Deciphering the ecg, the norm of indicators. Deciphering a cardiogram in children and adults: general principles, reading the results, an example of decoding Transition zone v3
7.2.1. Myocardial hypertrophy
The cause of hypertrophy is usually an excessive load on the heart, either by resistance (hypertension) or by volume (chronic renal and/or heart failure). Increased heart rate leads to increased metabolic processes in the myocardium and is further accompanied by an increase in the number of muscle fibers. The bioelectrical activity of the hypertrophied part of the heart increases, which is reflected in the electrocardiogram.
7.2.1.1. Left atrial hypertrophy
characteristic feature hypertrophy of the left atrium is an increase in the width of the P wave (more than 0.12 s). The second sign is a change in the shape of the P wave (two humps with a predominance of the second peak) (Fig. 6).
Rice. 6. ECG with left atrial hypertrophy
Left atrial hypertrophy is a typical symptom of mitral valve stenosis and therefore the P wave in this disease is called P-mitrale. Similar changes are observed in leads I, II, aVL, V5, V6.
7.2.1.2. Right atrial hypertrophy
With hypertrophy of the right atrium, the changes also affect the P wave, which acquires a pointed shape and increases in amplitude (Fig. 7).
Rice. 7. ECG with hypertrophy of the right atrium (P-pulmonale), right ventricle (S-type)
Hypertrophy of the right atrium is observed with atrial septal defect, hypertension of the pulmonary circulation.
Most often, such a P wave is detected in diseases of the lungs, it is often called P-pulmonale.
Hypertrophy of the right atrium is a sign of a change in the P wave in leads II, III, aVF, V1, V2.
7.2.1.3. Left ventricular hypertrophy
The ventricles of the heart are better adapted to the loads, and in the early stages of their hypertrophy may not appear on the ECG, but as the pathology develops, characteristic signs become visible.
With ventricular hypertrophy, there are significantly more changes on the ECG than with atrial hypertrophy.
The main signs of left ventricular hypertrophy are (Fig. 8):
Deviation of the electrical axis of the heart to the left (levogram);
Shift of the transition zone to the right (in leads V2 or V3);
The R wave in leads V5, V6 is high and larger in amplitude than RV4;
Deep S in leads V1, V2;
Extended QRS complex in leads V5, V6 (up to 0.1 s or more);
Shift of the S-T segment below the isoelectric line with a bulge upwards;
Negative T wave in leads I, II, aVL, V5, V6.
Rice. 8. ECG with left ventricular hypertrophy
Left ventricular hypertrophy is often observed in arterial hypertension, acromegaly, pheochromocytoma, as well as insufficiency of the mitral and aortic valves, congenital heart defects.
7.2.1.4. Right ventricular hypertrophy
Signs of right ventricular hypertrophy appear on the ECG in advanced cases. Diagnosis at an early stage of hypertrophy is extremely difficult.
Signs of hypertrophy (Fig. 9):
Deviation of the electrical axis of the heart to the right (rightogram);
Deep S wave in lead V1 and high R wave in leads III, aVF, V1, V2;
The height of the RV6 tooth is less than normal;
Extended QRS complex in leads V1, V2 (up to 0.1 s or more);
Deep S wave in lead V5 as well as V6;
S-T segment displacement below the isoline with a bulge upwards in the right III, aVF, V1 and V2;
Complete or incomplete blockade of the right leg of the bundle of His;
Shift of the transition zone to the left.
Rice. 9. ECG with right ventricular hypertrophy
Right ventricular hypertrophy is most often associated with an increase in pressure in the pulmonary circulation in lung diseases, mitral valve stenosis, parietal thrombosis and pulmonary artery stenosis, and congenital heart defects.
7.2.2. Rhythm disturbances
Weakness, shortness of breath, palpitations, rapid and labored breathing, irregular heartbeats, a feeling of suffocation, fainting, or episodes of loss of consciousness may be manifestations of a heart rhythm disorder due to cardiovascular diseases. An ECG helps to confirm their presence, and most importantly, to determine their type.
It should be remembered that automatism is a unique property of the cells of the conduction system of the heart, and the sinus node, which controls the rhythm, has the greatest automatism.
Rhythm disturbances (arrhythmias) are diagnosed when there is no sinus rhythm on the ECG.
Signs of normal sinus rhythm:
The frequency of the P waves is in the range from 60 to 90 (in 1 min);
The same duration of RR intervals;
Positive P wave in all leads except aVR.
Heart rhythm disturbances are very diverse. All arrhythmias are divided into nomotopic (changes develop in the sinus node itself) and heterotopic. In the latter case, excitatory impulses occur outside the sinus node, that is, in the atria, atrioventricular junction and ventricles (in the branches of the His bundle).
Nomotopic arrhythmias include sinus bradycardia and tachycardia and irregular sinus rhythm. To heterotopic - atrial fibrillation and flutter and other disorders. If the occurrence of arrhythmia is associated with a violation of the excitability function, then such rhythm disturbances are divided into extrasystole and paroxysmal tachycardia.
Considering all the variety of types of arrhythmias that can be detected on the ECG, the author, in order not to bore the reader with the intricacies of medical science, only allowed himself to define the basic concepts and consider the most significant rhythm and conduction disturbances.
7.2.2.1. Sinus tachycardia
Increased generation of impulses in the sinus node (more than 100 impulses per 1 min).
On the ECG, it is manifested by the presence of a regular P wave and a shortening of the R-R interval.
7.2.2.2. Sinus bradycardia
The frequency of pulse generation in the sinus node does not exceed 60.
On the ECG, it is manifested by the presence of a regular P wave and a lengthening of the R-R interval.
It should be noted that at a rate of less than 30 bradycardia is not sinus.
As in the case of tachycardia and bradycardia, the patient is treated for the disease that caused the rhythm disturbance.
7.2.2.3. Irregular sinus rhythm
Impulses are irregularly generated in the sinus node. The ECG shows normal waves and intervals, but the duration of the R-R intervals differs by at least 0.1 s.
This type of arrhythmia can occur in healthy people and does not need treatment.
7.2.2.4. Idioventricular rhythm
Heterotopic arrhythmia, in which the pacemaker is either the legs of the bundle of His or Purkinje fibers.
Extremely severe pathology.
A rare rhythm on the ECG (that is, 30–40 beats per minute), the P wave is absent, the QRS complexes are deformed and expanded (duration 0.12 s or more).
Occurs only in severe heart disease. A patient with such a disorder needs urgent care and is subject to immediate hospitalization in cardiological intensive care.
7.2.2.5. Extrasystole
Extraordinary contraction of the heart caused by a single ectopic impulse. Of practical importance is the division of extrasystoles into supraventricular and ventricular.
A supraventricular (it is also called atrial) extrasystole is recorded on the ECG if the focus that causes extraordinary excitation (contraction) of the heart is located in the atria.
Ventricular extrasystole is recorded on the cardiogram during the formation of an ectopic focus in one of the ventricles.
Extrasystole can be rare, frequent (more than 10% of heart contractions in 1 min), paired (bigemenia) and group (more than three in a row).
We list the ECG signs of atrial extrasystole:
Changed in shape and amplitude P wave;
Shortened P-Q interval;
The prematurely registered QRS complex does not differ in shape from the normal (sinus) complex;
The R-R interval that follows the extrasystole is longer than usual, but shorter than two normal intervals (incomplete compensatory pause).
Atrial extrasystoles are more common in the elderly against the background of cardiosclerosis and coronary disease heart, but can also be observed in practically healthy people, for example, if a person is very worried or experiencing stress.
If an extrasystole is seen in a practically healthy person, then the treatment consists in prescribing valocordin, corvalol and ensuring complete rest.
When registering an extrasystole in a patient, treatment of the underlying disease and taking antiarrhythmic drugs from the isoptin group are also required.
Signs of ventricular extrasystole:
The P wave is absent;
The extraordinary QRS complex is significantly expanded (more than 0.12 s) and deformed;
Complete compensatory pause.
Ventricular extrasystole always indicates damage to the heart (CHD, myocarditis, endocarditis, heart attack, atherosclerosis).
With ventricular extrasystole with a frequency of 3-5 contractions per 1 min, antiarrhythmic therapy is mandatory.
Most often, intravenous lidocaine is administered, but other drugs can also be used. Treatment is carried out with careful ECG monitoring.
7.2.2.6. Paroxysmal tachycardia
Sudden attack of hyper-frequent contractions lasting from a few seconds to several days. The heterotopic pacemaker is located either in the ventricles or supraventricularly.
With supraventricular tachycardia (in this case, impulses are formed in the atria or atrioventricular node), the correct rhythm is recorded on the ECG with a frequency of 180 to 220 contractions per 1 minute.
The QRS complexes are not changed or expanded.
With the ventricular form of paroxysmal tachycardia, the P waves can change their place on the ECG, the QRS complexes are deformed and expanded.
Supraventricular tachycardia occurs in Wolff-Parkinson-White syndrome, less often in acute myocardial infarction.
The ventricular form of paroxysmal tachycardia is detected in patients with myocardial infarction, with coronary artery disease, and electrolyte disturbances.
7.2.2.7. Atrial fibrillation (atrial fibrillation)
A variety of supraventricular arrhythmias caused by asynchronous, uncoordinated electrical activity of the atria, followed by a deterioration in their contractile function. The flow of impulses is not conducted to the ventricles as a whole, and they contract irregularly.
This arrhythmia is one of the most common cardiac arrhythmias.
It occurs in more than 6% of patients older than 60 years and in 1% of patients younger than this age.
Signs of atrial fibrillation:
R-R intervals are different (arrhythmia);
P waves are absent;
Flicker waves F are recorded (they are especially clearly visible in leads II, III, V1, V2);
Electrical alternation (different amplitude of I waves in one lead).
Atrial fibrillation occurs with mitral stenosis, thyrotoxicosis and cardiosclerosis, and often with myocardial infarction. Medical care is to restore sinus rhythm. Novocainamide, potassium preparations and other antiarrhythmic drugs are used.
7.2.2.8. atrial flutter
It is observed much less frequently than atrial fibrillation.
With atrial flutter, normal atrial excitation and contraction are absent, and excitation and contraction of individual atrial fibers are observed.
7.2.2.9. ventricular fibrillation
The most dangerous and severe violation of the rhythm, which quickly leads to circulatory arrest. It occurs with myocardial infarction, as well as in the terminal stages of various cardiovascular diseases in patients who are in a state of clinical death. Ventricular fibrillation requires immediate resuscitation.
Signs of ventricular fibrillation:
Absence of all teeth of the ventricular complex;
Registration of fibrillation waves in all leads with a frequency of 450-600 waves per 1 min.
7.2.3. Conduction disorders
Changes in the cardiogram that occur in the event of a violation of the conduction of an impulse in the form of a slowdown or complete cessation of the transmission of excitation are called blockades. Blockades are classified depending on the level at which the violation occurred.
Allocate sinoatrial, atrial, atrioventricular and intraventricular blockade. Each of these groups is further subdivided. So, for example, there are sinoatrial blockades of I, II and III degrees, blockades of the right and left legs of the His bundle. There is also a more detailed division (blockade of the anterior branch of the left leg of the bundle of His, incomplete blockade of the right leg of the bundle of His). Among the conduction disorders recorded by ECG, the following blockades are of the greatest practical importance:
Sinoatrial III degree;
Atrioventricular I, II and III degrees;
Blockade of the right and left legs of the bundle of His.
7.2.3.1. Sinoatrial block III degree
Conduction disorder, in which the conduction of excitation from the sinus node to the atria is blocked. On a seemingly normal ECG, another contraction suddenly drops out (blocks), that is, the entire P-QRS-T complex (or 2-3 complexes at once). In their place, an isoline is recorded. Pathology is observed in those suffering from coronary artery disease, heart attack, cardiosclerosis, with the use of a number of drugs (for example, beta-blockers). Treatment consists in the treatment of the underlying disease and the use of atropine, izadrin and similar agents).
7.2.3.2. Atrioventricular block
Violation of the conduction of excitation from the sinus node through the atrioventricular connection.
Slowing of atrioventricular conduction is a first-degree atrioventricular block. It appears on the ECG in the form of a prolongation of the P-Q interval (more than 0.2 s) with a normal heart rate.
Atrioventricular blockade II degree - incomplete blockade, in which not all impulses coming from the sinus node reach the ventricular myocardium.
On the ECG, the following two types of blockade are distinguished: the first is Mobitz-1 (Samoilov-Wenckebach) and the second is Mobitz-2.
Signs of blockade type Mobitz-1:
Constantly lengthening interval P
Due to the first sign, at some stage after the P wave, the QRS complex disappears.
A sign of blockade of the Mobitz-2 type is a periodic prolapse of the QRS complex against the background of an extended P-Q interval.
Atrioventricular blockade of the III degree - a condition in which not a single impulse coming from the sinus node is conducted to the ventricles. On the ECG, two types of rhythm are recorded that are not interconnected; the work of the ventricles (QRS complexes) and the atria (P waves) is not coordinated.
Blockade of the III degree is often found in cardiosclerosis, myocardial infarction, improper use of cardiac glycosides. The presence of this type of blockade in a patient is an indication for his urgent hospitalization in a cardiological hospital. Treatment is with atropine, ephedrine, and, in some cases, prednisolone.
7.2.3.3. Blockade of the legs of the bundle of His
In a healthy person, an electrical impulse originating in the sinus node, passing through the legs of the bundle of His, simultaneously excites both ventricles.
With the blockade of the right or left legs of the bundle of His, the path of the impulse changes and therefore the excitation of the corresponding ventricle is delayed.
It is also possible the occurrence of incomplete blockades and the so-called blockades of the anterior and posterior branches of the bundle of His bundle.
Signs of a complete blockade of the right leg of the bundle of His (Fig. 10):
Deformed and extended (more than 0.12 s) QRS complex;
Negative T wave in leads V1 and V2;
S-T segment offset from the isoline;
Widening and splitting of the QRS in leads V1 and V2 as RsR.
Rice. 10. ECG with complete blockade of the right leg of the bundle of His
Signs of a complete blockade of the left leg of the bundle of His:
The QRS complex is deformed and expanded (more than 0.12 s);
Offset of the S-T segment from the isoline;
Negative T wave in leads V5 and V6;
Expansion and splitting of the QRS complex in leads V5 and V6 in the form of RR;
Deformation and expansion of the QRS in leads V1 and V2 in the form of rS.
These types of blockades are found in heart injuries, acute myocardial infarction, atherosclerotic and myocardial cardiosclerosis, with the incorrect use of a number of medications (cardiac glycosides, procainamide).
Patients with intraventricular blockade do not need special therapy. They are hospitalized to treat the disease that caused the blockade.
7.2.4. Wolff-Parkinson-White Syndrome
For the first time such a syndrome (WPW) was described by the above-mentioned authors in 1930 as a form of supraventricular tachycardia, which is observed in young healthy people (“functional blockade of the bundle of His bundle”).
It has now been established that sometimes in the body, in addition to the normal path of impulse conduction from the sinus node to the ventricles, there are additional bundles (Kent, James and Maheim). Through these pathways, excitation reaches the ventricles of the heart faster.
There are several types of WPW syndrome. If excitation enters the left ventricle earlier, then type A WPW syndrome is recorded on the ECG. In type B, excitation enters the right ventricle earlier.
Signs of WPW syndrome type A:
The delta wave on the QRS complex is positive in the right chest leads and negative in the left (the result of premature excitation of a part of the ventricle);
The direction of the main teeth in the chest leads is approximately the same as with the blockade of the left leg of the bundle of His.
Signs of WPW syndrome type B:
Shortened (less than 0.11 s) P-Q interval;
The QRS complex is expanded (more than 0.12 s) and deformed;
Negative delta wave for the right chest leads, positive for the left;
The direction of the main teeth in the chest leads is approximately the same as with the blockade of the right leg of the bundle of His.
It is possible to register a sharply shortened P-Q interval with an undeformed QRS complex and the absence of a delta wave (Laun-Ganong-Levin syndrome).
Additional bundles are inherited. In about 30–60% of cases, they do not manifest themselves. Some people may develop paroxysms of tachyarrhythmias. In case of arrhythmia, medical care is provided in accordance with the general rules.
7.2.5. Early ventricular repolarization
This phenomenon occurs in 20% of patients with cardiovascular pathology (most often occurs in patients with supraventricular arrhythmias).
It is not a disease, but patients with cardiovascular disease who have this syndrome are 2-4 times more likely to suffer from rhythm and conduction disturbances.
Signs of early ventricular repolarization (Fig. 11) include:
ST segment elevation;
Late delta wave (notch on the descending part of the R wave);
High amplitude teeth;
Double-humped P wave of normal duration and amplitude;
Shortening of PR and QT intervals;
Rapid and sharp increase in the amplitude of the R wave in the chest leads.
Rice. 11. ECG in early ventricular repolarization syndrome
7.2.6. Cardiac ischemia
In coronary heart disease (CHD), the blood supply to the myocardium is impaired. In the early stages, there may be no changes on the electrocardiogram, in the later stages they are very noticeable.
With the development of myocardial dystrophy, the T wave changes and signs of diffuse changes in the myocardium appear.
These include:
Reducing the amplitude of the R wave;
S-T segment depression;
Biphasic, moderately dilated and flat T wave in almost all leads.
IHD occurs in patients with myocarditis of various origins, as well as dystrophic changes in the myocardium and atherosclerotic cardiosclerosis.
7.2.7. angina pectoris
With the development of an angina attack on the ECG, it is possible to detect a shift in the ST segment and changes in the T wave in those leads that are located above the zone with impaired blood supply (Fig. 12).
Rice. 12. ECG for angina pectoris (during an attack)
The causes of angina pectoris are hypercholesterolemia, dyslipidemia. In addition, arterial hypertension can provoke the development of an attack, diabetes, psycho-emotional overload, fear, obesity.
Depending on which layer of the heart muscle ischemia occurs, there are:
Subendocardial ischemia (over the ischemic area, the S-T shift is below the isoline, the T wave is positive, of large amplitude);
Subepicardial ischemia (elevation of the S-T segment above the isoline, T negative).
The occurrence of angina pectoris is accompanied by the appearance of typical pain behind the sternum, usually provoked by physical activity. This pain is of a pressing nature, lasts for several minutes and disappears after the use of nitroglycerin. If the pain lasts more than 30 minutes and is not relieved by taking nitropreparations, acute focal changes can be assumed with a high probability.
Emergency care for angina pectoris is to relieve pain and prevent recurrent attacks.
Analgesics are prescribed (from analgin to promedol), nitropreparations (nitroglycerin, sustak, nitrong, monocinque, etc.), as well as validol and diphenhydramine, seduxen. If necessary, inhalation of oxygen is carried out.
7.2.8. myocardial infarction
Myocardial infarction is the development of necrosis of the heart muscle as a result of prolonged circulatory disorders in the ischemic area of the myocardium.
In more than 90% of cases, the diagnosis is determined using an ECG. In addition, the cardiogram allows you to determine the stage of a heart attack, find out its localization and type.
An unconditional sign of a heart attack is the appearance on the ECG of a pathological Q wave, which is characterized by excessive width (more than 0.03 s) and greater depth(one third of the R wave).
Options QS, QrS are possible. S-T shift (Fig. 13) and T wave inversion are observed.
Rice. 13. ECG in anterolateral myocardial infarction (acute stage). There are cicatricial changes in the posterior lower parts of the left ventricle
Sometimes there is a shift in S-T without the presence of a pathological Q wave (small-focal myocardial infarction). Signs of a heart attack:
Pathological Q wave in leads located above the infarction area;
Displacement by an arc upward (rise) of the ST segment relative to the isoline in leads located above the infarction area;
Discordant shift below the isoline of the ST segment in leads opposite to the area of infarction;
Negative T wave in leads located above the infarction area.
As the disease progresses, the ECG changes. This relationship is explained by the staging of changes in a heart attack.
There are four stages in the development of myocardial infarction:
Acute;
subacute;
Scarring stage.
The most acute stage (Fig. 14) lasts several hours. At this time, the ST segment rises sharply on the ECG in the corresponding leads, merging with the T wave.
Rice. 14. The sequence of ECG changes in myocardial infarction: 1 - Q-infarction; 2 - not Q-infarction; A - the most acute stage; B - acute stage; B - subacute stage; D - cicatricial stage (post-infarction cardiosclerosis)
In the acute stage, a zone of necrosis is formed and an abnormal Q wave appears. The R amplitude decreases, the ST segment remains elevated, and the T wave becomes negative. The duration of the acute stage is on average about 1-2 weeks.
The subacute stage of infarction lasts for 1–3 months and is characterized by cicatricial organization of the focus of necrosis. On the ECG at this time, the ST segment gradually returns to the isoline, the Q wave decreases, and the R amplitude, on the contrary, increases.
The T wave remains negative.
The cicatricial stage can stretch for several years. At this time, the organization of scar tissue occurs. On the ECG, the Q wave decreases or disappears completely, the S-T is located on the isoline, the negative T gradually becomes isoelectric, and then positive.
Such staging is often referred to as the regular ECG dynamics in myocardial infarction.
A heart attack can be localized in any part of the heart, but most often occurs in the left ventricle.
Depending on the localization, the infarction of the anterior lateral and posterior walls of the left ventricle is distinguished. The localization and prevalence of changes are revealed by analyzing ECG changes in the corresponding leads (Table 6).
Table 6. Localization of myocardial infarction
Great difficulties arise in the diagnosis of re-infarction, when new changes are superimposed on an already changed ECG. Helps dynamic control with the removal of the cardiogram at short intervals.
A typical heart attack is characterized by burning, severe retrosternal pain that does not go away after taking nitroglycerin.
There are also atypical forms of a heart attack:
Abdominal (pain in the heart and abdomen);
Asthmatic (cardiac pain and cardiac asthma or pulmonary edema);
Arrhythmic (cardiac pain and rhythm disturbances);
Collaptoid (cardiac pain and a sharp fall blood pressure with profuse sweating);
Painless.
Treating a heart attack is a very difficult task. It is usually the more difficult, the greater the prevalence of the lesion. At the same time, according to the apt remark of one of the Russian zemstvo doctors, sometimes the treatment of an extremely severe heart attack goes unexpectedly smoothly, and sometimes an uncomplicated, simple micro-infarction makes the doctor sign his impotence.
Emergency care consists in stopping pain (narcotic and other analgesics are used for this), also eliminating fears and psycho-emotional arousal with the help of sedatives, reducing the infarct zone (using heparin), and eliminating other symptoms in turn, depending on their degree of danger.
After completion of inpatient treatment, patients who have had a heart attack are sent to a sanatorium for rehabilitation.
The final stage is a long-term observation in the clinic at the place of residence.
7.2.9. Syndromes in electrolyte disorders
Certain ECG changes make it possible to judge the dynamics of the electrolyte content in the myocardium.
In fairness, it should be said that there is not always a clear correlation between the level of electrolytes in the blood and the content of electrolytes in the myocardium.
Nevertheless, electrolyte disturbances detected by ECG serve as a significant help to the doctor in the process of diagnostic search, as well as in choosing the right treatment.
The most well-studied changes in the ECG in violation of the exchange of potassium, as well as calcium (Fig. 15).
Rice. 15. ECG diagnostics of electrolyte disorders (A. S. Vorobyov, 2003): 1 - normal; 2 - hypokalemia; 3 - hyperkalemia; 4 - hypocalcemia; 5 - hypercalcemia
7.2.9.1. Hyperkalemia
Signs of hyperkalemia:
High pointed T wave;
Shortening of the Q-T interval;
Reducing the amplitude of R.
With severe hyperkalemia, intraventricular conduction disturbances are observed.
Hyperkalemia occurs in diabetes (acidosis), chronic renal failure, severe injuries with crushing of muscle tissue, insufficiency of the adrenal cortex, and other diseases.
7.2.9.2. hypokalemia
Signs of hypokalemia:
Decrease in the S-T segment from top to bottom;
Negative or two-phase T;
The appearance of U.
With severe hypokalemia, atrial and ventricular extrasystoles, intraventricular conduction disturbances appear.
Hypokalemia occurs with the loss of potassium salts in patients with severe vomiting, diarrhea, after prolonged use of diuretic, steroid hormones, with a number of endocrine diseases.
Treatment consists in replenishing the deficiency of potassium in the body.
7.2.9.3. Hypercalcemia
Signs of hypercalcemia:
Shortening of the Q-T interval;
Shortening of the S-T segment;
Expansion of the ventricular complex;
Rhythm disturbances with a significant increase in calcium.
Hypercalcemia is observed with hyperparathyroidism, bone destruction by tumors, hypervitaminosis D and excessive administration of potassium salts.
7.2.9.4. hypocalcemia
Signs of hypocalcemia:
Increase in the duration of the Q-T interval;
S-T segment lengthening;
Decreased amplitude of T.
Hypocalcemia occurs with a decrease in the function of the parathyroid glands, in patients with chronic renal failure, with severe pancreatitis and hypovitaminosis D.
7.2.9.5. Glycoside intoxication
Cardiac glycosides have long been successfully used in the treatment of heart failure. These funds are indispensable. Their intake contributes to a decrease in heart rate (heart rate), more vigorous expulsion of blood during systole. As a result, hemodynamic parameters improve and manifestations of circulatory insufficiency decrease.
With an overdose of glycosides, characteristic ECG signs appear (Fig. 16), which, depending on the severity of intoxication, require either dose adjustment or drug withdrawal. Patients with glycoside intoxication may experience nausea, vomiting, interruptions in the work of the heart.
Rice. 16. ECG with an overdose of cardiac glycosides
Signs of glycoside intoxication:
Decreased heart rate;
Shortening of the electrical systole;
Decrease in the S-T segment from top to bottom;
Negative T wave;
Ventricular extrasystoles.
Severe intoxication with glycosides requires discontinuation of the drug and the appointment of potassium preparations, lidocaine and beta-blockers.
Einthoven proposed to determine the angle between the horizontal line (parallel to the axis I of the lead) drawn through the center of the triangle, and the electrical axis - angle a to describe the location of Aqrs in the frontal plane. The left end of the horizontal line (the positive pole of the axis I of the lead) he marked 00, the right end ± 180°. The lower end of the perpendicular, crossing the horizontal line in the center, he designated +90°, the upper -90°. Now, with a simple protractor laid along the horizontal axis, you can determine the angle a. In our example, the angle a=+40°.
the same method you can determine the position of the electrical axis (average vector) of ventricular repolarization (AT) - angle a. and the electrical axis of atrial excitation (Ar) - angle a in the frontal plane.
Electrical axis position can be determined by the Died scheme. Pre-calculate the algebraic sum of the amplitude of the teeth of I and III leads in millimeters. Then the obtained values are laid aside on the corresponding sides of the circuit. The intersections of the grid with the radial lines indicate the magnitude of the angle a.
For this purpose, the tables of R. Ya. Written and others are also used.
It is considered to be normal position of the electric axis in the segment from +30° to +69°. The location of the electrical axis in the segment from 0° to +29° is considered horizontal. If the electric axis is located to the left of 0° (in the -1°-90° quadrant), it is said to deviate to the left. The location of the electrical axis in the segment from +70° to + 90° is considered vertical. They talk about the deviation of the electric axis to the right when it is located to the right of + 90 ° (in the right half of the coordinate system).
Normal ECG reflects the correct sequence of excitation of the heart departments, characteristic of sinus rhythm, the normal orientation of the EMF vectors of their excitation, and therefore the standard relationship of the direction and amplitude of the teeth in various leads. as well as the normal duration of the intervals between cycles and within cycles.
The figure shows ECG healthy woman G., 32 years old. The sinus rhythm is correct, the heart rate is 62 in 1 min. (R - R = 0.95 sec.). P - Q = 0.13 sec. P = 0.10 sec. QRS = 0.07 sec. Q - T = 0.38 ex. RII>R>RIII. In the frontal plane, the location of AQRS=+52°. AT=+39°. QRS - T = 13°. AP=+50. P wave amplitude = 1.5 mm. PII>PI>PIII. The P wave is biphasic, the first (positive) phase is greater than the second (negative).
QRS complex I, II, aVL type qRs. QRSIII type R, q, „ aVL and SI, II are small. R,u slightly serrated at the descending knee. QRSV1-V3 complex type RS(rS). QRSV4_v6 type qRs. SV2=18 mm > SV3 > SV5, rv1 tooth
Normal electrocardiogram
A normal electrocardiogram, regardless of the lead system, consists of three upward (positive) P, R and T waves, two downward (negative) teeth and Q and S, and a non-constant upward U wave.
In addition, the ECG distinguishes P-Q, S-T, T-P, R-R intervals and two complexes - QRS and QRST (Fig. 10).
Rice. 10. Waves and intervals of a normal ECG
P wave reflects atrial depolarization. The first half of the P wave corresponds to the excitation of the right atrium, the second half - to the excitation of the left atrium.
P-Q interval corresponds to the period from the onset of atrial excitation to the onset of ventricular excitation. The P-Q interval is measured from the beginning of the P wave to the beginning of the Q wave, in the absence of a Q wave, to the beginning of the R wave. It includes the duration of atrial excitation (the P wave itself) and the duration of the spread of excitation mainly along the atrioventricular node, where the physiological delay in impulse conduction occurs ( segment from the end of the P wave to the beginning of the Q wave). During the passage of an impulse through a specifically conducting system, such a small potential difference arises that it is not possible to detect any of its reflections on the ECG taken away from the surface of the body. The P-Q interval is located on the isoelectric line, its duration is 0.12-0.18 s.
QRS complex reflects ventricular depolarization. The duration (width) of the QRS complex characterizes intraventricular conduction, which varies within the normal range depending on the heart rhythm (with tachycardia it decreases, with bradycardia it increases). The duration of the QRS complex is 0.06-0.09 s.
Q wave corresponds to excitation of the interventricular septum. Normally, it is absent in the right chest leads. A deep Q wave in lead III appears when the diaphragm is high, disappearing or decreasing with a deep breath. The duration of the Q wave does not exceed 0.03 s, its amplitude is no more than 1/4 of the R wave.
R wave characterizes the excitation of the main mass of the myocardium of the ventricles, the S wave - the excitation of the posterior superior sections of the ventricles and the interventricular septum. An increase in the height of the R wave corresponds to an increase in potential within the electrode. At the moment when the entire myocardium adjacent to the electrode depolarizes, the potential difference disappears and the R wave reaches the isoelectric line or passes into the S wave located below it (internal deviation, or internal deflexion). In unipolar leads, the segment of the QRS complex from the beginning of excitation (the beginning of the Q wave, and in its absence, the beginning of the R wave) to the top of the R wave reflects the true excitation of the myocardium at this point. The duration of this segment is called the internal deflection time. This time depends on the speed of propagation of excitation and the thickness of the myocardium. Normally, it is 0.015-0.035 s for the right ventricle, 0.035-0.045 s for the left ventricle. The internal deflection time lag is used to diagnose myocardial hypertrophy, pedicle block, and its localization.
When describing the QRS complex, in addition to the amplitude of its constituent teeth (mm) and duration (s), their letter designation is given. In this case, small teeth are indicated in lowercase letters, large ones in capital letters (Fig. 11).
Rice. 11. The most common forms of the complex and their letter designation
The S-T interval corresponds to the period of complete depolarization when there is no potential difference, and therefore is on the isoelectric line. A variant of the norm can be a shift of the interval in standard leads by 0.5-1 mm. Duration S-T interval varies widely with heart rate.
T wave is the final part of the ventricular complex and corresponds to the phase of ventricular repolarization. It is directed upwards, has a gentle ascending knee, a rounded top and a steeper descending knee, that is, it is asymmetrical. The duration of the T wave varies widely, averaging 0.12-0.16 s.
QRST complex(Q-T interval) corresponds in time to the period from the beginning of depolarization to the end of ventricular repolarization and reflects their electrical systole.
Calculation of the Q-T interval can be done using special tables. The duration of the QRST complex normally almost coincides with the duration of mechanical systole.
To characterize the electrical systole of the heart, the systolic indicator SP is used - the percentage ratio of the duration of the electrical systole Q-T to the duration of the cardiac cycle R-R:
An increase in the systolic rate by more than 5% above the norm may be one of the signs of an inferior function of the heart muscle.
U wave occurs 0.04 s after the T wave. It is small, with normal amplification it is not determined on all ECGs and mainly in leads V2-V4. The origin of this tooth is unclear. Perhaps it is a reflection of the trace potential in the phase of increased myocardial excitability after systole. The maximum amplitude of the U wave is normally 2.5 mm, the duration is 0.3 s.
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What does the ECG show
A typical electrocardiographic study includes registration of EMF in 12 leads:
- standard leads (I, II, III);
- enhanced leads (aVR, aVL, aVF);
- chest leads (V1..V6).
In each lead registers at least 4 complexes (full cycles) of the ECG. In Russia, the standard for the speed of the tape is 50 mm/s (abroad - 25 mm/s). At a tape speed of 50 mm/s, each small cell located between adjacent vertical lines (distance 1 mm) corresponds to an interval of 0.02 s. Every fifth vertical line on the electrocardiographic tape is thicker. The constant speed of the tape and the millimeter grid on the paper make it possible to measure the duration of the ECG waves and intervals and the amplitude of these teeth.
Due to the fact that the polarity of the lead axis aVR is opposite to the polarity of the axes of the standard leads, the EMF of the heart is projected onto the negative part of the axis of this lead. Therefore, normally in lead aVR, the P and T waves are negative, and the QRS complex looks like QS (rarely rS).
Activation time of the left and right ventricles- the period from the beginning of excitation of the ventricles to the excitation coverage of the maximum number of their muscle fibers. This is the time interval from the beginning of the QRS complex (from the beginning of the Q or R wave), to the perpendicular, lowered from the top of the R wave to the isoline. The activation time of the left ventricle is determined in the left chest leads V5, V6 (the norm is no more than 0.04 s, or 2 cells). The activation time of the right ventricle is determined in the chest leads V1, V2 (the norm is no more than 0.03 s, or one and a half cells).
ECG teeth are designated in Latin letters. If the tooth amplitude is more than 5 mm, such a tooth is indicated by a capital letter; if less than 5 mm - lowercase. As can be seen from the figure, a normal cardiogram consists of the following sections:
- P wave- atrial complex;
- PQ interval- the time of passage of excitation through the atria to the myocardium of the ventricles;
- QRS complex- ventricular complex;
- q wave- excitation of the left half of the interventricular septum;
- R wave- the main wave of the ECG, due to excitation of the ventricles;
- s wave- final excitation of the base of the left ventricle (non-permanent ECG wave);
- ST segment- corresponds to the period of the cardiac cycle, when both ventricles are covered by excitation;
- T wave- is recorded during ventricular repolarization;
- QT interval- electrical systole of the ventricles;
- u wave- the clinical origin of this tooth is not exactly known (it is not always recorded);
- TP segment- ventricular and atrial diastole.
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Electrocardiogram is a widely used method of objective diagnostics various pathologies of the human heart, which is used today almost everywhere. An electrocardiogram (ECG) is taken in a clinic, in an ambulance, or in a hospital department. An ECG is a very important recording that reflects the condition of the heart. That is why the reflection of a variety of options for cardiac pathology on the ECG is described by a separate science - electrocardiography. Electrocardiography also deals with the problems of correct ECG recording, decoding issues, interpretation of controversial and unclear points, etc.Definition and essence of the method
An electrocardiogram is a record of the work of the heart, which is represented as a curved line on paper. The cardiogram line itself is not chaotic, it has certain intervals, teeth and segments that correspond to certain stages of the heart.To understand the essence of the electrocardiogram, you need to know what exactly the device called the electrocardiograph records. The ECG records the electrical activity of the heart, which changes cyclically, in accordance with the onset of diastole and systole. The electrical activity of the human heart may seem like a fantasy, but this unique biological phenomenon exists in reality. In reality, there are so-called cells of the conduction system in the heart, which generate electrical impulses that are transmitted to the muscles of the organ. It is these electrical impulses that cause the myocardium to contract and relax with a certain rhythm and frequency.
An electrical impulse propagates through the cells of the conduction system of the heart in a strictly sequential manner, causing contraction and relaxation of the corresponding departments - the ventricles and atria. The electrocardiogram reflects exactly the total electrical potential difference in the heart.
decoding?
An electrocardiogram can be taken at any clinic or general hospital. You can contact a private medical center where there is a specialist cardiologist or therapist. After recording the cardiogram, the tape with curves is examined by the doctor. It is he who analyzes the recording, deciphers it and writes the final conclusion, which reflects all visible pathologies and functional deviations from the norm. An electrocardiogram is recorded using a special device - an electrocardiograph, which can be multi-channel or single-channel. The ECG recording speed depends on the modification and modernity of the device. Modern devices can be connected to a computer, which, if there is a special program, will analyze the recording and issue a ready-made conclusion immediately after the procedure.
Any cardiograph has special electrodes that are applied in a strictly defined order. There are four clothespins in red, yellow, green and black, which are placed on both hands and both legs. If you go in a circle, then the clothespins are applied according to the "red-yellow-green-black" rule, from the right hand. Remembering this sequence is easy thanks to the student saying: "Every-Woman-Worst-Hell." In addition to these electrodes, there are also chest electrodes, which are installed in the intercostal spaces.
As a result, the electrocardiogram consists of twelve curves, six of which are recorded from chest electrodes, and are called chest leads. The remaining six leads are recorded from electrodes attached to the arms and legs, with three of them called standard and three more reinforced. The chest leads are designated V1, V2, V3, V4, V5, V6, the standard ones are simply Roman numerals - I, II, III, and the reinforced leg leads are the letters aVL, aVR, aVF. Different leads of the cardiogram are necessary to create the most complete picture of the activity of the heart, since some pathologies are visible on the chest leads, others on the standard leads, and still others on the enhanced ones.
The person lies down on the couch, the doctor fixes the electrodes and turns on the device. While the ECG is being written, the person should be absolutely calm. We must not allow the appearance of any stimuli that can distort the true picture of the work of the heart.
How to make an electrocardiogram with the subsequent
decoding - video
The principle of decoding the ECG
Since the electrocardiogram reflects the processes of contraction and relaxation of the myocardium, it is possible to trace how these processes proceed and to identify the existing pathological processes. The elements of the electrocardiogram are closely related, and reflect the duration of the phases of the cardiac cycle - systole and diastole, that is, contraction and subsequent relaxation. The interpretation of the electrocardiogram is based on the study of the teeth, from the position relative to each other, duration, and other parameters. For analysis, the following elements of the electrocardiogram are studied:1. teeth.
2. intervals.
3. Segments.
All sharp and smooth bulges and concavities on the ECG line are called teeth. Each tooth is designated by a letter of the Latin alphabet. The P wave reflects the contraction of the atria, the QRS complex - the contraction of the ventricles of the heart, the T wave - the relaxation of the ventricles. Sometimes after the T wave on the electrocardiogram there is another U wave, but it does not have a clinical and diagnostic role.
An ECG segment is a segment enclosed between adjacent teeth. For diagnosing heart disease great importance play segments P - Q and S - T. The interval on the electrocardiogram is a complex that includes a tooth and an interval. The P-Q and Q-T intervals are of great importance for diagnosis.
Often in the conclusion of a doctor you can see small Latin letters, which also denote teeth, intervals and segments. Small letters are used if the prong is less than 5 mm long. In addition, several R-waves may appear in the QRS complex, which are commonly referred to as R ’, R ”, etc. Sometimes the R wave is simply missing. Then the whole complex is denoted by only two letters - QS. All this is of great diagnostic value.
ECG interpretation plan - a general scheme for reading the results
When deciphering the electrocardiogram, the following parameters are required to reflect the work of the heart: - the position of the electrical axis of the heart;
- determination of the correctness of the heart rhythm and the conductivity of the electrical impulse (blockades, arrhythmias are detected);
- determination of the regularity of contractions of the heart muscle;
- determination of heart rate;
- identification of the source of the electrical impulse (determine whether the rhythm is sinus or not);
- analysis of the duration, depth and width of the atrial P wave and the P-Q interval;
- analysis of the duration, depth, width of the complex of teeth of the ventricles of the heart QRST;
- analysis of the parameters of the RS-T segment and the T wave;
- analysis of the parameters of the interval Q - T.
In the conclusion on the electrocardiogram, the doctor must necessarily reflect the following parameters:
- sinus rhythm or not;
- rhythm regularity;
- heart rate (HR);
- position of the electrical axis of the heart.
An example of decoding an electrocardiogram
At the very beginning of the electrocardiogram tape there should be a calibration signal, which looks like a capital letter "P" 10 mm high. If this calibration signal is absent, then the electrocardiogram is uninformative. If the height of the calibration signal is below 5 mm in standard and enhanced leads, and below 8 mm in the chest leads, then the electrocardiogram voltage is low, which is a sign of a number of heart pathologies. For the subsequent decoding and calculation of some parameters, it is necessary to know how much time fits into one cell of graph paper. At a tape speed of 25 mm / s, one cell 1 mm long is 0.04 seconds, and at a speed of 50 mm / s - 0.02 seconds.Checking the regularity of heart beats
It is estimated by intervals R - R. If the teeth are located at the same distance from each other throughout the entire recording, then the rhythm is regular. Otherwise, it is called correct. Estimating the distance between the R-R waves is very simple: the electrocardiogram is recorded on graph paper, which makes it easy to measure any gaps in millimeters.Calculation of heart rate (HR)
It is carried out by a simple arithmetic method: they count the number of large squares on graph paper that fit between two R teeth. Then the heart rate is calculated by the formula, which is determined by the speed of the tape in the cardiograph: 1. The belt speed is 50 mm/s - then the heart rate is 600 divided by the number of squares.
2. The belt speed is 25 mm/s - then the heart rate is 300 divided by the number of squares.
For example, if 4.8 large squares fit between two R teeth, then the heart rate, at a tape speed of 50 mm / s, will be 600 / 4.8 = 125 beats per minute.
If the heart rate is incorrect, then the maximum and minimum heart rates are determined, also taking the maximum and minimum distances between the R waves as a basis.
Finding the Source of the Rhythm
The doctor studies the rhythm of heart contractions and finds out which node of nerve cells causes cyclic processes of contractions and relaxations of the heart muscle. This is very important for determining blockades.ECG interpretation - rhythms
Normally, the sinus ganglion is the pacemaker. And such a normal rhythm itself is called sinus - all other options are pathological. In various pathologies, any other node of the nerve cells of the conduction system of the heart can act as a pacemaker. In this case, cyclic electrical impulses are confused, and the rhythm of heart contractions is disturbed - an arrhythmia occurs.In sinus rhythm on the electrocardiogram in lead II, there is a P wave in front of each QRS complex, and it is always positive. On one lead, all P waves should have the same shape, length and width.
With atrial rhythm the P wave in the II and III leads is negative, but is present in front of each QRS complex.
Atrioventricular rhythms characterized by the absence of P waves on cardiograms, or the appearance of this wave after the QRS complex, and not before it, as is normal. With this type of rhythm, the heart rate is low, ranging from 40 to 60 beats per minute.
Ventricular rhythm characterized by an increase in the width of the QRS complex, which becomes large and rather intimidating. The P waves and the QRS complex are completely unrelated to each other. That is, there is no strict correct normal sequence - the P wave, followed by the QRS complex. The ventricular rhythm is characterized by a decrease in heart rate - less than 40 beats per minute.
Identification of the pathology of the conduction of an electrical impulse in the structures of the heart
To do this, measure the duration of the P wave, the P-Q interval and the QRS complex. The duration of these parameters is calculated from the millimetric tape on which the cardiogram is recorded. First, consider how many millimeters each tooth or interval occupies, after which the resulting value is multiplied by 0.02 at a writing speed of 50 mm / s, or by 0.04 at a writing speed of 25 mm / s.The normal duration of the P wave is up to 0.1 seconds, the P-Q interval is 0.12-0.2 seconds, the QRS complex is 0.06-0.1 seconds.
Electrical axis of the heart
Referred to as angle alpha. It can have a normal position, horizontal or vertical. Moreover, in a thin person, the axis of the heart is more vertical relative to the average values, and in full people it is more horizontal. The normal position of the electrical axis of the heart is 30-69 o , vertical - 70-90 o , horizontal - 0-29 o . Angle alpha, equal to from 91 to ±180 o reflects a sharp deviation of the electrical axis of the heart to the right. Angle alpha, equal to from 0 to -90 o , reflects a sharp deviation of the electrical axis of the heart to the left. The electrical axis of the heart can deviate in various pathological conditions. For example, hypertension leads to a deviation to the right, a conduction disorder (blockade) can shift it to the right or to the left.
Atrial P wave
The atrial P wave should be:- positive in I, II, aVF and chest leads (2, 3, 4, 5, 6);
- negative in aVR;
- biphasic (part of the tooth lies in the positive region, and part - in the negative) in III, aVL, V1.
Pathological forms of the P wave may indicate the following pathologies:
1.
High and sharp teeth in II, III, aVF leads appear with hypertrophy of the right atrium ("cor pulmonale");
2.
The P wave with two peaks with a large width in I, aVL, V5 and V6 leads indicates left atrial hypertrophy (for example, mitral valve disease).
P–Q interval
The P–Q interval has a normal duration of 0.12 to 0.2 seconds. An increase in the duration of the P-Q interval is a reflection of atrioventricular block. On the electrocardiogram, three degrees of atrioventricular (AV) blockade can be distinguished:- I degree: simple prolongation of the P-Q interval with the preservation of all other complexes and teeth.
- II degree: prolongation of the P-Q interval with partial loss of some QRS complexes.
- III degree: lack of communication between the P wave and QRS complexes. In this case, the atria work in their own rhythm, and the ventricles in their own.
Ventricular QRST complex
The ventricular QRST-complex consists of the QRS-complex itself and the S-T segment. The normal duration of the QRST-complex does not exceed 0.1 seconds, and its increase is detected with blockade of the Hiss bundle legs. QRS complex consists of three teeth, respectively Q, R and S. The Q wave is visible on the cardiogram in all leads except 1, 2 and 3 chest. A normal Q wave has an amplitude up to 25% of that of an R wave. The duration of the Q wave is 0.03 seconds. The R wave is recorded in absolutely all leads. The S wave is also visible in all leads, but its amplitude decreases from the 1st chest to the 4th, and in the 5th and 6th it may be completely absent. The maximum amplitude of this tooth is 20 mm.
The S–T segment is very important from a diagnostic point of view. It is by this tooth that one can detect myocardial ischemia, that is, a lack of oxygen in the heart muscle. Usually this segment runs along the isoline, in 1, 2 and 3 chest leads, it can rise up to a maximum of 2 mm. And in the 4th, 5th and 6th chest leads, the S-T segment can shift below the isoline by a maximum of half a millimeter. It is the deviation of the segment from the isoline that reflects the presence of myocardial ischemia.
T wave
The T wave is a reflection of the process of eventual relaxation in the cardiac muscle of the ventricles of the heart. Usually with a large amplitude of the R wave, the T wave will also be positive. Negative T wave is recorded normally only in lead aVR.Q-T interval
The Q - T interval reflects the process of ultimately contracting in the myocardium of the ventricles of the heart.ECG interpretation - norm indicators
The transcript of the electrocardiogram is usually recorded by the doctor in the conclusion. A typical example of a normal heart ECG looks like this:1. PQ - 0.12 s.
2. QRS - 0.06 s.
3. QT - 0.31 s.
4. RR - 0.62 - 0.66 - 0.6.
5. Heart rate is 70 - 75 beats per minute.
6. sinus rhythm.
7. the electrical axis of the heart is located normally.
Normally, the rhythm should be only sinus, the heart rate of an adult is 60-90 beats per minute. The P wave is normally no more than 0.1 s, the P-Q interval is 0.12-0.2 seconds, the QRS complex is 0.06-0.1 seconds, Q-T is up to 0.4 s.
If the cardiogram is pathological, then it indicates specific syndromes and deviations from the norm (for example, partial blockade of the left leg of the Hiss bundle, myocardial ischemia, etc.). Also, the doctor can reflect specific violations and changes in the normal parameters of the teeth, intervals and segments (for example, shortening of the P wave or Q-T interval, etc.).
Deciphering the ECG in children and pregnant women
In principle, in children and pregnant women, the normal values of the electrocardiogram of the heart are the same as in healthy adults. However, there are certain physiological features. For example, the heart rate in children is higher than in adults. The normal heart rate of a child under 3 years of age is 100 - 110 beats per minute, 3-5 years - 90 - 100 beats per minute. Then gradually the heart rate decreases, and in adolescence it is compared with that of an adult - 60 - 90 beats per minute.Pregnant women may have a slight deviation of the electrical axis of the heart by later dates gestation due to compression by the growing uterus. In addition, sinus tachycardia often develops, that is, an increase in heart rate to 110-120 beats per minute, which is a functional state, and passes on its own. An increase in heart rate is associated with a large volume of circulating blood and increased workload. Due to the increased load on the heart in pregnant women, an overload of various parts of the organ can be detected. These phenomena are not a pathology - they are associated with pregnancy, and will pass on their own after childbirth.
Deciphering an electrocardiogram in a heart attack
Myocardial infarction is a sharp cessation of oxygen supply to the cells of the heart muscles, as a result of which necrosis of a tissue site that has been in a state of hypoxia develops. The reason for the violation of oxygen supply can be different - most often it is a blockage of a blood vessel, or its rupture. A heart attack captures only part of the muscle tissue of the heart, and the extent of the lesion depends on the size of the blood vessel that is clogged or ruptured. On the electrocardiogram, myocardial infarction has certain signs by which it can be diagnosed. In the process of development of myocardial infarction, four stages are distinguished, which have different manifestations on the ECG:
- acute;
- acute;
- subacute;
- cicatricial.
Sometimes it is possible to catch the phase of myocardial ischemia preceding the most acute one, which is characterized by high T waves.
Acute stage myocardial infarction lasts 2-3 weeks. During this period, a wide and high-amplitude Q wave and a negative T wave are recorded on the ECG.
Subacute stage lasts up to 3 months. A very large negative T wave with a huge amplitude is recorded on the ECG, which gradually normalizes. Sometimes the rise of the S-T segment is revealed, which should have leveled off by this period. This is an alarming symptom, as it may indicate the formation of an aneurysm of the heart.
Cicatricial stage a heart attack is the final one, since a connective tissue is formed at the damaged site, incapable of contraction. This scar is recorded on the ECG in the form of a Q wave, which will remain for life. Often the T wave is flattened, has a low amplitude, or is completely negative.
Deciphering the most common ECGs
In conclusion, doctors write the result of ECG decoding, which is often incomprehensible, since it consists of terms, syndromes, and simply a statement of pathophysiological processes. Consider the most common ECG findings that are incomprehensible to a person without a medical education. Ectopic rhythm means not sinus - which can be both a pathology and a norm. The ectopic rhythm is the norm when there is a congenital abnormal formation of the conduction system of the heart, but the person does not make any complaints and does not suffer from other cardiac pathologies. In other cases, an ectopic rhythm indicates the presence of blockades.
Change in repolarization processes on the ECG reflects a violation of the process of relaxation of the heart muscle after contraction.
Sinus rhythm is the normal heart rate of a healthy person.
Sinus or sinusoidal tachycardia means that a person has a regular and regular rhythm, but an increased heart rate - more than 90 beats per minute. In young people under 30 years of age, it is a variant of the norm.
Sinus bradycardia- This is a low number of heartbeats - less than 60 beats per minute against the background of a normal, regular rhythm.
Nonspecific ST-T wave changes mean that there are minor deviations from the norm, but their cause may be completely unrelated to the pathology of the heart. A complete examination is required. Such non-specific ST-T wave changes can develop with an imbalance of potassium, sodium, chloride, magnesium ions, or various endocrine disorders, often during menopause in women.
Biphasic R wave in conjunction with other signs of a heart attack indicates damage to the anterior wall of the myocardium. If no other signs of a heart attack are detected, then a biphasic R wave is not a sign of pathology.
QT prolongation may indicate hypoxia (lack of oxygen), rickets, or overexcitation of the nervous system in a child, which is a consequence of birth trauma.
Myocardial hypertrophy means that the muscular wall of the heart is thickened, and works with a huge load. This may result in:
- heart failure;
- arrhythmias.
Moderate diffuse changes in the myocardium mean that the nutrition of tissues is disturbed, dystrophy of the heart muscle has developed. This is a reparable condition: you need to see a doctor and undergo an adequate course of treatment, including the normalization of nutrition.
Deviation of the electrical axis of the heart (EOS) left or right is possible with hypertrophy of the left or right ventricle, respectively. EOS can deviate to the left in obese people, and to the right in thin people, but in this case this is a variant of the norm.
Left type ECG- EOS deviation to the left.
NBPNPG- an abbreviation for "incomplete blockade of the right leg of the bundle of His". This condition can occur in newborns, and is a variant of the norm. In rare cases, NRBBB can cause arrhythmia, but generally does not lead to the development negative consequences. The blockade of the bundle of Hiss is quite common in people, but if there are no complaints about the heart, then this is absolutely not dangerous.
BPVLNPG- an abbreviation meaning "blockade of the anterior branch of the left leg of the bundle of His". It reflects a violation of the conduction of an electrical impulse in the heart, and leads to the development of arrhythmias.
Small R wave growth in V1-V3 may be a sign of ventricular septal infarction. To accurately determine if this is the case, another ECG study needs to be done.
CLC syndrome(Klein-Levy-Kritesko syndrome) is a congenital feature of the conduction system of the heart. May cause arrhythmias. This syndrome does not require treatment, but it is necessary to be regularly examined by a cardiologist.
Low voltage ECG frequently seen in pericarditis large volume connective tissue in the heart, replacing muscle). In addition, this symptom may be a reflection of exhaustion or myxedema.
Metabolic changes are a reflection of malnutrition of the heart muscle. It is necessary to be examined by a cardiologist and undergo a course of treatment.
Conduction retardation means that the nerve impulse passes through the tissues of the heart more slowly than normal. By itself, this condition does not require special treatment - it may be a congenital feature of the conduction system of the heart. Regular follow-up with a cardiologist is recommended.
Blockade 2 and 3 degrees reflects a serious violation of the conduction of the heart, which is manifested by arrhythmia. In this case, treatment is necessary.
Rotation of the heart with the right ventricle forward may be an indirect sign of the development of hypertrophy. In this case, it is necessary to find out its cause, and undergo a course of treatment, or adjust the diet and lifestyle.
The price of an electrocardiogram with a transcript
The cost of an electrocardiogram with decoding varies significantly, depending on the specific medical institution. So, in public hospitals and clinics, the minimum price for the procedure for taking an ECG and decoding it by a doctor is from 300 rubles. In this case, you will receive films with recorded curves and a doctor's conclusion on them, which he will make himself, or with the help of a computer program.If you want to get a thorough and detailed conclusion on the electrocardiogram, an explanation by the doctor of all parameters and changes, it is better to contact a private clinic that provides such services. Here, the doctor will be able not only to write a conclusion by deciphering the cardiogram, but also to calmly talk to you, slowly explaining all the points of interest. However, the cost of such a cardiogram with decoding in private medical center ranges from 800 rubles to 3600 rubles. You should not assume that bad specialists work in an ordinary clinic or hospital - it’s just that a doctor in a state institution, as a rule, has a very large amount of work, so he simply has no time to talk with each patient in great detail.
Transition zone (lead V3) in the precordial leads:
The direction of the electrical axis of the heart depends on many factors (the age of the child, hypertrophy of the heart, the position of the heart in the chest, etc.).
In children aged 3–14 years, the electrical axis is within +30° ÷ +70°. In children younger than 3 years, the electrical axis of the heart is in the +70° ÷ +100° sector.
Transition zone. When analyzing the ECG, the transition zone should be taken into account - it is determined by the lead, in which the R and S waves are equiphase, i.e., their amplitude on both sides of the isoelectric line is equal. In healthy older children, the QRS transition zone is usually defined in leads V3,4. When the ratio of vector forces changes, the transition zone moves in the direction of their predominance. For example, with right ventricular hypertrophy, the transition zone moves to the position of the left chest electrodes and vice versa. There is a gradual or spasmodic formation of the transition zone. The transition zone has no independent value in diagnostics. For example, in biventricular hypertrophy of the ventricular myocardium, there is no shift in the transition zone. However, in combination with other diagnostic features, the displacement of the transitional zone acquires a certain weight.
SI, II, III - ECG type. This is the designation of an ECG that has an S wave in three standard leads, the amplitude of which is equal to or greater than the amplitude of R, and a QRS complex of the RS shape without a Q wave. In this case, there are often a low-voltage curve and rSRV1. This type of ECG is found in a small number of observations (0.5 - 1%) in healthy children, relatively often in patients with pneumonia, with some congenital heart defects, etc. SI, II, III - ECG type, due to the rotation of the heart around the transverse axis top backwards. Diagnostic value SI, II, III-type ECG increases with its sudden appearance.
"Diseases of the heart and blood vessels in children", N.A. Belokon
Transition zone v3 v4
I. Determination of heart rate. To determine the heart rate, the number of cardiac cycles (RR intervals) in 3 seconds is multiplied by 20.
A. Heart rate< 100 мин –1: отдельные виды аритмий - см. также рис. 5.1.
1. Normal sinus rhythm. The correct rhythm with a heart rate of 60-100 min -1. The P wave is positive in leads I, II, aVF, negative in aVR. Each P wave is followed by a QRS complex (in the absence of AV block). PQ interval 0.12 s (in the absence of additional pathways).
2. Sinus bradycardia. Correct rhythm. heart rate< 60 мин –1 . Синусовые зубцы P. Интервал PQ 0,12 с. Причины: повышение парасимпатического тонуса (часто - у здоровых лиц, особенно во время сна; у спортсменов; вызванное рефлексом Бецольда-Яриша; при нижнем инфаркте миокарда или ТЭЛА); инфаркт миокарда (особенно нижний); прием medicines(beta-blockers, verapamil, diltiazem, cardiac glycosides, antiarrhythmic drugs of classes Ia, Ib, Ic, amiodarone, clonidine, methyldopa, reserpine, guanethidine, cimetidine, lithium); hypothyroidism, hypothermia, obstructive jaundice, hyperkalemia, increased ICP, sick sinus syndrome. Against the background of bradycardia, sinus arrhythmia is often observed (the spread of PP intervals exceeds 0.16 s). Treatment - see Ch. 6, p. III.B.
3. Ectopic atrial rhythm. Correct rhythm. Heart rate 50-100 min -1. The P wave is usually negative in leads II, III, aVF. The PQ interval is typically 0.12 s. It is observed in healthy individuals and with organic lesions of the heart. Usually occurs when sinus rhythm slows down (due to increased parasympathetic tone, medication, or sinus node dysfunction).
4. Migration of the pacemaker. Right or wrong rhythm. heart rate< 100 мин –1 . Синусовые и несинусовые зубцы P. Интервал PQ варьирует, может быть < 0,12 с. Наблюдается у здоровых лиц, спортсменов при органических поражениях сердца. Происходит перемещение водителя ритма из синусового узла в предсердия или АВ -узел. Лечения не требует.
5. AV-nodal rhythm. Slow regular rhythm with narrow QRS complexes (< 0,12 с). ЧСС 35-60 мин –1 . Ретроградные зубцы P (могут располагаться как до, так и после комплекса QRS, а также наслаиваться на него; могут быть отрицательными в отведениях II, III, aVF). Интервал PQ < 0,12 с. Обычно возникает при замедлении синусового ритма (вследствие повышения парасимпатического тонуса, приема лекарственных средств или дисфункции синусового узла) или при АВ -блокаде. Ускоренный АВ -узловой ритм (ЧСС 70-130 мин –1) наблюдается при гликозидной интоксикации, инфаркте миокарда (обычно нижнем), ревматической атаке, миокардите и после операций на сердце.
6. Accelerated idioventricular rhythm. Regular or irregular rhythm with wide QRS complexes (> 0.12 s). Heart rate 60-110 min -1. P waves: absent, retrograde (occur after the QRS complex), or not associated with QRS complexes (AV dissociation). Causes: myocardial ischemia, condition after restoration of coronary perfusion, glycoside intoxication, sometimes in healthy people. In slow idioventricular rhythm, the QRS complexes look the same, but the heart rate is 30–40 min–1. Treatment - see Ch. 6, p. V.D.
B. Heart rate> 100 min -1: certain types of arrhythmias - see also fig. 5.2.
1. Sinus tachycardia. Correct rhythm. Sinus P waves of the usual configuration (their amplitude is increased). Heart rate 100-180 min -1, in young people - up to 200 min -1. Gradual start and end. Causes: physiological reaction to stress, including emotional, pain, fever, hypovolemia, arterial hypotension, anemia, thyrotoxicosis, myocardial ischemia, myocardial infarction, heart failure, myocarditis, pulmonary embolism, pheochromocytoma, arteriovenous fistulas, the effect of drugs and other drugs (caffeine , alcohol, nicotine, catecholamines, hydralazine, thyroid hormones, atropine, aminophylline). Tachycardia is not relieved by massage of the carotid sinus. Treatment - see Ch. 6, p. III.A.
2. Atrial fibrillation. The rhythm is "wrong wrong". Absence of P-waves, random large- or small-wave oscillations of the isoline. The frequency of atrial waves is 350-600 min -1. In the absence of treatment, the frequency of ventricular contractions is 100-180 min -1. Causes: mitral valve disease, myocardial infarction, thyrotoxicosis, PE, condition after surgery, hypoxia, COPD, atrial septal defect, WPW syndrome, sick sinus syndrome, drinking large doses of alcohol, can also be observed in healthy individuals. If, in the absence of treatment, the frequency of ventricular contractions is small, then one can think of impaired conduction. With glycoside intoxication (accelerated AV nodal rhythm and complete AV block) or against the background of a very high heart rate (for example, with WPW syndrome), the rhythm of ventricular contractions may be correct. Treatment - see Ch. 6, item IV.B.
3. Atrial flutter. Regular or irregular rhythm with sawtooth atrial waves (f) most pronounced in leads II, III, aVF or V 1 . Rhythm is often regular with AV conduction 2:1 to 4:1, but may be irregular if AV conduction changes. The frequency of atrial waves is 250-350 min -1 with type I flutter and 350-450 min -1 with type II flutter. Reasons: see Ch. 6, item IV. With 1:1 AV conduction, the ventricular rate can reach 300 min–1, while due to aberrant conduction, expansion of the QRS complex is possible. At the same time, the ECG resembles that of ventricular tachycardia; this is especially often observed when using class Ia antiarrhythmic drugs without the simultaneous administration of AV blockers, as well as in WPW syndrome. Atrial fibrillation-flutter with chaotic atrial waves of various shapes is possible with one atrial flutter and another. Treatment - see Ch. 6, p. III.G.
4. Paroxysmal AV-nodal reciprocal tachycardia. Supraventricular tachycardia with narrow QRS complexes. Heart rate 150-220 min -1 , usually 180-200 min -1 . The P wave usually overlaps or follows the QRS complex (RP< 0,09 с). Начинается и прекращается внезапно. Причины: обычно иных поражений сердца нет. Контур обратного входа волны возбуждения - в АВ -узле. Возбуждение проводится антероградно по медленному (альфа) и ретроградно - по быстрому (бета) внутриузловому пути. Пароксизм обычно запускается предсердными экстрасистолами. Составляет 60-70% всех наджелудочковых тахикардий. Массаж каротидного синуса замедляет ЧСС и часто прекращает пароксизм. Лечение - см. гл. 6, п. III.Д.1.
5. Orthodromic supraventricular tachycardia in WPW syndrome. Correct rhythm. Heart rate 150-250 min -1. The RP interval is usually short, but may be prolonged with slow retrograde conduction from the ventricles to the atria. Starts and stops suddenly. Usually triggered by atrial extrasystoles. Causes: WPW syndrome, hidden additional pathways (see Chapter 6, p. XI.G.2). Usually there are no other heart lesions, but a combination with Ebstein's anomaly, hypertrophic cardiomyopathy, mitral valve prolapse is possible. Carotid sinus massage is often effective. With atrial fibrillation in patients with an obvious accessory pathway, impulses to the ventricles can be carried out extremely quickly; the QRS complexes are wide, as in ventricular tachycardia, the rhythm is irregular. There is a risk of ventricular fibrillation. Treatment - see Ch. 6, item XI.G.3.
6. Atrial tachycardia (automatic or reciprocal intraatrial). Correct rhythm. Atrial rhythm 100-200 min -1 . Non-sinus P waves. The RP interval is usually prolonged, but may be shortened in 1st-degree AV block. Causes: unstable atrial tachycardia is possible in the absence of organic lesions of the heart, stable - with myocardial infarction, cor pulmonale, and other organic lesions of the heart. The mechanism is an ectopic focus or reverse entry of an excitation wave inside the atria. It accounts for 10% of all supraventricular tachycardias. Massage of the carotid sinus causes a slowing of AV conduction, but does not eliminate the arrhythmia. Treatment - see Ch. 6, p. III.D.4.
7. Sinoatrial reciprocal tachycardia. ECG - as with sinus tachycardia (see Chapter 5, paragraph II.B.1). Correct rhythm. RP intervals are long. Starts and stops suddenly. Heart rate 100-160 min -1. The shape of the P wave is indistinguishable from the sinus. Reasons: can be observed in the norm, but more often - with organic lesions of the heart. The mechanism is the reverse entry of the excitation wave inside the sinus node or in the sinoatrial zone. It accounts for 5-10% of all supraventricular tachycardias. Massage of the carotid sinus causes a slowing of AV conduction, but does not eliminate the arrhythmia. Treatment - see Ch. 6, p. III.D.3.
8. Atypical form of paroxysmal AV nodal reciprocal tachycardia. ECG - as in atrial tachycardia (see Chapter 5, paragraph II.B.4). QRS complexes are narrow, RP intervals are long. The P wave is usually negative in leads II, III, aVF. The contour of the reverse entry of the excitation wave is in the AV node. Excitation is carried out anterograde along the fast (beta) intranodal pathway and retrograde - along the slow (alpha) pathway. Diagnosis may require an electrophysiological study of the heart. It accounts for 5-10% of all cases of reciprocal AV nodal tachycardias (2-5% of all supraventricular tachycardias). Massage of the carotid sinus can stop the paroxysm.
9. Orthodromic supraventricular tachycardia with delayed retrograde conduction. ECG - as in atrial tachycardia (see Chapter 5, paragraph II.B.4). QRS complexes are narrow, RP intervals are long. The P wave is usually negative in leads II, III, aVF. Orthodromic supraventricular tachycardia with slow retrograde conduction along an accessory pathway (usually posterior). The tachycardia is often persistent. It can be difficult to distinguish it from automatic atrial tachycardia and reciprocal intra-atrial supraventricular tachycardia. Diagnosis may require an electrophysiological study of the heart. Massage of the carotid sinus sometimes stops the paroxysm. Treatment - see Ch. 6, item XI.G.3.
10. Polytopic atrial tachycardia. Wrong rhythm. Heart rate > 100 min -1 . Non-sinus P waves of three or more different configurations. Different PP, PQ and RR intervals. Causes: in the elderly with COPD, with cor pulmonale, treatment with aminophylline, hypoxia, heart failure, after surgery, with sepsis, pulmonary edema, diabetes mellitus. Often misdiagnosed as atrial fibrillation. May progress to atrial fibrillation/flutter. Treatment - see Ch. 6, p. III.G.
11. Paroxysmal atrial tachycardia with AV block. Irregular rhythm with the frequency of atrial waves 150-250 min -1 and ventricular complexes 100-180 min -1. Non-sinus P waves. Causes: glycoside intoxication (75%), organic heart disease (25%). ECG usually shows atrial tachycardia with second-degree AV block (usually Mobitz type I). Massage of the carotid sinus causes a slowing of AV conduction, but does not eliminate the arrhythmia.
12. Ventricular tachycardia. Usually - the correct rhythm with a frequency of 110-250 min -1. QRS complex > 0.12 s, usually > 0.14 s. The ST segment and T wave are discordant to the QRS complex. Causes: organic heart damage, hypokalemia, hyperkalemia, hypoxia, acidosis, drugs and other drugs (glycoside intoxication, antiarrhythmic drugs, phenothiazines, tricyclic antidepressants, caffeine, alcohol, nicotine), mitral valve prolapse, in rare cases - in healthy individuals. AV dissociation (independent contractions of the atria and ventricles) may be noted. The electrical axis of the heart is often deviated to the left, confluent complexes are recorded. It may be nonsustained (3 or more QRS complexes but the paroxysm lasts less than 30 s) or persistent (> 30 s), monomorphic or polymorphic. Bidirectional ventricular tachycardia (with the opposite direction of the QRS complexes) is observed mainly with glycoside intoxication. Ventricular tachycardia with narrow QRS complexes has been described (< 0,11 с). Дифференциальный диагноз желудочковой и наджелудочковой тахикардии с аберрантным проведением - см. рис. 5.3. Лечение - см. гл. 6, п. VI.Б.1.
13. Supraventricular tachycardia with aberrant conduction. Usually - the right rhythm. The duration of the QRS complex is usually 0.12-0.14 s. There are no AV-dissociation and drain complexes. Deviation of the electrical axis of the heart to the left is not typical. Differential diagnosis of ventricular and supraventricular tachycardia with aberrant conduction - see fig. 5.3.
14. Pirouette tachycardia. Tachycardia with irregular rhythm and wide polymorphic ventricular complexes; a typical sinusoidal picture is characteristic, in which groups of two or more ventricular complexes with one direction are replaced by groups of complexes with the opposite direction. Occurs with prolongation of the QT interval. Heart rate - 150-250 min -1. Reasons: see Ch. 6, p. XIII.A. Attacks are usually short-lived, but there is a risk of transition to ventricular fibrillation. Paroxysm is often preceded by alternating long and short cycles of RR. In the absence of prolongation of the QT interval, such ventricular tachycardia is called polymorphic. Treatment - see Ch. 6, p. XIII.A.
15. Ventricular fibrillation. Chaotic irregular rhythm, QRS complexes and T waves are absent. Reasons: see Ch. 5, item II.B.12. In the absence of CPR, ventricular fibrillation quickly (within 4-5 minutes) leads to death. Treatment - see Ch. 7, item IV.
16. Aberrant conduction. It is manifested by wide QRS complexes due to delayed impulse conduction from the atria to the ventricles. This is most often observed when the extrasystolic excitation reaches the His-Purkinje system in the phase of relative refractoriness. The duration of the refractory period of the His-Purkinje system is inversely proportional to the heart rate; if, against the background of long RR intervals, an extrasystole occurs (short RR interval) or supraventricular tachycardia begins, then aberrant conduction occurs. In this case, excitation is usually carried out along the left leg of the bundle of His, and aberrant complexes look like blockade of the right leg of the bundle of His. Occasionally, aberrant complexes look like a left bundle branch block.
17. ECG with tachycardia with wide QRS complexes (differential diagnosis of ventricular and supraventricular tachycardia with aberrant conduction - see Fig. 5.3). Criteria for ventricular tachycardia:
b. Deviation of the electrical axis of the heart to the left.
B. Ectopic and replacement contractions
1. Atrial extrasystoles. Extraordinary non-sinus P wave followed by a normal or aberrant QRS complex. PQ interval - 0.12-0.20 s. The PQ interval of an early extrasystole may exceed 0.20 s. Causes: occur in healthy individuals, with fatigue, stress, smokers, under the influence of caffeine and alcohol, with organic heart disease, cor pulmonale. The compensatory pause is usually incomplete (the interval between the pre- and post-extrasystolic P waves is less than twice the normal PP interval). Treatment - see Ch. 6, p. III.B.
2. Blocked atrial extrasystoles. Extraordinary non-sinus P wave not followed by a QRS complex. Through the AV node, which is in the refractory period, atrial extrasystole is not carried out. The extrasystolic P wave sometimes overlaps the T wave and is difficult to recognize; in these cases, a blocked atrial extrasystole is mistaken for sinoatrial block or sinus node arrest.
3. AV nodal extrasystoles. Extraordinary QRS complex with retrograde (negative in leads II, III, aVF) P wave, which can be registered before or after the QRS complex, or superimposed on it. The shape of the QRS complex is normal; with aberrant conduction, it may resemble a ventricular extrasystole. Causes: occur in healthy individuals and with organic heart disease. The source of extrasystole is the AV node. The compensatory pause may be complete or incomplete. Treatment - see Ch. 6, p. V.A.
4. Ventricular extrasystoles. Extraordinary, wide (> 0.12 s) and deformed QRS complex. The ST segment and T wave are discordant to the QRS complex. Reasons: see Ch. 5, item II.B.12. The P wave may be unrelated to extrasystoles (AV dissociation) or be negative and follow the QRS complex (retrograde P wave). The compensatory pause is usually complete (the interval between the pre- and post-extrasystolic P waves is equal to twice the normal PP interval). Treatment - see Ch. 6, item V.B.
5. Substituting AV-nodal contractions. They resemble AV nodal extrasystoles, however, the interval to the replacement complex is not shortened, but lengthened (corresponding to a heart rate of 35–60 min–1). Causes: occur in healthy individuals and with organic heart disease. The source of the replacement impulse is a latent pacemaker in the AV node. Often observed when sinus rhythm slows down as a result of increased parasympathetic tone, medication (eg, cardiac glycosides), and sinus node dysfunction.
6. Replacement idioventricular contractions. They resemble ventricular extrasystoles, however, the interval to the replacement contraction is not shortened, but lengthened (corresponding to a heart rate of 20–50 min–1). Causes: occur in healthy individuals and with organic heart disease. The replacement impulse comes from the ventricles. Replacement idioventricular contractions are usually observed when the sinus and AV nodal rhythm slows down.
1. Sinoatrial blockade. The extended PP interval is a multiple of the normal one. Causes: some drugs (cardiac glycosides, quinidine, procainamide), hyperkalemia, sinus node dysfunction, myocardial infarction, increased parasympathetic tone. Sometimes there is a Wenckebach period (gradual shortening of the PP interval until the next cycle falls out).
2. AV blockade of the 1st degree. PQ interval > 0.20 s. Each P wave corresponds to a QRS complex. Causes: observed in healthy individuals, athletes, with an increase in parasympathetic tone, taking certain drugs (cardiac glycosides, quinidine, procainamide, propranolol, verapamil), rheumatic attack, myocarditis, congenital heart defects (atrial septal defect, patent ductus arteriosus). With narrow QRS complexes, the most likely level of block is the AV node. If the QRS complexes are wide, conduction disturbance is possible in both the AV node and the His bundle. Treatment - see Ch. 6, p. VIII.A.
3. AV blockade of the 2nd degree of the Mobitz type I (with Wenckebach's periodicals). Increasing lengthening of the PQ interval up to the loss of the QRS complex. Causes: observed in healthy individuals, athletes, when taking certain drugs (cardiac glycosides, beta-blockers, calcium antagonists, clonidine, methyldopa, flecainide, encainide, propafenone, lithium), with myocardial infarction (especially lower), rheumatic attack, myocarditis . With narrow QRS complexes, the most likely level of block is the AV node. If the QRS complexes are wide, the violation of impulse conduction is possible both in the AV node and in the bundle of His. Treatment - see Ch. 6, item VIII.B.1.
4. AV blockade of the 2nd degree of the Mobitz type II. Periodic prolapse of QRS complexes. The PQ intervals are the same. Causes: almost always occurs against the background of organic heart disease. The pulse delay occurs in the bundle of His. 2:1 AV block occurs in both Mobitz I and Mobitz II types: narrow QRS complexes are more typical for Mobitz I AV block, wide ones for Mobitz II AV block. With AV block high degree two or more consecutive ventricular complexes fall out. Treatment - see Ch. 6, item VIII.B.2.
5. Complete AV block. The atria and ventricles fire independently. The atrial contraction rate exceeds the ventricular rate. Same PP intervals and same RR intervals, PQ intervals vary. Causes: Complete AV block is congenital. The acquired form of complete AV blockade occurs with myocardial infarction, isolated disease of the conduction system of the heart (Lenegre's disease), aortic malformations, taking certain drugs (cardiac glycosides, quinidine, procainamide), endocarditis, Lyme disease, hyperkalemia, infiltrative diseases (amyloidosis, sarcoidosis ), collagenosis, trauma, rheumatic attack. Blockade of impulse conduction is possible at the level of the AV node (for example, with congenital complete AV blockade with narrow QRS complexes), the His bundle, or the distal fibers of the His-Purkinje system. Treatment - see Ch. 6, p. VIII.B.
III. Determination of the electrical axis of the heart. The direction of the electrical axis of the heart approximately corresponds to the direction of the largest total vector of depolarization of the ventricles. To determine the direction of the electrical axis of the heart, it is necessary to calculate the algebraic sum of the QRS complex amplitude teeth in leads I, II and aVF (subtract the amplitude of the negative part of the complex from the amplitude of the positive part of the complex) and then follow the table. 5.1.
A. Causes of deviation of the electrical axis of the heart to the right: COPD, cor pulmonale, right ventricular hypertrophy, blockade of the right leg of the His bundle, lateral myocardial infarction, blockade of the posterior branch of the left leg of the His bundle, pulmonary edema, dextrocardia, WPW syndrome. It happens in the norm. A similar picture is observed when the electrodes are applied incorrectly.
B. Causes of deviation of the electrical axis of the heart to the left: blockade of the anterior branch of the left leg of the His bundle, lower myocardial infarction, blockade of the left leg of the His bundle, left ventricular hypertrophy, atrial septal defect of the ostium primum type, COPD, hyperkalemia. It happens in the norm.
C. Causes of a sharp deviation of the electrical axis of the heart to the right: blockade of the anterior branch of the left leg of the His bundle against the background of right ventricular hypertrophy, blockade of the anterior branch of the left leg of the His bundle with lateral myocardial infarction, right ventricular hypertrophy, COPD.
IV. Analysis of teeth and intervals. ECG interval - the interval from the beginning of one wave to the beginning of another wave. An ECG segment is the gap from the end of one wave to the beginning of the next wave. At a writing speed of 25 mm/s, each small cell on the paper tape corresponds to 0.04 s.
A. Normal 12-lead ECG
1. P wave. Positive in leads I, II, aVF, negative in aVR, may be negative or biphasic in leads III, aVL, V 1 , V 2 .
3. QRS complex. Width - 0.06-0.10 s. Small Q wave (width< 0,04 с, амплитуда < 2 мм) бывает во всех отведениях кроме aVR, V 1 и V 2 . Переходная зона грудных отведений (отведение, в котором амплитуды положительной и отрицательной части комплекса QRS одинаковы) обычно находится между V 2 и V 4 .
4. ST segment. Usually on the isoline. In the leads from the extremities, a depression of up to 0.5 mm and an elevation of up to 1 mm are normally possible. In the chest leads, ST elevation up to 3 mm with a downward bulge is possible (syndrome of early repolarization of the ventricles, see Chapter 5, p. IV.3.1.d).
5. T wave. Positive in leads I, II, V 3 -V 6 . Negative in aVR, V 1 . May be positive, flattened, negative, or biphasic in leads III, aVL, aVF, V1, and V2. Healthy young people have a negative T wave in leads V 1 -V 3 (persistent juvenile type of ECG).
6. QT interval. Duration is inversely proportional to heart rate; usually fluctuates between 0.30-0.46 s. QT c \u003d QT / C RR, where QT c is the corrected QT interval; normal QT c 0.46 in men and 0.47 in women.
Below are some conditions, for each of which characteristic ECG signs are indicated. However, it must be borne in mind that ECG criteria do not have one hundred percent sensitivity and specificity, therefore, the listed signs can be detected separately or in different combinations, or absent altogether.
1. High pointed P in lead II: right atrial enlargement. P wave amplitude in lead II > 2.5 mm (P pulmonale). Specificity is only 50%, in 1/3 of cases P pulmonale is caused by an increase in the left atrium. It is noted in COPD, congenital heart defects, congestive heart failure, coronary artery disease.
2. Negative P in lead I
a. Dextrocardia. Negative P and T waves, an inverted QRS complex in lead I without an increase in the amplitude of the R wave in the chest leads. Dextrocardia can be one of the manifestations of situs inversus (reverse arrangement of internal organs) or isolated. Isolated dextrocardia is often associated with other congenital malformations, including corrected transposition of the great arteries, pulmonary artery stenosis, and ventricular and atrial septal defects.
b. The electrodes are incorrectly applied. If the electrode intended for the left hand is applied to the right hand, then negative P and T waves are recorded, an inverted QRS complex with a normal location of the transition zone in the chest leads.
3. Deep negative P in lead V 1: left atrial enlargement. P mitrale: in lead V 1, the end part (ascending knee) of the P wave is expanded (> 0.04 s), its amplitude is > 1 mm, the P wave is expanded in lead II (> 0.12 s). It is observed in mitral and aortic defects, heart failure, myocardial infarction. The specificity of these signs is above 90%.
4. Negative P wave in lead II: ectopic atrial rhythm. The PQ interval is usually > 0.12 s, the P wave is negative in leads II, III, aVF. See ch. 5, item II.A.3.
1. Prolongation of the PQ interval: AV blockade of the 1st degree. PQ intervals are the same and exceed 0.20 s (see Chapter 5, item II.D.2). If the duration of the PQ interval varies, then AV blockade of the 2nd degree is possible (see Chapter 5, p. II.D.3).
2. Shortening of the PQ interval
a. Functional shortening of the PQ interval. PQ< 0,12 с. Наблюдается в норме, при повышении симпатического тонуса, артериальной гипертонии, гликогенозах.
b. WPW syndrome. PQ< 0,12 с, наличие дельта-волны, комплексы QRS широкие, интервал ST и зубец T дискордантны комплексу QRS. См. гл. 6, п. XI.
in. AV - nodal or lower atrial rhythm. PQ< 0,12 с, зубец P отрицательный в отведениях II, III, aVF. см. гл. 5, п. II.А.5.
3. Depression of the PQ segment: pericarditis. Depression of the PQ segment in all leads except aVR is most pronounced in leads II, III, and aVF. Depression of the PQ segment is also noted in atrial infarction, which occurs in 15% of cases of myocardial infarction.
D. Width of the QRS complex
a. Blockade of the anterior branch of the left leg of the bundle of His. Deviation of the electrical axis of the heart to the left (from -30° to -90°). Low R wave and deep S wave in leads II, III, and aVF. High R wave in leads I and aVL. A small Q wave may be present. There is a late activation wave (R') in lead aVR. The shift of the transitional zone to the left in the chest leads is characteristic. It is observed in congenital malformations and other organic lesions of the heart, occasionally in healthy people. Does not require treatment.
b. Blockade of the posterior branch of the left leg of the bundle of His. Deviation of the electrical axis of the heart to the right (> +90°). Low R wave and deep S wave in leads I and aVL. A small Q wave may be recorded in leads II, III, aVF. It is noted in ischemic heart disease, occasionally in healthy people. Occurs infrequently. It is necessary to exclude other causes of deviation of the electrical axis of the heart to the right: right ventricular hypertrophy, COPD, cor pulmonale, lateral myocardial infarction, vertical position of the heart. Complete confidence in the diagnosis is given only by comparison with previous ECG. Does not require treatment.
in. Incomplete blockade of the left leg of the bundle of His. Serrated R wave or late R wave (R’) in leads V 5 , V 6 . Wide S wave in leads V 1 , V 2 . The absence of a Q wave in leads I, aVL, V 5 , V 6 .
d. Incomplete blockade of the right leg of the bundle of His. Late R wave (R’) in leads V 1 , V 2 . Wide S wave in leads V 5 , V 6 .
a. Blockade of the right leg of the bundle of His. Late R wave in leads V 1 , V 2 with slanting ST segment and negative T wave. Deep S wave in leads I, V 5 , V 6 . It is observed with organic lesions of the heart: cor pulmonale, Lenegra's disease, coronary artery disease, occasionally - normal. Masked blockade of the right bundle branch block: the form of the QRS complex in lead V 1 corresponds to the blockade of the right bundle branch block, however, in leads I, aVL or V 5 , V 6 the RSR complex is recorded. Usually this is due to the blockade of the anterior branch of the left leg of the His bundle, left ventricular hypertrophy, myocardial infarction. Treatment - see Ch. 6, p. VIII.E.
b. Blockade of the left leg of the bundle of His. Wide serrated R wave in leads I, V 5 , V 6 . Deep S or QS wave in leads V 1 , V 2 . The absence of a Q wave in leads I, V 5 , V 6 . It is observed with left ventricular hypertrophy, myocardial infarction, Lenegra's disease, coronary artery disease, sometimes normal. Treatment - see Ch. 6, p. VIII.D.
in. Blockade of the right leg of the bundle of His and one of the branches of the left leg of the bundle of His. The combination of two-bundle block with 1st degree AV block should not be regarded as a three-bundle block: prolongation of the PQ interval may be due to slow conduction in the AV node, and not blockade of the third branch of the His bundle. Treatment - see Ch. 6, p. VIII.G.
d. Violation of intraventricular conduction. Expansion of the QRS complex (> 0.12 s) in the absence of signs of blockade of the right or left bundle branch block. It is noted with organic heart disease, hyperkalemia, left ventricular hypertrophy, taking antiarrhythmic drugs of classes Ia and Ic, with WPW syndrome. Treatment usually does not require.
E. QRS complex amplitude
1. Low amplitude of teeth. Amplitude of the QRS complex< 5 мм во всех отведениях от конечностей и < 10 мм во всех грудных отведениях. Встречается в норме, а также при экссудативном перикардите, амилоидозе, ХОЗЛ, ожирении, тяжелом гипотиреозе.
2. High-amplitude QRS complex
a. Left ventricular hypertrophy
1) Cornell criteria: (R in aVL + S in V 3) > 28 mm in men and > 20 mm in women (sensitivity 42%, specificity 96%).
Medical Forum
In this forum topic, electrocardiograms will be posted. Let's decipher together.
Sinus rhythm, regular. Heart rate 62 beats per minute. Deviation of the electrical axis to the left. Transitional zone V 4. Ischemia in the anterior-septal, anterior-lateral region and partially posterior-diaphragmatic regions. Transmural ischemic injury in the anterior-apical and anterior-lateral regions of the left ventricle. Left ventricular hypertrophy. Blockade of the anterior branch of the left leg of the bundle of Giss.
A 60-year-old woman complains of general weakness, polyuria and high blood pressure.
People, help. I have no way to decipher the ECG - we have problems with cardiologists! I'm 30, it's constantly tight in my chest, shortness of breath and fatigue. And the ECG laboratory assistant said that everything was within the normal range, but he was not a specialist! Help. No strength to endure!
Dima! The laboratory assistant of the ECG room really said correctly that your ECG is within the normal range. I give a complete transcript of your ECG:
Р=0.08 PQ=0.14 QRS=0.10 QT=0.34 R-R=0.88-0.9.
The rhythm is sinus, regular. Heart rate 66 beats per minute. Normal position of the electrical axis of the heart. Transitional zone V 3. ST is elevated in leads V2-V3 seems to be 1 mm (not very clearly visible). ECG without features.
I would like to note that electrocardiography is not a 100% method for diagnosing heart diseases. And outside of the pain attack, the ECG can be completely normal. Dima You need to pass additional research. Echocardiography, make a survey X-ray, tell more about this pain. I can advise you to find a good therapist in your area and consult internally. And you can put the results of the research on the Forum and we will discuss it with our colleagues here at the Forum.
Transition zone v3 v4
Therefore, a small R wave is recorded in lead V1, and the presence of this tooth is required in the norm.
However, the main vector after excitation of the IVS is directed to the left, therefore, a negative wave is recorded in leads V1 and V2, namely, a deep S wave.
V3 and V4. As the ventricles are covered with excitation, the EMF vector (main vector), directed to the left, increases, therefore, the height of the S wave also increases in the left leads V3 and V4.
The S1 wave, on the contrary, gradually decreases.
Often in lead V3 or V4, the R and S waves are of equal amplitude.
These leads correspond to the so-called transition zone.
V5 and V6. The main EMF vector is directed towards leads V5 and V6, so the highest R waves are recorded in them. The T wave in leads V5 and V6 is positive.
Transition zone v3 v4
7.2.1. Myocardial hypertrophy
The cause of hypertrophy is usually an excessive load on the heart, either by resistance (hypertension) or by volume (chronic renal and/or heart failure). The increased work of the heart leads to an increase in metabolic processes in the myocardium and is subsequently accompanied by an increase in the number of muscle fibers. The bioelectrical activity of the hypertrophied part of the heart increases, which is reflected in the electrocardiogram.
7.2.1.1. Left atrial hypertrophy
A characteristic sign of left atrial hypertrophy is an increase in the width of the P wave (more than 0.12 s). The second sign is a change in the shape of the P wave (two humps with a predominance of the second peak) (Fig. 6).
Rice. 6. ECG with left atrial hypertrophy
Left atrial hypertrophy is a typical symptom of mitral valve stenosis and therefore the P wave in this disease is called P-mitrale. Similar changes are observed in leads I, II, aVL, V5, V6.
7.2.1.2. Right atrial hypertrophy
With hypertrophy of the right atrium, the changes also affect the P wave, which acquires a pointed shape and increases in amplitude (Fig. 7).
Rice. 7. ECG with hypertrophy of the right atrium (P-pulmonale), right ventricle (S-type)
Hypertrophy of the right atrium is observed with atrial septal defect, hypertension of the pulmonary circulation.
Most often, such a P wave is detected in diseases of the lungs, it is often called P-pulmonale.
Hypertrophy of the right atrium is a sign of a change in the P wave in leads II, III, aVF, V1, V2.
7.2.1.3. Left ventricular hypertrophy
The ventricles of the heart are better adapted to the loads, and in the early stages of their hypertrophy may not appear on the ECG, but as the pathology develops, characteristic signs become visible.
With ventricular hypertrophy, there are significantly more changes on the ECG than with atrial hypertrophy.
The main signs of left ventricular hypertrophy are (Fig. 8):
Deviation of the electrical axis of the heart to the left (levogram);
Shift of the transition zone to the right (in leads V2 or V3);
The R wave in leads V5, V6 is high and larger in amplitude than RV4;
Deep S in leads V1, V2;
Extended QRS complex in leads V5, V6 (up to 0.1 s or more);
Shift of the S-T segment below the isoelectric line with a bulge upwards;
Negative T wave in leads I, II, aVL, V5, V6.
Rice. 8. ECG with left ventricular hypertrophy
Left ventricular hypertrophy is often observed in arterial hypertension, acromegaly, pheochromocytoma, as well as insufficiency of the mitral and aortic valves, congenital heart defects.
7.2.1.4. Right ventricular hypertrophy
Signs of right ventricular hypertrophy appear on the ECG in advanced cases. Diagnosis at an early stage of hypertrophy is extremely difficult.
Signs of hypertrophy (Fig. 9):
Deviation of the electrical axis of the heart to the right (rightogram);
Deep S wave in lead V1 and high R wave in leads III, aVF, V1, V2;
The height of the RV6 tooth is less than normal;
Extended QRS complex in leads V1, V2 (up to 0.1 s or more);
Deep S wave in lead V5 as well as V6;
S-T segment displacement below the isoline with a bulge upwards in the right III, aVF, V1 and V2;
Complete or incomplete blockade of the right leg of the bundle of His;
Shift of the transition zone to the left.
Rice. 9. ECG with right ventricular hypertrophy
Right ventricular hypertrophy is most often associated with an increase in pressure in the pulmonary circulation in lung diseases, mitral valve stenosis, parietal thrombosis and pulmonary artery stenosis, and congenital heart defects.
7.2.2. Rhythm disturbances
Weakness, shortness of breath, palpitations, rapid and difficult breathing, interruptions in the work of the heart, a feeling of suffocation, fainting, or episodes of loss of consciousness may be manifestations of heart rhythm disturbances due to cardiovascular disease. An ECG helps to confirm their presence, and most importantly, to determine their type.
It should be remembered that automatism is a unique property of the cells of the conduction system of the heart, and the sinus node, which controls the rhythm, has the greatest automatism.
Rhythm disturbances (arrhythmias) are diagnosed when there is no sinus rhythm on the ECG.
Signs of normal sinus rhythm:
The frequency of the P waves is in the range from 60 to 90 (in 1 min);
The same duration of RR intervals;
Positive P wave in all leads except aVR.
Heart rhythm disturbances are very diverse. All arrhythmias are divided into nomotopic (changes develop in the sinus node itself) and heterotopic. In the latter case, excitatory impulses occur outside the sinus node, that is, in the atria, atrioventricular junction and ventricles (in the branches of the His bundle).
Nomotopic arrhythmias include sinus bradycardia and tachycardia and irregular sinus rhythm. To heterotopic - atrial fibrillation and flutter and other disorders. If the occurrence of arrhythmia is associated with a violation of the excitability function, then such rhythm disturbances are divided into extrasystole and paroxysmal tachycardia.
Considering all the variety of types of arrhythmias that can be detected on the ECG, the author, in order not to bore the reader with the intricacies of medical science, only allowed himself to define the basic concepts and consider the most significant rhythm and conduction disturbances.
7.2.2.1. Sinus tachycardia
Increased generation of impulses in the sinus node (more than 100 impulses per 1 min).
On the ECG, it is manifested by the presence of a regular P wave and a shortening of the R-R interval.
7.2.2.2. Sinus bradycardia
The frequency of pulse generation in the sinus node does not exceed 60.
On the ECG, it is manifested by the presence of a regular P wave and a lengthening of the R-R interval.
It should be noted that at a rate of less than 30 bradycardia is not sinus.
As in the case of tachycardia and bradycardia, the patient is treated for the disease that caused the rhythm disturbance.
7.2.2.3. Irregular sinus rhythm
Impulses are irregularly generated in the sinus node. The ECG shows normal waves and intervals, but the duration of the R-R intervals differs by at least 0.1 s.
This type of arrhythmia can occur in healthy people and does not need treatment.
7.2.2.4. Idioventricular rhythm
Heterotopic arrhythmia, in which the pacemaker is either the legs of the bundle of His or Purkinje fibers.
Extremely severe pathology.
A rare rhythm on the ECG (that is, 30–40 beats per minute), the P wave is absent, the QRS complexes are deformed and expanded (duration 0.12 s or more).
Occurs only in severe heart disease. A patient with such a disorder needs urgent care and is subject to immediate hospitalization in cardiological intensive care.
Extraordinary contraction of the heart caused by a single ectopic impulse. Of practical importance is the division of extrasystoles into supraventricular and ventricular.
A supraventricular (it is also called atrial) extrasystole is recorded on the ECG if the focus that causes extraordinary excitation (contraction) of the heart is located in the atria.
Ventricular extrasystole is recorded on the cardiogram during the formation of an ectopic focus in one of the ventricles.
Extrasystole can be rare, frequent (more than 10% of heart contractions in 1 min), paired (bigemenia) and group (more than three in a row).
We list the ECG signs of atrial extrasystole:
Changed in shape and amplitude P wave;
Shortened P-Q interval;
The prematurely registered QRS complex does not differ in shape from the normal (sinus) complex;
The R-R interval that follows the extrasystole is longer than usual, but shorter than two normal intervals (incomplete compensatory pause).
Atrial extrasystoles are more common in older people against the background of cardiosclerosis and coronary heart disease, but can also be observed in practically healthy people, for example, if a person is very worried or stressed.
If an extrasystole is seen in a practically healthy person, then the treatment consists in prescribing valocordin, corvalol and ensuring complete rest.
When registering an extrasystole in a patient, treatment of the underlying disease and taking antiarrhythmic drugs from the isoptin group are also required.
Signs of ventricular extrasystole:
The P wave is absent;
The extraordinary QRS complex is significantly expanded (more than 0.12 s) and deformed;
Complete compensatory pause.
Ventricular extrasystole always indicates damage to the heart (CHD, myocarditis, endocarditis, heart attack, atherosclerosis).
With ventricular extrasystole with a frequency of 3-5 contractions per 1 min, antiarrhythmic therapy is mandatory.
Most often, intravenous lidocaine is administered, but other drugs can also be used. Treatment is carried out with careful ECG monitoring.
7.2.2.6. Paroxysmal tachycardia
Sudden attack of hyper-frequent contractions lasting from a few seconds to several days. The heterotopic pacemaker is located either in the ventricles or supraventricularly.
With supraventricular tachycardia (in this case, impulses are formed in the atria or atrioventricular node), the correct rhythm is recorded on the ECG with a frequency of 180 to 220 contractions per 1 minute.
The QRS complexes are not changed or expanded.
With the ventricular form of paroxysmal tachycardia, the P waves can change their place on the ECG, the QRS complexes are deformed and expanded.
Supraventricular tachycardia occurs in Wolff-Parkinson-White syndrome, less often in acute myocardial infarction.
The ventricular form of paroxysmal tachycardia is detected in patients with myocardial infarction, with coronary artery disease, and electrolyte disturbances.
7.2.2.7. Atrial fibrillation (atrial fibrillation)
A variety of supraventricular arrhythmias caused by asynchronous, uncoordinated electrical activity of the atria, followed by a deterioration in their contractile function. The flow of impulses is not conducted to the ventricles as a whole, and they contract irregularly.
This arrhythmia is one of the most common cardiac arrhythmias.
It occurs in more than 6% of patients older than 60 years and in 1% of patients younger than this age.
Signs of atrial fibrillation:
R-R intervals are different (arrhythmia);
P waves are absent;
Flicker waves F are recorded (they are especially clearly visible in leads II, III, V1, V2);
Electrical alternation (different amplitude of I waves in one lead).
Atrial fibrillation occurs with mitral stenosis, thyrotoxicosis and cardiosclerosis, and often with myocardial infarction. Medical care is to restore sinus rhythm. Novocainamide, potassium preparations and other antiarrhythmic drugs are used.
7.2.2.8. atrial flutter
It is observed much less frequently than atrial fibrillation.
With atrial flutter, normal atrial excitation and contraction are absent, and excitation and contraction of individual atrial fibers are observed.
7.2.2.9. ventricular fibrillation
The most dangerous and severe violation of the rhythm, which quickly leads to circulatory arrest. It occurs with myocardial infarction, as well as in the terminal stages of various cardiovascular diseases in patients who are in a state of clinical death. Ventricular fibrillation requires immediate resuscitation.
Signs of ventricular fibrillation:
Absence of all teeth of the ventricular complex;
Registration of fibrillation waves in all leads with a frequency of 450-600 waves per 1 min.
7.2.3. Conduction disorders
Changes in the cardiogram that occur in the event of a violation of the conduction of an impulse in the form of a slowdown or complete cessation of the transmission of excitation are called blockades. Blockades are classified depending on the level at which the violation occurred.
Allocate sinoatrial, atrial, atrioventricular and intraventricular blockade. Each of these groups is further subdivided. So, for example, there are sinoatrial blockades of I, II and III degrees, blockades of the right and left legs of the His bundle. There is also a more detailed division (blockade of the anterior branch of the left leg of the bundle of His, incomplete blockade of the right leg of the bundle of His). Among the conduction disorders recorded by ECG, the following blockades are of the greatest practical importance:
Sinoatrial III degree;
Atrioventricular I, II and III degrees;
Blockade of the right and left legs of the bundle of His.
7.2.3.1. Sinoatrial block III degree
Conduction disorder, in which the conduction of excitation from the sinus node to the atria is blocked. On a seemingly normal ECG, another contraction suddenly drops out (blocks), that is, the entire P-QRS-T complex (or 2-3 complexes at once). In their place, an isoline is recorded. Pathology is observed in those suffering from coronary artery disease, heart attack, cardiosclerosis, with the use of a number of drugs (for example, beta-blockers). Treatment consists in the treatment of the underlying disease and the use of atropine, izadrin and similar agents).
7.2.3.2. Atrioventricular block
Violation of the conduction of excitation from the sinus node through the atrioventricular connection.
Slowing of atrioventricular conduction is a first-degree atrioventricular block. It appears on the ECG in the form of a prolongation of the P-Q interval (more than 0.2 s) with a normal heart rate.
Atrioventricular blockade II degree - incomplete blockade, in which not all impulses coming from the sinus node reach the ventricular myocardium.
On the ECG, the following two types of blockade are distinguished: the first is Mobitz-1 (Samoilov-Wenckebach) and the second is Mobitz-2.
Signs of blockade type Mobitz-1:
Constantly lengthening interval P
Due to the first sign, at some stage after the P wave, the QRS complex disappears.
A sign of blockade of the Mobitz-2 type is a periodic prolapse of the QRS complex against the background of an extended P-Q interval.
Atrioventricular blockade of the III degree - a condition in which not a single impulse coming from the sinus node is conducted to the ventricles. On the ECG, two types of rhythm are recorded that are not interconnected; the work of the ventricles (QRS complexes) and the atria (P waves) is not coordinated.
Blockade of the III degree is often found in cardiosclerosis, myocardial infarction, improper use of cardiac glycosides. The presence of this type of blockade in a patient is an indication for his urgent hospitalization in a cardiological hospital. Treatment is with atropine, ephedrine, and, in some cases, prednisolone.
7.2.3.3. Blockade of the legs of the bundle of His
In a healthy person, an electrical impulse originating in the sinus node, passing through the legs of the bundle of His, simultaneously excites both ventricles.
With the blockade of the right or left legs of the bundle of His, the path of the impulse changes and therefore the excitation of the corresponding ventricle is delayed.
It is also possible the occurrence of incomplete blockades and the so-called blockades of the anterior and posterior branches of the bundle of His bundle.
Signs of a complete blockade of the right leg of the bundle of His (Fig. 10):
Deformed and extended (more than 0.12 s) QRS complex;
Negative T wave in leads V1 and V2;
S-T segment offset from the isoline;
Widening and splitting of the QRS in leads V1 and V2 as RsR.
Rice. 10. ECG with complete blockade of the right leg of the bundle of His
Signs of a complete blockade of the left leg of the bundle of His:
The QRS complex is deformed and expanded (more than 0.12 s);
Offset of the S-T segment from the isoline;
Negative T wave in leads V5 and V6;
Expansion and splitting of the QRS complex in leads V5 and V6 in the form of RR;
Deformation and expansion of the QRS in leads V1 and V2 in the form of rS.
These types of blockades are found in heart injuries, acute myocardial infarction, atherosclerotic and myocardial cardiosclerosis, with the incorrect use of a number of medications (cardiac glycosides, procainamide).
Patients with intraventricular blockade do not need special therapy. They are hospitalized to treat the disease that caused the blockade.
7.2.4. Wolff-Parkinson-White Syndrome
For the first time such a syndrome (WPW) was described by the above-mentioned authors in 1930 as a form of supraventricular tachycardia, which is observed in young healthy people (“functional blockade of the bundle of His bundle”).
It has now been established that sometimes in the body, in addition to the normal path of impulse conduction from the sinus node to the ventricles, there are additional bundles (Kent, James and Maheim). Through these pathways, excitation reaches the ventricles of the heart faster.
There are several types of WPW syndrome. If excitation enters the left ventricle earlier, then type A WPW syndrome is recorded on the ECG. In type B, excitation enters the right ventricle earlier.
Signs of WPW syndrome type A:
The delta wave on the QRS complex is positive in the right chest leads and negative in the left (the result of premature excitation of a part of the ventricle);
The direction of the main teeth in the chest leads is approximately the same as with the blockade of the left leg of the bundle of His.
Signs of WPW syndrome type B:
Shortened (less than 0.11 s) P-Q interval;
The QRS complex is expanded (more than 0.12 s) and deformed;
Negative delta wave for the right chest leads, positive for the left;
The direction of the main teeth in the chest leads is approximately the same as with the blockade of the right leg of the bundle of His.
It is possible to register a sharply shortened P-Q interval with an undeformed QRS complex and the absence of a delta wave (Laun-Ganong-Levin syndrome).
Additional bundles are inherited. In about 30–60% of cases, they do not manifest themselves. Some people may develop paroxysms of tachyarrhythmias. In case of arrhythmia, medical care is provided in accordance with the general rules.
7.2.5. Early ventricular repolarization
This phenomenon occurs in 20% of patients with cardiovascular pathology (most often occurs in patients with supraventricular arrhythmias).
It is not a disease, but patients with cardiovascular disease who have this syndrome are 2-4 times more likely to suffer from rhythm and conduction disturbances.
Signs of early ventricular repolarization (Fig. 11) include:
ST segment elevation;
Late delta wave (notch on the descending part of the R wave);
High amplitude teeth;
Double-humped P wave of normal duration and amplitude;
Shortening of PR and QT intervals;
Rapid and sharp increase in the amplitude of the R wave in the chest leads.
Rice. 11. ECG in early ventricular repolarization syndrome
7.2.6. Cardiac ischemia
In coronary heart disease (CHD), the blood supply to the myocardium is impaired. In the early stages, there may be no changes on the electrocardiogram, in the later stages they are very noticeable.
With the development of myocardial dystrophy, the T wave changes and signs of diffuse changes in the myocardium appear.
These include:
Reducing the amplitude of the R wave;
S-T segment depression;
Biphasic, moderately dilated and flat T wave in almost all leads.
IHD occurs in patients with myocarditis of various origins, as well as dystrophic changes in the myocardium and atherosclerotic cardiosclerosis.
With the development of an angina attack on the ECG, it is possible to detect a shift in the ST segment and changes in the T wave in those leads that are located above the zone with impaired blood supply (Fig. 12).
Rice. 12. ECG for angina pectoris (during an attack)
The causes of angina pectoris are hypercholesterolemia, dyslipidemia. In addition, arterial hypertension, diabetes mellitus, psycho-emotional overload, fear, and obesity can provoke the development of an attack.
Depending on which layer of the heart muscle ischemia occurs, there are:
Subendocardial ischemia (over the ischemic area, the S-T shift is below the isoline, the T wave is positive, of large amplitude);
Subepicardial ischemia (elevation of the S-T segment above the isoline, T negative).
The occurrence of angina pectoris is accompanied by the appearance of typical pain behind the sternum, usually provoked by physical activity. This pain is of a pressing nature, lasts for several minutes and disappears after the use of nitroglycerin. If the pain lasts more than 30 minutes and is not relieved by taking nitropreparations, acute focal changes can be assumed with a high probability.
Emergency care for angina pectoris is to relieve pain and prevent recurrent attacks.
Analgesics are prescribed (from analgin to promedol), nitropreparations (nitroglycerin, sustak, nitrong, monocinque, etc.), as well as validol and diphenhydramine, seduxen. If necessary, inhalation of oxygen is carried out.
7.2.8. myocardial infarction
Myocardial infarction is the development of necrosis of the heart muscle as a result of prolonged circulatory disorders in the ischemic area of the myocardium.
In more than 90% of cases, the diagnosis is determined using an ECG. In addition, the cardiogram allows you to determine the stage of a heart attack, find out its localization and type.
An unconditional sign of a heart attack is the appearance on the ECG of a pathological Q wave, which is characterized by excessive width (more than 0.03 s) and greater depth (a third of the R wave).
Options QS, QrS are possible. S-T shift (Fig. 13) and T wave inversion are observed.
Rice. 13. ECG in anterolateral myocardial infarction (acute stage). There are cicatricial changes in the posterior lower parts of the left ventricle
Sometimes there is a shift in S-T without the presence of a pathological Q wave (small-focal myocardial infarction). Signs of a heart attack:
Pathological Q wave in leads located above the infarction area;
Displacement by an arc upward (rise) of the ST segment relative to the isoline in leads located above the infarction area;
Discordant shift below the isoline of the ST segment in leads opposite to the area of infarction;
Negative T wave in leads located above the infarction area.
As the disease progresses, the ECG changes. This relationship is explained by the staging of changes in a heart attack.
There are four stages in the development of myocardial infarction:
The most acute stage (Fig. 14) lasts several hours. At this time, the ST segment rises sharply on the ECG in the corresponding leads, merging with the T wave.
Rice. 14. The sequence of ECG changes in myocardial infarction: 1 - Q-infarction; 2 - not Q-infarction; A - the most acute stage; B - acute stage; B - subacute stage; D - cicatricial stage (post-infarction cardiosclerosis)
In the acute stage, a zone of necrosis is formed and an abnormal Q wave appears. The R amplitude decreases, the ST segment remains elevated, and the T wave becomes negative. The duration of the acute stage is on average about 1-2 weeks.
The subacute stage of infarction lasts for 1–3 months and is characterized by cicatricial organization of the focus of necrosis. On the ECG at this time, the ST segment gradually returns to the isoline, the Q wave decreases, and the R amplitude, on the contrary, increases.
The T wave remains negative.
The cicatricial stage can stretch for several years. At this time, the organization of scar tissue occurs. On the ECG, the Q wave decreases or disappears completely, the S-T is located on the isoline, the negative T gradually becomes isoelectric, and then positive.
Such staging is often referred to as the regular ECG dynamics in myocardial infarction.
A heart attack can be localized in any part of the heart, but most often occurs in the left ventricle.
Depending on the localization, the infarction of the anterior lateral and posterior walls of the left ventricle is distinguished. The localization and prevalence of changes are revealed by analyzing ECG changes in the corresponding leads (Table 6).
Table 6. Localization of myocardial infarction
Great difficulties arise in the diagnosis of re-infarction, when new changes are superimposed on an already changed ECG. Helps dynamic control with the removal of the cardiogram at short intervals.
A typical heart attack is characterized by burning, severe retrosternal pain that does not go away after taking nitroglycerin.
There are also atypical forms of a heart attack:
Abdominal (pain in the heart and abdomen);
Asthmatic (cardiac pain and cardiac asthma or pulmonary edema);
Arrhythmic (cardiac pain and rhythm disturbances);
Collaptoid (cardiac pain and a sharp drop in blood pressure with profuse sweating);
Treating a heart attack is a very difficult task. It is usually the more difficult, the greater the prevalence of the lesion. At the same time, according to the apt remark of one of the Russian zemstvo doctors, sometimes the treatment of an extremely severe heart attack goes unexpectedly smoothly, and sometimes an uncomplicated, simple micro-infarction makes the doctor sign his impotence.
Emergency care consists in stopping pain (narcotic and other analgesics are used for this), also eliminating fears and psycho-emotional arousal with the help of sedatives, reducing the infarct zone (using heparin), and eliminating other symptoms in turn, depending on their degree of danger.
After completion of inpatient treatment, patients who have had a heart attack are sent to a sanatorium for rehabilitation.
The final stage is a long-term observation in the clinic at the place of residence.
7.2.9. Syndromes in electrolyte disorders
Certain ECG changes make it possible to judge the dynamics of the electrolyte content in the myocardium.
In fairness, it should be said that there is not always a clear correlation between the level of electrolytes in the blood and the content of electrolytes in the myocardium.
Nevertheless, electrolyte disturbances detected by ECG serve as a significant help to the doctor in the process of diagnostic search, as well as in choosing the right treatment.
The most well-studied changes in the ECG in violation of the exchange of potassium, as well as calcium (Fig. 15).
Rice. 15. ECG diagnostics of electrolyte disorders (A. S. Vorobyov, 2003): 1 - normal; 2 - hypokalemia; 3 - hyperkalemia; 4 - hypocalcemia; 5 - hypercalcemia
High pointed T wave;
Shortening of the Q-T interval;
Reducing the amplitude of R.
With severe hyperkalemia, intraventricular conduction disturbances are observed.
Hyperkalemia occurs in diabetes (acidosis), chronic renal failure, severe injuries with crushing of muscle tissue, insufficiency of the adrenal cortex, and other diseases.
Decrease in the S-T segment from top to bottom;
Negative or two-phase T;
With severe hypokalemia, atrial and ventricular extrasystoles, intraventricular conduction disturbances appear.
Hypokalemia occurs with the loss of potassium salts in patients with severe vomiting, diarrhea, after prolonged use of diuretic, steroid hormones, with a number of endocrine diseases.
Treatment consists in replenishing the deficiency of potassium in the body.
Shortening of the Q-T interval;
Shortening of the S-T segment;
Expansion of the ventricular complex;
Rhythm disturbances with a significant increase in calcium.
Hypercalcemia is observed with hyperparathyroidism, bone destruction by tumors, hypervitaminosis D and excessive administration of potassium salts.
Increase in the duration of the Q-T interval;
S-T segment lengthening;
Decreased amplitude of T.
Hypocalcemia occurs with a decrease in the function of the parathyroid glands, in patients with chronic renal failure, with severe pancreatitis and hypovitaminosis D.
7.2.9.5. Glycoside intoxication
Cardiac glycosides have long been successfully used in the treatment of heart failure. These funds are indispensable. Their intake contributes to a decrease in heart rate (heart rate), more vigorous expulsion of blood during systole. As a result, hemodynamic parameters improve and manifestations of circulatory insufficiency decrease.
With an overdose of glycosides, characteristic ECG signs appear (Fig. 16), which, depending on the severity of intoxication, require either dose adjustment or drug withdrawal. Patients with glycoside intoxication may experience nausea, vomiting, interruptions in the work of the heart.
Rice. 16. ECG with an overdose of cardiac glycosides
Signs of glycoside intoxication:
Shortening of the electrical systole;
Decrease in the S-T segment from top to bottom;
Negative T wave;
Severe intoxication with glycosides requires discontinuation of the drug and the appointment of potassium preparations, lidocaine and beta-blockers.
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Small R wave growth is a common ECG symptom that is often misinterpreted by clinicians. Although this symptom is usually associated with an anterior myocardial infarction, it can be caused by other conditions that are not associated with a heart attack.
A small increase in the R wave is detected in approximately 10% of hospitalized adult patients and is the sixth most common ECG abnormality (19,734 ECGs were collected by the Metropolitan Life Insurance Company over a 5 ¼ year period). Besides, one third of patients with a previous anterior myocardial infarction may have only this ECG symptom. Thus, elucidation of specific anatomical equivalents of this electrocardiographic phenomenon is of great clinical importance.
Before analyzing the changes in the R waves, it is necessary to recall several theoretical foundations that are necessary to understand the genesis of ventricular activation in the chest leads. Ventricular depolarization usually begins in the middle of the left side of the interventricular septum, and proceeds anteriorly and from left to right. This initial vector of electrical activity appears in the right and middle chest leads (V1-V3) as a small r wave (the so-called " septal wave r").
A small increase in the R wave can occur when the initial depolarization vector decreases in magnitude or is directed backward. After septal activation, left ventricular depolarization dominates the rest of the depolarization process. Although the depolarization of the right ventricle occurs simultaneously with the left, its force is negligible in the heart of a normal adult. The resulting vector will be directed from leads V1-V3, and will show up as deep S waves on the ECG.
Normal distribution of R waves in the chest leads.
In lead V1, the ventricular beats are rS-type, with a steady increase in the relative size of the R waves to the left leads and a decrease in the amplitude of the S-waves. Leads V5 and V6 tend to show a qR-type complex, with R-wave amplitude greater in V5 than in V6. due to attenuation of the signal by the lung tissue.Normal variations include: narrow QS and rSr" patterns in V1, and qRs and R patterns in V5 and V6. At some point, usually in position V3 or V4, the QRS complex begins to change from predominantly negative to predominantly positive and the R/S ratio becomes >1. This zone is known as " transition zone ". In some healthy people, the transition zone can be seen as early as V2. This is called " early transition zone ". Sometimes the transition zone can be delayed until V4-V5, this is called " late transition zone ", or " transition zone delay ".
Normal R-wave height in lead V3 is usually greater than 2mm
. If the height of the R waves in leads V1-V4 is extremely small, it is said that there is "insufficient or small increase in the R wave."
There are various definitions of small R-wave gain in the literature, criteria such asR waves less than 2-4 mm in leads V3 or V4and/or the presence of R wave regression (RV4< RV3 или RV3 < RV2 или RV2 < RV1 или любая их комбинация).
In myocardial necrosis due to infarction, a certain amount of myocardial tissue becomes electrically inert and unable to generate normal depolarization. The depolarization of the surrounding ventricular tissues at this time increases (since they are no longer resisted), and the resulting depolarization vector reorients away from the area of necrosis (in the direction of unhindered propagation). With anterior myocardial infarction, Q waves appear in the right and middle leads (V1-V4). However, Q waves are not preserved in a significant number of patients.
In documented cases of previous anterior myocardial infarction, a small increase in the R wave is detected in 20-30% of cases . The average time for the complete disappearance of pathological Q waves is 1.5 years.
Attracts attention decrease in R wave amplitude in lead I . Up to 85% of patients with a previous anterior myocardial infarction and a small increase in the R wave have either R wave amplitude in lead I<= 4 мм , or R wave amplitude in lead V3<= 1,5 мм . The absence of these amplitude criteria makes the diagnosis of anterior myocardial infarction unlikely (with the exception of 10%-15% of cases of anterior myocardial infarction).
If there is a small increase in R waves in the chest leads, Impaired repolarization (ST-T wave changes) in leads V1-V3 will increase the likelihood of diagnosing old anterior myocardial infarction.
Other possible causes of insufficient growth of the R wave in the chest leads are:
- complete / incomplete blockade of the left leg of the bundle of His,
- blockade of the anterior branch of the left leg of the bundle of His,
- the Wolf-Parkinson-White phenomenon,
- certain types of right ventricular hypertrophy (especially those associated with COPD),
- left ventricular hypertrophy
- right ventricular hypertrophy type C.
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| Acute anterior MI |
Another common reason for a small increase in the R wave is the incorrect location of the electrodes: too high or too low location of the chest electrodes, the location of the electrodes from the limbs to the body.
Most often, the high position of the right chest electrodes leads to insufficient growth of the R waves. When the electrodes are moved to the normal position, the normal growth of the R waves is restored, however in old anterior myocardial infarction, QS complexes will persist
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Unfortunately, these criteria turned out to be of little use for diagnosis and give many false-negative and false-positive results.
A connection was found between a small increase in the R wave on the ECG and diastolic dysfunction in patients with diabetes mellitus, so this symptom may be an early sign of LV dysfunction and DCM in diabetics.
References.
- Electrocardiographic Poor R-Wave Progression. Correlation with Postmortem Findings. Michael I. Zema, M.D., Margaret Collins, M.D.; Daniel R. Alonso, M.D.; Paul Kligfield, M.D.CHEST, 79:2, FEBRUARY, 1981
- Diagnostic value of poor R-wave progression in electrocardiograms for diabetic cardiomyopathy in type 2 diabetic patients/ CLINICAL CARDIOLOGY, 33(9):559-64 (2010)
- Poor R Wave Progression in the Precordial Leads: Clinical Implications for the Diagnosis of Myocardial Infarction NICHOLAS L. DePACE, MD, JAY COLBY, BS, A-HAMID HAKKI, MD, FACC, BRUNOMANNO, MD, LEONARD N. HOROWITZ, MD, FACC , ABDULMASSIH S. ISKANDRIAN, MD, FACC. JACC Vol. 2. No. 6 December 1983"1073-9
- Poor R-Wave Progression. J InsurMed 2005;37:58–62. Ross MacKenzie, MD
- Dr. Smith's ECG Blog. Monday, June 6, 2011
- Dr. Smith's ECG Blog. Tuesday, July 5, 2011
- http://www.learntheheart.com/ Poor R Wave Progression (PRWP) ECG
- http://clinicalparamedic.wordpress.com/ R-Wave Progression: Is it important? YOU BET!!