Download "TRAINING GENERAL DOCTORS ENDOKRINALOGIEY

MINISTRY OF HEALTH REPUBLICAN UZBEKISTAN
TASHKENT MEDICAL ACADEMY
DEPARTMENT OF "TRAINING GENERAL DOCTORS
ENDOKRINALOGIEY"
Lecture theme:
SUDDEN DEATH. CAUSE OF SUDDEN DEATH. TACTICS GPS
(Students Medical pedagogical faculty)
ТАШКЕНТ – 2013
MINISTRY OF HEALTH REPUBLICAN UZBEKISTAN
TASHKENT MEDICAL ACADEMY
DEPARTMENT OF "TRAINING GENERAL DOCTORS
ENDOKRINALOGIEY"
"APPROVED"
Dean of the medical pedagogical faculty
Professor PS Zufarov
_________________
____ ________ 2013 y.
SUDDEN DEATH. CAUSE OF SUDDEN DEATH. TACTICS GPS
Lecturer: docent Rakhimov M.E.
Ташкент – 2013
TECHNOLOGY TRAINING
Number of Students
The structure of the training session
Plan of the lecture
Time - 2:00
Lecture - in the form of presentation
1. Give an explanation of the sudden death
2. The main causes of sudden death
3. Variants of sudden death
4. The pathogenesis of sudden death
5. Clinical variants of sudden death
6. Give explanation of sudden cardiac death
7. The causes of sudden cardiac death in young
8. Mechanisms at the basis of sudden cardiac death
9. The list of risks privodyashih to sudden death
10. Complications leading to death in MI
11. Typical signs for the syndrome Burgady
12. Tactics GPs in sudden death
Purpose uchubnogo lessons: to provide information to students about the sudden death, the main clinical
manifestations, classification, diagnostic criteria of major diseases causing sudden death, complications,
diagnosis, and some help on emergency prevention PRINCIPLE
Pedagogical obyazonnosti:
1. To provide full information to
students about classification, clinical
features and factors leading to sudden
death. To deepen their knowledge about
the diagnosis and emergency some help
with the sudden death.
2. Provide information about diseases
and their complications, leading to
sudden death.
3. Achieve whatever students have
mastered the skills to diagnose the
sudden death and disease leading to this
state of
4. Tell A students about preventive
measures
Teaching methods
Training forms
Training tools
Learning Environment
Learning outcomes
GPs should know
1. Determine the sudden death
2. Know the clinical signs of sudden death
3. Know about the main causes leading to sudden death
4. Know the diagnostic criteria for major diseases leading to
sudden death
5. Determine the risk factors leading to sudden death
6. In the case of sudden death diagnose and okozalos
emergency assistance conditional
7. Disease prevention and rehabilitation leading to sudden
death
The text of the lecture, video, brainstorm, solve situational
problems, competition between groups, the technique the "yes-no"
Laser projector, visual material on relations with specialized
equipment
Collective
Audience
Flow chart lectures
Stages, while
Stage 1
Input (5min)
Stage 2
Improve
knowledge (20
minutes)
stage 3
The main stage
(information)
(55 minutes)
Stage 4
final
(10 minutes)
Activities
Teacher
1. Tell theme intact and expected plans
2.1. Questions for students to improve their knowledge
1. Sudden death, what it means?
2. Key criteria for the diagnosis of sudden death?
3. List the group of diseases leading to sudden death?
4. List the causes of sudden death in young people?
5. Risk factors leading to sudden death?
6. What is the medical emergency is conducted in a
sudden death?
Conducts quick poll
2.2. Are referred to the purpose of the lecture
screening. Provide an explanation of the information
presented in lectures
Slide number 1, 2, ...
3.1. To familiarize with the essence of the lecture and
the criteria of forming a spiritual person. Improves
students' knowledge about the topic of the project and
carry out the "brainstorming"
1 - plan question: Give an explanation of sudden death?
2 - the question plan: list of clinical signs of sudden
death?
3 - question the plan: the main cause of sudden death?
4 - Plan question: Causes of sudden cardiac death in
young people?
5 - question the plan: a risk factor for sudden death
privodyashih?
6 - plan question: cause of sudden death syndrome
Burgada?
7 - the question plan: Emergency aid in the
development of sudden death?
Suggest to stop and write down the main points lectures
4.1. The question is asked:
1. Give an explanation of the sudden death
2. Variants of sudden death
3. The main causes of sudden cardiac death
4. Risk factors leading to the development of sudden
death
5. Emergency care for sudden death
4.2. Writing assignments for independent discounts:
Burgady syndrome and its treatment
Students
1. Listen
2.1. Answer questions
2.2. № 1 Familiarize with slides
2.3. Number 2 Familiarize with
slides
3.1. Ask questions and
discuss the materials specified
Writes highlights
4.1. answer questions
4.2. listen and write
SUDDEN DEATH. CAUSE OF SUDDEN DEATH.
The term "sudden death" is used in the literature for over 250 years, but until now there is no single
definition of it. By sudden death means either instant death or death occurring within a few minutes, 1 hour or 6
hours and even 24 hours after permanent symptoms ended lethal. (Gromov LI, Savina E., Wiechert AM, Culler
A). However, the use of the time factor as the main criterion does not provide a sufficiently high homogeneity
of the group died. In this approach, the group included patients who died suddenly, whose death occurs, though
in the early stages of the disease, but in the background of cardiogenic shock, pulmonary edema, heart failure.
Sudden cardiac death - is a non-violent, due to heart disease death, manifest by a sudden loss of
consciousness within 1 h after the onset of symptoms of acute, with prior heart disease may be known or
unknown, and death is always unexpected.
These definitions are also experts from WHO (1964, 1979), the difference lies only in the timing of the
onset of cardiac death. WHO experts believe that the sudden cardiac death of Pres-Paet within 1-6 hours after
the first signs of a heart attack.
Depending on the length of the interval between the onset of a heart attack and the time to death, crimes
distinguish instantaneous cardiac death (the patient dies within a few seconds, which is almost instantaneous)
and rapid cardiac death (the patient dies within hours). In the United States die suddenly about 300 000-400 000
people, which is about 0.1-0.2% of all residents. Almost 50% of all deaths from cardiovascular disease accounts
for sudden cardiac death.There are various definitions of sudden cardiac death. Myerburg and Castellanos
(2001) gives the following definition:
About 80% of cases of sudden cardiac death due to coronary heart disease (NA Mazur, 1999). This
sudden death can be labeled as sudden cardiac death. In the classification of coronary artery disease indicated
that a form of coronary artery disease is sudden cardiac death, which can be defined.
There are certain age and gender characteristics of sudden cardiac death.
There are two types of age-related sudden cardiac death: in infants (first 6 months of age) and adults
(aged 45-75 years) (Burch et al., 1965). Among infants the incidence of sudden cardiac death is about 0.1-0.3%.
At the age of 1-13 years, only 1 in 5 cases of sudden death due to heart disease, aged 14-21 years old, this figure
rises to 30%, and in the middle and old age, 88% of all cases of sudden death is sudden cardiac death.
There are sex differences in the frequency of sudden cardiac death. Sudden cardiac death in young and
middle aged men celebrated 4 times more often than women, aged 45-64 years in men sudden cardiac deaths
occur in 7 times more often than women, and only in the age group 65-74, the frequency of sudden cardiac
death in men and women is expressed as 2:1.
Thus, the incidence of sudden cardiac death increases with age and is higher for men than women.
Etiology
The main causes of sudden cardiac death, are shown below. The main causes of sudden cardiac death
(Myerburg, Castellanos, 2001, as amended.)
 Coronary atherosclerosis
 Chronic ischemic heart disease with transient imbalance in myocardial oxygen demand and its receipt
 Acute myocardial infarction
 Myocardial infarction
 Congenital abnormality of the coronary arteries
 Abnormal discharge from the pulmonary artery
 Discharge of the left coronary artery from the right sinus of Valsalva
 Coronary arteriovenous fistula
 Hypoplasia or aplasia of the coronary arteries
 Discharge of the right coronary artery from the left sinus of Valsalva
 Coronary intracardiac shunt
 Coronary Arteries
 Polyarteritis nodosa, systemic sclerosis, giant cell arteritis
 Kawasaki disease
 Syphilitic stenosis of the coronary arteries
 Coronary embolism
 Endocarditis with lesions aortic or mitral valve
 Artificial aortic or mitral valve thrombosis
 Blood clots in the valves or left ventricular parietal thrombus
 Mixed mechanical obstruction of the coronary arteries
 Stratification of coronary arteries in Marfan's syndrome
Stratification of the coronary artery in pregnancy
Aortic valve prolapse polyp at the mouth of the coronary arteries
Separation or rupture of sinus of Valsalva
Functional obstruction of the coronary arteries
Spasm of the coronary arteries against atherosclerosis or without atherosclerotic
Myocardial "bridges"
Diseases that cause cardiac hypertrophy
Hypertension without atherosclerosis of the coronary arteries
Left ventricular hypertrophy in patients with coronary artery disease
Myocardial hypertrophy with valvular heart
Hypertrophic kardiomiolatiya
Primary and secondary pulmonary hypertension
Myocardial diseases that lead to heart failure
Chronic congestive heart failure ischemic cardiomyopathy idiopathic dilated cardiomyopathy alcoholic
cardiomyopathy Hypertensive decompensated heart postmiokarditichesky cardiosclerosis postpartum
cardiomyopathy. Acute heart failure
 massive acute myocardial infarction
 acute myocarditis
 acute alcohol kardiolatiya
 exterior and interior of the heart breaks
Inflammatory, neoplastic and degenerative diseases of the myocardium
Viral myocarditis
Myocarditis with vasculitis
Sarcoidosis
Amyloidosis
Hemachromatosis
Gigantokpetochny idiopathic myocarditis
Chagas' disease
Intracardiac ganglionity
Arrhythmogenic right ventricular dysplasia
Neuromuscular diseases (muscular dystrophy, Friedreich's ataxia, myotonic dystrophy)
Tumors (benign, malignant, primary, metastatic, vnutrimiokardialnye, intracardiac obstructive)
Diseases of the heart valves
The narrowing of the mouth of the aorta, aortic valve insufficiency
Rupture of mitral valve
Mitral Valve Prolapse
Endocarditis
Prosthetic valve dysfunction
Congenital heart disease
Aortic stenosis or pulmonary artery
Eisenmenger syndrome
Pathology of electrophysiological processes in the heart
Violations of the conduction system (fibrosis Purkinje system - primary degeneration or disease Lenegre,
secondary fibrosis and calcification or disease Levy postvirusny fibrosis of the conducting system, congenital
vascular system)
Acquired and congenital forms of QT prolongation
Right bundle branch block and ST segment elevation in the absence of ischemia
Ventricular fibrillation known or unknown etiology, including fibrillation
Myocardial electric instability, due to the influence factors and the central nervous system
Kateholaminzavisimaya lethal arrhythmia due to the influence of the central nervous system
The reasons for the mixed nature
Sudden cardiac death due to extreme physical exertion
Injuries to the heart
Mechanical obstacles venous return of blood (acute cardiac tamponade, massive pulmonary embolism,
acute thrombosis)
Dissecting aortic aneurysm
Toxic-metabolic disorders (electrolyte, metabolic proarrhythmic effects of antiarrhythmic drugs and
equipment)
In young adults the most common cause of sudden cardiac death are inflammatory diseases of the
myocardium, cardiomyopathy syndrome extended interval QT, heart disease (eg, aortic constriction), anomalies
of the thoracic aorta in Marfan's syndrome, abnormalities of the coronary arteries, cardiac rhythm and
conduction, sometimes - undiagnosed coronary atherosclerosis.
The main factors causing sudden cardiac death in young adults are physically extreme overload (for
example, during a sporting event), alcohol and drug use (eg, cocaine causes severe and prolonged spasm of the
coronary arteries up to the development of myocardial infarction), receiving some medications (eg, tricyclic
antidepressants can cause significant slowing of conduction) expressed electrolyte disorders, alcoholic excesses
(particularly the use of alcoholic substitutes).
In persons older than 40 years, especially in the elderly and the elderly, the leading cause of sudden
cardiac death is coronary artery disease, and it is usually the difficult stenosing atherosclerosis of two or three
major coronary arteries. Usually these patients at autopsy revealed erosion or tears in the atherosclerotic
plaques, signs of aseptic inflammation and plaque instability, mural thrombosis of the coronary arteries and
significant myocardial hypertrophy. In 25-30% of patients revealed necrosis in the myocardium.
Since in most cases of sudden cardiac death due to coronary heart disease, it is clear that almost all of the
risk factors of coronary heart disease are both risk factors for sudden death. The highest value belongs to factors
such as advanced age, hypertension, left ventricular hypertrophy, cigarette smoking, high blood cholesterol,
overweight, non-specific ECG changes. The risk of sudden cardiac death increases significantly especially in
combination of several risk factors.
Myocardial infarction
Myocardial infarction is an important risk factor for sudden cardiac death. The potential risk of sudden
cardiac death in the first 72 hours after onset of infarction ranged from 15 to 20% of cases. The highest risk of
sudden cardiac death observed in patients with myocardial infarction during 3 days, 8 weeks, when the disease
was complicated by ventricular tachycardia or atrial fibrillation, or registered paired volley, early ventricular
beats, repeated episodes of ventricular premature volley. In post-MI important predictors of sudden cardiac
death is a violation of myocardial contractility and heart rate (ejection fraction <30% and a frequency of
ventricular premature 10-30 mph). The combination of these factors leads to an increased risk of sudden cardiac
death up to 20% per year. With the normalization of heart rate and left ventricular dysfunction eliminate the risk
of sudden death is significantly reduced.
A poor prognostic factor in post-MI depression is interval ST (painless or accompanied by pain) during
the exercise test. According to Mazur, NA (1999), the appearance of ST depression at a frequency range of heart
rate less than 115 min-1 indicates that the probability of dying in the next 2 years will be about 40%. Poor
prognostic value has a combination of subtotal stenosis of one or more coronary arteries, dyskinetic left
ventricular area (detected by echocardiography) and frequent ventricular premature politopnye. Significantly
increases the risk of sudden death, the presence of an aneurysm of the left ventricle, it marked hypertrophy, and
took place during the acute phase of myocardial infarction, ventricular fibrillation, successfully docked.
Impaired function of the left ventricular myocardium
Reduction of myocardial contractile function of the left ventricle is one of the major risk factors for
sudden cardiac death in heart patients. Considered to be a critical low ejection fraction less than 40%. After the
onset of congestive heart failure of various origins risk of sudden cardiac death is very high, can reach 35-40%
at 5 years.
Hypertrophy of the left ventricular myocardium
Hypertrophy of the left ventricular myocardium of any origin largely predispose to sudden cardiac death,
and the most common mechanism of death is a fatal arrhythmia. The reason is that with hypertrophy it violated
the kinetics of ions, there is pronounced heterogeneity of the medium propagation of depolarization and
repolarization of the myocardium, which contributes to the development of ventricular fibrillation and flutter.
High grade ventricular premature beats by Lown
Dramatically increases the likelihood of sudden cardiac death in premature ventricular 3 through Grade 5.
"Unexplained" decrease in exercise tolerance
Usually based on unreasonable reduction in exercise tolerance is myocardial ischemia, which is also often
associated with arrhythmias. The above factors greatly increase the risk of sudden cardiac death.
Comes first sudden cardiac death and attempted resuscitation
In patients who survived sudden cardiac death, a very high risk of recurrence of ventricular fibrillation
from 25% in the first year and about 5% in the second year (NM Shevchenko, 1992).
Violation of the autonomic regulation of the heart
In CHD, myocardial inflammatory diseases, diabetes and other diseases, there is loss of autonomic
nervous system, resulting in dysfunction and its causes, in particular, to reduce the effects on the heart and
increased sympathetic activity. Signs of impaired cardiac autonomic regulation are increasing the heart rate,
reduced heart rate variability, the lack of heart rate after administration mezatona.
Increased sympathetic activity increases the risk of sudden cardiac death, especially in the morning, after
waking up the patient. Sympathetic stimulation also contribute to various toxic effects on the myocardium
(smoking, alcohol, drugs proarrhythmic). Cardiac arrhythmias and ventricular fibrillation in acute stress may
develop due to increasing new blood and activation potential heterotopic foci of excitation in the heart under the
influence of high levels of catecholamines in the myocardium.
The influence of certain drugs
Some medicines can trigger sudden cardiac death or exacerbate the effects of other risk factors. To the
greatest extent it relates to anti-arrhythmic drugs class IA (quinidine) and 1C (mexiletine, encainide, flecainide,
etmozin) (study CAST, 1992). These drugs can have a pronounced effect proaritmogenny, cause the
development of ventricular tachycardia type "pirouette", frequent ventricular premature beats, and thus
contribute to the development of sudden cardiac death. The same effect can have aminophylline, adrenaline.
Electrolyte disturbances
Of sudden cardiac death in heart patients can contribute to hypokalemia (eg, overdose of
phosphodiesterase inhibitors and drugs with positive inotropic effect).
ECG markers of risk for sudden cardiac death
By ECG markers of risk for sudden cardiac death is the emergence of ventricular late potentials - lowamplitude high-frequency signals at the end of the QRS complex and the beginning of the segment ST
(registered with a high-resolution ECG), reducing variability circadian rhythm, increasing the interval
dispersion QTa more than 50 ms.
Pathology - Sudden Cardiac Death
As mentioned above, the basis of sudden cardiac death for persons 40-50 years of age is often CHD. Such
patients are usually detected heavy stenosing atherosclerosis of one or two (three) of the coronary arteries, their
parietal thrombosis, tear or rupture of an atherosclerotic plaque, in 20-30% of cases are found in myocardial
necrosis. Quite often, a hypertrophy of the left ventricular myocardium, especially when combined with
coronary heart disease and hypertension. Streets younger based on sudden cardiac death are often inflammatory
changes of the myocardium, cardiomyopathy, congenital vascular system and other pathological manifestations
according to etiologic factors for sudden cardiac death.
The main pathophysiological mechanisms
Lead the next model of sudden cardiac death.
It is due to the close interaction between structural and functional elements, and under the influence of
functional destabilizing structural elements.
The structural elements include myocardial infarction (the most common structural category), myocardial
hypertrophy, cardiomyopathy, structural, electrical disturbances (additional pathways with Wolff-ParkinsonWhite syndrome).
Functional disorders include transient ischemia and myocardial perfusion, systemic factors
(hemodynamic, hypoxemia, acidosis, electrolyte disturbances), neurophysiological interactions (dysfunction of
the autonomic nervous system that regulates the heart), toxic effects (proaritricheskie and cardiotoxic agents).
Risk factors of the category of structural defects interact with one or more precipitating factors function, which
leads to myocardial electrical instability (flutter or fibrillation).
The basis of sudden cardiac death is one of the following mechanisms:
ventricular fibrillation; ventricular flutter; asystole ventricular electromechanical dissociation of the heart.
The most common mechanism of sudden cardiac death is ventricular fibrillation (90% of all cases), which
is characterized by disorderly chaotic excitation of individual muscle fibers and lack of co-ordinated wholeventricular, irregular, chaotic motion of a wave of excitement.
When ventricular flutter coordinated ventricular occur, but their frequency is so high (250-300 min-1),
which does not occur in systolic ejection of blood into the aorta. Ventricular flutter by strong momentum in a
circular motion, the return of the excitation wave re-entry, localized in the ventricles.
Asystole heart - is a complete cessation of the heart, it stops. It is caused by dysfunction of the
automaticity pacemaker 1, 2, 3 order (weakness, cardiac sinus node function or lack of function of the
underlying drivers of depletion
Electromechanical dissociation of the heart - cessation of the pumping function of the left ventricle, while
maintaining evidence of electrical activity of the heart (gradually dwindling sinus node or rhythm, rolling in
asystole).
Approximately 3 minutes after sudden cardiac arrest in the cells of the cerebral cortex are irreversible
changes, so the diagnosis of sudden death and emergency care should be immediate.
Ventricular fibrillation always comes suddenly. After 3-4 seconds after the onset of atrial fibrillation
appears dizziness, weakness, the patient loses consciousness after 40 to develop the characteristic spasms single tonic contraction of skeletal muscles. At the same time, ie 40-45 with a pupil begins to expand and reach
a maximum size in 1.5 minutes. The maximum dilation of the pupils indicates that took half the time during
which the possible recovery of brain cells.
Noisy and fast breathing gradually slows and stops at the 2nd minute of clinical death.
The diagnosis of sudden death to be delivered immediately, within 10-15 s, we must not waste time on
measurement of blood pressure, listening to heart sounds, finding the pulse of the radial artery, the ECG.
Pulse should be determined only on the carotid artery. For this purpose, the index and middle fingers are
placed on the throat doctor patient, and then sliding down the side, with no hard pressure to probe the lateral
surface of the neck of the inner edge m.sternocleidomastoideus at the top of the thyroid cartilage.
Diagnosis
The diagnosis of clinical death is made by the following major diagnostic criteria: lack of awareness;
lack of breath or sudden appearance of breathing agonistic type (noisy, rapid breathing);
absence of a pulse in the carotid arteries;
mydriasis (if not taken drugs, never done leptoanalgesia not anesthetize, no hypoglycemia);
discoloration of the skin, the appearance of a pale gray color of the skin of the face. If the patient is on an
ECG-monitor observation, at the time of clinical death on the ECG recorded the following changes.
Ventricular fibrillation - is characterized by chaotic, irregular, sharply distorted waves of different height,
width and shape. These waves reflect the excitation of individual muscle fibers of the ventricles. At the
beginning of atrial fibrillation usually high-amplitude waves, occur with a frequency of about 600 min-1. At this
stage, the prognosis of defibrillation more favorable compared with the forecast for the next stage. Next wave
scintillations become low amplitude waves with a frequency of up to 1000 and even more in 1 minute. The
duration of this stage is about 2-3 minutes, then the duration of atrial waves increases, decreases the amplitude
and frequency (300-400 min-1). At this stage, defibrillation is not always effective. It should be emphasized that
the development of ventricular fibrillation often precede episodes of paroxysmal ventricular tachycardia,
ventricular tachycardia, sometimes bidirectional (type "pirouette"). Often, before the development of ventricular
fibrillation recorded politopnye frequent and early extrasystoles (type R on T).
When ventricular fibrillation ECG recorded curve resembling a sine wave with frequent rhythmic, very
large, broad and similar to each other in waves, reflecting the excitement of the ventricles. Highlight the
complex QRS, interval ST, T wave is not possible, there is no contour. Most often, ventricular flutter goes into
their flickering. ECG pattern of ventricular flutter is shown in Fig. 1.
Fig. 1. Ventricular flutter.
When asystole heart on an electrocardiogram recorded contour, are any waves or teeth are missing.
With electromechanical dissociation of the heart can be recorded on an electrocardiogram rare sinus nodal
rhythm, which moves to the rhythm, and then gives way to asystole.
Example ECG electromechanical dissociation of the heart is shown in Fig. 2.
Sudden cardiac death
By sudden cardiac death (SCD) understand death, it developed immediately or within one hour after the
manifestation of changes in the clinical status of the patient.
Cardiac arrest (Sardiac arrest) - is a condition accompanied by loss of consciousness due to asystole,
ventricular tachycardia or ventricular fibrillation. Obligatory condition diagnosis of cardiac arrest is the
registration of these episodes electrocardiographic method.
According to the WHO - today one million people a week died suddenly 30. In 1985 in the United States
about 400,000 deaths were classified as sudden in those over 25 years old (NIH Publication 83-2035). Out of
the total mortality in the share of sudden cardiac death accounts for about 10%. Sudden cardiac death accounts
for 15-20% of all non-violent deaths among residents of industrialized countries. The share of CHD accounts for
about 80% of all sudden deaths (Myerbug RJ et all., Heart disease: a textbook ...; 1992). In 25% of cases of
coronary heart disease manifests the development of BCC (Kennel WB et all., Circulation 1975). Suddenly 50%
of patients dying of CHD (Gillum RF., Circulation 1989). Approximately 400,000 BCC each year in Europe.
Among them: less than 10% are treated in hospital, (<40,000), half of these survivors died before discharge
(20,000) 20,000 survived to patients who need treatment (ESC, 2001).
In the Russian Federation, official statistics on the subject are contradictory to the objective and
subjective reasons. Taking into account the fact that the life expectancy of the male population in Russia is
much lower than in industrialized countries, and is 57 years old, it can be assumed that the absolute number of
sudden deaths in the general population will be great.
The mechanisms underlying the development of sudden cardiac death in the vast majority of cases,
ventricular tachycardia (VT) and ventricular fibrillation (VF) - 95%, and the remaining 5% are
bradyarrhythmias and asystole. The main cause of SCD is coronary heart disease. Other entities that in which
the BCC is the outcome of the disease, are dilated cardiomyopathy (DCM) and hypertrophic cardiomyopathy
(HCM), to arrhythmogenic right ventricular dysplasia (ADPZH) to Brugada syndrome and lengthened QT, the
anomalies of the coronary arteries, and so on. states, the list of which is presented in the table.
In 1984 J.T. Bigger identified predictors of SCD and analyzed the likelihood of its development,
depending on the specific clinical situation. Based on the analysis of the data obtained from the groups of high
and moderate risk of SCD.
The causes of sudden cardiac death by J. Ruskin, 1998 CHD
Dilated cardiomyopathy
Left ventricular hypertrophy
Hypertrophic cardiomyopathy
Acquired heart valvular disease
Congenital heart disease
Acute myocarditis
Anomalies of coronary arteries
Sarcoidosis
Amyloidosis
Heart tumors
Left ventricular diverticula
WPW syndrome
Long QT syndrome
Drug proarrhythmia
Cocaine intoxication
Severe electrolyte imbalance
Idiopathic ventricular tachycardia
Predictors of SCD.
Note: AMI - acute myocardial infarction, EF - ejection fraction, VE - frequent ventricular premature
beats, ventricular tachycardia - ventricular tachycardia, VSS - sudden cardiac death.
Prevention of cardiac death - is the health and social activities of the persons who have survived cardiac
arrest (secondary prevention) or have a high risk of developing cancer (primary).
Modern methods of preventing SCD:
- Implantation of a cardioverter-defibrillator;
- Holding constant antiarrhythmic drug therapy;
- Implementation of radiofrequency ablation of ventricular arrhythmias;
- Implementation of coronary revascularization;
- Surgical treatment of ventricular arrhythmias.
Implantation of a cardioverter-defibrillator
The effectiveness of ICDs for primary and secondary prevention of SCD in patients evaluated in these
studies as AVID, MADIT, MADIT II, MUSTT, CIDS, CASH. The results of the above studies showed a
statistically significant reduction in overall mortality in the group of patients treated with an ICD compared with
other methods of prevention of SCD in patients with a high risk of SCD. The effectiveness of ICDs for primary
and secondary prevention of SCD in patients with arrhythmogenic right ventricular dysplasia (ADPZH) was
demonstrated in a study DARVIN. In addition, according to a study in patients with ADPZH were isolated signs
of high risk for life-threatening arrhythmias. This cardiac arrest history, hemodynamically unstable ventricular
tachycardia, the youth involved in the left heart. In M. Zecchin demonstrated that ICD implantation is indicated
in patients DCM for secondary prevention of cardiac arrest. A combination of a reduced ejection fraction (below
30%), increased end-diastolic diameter of the left ventricle 70 mm, episodes of unstable ventricular tachycardia
and long history of the disease, according to recent data, is an indication for the primary prevention of sudden
cardiac death in these patients.
Analysis of the results of numerous works with a significant number of patients with different structural
pathology infarction showed that the precursors of sudden death, defined in 1984, JT Bigger by far are common.
The diagnosis of coronary heart disease, in fact, a risk factor for SCD and its prevention should be discussed at
an early stage of the disease.
Conducting ongoing antiarrhythmic drug therapy.
Survival of patients with ventricular arrhythmias with organic heart disease improved only by using Bblockers or drugs class III (kordaron, sotalol). Demonstrated that treatment with beta-blockers in patients with
postinfarction cardiosclerosis ZHNR significantly reduces mortality. Most clearly demonstrates this result in
patients with a high risk of SCD (Anderson JL, Platia EV). According to a study CAMIAT, EMIAT
appointment Cordarone patients with postinfarction cardiosclerosis ZHNR complicated, can significantly reduce
the risk of SCD. The use of drugs of class I, especially in Division I c studies CAST-I and CAST-II showed that
the purpose of these drugs in patients with postinfarction cardiosclerosis associated with increased risk of SCD.
Implementation of radiofrequency ablation of ventricular arrhythmias
Currently, radiofrequency ablation method used for destruction as focal ventricular arrhythmias, such as
ventricular tachycardia and PVCs from the area of the right ventricular outflow tract, and in patients with
ischemic ventricular tachycardia (which is based on the mechanism of re-entry).
The main indications for RFA is:
Class I (is shown):
1. Patients with hemodynamically significant sustained monomorphic VT refractory to or intolerant of
AAT AAT and / or do not wish to receive long-AAT.
2. Persons with VT in bundle-branch block;
3. Patients with long monomorphic VT and ICD experiencing frequent ryazryady ICDs prevent that can
not be carried out, or related ICD pereprogrammatsiey AAT. VT, resistant to the ongoing AAT or patients can
not tolerate or pharmacological agents do not want long-term use AARP.
Class III (no evidence)
1. Persons with VT, curable AAT ICD or surgery, preferring these treatments RFA.
2. Hemodynamically unstable, rapid, polymorphic ventricular tachycardia, which can not be adequately
mapped in the EPS.
3. Asymptomatic and benign variants VT.
Implementation of coronary revascularization
The main goal of treatment is to restore blood flow to ischemic myocardium (revascularization).
Revascularization is performed using the following: coronary artery bypass grafting autovenous; mammarocoronary bypass surgery, transluminal balloon angioplasty of the coronary arteries, laser angioplasty of the
coronary artery, coronary atherectomy Endoluminal, indirect revascularization.
Surgical treatment of ventricular arrhythmias.
To surgical treatment of ventricular tachycardia include operations: circular endocardial resection,
extended endocardial resection in combination with or without cryodestruction. The choice of surgical removal
of ventricular tachycardia is made depending on the localization of arrhythmogenic area.
If we talk about all the available methods of preventing SCD, we should not forget about the heart
transplant, which certainly is the most effective in patients with postinfarction cardiosclerosis and with reduced
inotropic myocardial function, in patients with dilated cardiomyopathy and ADPZH and other diseases (survival
to 60 - 70% within 5 years).
We should not forget that the modern approach to identification of high risk groups, based on the results
of these studies as AVID, MADIT-I, MADIT-II, CASH inadequate and covers less than half of the patients who
eventually die suddenly. This fact focuses on the need for further research aimed at identifying predictors of
SCD, and makes a major focus of the category of persons in need of primary prevention of SCD. Prevention of
sudden cardiac death is one of the main problems of modern electrophysiology. This, ultimately, determines the
necessity for this section of cardiology in our country and in the Armed Forces in particular.
Villmed
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Design www.happyAtrial flutter. Atrial fibrillation (atrial fibrillation)
Atrial flutter (TA) - is one of the most common cardiac arrhythmia, it accounts for about 10% of
paroxysmal supraventricular tachyarrhythmias. It is a common complication of acute myocardial infarction and
surgery open heart surgery. Other causes of atrial flutter include chronic lung disease, pericarditis,
thyrotoxicosis, rheumatic fever (especially in patients with mitral stenosis), sinus node dysfunction (tachy-brady
syndrome), as well as other diseases that contribute to atrial dilation. Atrial flutter can occur in patients of all
ages. However, those who have heart disease, it is much more common.
Atrial fibrillation (AF) - is a supraventricular tachyarrhythmia characterized by uncoordinated atrial
activation with electrical frequency 350-700 per minute, which causes deterioration of the contractile ability of
the atria and the actual loss of phase predsernogo ventricular filling.
Atrial fibrillation is one of the most common and most common arrhythmia in clinical practice.
Clinical manifestations
Typically, patients with atrial flutter complain of suddenly arisen palpitations, shortness of breath,
weakness, exercise intolerance, or pain in the chest. However, there are more severe clinical manifestations syncope, dizziness, hypotension, and against the background even cardiac arrest due to a higher incidence of
ventricular contraction. Pathophysiological basis of this system is to reduce the symptoms of release, systemic
blood pressure and a decrease in coronary blood flow. According to some data reduction of coronary blood flow
can reach 60% with increasing myocardial oxygen demand. Due to severe hemodynamic disorders develop
systolic dysfunction of the heart, followed by dilation of its cavities, leading eventually to heart failure.
Classification of atrial flutter
Atrial flutter - a fast, regular atrial tachyarrhythmia with the frequency of excitation and atrial contraction
of more than 200 per minute. Is now generally recognized that the basis of this arrhythmia is a mechanism for
re-entry of excitation.
Typical TP due pravopredserdnym around Macrory-entri, limited front ring of the tricuspid valve, and the
rear anatomical obstacles (holes of the upper and lower vena cava, the Eustachian ridge) and a functional barrier
in the form of terminal crista. In this wave of excitement passes through the lower isthmus (the zone of slow),
located between the inferior vena cava and the perimeter of tricuspid valve. This so-called istmuszavisimoe
systems: it can be oversaw by RF exposure in the area.
Depending on the direction of the wave of depolarization in the atrium are two typical types of systems:
- TP with atrial septal activation (WFP) in kaudokranialnom direction and the lateral portion of the right
atrium (PP) - in craniocaudal, ie circulating excitation wave around the tricuspid valve counter-clockwise
(counterclockwise - CCW) when viewed from the top side heart. On the ECG is characterized by negative F
waves in leads II, III, aVF, reflecting synchronous activation of the MPP from the bottom up, and positive
flutter waves in lead V1. Descending knee F-waves in the inferior leads of standard and reinforced is long (very
shallow) than ascending (steeper). The important point is much smaller amplitude of atrial electrical activity of
the complexes in lead V1, projected onto the upward phase of the waves TA in lead aVF;
- TP with the other structures of the activation of the right atrium, that is, with the circulation of the
excitation wave in the clockwise direction (clockwise - CW), characterized by the positive direction
elektorokardiografice flutter waves in the inferior leads and enhanced standard and comparable in amplitude
with the F-wave in lead V1 .
However, the characteristic ECG findings in patients may not always be so only when it can be proved
endo EFI interest kavatrikuspidalnogo Isthmus.
Istmuszavisimymi tachycardias addition to a typical two-wave and TAs are nizhnepetlevoe atrial flutter.
For two-wave TA characterized by the formation of two waves of depolarization in PP circulating each other
around the tricuspid valve ring in one direction, resulting in an acceleration of the TA. The geometry of the
atrial activation on the surface ECG showed no significant change. This type of arrhythmia, probably has little
clinical importance, as it saves a short period of time (up to 11 systems), the subsequent transfer of a typical TA,
at least in atrial fibrillation.
Nizhnepetlevoe TP characterized breakthrough excitation wave through a terminal Christie (TC) at its
different sites to form a circle around the re-entri mouth of the inferior vena cava loop momentum
counterclockwise (CWW). In this case, electrocardiographic characteristics TA will depend on the level of a
border furrow. It will vary from ECG pattern identical to a typical TP / CWW, with a slight decrease in the
amplitude of the positive phase flutter waves in the inferior leads and P wave in lead V1, reflecting the clash of
counter fronts depolarization in a set PP (in breaking waves TA in caudal TC) to the ECG pattern similar to that
of a typical TP / CW, which will be a reflection of the activation of WFP in craniocaudal direction (the break in
the cranial TC). These forms of TA as well as the typical form of TA amenable to radiofrequency ablation in the
lower isthmus.
By istmusnezavisimym TP are verhnepetlevoe, mnozhestvennotsiklovoe levopredserdnye and atrial
flutter. When verhnepetlevom TP wave of depolarization, breaking through the TC forms a circle re-entri in PP
arch perimeter of the superior vena cava with the circulation of the pulse in the clockwise direction, and the
lower parts of PP are not involved in the cycle of the TA. The geometry of the atrial activation on the surface
ECG is similar to a typical TP / CW.
Mnozhestvennotsiklovoe TP is characterized by simultaneous activation of several cycles of the atria
because of the possibility of multiple breaches of excitation waves through the TC.
In more rare cases, community-Macrory entri can form in the left atrium and are more common in
patients who have had surgery on the left atrium. Electrocardiographic pattern at these options TA will be very
variable.
Treatment of atrial flutter
Emergency treatment
Emergency care for m depends on the clinical manifestations. Patients with acute circulatory collapse,
cerebral ischemia, angina, or with an increase in symptoms of heart failure shows emergency synchronized
cardioversion. Successful restoration of sinus rhythm can be achieved less than 50 J discharge using singlephase currents, and with biphasic currents - even less energy. The use of drugs Ia, Ic and III classes use
increases the chances of cardioversion.
Frequent atrial pacing as transesophageal and intraatrial is the method of choice in restoring sinus rhythm.
According to medical literature, its efficiency is on average 82% (from 55 to 100%). -Frequent stimulation is
particularly justified in TA after heart surgery, as these patients in the postoperative period is often left atrial
epicardial electrodes. Pacing (pacing) fibrillation should begin with the frequency of 10 pulses exceeding the
spontaneous electrical activity of the atria in the TA. The growth rate for the pacemaker to verify the effective
entry tachycardia cycle is recommended to inkrementsiey 10 ekstrastimulov. The dramatic change in the
morphology of the surface waves TA lower standard ECG leads and enhanced switching points (resetting) TA.
Termination of pacing at this point may be associated with restoration of sinus rhythm. The critical frequency
required for the termination of the first type of TA is more than usually flutter frequency of 15-25%. The use of
quinidine, disopyramide, procainamide, propafenone, ibutilide increases the chances of effectiveness-frequent
stimulation to restore sinus rhythm. Attempts to stop using TP-frequent stimulation can often lead to the
induction of atrial fibrillation, which is often preceded by a spontaneous conversion to sinus rhythm. Induction
of atrial fibrillation, probably using a more "high-speed" mode-frequent stimulation (cycle length of the
stimulation cycle is superior TP by 50% and more).
A number of drugs (Ibutilide, flecainide) effectively restore sinus rhythm with TP, however, significantly
increase the risk of ventricular tachycardia spindle. No drugs that slow AV-holding or kordaron not been
effective in restoring sinus rhythm, although they can effectively monitor your heart rate.
In most cases, the AV-conducting 2:1 and above patients have hemodynamic disturbances. In this
situation, the clinician may opt for the drugs that slow AV conduction. Drugs of choice should be considered
calcium antagonists (nedigidroperidinovogo series) and blockers. Adequate, though elusive, frequency control
rhythm is particularly important if sinus rhythm is delayed (for example, the need for anticoagulation therapy).
Moreover, if you plan to cardioversion drug monitoring may be required tachysystole as antiarrhythmic drugs,
such as drugs of class Ic, can reduce the incidence of atrial and cause a paradoxical increase in the frequency of
ventricular hidden because of slowing AV conduction and affect the clinical status of the patient. If TP lasts
more than 48 hours, the patients showed an anticoagulant to electrical or pharmacological cardioversion.
Constant medical therapy
Chronic pharmacological prophylactic therapy with TP is usually empirically, the efficiency is
determined by trial and error. Traditionally recommended dual therapy with a drug effective in blocking an
atrioventricular connection, and membrane-active agent. The exception is the class III drugs (sotalol, kordaron),
combines the features of all classes of antiarrhythmic therapy.
Catheter ablation of the isthmus at kavotrikuspidalnogo istmuszavisimom flutter
It is now recognized that the creation of a complete bidirectional block in the isthmus between the inferior
vena cava and the perimeter of tricuspid valve using radiofrequency catheter ablation (RFA) is a highly effective
and safe procedure to remove TP and gradually occupies a leading position in the structure of different ways to
treat these arrhythmias. Radiofrequency ablation can be performed or the period of TA or during sinus rhythm.
Previously it was thought that the end point of surgery is relief of TP. Later developed rigorous criteria to
achieve bidirectional block in the bottom of the neck, which significantly increased the long-term efficacy RFA.
In endovascular center GVKG them. Acad. State Medical Academy from 1999. to 2004. made more than
a hundred interventions for typical atrial flutter. Verification of the block in the lower isthmus was carried out
on the basis of local criteria to achieve conduction block in the area of interest and on the basis of the traditional
technique of verification unit (indirectly). Effectiveness of the procedure without the support of AAT on the
results of a prospective follow-up was 88%. Combined management of patients included: the implantation of a
permanent pacemaker system, the repeated interventions of the pulmonary veins, the resumption of AAT. In
these conditions, the effective control of sinus rhythm in a calendar year was achievable in 96% of all clinical
cases. We have shown a significant improvement in the pumping function of the atria, which can ultimately
explain a significant positive clinical dynamics. Quality of life was significantly higher in patients after RFA.
In a prospective randomized study comparing continuous oral AAT (61 patients with TA) and
radiofrequency ablation. In the dynamic follow-up of 21 ± 11 months, sinus rhythm was maintained only 36%
of patients treated with AAT, whereas after RFA - 80% of patients. In addition, 63% of patients receiving
continuous drug therapy, took one or more hospitalizations, compared with 22% of patients after RFA.
Absolute indication for RFA TAs are times when develop resistance to multiple AAT or intolerance, or
when the patient does not wish to receive long-AAT. However, the development of resistance - the result, in
many cases, long-term use of AAT, which is impractical for financial reasons and because of the risk of
proaritmogennogo of the AAT. Therefore, we believe that RFA is shown at the time when the patient agrees to
the examination, and the first long paroxysm of TA is an absolute indication for RFA.
Indications for ICD implantation
History of ICDs in clinical practice has not more than thirty years, and today the effectiveness of modern
devices for VF and VT is close to 100%.
In 1970, Michel Mirowski and Morton Mower, sudden death shocked his colleagues, proposed the
concept of creating an implantable device that would automatically carry out emergency treatment in the event
of life-threatening ventricular tachyarrhythmias. In 1980, Michel Mirowski conducted the world's first
successful surgery to implant a cardioverter-defibrillator, a young woman with recurrent episodes of cardiac
arrest due to ventricular fibrillation. Subsequently, this therapy has become one of the most effective methods of
prevention of SCD.
Modern ICDs is a system consisting of a device, a prisoner in a small titanium case and connected with it
one or more electrodes placed in the chambers of the heart. ICD is implanted in the left or right subclavian area
under general anesthesia. During the operation, after the installation of an ICD defibrillation threshold
determination is made. The device includes a power supply - Lithium-silver-vannadievuyu battery voltage
converter, resistors, capacitors, chip and system analysis of heart rate, release the discharge database
electrograms arrhythmic events. In clinical practice, applied ventricular and atrial electrodes with passive and
active fixation for cardioversion defibrillation antitahikardicheskoy, antibradikardicheskoy pacing. At present,
we use one-, two-chamber system.
The basis of the detection of arrhythmias is an analysis of the frequency of its own rhythm, ventricular
morphology, signal stability of RR-interval, the ratio of the characteristics of atrial and ventricular activity (in
the two-chamber system). Those characteristics allow the device to differentiate between ventricular and
supraventricular tachyarrhythmias.
In defibrillators are so-called zone of detection of fast and slow ventricular tachycardia. In that case, if the
frequency of arrhythmias enters the first zone, then there is a discharge defibrillator for relief VF or rapid
ventricular tachycardia. In the second zone may hold different types antitahikardicheskoy ventricular pacing to
suppress arrhythmias. Parameters detection and treatment algorithms for each zone is defined by the
characteristics of ventricular tachycardia and puts using the programming device. At follow-up, depending on
the clinical situation, ongoing medical treatment, these values can be corrected.
Treatment algorithm, implemented device is set individually, based on patient tolerability clinical
tachycardia. When hemodynamically insignificant, relatively slow VT may be effective antitahikarditicheskaya
stimulation burst (stimulation of short bursts at a frequency of 10-30% above the rate of tachycardia) or ramp
(stimulation pulses with gradually increasing frequency at which each pulse shortens the cycle of stimulation as
compared to the previous one) , and in their failure mode can be used cardioversion. With the development of
ventricular fibrillation or rapid ventricular tachycardia first step in treatment is defibrillation immediately. The
power level must exceed 10 J intraoperative defibrillation threshold, followed by stepwise increases aggressive
therapy in the form of increase of the discharge power to the maximum value (30 J), and a change in the polarity
of the circuit from the case of ICD defibrillation to intracardiac electrode and vice versa.
Indications for ICD implantation.
Based on the results of multicenter studies, Joint Task Force - North American Society of
Electrophysiology / American College of Cardiology / American Heart Association (NASPE / ACC / AHA) in
2002 developed the indications for implantation, and recommendations for the clinical management of patients
with cardioverter-defibrillators. In our opinion, they are acceptable to the Russian Federation.
Class I
1. Cardiac arrest due to VT / VF, but not due to the temporary or reversible cause (level of evidence - A).
2. Spontaneous resistant VT associated with organic heart disease (level of evidence - B).
3. Syncope of unknown origin in cases where at EPS induced hemodynamically significant VT or VF
resistant and drug therapy is ineffective or intolerable no advantage (level of evidence - B).
4. Unstable ventricular tachycardia due to coronary artery disease, myocardial infarction, left ventricular
dysfunction, and inducible VF or VT stand at EPS, which is not inhibited by AARP class I (level of evidence A).
5. Spontaneous resistant VT in patients without organic heart disease, and are not subject to other
methods of treatment (level of evidence - C).
Class II and
1. Patients with an ejection fraction <30%, at least 1 month after MI and 3 months after surgical
revascularization (level of evidence - B).
Class II b
1. Heart failure, probably due to ventricular fibrillation, but conducting electrophysiological testing
excluded for other medical conditions (level of evidence - C).
2. Severe symptoms (eg, syncope), attributed to sustained ventricular tachyarrhythmias in patients
awaiting heart transplantation (level of evidence - C).
3. Family or congenital disease with a high risk of developing life-threatening ventricular
tachyarrhythmias such as long QT syndrome or hypertrophic cardiomyopathy (level of evidence - B).
4. Unstable ventricular tachycardia in patients with coronary heart disease, myocardial infarction, left
ventricular dysfunction, which are induced at EPS stable VT or VF (level of evidence - B).
5. Recurrent syncope in the presence of left ventricular dysfunction and inducible ventricular arrhythmia
at EPS, when other causes of syncope are excluded (level of evidence - C).
6. Syncope of unknown etiology or unexplained sudden cardiac death in the family history, combined
with typical and atypical BPNPG segment elevation and ST (Brugada syndrome) (level of evidence - C).
7. Syncope in patients with advanced heart disease who have a thorough invasive and noninvasive study
could not determine the cause (level of evidence - C).
Class III
1. Syncope of unknown origin in patients without inducible ventricular tachyarrhythmias and without
organic heart disease (level of evidence - C).
2. Continuously recurrent ventricular tachycardia or ventricular fibrillation (level of evidence - C).
3. VT or VF due Syndrome WPW, VT with the source of the right ventricular outflow tract, idiopathic
left ventricular tachycardia or ventricular tachycardia fastsikulyarnaya to be surgical or catheter ablation (level
of evidence - C).
4. Ventricular tachycardia or ventricular fibrillation associated with temporary or reversible disorders (eg,
myocardial infarction, electrolyte imbalance, drug action, trauma) when correction violations considered
feasible, and probably significantly reduce the risk of recurrence of arrhythmia (level of evidence - B).
5. Serious mental illness, which may be exacerbated by device implantation or may preclude systematic
follow-up (level of evidence - C).
6. A terminal illness with a life expectancy of <6 months (Level of evidence - C).
7. CHD patients with left ventricular dysfunction and a wide QRS complex in the absence of spontaneous
or inducible stable or unstable ventricular tachycardia, undergoing surgery for coronary artery bypass surgery
(level of evidence - B).
8. FC IV CHF (NYHA), drug resistance in patients who are not candidates for heart transplantation (level
of evidence - C).
Atrioventricular reciprocating tachycardia
Epidemiology tachycardia
The share of atrioventricular nodal reciprocating tachycardia (AVNRT) accounts for 85% of all
supraventricular arrhythmias, with the deletion of atrial fibrillation. In a population of patients suffering from
this arrhythmia (ie, tachycardia), the ratio between men and women is 3:2. AVNRT is found in all age groups.
However, in most cases, significant clinical symptoms between the ages of 28 and 40.
Clinic
In a patient with AVNRT is usually no sign of structural pathology infarction. Disease (tachycardia)
occurs in the form of frequent bouts of rhythmic heartbeat that starts and stops abruptly. Duration paroxysm
AVNRT from a few seconds to several hours, and the frequency of occurrence of the daily arrhythmia to 1-2
times a year. Symptoms during an attack depends on the heart rate (usually 140 to 250 per minute), the
functionality of the cardiovascular system, the presence of comorbidity. During the paroxysm patients usually
complain of weakness, dizziness, feeling of pulsation in the neck vessels in the head. Sometimes the attack is
accompanied by the development of syncope, hypotension.
Pathogenesis
The pathogenesis is the functional separation of atrioventricular connection to 2 channels with different
electrophysiological properties, "fast" and "slow." These channels form the two anterograde atrial entry into the
compact part of the atrioventricular connections in the triangle of Koch (anatomic site located in the atrial
septum in the right atrium and the limited band of Todaro, the top edge of the mouth of the coronary sinus and
the fibrous ring of tricuspid valve). The "fast" part of the ABC is in the upper part of the triangle of Koch, has
the properties of a "fast" event (when sinus rhythm is holding it on it) and the relatively high values of
refractoriness. At the same time, the fibers 'slow' parts are located in the lower part of the triangle extending
from the upper edge of the coronary sinus along the tricuspid valve annulus to the compact part of the FAA.
These fibers are characterized by a "slow" holding and low values of refractoriness. Different
electrophysiological properties of two groups of fibers in this area are the basis for the formation of re-entry
field (re-entri) and the existence of tachycardia. At an extraordinary reduction fibrillation (such as atrial
premature beat) occurs in the blockade of the fast part and the momentum slowly carried the ventricles in the
lower triangle of Koch. During this time of anxiety in quick time to recover, and the wave of depolarization is
retrograde applies to a "fast" part, and then again at a "slow".