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When an excitation pulse leaves the sinus node, it begins to be recorded by the cardiograph. Normally, excitation of the right atrium (curve 1) begins somewhat earlier than the left (curve 2) atrium. The left atrium starts later and finishes arousal later. The cardiograph registers total vector both atria by drawing P wave: The ascent and descent of the P wave is usually gentle, the apex is rounded.

• A positive P wave is indicative of sinus rhythm.
• The P wave is best seen in 2 standard lead, in which it must be necessarily positive.
• Normally, the duration of the P wave is up to 0.1 seconds (1 large cell).
• The amplitude of the P wave should not exceed 2.5 cells.
• The amplitude of the P wave in standard leads and in leads from the limbs is determined by the direction of the electrical axis of the atria (they will be discussed later).
• Normal amplitude: P II> P I> P III.

The P wave can be serrated at the apex, while the distance between the teeth should not exceed 0.02 s (1 cell). The activation time of the right atrium is measured from the beginning of the P wave to its first apex (no more than 0.04 s - 2 cells). The activation time of the left atrium is from the beginning of the P wave to its second apex or to the highest point (no more than 0.06 s - 3 cells).

The most common variants of the P wave are shown in the figure below:

The table below describes how the P wave should be in different leads.

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R wave(basic ECG wave) is caused by excitation of the ventricles of the heart (for more details, see "Excitation in the myocardium"). The amplitude of the R wave in standard and reinforced leads depends on the location of the electrical axis of the heart (EOS). With a normal arrangement of the e.o. R II> R I> R III.

• The R wave may be absent in enhanced lead aVR;
• With a vertical arrangement of the e.o. R wave may be absent in lead aVL (on the ECG on the right);
• Normally, the amplitude of the R wave in lead aVF is greater than in standard lead III;
• V chest leads V1-V4 the amplitude of the R wave should increase: R V4> R V3> R V2> R V1;
• Normally, in lead V1, the r wave may be absent;
• In young people, the R wave may be absent in leads V1, V2 (in children: V1, V2, V3). However, such an ECG is often a sign of myocardial infarction of the anterior interventricular septum of the heart.

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Small R-wave gains are common symptomatic ECG, which is often misinterpreted by doctors. Although this symptom is usually associated with anterior myocardial infarction, it can also be caused by other non-infarction conditions.

A small increase in the R wave is detected approximately in 10% of hospitalized adult patients and is the sixth most common ECG abnormality (19,734 ECGs were collected by Metropolitan Life Insurance Company over a 5 ¼ year period). Moreover, one third of patients with previous anterior myocardial infarction may only have this symptom on the ECG. Thus, the elucidation of specific anatomical equivalents of this electrocardiographic phenomenon is of great clinical importance.

Normal distribution of R-waves in the chest leads.

Normal R wave height in lead V3 is usually more than 2 mm ... 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 low R-wave gain in the literature, criteria such asR waves less than 2-4 mm in leads V3 or V4and / or the presence of a reverse growth of the R wave (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. Depolarization of the surrounding tissues of the ventricles at this time increases (since they no longer have resistance), and the resulting depolarization vector is reoriented in the direction from the necrosis zone (in the direction of unhindered propagation). With anterior myocardial infarction, Q waves appear in the right and middle leads (V1-V4). However, in a significant number of patients, Q waves are not preserved.

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.

Noteworthy decrease in the amplitude of the R wave in lead I ... Up to 85% of patients with anterior myocardial infarction and low R-wave growth have either the amplitude of the R waves 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 (except for 10% -15% of cases of anterior myocardial infarction).

In the presence of a small increase in the R waves in the chest leads, violation of repolarization (ST-T changes) in leads V1-V3 will increase the likelihood of diagnosing old anterior myocardial infarction.

Other possible causes of insufficient R-wave growth in the chest leads are:

• complete / incomplete left bundle branch block,
• blockade of the anterior branch of the left bundle branch,
• Wolff-Parkinson-White phenomenon,
• some types of right ventricular hypertrophy (especially those associated with COPD),
• left ventricular hypertrophy
• right ventricular hypertrophy type C.

Acute anterior MI

Another common reason for a small increase in the R wave is improper placement of the electrodes: too high or too low location of the chest electrodes, the location of the electrodes from the limbs on the trunk.

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 with old anterior myocardial infarction, QS complexes will persist .

A relationship was found between a small increase in the R wave on the ECG and diastolic dysfunction in patients with diabetes mellitus; therefore, this symptom may be an early sign of LV dysfunction and DCM in diabetics.

References.

1. 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
2. Diagnostic value of poor R-wave progression in electrocardiograms for diabetic cardiomyopathy in type 2 diabetic patients / CLINICAL CARDIOLOGY, 33 (9): 559-64 (2010)
3. 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
4. Poor R-Wave Progression. J Insur Med 2005; 37: 58-62. Ross MacKenzie, MD
5. Dr. Smith "s ECG Blog. Monday, June 6, 2011
6. Dr. Smith "s ECG Blog. Tuesday, July 5, 2011
7. http://www.learntheart.com/ Poor R Wave Progression (PRWP) ECG
8. http://clinicalparamedic.wordpress.com/ R-Wave Progression: Is it important? YOU BET !!

P wave- is formed as a result of excitation of two atria. It begins to register immediately after the impulse leaves the sinus node. The left atrium begins and ends later its excitement, as a result of overlapping excitations of the left and right atrium, a tooth is formed. The amplitude of the P wave is usually greatest in the II century. lead. Normally, the duration of P is up to 0.1 s, the amplitude should not exceed 2.5 mm. In lead aVR, the wave is always negative. The P wave may be serrated at the apex, but the distance between the notches should not exceed 0.02 s.

PQ interval- from the beginning of the P wave to the beginning of the Q wave. It corresponds to the time of passage of excitation through the atria and the AV connection to the ventricular myocardium. Changes depending on the heart rate, on the age and body weight of the patient. Normally, the PQ interval is 0.12 - 0.18 (up to 0.2 s). Thus, the PQ interval includes the P wave and the PQ segment.

Macruz Index... This is the ratio of the duration of the P wave to the duration of the PQ segment. Normally -1.1 - 1.6. This index helps in the diagnosis of atrial hypertrophy.

QRS complex- ventricular complex. This is usually the largest ECG deviation. The width of the QRS complex is normally 0.06 - 0.08 s and indicates the duration of intraventricular conduction of excitation. With age, the width of the QRS complex. The amplitude of the QRS complex waves usually varies. Normally, in at least one of the standard leads or in the limb leads, the amplitude of the QRS complex should exceed 5 mm, and in the chest leads - 8 mm. In any of the chest leads in adults, the amplitude of the QRS complex should not exceed 2.5 cm.

Q wave- the initial tooth of the QRS complex. it is recorded during excitation of the left half of the interventricular septum. Registration of the q wave of even a small amplitude in leads V1-V3 is a pathology. Normally, the width of the q wave should not exceed 0.03 s, and its amplitude in each lead should be less than 1/4 of the amplitude of the following R wave in this lead.

R wave- usually the main wave of the ECG. It is caused by excitation of the ventricles, and its amplitude in standard leads and in leads from the limbs depends on the position of the electrical axis of the heart. With the normal position of the electrical axis and RII> RI> RIII. The R wave may be missing in lead aVR. In the chest leads, the R wave should grow in amplitude from V1 to V4.

S wave- mainly due to the final excitation of the base of the left ventricle. This tooth may be absent normally, especially in the limb leads. In the chest leads, the largest amplitude of the S wave is in leads V1 and V2. The width S in any case should not exceed 0.03 s.

The ST segment - corresponds to that period of the cardiac cycle when both ventricles are completely engulfed in excitement. The point where the QRS complex ends is designated as ST - connection, or point J. The ST segment directly passes into the T wave. The ST segment is normally located on the isoline, but it can be slightly raised or lowered. Normally, the ST segment can be located even 1.5 - 2 mm above the isoline. In healthy people, this is combined with a subsequent high positive T wave and has a concave shape. In cases where the ST segment is not located on the contour, its shape is described as concave, convex, or horizontal. The duration of this segment is not of great diagnostic value, and is usually not determined.

T wave... Recorded during ventricular repolarization. This is the most labile ECG wave. The T wave is normally usually positive. normally, the T wave is not serrated. The T wave is usually positive in those leads where the QRS complex is mainly represented by the R wave. In leads. where in this complex mainly negative teeth are recorded, there is a tendency to register negative S. In lead aVR, T should always be negative. The duration of this wave is from 0.1 to 0.25 s, but it has little diagnostic value. The amplitude usually does not exceed 8 mm. Normally, TV1 is necessarily higher than TV6.

QT interval... This is the electrical systole of the ventricles. The QT interval is the time in seconds from the beginning of the QRS complex to the end of the T wave. Depends on gender, age and heart rate. Normally, the duration of the QT interval is 0.35 - 0.44 s. QT is a constant for a given heart rate separately for males and females. There are special tables in which the standards for the electric systole of the ventricles for a given gender and rhythm frequency are presented. To identify gross violations in the duration of the QT interval in this patient, various formulas are presented, the most common in practical use is the Bazett formula. This formula compares the conditional calculated QT interval with its duration in a given patient and with the duration of the cardiac cycle (the distance between two adjacent R waves in seconds).

Normally, the mass of the left ventricle is approximately 3 times the mass of the right ventricle. With left ventricular hypertrophy, its predominance is even more pronounced, which leads to an increase in EMF and the excitation vector of the left ventricle. The duration of excitation of the hypertrophied ventricle also increases due to not only its hypertrophy, but also the development of dystrophic and sclerotic changes in the ventricle.

Characteristic features of the ECG during the period of excitation of the hypertrophied left ventricle:

in the right chest leads V1, V2, an ECG of the rS type is recorded: the r V1 wave is caused by the excitation of the left half of the interventricular septum; S wave V1 (its amplitude is more than normal) is associated with the excitation of a hypertrophied left ventricle;

in the left chest leads V5, V6, an ECG of the qR type (sometimes qRs) is recorded: the q wave of V6 (its amplitude is higher than normal) is caused by the excitation of the hypertrophied left half of the interventricular septum; R V6 wave (its amplitude and duration are higher than normal) is associated with the excitation of a hypertrophied left ventricle; the presence of the s wave of V6 is associated with excitation of the base of the left ventricle.

Characteristic features of the ECG during repolarization of the hypertrophied left ventricle:

the ST V1 segment is above the isoline;

T wave V1 positive;

the ST V6 segment is below the isoline;

T wave V6 negative asymmetric.

Diagnosis "left ventricular hypertrophy" is set based on the analysis of the ECG in the chest leads:

high teeth R V5, R V6 (R V6> R V5> R V4 - a clear sign of left ventricular hypertrophy);

deep teeth S V1, S V2;

the more hypertrophy of the left ventricle, the higher R V5, R V6 and deeper S V1, S V2;

segment ST V5, ST V5 with an arc facing upward convexity, located below the isoline;

T wave V5, T V6 negative asymmetric with the greatest decrease at the end of the T wave (the greater the height of the R V5, R V6 wave, the more pronounced the decrease in the ST segment and the negativity of the T wave in these leads);

segment ST V1, ST V2 with an arc facing downward convexity, located above the isoline;

tooth T V1, T V2 positive;

in the right chest leads, there is a rather significant rise in the ST segment and an increase in the amplitude of the positive T wave;

the transition zone with left ventricular hypertrophy is often displaced to the right chest leads, while the T V1 wave is positive, and the T V6 wave is negative: T V1> T V6 syndrome (normally the opposite). Syndrome T V1> T V6 is an early sign of left ventricular hypertrophy (in the absence of coronary insufficiency).

The electrical axis of the heart with left ventricular hypertrophy is often moderately deviated to the left or located horizontally (a sharp left deviation is not typical for isolated left ventricular hypertrophy). The normal position of the EOS is less often observed; even more rarely, the semi-vertical position of the e.s.s.

Typical signs of ECG in the leads from the extremities with left ventricular hypertrophy (e.o. is located horizontally or deviated to the left):

The ECG in leads I, aVL is similar to the ECG in leads V5, V6: it looks like qR (but the teeth are of smaller amplitude); the ST I, aVL segment is often located below the isoline and is accompanied by a negative asymmetric T I, aVL wave;

An ECG in leads III, aVF is similar to an ECG in leads V1, V2: it looks like rS or QS (but with a smaller amplitude); segment ST III, aVF is often elevated above the isoline and merges with the positive wave of T III, aVF;

the T III wave is positive, and the T I wave is low or negative, therefore, T III> T I is characteristic of left ventricular hypertrophy (in the absence of coronary insufficiency).

Typical signs of ECG in the leads from the extremities with left ventricular hypertrophy (e.o. is located vertically):

in leads III, aVF there is a high R wave; as well as a decrease in the ST segment and a negative T wave;

in leads I, aVL there is a r wave of small amplitude;

in lead aVR ECG looks like rS or QS; T wave aVR positive; the ST aVR segment is located on the isoline or slightly above it.

An exercise test is used to detect latent coronary insufficiency, for differential diagnosis of coronary heart disease with other diseases, assessment of coronary circulation reserves, physical ability, detection of transient arrhythmias and conduction disturbances and differentiation of their functional and organic nature, determination of the prognosis of the disease, etc. ... Physical activity increases myocardial oxygen demand and blood flow through the coronary vessels.

The standardized method is the test of the Master. Taking into account the sex, age and body weight of patients.

The non-standardized method is based on determining the magnitude of the load, depending on the capabilities of the individual: Bicycle ergometric test and treadmill test.

SSSU, principles of treatment.

ECG-diagnostics of SSSS In case of dysfunctions of the CA-node, electrocardiographic signs of sinus dysfunctions can be registered long before the onset of clinical symptoms. 1. Sinus bradycardia - slowing down of sinus rhythm with a heart rate of less than 60 per minute. due to the reduced automatism of the sinus node. In SSSS, sinus bradycardia is persistent, long-lasting, refractory to exercise and the administration of atropine (Fig. 1). 2. Bradystolic form of atrial fibrillation (MA, atrial fibrillation, atrial fibrillation, absolute arrhythmia, atrial fibrillation, vorhofflimmern, arrhythmia perpetua, delirium cordis, arrhythmia completa) - chaotic, fast and irregular non-coordinated atrial fibrillation atrial impulses with a frequency of 350 to 750 per minute, causing a complete disorder of ventricular contractions. In the bradystolic form of MA, the number of ventricular contractions is less than 60 per minute. (fig. 2). 3. Migration of the pacemaker through the atria (wandering rhythm, sliding rhythm, migrating rhythm, migration of the pacemaker, wandering pacemaker). There are several variants of the wandering (wandering) rhythm: a) wandering rhythm in the sinus node. The P wave has a sinus origin (positive in leads II, III, AVF), but its shape changes with different heartbeats. The PR interval remains relatively constant. There is always pronounced sinus arrhythmia; b) a wandering rhythm in the atria. The P wave is positive in leads II, III, AVF, its shape and size change with different heartbeats. Along with this, the duration of the PR interval is changed; c) a wandering rhythm between the sinus and AV nodes. This is the most common wandering rhythm. With it, the heart contracts under the influence of impulses that periodically change their place, gradually moving from the sinus node, along the atrial muscles to the AV-connection, and again return to the sinus node. ECG criteria for the migration of the pacemaker along the atria are three or more different P waves on a series of cardiac cycles, a change in the duration of the PR interval. The QRS complex does not change (Fig. 3 and 4). 4. Passive ectopic rhythms. Decreased activity of the sinus node or complete blockade of sinus impulses due to functional or organic damage to the sinus node causes the activation of automatic centers of the II order (cells of atrial pacemakers, AV-connection), III order (His system) and IV order (Purkinje fibers, ventricular musculature ). Automatic centers of the II order cause unchanged ventricular complexes (supraventricular type), while centers of the III and IV order generate dilated and deformed ventricular complexes (ventricular, idioventricular type). The following rhythm disturbances have a substituting character: atrial, nodal, pacemaker migration along the atria, ventricular (idioventricular rhythm), jumping out contractions. 4.1. Atrial rhythm (slow atrial rhythm) is a very slow ectopic rhythm with foci of generation of impulses in the atria (Table 2): a) right atrial ectopic rhythm - the rhythm of an ectopic foci located in the right atrium. On the ECG, a negative P wave is recorded in leads V1-V6, II, III, aVF. P – Q interval of usual duration, QRST complex is not changed; b) the rhythm of the coronary sinus (the rhythm of the coronary sinus) - impulses to excite the heart come from the cells located in the lower part of the right atrium and the coronary sinus vein. The impulse propagates along the atria retrogradely from the bottom up. This leads to the registration of negative P waves in II, III, aVF leads. The P ’aVR tooth is positive. In leads V1-V6, the P wave is positive or biphasic. The PQ interval is shortened and is typically less than 0.12 s. The QRST complex is not changed. The rhythm of the coronary sinus may differ from the right atrial ectopic rhythm only by the shortening of the PQ interval; c) left atrial ectopic rhythm - impulses to excite the heart come from the left atrium. At the same time, a negative P wave is recorded on the ECG in leads II, III, aVF, V3 – V6. The appearance of negative P waves in I, aVL is also possible; P wave in aVR is positive. A characteristic sign of the left atrial rhythm is the P wave in lead V1 with an initial rounded dome-shaped part, followed by a pointed peak - "shield and sword" ("dome and spire", "bow and arrow"). The P wave 'precedes the QRS complex with a normal PR interval of 0.12–0.2 s. The atrial rate is 60–100 per minute, rarely below 60 (45–59) per minute. or more than 100 (101–120) per min. The rhythm is correct, the QRS complex is not changed (Fig. 5); d) lower atrial ectopic rhythm - the rhythm of an ectopic focus located in the lower parts of the right or left atrium. This leads to the registration of negative P 'waves in II, III, aVF leads and a positive P' wave in aVR. The PQ interval is shortened (Fig. 6). 4.2. Nodal rhythm (AV-rhythm, replacing AV nodal rhythm) - heart rate under the influence of impulses from the AV-connection with a frequency of 40-60 per minute. There are two main types of AV rhythm: a) nodal rhythm with simultaneous excitation of the atria and ventricles (nodal rhythm without P 'wave, nodal rhythm with AV dissociation without P' wave): an unchanged or slightly deformed QRST complex, P wave is recorded on the ECG absent (fig. 7); b) the junctional rhythm with different-temporal excitation of the ventricles and then the atria (junctional rhythm with a retrograde P ’wave, an isolated form of the AV rhythm): an unchanged QRST complex is recorded on the ECG, followed by a negative P wave (Fig. 8). 4.3. Idioventricular (ventricular) rhythm (intrinsic ventricular rhythm, ventricular automatism, intraventricular rhythm) - impulses of ventricular contraction occur in the ventricles themselves. ECG criteria: widened and deformed QRS complex (more than 0.12 s), rhythm with a heart rate of less than 40 (20-30) per minute. Terminal idioventricular rhythm is very slow and unstable. The rhythm is more often correct, but may be incorrect in the presence of several ectopic foci in the ventricles or one foci with varying degrees of impulse formation or blockade at the exit ("exit block"). If atrial rhythm is present (sinus rhythm, atrial fibrillation / flutter, ectopic atrial rhythm), then it does not depend on the ventricular rate (AV dissociation) (Fig. 9). 5. Sinoauricular block (blockade of the exit from the CA-node, dissociatio sino-atriale, SA-block) - a violation of the formation and / or conduction of an impulse from the sinus node to the atria. SA blockade occurs in 0.16–2.4% of people, mainly in people over 50–60 years old, more often in women than in men. 5.1. Sinoauricular block of the 1st degree is manifested by a slowed-down formation of impulses in the sinus node or a slower conduction of them to the atria. A conventional ECG is uninformative, diagnosed by electrical atrial stimulation or by recording the potentials of the sinus node and based on changes in conduction time in the sinus node. 5.2. Sinoauricular block II degree is manifested by partial conduction of impulses from the sinus node, which leads to loss of atrial and ventricular contractions. There are two types of II degree sinoauricular block: II degree sinoauricular block of type I (with the Samoilov – Wenckebach period): a) progressive shortening of the PP intervals (Samoilov – Wenckebach period), followed by a long PP pause; b) the greatest distance PP - during a pause at the time of loss of heart contraction; c) this distance is not equal to two normal PP intervals and less than their duration; d) the first PP interval after the pause is longer than the last PP interval before the pause (Fig. 10). Sinoauricular block II degree II type: a) asystole - lack of electrical activity of the heart (P wave and QRST complex are absent), atrial and ventricular contraction falls out; b) a pause (asystole) is a multiple of one normal RR (PP) interval or equal to two normal RR (PP) periods of the main rhythm (Fig. 11). Far-reaching sinoauricular block II degree II type. By analogy with AV block, prolonged SA blockade 4: 1, 5: 1, etc. should be called a distant SA-blockade of the II degree of type II. In some cases, the pause (isoelectric line) is interrupted by slipping out complexes (rhythms) from the atrial centers of automatism or, more often, from the area of ​​the AV connection. Sometimes lagging sinus impulses meet (coincide) with AB slip impulses. On the ECG, rare P waves are located in close proximity to the escape QRS complexes. These P waves are not held to the ventricles. The emerging AV dissociation can be complete and incomplete with ventricular seizures. One of the variants of incomplete AV dissociation, when each escaping complex is followed by the capture of the ventricles by a sinus impulse, is called escape-capture-bigemini (bigeminy of the "slip-capture" type). 5.3. Grade III sinoauricular block (complete sinoauricular block) is characterized by the absence of excitation of the atria and ventricles from the sinus node. Asystole occurs and continues until the automatic center of the II, III or IV order begins to operate (Fig. 12). 6. Stopping the sinus node (sinus node failure, sinus arrest, sinus pause, sinus – inertio) - periodic loss of the sinus node's ability to generate impulses. This leads to loss of excitement and contraction of the atria and ventricles. There is a long pause on the ECG, during which the P, QRST waves are not recorded and the isoline is recorded. The pause when stopping the sinus node is not a multiple of one RR (PP) interval (Fig. 13). 7. Atrial arrest (atrial asystole, atrial standstill, partial asystole) - the absence of atrial excitation, which is observed during one or (more often) more cardiac cycles. Atrial asystole can be combined with asystole of the ventricles, in such cases there is complete asystole of the heart. However, during atrial asystole, pacemakers of the II, III, IV order usually begin to function, which cause excitation of the ventricles (Fig. 14). There are three main options for stopping the atria: a) stopping the atria together with the failure (stopping) of the CA-node: the P waves are absent, as are the electrograms of the CA-node; a slow replacement rhythm is recorded from the AV connection or from the idioventricular centers. A similar phenomenon can be encountered with severe quinidine and digitalis intoxication (Fig. 14); b) the absence of electrical and mechanical activity (arrest) of the atria while maintaining the automatism of the CA-node, which continues to control the excitation of the AV- node and ventricles. Such a picture is observed in severe hyperkalemia (> 9-10 mm / l), when the correct rhythm appears with broadened QRS complexes without P waves. This phenomenon is called synoventricular conduction; c) maintaining the automatism of the CA-node and electrical activity of the atria (P waves) in the absence of their contractions. Syndrome Electromechanical dissociation (disconnection) in the atria can sometimes be observed in patients with dilated atria after their electrical defibrillation. Permanent stop, or paralysis, of the atria is rare. In the literature, there are reports of atrial paralysis in cardiac amyloidosis, widespread atrial fibrosis, fibroelastosis, fat infiltration, vacuolar degeneration, neuromuscular dystrophies, in the terminal period of heart disease. 8. Syndrome of bradycardia / tachycardia (tachy / brady syndrome). With this option, there is an alternation of a rare sinus or replacement supraventricular rhythm with attacks of tachysystole (Fig. 15). The clinical assessment of the function of the sinus node of the SSS should be considered as a probable diagnosis in patients with the symptoms described above. The most complex electrophysiological studies should be carried out only when the diagnosis of sinus node dysfunction raises certain doubts. Valsalva test. The simplest vagal tests with a breath holding on a deep inspiration (including the Valsalva test), carried out in isolation or in combination with straining, sometimes reveal sinus pauses exceeding 2.5-3.0 s, which must be differentiated with pauses caused by violations AB-conducting. The identification of such pauses indicates an increased sensitivity of the sinus node to vagal influences, which can occur both with VDSU and with CVS. If such pauses are accompanied by clinical symptoms, an in-depth examination of the patient is required in order to determine tactics. treatment ... Massage of the carotid sinus. The carotid sinus is a small formation of the autonomic nervous system located at the beginning of the internal carotid artery above the bifurcation of the common carotid artery. Carotid sinus receptors are associated with the vagus nerve. The reflex of the carotid sinus under physiological conditions causes bradycardia and hypotension due to irritation of the vagus nerve and the vascular regulatory center in the medulla oblongata. With a hypersensitive (hypersensitive) carotid sinus, pressure on it can cause sinus pauses in excess of 2.5–3.0 s, accompanied by a short-term disorder of consciousness. Before massage of the carotid zones, such patients are shown to assess the state of blood flow in the carotid and vertebral arteries, because massage of arteries with pronounced atherosclerotic changes can lead to sad consequences (severe bradycardia up to loss of consciousness and asystole!). It is important to emphasize that carotid sinus syndrome can, on the one hand, develop against the background of the normal function of the sinus node, and on the other hand, it does not exclude the presence of SSS. Tilt test. Tilt-test (passive orthostatic test) is considered today as the "gold standard" in the examination of patients with syncope conditions of unknown etiology. Load testing (bicycle ergometry, treadmill test). Exercise testing evaluates the ability of the sinus node to accelerate the rhythm in accordance with the internal physiological chronotropic stimulus. Holter monitoring. Ambulatory Holter monitoring, if performed during normal daytime activity, appears to be a more valuable physiological method for assessing sinus node function than exercise testing. The alternating appearance of bradyarrhythmias and tachyarrhythmias in patients with CVS is often not detected on a conventional electrocardiogram at rest. Study of the sinus node function by the CPES method. An indicator of the automatic activity of the sinus node is the duration of the sinus pause from the moment of termination of stimulation (the last artifact of the electrical stimulus) to the beginning of the first independent wave of P. This period of time is called the recovery time of the sinus node function (VFSU). Normally, the duration of this period does not exceed 1500-1600 ms. In addition to VVFSU, one more indicator is calculated - the corrected time of restoration of the sinus node function (CVVFSU), which takes into account the duration of the VVFSU indicator in relation to the initial frequency of the sinus rhythm. Treatment SSSU At the beginning of SSSU therapy, all drugs that can contribute to conduction disturbances are canceled. In the presence of tachy-brady syndrome, tactics can be more flexible: with a combination of moderate sinus bradycardia, which is not yet an indication for the installation of a permanent pacemaker, and frequent brady-dependent paroxysms of atrial fibrillation, in some cases, it is possible to prescribe allapinin in a small dose (1/2 tab 3-4 r. / Day) followed by mandatory control during Holter monitoring. However, over time, the progression of conduction disorders may require discontinuation of drugs, followed by the installation of a pacemaker. While maintaining bradycardia, the simultaneous use of belloid 1 tab is permissible. 4 rubles / day or teopeka 0.3 g 1/4 tab. 2-3 rubles / day It is necessary to exclude hyperkalemia or hypothyroidism, in which the patient may be mistakenly directed to the installation of a permanent pacemaker. If you suspect SSS, you should refrain from prescribing sinus node suppressants before Holter monitoring and special tests. Appointment of β-blockers, calcium antagonists (verapamil, diltiazem), sotalol, amiodarone, cardiac glycosides is inappropriate. In cases of acute development of SSSU, first of all, etiotropic treatment... If its inflammatory genesis is suspected, administration of prednisolone 90–120 mg IV or 20–30 mg / day is indicated. inside. In acute myocardial infarction, anti-ischemic drugs (nitrates), antiplatelet agents (acetylsalicylic acid, clopidogrel), anticoagulants (heparin, low molecular weight heparins), cytoprotectors (trimetazidine) are prescribed. Emergency therapy of the actual SSS is carried out depending on its severity. In cases of asystole, MAS attacks, resuscitation measures are required. Severe sinus bradycardia, which worsens hemodynamics and / or provokes tachyarrhythmias, requires the appointment of atropine 0.5–1.0 ml of 0.1% s / c solution up to 4–6 r. / Day, infusion of dopamine, dobutamine or aminophylline under the control of a cardiac monitor ... For prophylactic purposes, a temporary endocardial stimulator can be installed.

The table on the right shows the ECG (in 12 leads) of two patients: a healthy person and a patient with a diagnosis " severe right ventricular hypertrophy"(bases: deviation of the EOS to the right; dominant R wave V1; inversion of the T wave in the right chest leads V1, V2). ECG tape speed - 25 mm / s (1 cell horizontally = 0.04 s).

Quantitative signs of right ventricular hypertrophy

R V1> 7 mm;

S V1, V2 ≤ 2 mm;

1. R V5, V6< 5 mm;

   R V1 + S V5 (V6)> 10.5 mm;

   R aVR> 4 mm;

   negative T V1 with a decrease in ST V1, V2 (R V1> 5 mm) in the absence of coronary insufficiency.

ECG conclusion

Right ventricular hypertrophy- if with ECG signs of right ventricular hypertrophy there is a high R V1, V2 wave without changes from the ST segment V1, V2 and T wave V1, V2.

Right ventricular hypertrophy with overload- if with ECG signs of right ventricular hypertrophy, a high R V1, V2 wave is observed in combination with a decrease in the ST segment V1, V2 and a negative T V1, V2 wave.

Hypertrophy of the right ventricle with its overload and pronounced changes in the myocardium- if a high R wave with a decrease in the ST segment and a negative T wave is observed not only in leads V1, V2, but also in other chest leads.

Systolic overload of the right ventricle is manifested by spatial displacement of the QRS loop to the right and anteriorly, the T loop to the left and back. The centripetal part of the QRS loop moves anteriorly from the isoelectric point, as a result of which the QRS loop is recorded clockwise in the horizontal plane.

"Diastolic" overload of the right ventricle is manifested by an increase in the final deviation of the QRS loop, directed to the right and upward (forward or backward), in the absence of changes from the other parts of the QRS loop and T.

ECG signs of extrasystoles:

Premature ventricular QRST complex and / or P wave (main symptom);

full compensatory pause - a pause that occurs after a ventricular extrasystole, while the distance between two sinus complexes P-QRST is equal to twice the R-R interval of the main rhythm;

incomplete compensatory pause - a pause that occurs after an atrial extrasystole (extrasystoles from the atrioventricular junction), while the duration of the pause is slightly longer than the usual P-P interval of the main rhythm;

allorhythmy - the correct alternation of extrasystoles and normal contractions:

• bigeminia - the occurrence of extrasystoles after each normal contraction;

  trigeminia - after every two normal heart contractions;

  quadrigimation - after every three normal contractions.

Treatment of supraventricular extrasystoles

adherence to a rational regime: quitting smoking, alcohol, strong tea and coffee, creating a favorable psycho-emotional environment;

potassium diet and potassium salts;

sedatives (tinctures of valerian, motherwort, corvalol - 20-30 drops 3-4 times a day);

antiarrhythmic drugs:

• beta blockers (propranolol 10 mg 4 times a day; metoprolol- 50 mg 2 times a day);

  calcium antagonists (verapamil- 40 mg 3-4 times a day);

  cardiac glycosides in the event of heart failure ( digoxin, isolanide- 0.25 mg 2 times a day);

  Class Ia drugs (quinidine 0.25 g 1-3 times a day).

1. Normal sinus rhythm

Sinus rhythm is the rhythm that leaves the sinus node, which is an automatic center of the first order (for more details, see "The conduction system of the heart"). In healthy people, the rhythm is always sinus. However, sinus rhythm can also be observed in patients. The rhythm frequency (heart rate - HR) is normally in the range of 60-80 beats per minute.

Criteria for normal sinus rhythm are:

1. The presence of a p wave of sinus origin, which precedes the qrs complex:

the P wave must be positive in standard lead II and negative in lead aVR;

in the rest of the limb leads, the shape of the P wave can be different depending on the orientation of the electrical axis of the heart (e.s.) - in most cases, the P wave is positive in leads I, aVF;

in the chest leads V1, V2, the P wave, as a rule, is biphasic;

in the rest of the chest leads V3-V6, the P wave is usually positive at normal sinus rhythm, but there may be options depending on the location of the EOS.

constant and normal (0.12-0.2 s) distance of the PQ interval (each P wave must be followed by a QRS complex and a T wave);

constant shape of the P wave in all leads (the shape of the P wave can change in some leads during breathing, in this case, an ECG is recorded while holding the breath);

Heart rate within 60-80 beats per minute;

constant distance between teeth P (R) - differences in distance between teeth should not exceed 10%.

1. With atrial fibrillation, frequent (350-700 per minute) random, chaotic excitation and contraction of individual groups of atrial muscle fibers is observed.

ECG signs:

Absence in all leads of the P wave;

The presence throughout the entire cardiac cycle of random small waves f, having a different shape and amplitude. Best in leads (V1, V2, II, III, and aVF)

Irregularity of ventricular complexes QRS - irregular ventricular rhythm

The presence of QRS complexes, which in most cases have a normal unchanged appearance without deformation and widening.

Drug therapy

The following areas of drug therapy for atrial fibrillation are distinguished: cardioversion (restoration of normal sinus rhythm), prevention of repeated paroxysms (episodes) of supraventricular arrhythmias, control of the normal heart rate. Also, an important goal of drug treatment for AF is to prevent complications - various thromboembolisms. Drug therapy is carried out in four directions.

Treatment with antiarrhythmics. It is used if a decision is made to attempt drug cardioversion (rhythm restoration with medication). Drugs of choice - propafenone, amiodarone.

Propafenone Is one of the most effective and safest medicines used to treat supraventricular and ventricular heart rhythm disturbances. The action of propafenone begins 1 hour after ingestion, the maximum plasma concentration is reached after 2-3 hours and lasts 8-12 hours.

Heart rate control. If it is impossible to restore the normal rhythm, it is necessary to bring the atrial fibrillation to the norm. For this purpose, beta-blockers, calcium antagonists of the nondihydropyridine series (verapamil group), cardiac glycosides, etc. are used.

Beta-blockers... Drugs of choice for monitoring heart function (frequency and strength of contractions) and blood pressure. The group blocks beta-adrenergic receptors in the myocardium, causing a pronounced antiarrhythmic (decrease in heart rate), as well as hypotensive (decrease in blood pressure) effect. Beta blockers have been shown to statistically increase life expectancy in heart failure. Among the contraindications for admission is bronchial asthma (since the blocking of beta 2-receptors in the bronchi causes bronchospasm).

Anticoagulant therapy. To reduce the risk of thrombus formation in persistent and chronic forms of AF, blood thinners must be prescribed. Anticoagulants are prescribed direct (heparin, fraxiparin, fondaparinux, etc.) and indirect (warfarin) action. There are schemes for taking indirect (warfarin) and so-called new anticoagulants - antagonists of blood coagulation factors (pradaxa, xarelto). Treatment with warfarin is accompanied by mandatory monitoring of clotting parameters and, if necessary, careful adjustment of the dosage of the drug.

Metabolic therapy. Metabolic drugs include drugs that improve nutrition and metabolic processes in the heart muscle. These drugs allegedly have a cardioprotective effect, protecting the myocardium from the effects of ischemia. Metabolic therapy for AF is considered an adjunctive and optional treatment. According to the latest data, the effectiveness of many drugs is comparable to placebo. These medicines include:

• ATP (adenosine triphosphate);

  ions K and Mg;

  cocarboxylase;

  riboxin;

  mildronate;

  predicted;

  A normal ECG consists mainly of P, Q, R, S, and T waves.
  Between the individual teeth are the PQ, ST and QT segments, which are of clinical importance.
  The R wave is always positive, and the Q and S waves are always negative. P and T waves are normally positive.
  The spread of excitation in the ventricle on the ECG corresponds to the QRS complex.
  When they talk about the restoration of myocardial excitability, they mean the ST segment and the T wave.

  Normal ECG usually consists of P, Q, R, S, T and sometimes U waves. These designations were introduced by Einthoven, the founder of electrocardiography. He chose these lettering at random from the middle of the alphabet. The Q, R, S waves together form a QRS complex. However, depending on the lead in which the ECG is being recorded, the Q, R, or S waves may be missing. There are also PQ and QT intervals and PQ and ST segments that connect separate teeth and have a certain meaning.

  Same part of the curve ECG can be called differently, for example, the atrial wave can be called a wave or a P wave. Q, R and S can be called a Q wave, an R wave and an S wave, and P, T and U can be called a P wave, a T wave and a U wave. for convenience, P, Q, R, S and T, with the exception of U, will be called teeth.

  Positive prongs are located above the isoelectric line (zero line), and negative - below the isoelectric line. The P and T waves and the U wave are positive. These three waves are normally positive, but with pathology they can also be negative.

  Q and S waves is always negative and the R wave is always positive. If a second R or S wave is registered, it is designated as R "and S".

  QRS complex begins with a Q wave and lasts until the end of the S wave. This complex is usually split. In the QRS complex, high teeth are indicated by an uppercase letter, and low ones by a lowercase letter, for example, qrS or qRs.

  The end of the QRS complex is indicated by point J.

  For a beginner, the exact tooth recognition and segments is very important, so we dwell on them in detail. Each of the teeth and complexes is shown in a separate figure. For better understanding, next to the figures are the main features of these teeth and their clinical significance.

  After describing the individual teeth and segments ECG and the corresponding explanations, we will get acquainted with the quantitative assessment of these electrocardiographic indicators, in particular the height, depth and width of the teeth and their main deviations from normal values.

  P wave is normal

  The P wave, which is a wave of atrial excitation, normally has a width of up to 0.11 s. The height of the P wave changes with age, but should normally not exceed 0.2 mV (2 mm). Usually, when these parameters of the P wave deviate from the norm, we are talking about atrial hypertrophy.

  PQ interval is normal

  The PQ interval, which characterizes the time of excitation to the ventricles, is normally 0.12 ms, but should not exceed 0.21 s. This interval is lengthened in AV blocks and shortened in WPW syndrome.

  Q wave is normal

  The Q wave in all assignments is narrow and its width does not exceed 0.04 s. The absolute value of its depth is not standardized, but the maximum is 1/4 of the corresponding R wave. Sometimes, for example, with obesity, a relatively deep Q wave is recorded in lead III.
  A deep Q wave is primarily suspected of having an MI.

  R wave normal

  The R wave among all the ECG waves has the greatest amplitude. A high R wave is normally recorded in the left chest leads V5 and V6, but its height in these leads should not exceed 2.6 mV. A taller R wave indicates LV hypertrophy. Normally, the height of the R wave should increase with the transition from lead V5 to lead V6. With a sharp decrease in the height of the R wave, MI should be excluded.

  Sometimes the R wave is split. In these cases, it is denoted by uppercase or lowercase letters (for example, the R or r wave). An additional R or r wave is denoted, as already mentioned, as R "or r" (for example, in lead V1.

  S wave normal

  The S wave in its depth is characterized by significant variability depending on the lead, the position of the patient's body and his age. With ventricular hypertrophy, the S wave is unusually deep, for example, with LV hypertrophy, in leads V1 and V2.

  QRS complex is normal

  The QRS complex corresponds to the spread of excitation through the ventricles and normally should not exceed 0.07-0.11 s. Expansion of the QRS complex (but not a decrease in its amplitude) is considered pathological. It is observed, first of all, with blockages of the legs of the PG.

  J-point is normal

  Point J corresponds to the point at which the QRS complex ends.

  
  P wave... Features: the first short, semicircular tooth that appears after the isoelectric line. Meaning: excitation of the atria.
  Q wave... Features: the first negative small wave following the P wave and the end of the PQ segment. Meaning: the beginning of ventricular excitation.
  R wave... Features: The first positive wave after the Q wave or the first positive wave after the P wave if there is no Q wave. Meaning: excitement of the ventricles.
  S wave... Features: The first negative small wave after the R wave. Meaning: excitation of the ventricles.
  QRS complex... Features: Usually a cleaved complex following the P wave and PQ interval. Meaning: The spread of excitation through the ventricles.
  Point J... Corresponds to the point at which the QRS complex ends and the ST segment begins.
  T wave... Features: The first positive semicircular wave that appears after the QRS complex. Value: Restoration of ventricular excitability.
  Wave U... Features: Positive small tooth that appears immediately after the T wave. Meaning: Potential aftereffect (after restoration of ventricular excitability).
  Zero (isoelectric) line... Features: the distance between individual waves, for example, between the end of the T wave and the beginning of the next R wave. Meaning: the baseline, relative to which the depth and height of the ECG waves are measured.
  PQ interval... Features: the time from the beginning of the P wave to the beginning of the Q wave. Meaning: the time of conduction of excitation from the atria to the AV node and further through the PG and its legs.
  PQ segment... Features: the time from the end of the P wave to the beginning of the Q wave. Significance: of no clinical significance ST segment... Features: the time from the end of the S wave to the beginning of the T wave. Meaning: the time from the end of the propagation of excitation through the ventricles to the beginning of restoration of ventricular excitability. QT interval... Features: the time from the beginning of the Q wave to the end of the T wave. Meaning: the time from the beginning of the propagation of excitation until the end of the restoration of the excitability of the ventricular myocardium (electrical systole of the ventricles).
  

  ST segment is normal

  Normally, the ST segment is located on the isoelectric line, in any case, it does not deviate significantly from it. Only in leads V1 and V2 can it be above the isoelectric line. With a significant rise in the ST segment, a fresh MI should be ruled out, while a decrease in it indicates an ischemic heart disease.

  The T wave is normal

  The T wave is of clinical importance. It corresponds to the restoration of myocardial excitability and is usually positive. Its amplitude should not be less than 1/7 of the R wave in the corresponding lead (for example, in leads I, V5 and V6). With clearly negative T waves, combined with a decrease in the ST segment, MI and coronary heart disease should be excluded.

  QT interval is normal

  The width of the QT interval depends on the heart rate; it has no constant absolute values. Prolongation of the QT interval is observed with hypocalcemia and prolonged QT interval syndrome.