changes in the complex QRS(for example, with bundle branch blocks). And these are not all the reasons.
Features of the ST segment and T wave
for various pathological conditions.
ST segment Maybe rise above the isoline not only with myocardial damage or infarction, but also with:
- heart aneurysm,
- PE (pulmonary embolism),
- Prinzmetal's angina,
- acute pancreatitis,
- pericarditis,
- coronary angiography,
- secondary - with bundle branch block, ventricular hypertrophy, early ventricular repolarization syndrome, etc.
ECG option for pulmonary embolism: McGean-White syndrome
(deep S wave in lead I, deep Q and negative T wave in lead III).
ST segment depression cause not only a heart attack or myocardial damage, but also other reasons:
- myocarditis, toxic myocardial damage,
- taking cardiac glycosides, aminazine,
- post-tachycardia syndrome,
- hypokalemia,
- reflex causes - acute pancreatitis, cholecystitis, gastric ulcer, hernia hiatus diaphragms, etc.,
- shock, severe anemia, acute respiratory failure,
- acute cerebrovascular accidents,
- epilepsy, psychosis, tumors and inflammation in the brain,
- hunger or overeating
- carbon monoxide poisoning,
- secondary - with bundle branch block, ventricular hypertrophy, etc.
Q wave most specific for myocardial infarction, but it can also temporarily appear and disappear in the following cases:
- cerebral infarctions (especially subarachnoid hemorrhages),
- acute pancreatitis,
- coronary angiography,
- uremia (end stage of acute and chronic renal failure),
- hyperkalemia,
- myocarditis, etc.
As I noted above, there are heart attacks without Q waves on the ECG. For example:
- when subendocardial infarction when a thin layer of myocardium dies near the endocardium of the left ventricle. Due to the rapid passage of excitation in this zone the Q wave does not have time to form. On ECG R wave height decreases(due to loss of excitation of part of the myocardium) and the ST segment descends below the isoline with convexity downward.
- intramural infarction myocardium (inside the wall) - it is located in the thickness of the myocardial wall and does not reach the endocardium or epicardium. Excitation bypasses the infarction zone on both sides, and therefore the Q wave is absent. But around the infarction zone a transmural ischemia, which appears on ECG negative symmetrical “coronary” T wave. Thus, intramural myocardial infarction can be diagnosed by the appearance negative symmetrical T wave.
You also need to remember that ECG is just one of the research methods when establishing a diagnosis, although it is a very important method. In rare cases (with atypical localization of the necrosis zone), myocardial infarction is possible even with a normal ECG! I’ll dwell on this a little further.
How do ECGs distinguish heart attacks from other pathologies?
By 2 main features.
1) characteristic ECG dynamics. If the ECG shows changes in the shape, size and location of teeth and segments typical of a heart attack over time, we can speak with a high degree of confidence about a myocardial infarction. In heart attack departments of hospitals ECG is done daily. To make it easier to assess the dynamics of a heart attack on an ECG (which is the most expressed on the periphery of the affected area), it is recommended to apply markings for placement of chest electrodes so that subsequent hospital ECGs are taken in the chest leads completely identically.
An important conclusion follows from this: if pathological changes were detected in a patient’s cardiogram in the past, It is recommended to have a “control” copy of the ECG at home so that the emergency doctor can compare the new ECG with the old one and draw a conclusion about the age of the detected changes. If the patient has previously suffered a myocardial infarction, this recommendation becomes iron rule. Every patient who has had a heart attack should receive a follow-up ECG upon discharge and keep it where they live. And on long trips, take it with you.
2) presence of reciprocity. Reciprocal changes are “mirror” (relative to the isoline) ECG changes on the opposite wall left ventricle. Here it is important to consider the direction of the electrode on the ECG. The center of the heart (the middle of the interventricular septum) is taken as the “zero” of the electrode, so one wall of the heart cavity lies in the positive direction, and the opposite wall lies in the negative direction.
The principle is this:
- for the Q wave the reciprocal change will be R wave enlargement, and vice versa.
- if the ST segment moves above the isoline, then the reciprocal change will be ST offset below isoline, and vice versa.
- for a high positive "coronal" T wave, the reciprocal change would be negative T wave, and vice versa.
.
Direct signs are visible in leads II, III and aVF, reciprocal- in V1-V4.
Reciprocal changes on the ECG in some situations they are the only ones, which can be used to suspect a heart attack. For example, with posterobasal (posterior) infarction myocardium, direct signs of infarction can be recorded only in the lead D (dorsalis) across the Sky[reads e] and in additional chest leads V7-V9, which are not included in the standard 12 and are performed only on demand.
Additional chest leads V7-V9.
Concordance ECG elements- unidirectionality in relation to the isoline of the same ECG waves in different leads (that is, the ST segment and the T wave are directed in the same direction in the same lead). It happens with pericarditis.
The opposite concept is discordance(multi-directional). Typically, this implies discordance of the ST segment and T wave in relation to the R wave (ST is deviated in one direction, T in the other). Characteristic of complete blockades of the His bundle.
ECG at the onset of acute pericarditis:
there is no Q wave and reciprocal changes, characteristic
concordant changes in the ST segment and T wave.
It is much more difficult to determine the presence of a heart attack if there is intraventricular conduction disorder(bundle branch block), which in itself changes a significant part of the ECG beyond recognition from the ventricular QRS complex to the T wave.
Types of heart attacks
A couple of decades ago they divided transmural infarctions(ventricular complex type QS) and non-transmural large-focal infarctions(like QR), but it soon became clear that this does not give anything in terms of forecast and possible complications. For this reason, heart attacks are currently simply divided into Q-infarctions(Q-wave myocardial infarctions) and non-Q heart attacks(myocardial infarction without Q wave).
Localization of myocardial infarction
The ECG report must indicate infarction zone(for example: anterolateral, posterior, inferior). To do this, you need to know in which leads ECG signs appear. various localizations heart attack.
Here are a couple of ready-made schemes:
Diagnosis of myocardial infarction by location.
Topical diagnosis of myocardial infarction
(elevation- rise, from English. elevation; depression- reduction, from English. depression)
Finally
If you did not understand anything from what was written, do not be upset. Myocardial infarction and, in general, ECG changes in coronary artery disease - the most difficult topic in electrocardiography for students medical university At the Faculty of Medicine, ECG begins to be studied from the third year of study. propaedeutics of internal diseases and study for another 3 years before receiving a diploma, but few graduates can boast of stable knowledge on this topic. I had a friend who (as it turned out later) after the fifth year was specially assigned to a subordination in the obstetrics and gynecology department in order to have fewer encounters with ECG tapes that were difficult for her to understand.
If you want to more or less understand ECG, you will have to spend many tens of hours of thoughtful reading teaching aids And view hundreds of ECG tapes. And when you can draw an ECG from memory of any heart attack or rhythm disorder, congratulate yourself - you are close to the goal.
In this publication I would like to talk about such a necessary and effective method diagnostics, such as ECG for myocardial infarction. After reading the information provided, everyone will be able to determine a heart attack on an ECG, as well as its stage and degree of damage.
Many, faced with this type of disease, increasingly understand that myocardial infarction is one of the most terrible and popular heart pathologies, the consequences of which can lead to great problems with health in general, not excluding death.
During the onset of symptoms, many, having read information from many sources, often confuse the symptoms of a heart attack with angina. In order not to make your own mistakes, you should go to the hospital at the first symptoms, where specialists can determine the exact condition of the heart using an ECG.
What is a heart attack and its types
Myocardial infarction is one of the clinical types of ischemic heart disease, which occurs with the formation of ischemic necrosis of the myocardial area, subsequently leading to absolute or relative insufficiency of its blood supply.
Important! An ECG during a heart attack is one of the main types of diagnosing and determining signs of the disease. At the first symptoms of myocardial infarction, you must immediately contact a cardiologist to undergo an ECG test in the first 60-120 minutes, which are very important!
The main reasons for visiting a doctor include:
- Shortness of breath;
- Pain syndromes behind the sternum;
- Malaise;
- Frequent pulse when listening, and unstable heart rhythms are also possible;
- A feeling of fear, accompanied by severe sweating.
You should know! Myocardial infarction is the first sign of development against the background arterial hypertension, a strong decrease or increase in glucose, as well as against the background of atherosclerosis, smoking, excess weight or a sedentary lifestyle.
The following factors provoke a heart attack:
- Frequent anxiety, depression, stress, anxiety;
- Work related to physical exertion or sports activities (weightlifters);
- Surgical interventions;
- Frequent changes in atmospheric pressure.
To ensure your health and your life, you should be diagnosed at the first sign. With the help of an ECG, during the formation of a heart attack, the specialist will use special electrodes attached to the cardiogram machine, after which a certain kind of signals will occur from the heart muscle. To conduct a regular ECG, 6 sensors should be used, in the case when it comes to determining a heart attack using an ECG - as many as 12.
Types of MI
The pathology of MI is possible in most forms, but an ECG when examining this organ can only reveal the following:
- Transmural infarction (has indicators of large-focal necrosis of the walls of the left ventricle of the heart, which can reach up to 55-70% of the affected area);
- Subendocardial (in 90% of cases it occurs extensively; ECG often shows blurred edges of the affected area of the myocardium, which makes it difficult for the ultrasound specialist to see this problem);
- Intramural (considered one of the small focal types of pathologies).
According to the identified symptoms, the following forms of MI can be distinguished:
- Anginal is one of the most common types of infarction. Manifests itself as severe pain behind the chest, which often radiates to the left top part body (face, arm, hypochondrium). The patient feels unwell, lethargic, a sharp deterioration in general condition, and sweating.
- Asthmatic - manifests itself as shortness of breath, lack of oxygen for inhalation. With these symptoms in adults and elderly people, this indicates that an MI has already been suffered;
- Gastralgic – unpleasant localization pain in the upper abdomen. There may also be an unpleasant feeling of tightness in the shoulder blades and back. All this causes hiccups, a feeling of nausea, “bloating” of the abdomen, and pain in some areas of the intestines.
- Cerebrovascular - manifests itself as dizziness, severe pain in the temples and occipital region, nausea, vomiting. The diagnosis of this type can only be determined using an ECG.
- Arrhythmic – constant feeling that the pulse disappears or is temporarily absent. May be lightheaded, severe headache, a sharp decline HELL.
- Asymptomatic - the localization of the heart attack is characterized by severe weakness and shortness of breath.
Something to remember! To better recognize these symptoms, an ECG should be taken immediately.
Role of ECG in the study of myocardial infarction
An ECG is an integral part in recognizing a particular symptom of MI, and its diagnostic technique is simple and explains a lot for both cardiologists and doctors. Thanks to the latest technologies, everyone has a chance to quickly and effectively diagnose the heart and identify heart attack pathologies, both at home and in specially designated institutions.
Any ECG performed is direct evidence for doctors of the existence of a particular disease in a person. MI can easily be confused with pancreatitis or cholecystitis, so an electrocardiogram should be performed immediately.
Although the following fact should be noted - in almost 8-9% of this diagnosis, there may be incorrect data. Therefore, in order to more accurately identify a particular pathology, an ECG should be performed several times, as well as interpretation.
Overview of Heart Attack on ECG
Carrying out an ECG in the event of the development of an acute disturbance of blood flow in the myocardium is an integral part of the study of the organ. The decoding of the diagnosis increases several times during the first few hours of the formation of MI, because it is at this time that the symptoms of this disease begin to manifest themselves.
On film, during the first stages of the development of the disease, only initial disturbances in the blood supply can be observed, and then only if these disturbances were revealed during an electrocardiogram. In the photo this is expressed as changes in the S – T segment.
Let us present to you visual indicators of changes in ECG waves:
This type of abnormality in the electrocardiogram is associated with 3 factors occurring in the infarction area, thereby dividing it into certain zones:
- Tissue necrosis - but only with the development of a Q-infarction;
- Violation of cell integrity, which subsequently threatens death;
- Insufficient amount of blood flow, which is completely recoverable.
There are certain signs that when ECG description development of MI was revealed:
- The R wave (зR) is small or completely absent;
- Q wave (zQ) deep;
- T wave (zT) negative;
- the S–T segment is lower than the isoline.
Temporary stages of infarction development on a cardiogram
Table of stages of MI formation
ECG signs depending on the size of the lesion
| Type of heart attack | Subspecies | ECG signs |
| Q-infarction | Transmural (circular) - damage occurs along the entire heart wall | No zR zQ – deep the S–T segment is much higher than the isoline, merging with the EZ during a subacute type of infarction – sT negative |
| Subepicardial – the lesion occurs near the outer membrane | The R wave is quite enlarged, sT becomes negative during this period, being in the subacute stage |
|
| Intramural - damage occurs inside the cardiac muscle layer | Pathologies do not occur in the R, Q waves segment S – T without visible changes zT negative |
|
| Subendocardial - lesion near the inner lining of the muscle | Pathologies do not occur in the R, Q and T waves segment S – T is below the isoline by at least 0.02 mV |
ECG changes during different MI positions
In order to accurately establish a diagnosis, a specialist must use all twelve electrodes for the ECG. Let's imagine this in the form of a photo:
And depending on the position of the lesion, the disease is displayed differently on film. Let's look at the types of heart attacks.
Anteroseptal Q-infarction
| Leads | Signs of pathologies |
| Standard. I, II and left hand | zQ – deep the S–T segment slowly rises above the isoline zT - positive, and becomes close to the segment |
| Standard. III and from right leg | the S-T segment slowly decreases above the E-T isoline during this period and becomes negative |
| Chest I-III (during the transition to the top, IX chest) | Without zR, but instead there is a QS segment S - T located above the isoline by at least 1.8-2.8 mm |
| From right hand and chest (IX-VI) | zT – flat segment S – T is located in the lower part of the isoline by at least 0.02 mV shifted |
Lateral MI
Lead is standard. III from the left hand, right leg and chest V-VI
Signs of pathologies - zQ - deep, widened, segment S - T slowly rises above the isoline.
Anteroposterior Q-infarction
Lead is standard. III from the left arm, right leg and chest III - VI
Signs of pathologies - zQ – deep, widened, the S-T segment rises significantly above the isoline, while the zT is positive, merging with the segment.
Posterior diaphragmatic
Q-infarction anterior subendocardial
Posterior subendocardial non-Q infarction
Lead standard. II,III, from the right leg, thoracic V-VI.
Signs of pathologies - z R – reduced, zT – positive, then there is a slight decrease in the segment, without the Q wave.
Difficulties in performing an ECG
The location of the teeth and spaces can be caused by the following factors:
- at overweight the patient's electroposition of the heart may be changed;
- scars on the heart from a previous MI prevent the detection of new changes;
- It is almost impossible to identify IHD in case of conduction disorders in the form of blockade along the left bundle branch;
- A “frozen” ECG during an aneurysm will not reveal new changes in the functioning of the heart.
With the help of an ECG there is a chance to determine the location of ischemia. Let's present you a table:
In conclusion, I would like to remind you that in the modern world, thanks to innovative technologies, it is quite easy and quick to determine a heart attack on an ECG. It is also effectively possible to decipher all the indicators identified on the electrical tape, recording the work of the heart muscle for 24 hours or more. The improved wards have cardiac monitoring, as well as audible alarms, which allows doctors to immediately respond to the situation in the event of serious changes, providing the necessary assistance quickly.
