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MINISTRY OF HEALTH OF REPUBLIC OF UZBEKISTAN
TASHKENT MEDICAL ACADEMY
DEPARTMENT OF DEPARTMENT OF INTERNAL DISEASES № 3
OF MEDICAL AND PEDAGOGICAL FACULTY
LECTURE TOPIC:
« ARRHYTHMIA AND BLOCKADES. DIFFERENTIAL DIAGNOSIS.
CLINIC AND ECG SIGNS. EMERGENCY. TACTICS OF GENERAL
PRACTITIONER »
(for the students of medical-pedagogical faculty)
TASHKENT – 2016
MINISTRY OF HEALTH OF REPUBLIC OF UZBEKISTAN
TASHKENT MEDICAL ACADEMY
DEPARTMENT OF DEPARTMENT OF INTERNAL DISEASES № 3
OF MEDICAL AND PEDAGOGICAL FACULTY
«APPROVED»
Dean of medical-pedagogical faculty,
professor Khamraev A.A..
___________________
____ _____________ 2016 y
LECTURE TOPIC:
«ARRHYTHMIA AND BLOCKADES. DIFFERENTIAL DIAGNOSIS.
CLINIC AND ECG SIGNS. EMERGENCY. TACTICS OF GENERAL
PRACTITIONER »
(for the students of medical-pedagogical faculty)
LECTURER: professor Gadaev A.G.
TASHKENT – 2016
TECHNOLOGY OF THE EDUCATION
Amount student
Form of the
occupation
Time - 2 hours
scholastic Lecture - a visualization
Plan to lectures
1.The сonducting system heart. Determination of
the notion aritmias, blocades
2.Reasons and conditions, bring about origin
aritmias and blocades
3.Categorization of aritmias
4.Notion, determination and clinical current
different type aritmias and blocades
5.Particularities of the treatment different type
blocades and aritmias, tactics squall, urgent help
Purpose of the scholastic occupation: acquaint student with reasons, patogenesis
of the diseases, being accompanied origin aritmias and blocades, modern
categorization of aritmias, train principle of the differential diagnostics and urgent
help under different type of aritmias
The Pedagogical problems
1.Consolidate and deepen
knowledges a student about
disease, being accompanied
aritmias
and blocade
2. Teach student it is correct
to install diagnosis in
accordance with modern
categorization
3. Train student to skill to
differentiate different types
aritmias
The results of the scholastic process:
the general practitioner must know:
1.Construction conducting systems heart
2.Diseases, being accompanied arising the blocades
and aritmias
3.Categorization of aritmias
4.Principles of the differential diagnostics different
type aritmias
5. Tactician of conduct, principles of the treatment
sick different type of aritmias
4. Train student to conduct,
urgent help and treatment
sick with aritmias
Methods of teaching
Text to lectures, video film, questions, technology
"yes-no"
Form of the education
Lazer projector, visual material, special technical
equipment, show thematic sick
Facilities of the education
Group
Conditions
of
the Auditorium
undertaking the scholastic
process
PRODUCTION CHART TO LECTURES
Stages, time
Activity
Teacher
1 stage
Introductory part
(5 mines)
1. Tells about subject of the
lectures, her purposes and plan
Students
1.
Listen
2.1. In purpose of increasing to 2.1. Answer questions
2 stages
actualizations (increasing to value)
Actualization
(increasing
to of the knowledges student will
value ) of the assign the questions:
knowledges
1.Tell construction conducting
(20 mines)
systems heart
2. Enumerate diseases, being
accompanied blocade and aritmias
3. Enumerate groups a preparation,
using for treatment of the blocades
and aritmias
2.2. Showing on screen offers to
get acquainted the student with
purpose and problem to lectures.
2.2 Study slide 1
Slide 1, 2
2.3. Study slide 2
3 stages
Main
(information)
mines)
3.1. Introduces the student with 3.1. Together analyse
lecture material, value of the heard lecture material,
part subject and principle of the shaping will assign questions
(55 intelegent cultural personality, in
particular squall-teacher.
In purpose of increasing to
actualizations of the knowledges
conducts quick questioning a
student:
On 1 point of the plan to lectures:
tell
construction
conducting
systems heart
On 2 points of the plan to lectures:
enumerate
diseases,
being
accompanied arising the blocades
and aritmias
On 3 points of the plan to lectures:
tell categorization aritmias
On 4 points of the plan to lectures:
enumerate differential diagnostic
signs different type of aritmias
On 5 points of the plan to lectures:
tell tactician of conduct, principles
of the treatment sick different type
of aritmias
Sopping for important moment of
the lectures offers to write main Main moments write in
copy-book
positions in copy-book
4 stages
final (10 mines)
4.1. Will Assign questions:
4.1. Answer questions
1.Enumerate most often meeting
diseases,
being
accompanied
aritmias and blocade
2. Tell main diagnostic пизнаки
different
type
aritmias
(мерцательная
aritmias,
экстрасистолии,blocades )
4.2. Listen, write
3. Name cardinal principles of the
treatment, urgent help under
different type aritmias
4.2. Gives task for independent
work student: Study EKG signs of
the blocades
Arrhythmias and heart block. Cardiac arhythmias and conduction - a large group of
transient or permanent heart rhythm disorders, mainly arising from the organic
lesions of the cardiovascular system. They are caused by violations of the most
important functions of myocardium: automatism, excitability and conductivity.
Organic lesions of the cardiovascular system are the most common arrhythmia in
ischemic heart disease, myocarditis, cardiomyopathy, heart defects, disease of
large vessels (thrombosis boemboliyah pulmonary artery aneurysms of the aorta
and its tears, Takayasu's disease), hypertension, pericarditis, cardiac tumors.
Arrhythmias are also seen in endocrinopathy (pheochromocytoma, thyrotoxicosis),
intoxication drugs (glycosides, catecholamines), acute infectious diseases, anemia,
and
other
pathological
conditions.
Arrhythmias may be associated with features of the conduction system, such as in
cases
of
the
syndrome
Wolff-Parkinson-White
steam.
Often arrhythmias develop disorders of electrolyte balance, especially potassium,
calcium
and
magnesium.
Sometimes arrhythmias occur under the influence of excessive consumption of
coffee, alcohol, and smoking, often hidden in the affected myocardium. Some
types of arrhythmias can develop in healthy people in response to exercise or
stress.
The diagnosis of cardiac arrhythmias is based on clinical and electrocardiographic
data.
For
a
healthy
person,
it
is
typical
sinus
rhythm.
Sinus tachycardia is diagnosed in conditions, if the heart rate at rest is higher than
100 in 1 min, while maintaining the right sinus rhythm. The main reason neurosis, hyperthyroidism, heart failure, rheumatic heart disease and myo,
intoxication, fever, anemia. In healthy people, it occurs in the emotional and
physical stress. As noncardiac causes of sinus tachycardia may be an imbalance of
autonomic
nervous
system
tone
dominated
sympathic.
There clinically manifested sinus tachycardia palpitations, feeling of heaviness in
the chest, shortness of breath sometimes. It usually begins slowly and gradually
ends in contrast to that in paroxysmal tachycardia. In ischemic heart disease sinus
tachycardia can cause chest pain due to an increase in myocardial oxygen demand.
Diagnosis of sinus tachycardia is on ECG - the presence of P wave of sinus origin,
which precede each complex QRS, if the duration of the interval P-P less than 0.6
s, and the results of vagal samples that cause the gradual decrease in rate of
tachycardia, and in case of paroxysmal ends abruptly attack or ineffective.
In cases of severe sinus tachycardia often decreases the duration of electrical
ventricular systole (Q-7), ST segment can be moved below the contour.
Treatment is aimed at addressing the root causes: anemia, fever, hyperthyroidism,
etc. If the tachycardia itself serves as a pathogenetic factor, such as angina pectoris,
myocardial infarction, appointed blockers p-adrenergic receptors (propranolol
inside of 10-40 mg every 6 hours atenrlol or 25-50 mg 2 times a day), calcium
antagonists, verapamil (Isoptin, verapamil by 40-80 mg 2-3 times a day). Often
sinus
tachycardia
persists
vagotropic
samples.
Sinus bradycardia is characterized by slowing the heart rate below 60 sinoatrial
origin in 1 min. Reasons - increased tone of the vagus nerve or sinus node function
changes in a number of infections (influenza, typhoid fever), myocardial infarction,
increased intracranial pressure, and other micro sedema Sinus bradycardia may be
a consequence of medical treatment in the case of p-blockers ,quinidine drugs
Cordarone, verapamil, tranquilizers. Athletes incidence rate is between 40-45 beats
per
1
min.
Often, it is clinically manifested. Sometimes patients complain of a rare heart rate,
weakness, a feeling of "fading" of the heart, dizziness. Excessive bradycardia can
cause
cerebral
ischemia
with
symptoms
of
syncope.
Diagnosed by ECG on the basis of normal sinus rhythm, in addition to reducing its
frequency,
sometimes
forms
tall
spiky
tooth
T.
Heart rate during sinus bradycardia unlike bradycardia due to various types of
blockades, becomes more frequent in the case of exercise, the injection of atropine.
Treatment in the absence of clinical signs is not required. If sinus bradycardia
causing hemodynamic instability and other clinical manifestations, appointed
atropine (0.5-2.0 mg / v or s / c), isoproterenol (1.4 micrograms / min in / infusion).
In case of mild bradycardia, there may be applied drugs belladonna. In case of
severe sinus bradycardia, and no effect of drug treatment is carried out pacing.
Sinus arrhythmia is called irregular sinus rhythm, characterized by variable
frequency. Small fluctuations in the frequency (the value of P-P intervals of 0.1 s)
are physiological and are usually associated with the act of breathing during
inspiration some rhythm quickens, exhalation-rate slows. Sinus arrhythmia is not
related to the phases of respiration, indicating autonomic dysfunction or
cardiovascular disease. Difference between the P-P intervals in such cases is 0.12
or more.
Sinus arrhythmia in most cases does not cause discomfort because they do not have
a significant effect on hemodynamics, except when it is combined with a sharp
sinus bradycardia. Diagnosis is by ECG on the basis of normal sinus rhythm with a
difference in the intervals of the PP or RR. Secondary importance for the diagnosis
of a sinus arrhythmia after the disappearance of breath and, conversely, increased
arrhythmia amid deep breathing.
No specific treatment for this type of arrhythmia is not required.
Migratory atrial fibrillation rhythm is characterized by a different shape and
polarity of the P wave, different duration of the interval PR. The underlying source
offset formation of pulses within the vascular system, or the atria from the
sinoatrial node to the atrioventricular connection area or, conversely, different rates
of diastolic depolarization in sinoatrial node in specialized cells of the atria and
atrioventricular connection.
If you change the tone of the vagus nerve, migratory rhythm can occur in healthy
people. In patients with organic heart disease (myocarditis, heart defects, coronary
artery disease) migratory rhythm, apparently - the result of the activation of ectopic
rhythm.
Clinically migration supraventricular rhythm usually does not occur. Diagnosis is
by ECG studies: P wave of sinus origin alternating with right left atrial teeth and
precede complex QRS; magnitude R-R intervals in the range from 0.12 to 0.20
seconds.
Treatment is directed at the underlying disease.
RHYTHM CONNECTIONS atrioventricular (nodal rhythm) occurs during the
suppression of the sinoatrial node automaticity and retrograde propagation of the
pulse of the atrioventricular connection. As a result of the ECG, there is recorded
negative prong R. It precedes the complex QRS, appears simultaneously with or
after. This rhythm often recorded by organic disease of the heart (myocarditis,
coronary heart disease, myocardiopathy) and intoxicated with some drugs
(glycosides, reserpine, quinidine, and others). However, sometimes the nodal
rhythm may occasionally be observed in healthy individuals with severe vagotonic.
The clinical picture. Nodal rhythm in patients with heart disease may exacerbate
the severity of their condition. Healthy people usually do not notice it. There is
diagnosed rhythmof atrioventricular connections only on ECG, in the presence of a
row of 3 or more nodal impulses. The pulse rate at this rhythm within 40-65 in 1
min.
Treatment of the underlying disease.
Extrasystole - a premature contraction of the heart, the atria or ventricles only
caused by impulses arising outside the sinoatrial node. Accordingly, depending on
the location of different beats atrial, ventricular, and emanating from the
atrioventricular connection. Cause of arrhythmia - inflammatory, degenerative,
sclerotic processes in the myocardium, valvular lesions, coronary artery disease,
intoxication. Extrasystoles also appears in reflex action of other organs (gall and
kidney stones, diaphragmatic hernia, ulcer, stomach, etc.).
Depending on the time of appearance, there are distinguished early, middle, late
extrasystoles. Depending on the frequency, there are rare (less than 5, and at 1
min), moderate (6 to 15) and frequent (more than 15 in one minute). A group of
two extrasystolesare called pair of three or more - a paroxysm of tachycardia.
Adverse prognostic beats are early type A to D. This category should include
multiple, group (there are several consecutive extrasystoles) and politopnye beats,
indicating significant changes in the myocardium.
The clinical picture. Usually when arrhythmia, patients complain of disruption of
the heart, pushes and fades behind the breastbone. For continuous allodromy
(bigeminy, Trigeminy) such complaints are often not available. A number of
patients in the foreground fatigue, shortness of breath, dizziness, general weakness.
On physical examination, there are defined as premature beats kick followed
compensatory pause.
There is diagnosed by ECG beats by premature appearance extrasystolic complex.
In this case, supraventricular arrhythmias are continuing form of ventricular
complex and incomplete compensatory pause. When atrial extrasystoles,
sometimes there are several deformed tooth R. Extrasystoles of atrioventricular
connection due to retrograde spread of the pulse at the atrium has a negative P
wave forms. Ventricular premature is different from deformation, high amplitude
ventricular complex, width exceeding 0.12 seconds, and a full compensatory
pause. The largest tooth beats sent discordant with respect to the segment ST, as
well as the T wave.
Interpolated (intercalary) ventricular ectopic beats occur between two normal
contractions, with extrasystole appears very early.
Atrial extrasystoles and emanating from the atrioventricular connections are called
supraventricular.
The appearance of the ECG extrasystoles with various forms of ventricular
complex (politopnye) points to several ectopic foci. Politopnye and multiple beats
inherent organic damage to the myocardium.
Differential diagnosis with ventricular extrasystolesis based on the presence of
supraventricular arrhythmias with strain P wave and the absence of the complex
QRS.
When supraventricular arrhythmia P wave, there may be biphasic or negative, in
front of the complex OLO (when the momentum of the atrioventricular leads),
there can also be merged with the complex ORS. The emergence of beats after
each stroke is called "bigeminy" after every second - "trigeminy" etc.
The appearance of extrasystolesmonofokustype of bigeminyare more prevalent in
sinus bradycardia. Polifocusbeats are observed in most cases, in violation of
electrolyte
metabolism
and
acid-base
balance.
Right ventricular arrythmia attaches high serrated barb R1-5 in the chest leads.
When there is a high left ventricular arrhythmia RV, in the right precordial leads,
deep SV, in the left chest leads. To register, occasionally appearing extrasystoles,
extrasystoles and wearing paroxysmal character, the best effective isHolter
monitoring. If you are using for this purpose an ordinary ECG detection,
probability increases with extrasystoles provocation of the Valsalva maneuver,
physical
activity,
in
particular
the
cycle
ergometer.
Arrythmia treatment is shown in violation of her influence treatment effects when
exposed to it on hemodynamics and adverse prognostic beats, which can lead to
fatal arrhythmias (ventricular fibrillation or asystole). Asymptomatic atrial
extrasystoles without signs of stable atrial tachycardia (ie, with a duration of less
than 2 minutes paroxysm) do not require antiarrhythmic therapy, unless the
patients' illness or eliminate trigger factors. Necessary to eliminate the influence of
external arrhythmogenic factors (strong tea, coffee, smoking, alcohol consumption,
use of certain drugs - ephedrine, aminophylline, astmopenta etc.).
With the development of beats in the background of tachycardia and hypertension,
there are shown blockers p-adrenergic receptor type propranolol (Inderal, Inderal,
obzidan by 40-80 mg 2-3 times a day), atenolol (tenormina) 50-100 mg two times a
day.
Atrial extrasystolesare better to eliminate with antiarrhythmics class 1a (ritmilen
100-200 mg three times a day, procainamide 250-500 mg three times a day) and 1c
(rhythm norms 150-300 mg three times a day, 500 etatsizin mg three times a day,
VFS
25
mg
3
times
daily).
If the atrial arrhythmia had a history of paroxysmal atrial fibrillation or atrial
flutter, there should be simultaneously designated drugs that suppress the AVconducting (digoxin, p-blockers, verapamil) for ventricular shortening in case of
paroxysm.
In cases of ventricular arrhythmias, there should be preferred beta-blockers and
anti-arrhythmic drugs class III: amiodarone, Cordarone in the initial dose of 600
mg per day in 3 divided doses, followed by a decrease in the dose of 200 mg every
5-6 days and the transition to a maintenance dose of 200 mg per day and sotalol for
80-120
mg
2
times
a
day.
For the acute treatment of ventricular premature beats (myocardial infarction), it is
best used intravenous lidocaine or trimekaina to 40-120 mg (initially intravenously
for 2-3 minutes and then drop at a rate of 1-2 mg in 1 min.)
If there is no effect of the individual drugs, there combined several
antiarrhythmics. There are justified and approved in the clinic the following
combinations: kordaron, 100-200 mg 2-3 times a day + ritmilen, 100 mg 2-4 times
or etatsizin +, 50 mg 2-3 times, or + etmozin, 100 mg 2-3 times; ritmilen, 100 mg
three times daily + etmozin, 100 mg 3 times, or VFS +, 25 mg 1-2 times, or +
meksitil,
200
mg
2
times
n
day.
In the combined therapy of extrasystole, it isappropriate to include preparations of
potassium and magnesium (PananginAsparcam or 2 tablets 3 times after meals).
Paroxysmal tachycardia is a rapid heartbeat seizures, usually from 140 to 220 in 1
min, with a sudden start and end. The attack can last from seconds to hours and
many
days.
Different supraventricular paroxysmal tachycardia and ventricular. The first is the
atrial and atrioventricular (AV) of its form. Frequency rate - 200-300 in 1 min
corresponds to flutter, and more than 300 - atrial fibrillation.
Supraventricular paroxysmal tachycardia is characterized by correct timing and
intact ventricular complex in the case of an absent intraventricularblockade.
According to the mechanism, there are ectopic and reciprocal (return type reentry),
atrial
tachycardia
and
AV.
Ventricular paroxysmal tachycardia originating in the contractile ventricular
myocardium or in Purkinje fibers and bundle branch block, a special place, as they
inherent tendency to move into ventricular fibrillation and to the appearance of
heavy hemodynamic disturbances, including arrhythmogenic shock and pulmonary
edema.
The reason for the development is the same, as at beats. Ventricular tachycardia
can sometimes be the result of arrhythmogenic right ventricular dysplasia and
digitalis
intoxication.
The clinical picture. During the paroxysm patients feel frequent palpitations, often
beginning with a sharp jerk of the sternum. In many cases, the heart is
accompanied by shortness of breath, pain in the heart or in the chest, dizziness,
weakness. Blood pressure is somewhat reduced, and with increased
sympathoadrenal crises. Such crises but also has a sense of fear, fever, frequent
urination, lack of air. During the attack patients are scared, there is restlessness.
Jugular veins were swollen, throbbing arterial pulses synchronously.
Diagnostics.The basic method - electrocardiography.Informativeness increases
with the use of transesophagealECG, reveals the shape and location of the atrial P
wave in the case of rare and brief bouts of diagnosis is improved when applied
ECG monitoring. By electrocardiographic signs, ventricular tachycardia include:
expansion of QRS with a 0,12-0,14 against tachycardia of 120 to 200 cuts in 1 min
following the P wave in a rare sinus rhythm (best detected at the esophageal ECG),
the phenomenon of a full and partial capture of the ventricles. When left
ventricular tachycardia QRS, complexes have a form typical of right bundle branch
block, right heart and when – for the blocks of
the left leg.
Treatment. When a paroxysm of supraventricular tachycardia applied vagal tests:
1) Carotid sinus massage first right - from 1-20, with no effect - on the left, it is
carefully monitored and the activity of the heart (auscultation or ECG) test should
not be used elderly patients because it can impair the brain circulation (massage is
contraindicated in the presence of noise in the carotid arteries and cerebral blood
flow), 2) moderate pressure on the eyeballs for a few seconds, and 3) artificial
induction of vomiting, and 4) Valsalva (deep breath with a maximum exhalation
While
pressing
the
nose,
the
mouth
is
closed).
If there is no effect, most actions verapamil (finoptin, Isoptin) slow intravenous
bolus - 0.25% solution, 4 ml (10 mg), and possibly re-introduce it in 20 minutes in
the same dose (not recommended to verapamil in patients receiving r blockers).
High efficiency also has a 1% solution of adenosine triphosphate (ATP),
intravenous
bolus
of
2-3
ml.
During an episode of supraventricular tachycardia, it is commonly used blockers padrenergic receptors (slow intravenous). Obzidanis introduced to 1 mg over 1-2
minutes to a total dose of 3-10 mg (must have ready syringe mezatonom), cardiac
glycosides are introduced slowly bolus of 5% glucose solution and isotonic sodium
chloride solution (strophanthin - 0,25-0 , 5 ml, korglikon - 0.5-1 ml) aymalin -2,5-2
ml intravenously slowly over 5 minutes (to avoid severe complications),
procainamide intravenously slowly to a total dose of 0.5-1 g (in no blockade
bundle-branch block and cardiac decompensation), kordaron - 300-450 mgslow
intravenous isotonic solution. Etmozinetatsizinis usually used in a hospital in 2 ml
of 2.5% solution in saline sodium chloride intravenous slowly under the control of
blood pressure and ECG desirable. You can use a combination of therapies pblockers and low dose quinidine. Quinidine is used in the first intake in a dose of
0.2 g, followed by 0.2 g every 2 hours (total dose - 1.2 g).
Ciliary arrhythmia is characterized by very frequent (more than 350 in 1 min),
irregular (with flutter - regular) atrial impulses, leading to uncoordinated
contractions of individual muscle fibers. The prevalence is second beats. In this
disorder, the effective reduction of atrial rhythm is absent. In the ventricles, there
are received frequent and irregular series of electrical pulses, most of them are
blocked in the atrioventricular connection, but often reaches ventricular
myocardium,
causing
a
reduction
in
arrhythmic
them.
When atrial flutter to the ventricles, there can be held every second and third pulses
- the so-called right form of atrial flutter. If the conductivity of the atrioventricular
connection varies, the ventricles are reduced arhythmically as atrial fibrillation.
Atrial fibrillation can be permanent and paroxysmal. There are taken to distinguish
taking-, hypo-and tachysystolic atrial fibrillation, in which the heart rate at rest is
60
and
less
than
90
and
61-90
in
1
min.
Atrial fibrillation occurs against a background of various organic heart disease: the
elderly against coronary heart disease in young - against rheumatism with damage
to valvular or congenital heart disease, myocarditis, myocardiopathy,
thyrotoxicosis.
Clinical presentation and diagnosis. Feeling sick and hemodynamic instability
during atrial flutter is largely dependent on the shape of atrioventricular. During
the 2:1 or 1:1 (rare), there are concernedpalpitations, fatigue, increases
cardiovascular failure. The emergence of forms of 3:1 and 4:1, and the patient may
not
notice.
In atrial flutter waves on ECG, there are detected F, located at equal intervals,
close to each other. They are the same height and width, frequency - 200-350 in 1
min. The shape and width of the ventricular complexes are usually normal. The
most frequently observed varying degrees of atrioventricular block, and is not
always possible to establish the existence of a pair of atrial complexes because of
its lamination to the ventricular complex. In this situation, atrial flutter can be
taken
for
paroxysmal
atrial
tachycardia.
Atrial fibrillation hemodynamic instability is due to the absence of coordinated
atrial and ventricular arrhythmias. In such a situation, the cardiac output falls by
20-30%.
Subjective feelings of the patient depends on the frequency of contractions of the
ventricles and their duration. With tachycardia (100-200 cuts in 1 min), patients
complain of palpitations, weakness, shortness of breath, fatigue. In cases
bradiarrhythmic form (less than 60 cuts of 1 min) dizziness, fainting.
Innormoarrhythmic form (60-100 contractions in 1 minute) the complaint is often
absent.
Treatment. For relief of paroxysmal atrial fibrillation, there are used cardiac
glycosides, p-blockers, procainamide, verapamil (finoptin, Isoptin), etmozin,
etatsizin, aymalin, quinidine. Cardiac glycosides are administered intravenously by
slow bolus of 5% glucose solution and isotonic sodium chloride solution (0.05%
solution of strophanthin - 0.25-0.5 ml korglikon - 0.5-1 ml) obzidan 1 mg for 1 -2
min, the total dose - 3-10 mg, if it is necessary to have a syringe with mezatonom
when administered to control blood pressure. You can also apply aymalin (2.5%
solution - 2 ml intravenously slowly over 5 min) or slow intravenous procainamide
to a total dose of 0.5-1 g (condition: no block bundle-branch block and severe heart
failure), or kordaron to 6.9 ml (300-450 mg) undiluted intravenously over 5-10
minutes. Verapamil (finoptin, Isoptin) is introduced at a dose of 5.10 mg
intravenous bolus, and etmozinetatsizin (usually in hospital) - 2 ml of 2.5%
solution intravenously slowly drip of isotonic sodium chloride solution. You can
use quinidine (0.2 g every 2 h, the total dose - 1.2 g). There are appointed and
concomitant therapy p-blockers and cardiac glycosides, p-blockers and low dose
quinidine.
Weakness syndrome (dysfunction) of sinus syndrome (brady-and tachycardia) is
characterized by alternating periods of bradycardia and tachycardia, is due to
reduction in the number of specialized cells in the sinus node, proliferation of
connective tissue. In the development of sick sinus syndrome (SSS) play the role
of organic changes in the myocardium (with myocarditis, rheumatic heart disease,
valvular heart disease, coronary artery disease, cardiomyopathy, etc.), cardiac
glycoside intoxication, quinidine, household poisoning trichlorfon, karbofosom
poisonous mushrooms. Congenital or hereditary deficiency of the sinus node
(idiopathic
SSS)
occurs
in
40-50%
of
cases.
The clinical manifestations of dysfunction SU are dizziness, short-term loss or
confusion, blackouts, staggering, fainting (50-70% of cases), persistent weakness,
fatigue. When bradycardia-tachycardia syndrome increases the risk of intracardiac
thrombus and thromboembolic complications, including frequent ischemic strokes.
Extreme dysfunctions SU are attacks of Morgagni-Adams-Stokes (MAC) and
sudden
death.
Syncope caused by attacks MAC, characterized surprise, no lightheadedness
reactions expressed pale when he lost consciousness and reactive hyperemia of the
skin after the attack, the rapid restoration of the initial state of health. Loss of
consciousnesscomes to the sudden deceleration of the heart rate less than 20 in 1
min
or
during
asystole
lasting
more
than
5-10
seconds.
Diagnostics. SSS for the most characteristic features of the following ECG:
constant sinus bradycardia with resting heart rate less than 45-50 in 1 minute stop
SU
with
sinus
pauses
over
2-2.5
s;
sinus
block
with
sinus
pauses
over
2-2.5
s;
slow recovery of function after SU electrical or pharmacological cardioversion, as
well as in the spontaneous termination of supraventricular tachycardia episode
(pause before restoration of sinus rhythm more than 1.6 s);
alternating sinus bradycardia (pause 2.5-3 s) with paroxysms of atrial fibrillation or
atrial
tachycardia
(bradycardia-tachycardia
syndrome).
Holter monitoring - the most informative method of verification and
documentation of communication between clinical and electrocardiographic
manifestations of dysfunction of the SS. The assessment should take into account
the results of monitoring heart rate limits. In patients with SSS maximum heart rate
for the day, as a rule, does not reach 90 in 1 min, and the minimum is less than 40
during
the
day
and
less
than
30
at
night.
Treatment. In the early stages of the SSS, there can be achieved short-term
cancellation rate increased frequency of unstable drugs that slow the heart rate, and
the appointment holinoliticheskih (atropine drops) or sympatholytic (izadrin 5 mg
from 1/4-1 / 2 tablets, the dose is gradually increased to prevent the occurrence of
ectopic arrhythmias). In some cases you can get a temporary effect of the
appointment of drugs belladonna. Some patients are marked with an effect in
primeneniinifedipina, nicotinic acid, and heart failure - ACE inhibitors.
Primary treatment for SSS - constant electrical stimulation of the heart.
Atrial flutter and ventricular fibrillation. Flutter - part of the regular activities of
the ventricles (over 250 cuts of 1 min), are accompanied by cessation of circulatory
flickering (fibrillation) - a frequent and indiscriminate action of the ventricles. In
this case, blood flow stops immediately. In paroxysmal atrial flutter or fibrillation
occur
syncope,
seizures,
Morgagni-Adams-Stokes
equations.
Typically, this is a terminal arrhythmias in most patients dying from various
serious diseases. The most common cause - acute coronary insufficiency.
Clinic and diagnostics. Since the beginning of atrial or ventricular fibrillation,
disappearspulse, nolistening heart tones, blood pressure is not determined, the skin
becomes pale with a bluish tinge. In the 20-40s the patient loses consciousness,
there may be convulsions, pupils dilate, breathing becomes noisy and frequent.
To ventricular fibrillation ECG, there are recorded regular rhythmic waves,
resembling a sine curve with a frequency of 180-250 in 1 min. Tines Ri T is not
defined. In cases of ventricular fibrillation observed in the ECG continuously
changing shape length, height and direction of waves with a frequency of 130-150
in
1
min.
Treatment. Must quickly, there are carried out the electrical defibrillation of the
ventricles, external cardiac massage, very punch in the chest or sternum. Electrical
defibrillation begins with a maximum voltage of 7 kV (360 J). If there is no effect,
bits are repeated, in between used external cardiac massage and artificial
ventilation. Intravenously orintracardiac bolus injected adrenaline - 0.5-1 mg,
calcium chloride - 0.5-1 g, procainamide - 250-500 mg -100 mg lidocaine, obzidan
- 5.10 mg. Effectiveness of the measures depends on the time in which they started,
and
the
possibility
of
electrical
defibrillation.
Weather is mostly unfavorable, especially in the event of atrial fibrillation in
patients
with
severe
heart
failure,
cardiogenic
shock.
Ventricular asystole - full stop ventricles, associated with the loss of their electrical
activity. Most often it is the outcome of ventricular fibrillation. ECG recorded on a
straight
line.
Treatment is not very different from that described. After defibrillation is
administered intravenously bolus adrenaline -0,5-1 mg, then atropine - 1 mg,
repeated their introduction every 5 minutes. Sodium bicarbonate in cardiac arrest
should not be entered. There may be applid a temporary electrical stimulation.
Sinoauricular block (SAB) is developed in violation of the impulse from the sinus
node (SA) to the atria. It can be observed in cases of severe vagotonia, organic
heart disease (CHD, myocarditis, cardiomyopathy, digitalis intoxication, quinidine,
hypokalemia).
There are 3 degrees SAB. InI,extended the transition pulse from the SA-node to the
atria.
ECG
is
not
detected.
The blockade of II degree is falling entirely heartbeat - no complex P-QRST. Pause
on the ECG is recorded equal to the duration of double-spaced RR. A roll of more
complex, the pause will be equal according to their total duration. You may
experience
dizziness,
irregular
heart
activity,
fainting.
Third-degree block (full ABS) is actually asystole: no impulse from the SA node,
the atria are not carried out, or is not formed in the sinus node. Heart activity is
supported
by
the
underlying
sources
of
activation
rate.
Treatment.Treatment of the underlying disease. In severe hemodynamic
disturbances, there are applied atropine, belladonna, ephedrine, alupent. The
appearance of syncope is an indication for pacing the heart.
Atrioventricular block (AVB) - a slowing or stopping of impulses from the atria to
the ventricles. Accordingly, the level of damage to the conduction system, there
can occur in the atria, the atrioventricular connection and even in the ventricles.
Causes of AVB are the same as for other violations of conduct. However, there are
self-developing and degenerative sclerotic changes of the conducting system of the
heart, leading to AVB in the elderly (illness Lenegre and left). AVB can
accompany ventricular septal defect, tetralogy of Fallot, aortic membranous part of
the
partition,
etc.
There are 3 degrees of blockade. The first degree is characterized by lengthening
the time of the AV, the interval P-Q is equal to or greater than 0.22 sec. In II
degree AVB type 2 blocks allocated to Mobittsu. Type-I Mobittsa gradual
lengthening of the interval PQ with the fallout of one ventricular complex Samoilov-Wenckebach phenomenon. The blockade of type II Mobittsa - consistent
prolongation P-Q is preceded by loss of ventricular complex. With this type may
drop several consecutive ventricular complexes, which leads to a significant
reduction in heart rate, often at the same time there are attacks of MorgagniAdams-Stokes
equations.
Inatrioventricular block I and II degree with periods Samoilov-Wenckebach
clinical signs were observed. Major importance is the dynamic monitoring of ECG
data.
Treatment.In AV block I degree, if the PQ interval is less than 400 ms, and there
are no clinical manifestations, treatment is needed. AV block type II degree
Mobittsa I no clinical manifestations also does not require treatment. In the case of
hemodynamic: atropine, 0.5-2.0 mg intravenously, then pacing. If AV block due to
myocardial ischemia (in the tissues increases the level of adenosine), then assigned
adenosine antagonist aminophylline. When AV block II degree Mobittsa type II
regardless of clinical manifestations is a time, then the constant pacing (pacing).
Complete transverse block (atrioventricular block III degree) is characterized by
the complete absence of impulses through the atrioventricular connection from the
atria to the ventricles. The atria are excited from the sinus node, the ventricles under the influence of impulses from the atrioventricular connections below the
center of the block or automatism III order. In this regard, the atria and ventricles
are excited and contract independently of each other. In this case, the right atrial
rhythm is higher than the number of contractions of the ventricles.
The number of contractions of the ventricles depends on the location of the
pacemaker. If it reaches (or exceeds) 45 in 1 min, it is believed that the pacemaker
is located in the atrioventricular connection (proximal type blockade). With this
type of path, pulse is normal ventricles, because the QRS complex is not changed.
R-R distance is constant. Because the atria reduced more than the ventricles, the
distance
is
P-P
<RR.
Complete transverse blockade may be transient and permanent.
The combination of a full cross-blockade with atrial flutter or fibrillation is called
syndrome or phenomenon Frederick. In deceleration of the heart rate to 20 and less
than a 1 minute, there occur periods of unconsciousness with convulsions due to
cerebral ischemia (seizures Morgagni-Adams-Stokes).
Treatment.Electrocardiographic constant stimulation (ECS). If the causes of
reversible blockade (eg, hyper potassium), if there is a blockage in the early
postoperative period or at the lower heart attack, there can be prescribed
medications that increase ventricular automaticity: izadrin 5 mg (under the tongue),
or infusion into a vein alupenta - 0.5 - 1 ml of 0.05% solution drip or stream
slowly. But most often, in such cases, resorted temporary pacing, especially when
the
replacement
rhythm
with
wide
complex
QRS.
Intraventricular block can develop in any part of the cardiac conduction system
distal to the AV connection (from the bundle-branch block to the Purkinje fibers).
The main reasons are: coronary artery disease, myocarditis, valvular lesions,
cardiomyopathy. The blockade of the right leg may develop pulmonary heart.
The main electrocardiographic signs of intraventricular block (VZHB) broadening ventricular complex. VZHB are complete when the QRS complex is
0.12 or greater, and incomplete - (QRS wider than 0.09 sec, not more than 0.12
seconds. During blockade of bundle-branch block of the blocked ventricle excited
legs later, as the excitation pulse bypasses the affected area. In the left leg
(LBBB), the first will be excited by the right ventricle, and the blockade of the
right
leg
(BPN)
left
ventricle.
Preexcitation syndrome, due to the presence of additional pathways by which the
momentum spread from the atria to the ventricles, the ECG shows a shortening of
the interval P-Q to 0,08-0,11 a broadening of the QRS complex and larger than
normal (up to 0.12-0.15). In this regard, the QRS complex resembles blockade
bundle branch block. At the beginning of the QRS complex is registered as a
«stairway" additional wave (D-wave). Depending on the location of the D-wave
syndrome, varies several options: a positive D-wave in lead V,-type A negative Dwave in V, - type B. Despite the shortening of the interval P-Q and the broadening
of the complex QRS, the total duration of the interval PQRS is usually within
normal limits, ie, the QRS complex is broadened as much shortened interval PQ.
Syndrome W-P-W meets at 0.15-0.20% of people, and in 40-80% of those
observed in various cardiac arrhythmias, predominantly supraventricular
tachycardia. There may be paroxysmal atrial fibrillation or flutter (approximately
10%
of
patients).
In 1/4 people with the syndrome of W-P-W, there noted arrhythmias,
predominantly supraventricular. This pathology is more common in men and can
occur
at
any
age.
Often there is a family history. Perhaps, there is a combination of the syndrome WP-W
with
congenital
heart
anomalies.
Treatment. Syndrome W-P-W, is not accompanied by bouts of tachycardia and
requires no treatment. In the event of cardiac rhythm, and it is most often
paroxysmal supraventricular tachycardia, the principles of treatment are the same
as in similar tachyarrhythmia another genesis - vagotropic sample intravenous
cardiac glycosides, P-blockers adrenergic receptor izoptina, procainamide. If the
effect of pharmacotherapy is missing, there is conducted electrical defibrillation.
With frequent paroxysmal tachyarrhythmia refractory to medical therapy, there
conducted surgical treatment: the intersection of complementary ways.
List of the literature
1. Jeffrey Bender, Kerry Russell, Lynda Rosenfeld, Sabeen Chaudry-Oxford
American Handbook of Cardiology, 2011
2. A.Zaza An introduction to cardiac electrophysiology
3.ABC of Interventional Cardiology - Ever D. Grech, 2004
4. Cardiovascular Disease in the Elderly - Wilbert S.Aronow, Jerome L.Fleg,
5.www.аritmia.info/
6.ru.wikipedia.org/wiki/аритмия
7.medportal.ru.>…> Кардиология