Материал: General propedeutics of internal diseases_Nemtsov-LM_2016

Interpretation of ECG

In the beginning of interpretation of ECG technical conditions of tape recording must be defined (voltage of the ECG and speed of a tape). The ECG graph paper records the time (interval) between cardiac electrical events along the horizontal axis and their amplitude (voltage) along the vertical axis (Fig. Suppl. 4). . It is important for correct estimation of heart rate, amplitude and duration of ECG waves and intervals (Fig. Suppl. 4).

The sequence of ECG analysis:

1.Voltage of the ECG is estimated in compliance with standard size of 1 mv =10 mm. To that end, the amplitude of R waves is measured in standard leads. Normal amplitude is 5- 15 mm. If the amplitude of the highest R wave does not exceed 5 mm in standard leads, or the sum of amplitudes of these waves in all three leads is less than 15 mm, the ECG voltage is considered decreased.

2.Speed of tape. If speed of tape is 50 mm/min – 0.02 s in 1 mm of

tape (width of QRS=3-4 mm). If speed of tape 25 mm/min – 0.04 s in 1 mm of tape (width of QRS=1-2 mm).

3. Regularity and pacemaker of the cardiac rhythm.

Since the sinoatrial node is the pacemaker of a normal heart, and the excitation of the ventricles is preceded by excitation of the atria, the P wave should come before the ventricular complex. The R-R intervals should be equal. Its fluctuations normally do not exceed 0.1 s. Greater variations in the length of the R-R intervals indicate disordered cardiac rhythm.

Sinus rhythm signs - Р-wave positive in II standard lead and corresponds (previous) to complexes QRS.

4. Heart rate (HR)

60 (seconds in 1 minutes) _____________

[R-R] (in seconds, i.e. to - in divisions х 0.02)

To that end, duration of one cardiac cycle (the R-R interval) and the number of such cycles in one minute length should be determined. For example, if one cycle lasts 0.8 s, there will be 75 such cycles in a minute (60 : 0.8 = 75). If the cardiac rhythm is irregular, the length of five or ten R-R intervals is determined, the mean R-R interval found, and the cardiac rate is finally determined as for regular cardiac rhythm. Lengths of the maximum and minimum R-R intervals are given in parentheses. Other variant of HR determination - multiply in 20 times (×20) the number of R-R intervals during 3 seconds (Fig. Suppl. 5).

5. Analysis of myocardial conduction depending duration of:

-P wave (≤0.10-0.12 s)– intraatrial conduction;

-PQ interval (0.12-0.20 s) – conduction in atrioventricular node;

-QRS complex (0.06-0.10 s) - intraventricular conduction.

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6.The position of the electrical axis of heart changes with changes of the position of the heart in the chest. The relation between the electrical axis and the magnitude of the QRS complexes in standard leads is described by the so-called Einthoven triangle. The electrical axis of the heart is determined by the shape of ventricular complexes in standard leads:

-normal electrical axis - RII> RI> RIII;

-horisontal electrical axis (levogram)- RI> RII> RIII;

-vertical electrical axis (dextrogram) - RIII> RII> RI.

7.Analysis of waves and intervals. The length and size of ECG

elements (P wave, R-Q interval and QRST complexes) are then determined in those leads where the waves are the largest (usually in lead II). Moreover, the direction of the P and T waves is determined (they can be positive and negative). Smaller and split waves can be present as well. Additional waves can appear. The shape of the ventricular complex in all leads is thoroughly examined, character of the S-T interval is noted (see Table 9-2). The length of the QRST complex (Q-T interval) depends on rate: the higher the rate, the shorter the interval.

The ECG of healthy persons depend on their age and constitution, on the posture at the moment of taking an ECG (sitting, lying), on the preceding exercise, etc. ECG may change during deep breathing (the position of the heart in the chest is changed during deep inspiration and expiration), in increased tone of the sympathetic and parasympathetic nervous systems and in some other conditions.

It is difficult to overestimate the clinical importance of electrocardiography. It is used to reveal disorders of heart activity, enlargement of heart chambers and to diagnose coronary circulatory disorders.

ECG in hypertrophy of atriums

Hypertrophy of auricles is determined by changes of P-wave.

Left atrium hypertrophy is detected by “P mitrale”: wide (>0.1 s), splitted Р-wave in I, II, AVL, left chest leads (V5-6); flat or negative Р in III, biphasic or negative (>1 mm) Р V1 (Fig. Suppl. 6). Left atrium hypertrophy is typical in mitral valves diseases (mitral stenosis and mitral incompetence).

Right atrium hypertrophy is detected by “P pulmonale”: high (>2.5 mm) acute Р in II, III, AVF and right chest leads (V1-2). Right atrium hypertrophy is typical in chronic pulmonary diseases (pulmonary heart) and tricuspid valves incompetence.

ECG in hypertrophy of ventricles

Hypertrophy of ventricles is determined mainly by changes of ventricular complex QRS (Fig. Suppl. 7). Ventricular hypertrophy causes the following changes in ECG:

(I) the position of the electrical axis is changed: in left-ventricular hypertrophy - levogram,

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in right-ventricular hypertrophy dextogram;

(2)the amplitude of the ventricular complex and its length increase,

(3)changed terminal part of the ventricular complex of the ECG because of repolarization abnormalities:

ST-segment depression and T-wave inversion in leads with a prominent R wave;

(4)in left-ventricular hypertrophy -

amplitude of the S wave increases in V1-2; amplitude of the R wave increases >20-25 mm in V4-6 sum of amplitude SV1 + RV5 (or RV6)≥35 mm;

(5)In right-ventricular hypertrophy the changes in the S and R waves are the reverse:

high R wave ≥ 7 mm appears in V1-2, deep S wave in V4-6 .

ECG in ischemic heart disease (IHD)

Acute ischemia of myocardium causes a current of injury of myocardium (Fig. Suppl. 8):

Subendocardial ischemia - the resultant ST vector directs toward the inner layer of the affected ventricle. Overlying leads therefore will record ST depression.

Transmural or epicardial ischemia - the ST vector is usually shifted in the direction of the outer (epicardial) layers, producing ST elevations and sometimes, in the earliest stages of ischemia, tall, positive so-called hyperacute T waves over the ischemic zone.

ECG in myocardial infarction

Electrocardiographic examination is especially important. It establishes the presence of myocardial infarction and also some important details of the process such as localization, depth of the process, and the size of the affected area.

Three zones of myocardial damage in acute myocardial infarction can be detected by ECG: necrotic zone, ischemic myocardium injury zone, and zone of ischemia.

Myocardial necrosis is detected by pathological Q-wave:

Pathological Q-wave is characterized by width≥0.04 s (in V4-6 >0.025 s), depth>2 mm or>1/4 R-wave (in V4-6 >15%R) (Fig. Suppl. 8).

Ischemic myocardium injury is detected by ST-interval:

-Transmural or epicardial injury - convexing elevation ST with transmission in T-wave (Fig. Suppl. 9a-b);

-Subendocardial injury – horizontal or concaving depression ST.

Ischemia of myocardium is detected by T-wave:

-Subendocardial ischemia – symmetrical acute high T-wave in overlying leads (>6 mm in standard and augmented leads, >8-10 mm in chest leads) (Fig. Suppl. 10);

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- Transmural or epicardial ischemia - symmetrical acute deep T-wave. The S-T segment and T wave change during the first hours of the disease (Table 9). The descending limb of the R wave transforms into the S-T segment without reaching the isoelectric line. The S-T segment rises above the isoelectric line to form a convexing arch and to coincide with the T wave. A monophase curve is thus formed. These changes usually persist for 3—5 days. Then the S-T segment gradually lowers to the isoelectric line while the

T wave becomes negative and deep.

A deep Q wave appears, the R wave becomes low or disappears at all. The QS wave is then formed, whose appearance is characteristic of transmural infarction.

Depending on localization of infarction, changes in the ventricular complex are observed in the corresponding leads (Table 10, Fig. Suppl. 1112). The initial shape of ECG can be restored during cicatrization, or the changes may remain for the rest of life.

Variability of ECG patterns with acute myocardial ischemia:

-Non–infarction subendocardial ischemia – transient ST depressions;

-Non–infarction transmural ischemia - transient ST elevation or

paradoxical T-wave normalization, some times followed by T-waves inversions;

-Non–Q-wave (non-ST elevation) infarction - ST depressions or T- inversions without Q-wave;

-Q-wave – infarction - Q-wave with hyperacute T-waves/ST-elevations

followed by T-waves inversions.

Exercise stress ECG testing:

Because the diagnosis of angina pectoris is usually primarily based on the patient's history, exercise testing in a patient with typical symptoms is generally used to determine functional and ECG response to graded stress (for exercise stress testing using radionuclide imaging; for exercise testing in asymptomatic persons to determine fitness for exercise programs, see below).

The patient exercises to a predetermined goal (e.g., 80 to 90% of maximal heart rate, which can be approximated as 220 less the age in years), unless distressing cardiovascular symptoms (dyspnea, reduced endurance, fatigue, hypotension, or chest pain) supervene. The ischemic ECG response during or after exercise is characterized by a flat or downward-sloping ST segment depression>0.1 millivolts (1 mm on the ECG when properly calibrated) lasting > 0.08 sec.

ECG diagnosis of sinus node automatism disorders, disordered myocardial conduction and excitability

Cardiac arrhythmia

Arrhythmias are deviations from the normal rhythm of the heart. Cardiac arrhythmias are common in many organic and functional disorders of circulatory system.

Causes of cardiac arrhythmias include:

(1)Affected automaticity of the sinus node;

(2)Foci of increased activity in the myocardium can generate impulses to initiate heart contractions apart sinus node (ectopic arrhythmia);

(3) Disorders of cardiac conduction system, local conduction disorder (re-entry mechanism);

(4) Combined changes in several functions of the heart such as automaticity, excitability, conduction or contractility.

Re-entry mechanism according to up-to-date view of point is a most common cause of cardiac arrhythmia. Re-entry mechanism means a pathological circuit of impulse because of:

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