To assess heart rate and conduction, it is necessary to determine:

1) the frequency of the rhythm;

2) the regularity of excitation of the atria and ventricles;

3) the type of atrial excitation;

4) the shape and duration of the ventricular complexes;

5) the relationship between atrial excitation and ventricular excitation;

6) for what arrhythmias are the signs identified on the ECG characteristic?

The rhythm frequency can be normal (60-90 per minute), less SCH in 1 min or more 90 in 1 min.

Regularity of rhythm. The rhythm can be regular, irregular (chaotic), regular with episodic disturbances.

The regularity of the rhythm can be periodically disrupted:

Gradual or abrupt decrease and increase in frequency;

Premature complexes;

Delay or absence of regular complexes;

The presence of the second rhythm.

Atrial excitation is reflected on the ECG by sinus P waves, ectopic P 'waves (constant or changing shape), atrial flutter (F) or fibrillation (f) waves.

The shape of the ventricular complexes in one ECG lead can be constant or unstable, change due to the initial or final parts of the QRS complex, have a form characteristic of a blockade of one or another bundle branch or its branch. The duration of the ventricular complex is either normal (up to 0.1 s inclusive), or increased moderately (0.11-0.13 s) or significantly (0.14 s and more).

The connection between the excitation of the atria and ventricles may be constant, intermittent, or absent:

P waves are recorded before each QRS complex at constant P-Q intervals of 0.12-0.20 (0.21) s;

P waves are found in front of each QRS complex at constant P-Q intervals in excess of 0.20-0.21 s;

After the P waves, the QRS complex is not always determined, and the P-Q intervals are constant or change;

P waves are fixed in front of each QRS complex with a constant P-Q interval of less than OD 2 s;

P waves are registered in front of the QRS complex, on it, after it at a constant distance;

There is no connection between atrial teeth or waves with ventricular excitation.

The analysis of the ECG in the specified sequence allows you to identify the existing violations of the heart rhythm and conduction, or, at least, to outline the circle of arrhythmias for differential diagnosis.

Recognition of arrhythmias is assisted by extended ECG recording in one lead. To assess the excitation of the atria, special leads are used (S 5. No to Lewis et al., The recording of the esophageal derivation of the ECG is even more informative).

To record the Ss lead, the electrode for the right hand (red) is placed on the handle of the sternum, the electrode for the left hand (yellow) is placed in the fifth intercostal space at the left edge of the sternum, the commutator is switched to I.

To register an ECG according to Lewis, the electrode for the left hand (yellow) is fixed in the area of ​​the apical impulse, the electrode

for the right hand (red) - to the right of the sternum at the level of the second-fourth intercostal space, the lead switch is switched to I.

To record the transesophageal lead, an electrode is used for endocardial or transesophageal pacemaker, which is connected to the chest electrode of the electrocardiograph, and the lead switch is set to V. activity (the duration of the atrial complexes is less than the duration of the ventricular complexes), the ECG is recorded at the time of holding the breath.

On a transesophageal ECG, the electrical activity of the atria is not determined only in its absence (stop of the sinus node, idioventricular rhythm) or when the rhythm is from the AV connection with simultaneous excitation of the atria and ventricles. In the first half of the RR interval, the atrial complex can be recorded either with tachycardia from the AV junction (the R-P 'interval is usually less than 0.1 s), or with tachycardia that develops against the background of WPW syndrome (the R-P' interval is usually more than OD with ). In the second half of the R-R interval, the P 'waves are determined with atrial tachycardia.

In conclusion of this chapter, we present tables for the differential diagnosis of the most common paroxysmal tachycardia and tachyarrhythmias (Table 3.2-3.6).

Grishkin Yu.N. Differential diagnosis of arrhythmias. ECG Atlas DJVU

SPb. Folio, 2000 .-- 480 p. silt - ISBN 5-93929-006-X.

Diagnosis of arrhythmias and blockages is carried out almost exclusively by electrocardiography data, and in difficult cases - using transesophageal and endocardial electrograms. This manual presents 250 electrocardiograms recorded in patients with cardiac arrhythmias and conduction disorders, covering most types of arrhythmias. Almost all of them were registered synchronously with intracardiac electrograms - atria, His bundle, less often - with transesophageal electrocardiograms. Since most practicing doctors in their daily activities do not come across such records, the beginning of the book provides basic information that allows you to more freely navigate in them. Comparison of a conventional ECG with intracardiac electrograms will allow the reader to understand the features of the formation of a conventional surface ECG in complex rhythm disturbances.

The book is divided into several chapters, each of which is devoted to a separate group of arrhythmias.

All chapters are structured in the same way: first, the main electrocardiographic (and electrophysiological) characteristics of arrhythmias and blockages are given, then electrocardiograms are given, after which detailed comments are given for each of these electrocardiograms. ECG number and comment number are the same. All ECGs were recorded at a speed of 50mm / s, on each electrocardiogram the intervals are indicated in fractions of a second and in milliseconds (ms). Each ECG has a scale bar that allows, if desired, to measure any interval independently.

Violations of the automatism of the sinus node.

Sinus tachycardia.

Sinus bradycardia.

Sinus arrhythmia.

Rigid sinus rhythm.

Manifestations of automatism of latent pacemakers.

Slip-out (replacement) complexes and rhythms.

Atrial escape complexes and rhythms.

Escaping complexes and rhythms from the AV junction.

Idioventricular (ventricular) replacement complexes and rhythms.

Accelerated slip out complexes and rhythms.

Migration of the supraventricular pacemaker.

Atrioventricular dissociation.

Electrocardiograms from No. 1.1 to No. 1.16.

Comments to ECG from no. 1.1 to no. 1.16.

Extrasystole

Sinus extrasysty.

Atrial extrasystoles.

Extrasystoles from the AV connection.

Ventricular extrasystoles.

Electrocardiograms from No. 2.1 to No. 2.39.

State educational institution of higher

Vocational education

Stavropol State Medical Academy

Ministry of Health and Social Development of the Russian Federation

I approve

head chair

internal diseases No. 1

with a course of outpatient

therapy A.V. Berry

"___" _____________ 200__

METHODOLOGICAL DEVELOPMENT

to a practical lesson for students

6 courses of the specialty "General Medicine"

on the discipline "internal diseases"

TOPIC №3. DIFFERENTIAL DIAGNOSTICS AND TREATMENT OF HEART RATE AND CONDUCTIVITY DISORDERS

LESSON # 2. DIFFERENTIAL DIAGNOSTICS AND TREATMENT OF HEART CONDUCTIVITY DISORDERS

Discussed at the meeting

Department of Internal Medicine №1

with a course of outpatient therapy

"___" _____________ 200__

Protocol No. ___

Methodical development compiled

Shnyukova T.V.

Stavropol, 200__

Topic 3. Differential diagnosis and treatment of cardiac arrhythmias and conduction disorders

Lesson 2. Differential diagnosis and treatment of cardiac conduction disorders

Study questions of the lesson:

Questions for independent work (self-study) of students:

Algorithm for differential diagnosis of cardiac conduction disorders;

Differential diagnostic signs of sinoauricular and intra-atrial blocks;

Differential diagnostic signs of atrioventricular blockade;

Differential diagnostic signs of intraventricular blockade;

Differential diagnostic signs of sick sinus syndrome;

Principles of differentiated therapy for cardiac conduction disorders. Temporary and permanent pacing;

Emergency therapy for asystole.

Questions for self-study by students:

Surgical methods for the treatment of cardiac conduction disorders.

List of studied diseases and conditions:

Sinoauricular (sinoatrial) blockade;

Intra-atrial blockade;

Atrioventricular block;

Intraventricular blockade;

Sick sinus syndrome.

Location of the lesson: the clinical base of the Department of Internal Diseases No. 1 with a course of polyclinic therapy is the cardiology department No. 2 of the State Healthcare Institution SKKKD.

Material and laboratory support:

Training tables;

Sets of electrocardiograms;

Sets of test items;

Sets of situational tasks.

Educational and educational goals:

A) common goal- the student needs to master the algorithm for differential diagnosis of various forms of cardiac conduction disorders, study the differential diagnostic signs of various forms of cardiac conduction disorders, and learn to apply the knowledge gained in their future profession.

B) private purposes- as a result of studying the educational issues of the lesson, the student must

Etiology, pathogenesis, clinical picture and diagnosis of various forms of cardiac conduction disorders;

Algorithm for differential diagnosis of cardiac conduction disorders;

Diagnostic capabilities of 12-channel ECG, exercise ECG, 24-hour and 24-hour ECG monitoring in case of cardiac conduction disorders;

Basic principles of medical care in case of emergency conditions arising from cardiac conduction disorders (ventricular asystole).

Draw up a program for examining a patient with cardiac conduction disorders;

Conduct a physical examination of the patient (examination, palpation, auscultation, blood pressure measurement, determination of pulse properties) and identify signs of cardiac conduction disorders;

Establish and substantiate the clinical diagnosis of a patient with intracardiac conduction disorders;

To decipher the ECG in 12 leads of patients with the identification of various forms of cardiac conduction disorders;

Draw up a plan for examining a patient with cardiac conduction disorders;

Provide emergency care in conditions (asystole of the ventricles) complicating the violation of intracardiac conduction;

Conduct resuscitation measures in cases of clinical death;

Methods of auscultation of the heart and blood vessels;

Interpretation of the results of instrumental methods of examination of a patient with cardiac conduction disorders;

Algorithm for setting a preliminary and detailed clinical diagnosis (main, concomitant, complications) of a patient with cardiac conduction disorders;

Implementation of basic medical treatment measures for the provision of first aid for ventricular asystole;

HAVE A SET OF COMPETENCIES:

Ability and willingness to implement primary and secondary prevention of cardiac conduction disorders;

The ability and willingness to establish deviations in the health of a patient with cardiac conduction disorders, taking into account the laws of the course of pathology in systems, regions and the body as a whole; using knowledge of fundamental and clinical disciplines;

Ability to comply with the requirements of medical ethics and deontology when communicating with patients, as well as their relatives and friends;

The ability and willingness to conduct a qualified diagnostic search to detect cardiac conduction disorders in the early stages, typical, as well as low-symptom and atypical manifestations of the disease, using clinical, laboratory and instrumental methods in an adequate volume;

the ability and willingness to correctly formulate the established diagnosis, taking into account the ICD-10, with an additional examination and the appointment of adequate treatment;

The ability and willingness to assess the need to choose an outpatient or inpatient treatment regimen, to resolve issues of examination of working capacity; draw up primary and current documentation, evaluate the effectiveness of dispensary observation.

The ability and willingness to assess the possibilities of using drugs for the treatment and prevention of cardiac conduction disorders; to analyze the action of drugs in terms of the totality of their pharmacological properties; possible toxic effects of drugs;

Ability and willingness to interpret the results of modern diagnostic technologies, to understand the strategy of a new generation of therapeutic and diagnostic drugs;

The ability and willingness to perform basic diagnostic and therapeutic measures, as well as to make the optimal choice of drug therapy for providing first aid in urgent and life-threatening conditions that complicate the course of cardiac conduction disorders;

The ability and readiness to analyze the performance indicators of various types of health care facilities in order to optimize their functioning, to use modern organizational technologies for diagnostics, treatment, rehabilitation, prevention in the provision of medical services in the main types of medical and prophylactic institutions;

Ability and willingness to maintain accounting and reporting medical records;

Ability for independent analytical work with various sources of information, willingness to analyze the results of their own activities to prevent professional mistakes;

HAVE REPRESENTATIONS:

Surgical methods for correcting cardiac conduction disorders.

Integrative relationships (elements of a unified lifelong learning program):

- normal anatomy: the structure of the cardiovascular system;

- normal physiology: intracardiac conduction of an electrical impulse is normal;

- pathological physiology: intracardiac conduction of an electrical impulse in case of conduction disturbances;

- propedeutics of internal diseases: methods of research of the cardiovascular system;

- pharmacology: antiarrhythmic drugs, metabolic drugs.

main:

1. Internal diseases: textbook / Ed. S.I. Ryabova, V.A. Almazova, E.V. Shlyakhtova. - SPb., 2001.

2. Internal medicine: textbook: in 2 volumes / Ed. N.L. Mukhina, V.S. Moiseeva, A.I. Martynov. - 2nd ed., Rev. and add. - M: GEOTAR-Media, 2004.

3. Internal medicine: textbook: in 2 volumes / Ed. N.L. Mukhina, V.S. Moiseeva, A.I. Martynov. - 1st ed. - M: GEOTAR-Media, 2001.

4. Internal medicine: textbook: in 2 volumes / Ed. N.L. Mukhina, V.S. Moiseeva, A.I. Martynov. - 2nd ed., Rev. and add. - M: GEOTAR-Media, 2005.

5. Internal diseases: textbook / Ed. IN AND. Makolkin, S.I. Ovcharenko. - 5th ed. - M: Medicine, 2005.

additional:

1. 2000 diseases from A to Z / Ed. I.N. Denisova, Yu.L. Shevchenko. - M., 2003.

2. Mukhin, N.A. Selected lectures on internal medicine / N.A. Mukhin. - M., 2006.

3. Cardiology: Manual for Physicians / Ed. R.G. Oganova, I. G. Fomina. - M .: Medicine, 2004.

4. Diagnosis in cardiovascular diseases. Formulation, classification. Practice. manual / Ed. I.N. Denisova, S.G. Gorokhovoy. - M .: Geotar-Media, 2005.

Familiarize yourself with the educational (general and specific) objectives and educational questions of the lesson;

Restore the acquired knowledge of basic disciplines within the framework of integrative relations on the studied topic of the lesson;

Analyze the work done by answering questions for self-study (self-study) and self-study;

Complete test tasks (Appendix 2) and solve situational tasks (Appendix 3).

Appendix 1. Abstract (current state of the art):

Sinoauricular (SA) block represents a deceleration
or the termination of the impulse from the sinus node through
sinoatrial connection to the atria.

The most common cause of SA blockade is coronary artery disease, especially
with damage to the right coronary artery. Also, CA blockade occurs with myocarditis, hypertension or as a result of the action
medicines (cardiac glycosides, quinidine,
β-blockers, cordarone, isoptin). Cause of SA blockade
there may also be an increased vagus nerve tone.

Classification of SA blockade

The first degree of SA block does not cause any changes
cardiac activity and does not appear on a normal ECG. Wherein
in the form of a blockade, all sinus impulses pass to the atria.

With SA blockade of the II degree, sinus impulses through the SA
the connection does not pass at times. This is followed by loss
one or more atrioventricular complexes in a row. With II degree SA blockade, dizziness may occur,
feeling irregular heart activity or fainting. During the period
pauses of the sinoauricular block, the appearance of slipping out
contractions or rhythms from underlying sources (AV connection,
Purkinje fibers);

With SA blockade of the III degree, impulses from the side
sinus node does not pass through the CA junction and activity
heart is associated with the activation of underlying sources of rhythm.

Currently, only grade 2 CA block is diagnosed, since the rest are not diagnosed.

SA blockade clinic

Heart sinking if there is one impulse. Vertigo if there are several impulses. Morgagni-Edems-Stokes syndrome (loss of consciousness), if 6-8 complexes fall out.

ECG the whole heart complex is absent. There is no P, T, QRS, instead of them a long pause is visible, which can be a multiple of any R-R number and is equal to 2, 3, 4, etc., respectively. normal R-R. Sliding, replacement complexes are often visible: during
a long pause to the aid of its own impulse jumps out (the artioventricular node helps); there will be no P wave. Auscultatory at this time, a loud tone can be heard - a strong contraction of the heart.

Tactics for the treatment of disorders of the SA conduction related to treatment
the underlying disease causing conduction disturbance. Specific therapy for CA blockade:

1. Increase in heart rate:

Anticholinergics (belladonna extract, platifilin)

· Sympatholytics, but they are few to be prescribed, with great caution, since they can provoke an attack of angina pectoris: sublingual izadrin or in the form of inhalation;

2. Antiarrhythmic therapy. Prescribe very mild remedies: Delagil at night.

3. Calcium antagonists: isoptin.

4. With frequent loss of consciousness, the patient is transferred to continuous electrical impulse therapy... But more often you have to spend a temporary pacing "on demand".

Intra atrial block

Often associated with organic lesions, often a harbinger of atrial fibrillation.

It can also be with a sharp dilatation of the atria.
Etiology: heart defects, ischemic heart disease, overdose of antiarrhythmic drugs.

Clinical manifestations practically does not.

The only one diagnostic method- ECG: widening and splitting of the P wave (normally no more than 0.10 sec.). Often, the P wave becomes biphasic (+/-).

There may be a deeper lesion - damage to the Bachmann bundle - atrial parasystole syndrome (the right atrium works on the rhythm of the sinus node, and the left one from its own impulses from heterotopic foci of excitation). This leads to severe hemodynamic disturbances. Rare.

Atrioventricular block

occurs due to a violation of the conduction of an electrical impulse from the atria to the ventricles through the AV connection.

The causes of conduction disturbances through the AV connection can be coronary artery disease, myocarditis, heart defects, electrolyte imbalance, or damage to the atrioventricular node during surgical procedures. In some cases, AV block is hereditary and occurs in members of the same family. There are hereditary degenerative changes in the conduction system, such as Lev's disease (calcification and sclerosis of the fibrous heart with the involvement of the valve apparatus) and Lenegra's disease (primary sclerosing lesion of the cardiac conduction system, not involving the myocardium and fibrous skeleton of the heart).

Classification of AV blocks

· AV blockade of the 1st degree (slowing down of the impulse conduction from the atria to the ventricles through the AV node);

II degree (slowing the conduction of the impulse from the atria to the ventricles through the AV node with periodic development of complete blockade with loss of ventricular contraction);

III degree (complete absence of impulse conduction from the atria to the ventricles through the AV node with a contraction of the ventricles due to the appearance of a pacemaker of the 2nd or 3rd order).

Separately distinguish artificially created AV block... Share also proximal(AV node only) and distal(with damage to the Gisa-Purkinje system) AV blockade. Distal AV blocks are prognostically less favorable.

Clinical manifestations with AV blockade depend on the etiology of the underlying disease and the degree of heart rate slowdown.

With AV block of the 1st degree, the state of health may not change, less often there are sensations of a rare rhythm or interruptions in the work of the heart.

With AV block II degree, attacks of severe weakness, dizziness with darkening of the eyes, lightheadedness or syncope may occur.

· AV block of III degree in all patients is accompanied by a deterioration in hemodynamic parameters due to a decrease in myocardial contractility and a decrease in ventricular ejection fraction. This is manifested by a deterioration in the blood supply to all organs and, first of all, to the brain, heart and others. In addition, conditions are created for the occurrence of ventricular extrasystole and tachycardia, flutter and fibrillation of the ventricles, asystole of the heart. Patients have attacks of Morgagni-Edems-Stokes, and in some cases, sudden death.

Electrocardiographic signs of 1st degree AV block:

Lengthening of the P-R (Q) interval more than 0.21 seconds at a normal frequency and more than 0.22 seconds with sinus bradycardia;

· The increase in the interval is due to the lengthening of the segment from the end of the P to the beginning of the R or Q wave. Normally, the AV delay and the P-R (Q) segment is 0.07 seconds.

Electrocardiographic signs of 2nd degree AV block:

· Type I or Mobitz type I is characterized by the Samoilov-Wenckebach period: a gradual lengthening of the P-R (Q) interval with each cardiac cycle; loss of the QRS complex, which occurs after the longest R-R (Q), after which the normal R-R (Q) interval is again recorded. In the absence of a QRS complex loss, the same pattern is observed when, after the longest P-R (Q) interval, the normal duration of this interval is restored;

Type II or Mobitz type II: loss of the QRS complex with a normal duration of the P-R (Q) interval in a ratio of 2: 1, 3: 1, 4: 1, etc. Constant increase in the P-R (Q) interval, i.e. AV block of the 1st degree, in combination with a loss of the QRS complex in a ratio of 2: 1.3: 1.4: 1, etc.

Electrocardiographic signs of grade III AV block (complete transverse heart block):

· Cessation of impulses from the atria to the ventricles, in connection with which the atria are excited and contract in their rhythm with a frequency of 60-80 beats / min, and the ventricles - 30-60 beats / min;

· A change in the shape and size of the ventricular QRS complexes in comparison with the sinus rhythm that existed earlier, since the sources of excitation of the ventricles are the AV connection or the conduction system of the ventricles, which are designated as ectopic centers of automatism of the II or III order;

· In separate complexes, P is superimposed on the ST and T segment of the QRST complex, deforming them;

· There is no relationship between P and the subsequent QRTS complex, while the P-P intervals are always less and remain constant, and R-R is greater than P-P and can be different in size;

· There is a regularity that at the centers of automatism of the III order there is a more rare rhythm, less than 40 beats / min, and an extended, deformed QRS complex.

In the overwhelming majority of cases, when a third-degree AV block appears, temporary transvenous electrical stimulation of the heart is performed, and then permanent - with the installation of an artificial pacemaker that works on demand.

Indications for implantation of pacemaker with AV blockade divided into three groups: A - implantation is necessary, B - implantation is desirable, C - implantation is undesirable. Asymptomatic patients with grade I AV block should be evaluated frequently due to the possibility of a sudden increase in grade. With AV block II degree with clinical manifestations, pacemaker implantation is indicated. In asymptomatic II degree proximal AV block, implantation is usually not required. In asymptomatic II degree distal AV block, pacemaker implantation is desirable due to the risk of asystole and progression of the block. With complete AV block with clinical manifestations, pacemaker implantation is indicated. Asymptomatic patients with complete AV block may not need pacemaker implantation if the secondary pacemaker has adequate frequency and stability and is not suppressed by high-frequency pacing after autonomic heart block. In patients with complete AV block in acute myocardial infarction (regardless of its location and at any width of the QRS complex), temporary pacing is indicated. In case of AV block, it is preferable to implant a two-chamber stimulation system. Isolated pacing of the ventricles, without preserving the coordinated atrial contribution to hemodynamics, is prognostically less favorable in AV block.

Complications of grade III AV block and other life-threatening arrhythmias include Morgagni-Edems-Stokes syndrome.

Morgagni-Edems-Stokes syndrome is manifested by attacks of loss of consciousness with the rapid development of severe cerebral ischemia due to a significant decrease in cardiac output in patients with cardiac arrhythmias. This syndrome occurs due to the sudden cessation of effective cardiac activity during asystole, flutter and fibrillation of the ventricles. Severe cerebral ischemia occurs when cardiac output drops below two liters per minute due to an abnormal heart rhythm.

Depending on the type of heart rhythm disturbances, three pathogenetic forms of Morgagni-Edems-Stokes are distinguished: bradycardic, tachyarrhythmic and mixed forms.

Clinical manifestations of Morgagni-Edems-Stokes syndrome are determined by the duration of life-threatening arrhythmias and the resulting severe hemodynamic disorders and cerebral ischemia.

Clinical manifestations of Morgagni-Edems-Stokes syndrome depending on the duration of life-threatening cardiac arrhythmias:

· Within 3-5 seconds. Sudden onset of a light-headed (lipotimic) state: severe weakness, dark circles before the eyes, slow speech, impaired coordination, indifference to the environment and disorientation, increasing noise or ringing in the ears and head, nausea, vomiting, pallor of the skin, decreased blood pressure, disturbances heart rate (which can be determined by the pulse and auscultation of the heart, but the type of arrhythmia is diagnosed only when the ECG is taken at this moment).

· Within 10-20 seconds. Fainting (syncope): loss of consciousness, pallor of the skin, cyanosis of the lips, acrocyanosis, drop in blood pressure, decreased muscle tone, the patient lies motionless, clonic twitching of the face and trunk, weakened, almost imperceptible breathing, heart rhythm disturbances (which can be determined by pulse and auscultation of the heart, but the type of arrhythmia is diagnosed only when the ECG is taken at this moment).

· Within 20-40 seconds. Deep fainting persists: hemodynamic disorders progress, breathing disorders persist, generalized epileptiform seizures appear, patients who have suffered a brain injury may have tongue biting, involuntary urination and defecation, cardiac arrhythmias (which can be determined by pulse and auscultation of the heart, but the type of arrhythmia is diagnosed only when taking an ECG at this moment).

· Within 1-5 minutes. The state of clinical death: periodic breathing, such as Cheyne-Stokes with an increase in the period of apnea, bubbling breathing, as with increasing pulmonary edema, intense cyanosis, most often the entire upper half of the body, deaf heart sounds, rare rhythm, periods of asystole alternating with periods of arrhythmias, pulse and blood pressure is not determined, the pupils are dilated, corneal reflexes, cardiac arrhythmias decrease and disappear (which can only be determined when the ECG is taken at this moment).

· After 5-10 minutes. Coma or biological death: periodic breathing, such as Cheyne-Stokes, with an increase in the period of apnea, bubbling breathing, as with increasing pulmonary edema, intense cyanosis, deaf heart sounds, rare rhythm, periods of asystole, alternating with periods of arrhythmias, pulse and blood pressure are not are determined, the pupils are dilated, corneal reflexes, cardiac arrhythmias decrease and disappear (which can only be determined when the ECG is taken at this moment).

An attack of Morgagni-Edems-Stokes can be stopped at all stages of emergency care, resuscitation. Treatment tactics are determined by the type of heart rhythm disorder. Treatment programs of one type or another are almost always implemented, including resuscitation measures for asystole or atrial fibrillation, etc.

Intraventricular conduction disorders

(intraventricular block)

Intraventricular blockade occurs when the impulse propagation from the sinus node and atria through the ventricles is disturbed due to the absence or slowing down of conduction along one of the legs of the bundle of His. One ventricle is activated through the interventricular septum later than the other by about 0.04-0.06 seconds. Therefore, the ventricular QRS complex becomes abnormally wide (over 0.12 seconds) and deformed. The most common are blockades of the right or left bundle branch block.

ECG signs of complete right bundle branch block:

· Cleavage of the QRS complex in the form of the letter M - rsR, rsR ", RSR" RsR ", rR" forms and increased time of internal deflection (intrinsicoid deflection) in leads V 1, V 2, V 3 R, aVR more than 0.06 seconds;

· Deep, serrated S wave with a duration of more than 0.04 seconds in leads I, V 5, V 6, sometimes in leads II, aVL. Leads I and II have a predominantly positive QRS complex in which R> S;

• downward shift of the ST segment and negative T wave in leads V 1, V 2, V 3 R, possibly in leads III and aVF;

· The electrical axis of the heart most often occupies an indifferent position, or there is a slight deviation to the right or left.

Left bundle branch consists of two branches and is a powerful formation of the cardiac conduction system, therefore, its blockade occurs with significant anatomical damage.

ECG signs of complete left bundle branch block:

· Expansion of the QRS complex up to 0.12 seconds or more;

· Wide and split R wave (there are no Q and S teeth) in the form of a wide letter "L" in lead I, increased time of internal deflection (intrinsicoid deflection) up to 0.08 seconds and more in leads I, V 5, V 6 , aVL;

· Widened and jagged S wave or QS complex in opposite leads V 1, V 2, sometimes in leads III and aVF;

· Downward shift of the ST segment with a negative asymmetric T wave in leads V 5, V 6, I, aVL. An upwardly displaced ST segment with high asymmetric T in leads V 1, V 2 and sometimes in leads III and aVF;

· In the overwhelming majority of cases, there is a horizontal position of the electrical axis of the heart (forms I, aVL leads correspond to V 5, V 6) or pathological deviation of the axis to the left.

Sick sinus syndrome (SSS)

more often occurs at a certain stage in the evolution of certain diseases. In the overwhelming majority of cases, with this violation of the heart rhythm, significant morphological changes in the atrial myocardium or atherosclerosis of the artery of the sinus node are found. Dysfunction of the sinus node is manifested by a violation of automatism with inhibition of pacemaker activity, blockade of excitation output and deterioration of conduction in the perinodal zone.

In the development of sick sinus syndrome in some patients, two periods can be distinguished - transient changes that occur under the influence of exogenous factors, more often drugs, and permanent changes. In elderly patients with coronary artery disease, sick sinus syndrome can debut. The overwhelming majority of the onset of sick sinus syndrome is observed against the background of severe organic pathology of the heart and characterizes a prognostically unfavorable course.

Sick sinus syndrome can manifest itself in various types of arrhythmias, while they often alternate in the same patient and are detected for the first time during antiarrhythmic therapy. Allocate the following cardiac arrhythmias in SSS: sinus bradycardia with escaping contractions; sinoauricular block; atrial pacemaker migration; atrial and ventricular asystole; bradytachycardia syndrome, when there is an alternation of the above-mentioned cardiac arrhythmias with attacks of supraventricular tachycardia, atrial flutter-fibrillation; delayed restoration of sinus rhythm after the termination of tachyarrhythmia - asystole, pronounced sinus bradycardia, idioventricular rhythm.

Clinical manifestations are determined by the type of heart rhythm disturbance, the nature of the heart disease and the state of cerebral blood flow. In the vast majority of patients, during the development of sick sinus syndrome, there is also a progression of cardiovascular diseases, for example, an increase in angina attacks, progression of heart failure or arterial hypertension. In elderly patients suffering from atherosclerosis of cerebral vessels, attacks of severe weakness, dizziness, gait instability, a feeling of approaching fainting more often occur, at the same time the phenomena of discirculatory encephalopathy increase, new neurological symptoms and syndromes appear that make one think about the development of a transient ischemic attack or acute cerebrovascular accident. With short-term severe hemodynamic disturbances during transient asystole, episodes of severe bradycardia up to 40 beats / min, fainting and other manifestations of Morgagni-Edems-Stokes syndrome may occur. Prolonged attacks of atrial fibrillation in sick sinus syndrome can transform into a permanent form of atrial fibrillation.

One of the reliable methods for diagnosing sick sinus syndrome is Holter ECG monitoring, after which it is decided to conduct transesophageal electrical stimulation of the heart and further treatment tactics.

Conducting arresting antiarrhythmic therapy for bradytachycardia syndrome is very dangerous due to the possibility of asystole and death of the patient.

To determine the tactics of treatment, it is necessary to carry out a differential diagnosis between sick sinus syndrome and autonomic dysfunction of the sinus node. The main criterion is the result of an atropine test or a drug denervation test. A test with atropine is carried out against the background of taking an ECG or conducting daily monitoring of an ECG. The patient is injected intravenously (or subcutaneously) with a solution of atropine sulfate at a dose of 0.025 mg / kg of the patient's body weight. An increase in heart rate after the administration of atropine and the disappearance of clinical symptoms speak in favor of autonomic dysfunction of the sinus node. A more reliable test with drug denervation of the heart (complete autonomic blockade) during transesophageal (or intracardiac) electrophysiological examination. Initially, the patient is determined by the sinus node recovery time (VVFSU) and corrected VVFSU. Then, intravenously injected sequentially solutions of propranolol at the rate of 0.2 mg / kg of the patient's body weight and atropine sulfate at the rate of 0.04 mg / kg of the patient's body weight, after which the recovery time of the sinus node is again determined. If after medication denervation of the heart VVFSU (the interval from the last electrical stimulus to the first natural P wave) is more than 1500 ms or CVVFSU (the difference between the value of VVFSU and the average duration of the initial cardiac cycle) is more than 525 ms, then the patient has a sick sinus syndrome. If the indicated values ​​are less than the indicated values, then there is a vegetative dysfunction of the sinus node.

Treatment for sick sinus syndrome consists of the implantation of a pacemaker (PAC). Currently, indications for pacemaker implantation are divided into three groups: A - implantation is necessary, B - implantation is desirable, C - implantation is undesirable. With regard to the syndrome of weakness of the sinus node, patients with its presence fall into group B, and if the patient has a clinic (MES syndrome), then he falls into the group of indications for implantation A. study). The presence of impaired AV conduction indicates the need for implantation of a two-chamber stimulation system. With preserved AV conduction, atrial stimulation is performed. Implantation of a single-chamber pacemaker with ventricular stimulation in sick sinus syndrome is undesirable. Preferred are the implantation of physiological pacemakers (frequency-adaptive, i.e. increasing heart rate during physical activity) with bipolar intracardiac electrodes. In the case of tachy-brady syndrome, it is advisable to install the atrial electrode in the interatrial septum (for the prevention of tachycardia paroxysms) and set a slightly higher stimulation frequency (75-80 per minute) during programming.

Autonomic dysfunction of the sinus node is well treated with anticholinergics. Most often, belladonna preparations (bellataminal, besalol, bacarbon, belloid) are used for its treatment. In isolated cases of severe dysfunction, implantation of a pacemaker is possible.

Appendix 2. Test tasks:

1. In what diseases are Morgagni-Adams-Stokes attacks occurring?

1) ventricular premature beats

2) ventricular fibrillation

3) atrial fibrillation

4) atrioventricular block

2. What are the characteristics of sick sinus syndrome?

1) ventricular extrasystoles

2) sinoauricular (sinoatrial) block

3) atrioventricular block

3. The test with atropine is used in patients with the following purposes:

1) to diagnose existing disorders of atrioventricular conduction

2) to assess the class of coronary insufficiency

3) to identify violations of the rheological properties of blood

4) to detect latent coronary insufficiency

5) for the diagnosis of sick sinus syndrome

4. Indications for electro-pulse therapy are:

1) rapid progression against the background of an attack of tachyarrhythmia of signs of heart failure, insufficiency of the coronary or cerebral circulation

2) bradystolic form of atrial fibrillation

3) tachyarrhythmias that developed against the background of intoxication with cardiac glycosides

5. AV blockade of the 1st degree is characterized by:

1) P-R (Q) interval 0.21 s or more at normal heart rate

2) P-R (Q) interval more than 0.22 s with sinus bradycardia

3) gradual lengthening of the P-R (Q) interval with each cardiac cycle

4) heart rate 36 per minute

5) correct 1 and 2

6. For AV block II degree I type is characterized by:

1) lengthening of the P-R (Q) interval more than 0.35 s

2) a gradual lengthening of the P-R (Q) interval with each cardiac cycle

3) loss of the QRS complex with a normal duration of the P-R (Q) interval

4) loss of the QRS complex occurs after the longest P-R (Q), after which the normal P-R (Q) interval is again recorded

5) 2 and 4 are correct

7. For AV block II degree II type is characterized by:

1) there is no relationship between P and subsequent QRST

2) loss of the QRS complex with a normal duration of the P-R interval (Q)

3) a constant increase in the interval P-R (Q)

4) gradual lengthening of the P-R (Q) interval with each cardiac cycle

5) 2 and 3 are correct

8. ECG signs of grade III AV block are:

1) termination of impulses from the atria to the ventricles

2) in separate complexes, P is superimposed on the ST and T segment of the QRST complex, deforming them

3) there is no relationship between P and the subsequent QRST complex, while R-R is greater than P-R

4) everything is correct

9. The clinical manifestations of the Morgagni-Adams-Stokes syndrome are:

1) loss of consciousness

2) increase in blood pressure

3) the presence of a paradoxical pulse

10. Indications for temporary pacing are:

1) asystole

2) AV block II degree II type and III degree in acute myocardial infarction

3) intoxication with cardiac glycosides, which is complicated by significant bradyarrhythmias

4) everything is correct

11. Indications for permanent pacing are:

1) AV block II degree II type with attacks of Morgagni-Adams-Stokes

3) AV block III degree

4) everything is correct

12. A patient with ischemic heart disease has postinfarction cardiosclerosis. The syndrome of weakness of the sinus node was revealed, for the last 2 weeks, attacks of atrial fibrillation occur every day, episodes of bradycardia, accompanied by dizziness, are noted. Your tactics:

1) prescribe quinidine

2) prescribe novocainamide

3) to implant a permanent artificial pacemaker

4) prescribe digoxin

5) carry out temporary cardiac stimulation

13. Contraindications for the appointment of beta-blockers are:

1) arterial hypertension

2) sick sinus syndrome

3) bronchial asthma

4) 2 and 3 are correct

5) everything is correct

14. ECG signs of SA blockade are:

1) periodic loss of the P-QRS-T complex

2) lengthening of the interval P-R (Q) more than 0.20 s

3) periodic loss of the QRS complex

15. ECG signs of right bundle branch block are:

1) expansion and deformation of the QRS complex in the form of the letter M in the right chest leads, wide and deep S in the left chest leads;

2) expansion and deformation of the QRS complex in the form of the letter M in the left chest leads, wide and deep S in the right chest leads;

16. ECG signs of left bundle branch block are:

1) expansion and deformation of the QRS complex in the form of the letter L in the right chest leads, wide and deep S in the left chest leads;

2) expansion and deformation of the QRS complex in the form of the letter L in the left chest leads, wide and deep S in the right chest leads;

3) periodic loss of the QRS complex.

17. The worst forecast has:

1) intra-atrial block;

2) 1st degree AV block;

3) AV block of the III degree;

18. Has an asymptomatic course and often occurs in athletes:

1) intra-atrial block;

2) 1st degree AV block;

3) AV block of the III degree;

4) right bundle branch block.

19. In the treatment of cardiac conduction disorders, DO NOT use:

1) temporary cardiac stimulation;

2) constant cardiac stimulation;

3) all classes of antiarrhythmic drugs;

4) vegetative correctors.

20. Sick sinus syndrome includes everything except:

1) sinus bradycardia;

2) SA blockade;

3) sinus tachycardia.

Answers to test tasks: 1 – 4; 2 – 2; 3 – 5; 4 – 2; 5 – 5; 6 – 5; 7 – 5; 8 – 4; 9 – 1; 10 – 4; 11 – 4; 12 – 5; 13 – 4; 14 – 1; 15 – 1; 16 – 2; 17 – 3; 18 – 4; 19 – 3; 20 – 3.

Appendix 3. Situational tasks:

Objective 1.

Patient M., 23 years old, consulted a cardiologist. During a routine examination before the competition (an athlete, weightlifting for 11 years), the ECG revealed a complete blockade of the right bundle branch. No complaints. Echocardiography, blood and urine tests - no pathology.

1. What is the genesis of conduction disturbance in this patient?

2. Management tactics.

3. Is it possible to participate in sports competitions?

4. Is an additional examination shown?

5. What therapy can be given to this patient?

Objective 2.

Patient S., 81, is under dispensary observation with a diagnosis of ischemic heart disease, angina pectoris FC II. Postinfarction cardiosclerosis. For the last 2 weeks, he began to notice unmotivated attacks of acute weakness, accompanied by tinnitus, dizziness, darkening of the eyes, sweating, and a decrease in blood pressure. Once - loss of consciousness. On the ECG - without fundamental dynamics, the sinus rhythm, cicatricial changes in the anterior septal region are preserved. When performing Holter ECG monitoring, transient I and II degree AV block Mobitz type 1 was detected. For the existing ischemic heart disease and postinfarction cardiosclerosis, the patient receives an ACE inhibitor (ramipril), a β-blocker (metoprolol), a disaggregant (aspirin) and statin (simvastatin).

1. What genesis of cardiac conduction disturbances can be assumed in this patient?

2. How to interpret complaints that have appeared 2 weeks ago?

3. Is it possible to continue cardiotropic therapy in the same volume?

5. Tactics of further management of the patient.

Objective 3.

4. Are there any indications for pacing?

Task 4.

1. What type of conduction disturbance is presented on the ECG?

2. Is normal hemodynamics possible with this conduction disturbance?

3. Is it possible for this patient to develop Morgagni-Edems-Stokes syndrome?

4. Are there any indications for pacing?

5. Is antiarrhythmic therapy indicated and why?

Task 5.

Compile in the form of a table the main differential diagnostic differences in cardiac conduction disorders, indicating such characteristics as etiological factors, complaints, clinical manifestations, ECG data, indicated and contraindicated drugs, the possibility of surgical correction.

  • Algorithms: basic characteristics, types. The executor of the algorithm. Basic syntactic constructions of the C language that implement algorithms.
  • An aynalymy zhetispeushiligi syndromes (zhedel zhene sozylmaly). Symptoms, gifts, old mechanisms. Diagnostics of the maңyzy.

    • Differential diagnosis of atrial fibrillation is presented as a result of laboratory studies, based on the clinical picture of the disease and some mathematical techniques.

    Arrhythmia symptoms and diagnosis

    The diagnosis of atrial fibrillation is based on electrocardiographic data.

    On the electrocardiogram, when blinking, instead of one distinct tooth, small multiple teeth are visible. 3-5-8 and more atrial waves fall on one gastric complex. Sometimes on the cardiogram, only a slight undulation is noted. The ventricular teeth are in the wrong order, although they are normal in both shape and direction. The venous pulse with atrial fibrillation is distinguished by the disappearance of the wave and the same irregularity in the alternation of ventricular waves.

    Diagnosis of arrhythmia consists in the fact that, usually, when flickering, the pulse is quickened, but it can also be slow (tachysystolic and bradystolic forms).

    Sometimes, with a slow pulse, its irregularity is smoothed out, and the pulse seems rhythmic; in such cases, it is easy to diagnose flicker on the electrocardiogram.

    The importance of atrial fibrillation for clinical trials is great. This type of rhythm disorder, when encountered with serious anatomical changes in the heart, should accordingly influence the assessment of the patient's position. Sometimes patients have atrial fibrillation for many years and yet people continue to be able to work. But more often the appearance of atrial fibrillation indicates that the heart disease is becoming severe.

    A doctor can detect an abnormal heart rhythm during a physical exam by feeling for a pulse. Symptoms of arrhythmia can be: irregular heartbeat, a feeling that the heart is running very quickly, dizziness, shortness of breath, chest discomfort, feeling very tired.

    All these signs make it possible to make the correct diagnosis of the disease and prescribe an effective treatment.

    Differential diagnosis includes ECG, Holter monitor, echocardiogram, cardiac catheterization, electrophysiological examination, and stress test, which records the electrical activity of the heart. The diagnosis is determined by a cardiologist based on the examinations performed. The cardiologist may perform further diagnostic procedures to determine the cause and select the correct treatment.

    The main condition for the occurrence of atrial fibrillation is an increase in their excitability, and the latter is obtained mainly when the nutrition of the atrial neuromuscular tissue is disturbed. Therefore, all the reasons leading to metabolic disorders in the atrial muscle can cause atrial fibrillation.

    Year of issue: 2000

    Genre: Cardiology

    Format: DjVu

    Quality: Scanned pages

    Description: Heart rhythm and conduction disorders are one of the most difficult areas of modern cardiology and therapy. Diagnosis of arrhythmias and blockages is carried out almost exclusively by electrocardiography data, and in difficult cases - using transesophageal and endocardial electrograms. This manual presents 250 electrocardiograms recorded in patients with cardiac arrhythmias and conduction disorders, covering most types of arrhythmias. Almost all of them were recorded synchronously with intracardiac electrograms - atria, Tis's bundle, less often - with transesophageal electrocardiograms. Since most practicing doctors in their daily activities do not come across such records, the beginning of the book provides basic information that allows you to more freely navigate in them. Comparison of a conventional ECG with intracardiac electrograms will allow the reader to understand the features of the formation of a conventional surface ECG in complex rhythm disturbances.
    The book is divided into several chapters, each of which is devoted to a separate group of arrhythmias. All chapters are structured in the same way: first, the main electrocardiographic (and electrophysiological) characteristics of arrhythmias and blockages are given, then electrocardiograms are given, after which detailed comments are given for each of these electrocardiograms. ECG number and comment number are the same. All ECGs were recorded at a speed of 50mm / s, on each electrocardiogram the intervals are indicated in fractions of a second and in milliseconds (ms). Each ECG has a scale bar that allows, if desired, to measure any interval independently.
    When working with the book, first it is advisable to familiarize yourself with the ECG characteristics of the arrhythmias included in this chapter, then make your own impression on each electrocardiogram, and only then compare your conclusion with the comments given to each specific electrocardiogram.
    The book is intended for therapists, cardiologists, doctors of functional diagnostics, as well as for electrophysiologists. I hope this guide will be useful in improving the diagnosis and, therefore, the treatment of cardiac arrhythmias and conduction disorders.

    Chapter 1. Violations of the formation (formation) of the heart impulse
    Sinus node automatism disorders
    Sinus tachycardia
    Sinus bradycardia
    Sinus arrhythmia
    Rigid sinus rhythm
    Manifestations of automatism of latent pacemakers
    Slip-out (replacement) complexes and rhythms
    Atrial escape complexes and rhythms
    Escaping complexes and rhythms from the AV junction

    Idioventricular (ventricular) replacement complexes and rhythms
    Accelerated slip beats and rhythms
    Migration of the supraventricular pacemaker
    Atrioventricular dissociation
    Electrocardiograms from No. 1.1 to No. 1.16




    Common causes of arrhythmias 1.Diseases of the cardiovascular system (congenital, acquired) 2.Disregulation of CVS in a noncardiac pathological process - in case of gastrointestinal tract damage (gallstone disease, diaphragmatic hernia) - in case of damage to the central nervous system - in endocrine diseases




    Electro-pathophysiological mechanisms of cardiac arrhythmias 1.Disruption of the mechanisms of impulse formation - violation of the automatism of the sinus node and latent centers of automatism - the formation of pathological automatism - mechanisms of oscillatory or trigger (trigger) activity


    2. Violation of impulse conduction - lengthening of refractoriness and decaying (decremental) conduction in the cardiac conduction system - anatomical damage to the cardiac conduction system - re-entry phenomenon 3. Combined mechanisms of formation and conduction of impulses


    CLINICAL AND ELECTROCARDIOGRAPHIC CLASSIFICATION OF ARRHYTHMAS (1) I. IMPACT OF IMPULSE FORMATION: AUTOMATIC MECHANISMS: Changes or disturbances in the automatism of the sinus node: sinus tachycardia - bradycardia - arrhythmia of the sinus node (refusal) sinus arrhythmia or accelerated escape beats or AV dissociation rhythms supraventricular pacemaker migration




    CLINICAL AND ELECTROCARDIOGRAPHIC CLASSIFICATION OF ARRHYTHMIAS (2) II. IMPULSE DISORDERS AND ANOMALIES: BLOCADES: sinoatrial blockade, atrial and intra-atrial blockade, atrio-ventricular blockade, intraventricular blockade. PREMATURE VENTRICULAR EXCITATION: Wolff-Parkinson-White syndrome and phenomenon. shortened P-R interval syndrome. III. COMBINED DISORDERS OF EDUCATION AND CONDUCTING AN IMPULSE: Parasystole Ectopic activity of centers with blockade of exit.


    Normal sinus rhythm. Correct rhythm with heart rate per minute. 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 conduction pathways)




    Sinus bradycardia. Correct heart rate rhythm


    Causes: increased parasympathetic tone (often in healthy individuals, especially during sleep; in athletes; myocardial infarction (especially the lower one); taking medications (beta-blockers, verapamil, diltiazem, cardiac glycosides, antiarrhythmics of classes Ia, Ib, Ic, amiodarone, clonidine, methyldopa, reserpine, guanethidine, cimetidine, lithium); verapamadylthiazema amiodarone clonidine methyldofyreserpine guanethidine cimetidine lithium






    Treatment Only if it is proven that it causes angina pectoris, arterial hypotension, fainting, heart failure, ventricular arrhythmias! ATROPINE mg IV ISOPRENALINE 2-20 μg / min IV atrial pacemaker in the absence of AV block.


    Pacemaker migration. Correct or incorrect heart rate rhythm






    Sinus tachycardia. Correct rhythm. Sinus P waves of the usual configuration (their amplitude can be increased). Heart rate min – 1, in young people up to 200 min – 1. Gradual start and stop.




    Causes: thyrotoxicosis, myocardial ischemia, myocardial infarction, heart failure, myocarditis, PE, pheochromocytoma, arteriovenous fistulas, the effect of drugs and other drugs (caffeine, alcohol, nicotine, catecholamines, hydralazine, thyroid hormones, atropine). Tachycardia is not relieved by massage of the carotid sinus.








    SSSU The syndrome is characterized by fainting or other manifestations of cerebral dysfunction, accompanied by: sinus bradycardia, sinus arrest (sinus arrest), sinoatrial blockade, alternating bradyarrhythmias and tachyarrhythmias (tachycardia syndrome), increased sensitivity of the carotid sinus.


















    AV nodal extrasystoles. An extraordinary QRS complex with a retrograde (negative in leads II, III, aVF) P wave, which can be registered before or after the QRS complex or layered on it. The shape of the QRS complex is normal; with aberrant conduction, it may resemble a ventricular extrasystole.





    Ventricular extrasystoles. Extraordinary, wide (> 0.12 s) and deformed QRS complex. The ST segment and T wave are discordant to the QRS complex. 0.12 s) and a deformed QRS complex. The ST segment and T wave are discordant to the QRS complex. "> 0.12 sec) and the deformed QRS complex. The ST segment and T wave are discordant to the QRS complex."> 0.12 sec) and the deformed QRS complex. The ST segment and T wave are discordant to the QRS complex. "Title =" (! LANG: Ventricular extrasystoles. Extraordinary, wide (> 0.12 s) and deformed QRS complex. The ST segment and T wave are discordant to the QRS complex."> title="Ventricular extrasystoles. Extraordinary, wide (> 0.12 s) and deformed QRS complex. The ST segment and T wave are discordant to the QRS complex."> !}


    Diagnosis The P wave may not be associated with extrasystoles (AV dissociation) or be negative and follow the QRS complex (retrograde P wave). The compensatory pause is usually complete (the interval between pre- and post-extrasystolic P waves is equal to twice the normal PP interval).


    Classification of ventricular extrasystoles (according to B.Lown, M. Wolf, M. Ryan, 1975): 0. - no ventricular extrasystoles in 24 hours. Monitoring 1. - no more than 30 ventricular extrasystoles in any hour of monitoring more than 30 ventricular extrasystoles in any hour monitoring polymorphic ventricular extrasystoles. 4. A - monomorphic paired ventricular extrasystoles. 4. B - polymorphic paired ventricular extrasystoles. 5. ventricular tachycardia (more than 3 in a row extrasystoles).





    Treatment In most cases, specific antiarrhythmic therapy for extrasystole is not required. Prognostically the most unfavorable are ventricular extrasystoles of high gradations according to B. Lown - grade 2 and higher. Preventive treatment of high-grade ventricular premature beats corresponds to the treatment of ventricular tachycardia




    Diagnosis of tachyarrhythmias Diagnosis is assisted by: long-term recording of leads II, aVF, or Vd. Doubled ECG voltage and increasing paper tape speed up to 50 mm / s help to identify P waves; additional ECG leads (right side of the chest, esophageal ECG, right atrial area) facilitate the recognition of P waves.


    Atrial fibrillation. The rhythm is "wrong wrong". Absence of P waves, random large or small-wave oscillations of the isoline. Atrial wave frequency min In the absence of treatment, ventricular rate min – 1 Electrical alternation (different heights of QRS complexes)


    Causes: mitral defects, myocardial infarction, thyrotoxicosis, PE, postoperative condition, hypoxia, COPD, atrial septal defect, WPW syndrome, sick sinus syndrome, drinking large doses of alcohol, can also be observed in healthy individuals.


    Causes If, in the absence of treatment, the frequency of ventricular contractions is low, then one can think of impaired conduction. With glycosidic intoxication (accelerated AV nodal rhythm and complete AV block) or against a background of very high heart rate (for example, with WPW syndrome), the rhythm of ventricular contractions may be correct.



    12 months Severe symptoms Minimal symptoms Minimal symptoms Severe symptoms Direct Cardio version Digoxin BB Verapamil FOR 3 weeks Digoxin BB Verapamil BB Verapamil Permanent "title =" (! LANG: ALGORITHM FOR TREATMENT OF ATIBLE ARRHYTHMIA Acute 12 months Severe symptoms Severe symptoms Direct Cardio version Digoxin BB Verapamil ON 3 weeks Digoxin BB Verapamil BB Verapamil Permanent p" class="link_thumb"> 50 !} ALGORITHM FOR TREATMENT OF ATIBLE ARRHYTHMIA Acute 12 months Severe symptoms Minimal symptoms Minimal symptoms Severe symptoms Direct Cardio version Digoxin BB Verapamil for 3 weeks Digoxin BB Verapamil BB Verapamil Continuous use of NA or Aspirin Selective cardioversion Episodes of long-term therapy AAropaphism None Sotalol Continuous use of NA or Aspirin 12 months Severe symptoms Minimal symptoms Minimal symptoms Severe symptoms Direct Cardio version Digoxin BB Verapamil ON 3 weeks Digoxin BB Verapamil BB Verapamil Permanent p "> 12 months Severe symptoms Minimal symptoms Minimal symptoms Severe symptoms Direct Cardio version Digoxin BB Verapamil ON 3 weeks BB Verapamil BB Verapamil Continuous use of NA or Aspirin Selective cardioversion Long-term AA therapy Isolated Episodes - None Paroxysmal seizures Propafenone, Amiodarone, Sotalol Continuous use of NA or Aspirin "> 12 months Severe symptoms Minimal symptoms Minimal symptoms Severe symptoms Direct Cardioplastic version Vibroxamil 3 weeks Digoxin BB Verapamil BB Verapamil Constant n "title =" (! LANG: ALGORITHM FOR TREATMENT OF ATIBLE ARYTHMIA Acute 12 months Severe symptoms Minimum symptoms Minimal symptoms Severe symptoms Direct Cardio version Digoxin BB Verapamil ON 3 ned Digoxin Bb"> title="ALGORITHM FOR TREATMENT OF ATIBLE ARRHYTHMIA Acute 12 months Severe symptoms Minimal symptoms Severe symptoms Direct Cardio version Digoxin BB Verapamil FOR 3 weeks Digoxin BB Verapamil BB Verapamil Permanent p"> !}


    Atrial flutter. ECG criteria 1. F waves of a sawtooth shape with a frequency of 1 min 2. F waves pass into one another without an isoelectric line in II, III, AVF 3. Absence of P waves 4.QRS complex is not changed 5. HRF is usually about 150 per 1 min 6. Distinguish between regular and irregular forms of TP


    Diagnostics With 1: 1 AV conduction, the ventricular rate can reach 300 min – 1, while the QRS complex may expand due to aberrant conduction. ECG as for ventricular tachycardia; observed with the use of class Ia antiarrhythmic drugs without the simultaneous administration of AV blockers, with WPW syndrome



    Electric impulse therapy is used for: - Atrial flutter, ventricular fibrillation - Ventricular paroxysmal tachycardia, especially in patients with acute myocardial infarction - Atrial flutter 1: 1 - Nonventricular paroxysmal tachycardia, tachyarrhythmic form of atrial fibrillation A (with papillomavirus failure) A or papudin ineffectiveness form of atrial fibrillation after mitral commissurotomy, if MA is not more than 3 years




    Causes of flutter and ventricular fibrillation - organic heart disease - increased tone of sympathetic NS - hypoxia - violation of homeostasis - decrease in body temperature, trauma - drugs (antiarrhythmics, cardiac glycosides) - electric current



    WOLF-PARKINSON-WHITE syndrome (WPW) -Ventricular premature excitation syndrome - Excitation wave is conducted from the atria to the ventricles along an additional Kent beam On the ECG: - delta wave - shortening of P-Q less than 0.12 sec - expansion of the QRS complex more than 0.11 sec



    Sinoatrial blockade. The extended PP spacing is a multiple of normal. Causes: some drugs (cardiac glycosides, quinidine, procainamide), quinidine procainamide, hyperkalemia, sinus node dysfunction, myocardial infarction, increased parasympathetic tone. Sometimes the Wenckebach period is noted (a gradual shortening of the PP interval until the next cycle falls out).



    0.20 s. Each P wave has a corresponding QRS complex. Causes: observed in healthy individuals, athletes, with an increase in parasympathetic tone, taking certain drugs (cardiac glycosides, quinidine, "title =" (! LANG: 1st degree AV block. PQ ​​interval> 0.20 s. Each P wave corresponds QRS complex Causes: observed in healthy individuals, athletes, with an increase in parasympathetic tone, taking certain medications (cardiac glycosides, quinidine," class="link_thumb"> 62 !} 1 degree AV block. PQ interval> 0.20 s. Each P wave has a corresponding QRS complex. Causes: observed in healthy individuals, athletes, with an increase in parasympathetic tone, taking certain drugs (cardiac glycosides, quinidine, procainamide, propranolol, verapamil), quinidine-procainamide propranololaverapamil, rheumatic attack, myocarditis, congenital heart disease, open heart disease ... 0.20 s. Each P wave has a corresponding QRS complex. Causes: observed in healthy individuals, athletes, with an increase in parasympathetic tone, taking certain medications (cardiac glycosides, quinidine, "> 0.20 s. Each P wave corresponds to a QRS complex. Reasons: observed in healthy individuals, athletes, with an increase in parasympathetic tonus, taking certain medications (cardiac glycosides, quinidine, procainamide, propranolol, verapamil), quinidine-procainamide propranololaverapamil for rheumatic fever, myocarditis, congenital heart defects (atrial septal defect, P corresponds to an open ductus arteriosus). QRS complex Causes: observed in healthy individuals, athletes, with an increase in parasympathetic tone, taking certain medications (cardiac glycosides, quinidine, "title =" (! LANG: 1st degree AV block. PQ ​​interval> 0.20 s. Each the P wave corresponds to the QRS complex.Causes: observed in healthy individuals, athletes, with an increase in the parasympathetic tone sa, taking certain medications (cardiac glycosides, quinidine,"> title="1 degree AV block. PQ interval> 0.20 s. Each P wave has a corresponding QRS complex. Causes: observed in healthy individuals, athletes, with an increase in parasympathetic tone, taking certain medications (cardiac glycosides, quinidine,"> !}





    AV block of the 2nd degree of the Mobitz type I (with the Wenckebach period). Increasing lengthening of the PQ interval up to the loss of the QRS complex. Causes: observed in healthy individuals, athletes, while taking certain medications (cardiac glycosides, beta-blockers, calcium antagonists, clonidine, methyldopa, flecainide, encainide, propafenone, lithium), clonidine methyldopa flecainide encainidapropafenonalitia (especially rheumatoid arthritis in case of myocardial infarction) , myocarditis.








    Reasons: complete AV block is congenital. The acquired form of complete AV blockade occurs with myocardial infarction, isolated disease of the conducting system of the heart (Lenegra's disease), aortic defects, taking certain medications (cardiac glycosides, quinidine, procainamide), quinidine procainamide, endocarditis, Lyme disease, hyperkalemia, infiltrative diseases (amyloidosis sarcoidosis), collagenosis, trauma, rheumatic attack.



    Paroxysmal supraventricular heart rate tachycardia P wave is pointed or inverted in leads II, III, aVF Sharply replaced by sinus rhythm Can be in healthy people and with WPW Tactics: Stimulation of the vagus; if there is no effect: adenosine, verapamil, beta-blocker, group IA drug, electro-pulse therapy (150 J)




    Ventricular PT Usually correct rhythm with a rate of min – 1. QRS complex> 0.12 s, usually> 0.14 s. The ST segment and T wave are discordant to the QRS complex. 0.12 s, typically> 0.14 s. The ST segment and T wave are discordant to the QRS complex. "> 0.12 s, usually> 0.14 s. The ST segment and T wave are discordant to the QRS complex."> 0.12 s, usually> 0.14 s. ST segment and T wave discordant to the QRS complex. "Title =" (! LANG: Ventricular PT Usually regular at 110-250 min – 1. QRS complex> 0.12 s, usually> 0.14 s. ST segment and T wave discordant complex QRS."> title="Ventricular PT Usually 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 (glycosidic intoxication, antiarrhythmic drugs, phenothiazines, tricyclic antidepressants, caffeine, alcohol, nicotine), mitral valve prolapse, in rare cases in healthy individuals.



    Restoration of sinus rhythm (step-by-step approach): 1) vagotropic techniques (Valsalva test, massage of the carotid sinus); 2) adenosine, verapamil or diltiazem IV. In heart failure, digoxin is administered instead of calcium antagonists; adenosineverapamyldyltiazem digoxin 3) procainamide or propafenone. Procainamidepropafenone.


    B. Prevention of paroxysms: 1) rare, short paroxysms, proceeding without hemodynamic disturbances: only vagotropic techniques. Otherwise, catheter destruction or constant intake of AV blockers; 2) in case of ineffectiveness of AV-conduction blockers, drugs of class Ia or Ic are added.