Differential diagnosis and treatment of heart rhythm disorders. Differential diagnosis of atrial fibrillation Differential diagnosis of arrhythmias
State educational institution higher
Stavropol State medical Academy
Ministry of Health and Social Development of the Russian Federation
I approve
head department
internal medicine №1
with a polyclinic course
therapy A.V. Berry
"___" _____________ 200__
METHODOLOGICAL DEVELOPMENT
To practical lesson for students
6th year specialty "General Medicine"
By academic discipline"internal illnesses"
TOPIC No. 3. DIFFERENTIAL DIAGNOSTICS AND TREATMENT OF HEART RHYTHM AND CONDUCTION DISORDERS
LESSON No. 2. DIFFERENTIAL DIAGNOSTICS AND TREATMENT OF HEART CONDUCTION DISORDERS
Discussed at the meeting
Department of Internal Medicine No. 1
with a course of outpatient therapy
"___" _____________ 200__
Protocol No.___
Methodological development compiled
Shnyukova T.V.
Stavropol, 200__
Topic 3. Differential diagnosis and treatment of heart rhythm and conduction disorders
Lesson 2. Differential diagnosis and treatment of cardiac conduction disorders
Study questions for the lesson:
Questions for independent work(self-training) students:
Algorithm for differential diagnosis of cardiac conduction disorders;
Differential diagnostic signs of sinoauricular and intraatrial blocks;
Differential diagnostic signs of atrioventricular block;
Differential diagnostic signs of intraventricular blockades;
Differential diagnostic signs of sick sinus syndrome;
Principles of differentiated therapy for cardiac conduction disorders. Temporary and permanent cardiac pacing;
Emergency treatment of asystole.
Questions for self-study by students:
Surgical methods for treating cardiac conduction disorders.
List of diseases and conditions studied:
Sinoauricular (sinoatrial) blocks;
Intraatrial blocks;
Atrioventricular block;
Intraventricular blocks;
Sick sinus syndrome.
Location of the lesson: clinical base of the Department of Internal Medicine No. 1 with a course of outpatient therapy - cardiology department No. 2 of the State Health Institution SKKKD.
Materials and laboratory support:
Educational tables;
Electrocardiogram sets;
Sets of test tasks;
Sets of situational problems.
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 acquired knowledge 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, stress ECG, daily and multi-day ECG monitoring for cardiac conduction disorders;
Basic principles of medical care in emergency conditions arising from cardiac conduction disturbances (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 justify the clinical diagnosis of a patient with intracardiac conduction disorders;
Decipher the ECG in 12 leads of patients to identify various forms of cardiac conduction disorders;
Draw up a plan for examining a patient with cardiac conduction disorders;
Provide emergency care for conditions (ventricular asystole) complicating intracardiac conduction disturbances;
Carry out resuscitation measures in cases of clinical death;
Methods of auscultation of the heart and blood vessels;
Interpretation of the results of instrumental methods of examining a patient with cardiac conduction disorders;
An algorithm for making a preliminary and detailed clinical diagnosis (main, concomitant, complications) of a patient with cardiac conduction disorders;
Carrying out basic medical treatment measures to provide first aid medical care with ventricular asystole;
HAVE A SET OF COMPETENCIES:
Ability and readiness to carry out primary and secondary prevention of cardiac conduction disorders;
The ability and willingness to identify deviations in the health of a patient with cardiac conduction disorders, taking into account the laws of the flow of pathology across systems, areas and the body as a whole; using knowledge of fundamental and clinical disciplines;
The 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 identify cardiac conduction disorders on early stages, typical, as well as low-symptomatic and atypical manifestations of the disease, using clinical, laboratory and instrumental methods to an adequate extent;
the ability and willingness to correctly formulate the established diagnosis, taking into account ICD-10, with additional examination and prescription of adequate treatment;
The ability and willingness to assess the need to choose an outpatient or inpatient treatment regimen and resolve issues of assessing work capacity; draw up primary and current documentation, evaluate the effectiveness of dispensary observation.
Ability and willingness to evaluate application possibilities medicines for the treatment and prevention of cardiac conduction disorders; analyze the effect of drugs based on the totality of their pharmacological properties; possible toxic effects of drugs;
The ability and willingness to interpret the results of modern diagnostic technologies, understand the strategy of the new generation of therapeutic and diagnostic drugs;
The ability and willingness to perform basic diagnostic and therapeutic measures, as well as to carry out optimal choice drug therapy to provide first aid for emergency and life-threatening conditions that complicate the course of cardiac conduction disorders;
Ability and readiness to analyze performance indicators of health care facilities various types in order to optimize their functioning, to the use of modern organizational technologies for diagnosis, treatment, rehabilitation, prevention in the provision of medical services in the main types of treatment and preventive institutions;
Ability and readiness to maintain medical records and records;
The ability to independently analytically work with various sources of information, the willingness to analyze the results of one’s own activities to prevent professional errors;
HAVE SUGGESTIONS:
On surgical methods for correcting cardiac conduction disorders.
Integrative connections (elements of a unified lifelong learning program):
- normal anatomy: structure of cardio-vascular system;
- normal physiology: intracardiac conduction of electrical impulse is normal;
- pathological physiology: intracardiac conduction of electrical impulses in case of conduction disorders;
- propaedeutics 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. – St. Petersburg, 2001.
2. Internal diseases: textbook: in 2 volumes / Ed. N.L. Mukhina, V.S. Moiseeva, A.I. Martynov. – 2nd ed., rev. and additional – M: GEOTAR-Media, 2004.
3. Internal diseases: textbook: in 2 volumes / Ed. N.L. Mukhina, V.S. Moiseeva, A.I. Martynov. – 1st ed. – M: GEOTAR-Media, 2001.
4. Internal diseases: textbook: in 2 volumes / Ed. N.L. Mukhina, V.S. Moiseeva, A.I. Martynov. – 2nd ed., rev. and additional – M: GEOTAR-Media, 2005.
5. Internal diseases: textbook / Ed. IN AND. Makolkina, 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 diseases / N.A. Mukhin. – M., 2006.
3. Cardiology: A Guide for Doctors / Ed. R.G. Oganova, I.G. Fomina. – M.: Medicine, 2004.
4. Diagnosis of cardiovascular diseases. Formulation, classifications. Pract. manual / Ed. I.N. Denisova, S.G. Gorokhova. – M.: Geotar-Media, 2005.
Familiarize yourself with the learning objectives (general and specific) and educational issues classes;
Restore acquired knowledge of basic disciplines within the framework of integrative connections on the topic being studied;
Analyze the work done by answering questions for independent work (self-preparation) and independent study;
Execute test tasks(Appendix 2) and solve situational problems (Appendix 3).
Appendix 1. Abstract (current state of the issue):
Sinoauricular (SA) block represents a deceleration
or cessation of impulse transmission from the sinus node through
sinoatrial connection to the atria.
The most common cause of SA block is ischemic heart disease, especially
with damage to the right coronary artery. Also, SA blockade occurs with myocarditis, hypertension, or as a result of the action
medications (cardiac glycosides, quinidine,
β-blockers, cordarone, isoptin). Cause of SA blockade
There may also be increased vagal tone.
Classification of SA blockade
· The first degree of SA block does not cause any changes
cardiac activity and does not appear on a regular ECG. Wherein
In the form of blockade, all sinus impulses pass to the atria.
· With SA block of the second degree, sinus impulses through the SA
The connection sometimes fails. This is accompanied by loss
one or more atrioventricular complexes in a row. With second degree SA blockade, dizziness may occur,
feeling of irregular heart activity or fainting. During
Pauses of sinoauricular block may cause slipping
contractions or rhythms from underlying sources (AV connection,
Purkinje fibers);
· With SA block of the third degree, impulses from the side
sinus node does not pass through the SA connection and activity
heart rate is associated with the activation of underlying rhythm sources.
Currently, only 2 degrees of SA block are diagnosed, since the rest are not diagnosed.
SA blockade clinic
Freezing of the heart if one pulse falls. Dizziness if several pulses fall out. Morgagni-Edams-Stokes syndrome (loss of consciousness), if 6-8 complexes fall out.
On ECG the entire cardiac complex is missing. There is no P, T, QRS, instead of them a long pause is visible, which can be a multiple of any number R-R and is equal to 2, 3, 4, etc., respectively. normal R-R. Sliding, replacing complexes are often visible: during
after a long pause, its own impulse jumps out to help (the artioventricular node helps); there will be no P wave. Auscultation At this time, a loud tone can be heard - a strong contraction of the heart.
Treatment tactics for SA conduction disorders related to treatment
underlying disease causing conduction disturbances. Specific therapy for SA blockade:
1. Increased heart rate:
· anticholinergics (belladonna extract, platifilin)
· sympatholytics, but they should be prescribed in small quantities, with great caution, as they can provoke an attack of angina pectoris: isadrin sublingually or in the form of inhalations;
2. Antiarrhythmic therapy. Very mild medications are prescribed: delagil at night.
3. Calcium antagonists: isoptin.
4. If there is frequent loss of consciousness, the patient is transferred to continuous electropulse therapy. But more often it is necessary to spend temporary on-demand pacing.
Intraatrial block
Often associated with organic lesions, often a harbinger of atrial fibrillation.
It can also occur with sharp dilatation of the atria.
Etiology: heart defects, ischemic heart disease, overdose of antiarrhythmic drugs.
Clinical manifestations practically does not give.
The only one diagnostic method– ECG: widening and splitting of the P wave (normally no more than 0.10 seconds). Often the P wave becomes biphasic (+/-).
There may be a deeper lesion - damage to the Bachmann bundle - atrial parasystole syndrome ( 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. Rarely seen.
Atrioventricular block
occurs due to a disruption in the conduction of electrical impulses from the atria to the ventricles along the AV junction.
The causes of conduction disturbances through the AV junction may be ischemic heart 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 skeleton of the heart involving the valve apparatus) and Lenegra's disease (primary sclerosing lesion of the conduction system of the heart, not involving the myocardium and fibrous skeleton of the heart).
Classification of AV blocks
· AV blockade of the first degree (slowing of impulse conduction from the atria to the ventricles through the AV node);
· II degree (slowing of impulse conduction 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 contraction of the ventricles due to the appearance of a 2nd or 3rd order pacemaker).
Separately allocate artificially created AV block. They also share proximal(AV node only) and distal(with damage to the His-Purkinje system) AV block. Distal AV blocks have a less favorable prognosis.
Clinical manifestations with AV block depend on the etiology of the underlying disease and the degree of heart rate slowdown.
· With AV block of the first degree, the state of health may not change; less often, sensations of a rare rhythm or interruptions in the work of the heart appear.
· With second degree AV block, attacks of severe weakness, dizziness with darkening of the eyes, presyncope or syncope may occur.
· Third degree AV block in all patients is accompanied by deterioration of hemodynamic parameters due to decreased myocardial contractility and a decrease in ventricular ejection fraction. This is manifested by a deterioration in the blood supply to all organs, primarily the brain, heart and others. In addition, conditions are created for the occurrence of ventricular extrasystole and tachycardia, ventricular flutter and fibrillation, and cardiac asystole. Patients experience Morgagni-Edams-Stokes attacks, and in some cases sudden death.
Electrocardiographic signs of 1st degree AV block:
· prolongation of the PR (Q) interval by more than 0.21 seconds at normal frequency and more than 0.22 seconds with sinus bradycardia;
· the interval increases due to the lengthening of the segment from the end of 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 second degree AV block:
· Type I or Mobitz type I is characterized by the Samoilov-Wenckebach periodicity: gradual lengthening of the PR (Q) interval with each cardiac cycle; loss of the QRS complex that occurs after the longest P-R (Q), after which the normal P-R (Q) interval is recorded again. In the absence of loss of the QRS complex, 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 PR (Q) interval in a ratio of 2:1, 3:1, 4:1, etc. Constant increase in the Р-R (Q) interval, i.e. AV block of the first degree, in combination with loss of the QRS complex in the ratio 2: 1, 3: 1, 4: 1, etc.
Electrocardiographic signs of third degree AV block (complete transverse heart block):
· cessation of conduction of impulses from the atria to the ventricles, due to which the atria are excited and contract in their own 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 compared to the previously existing sinus rhythm, since the sources of excitation of the ventricles become the AV connection or the ventricular conduction system, which are designated as ectopic centers of automaticity of the second or third order;
· in individual complexes P is superimposed on the ST and T segments of the QRST complex, deforming them;
· there is no relationship between P and the subsequent QRTS complex, while the P-P intervals are always smaller and remain constant, a R-R moreР-Р and can be different in size;
· there is a pattern that with foci of third-order automatism there is a rarer rhythm, less than 40 beats/min, and an expanded, deformed QRS complex.
In the vast majority of cases, when third-degree AV block occurs, 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 pacemaker implantation for AV blockade divided into three groups: A – implantation is necessary, B – implantation is desirable, C – implantation is undesirable. Asymptomatic patients with first-degree AV block should be examined frequently because of the possibility of sudden worsening of the degree. In case of second degree AV block with clinical manifestations, pacemaker implantation is indicated. For proximal asymptomatic second-degree AV block, implantation is usually not required. In case of distal asymptomatic second-degree AV block, pacemaker implantation is desirable due to the risk of asystole and progression of the degree of block. In case of complete AV block with clinical manifestations, pacemaker implantation is indicated. Asymptomatic patients with complete AV block may not require pacemaker implantation if the secondary pacemaker has adequate rate and stability and is not suppressed by high-frequency pacing after autonomic heart block. In patients with complete AV block during acute myocardial infarction (regardless of its location and at any width of the QRS complex), temporary cardiac pacing is indicated. For AV blockades, it is preferable to implant dual-chamber pacing systems. Isolated ventricular stimulation, without maintaining the coordinated atrial contribution to hemodynamics, with AV blockade is prognostically less favorable.
Among the complications of third degree AV block and other life-threatening arrhythmias is Morgagni-Edams-Stokes syndrome.
Morgagni-Edams-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 due to asystole, flutter and ventricular fibrillation. Severe cerebral ischemia occurs when cardiac output decreases below two liters per minute due to cardiac arrhythmias.
Depending on the type of cardiac arrhythmia, three pathogenetic forms of Morgagni-Edams-Stokes are distinguished: bradycardic, tachyarrhythmic and mixed forms.
Clinical manifestations of Morgagni-Edams-Stokes syndrome are determined by the duration of life-threatening arrhythmias and the resulting severe hemodynamic disorders and cerebral ischemia.
Clinical manifestations of Morgagni-Edams-Stokes syndrome depending on the duration of life-threatening cardiac arrhythmias:
· Within 3-5 seconds. Sudden onset of a presyncope (lipothymic) state: severe weakness, dark circles before the eyes, slow speech, lack of coordination, indifference to the environment and disorientation, increasing noise or ringing in the ears and head, nausea, vomiting, pallor skin, decreased blood pressure, heart rhythm disturbances (which can be determined by the pulse and auscultation of the heart, but the type of arrhythmia is diagnosed only when an 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 torso may occur, 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 an ECG is taken at this moment).
· Within 20-40 seconds. Deep fainting persists: hemodynamic disorders progress, breathing disorders persist, generalized epileptiform convulsions appear, patients who have suffered a brain injury may have tongue biting, involuntary urination and defecation, heart rhythm disturbances (which can be determined by the 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. State of clinical death: periodic breathing, Cheyne-Stokes type with increasing period of apnea, bubbling breathing, as with increasing pulmonary edema, intense cyanosis, most often of the upper half of the body, muffled heart sounds, rare rhythm, periods of asystole alternating with periods of arrhythmia, pulse and blood pressure are not determined, the pupils are dilated, corneal reflexes decrease and disappear, and heart rhythm disturbances (which can only be determined by taking an ECG at this moment).
· After 5-10 minutes. Comatose state or biological death: periodic breathing, Cheyne-Stokes type, with an increase in the period of apnea, bubbling breathing, as with increasing pulmonary edema, intense cyanosis, muffled heart sounds, rare rhythm, periods of asystole alternating with periods of arrhythmia, pulse and blood pressure are not are determined, the pupils are dilated, corneal reflexes decrease and disappear, heart rhythm disturbances (which can only be determined by taking an ECG at this moment).
Morgagni-Edems-Stokes attack can be stopped at all stages of treatment emergency care, carrying out resuscitation measures. Treatment tactics are determined by the type of heart rhythm disorder. Treatment programs of one kind or another are almost always implemented, including resuscitation measures for asystole or ventricular flutter-fibrillation, etc.
Intraventricular conduction disorders
(intraventricular block)
Intraventricular blockades occur when the propagation of an impulse from the sinus node and atria through the ventricles is disrupted due to the absence or slowdown of conduction along one of the bundle branches. One ventricle is activated through the interventricular septum later than the other by approximately 0.04-0.06 seconds. Therefore, the ventricular QRS complex becomes abnormally wide (more than 0.12 seconds) and distorted. The most common are right or left bundle branch blocks.
ECG signs of complete block of the right bundle branch:
· splitting of the QRS complex in the form of the letter M - rsR, rsR", RSR" RsR", rR" forms and increased time of internal deviation (intrinsicoid deflection) in leads V 1, V 2, V 3 R, aVR more than 0.06 seconds;
· deep, jagged 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 displacement of the ST segment and a 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 conduction system of the heart, so its blockade occurs with significant anatomical damage.
ECG signs of complete block of the left bundle branch:
· expansion of the QRS complex to 0.12 seconds or more;
· wide and split R wave (Q and S waves are absent) 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 displacement of the ST segment with a negative asymmetric T wave in leads V 5, V 6, I, aVL. Shifted upward ST segment with high asymmetric T wave in leads V 1, V 2 and sometimes in leads III and aVF;
· in the vast 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 a pathological deviation of the axis to the left.
Sick sinus syndrome (SSNS)
occurs more often at a certain stage in the evolution of certain diseases. In the vast majority of cases, this heart rhythm disturbance reveals significant morphological changes in the atrial myocardium or atherosclerosis of the artery of the sinus node. 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, often drugs, and permanent changes. In elderly patients, coronary artery disease may debut with sick sinus syndrome. The occurrence of sick sinus syndrome in the overwhelming majority is observed against the background of severe organic pathology of the heart and characterizes a prognostically unfavorable course.
Sick sinus syndrome may occur various types arrhythmias, while they often alternate in the same patient and are detected for the first time during antiarrhythmic therapy. Highlight the following cardiac arrhythmias in SSSS: sinus bradycardia with escape contractions; sinoauricular block; migration of the pacemaker through the atria; asystole of the atria and ventricles; bradytachycardia syndrome, when there is an alternation of the above-mentioned heart rhythm disturbances with attacks of supraventricular tachycardia, atrial flutter-fibrillation; slow recovery of sinus rhythm after cessation of tachyarrhythmia - asystole, severe sinus bradycardia, idioventricular rhythm.
Clinical manifestations 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, progression of cardiovascular diseases is also observed, for example, an increase in angina attacks, progression of heart failure or arterial hypertension. Elderly patients suffering from atherosclerosis of the cerebral vessels more often experience attacks of severe weakness, dizziness, unsteady gait, a feeling of impending fainting, while the phenomena of discirculatory encephalopathy intensify, new neurological symptoms and syndromes arise 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-Edams-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 the issue of transesophageal electrical stimulation of the heart and further treatment tactics are decided.
Carrying out relief antiarrhythmic therapy for bradytachycardia syndrome is very dangerous due to the possibility of asystole and death of the patient.
To determine treatment tactics, it is necessary to make a differential diagnosis between sick sinus syndrome and autonomic sinus node dysfunction. The main criterion is the result of a test with atropine or a test with drug denervation of the heart. A test with atropine is carried out against the background of an ECG or 24-hour ECG monitoring. 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. The 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 is a drug-induced denervation of the heart (complete autonomic blockade) during a transesophageal (or intracardiac) electrophysiological study. Initially, the patient is determined by the time of recovery of the sinus node (SVFSU) and corrected VVFSU. Next, solutions of propranolol in the amount of 0.2 mg/kg of the patient’s body weight and atropine sulfate in the amount of 0.04 mg/kg of the patient’s body weight are administered intravenously, after which the recovery time of the sinus node is again determined. If, after drug denervation of the heart, the VVFSU (the interval from the last electrical stimulus to the first intrinsic P wave) is more than 1500 ms or the VVFSU (the difference between the value of the VVFSU and the average duration of the initial cardiac cycle) is more than 525 ms, then the patient is confirmed to have sick sinus syndrome. If the indicated values are less than the given values, then autonomic dysfunction of the sinus node occurs.
Treatment for sick sinus syndrome involves implantation of a pacemaker (pacemaker). 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 sick sinus syndrome, patients with its presence fall into group B, and if the patient has a clinical picture (MES syndrome), then he falls into group A of indications for implantation. Before placing a pacemaker, it is necessary to assess the state of AV conduction in the patient (transesophageal electrophysiological study). The presence of impaired AV conduction indicates the need for implantation of a dual-chamber stimulation system. If AV conduction is preserved, atrial stimulation is performed. Implantation of single-chamber pacemakers 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 (to prevent paroxysms of tachycardia) and during programming set a slightly higher stimulation frequency (75-80 per minute).
Autonomic dysfunction of the sinus node is well treated with anticholinergic drugs. Most often, belladonna preparations (bellataminal, besalol, becarbon, belloid) are used for its treatment. In isolated cases of severe dysfunction, implantation of a pacemaker is possible.
Appendix 2. Test tasks:
1. What diseases cause Morgagni-Adams-Stokes attacks?
1) ventricular extrasystole
2) ventricular fibrillation
3) atrial fibrillation
4) atrioventricular block
2. What signs are characteristic of sick sinus syndrome?
1) ventricular extrasystoles
2) sinoauricular (sinoatrial) blockade
3) atrioventricular block
3. The atropine test is used in patients for 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 identify hidden coronary insufficiency
5) for diagnosing sick sinus syndrome
4. Indications for electropulse therapy are:
1) rapid progression of signs of heart failure, coronary or cerebral circulatory insufficiency against the background of an attack of tachyarrhythmia
2) bradysystolic form of atrial fibrillation
3) tachyarrhythmias that developed against the background of intoxication with cardiac glycosides
5. I degree AV block is characterized by:
1) P-R interval (Q) 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 P-R interval(Q) at each cardiac cycle
4) pulse rate 36 per minute
5) correct 1 and 2
6. Type I II degree AV block is characterized by:
1) prolongation of the P-R (Q) interval more than 0.35 s
2) 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 recorded again
5) correct 2 and 4
7. Second degree AV block type II 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 (Q) interval
3) constant increase in the P-R (Q) interval
4) gradual lengthening of the P-R (Q) interval with each cardiac cycle
5) correct 2 and 3
8. ECG signs of third degree AV block are:
1) cessation of conduction of impulses from the atria to the ventricles
2) in individual 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 more R-R
4) everything is correct
9. Clinical manifestations of Morgagni-Adams-Stokes syndrome are:
1) loss of consciousness
2) increased blood pressure
3) presence of paradoxical pulse
10. Indications for temporary cardiac pacing are:
1) asystole
2) AV block of the second degree, type II and third degree in acute myocardial infarction
3) intoxication with cardiac glycosides, which is complicated by significant bradyarrhythmias
4) everything is correct
11. Indications for permanent cardiac pacing are:
1) AV block II degree II type with Morgagni-Adams-Stokes attacks
3) AV block of the third degree
4) everything is correct
12. A patient with ischemic heart disease has post-infarction cardiosclerosis. Sick sinus syndrome has been identified; for the last 2 weeks, attacks of atrial fibrillation have been occurring daily, and episodes of bradycardia accompanied by dizziness have been noted. Your tactics:
1) prescribe quinidine
2) prescribe novocainamide
3) implant a permanent artificial pacemaker
4) prescribe digoxin
5) perform temporary cardiac stimulation
13. Contraindications for the use of beta-blockers are:
1) arterial hypertension
2) sick sinus syndrome
3) bronchial asthma
4) correct 2 and 3
5) everything is correct
14. ECG signs of SA blockade are:
1) periodic loss of the P-QRS-T complex
2) prolongation of the P-R (Q) interval 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 prognosis is:
1) intraatrial block;
2) AV block of the first degree;
3) AV block of the third degree;
18. Has an asymptomatic course and is often found in athletes:
1) intraatrial block;
2) AV block of the first degree;
3) AV block of the third degree;
4) right bundle branch block.
19. When treating cardiac conduction disorders, DO NOT use:
1) temporary cardiac stimulation;
2) permanent cardiac pacing;
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:
Task 1.
Patient M., 23 years old, consulted a cardiologist. During a preventive examination before competitions (athlete, weightlifting for 11 years), the ECG revealed a complete block of the right bundle branch. He makes no complaints. EchoCG, blood and urine tests - without pathology.
1. What is the genesis of the conduction disorder in this patient?
2. Lead tactics.
3. Is it possible to participate in sports competitions?
4. Is further examination indicated?
5. What therapy can be performed for this patient?
Task 2.
Patient S., 81 years old, is under clinical observation with a diagnosis of coronary artery disease, angina pectoris FC II. Post-infarction cardiosclerosis. Over the last 2 weeks, he began to notice unmotivated attacks of acute weakness, accompanied by tinnitus, dizziness, darkening of the eyes, sweating, and decreased blood pressure. One time – loss of consciousness. The ECG shows no fundamental dynamics, sinus rhythm remains, cicatricial changes in the anteroseptal region. Holter ECG monitoring revealed transient AV block I degree and II degree Mobitz type 1. For existing ischemic heart disease and post-infarction cardiosclerosis, the patient receives an ACE inhibitor (ramipril), a β-blocker (metoprolol), a disaggregant (aspirin) and a statin (simvastatin).
1. What genesis of the cardiac conduction disorder can be assumed in this patient?
2. How to interpret complaints that appeared 2 weeks ago?
3. Is it possible to continue cardiotropic therapy at the same level?
5. Tactics for further management of the patient.
Task 3.
4. Are there indications for cardiac stimulation?
Task 4.
1. What type of conduction disorder is shown on the ECG?
2. Is normal hemodynamics possible with this conduction disorder?
3. Is it possible for this patient to develop Morgagni-Edams-Stokes syndrome?
4. Are there indications for cardiac stimulation?
5. Is antiarrhythmic therapy indicated and why?
Task 5.
Make a table in the form of a table of the main differential diagnostic differences in cardiac conduction disorders, indicating such characteristics as etiological factors, complaints, clinical manifestations, ECG data, indicated and contraindicated drugs, and possibilities of surgical correction.
Cardiac cough is a much discussed and rather conventional term in the clinic of heart disease. It is used by both doctors and patients to indicate a manifestation that signals diseases of the cardiovascular system.
The primary concept - cough in heart disease - implied a symptom of left ventricular failure of the heart and arose as a result of the accumulation and stagnation of fluid in the pulmonary circulation (in the lungs). The consequences of this pathological process are cardiac asthma and swollen lungs, in which transudate (liquid) causes defense mechanism- cough.
Therefore, the symptoms and treatment of cardiac cough constitute an urgent and sought-after problem in the healthcare system.
Provoking factors
The causes of cardiac cough are diseases that disrupt and exhaust the functioning of the heart to the stage of decompensation and the development of heart failure. The main ones:
- cardiac ischemia;
- cardiosclerosis after a heart attack;
- cardiomyopathy;
- myocarditis;
- arterial hypertension;
- arrhythmias;
- defeat and birth defects heart valves (especially the mitral valve);
- heart defects, most often acquired.
Often simultaneous problems from both respiratory system are the cause of worsening cardiac cough.
Characteristics and symptoms
Symptoms of cardiac cough appear in certain conditions and are directly dependent on physical activity. In the initial stage of the disease, the cough becomes more intense with muscle exertion, with the progression of the pathological process - with any physical stress.
The distinctive signs of cardiac cough from other types of cough are illustrated by the question “cardiac cough - what is it?”:
- Causes discomfort and pain in the heart and chest area during coughing.
- It is inevitably accompanied by a strong heartbeat in most cases.
- As a rule, it is dry, without phlegm, in contrast to bronchial cough and in smokers. The appearance of bloody discharge indicates an acute course or an advanced form of heart failure (impaired functioning of the left ventricle).
- Patients experience hoarse and ineffective breathing, which is manifested by shortness of breath, a feeling of lack of oxygen and cyanosis. First, this condition occurs under significant loads, followed by minimal physical activity (climbing stairs, accelerating steps) or significant monologue during conversation.
- Loss of consciousness (fainting) and possible swelling of the neck veins reveal poor circulation and an increase in chest pressure.
Cough in heart failure has special characteristics. With left ventricular damage, it is loud, exhausting, predominantly dry and irritable, occurs mainly in the evening and interferes with sleep. The patient's position during sleep in the horizontal plane also provokes a cough; he instinctively sits down and lowers his legs down to reduce the load on the heart and lungs. Over time, hemoptysis develops.
This set of signs will help distinguish it from a cough of another nature and refer you for consultation to a cardiologist.
Treatment
Basic principles and methods of therapy include:
- detailed examination of the patient and differential diagnosis with pathology of the respiratory system;
- identification and elimination of the underlying cardiac disease that provokes cough;
- an integrated approach to treatment instead of symptomatic cough suppression, which clears the bronchi of fluid.
Treatment of cardiac cough includes a combination of an optimal work and rest schedule, a diet in accordance with the underlying disease, a healthy lifestyle and the prescription of medications. To reduce pressure on the pulmonary circulation, diuretics and vasodilators are used. If necessary, antitussive and expectorant medications are used. Combination with oxygen therapy and drugs to strengthen the myocardium and improve its function leads to visible results.
Treatment of cardiac cough with folk remedies during the acute period of the disease and during severe course Not recommended. Decoctions and infusions, which include mint, lemon balm, valerian root, yarrow, are used under the supervision of a doctor in full courses during the recovery stage and for the purpose of prevention.
Thus, the answer to the question “how to treat cardiac cough?” serves as an integrated approach, which is based on drug treatment of the underlying disease, maintaining the structure and function of the heart muscle and relieving the load on the circulatory system in combination with a healthy lifestyle and nutrition. Application of funds traditional medicine possible with the permission of the attending physician.
As a result, “is there a cardiac cough?” we can say that it not only exists, but its presence is a signal to immediately seek medical advice without self-medicating.
Symptoms and treatment of paroxysmal atrial fibrillation
The heart works constantly, without stopping. The strong muscular walls of the heart sections - the atria and ventricles - help it pump blood. During contractions of muscle tissue, the heart contracts and pushes the blood flow.
- Atrial fibrillation - concept
- Classification of the disease
- Causes of atrial fibrillation
- Clinical picture of the pathology
- Diagnosis of atrial fibrillation
- Emergency assistance for an arrhythmia attack
- Treatment of atrial fibrillation
- Conservative treatment
- Electropulse therapy
- Surgery
- Traditional methods of therapy
- Complications of the disease
- Prevention measures
- Prognosis for atrial fibrillation
A clear rhythm of heart contractions is set by the sinus (sinoatrial) node, located in the right atrium. This pacemaker sends impulses to the atrioventricular node, located between the atria and ventricles.
When the AV node receives too many impulses, a person experiences irregular heartbeat and is diagnosed with paroxysmal atrial fibrillation.
Atrial fibrillation - concept
PMA - paroxysmal atrial fibrillation (synonymous with atrial fibrillation, or AF) - is a type of arrhythmia, a widespread disorder of atrial contraction.
This form of arrhythmia is distinguished by the occurrence of tachycardic attacks (paroxysms) with a heart rate of 350 – 700 beats per minute.
With this type of atrial fibrillation, the upper chambers of the heart contract at a high frequency and irregularly, and the attack can last from a couple of minutes to several days.
The specific rate of heart contraction will depend on individual indicators:
- level of activity of the nervous system;
- physiological properties of the atrioventricular node;
- taking medications;
- presence/absence of organic heart pathologies, etc.
Paroxysmal atrial fibrillation (PFAF) is a common diagnosis among other heart rhythm disorders (heart rhythm disorders). The disease occurs in 1 - 2% of the population, and after 80 years - already in 8%; the risk of developing arrhythmia in men and women is approximately the same. In stroke survivors, such a heart rhythm disorder is recorded in 20% of cases. Atrial fibrillation
Danger sudden death with atrial fibrillation it increases 2 times compared to a healthy person. The lethal outcome is caused by severe hemodynamic and thromboembolic complications. A person with AF is exempt from military service.
Classification of the disease
Depending on the specific heart rate per minute, the following types of pathology are distinguished:
- Fluttering with a contraction frequency of up to 200 beats.
- Flickering with a contraction frequency of 200 beats.
Since the ventricles begin to contract more intensely against the background of arrhythmia, the classification takes into account the following forms of the disease:
- Tachysystolic (tachyform) - the ventricles contract more than 90 times per minute.
- Bradysystolic - the rate is less than 60 times per minute.
- Normosystolic - the contraction rate is between 60 and 90.
Another classification divides arrhythmia into the following forms:
- ventricular, with severe disturbances of heart rhythms, clearly expressed by ECG;
- atrial, with changes in His bundle conductivity;
- mixed, with a combination of the two indicated forms.
The first identified episode of the disease should be distinguished from paroxysmal fibrillation itself, in which the paroxysm is repeated and lasts up to 7 days (usually up to 2 days).
The disease can persist (last more than a week) or become a long-persistent type (the attack lasts up to a year).
With frequent exacerbations of cardiac arrhythmia, they speak of the recurrent type. The permanent type of the disease implies the persistence of symptoms of atrial fibrillation for more than a year with the ineffectiveness of the therapy.
According to the signs, AF is divided into classes:
- The first is that there is no clinical picture.
- Second, the quality of life does not suffer, but there are mild signs of illness.
- Third - there are numerous complaints, the patient has to limit himself in life.
- Fourth - the clinic is bright, there are disabling complications.
Causes of atrial fibrillation
Young people often develop an idiopathic form of the disease, the cause of which cannot be determined. In other cases, drug addiction and alcoholism, hereditary predisposition and genetic diseases can disrupt the functioning of the heart in a patient under 30 years of age.
In older people, ischemic heart disease (CHD) is considered the main cause of atrial fibrillation.
The etiology of paroxysms of atrial fibrillation may be as follows:
- diseases of the thyroid gland, especially thyrotoxicosis;
- rheumatism;
- valvular heart failure;
- cardiomyopathies of various types;
- inflammation of the heart membrane - pericarditis;
- long-term hypertension;
- obstructive apnea syndrome;
- previous ischemic stroke, heart attack;
- amyloidosis;
- myxoma and sarcoma of the heart;
- hemochromatosis;
- serious types of anemia;
- low potassium levels in the body;
- lung cancer, emphysema, pneumonia, pulmonary embolism;
- severe poisoning;
- electric shock;
- SVC syndrome (Wolf-Parkinson-White syndrome).
Paroxysmal arrhythmias sometimes become a consequence of unsuccessful heart surgery. Risk factors against which situational arrhythmia with paroxysm may occur:
- smoking;
- abuse of coffee, energy drinks;
- severe stress.
The pathogenesis of paroxysmal contractions of the heart is associated with a combination of the appearance of multiple waves and focal changes. Several rhythm centers are formed in the atria, and impulses are formed in them, and not in the pacemaker. Due to the presence of additional conduction pathways, the atria contract in an enhanced manner, transmitting impulses to the ventricles.
Clinical picture of the pathology
Symptoms in mild forms of heart damage may be completely absent. Episodes of atrial fibrillation may occur without obvious manifestations, or a person may notice slight discomfort in the chest. The symptoms are not the same in each specific case of arrhythmia attacks.
The clinical picture of cardiac arrhythmia can be highly variable and include the following components:
- chest pain;
- hypotension (pressure drop);
- feeling of rapid heartbeat;
- general weakness, dizziness;
- feeling of shortness of breath and lack of air;
- cold hands and feet;
- the appearance of cold sweat;
- chills, trembling;
- faintness, loss of consciousness;
- increased urination;
- arrhythmia (irregularity) of the pulse in the arm, neck;
- panic, fear, feeling of imminent death;
- pale skin, blue lips.
The main symptom of atrial fibrillation with paroxysmal manifestations in a number of patients is the sudden development of a stroke, which can occur after a long asymptomatic course of atrial fibrillation. This type of AF development is the most severe and can be fatal.
Diagnosis of atrial fibrillation
If a patient is admitted to the hospital with an acute attack of arrhythmia, the examination is carried out in the hospital. Pre-hospital diagnostics are performed when a person seeks help from a cardiologist for a routine examination with a number of complaints.
A cardiogram (ECG) is the main method for detecting atrial fibrillation. The procedure should be done once a year even if there are no complaints over the age of 45 years. According to the ECG, signs of atrial fibrillation with attacks of paroxysms are the absence of the P wave in all leads, which is replaced by chaotic waves of tachysystoles f. R-R intervals are not the same in duration.
If the patient indicates characteristic symptoms in the anamnesis, but there are no obvious changes in the ECG, Holter monitoring is performed. An exercise ECG can help identify AF.
Organic causes of atrial fibrillation are identified after an ultrasound of the heart. Transesophageal ultrasound is indicated for suspected cardiac thrombus but is rarely performed.
Differential diagnosis is made with other types of arrhythmias and heart blocks. An example of a diagnosis: paroxysm of atrial fibrillation, tachysystolic form.
Emergency assistance for an arrhythmia attack
If an attack of cardiac arrhythmia develops, the task of the patient and his relatives is to consult a doctor as soon as possible, no later than 48 hours. After 2 days, there is a high risk of blood clots appearing inside the heart and the development of heart attack and stroke.
Algorithm for providing emergency care at home:
- Lay the person on the bed, sofa, floor.
- Open the window and provide air access.
- Advise the patient to take a deep breath, then puff out his cheeks with his mouth closed and nose pinched. This attempt is designed to act on the vagus nerve and is aimed at stopping the attack. You can press on the eyeballs, on the abdominals.
- Have the person take Warfarin or another previously prescribed anticoagulant to reduce the risk of blood clots.
At the same time, you should call the emergency team. To relieve paroxysmal arrhythmia, the doctor urgently administers a cardiac glycoside (Korglikon, Strophanthin) or a Novocainomide solution, a Lidocaine solution on glucose (intravenously).
Treatment of atrial fibrillation
After receiving the conclusion, the necessary therapy is selected for the patient, recommendations are given on healthy image life, avoiding heavy physical activity, proper nutrition. It is important to find the cause of the pathology and act on it, for example, treat hyperfunction of the thyroid gland, inflammation of the pericardium, etc.
For mild forms, treatment can be done on an outpatient basis. Indications for hospitalization are:
- first episode of fibrillation to occur;
- heart rate - more than 200 per minute;
- signs of heart failure;
- a sharp drop in pressure;
- the presence of thrombotic complications.
Conservative treatment
The goal of treatment is to restore the rhythm or maintain the arrhythmia, but with a normal heart rate. It is important to eliminate the symptoms of the disease and reduce the risk of blood clots and further complications. For anyone diagnosed with a paroxysmal form of arrhythmia, the doctor is required to write a prescription for anticoagulants and antiplatelet agents.
If a person is under 60 years of age and there is no organic damage to the myocardium, drug treatment should include constant intake of acetylsalicylic acid (Aspirin-Cardio, Cardiomagnyl).
In the presence of coronary artery disease and other aggravating diseases, Warfarin is indicated with regular monitoring of tests. In acute cases, low molecular weight heparins are prescribed for a short period of time.
To restore the rhythm, medical assistance (cardioversion) is prescribed, which can be pharmacological or instrumental.
There are a number of effective antiarrhythmic drugs that prevent repeated attacks of paroxysmal fibrillation:
- Cordarone;
- Nibentan;
- Propafenone;
- Amiodarone;
- Allapinin;
- Sotalex.
If a heart rate control strategy is chosen without eliminating arrhythmia, then these drugs are not prescribed, but are replaced with beta-blockers (Carvedilol, Metoprolol, Betaloc), calcium channel blockers (Lerkamen, Amlodipine).
Electropulse therapy
Electrical cardioversion involves bringing the heart rhythm back to normal by applying an electric current. Due to high pain, the procedure is performed under general anesthesia. A device (cardioverter-defibrillator) with electrodes is installed in the area of the right collarbone, which sends an impulse to the heart, which reboots the functioning of the organ.
Cardioversion can be done on an emergency or elective basis. If the procedure is planned, the person should take Warfarin for a month before and after it. Before emergency cardioversion, the patient is urgently administered Heparin.
Surgery
In case of a recurrent form of the disease and the ineffectiveness of other methods, an operation - radiofrequency catheter ablation - is indicated. This is a minimally invasive intervention.
The electrode is inserted through the femoral vein into the heart, and with the help of an electric shock, pathological foci of excitation are destroyed. If it is necessary to destroy the AV node or His bundle, a pacemaker must be installed during the operation.
Traditional methods of therapy
Paroxysmal forms of arrhythmia are very life-threatening, so their treatment should only be done under the supervision of a doctor. Folk remedies can only serve as auxiliary measures to maintain and strengthen the heart muscle.
For this purpose, it is recommended to take infusions of hawthorn and rose hips, it is useful to eat lemons with honey, and add natural vegetable oils to food.
Complications of the disease
The transition of the disease to a permanent form threatens a serious decrease in the quality of life.
The most common complication is the appearance of blood clots in the heart, because the blood does not leave the atria in full, so it stagnates. When a thrombus embolizes, it can cause an ischemic stroke.
Prevention measures
In order not to encounter atrial fibrillation in its paroxysmal form, it is important:
- give up a lot of coffee and energy drinks;
- do not abuse alcohol, do not smoke;
- Do not take medications containing pseudoephedrine without a doctor’s prescription;
- Healthy food;
- take vitamins, omega-3,6,9 acids;
- treat hypertension, ischemic heart disease.
Prognosis for atrial fibrillation
The prognosis will depend on the severity of the heart disease or other disease that caused the arrhythmia. With AF, the risk of stroke is 1.5% before age 60, 25% after age 80.
The risk of sudden death increases from year to year. With proper therapy, patients live 10–20 years; after a successful operation, a person can live a full life.
Federal State Budgetary Educational Institution
higher education
"Bashkir State Medical University"
Ministry of Health of the Russian
Federation
Department of Hospital Therapy No. 2
I APPROVED
Head department,
Professor Davletshin R.A.
METHODOLOGICAL INSTRUCTIONS FOR STUDENTS
to the practical lesson
on the topic “Differential diagnosis of rhythm and conduction disorders.
ECG interpretation »
Discipline Hospital therapy
Specialty (code, name) 05/31/01 – medical practice
Semester XII
Number of hours 6 o'clock
Topic: “Differential diagnosis of rhythm and conduction disorders. ECG interpretation »
»
based work program disciplines hospital therapy, approved November 24, 2016
Reviewers:
1) manager Department of Polyclinic Therapy with IDPO course
Doctor of Medical Sciences, Professor L.V. Volevach
2) manager Department of Faculty Therapy
Doctor of Medical Sciences, Professor G.Kh. Mirsaeva
Protocol No. 6 dated January 23, 2017 was approved at a meeting of the Department of Hospital Therapy No. 2.
1. Topic and its relevance: Heart rhythm disturbances, as is known, are a consequence of changes in the basic functions of the heart: automaticity, excitability and conductivity. The relevance of the problem is due to the existence of various forms of heart rhythm disturbances, the influence of arrhythmias on the quality of life and prognosis. Heart rhythm disturbances occupy one of the leading places among the causes of cardiac death, including sudden death. The incidence of sudden cardiac death (SCD), according to various studies, is 0.36 - 1.28 per 1000 inhabitants per year. Approximately 5 - 10% of cases of VCS occur in the absence of coronary heart disease (CHD) and heart failure (HF).
Introduced into clinical practice modern methods Research such as Holter ECG monitoring, pre- and intraoperative mapping, transesophageal pacing, invasive intracardiac electrophysiological study (EPS) and others have opened up wide opportunities for a more in-depth study of the mechanisms of heart rhythm disturbances, their diagnosis, treatment and prognosis.
2. Purpose of the lesson: Master the medical skills of ECG diagnostics of various cardiac rhythm and conduction disorders
know(initial basic knowledge and skills):
age-related characteristics of the cardiovascular system.
To develop professional competencies, a student must be able to:
collect anamnesis, examine the patient’s organs and systems;
prescribe a plan for additional examination;
evaluate the results of clinical and laboratory-instrumental data;
formulate a diagnosis in accordance with the modern classification;
prescribe treatment;
conduct a work ability examination;
assign primary and secondary preventive actions and etc.
anatomical and physiological features of the cardiovascular system;
histological features of the myocardium, vessel walls
research methods for diseases of the cardiovascular system;
MAIN QUESTIONS OF THE TOPIC.
Types of LDCs.
NRS associated with sinus node dysfunction: sinus bradycardia, sinus tachycardia.
LDCs associated with the re-entry mechanism.
NDCs associated with electrolyte disturbances.
LDCs associated with conduction disorders: a-c blockades.
NRS associated with congenital anomalies of the cardiac conduction system.
Clinical signs of the main groups of LDCs:
a) extrasystole
b) atrial fibrillation
c) paroxysmal supraventricular tachycardia
d) paroxysmal ventricular tachycardia
ECG diagnostics of NRS: extrasystole, atrial fibrillation and flutter, paroxysmal tachycardia, heart block.
1) Main groups of antiarrhythmic drugs.
2) Treatment of NRS.
BASELINE CONTROL ISSUES.
3.1. Types of LDCs.
Clinical manifestations of NRS.
Mechanism of heart rhythm disturbances: disturbance of automaticity, appearance of pathological foci, re-entry mechanism, electrolytes.
Extra asystole: benign and non-benign pacemaker, gradation of pacemaker according to Lown.
Atrial fibrillation and atrial flutter: constant and paroxysmal forms. Pathology of the conduction system: a-c blockade.
Anomalies of the conduction system and their role in NRS.
Paroxysmal supraventricular and ventricular tachycardia.
Groups of antiarrhythmic drugs.
Treatment of NRS.
4.Type of lesson:practical lesson, seminar, laboratory session, colloquium, etc.).
5.Lesson duration: 6(in academic hours)
6. Equipment:
6.1. Didactic material (films and videos, training and control computer programs, multimedia atlases and situational tasks, business games, phantoms, simulators, etc.);
6.2. TSO(computers, video duals, multimedia projectors, etc.)
7. Lesson content:
7.1. Monitoring the initial level of knowledge and skills.
Self-control tasks: (students solving individual sets of tests on the topic)
Task (tests) 1.
Task (tests) 2.
Typical tasks.
7.2. Analysis with the teacher of key issues necessary to master the topic of the lesson.
Self-training location:
a training room for independent work of students, patient rooms, functional diagnostic rooms, etc. for mastering practical skills, equipped with the necessary educational and methodological materials.
Educational and research work of students on this topic: tests, situational tasks.
Forms and methods of control the initial and final level of knowledge of students, additional educational material is presented in the appendices to the methodological instructions (sets of tests for the initial and final level of knowledge and skills of students with standards of answers, with instructions for performing test control tasks, situational tasks).
Definition. Cardiac arrhythmias are disturbances in the frequency, rhythm and sequence of contractions of the heart. Disturbances in the conduction of excitation can occur at different levels of the conduction system of the heart and are called blockades
Highlight:
neurogenic rhythm disturbances,
medications (atropine, adrenaline, caffeine cause tachycardia, cardiac glycosides, opiates, lidocaine, procainamide, beta-blockers, tranquilizers, reserpine cause bradycardia),
toxic (alcohol, nicotine),
hormonal (pregnancy, menopause, thyrotoxicosis, myxedema, pheochromocytoma),
infectious-toxic (angina, sepsis, pneumonia, etc.),
electrolytic (hypokalemia, hypomagnesemia, hyperkalemia, hypercalcemia),
in some cases, the cause of arrhythmias is congenital defects of the conduction system (Wolf-Parkinson-White syndrome).
Arrhythmias occur in cardiovascular diseases with inflammatory (myocarditis) and degenerative (atherosclerotic cardiosclerosis) myocardial damage, valvular malformations, heart failure, AMI, chronic cor pulmonale, shock, collapse, hypertension.
There are disturbances in the formation of myocardial excitation and conduction disturbances. Disturbances in the formation of arousal are associated with an increase or decrease in automaticity.
Increased automation- noted with an increase in sympathetic tone, a decrease in the tone of the vagus nerve, a direct effect on the cells of the sinus node during hypoxia, acidosis, elevated body temperature, intoxication and infections. Permeability is of particular importance cell membrane for potassium ions and a change in the ratio of potassium content inside and outside the cell.
The consequence of all of the above is an increase in spontaneous diastolic depolarization and (or) a decrease in the threshold potential. When the threshold potential level is reached, increased permeability of the cell membrane for sodium ions occurs and a sudden movement of ions occurs - sodium ions enter the cell and create an electrical impulse, which, when entering the refractory period, causes premature contraction of the heart.
Disorders associated with increased automaticity include:
sinus tachycardia,
extrasystole,
ectopic tachycardias (atrial, nodal, ventricular - paroxysmal and non-paroxysmal),
atrial flutter and fibrillation,
ventricular flutter and fibrillation.
According to the place of origin (topically) they are distinguished:
supraventricular rhythm disturbances:
extrasystoles (atrial, nodal),
atrial fibrillation,
paroxysmal atrial tachycardia
and ventricular:
ventricular extrasystoles,
paroxysmal ventricular tachycardia.
In accordance with the effect of drugs on electrical processes in the myocardium, there are four classes of antiarrhythmic drugs:
class I (A, B, C): membrane stabilizing agents (sodium channel blockers) - quinidine, procainamide, lidocaine, etc.,
class II: beta-blockers,
class III: drugs that slow down repolarization - amiodarone, bretylium tosylate, ibutilide, sotalol (also has the properties of drugs of class 2),
class IV: calcium channel blockers (excluding dihydropyrine derivatives).
Heart rhythm disturbances
Arrhythmias are divided into supraventricular and ventricular. With supraventricular arrhythmias, a complex is usually recorded on the ECG QRS normal duration, since ventricular depolarization occurs in the usual way when excitation propagates through the AV junction, bundle branches and Purkinje fibers. For ventricular arrhythmias, the complex QRS expanded, since the spread of excitation occurs in an abnormal way, partly through the ventricular myocardium.
All arrhythmias are based on three mechanisms.
1. High pathological automatism of the structures of the conduction system of the heart, which is closely related to the pathology of membranes and electrolytes: sodium, potassium, magnesium, calcium.
2. Conduction disturbances are the basis of one of the most common mechanisms of arrhythmia; re-entry mechanism.
3. Trigger activity, closely related to membrane pathology and electrolytes, which is a common cause of extrasystole.
All these mechanisms are closely intertwined. All three mechanisms can trigger extrasystoles, and those can trigger new re-entry circles.
Classification of cardiac rhythm and conduction disorders
Rhythm formation disorders.
Disorders of sinus node automaticity (nomotopic arrhythmias):
P sinus tachycardia;
P sinus bradycardia;
P sinus arrhythmia;
P sick sinus syndrome.
Ectopic (heterotopic) rhythms caused by the predominance of automatism of ectopic centers:
P slow (replacing) slipping complexes and rhythms:
Atrial;
From the AV connection;
Ventricular;
P migration of the supraventricular pacemaker; P accelerated ectopic rhythms (non-paroxysmal tachycardia):
Atrial;
From the AV connection;
Ventricular
Ectopic (heterotopic) rhythms, mainly not associated with a violation of automaticity (mechanism re-entry and etc.):
P extrasystole (atrial, from the AV junction, ventricular);
P paroxysmal tachycardia (supraventricular, ventricular);
P atrial flutter; P FP;
P flutter and ventricular fibrillation.
Conduction disorders.
Sinoatrial block.
Intraatrial block.
AV block (I, II, III degrees).
Intraventricular blockades (blockades of the branches of the His bundle): P of one branch (monofascicular);
P two branches (bifascicular);
P three branches (trifascicular).
Ventricular asystole.
Premature ventricular excitation syndrome: Wolff-Parkinson-White syndrome;
P short interval syndrome PQ: Clerka-Levi-Christesco or Lawn-Genong-Levine.
Combined rhythm disturbances.
Parasystole.
Ectopic rhythms with exit block.
1) Sinus tachycardia (ST)
In normal sinus rhythm, impulses are created in the sinus system and travel to A-B node, into the His bundle, the branches of the His bundle and cause contractions of the ventricles.
Rice. 1. ECG for sinus tachycardia
With TS, cardiac activity increases at rest, exceeding 90 contractions per minute. with the correct rhythm (up to 150-160 beats per 1 min., during maximal physical activity up to 190-200 beats per 1 min.). SU pacemaker. ECG signs: the presence of a positive P wave in the second standard lead, having the same shape as without tachycardia. Heart rate correction is carried out with beta-blockers, calcium antagonists (verapamil, diltiazem), and an inhibitor of SU activity - coraxan.
2) Supraventricular paroxysmal tachycardia (SVT)
Paroxysmal supraventricular tachycardia:
A. Supraventricular nodal reciprocal tachycardia (NURT).
B . Supraventricular nodal reciprocal tachycardia with the participation of additional pathways: WPW.CLC syndrome. (NURT dp).
IN. Focal atrial tachycardia (OPT).
D. Sino-auricular reciprocal tachycardia.
For all NVT The following clinical picture is typical:
1. A sudden, causeless attack of palpitations with a sudden start and end.
2. If SVT occurs in people without pathology of the heart muscle and the rhythm does not exceed 180 per minute, then their general condition can be quite satisfactory. If NVT occurs against the background of heart disease or against the background of preserved myocardium, but with a rhythm of more than 200, t o possible:
A. Arrhythmogenic collapse or arrhythmogenic shock.
b. Semi-syncope or syncope syndrome.
V. Shortness of breath, suffocation, signs of acute left ventricular failure.
d. Anginal pain behind the sternum, appearing after the onset of tachycardia due to subendocardial ischemia provoked by tachycardia. Typically, in such cases, the ECG shows a deep horizontal downward displacement of the ST segment. After an attack, deep negative T waves and a positive troponin test may appear. This condition is called posttachycardial Cossio syndrome.
Patients with SVT often find ways to stop attacks by coughing or holding their breath. This does not happen with paroxysms of ventricular tachycardia. With NVT in the supine position, you can see the pulsation of the neck veins, equal in frequency to the heart rhythm. This fundamentally distinguishes NT from ventricular tachycardia, in which venous pulsation is always much slower than the heart rate.
Supraventricular nodal reentrant tachycardia (NURT)
NURT occurs with congenital or acquired disorders of impulse conduction in the A-V node. A circular wave of excitation occurs, leading to a paroxysm of SVT. The atria are also involved retrogradely in this circular process (Fig. 2.).
Rice. 2. The mechanism of re-entry of excitation during NURT (G.V. Roitberg, A.V. Strutynsky, 2003)
ECG signs of NURT ( rice. 3 ):
A. Sudden onset and sudden end of tachycardia with a heart rate of 140-240 per minute with a clear, regular rhythm.
B. Absence of the P wave, which merges with the QRS complex.
B. Normal narrow QRS complexes with a duration of no more than 0.12 s. This attribute is optional. In the case of bundle branch blocks, the QRS complex will be wide.
D. An ECG taken outside of an attack shows no signs of pre-excitation syndrome.
Fig 3. Upper ECG: NURT. Average ECG: NURT for WPW syndrome with wide QRS.
ECG signs of atrial HT:
1. A sudden attack of heart rate from 140 to 250 per minute with a sudden end.
2. The presence of a deformed or negative P wave in front of the QRS complex.
3. Normal, unchanged narrow QRS complexes, similar to the QRS complexes before the attack.
4. In case appearance of A-B blockade, loss of individual QRS complexes is possible (Fig. 4). In this case, atrial tachycardia resembles an attack of atrial fibrillation. However, the presence of clear atrial waves allows us to exclude this. Atrial tachycardias can be acute or chronic, leading after a few years to arrhythmogenic dilated cardiomyopathy.
Rice. 4. ECG first upper: atrial focal tachycardia. The second ECG shows atrial tachycardia with transient A-V block.
Table 1.
Treatment of supraventricular tachycardias with a narrow QRS complex
If the type of SVT is known, then a previously effective antiarrhythmic drug (AAP) must be administered; if not, then the sequence of actions is as follows.
Stopping an attack:
1. Vagal tests:
A. Deep breathing.
b. Valsalva maneuver: straining for 15-20 seconds.
V. Pressing on side surfaces eyeballs for 5 seconds (contraindicated for glaucoma and high myopia).
d. Sudden lowering of the face into cold water
d. Squatting with straining.
e. Inducing vomiting.
and. Massage one carotid sinus for 5 seconds.
Vagal tests are contraindicated in case of conduction disorders and in elderly people with dyscirculatory encephalopathy. Patients must be taught to perform these tests independently.
2. In case of unstable hemodynamics (collapse, cardiac asthma), EIT or transesophageal electrical stimulation is performed.
3. In the absence of injectable forms of AAP, one of the following drugs can be chewed and washed down with water: 20-40 mg of propronalol (Inderal, Anaprilin, Obzidan), 25-50 mg of atenolol, 200-400 mg of quinidine, 80-120 mg of verapamil (not give for WPW and CLC syndromes), sotalol 80 mg, propafenone 300 mg, etacizine 25-50 mg
4. ATP 2.0 ml of 1% solution bolus over 2 seconds intravenously. If there is no effect, repeat the administration. Stops reciprocal nodal tachycardia, sino-auricular reciprocal tachycardia and, in some patients, focal atrial tachycardia.
The administration of ATP is accompanied by an unpleasant, non-hazardous reaction: nausea, flushing of the face. It goes away within a few minutes due to the rapid destruction of ATP. There is no need to administer ATP to elderly patients with suspected sinus node weakness (there is no need to be afraid of this in the ICU). After the attack stops, a pause lasting 3-5 seconds or asystole may occur.
5. If there is no effect from ATP, you can immediately administer 5-10 mg of isoptin in a slow stream under blood pressure control. Effective for reciprocal and focal ectopic SVT. Should not be administered to patients with pre-excitation syndrome (WPW and CLC).
6. Before isoptin or an hour after it, novocainamide 1000 mg can be administered intravenously over 5-10 minutes under blood pressure control with mezaton 0.3-05 ml, or one of the following AAPs:
7. Propronalol (obzidan) 5-10 mg IV. Undesirable for initial hypotension.
8. Propophenone 1.0 mg per kg of body weight in a stream for 4-6 minutes. It makes no sense to introduce it if there was no effect from procainamide.
9. Amiodarone 300 mg IV over 5 minutes.
After ineffective administration of two drugs (not counting ATP), it is necessary to carry out EIT.
Table 2 - Differential diagnostic signs of supraventricular and ventricular AT(according to F.I. Belyalov, 2006)
| Signs | Supraventricular PT | Ventricular PT |
| Probability | 9:1 | 1:9 |
| Age | Most often young | Mostly mature and elderly |
| Heart rate | Usually above 160 beats/min, often 200-220 or more | Usually no higher than 160 beats/min, rarely 180-200 |
| Rhythm of contractions | Strictly regular rhythm or periodic loss of pulse wave | Some rhythm irregularity |
| Course of the attack | Most often relatively mild | Often more severe |
| Pulsation of neck veins | Frequent, synchronous with arterial pulse | Rare, with periodic appearance of enhanced waves |
| 1 tone above the top | Normal strength | Periodic appearance of “cannon” 1 tone |
| The phenomenon of “spastic urine” | Typical | Absent |
| Increased intestinal motility | Typically, with the urge to defecate | Absent |
| Reflex stimulation of the vagus | Slows down the rhythm or interrupts an attack | Has no effect |
| QRS complex on ECG | Narrow (less than 0.1 s), normal shape | Wide (0.12-0.14 s or more), deformed |
| Relieving effect of verapamil | High | Absent |
| Relieving effect of ATP | High | Absent |
| Relieving effect of lidocaine | Absent | High |
Paroxysmal ventricular tachycardia (PVT). PVT is understood as a section of rhythm consisting of three or more ectopic complexes emanating from the His bundle and its branches, Purkinje fibers or ventricular myocardium.
Etiology. PVT usually indicates severe myocardial pathology.
Coronarogenic PVT: acute myocardial infarction, post-infarction left ventricular aneurysm, ischemic heart disease.
Non-coronarogenic PVT: acute myocarditis, post-myocardial cardiosclerosis, cardiomyopathies, heart defects, amyloidosis, sarcoidosis, heart surgery, thyrotoxicosis, digitalis intoxication, arrhythmogenic effect of drugs (class IC and III antiarrhythmics), etc.
On the ECG ( rice. 5, 6) available:
1. Tachycardia with heart rate 140-220 beats/min
2. Wide (0.12-0.14 s or more) deformed QRS complexes, reminiscent of bundle branch block and often turning into discordant ST segment and T wave.
3. Atrioventricular dissociation.
Rice. 5. Short paroxysm of ventricular tachycardia ( V= 25 mm/sec).
Rice. 6. Paroxysmal ventricular tachycardia ( V= 50 mm/sec).
Relief of VT paroxysm.
1. Severe hemodynamic instability requires emergency EIT (discharge 360-400 J), which, if it is impossible to immediately use a defibrillator, is preceded by a precordial shock, chest compressions and artificial ventilation. If it is ineffective, defibrillation is repeated against the background of intravenous jet injection (in the absence of a pulse - into the subclavian vein or intracardiacly) of adrenaline 1 ml of a 10% solution per 10 ml of saline and antiarrhythmics:
Lidocaine 50-75 mg;
Amiodarone 300-450 mg;
Bretylium tosylate 5-10 mg/kg.
Drug relief of VT paroxysm is carried out by intravenous administration of the following drugs:
The drug of choice is lidocaine (compared to procainamide, lidocaine begins to act faster, it has a negative inotropic effect, and has less effect on conductivity) is administered 1-1.5 mg/kg, on average 80-120 mg, as a bolus - quickly, in one or two minutes;
If there is no effect, novocainamide 1 g (10 ml of 10% solution), slowly, over 20 minutes (with rapid administration, a drop in pressure and expansion of the QRS complex);
It is possible to use ethmosin 6 ml 2.5% solution, disopyramide 15 ml 1% solution;
Third place - amiodarone 5 mg/kg, slowly, over 10 minutes ( side effect: decreased pressure, impaired intraventricular conduction).
Verapamil, as a rule, is not indicated (there may be a transition to ventricular fibrillation or acceleration of tachycardia).
If there is no effect: magnesium sulfate 1-2 g - 10-20 ml of 25% solution in one to two minutes (the drug of choice for tachycardia of the “pirouette” type with QT prolongation).
Maintenance antiarrhythmic therapy for PVT is carried out mainly with amiodarone or sotalol, especially in patients with coronary artery disease. For non-coronarogenic PVT, therapy with class I antiarrhythmics can be carried out (see algorithm for the use of antiarrhythmic drugs).
For idiopathic PVT, verapamil 240-360 mg/day is prescribed; for congenital long QT syndrome, β-blockers are prescribed.
Indications for installation of implantable cardioverter-defibrillators (ICD):
1) clinical death caused by PVT;
2) spontaneous paroxysms of sustained VT;
3) syncope of unknown origin in combination with the induction of significant PVT during EPS and the ineffectiveness/impossibility of prescribing antiarrhythmics;
4) unstable VT, which is reproduced during EPI, is not relieved by novocainamide and is combined with post-infarction cardiosclerosis and left ventricular dysfunction.
Indications for surgical treatment(radiofrequency ablation) PVT:
1. Hemodynamically significant prolonged monomorphic PVT, resistant to antiarrhythmics (or there are contraindications to their use), including idiopathic.
2. PVT with a relatively narrow QRS, caused by re-entry along the bundle branch system.
3. Frequent ICD discharges in patients with prolonged monomorphic PVT, which cannot be suppressed by ICD reprogramming and the prescription of antiarrhythmics.
Extrasystole- the most common form of arrhythmias. Based on etiopathogenetic characteristics, the following variants of extrasystoles are distinguished:
- functional(dysregulatory) - in people with a healthy heart;
- organic, caused by damage to the myocardium and valvular apparatus of the heart;
- toxic: for intoxication, feverish conditions, overdose of cardiac glycosides, arrhythmogenic effect of antiarrhythmic drugs (AS).
In turn, within the framework of functional extrasystole there are 2 subgroups:
a) neurogenic extrasystoles - in case of neurosis with vegetative dystonia: an arrhythmic variant of disregulatory cardiopathy;
b) neuroreflex extrasystoles - in the presence of a focus of irritation in one of internal organs, more often abdominal cavity; for cholelithiasis and urolithiasis, gastric and duodenal ulcers, bloating, kidney prolapse, etc. They are realized through the mechanism of viscero-visceral reflexes, through the vagus nerve.
Based on the localization of the heterotopic focus, extrasystoles are divided into supraventricular (atrial and atrioventricular) and ventricular.
ECG criteria. A common sign of any extrasystole is premature excitation of the heart - shortening of R-R on the ECG. The interval between the sinus and extraordinary complexes is called the pre-extrasystolic interval or the coupling interval. After the extracomplex there is a compensatory pause - lengthening R-R. The exception is intercalated or interpolated extrasystoles that are approximately equidistant from adjacent sinus activations.
Supraventricular (supraventricular) extrasystole. Supraventricular pacemaker is an excitation of the heart caused by an extraordinary impulse emanating from the atria or atrioventricular node. The main mechanism of extrasystole is the mechanism of micro-reentry in areas of the myocardium or conduction system with different conductivity and unidirectional blockade of impulse conduction.
ECG signs of supraventricular pacemaker:
1. Premature appearance of the P wave with the QRS complex.
2. Deformation and change in the polarity of the P wave of the extrasystole.
3. The presence of an incomplete compensatory pause: the sum of the time interval before and after the extrasystole is less than two normal intervals before the extrasystole.
4. The presence of a slightly changed extrasystolic QRS complex. An aberrant complex during supraventricular pacemaker may resemble a widened and deformed ventricular complex, but there is a deformed P wave before the pacemaker, and the compensatory pause is incomplete (Fig. 7)
Fig 7. Supraventricular pacemaker, incomplete compensatory pause.
If a supraventricular extrasystole occurs before the end of the refractory period, then it is not carried out to the ventricles and there is no QRS. Such an pacemaker is called blocked (Fig. 8).
Fig.8. The first ECG from above: before the atrial pacemaker, a slightly changed P wave. On the second ECG after the atrial pacemaker, QRS did not appear: the atrial pacemaker was blocked. On the third ECG, the P wave overlapped the QRS. On the fourth ECG, retrogradely excited atrial P layered onto the ST segment.
If the shape of the P wave changes from complex to complex, such pacemakers are called polymorphic supraventricular.
With extrasystoles from the AV junction, the P wave either merges with the QRS and is therefore not visible, or is recorded as a negative wave on the RS-T segment. It is not always possible to distinguish atrial extrasystoles from atrioventricular extrasystoles. In controversial cases, it is permissible to limit ourselves to indicating the supraventricular nature of the extrasystoles.
Ventricular extrasystoles(Fig. 9)
ECG signs of PVCs::
1. Absence of the P wave before the PVC. In early PVCs that occur immediately behind the P wave, the P wave is present, but the PQ is shortened.
2. QRS more than 0.12 seconds, has the form of a bundle branch block (sharp widening and deformation of the QRS-T complex with discordance (multidirectionality) of the maximum wave of the QRS triad and its terminal part - the RS-T segment and the T wave).
3. The pacemaker is followed by a complete compensatory pause. If the rhythm is rare, there may be no compensatory pause - intercalated PVC
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Fig.9. Ventricular extrasystole ( V= 25 mm/sec)
Depending on the number of functioning ectopic centers, monotonic (monofocal, monoform) and polytopic (polyfocal, polyform) extrasystoles are distinguished.
Polytopic supraventricular extrasystole is characterized by the following features: P waves within one lead vary in shape and polarity; P-Q intervals of extracomplexes have different durations, pre-extrasystolic intervals are not the same.
Polytopic ventricular extrasystole is recognized by the following characteristics: different shapes of QRS-T complexes of extraordinary activations within one lead, changing duration of coupling intervals even with external similarity of extrasystoles.
Extrasystoles can be single, paired (two in a row) and group (three or four in a row) (Fig. 10, 11).
Rice. 10. Group ventricular extrasystoles (triplet and couplet) ( V= 25 mm/sec).
Rice. eleven. Allorhythmia according to the type of bigemeny ( V= 50 mm/sec). 
Rice. 12. Atrial extrasystoles.
A. blocked atrial extrasystole (PE), B. PE with aberrant conduction to the ventricles (right bundle branch block). NVEs are usually asymptomatic or oligosymptomatic.The prognostic significance of PVCs depends on the background of their occurrence. If PVCs occur in individuals without signs of heart disease, their prognostic significance is quite favorable. If they do not bother the patient much, then there is no need to be persistent in their treatment. The prognostic significance of PVCs is worse the more often they occur and the more severe the heart pathology.
The Laun-Wolf classification has been compiled on a quantitative and morphological basis and makes it possible to assess the prognostic significance of PVCs in patients who have had myocardial infarction:
0 - absence of PVCs;
1 - rare, monomorphic (up to 30 per hour);
2 - frequent, monomorphic (more than 30 per hour);
3 - polymorphic;
4A - paired;
4B - salvo (VT runs of 3 or more complexes);
5 - early PVCs (“R to T”).
The higher the class of PVCs according to this classification, the higher the risk of sudden death. This risk classification does not apply to PVCs in other heart diseases, and especially not in idiopathic, functional autonomic PVCs.
There is a prognostic classification of PVCs according to Bigger:
Benign PVCs– no history of fainting, myocardial pathology, as a rule, is absent (including post-infarction scar and myocardial hypertrophy of more than 14 mm), frequency of PVCs is 1-10 per hour, there are no episodes of non-continuous ventricular tachycardia (VT).
Malignant VTs– there is a history of fainting or cardiac arrest, there is heart disease, the frequency of PVCs is 10-100 per hour, persistent paroxysms of VT are often detected.
Potentially malignant– differ from malignant ones by the absence of a history of fainting and cardiac arrest, and the absence of attacks of unstable VT.
The risk of sudden death in the last two classes is higher with an ejection fraction of less than 40%, with PVCs occurring with physical activity, when it appears during the appearance of ischemic ST-T changes in angina pectoris
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Atrial fibrillation and atrial flutter
In the pathogenesis of MA and TP the main role belongs to the appearance of zones of heterogeneity in the myocardium due to dystrophic changes. Areas with different levels of conductivity and refractoriness appear, which creates conditions for the emergence of a mosaic of macro- and micro-reentry fields with the formation of leading excitation circles. Sometimes the leading wave acquires an ordered character in the form of a circular excitation wave circulating through the atria around the valve rings up to 300 per second. - Atrial flutter develops. Depending on how many waves the A-V node can transmit, TP is distinguished 1:1 (very rarely, only with pre-excitation syndrome); 2:1; 3:1; 4:1.
The main reasons for the appearance of heterogeneity in conduction in the atria in the myocardium are: age-related changes in the atria, abnormal structural features of the mouths of the pulmonary veins with many arrhythmogenic zones, as well as dilatation of the left atrium.
Etiological factors of MA:
1. IHD. The most common cause of MA.
2. Arterial hypertension. Diastolic dysfunction of the left ventricle in the presence of myocardial hypertrophy leads to enlargement of the left atrium, which contributes to the appearance of AF.
3. Congenital and acquired heart defects with atrial dilatation.
4. Dilated, and less commonly, hypertrophic cardiomyopathy.
5. Primary cardiac amyloidosis (in persons over 70 years of age).
6. Hemochromatosis (pigmentation and diabetes mellitus).
7. Constrictive pericarditis (MA is combined with nonspecific ST-T changes, isolated venous congestion in the systemic circle and small heart size).
8. Infective endocarditis.
9. Thyrotoxicosis.
10. Alcoholic myocardial dystrophy.
11. Dyshormonal myocardial dystrophy (menopause).
12. Mitral valve prolapse with left atrium enlargement. 13. Chronic cor pulmonale. 14. Myxoma of the left atrium. 15. MA in athletes. 16. In the absence of all of the above, a diagnosis of the idiopathic form of AF is made (most often the reason is the presence of arrhythmogenic foci at the mouths of the pulmonary veins).
MA has the following clinical types:
1. Paroxysmal - lasting 7 days.
2. Persistent - more than 7 days.
3. Permanent form of MA. The permanent form of AF can be: bradyarrhythmic - with a heart rate of less than 60 per minute, normoarrhythmic with a heart rate of up to 100, tachyarrhythmic - with a heart rate of more than 100 per minute.
ECG signs of MA: 1. The P wave is not detected. Small or large F waves may be observed, sometimes looking like a P wave.
2. Interval R-R are different(Figure 13).
3. Depending on the magnitude of the F waves, MAs are divided into small-wave or large-wave.
Rice. 13. ECG first: tachysystolic MA. ECG second: bradysystolic MA. ECG third: large-wave MA. ECG fourth: small-wave MA.
When a complete A-V block occurs, the rhythm against the background of MA becomes ventricular, regular, less than 50 (Fig. 14. Frederick's syndrome).
Rice. 14. Atrial fibrillation against the background of complete A-V block (Frederick's syndrome).
Signs of TP: 1. The presence of smooth sawtooth F waves with a heart rate of up to 300 per minute, clearly visible in standard leads 2 and 3 (Fig. 15). Each flutter wave cannot reach the ventricles. Either every 2nd, or every 3rd, 4th reaches.
2. The rhythm of the ventricular complexes is correct. If there is an alternating blockade 2:1,3:1,4:1, the rhythm becomes abnormal.
Rice. 15. TP options. Upper ECG: TP 1 to 2. Second ECG: TP 1 to 3. Third ECG: 1 to 4. Fourth ECG: TP 1 to 3, 1 to 4, 1 to 5.
Atrial fibrillation and atrial flutter are similar in the mechanism of their formation and can be observed in the same patient at different times. TP is 2 to 1 less well tolerated than MA. TP 3 to 1, or 4 to 1 may not be felt.
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Diagnosis of atrial fibrillation is generally simple; difficulties arise only in isolated cases.
Sometimes atrial fibrillation can be mistaken for frequent group extrasystoles, sinus arrhythmia, paroxysmal tachycardia, atrial flutter. During auscultation, several successive rhythmic heart contractions can be detected between extrasystoles, with extraordinary contractions followed by a compensatory pause. This is not observed with atrial fibrillation. In difficult cases, an ECG study is necessary to clarify the diagnosis.
Sometimes it is necessary to differentiate between atrial fibrillation and paroxysmal tachycardia.
During auscultation in patients with paroxysmal tachycardia, the rhythm of cardiac activity is correct, the sonority of tones does not change. At the same time, with atrial fibrillation, an arrhythmic appearance of tones and a change in their volume are noted. With paroxysmal tachycardia, the pulse is regular, without deficit; with atrial fibrillation it is irregular, uneven filling, with a pronounced deficiency. After vagal tests (pressure on the carotid sinus), the attack of paroxysmal tachycardia very often stops, while atrial fibrillation is not relieved, but only temporarily slows down cardiac activity. It is impossible to distinguish irregularly shaped atrial flutter from atrial fibrillation based on clinical signs. An accurate diagnosis can only be made using an ECG.
Prof. A.I. Gritsyuk
“Diagnostics of atrial fibrillation, differential diagnosis” section
Differential diagnosis atrial fibrillation sometimes you have to carry out sinus tachycardia, supraventricular form of paroxysmal tachycardia, atrial flutter and ventricular paroxysmal tachycardia. It should be taken into account that in the ventricular form of paroxysmal tachycardia, the QRS complex is always widened by more than 0.12 s and deformed. However, if atrial fibrillation is associated with a preexisting bundle branch block or aberrant ventricular conduction, the shape of the QRS complex is of little help in the differential diagnosis.
If a positive P wave is recorded before each QRS complex, this indicates the supraventricular nature of the tachycardia (sinus or atrial paroxysmal) and allows us to reject both ventricular paroxysmal tachycardia and atrial fibrillation. The differential diagnosis should take into account the nature of the rhythm. The rhythm of ventricular tachycardia may be somewhat irregular. In such cases, the differential diagnosis with atrial fibrillation and aberrant complexes or with concomitant leg block is especially difficult with a high heart rate.
Large-wave atrial fibrillation must be differentiated from atrial flutter. With small-wave fibrillation, signs of electrical activity of the atria on the ECG may not be detected, which, with a tendency to bradycardia, may resemble an escape rhythm from the atrioventricular junction. Distinctive features Atrial fibrillation in this case is the variability of the RR interval, as well as the detection of flicker f waves during recording of an enhanced ECG or transesophageal ECG.
The differential diagnosis of atrial fibrillation with individual aberrant QRS complexes and ventricular extrasystole accompanying atrial fibrillation may present certain difficulties. The following evidence supports aberrant intraventricular conduction of impulses:
1) the appearance of aberrance in a short cardiac cycle, which is preceded by a long cardiac cycle (Ashman phenomenon);
2) blockade of the right bundle branch (often, but not necessarily);
3) absence of a compensatory pause;
4) absence of aberration in short cardiac cycles without a previous pause;
5) disappearance of aberrance with minimal changes in the duration of the cardiac cycle.
Even greater problems arise in the differential diagnosis of atrial fibrillation with wide QRS complexes due to the “old” concomitant bundle branch block or Wolff-Parkinson-White syndrome and ventricular tachycardia, especially with a rapid ventricular rhythm when fluctuations in the RR interval are minimal. It should be taken into account that ventricular tachycardia, as a rule, is accompanied by hemodynamic disturbances and, characterized by instability, quite quickly turns into ventricular fibrillation. In contrast, the relative stability of hemodynamics with relatively long-term persistence of tachyarrhythmia is more typical for atrial fibrillation. The diagnosis can be clarified only by recording an intracardiac ECG.
Based on the above and taking into account the following: the patient’s complaints about fluctuations in blood pressure from 130/70 mmHg to 210/120 mmHg, pain in the heart area of a compressive nature at night (relieved by nitroglycerin), shortness of breath with insignificant physical activity, memory loss, periodic headaches, dizziness, weakness; history data - considers himself sick for 2 weeks, when complaints appeared about fluctuations in blood pressure from 130/70 mmHg to 210/120 mmHg, pain in the heart area of a compressive nature (relieved by nitroglycerin), shortness of breath with physical activity, periodic headaches, dizziness, weakness, observed in the student. rarely sees a therapist, does not take medications regularly (dibazol, adelfan), has been suffering from hypertension for about 5-7 years, heart rhythm disturbances, according to the patient, appeared about a year ago, the patient’s mother suffered from hypertension and had arrhythmia; objective examination data - expansion of the boundaries of relative dullness to the left, increased apical impulse, blood pressure 150/95 mmHg, arrhythmic pulse, pulse deficit; further clinical and laboratory examination, which revealed Echography of the heart:ECG: X-ray signs of stagnation in the ICC; the following diagnosis can be made:
Basic
clinical diagnosis:
Basic: Arterial hypertension stage III, degree 3, risk 4. Coronary heart disease. Heart rhythm disturbances, permanent form of atrial fibrillation (normosystole)
Complications: CHF IIA FCIII.
Related: Peptic ulcer stomach.
Rationale for clinical diagnosis:
Based on the patient's complaints of: fluctuations in blood pressure from 130/70 mmHg to 210/120 mmHg, pain in the heart area of a compressive nature at night (relieved by nitroglycerin), shortness of breath with slight physical exertion, decreased memory , periodic headaches, dizziness, weakness; history data - considers himself sick for 2 weeks, when complaints appeared about fluctuations in blood pressure from 130/70 mmHg to 210/120 mmHg, pain in the heart area of a compressive nature (relieved by nitroglycerin), shortness of breath with physical activity, periodic headaches, dizziness, weakness, observed in the student. rarely sees a therapist, does not take medications regularly (dibazol, adelfan), has been suffering from hypertension for about 5-7 years, heart rhythm disturbances, according to the patient, appeared about a year ago, the patient’s mother suffered from hypertension and had arrhythmia; objective examination data - expansion of the boundaries of relative dullness to the left, increased apex impulse, blood pressure 150/95 mmHg, arrhythmic pulse, pulse deficit; further clinical and laboratory examination, which revealed Echography of the heart: Conclusion: Left ventricular systolic dysfunction. ECG: EOS is not rejected. Atrial fibrillation. Heart rate = 55-90 beats/min. Hypertrophy of the left ventricular myocardium with secondary disorders of repolarization processes. Chest X-ray: X-ray signs of stagnation in the ICC; data from the performed differential diagnosis; The following diagnosis can be made:
Basic: Arterial hypertension stage III, degree 3, risk 4.
Cardiac ischemia. Heart rhythm disturbances, constant form of atrial fibrillation (normosystole because heart rate is 60-90).
Stage III is characterized by a pronounced clinical picture. Signs found in the patient indicating stage III of hypertension: complaints of increased fatigue; Blood pressure is constantly elevated (at about 150/90 with an increase to 210/120 mmHg; hypertension decreases under the influence of drug treatment; physical examination revealed signs of left ventricular hypertrophy; ECG shows signs of left ventricular hypertrophy and rhythm disturbance (atrial fibrillation).
Stage 3 (severe) is assigned in accordance with the blood pressure level = 210 mm Hg. Art.
Risk 4, because there is a blood pressure>180/110 mm Hg. Art. and the presence of risk factors (genetic predisposition, overweight body) and ACS (CHF).
Complications: CHF IIA FCIII.
CHF IIA FCIII can be diagnosed based on: characteristic symptoms and complaints - shortness of breath with slight physical exertion, fatigue, palpitations; physical examination data - wheezing and hard breathing, cardiomegaly (damage to the 1st (lesser) circulation - IIA); objective examination data - ECG, EchoCG, chest X-ray, 6-minute test data (200m - FCIII).
EPICRISIS
Zharovnya Vasilina Semenovna, 63 years old, was treated in City Hospital No. 4 from November 7, 2012 to November 17. 2012. She was admitted urgently to the emergency room with a diagnosis of acute bilateral lower lobe congestive pneumonia. After clinical, laboratory and instrumental studies, the following diagnosis was made:
Basic: Arterial hypertension stage III, degree 3, risk 4. Coronary heart disease. Heart rhythm disturbances, permanent form of atrial fibrillation (normosystole).
Complications: CHF IIA FCIII.
Related: Stomach ulcer.
This diagnosis was made based on:
Complaint:
for fluctuations in blood pressure from 130/70 mmHg to 210/120 mmHg, heart palpitations, interruptions, pain in the heart area of a compressive nature at night (self-limiting), shortness of breath with slight physical exertion, decreased memory, recurrent headaches, dizziness, weakness
History of present illness:
considers himself sick for 2 years, when there were complaints of fluctuations in blood pressure from 130/70 mmHg to 210/120 mmHg, pain in the heart area of a compressive nature (self-limiting), shortness of breath on exercise, periodic headaches, dizziness, weakness, medications taken independently (dibazol, adelfan), heart rhythm disturbances, according to the patient, appeared about a year ago, the patient’s mother suffered from hypertension and had arrhythmia.
Objective data:
expansion of the boundaries of relative dullness to the left, increased apical impulse, blood pressure 150/95 mmHg, arrhythmic pulse, pulse deficiency, subcutaneous tissue is overdeveloped.
Results of laboratory and instrumental research:
General analysis blood:
Biochemical analysis blood:
General urine analysis:
color light yellow
acidic reaction
specific gravity 1024
transparency transparent
no protein
ketone bodies no
glucose no
Epithelial cells
Flat 3-4 in sight;
3 leukocytes in field of view
No red blood cells
Mucus neg.
Blood test for coagulogram:
Blood test for RW: negative.
Blood test for HbsAg and HCV: negative.
Blood test for HIV: negative.
Echography of the heart:
Conclusion: Left ventricular systolic dysfunction.
ECG:
EOS is not rejected. Atrial fibrillation. Heart rate = 55-90 beats/min. Hypertrophy of the left ventricular myocardium with secondary disorders of repolarization processes.
Chest X-ray:
X-ray signs of stagnation in the ICC.
Kidney ultrasound:
The kidneys are not enlarged, their topography is not changed, the parenchyma is of a homogeneous structure, of average echogenicity, up to 17 mm wide, without ecstasy and stones, up to 10 mm wide.
Doppler ultrasound of blood vessels kidney:
An angiorenoscintigram performed with the patient in an upright position showed an image of both kidneys located at a typical level. The vertical size of the image of both kidneys is normal, the contours of the kidney image are clear.
The flow of radiopharmaceuticals into the arterial bed of both kidneys is within normal limits. The volume of renal perfusion on both sides and the rate of renal perfusion on both sides were within normal limits. The filtration and excretory capacity of both kidneys is within normal limits. Blood purification from RF is timely.
Result of analysis for metanephrine and normetanephrine in urine:
50 mcg/day - metanephrine; (normal)
40 mcg/day - normetanephrine (normal)
(in daily urine [mcg/day] - metanephrine<350, норметанеферин <600)
TSH study:
TSH – 2 Med/l (normal 1-4 Med/l);
ARS test:
25 units (20-40 normal) – within normal limits.
6 minute test results:
Parameters of physical activity and oxygen consumption in patients with CHF
The patient walks 200 meters, which indicates FC III CHF.
Conducted differential diagnosis.
She was discharged in satisfactory condition for outpatient treatment with a general practitioner at her place of residence.
Drug therapy was carried out:
1.Selective beta blockers block beta1 receptors of the heart, reduce the secretion of renin, increase the synthesis of vasodilating prostaglandins, increase the secretion of atrial natriuretic factor.
Rp.: Bisoprololi 1.5
D.t.d. No. 20 in tab.
S. One tablet 2 times a day
2.Diuretics inhibit the reabsorption of sodium ions in the cortical part of the loop of Henley, reduce arterial tone and reduce total peripheral vascular resistance.
Rp.: Sol. Furosimidi - 4.0 ml
D.t. d. №5 in amp..
S. intravenous injection for diuretic purposes.
Rp.: Veroshpironi 0.5
D.t.d. No. 20 in tab.
3.ACE inhibitors block the conversion of angiotensin 1 to angiotensin 2, which leads to a weakening of the vasoconstrictor effect and inhibition of aldosterone secretion.
Rp.: Tab. Enalaprili 0.01
S. 1 tablet 2 times a day, morning and evening.
4. Cardiac glycosides- in small doses. In case of atrial fibrillation, they remain a “first-line” treatment, and in case of sinus rhythm and ischemic etiology of CHF, the use requires caution and control.
Rp.: Digoxini 0.125
D.t. d. No. 10 in amp.
S. Inject intravenously the contents of 1 ampoule in 200 ml of physiological solution once a day at 18.00.
5. Polarizing mixture has a beneficial effect, including on rhythm stability, both indirectly by improving the metabolism of affected tissues and by increasing the content of intracellular potassium, since myocardial hypoxia causes the release of potassium from the cell into the extracellular space.
Insulin enhances the utilization of glucose and promotes the entry of potassium into the cell. Even without additional glucose, insulin ensures the accumulation of potassium in the cell. This should normalize polarization processes in the myocardial fibers and thus create a favorable basis for rhythm stabilization. It is also prescribed during diuretic therapy to replenish the loss of magnesium and potassium.
Rp.: Sol.Glu 5% - 200.0
Sol.Actropidi 4ED
D.t. d. No. 5 in amp.
6. For the prevention of thrombosis, thromboembolism and to improve hemorheology.
Clopidogrel 75 mg 1 tab. 1 time a day.
Treatment:
Bisoprolol 1.5 mg One tablet 2 times a day
Hypothiazide 12.5 1 tab once a day