Atrial fibrillation – what is it

Extrasystole – premature extraordinary
excitement of the heart due to
re-entry mechanism or
increased oscillatory activity
cell membranes originating in
atria and AV connection or in
different parts of the conductive system
ventricles.

ECG signs:
premature onset of cardiac
P-QRST cycle on an ECG. Distance from previous
extrasystole of the next cycle P-QRST of the main rhythm to
extrasystoles is called pre-extrasystolic interval
(clutch interval); distance
from extrasystoles to the next normal
cycle called post extrasystolic
interval or compensatory
a pause.

Compensatory Pause
regarded as full if the amount
pre-extrasystolic and
post extrasystolic intervals
equal to exactly two R-R intervals of the main rhythm. Compensatory Pause
considered incomplete if the amount
pre-extrasystolic and
post extrasystolic intervals
less than the distance of two intervals R-R of the main rhythm.

If the amount
pre-extrasystolic and
post extrasystolic intervals
equal to the distance R-R of the main rhythm, then extrasystole
considered interpolated (insertion).

The basic one
the mechanism of extrasystole is
wave re-entry mechanism
excitation (re-entry).

Essence
wave re-entry mechanism
excitation (re-entry).

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development in certain areas of the heart
muscle ischemia, dystrophy, necrosis,
cardiosclerosis or significant
metabolic disorders electrical
properties of various parts of the myocardium
and the conduction system of the heart can
differ significantly from each other,
leading to electrical
inhomogeneity of the heart muscle, which
manifested by uneven speed
holding an electrical impulse in
different parts of the heart.

Eventually
foci of the heart muscle appear,
which is excited not ordinary, but
in a roundabout way with a big time
delay when all other sections
not only did the heart muscle
get excited but also get out of the state
refractoriness
(excitability).
In this case, the excitation of this site
may reapply to
adjacent sections of the heart before arrival
the next impulse from the CA node.

Are described
and other mechanisms of the development of extrasystole:
increase in trace potential amplitude
(oscillations in phase 4 PD), asynchronous
repolarization of individual sites
myocardium creating inhomogeneity
myocardial electrical condition.

Extrasystole
– this is one of the most common violations
heart rate. Allocate functional
and organic
extrasystoles.

У
healthy people extrasystole wears
functional
character,
provoked
emotional stress, smoking,
the abuse of strong tea, coffee,
alcohol, etc. Such an extrasystole
does not require special
antiarrhythmic drugs passes
independently after elimination
exposure to the patient indicated
provoking factors.

Extrasystoles
organic
origin attests
about profound changes in the heart muscle
in the form of foci of ischemia, dystrophy, necrosis
or cardiosclerosis contributing
the formation of electrical inhomogeneity
heart muscle. Often extrasystole
observed in acute myocardial infarction
(in 80-100% of cases), chronic ischemic
heart disease, arterial hypertension,
rheumatic heart diseases, myocarditis,
congestive circulatory failure.
Various options for persistent ventricular
allorhythmias – bigeminias, trigeminias
characteristic for overdose of cardiac
glycosides.

Atrial fibrillation refers to a mixed group of cardiac arrhythmias, in which there is an increase in cardiac activity from 350 to 700 beats per minute. The name of the disease comes from Latin and means “madness of the heart.” It can occur in adults, children, men and women, but the risk group for the disease is people after 60 years, since it is the degenerative changes in the myocardium that lead to the occurrence of supraventricular tachycardia.

Up to 60 years, flickering arrhythmia is diagnosed in 1% of patients, in the elderly it is determined in 6-10% of cases.

Why is atrial fibrillation dangerous? First of all, by insufficient cardiac output, because the ventricles cannot provide a sufficient amount of blood to organs through the small and large circle of blood circulation. At first, the disorder is compensated, but with a long course of the disease, acute circulatory failure occurs. With some ailments, such as mitral stenosis or hypertrophic cardiomyopathy, heart failure develops very quickly.

A strong drop in cardiac output causes an arrhythmogenic form of cardiogenic shock. In the absence of emergency medical care, a fatal outcome is possible.

Asynchronous atrial contraction leads to stagnation of blood. Against this background, the risk of thrombosis increases, especially in the left atrium, from where they easily enter the cerebral vessels and cause ischemic stroke. An uncoupled attack of atrial fibrillation, lasting more than 2 days, primarily threatens with acute thrombosis of the vessels located in the brain.

1. Definition, development mechanisms, etiology, clinic of cardiac arrhythmias and conduction

Under
the term “rhythm disturbance
hearts “understand arrhythmias and blockades
hearts. Arrhythmias are a violation
frequency, regularity and sequence
heart
abbreviations. Violations
conducting arousal cause development
heart block.

All
arrhythmias are the result of a change
main functions of the heart: automatism,
excitability and conductivity. They are
develop in violation of the formation
cell action potential and change
its speed as a result
changes in potassium, sodium and calcium
channels. Impaired potassium activity,
sodium and calcium channels depends
from sympathetic activity, level
acetylcholine, muscarinic-like
M2 receptors
ATP.

1.
Impulse formation disorders: –
violations of the automatism of the sinus node
(SU); – abnormal automatism and trigger
activity (early and late depolarization).

2.
Excitation wave circulation (re – entry).

3.
Impulse conduction impairment.

Violations
pulse formation.
Ectopic foci of automatic
activity (abnormal automatism)
may be in the atria, coronary
sinus, along the perimeter of the atrioventricular
valves, in AV– unit, in the beam system
His and Purkinje fibers. Occurrence
ectopic activity promotes
decreased automatism of SU (bradycardia,
dysfunction, sinus weakness syndrome
node (SSSU)).

Violation
holding an impulse.
Impulse conduction can
occur in any areas of the conducting
heart systems. Blockade on the way
impulse is manifested by asystole,
bradycardia, sinoatrial, AB– and
intraventricular blockade. At
this creates conditions for circular
re – entry movements.

Circular
movement.
To form re – entry
necessary
the presence of a closed loop,
unidirectional blockade in one of
contour sections and slow motion
excitement spread in another
section of the contour. Impulse is slow
extends along the knee of the contour with
preserved conductivity, commits
turn and enters the knee where there was
blockade of conduct.

If conductivity
restored then the momentum moving along
a vicious circle, returns to the place
of its occurrence and repeats again
your movement. Waves re – entry
can occur in the sinus and AV nodes,
atria and ventricles, if any
additional pathways and in
any part of the conduction system of the heart,
where dissociation may appear
conducting excitement. This mechanism
plays an important role in development
paroxysmal tachycardia flutter
and atrial fibrillation.

Trigger
activity.
When trigger activity occurs
development of trace depolarization at the end
repolarization or the beginning of the resting phase.
This is due to transmembrane disturbance
ion channels.

В
the development of arrhythmias that occur during
various diseases and conditions
an important role is played by exogenous and endogenous
factors like psychosocial
life-threatening stress
arrhythmias in 20-30% of cases, neurovegetative
imbalance, with a predominance of activity
sympathetic or parasympathetic
departments of the autonomic nervous system,
toxic effects (alcohol,
nicotine, drugs
pharmaceuticals industrial
poisons, etc.), internal diseases
organs.

Etiology
heart rhythm disturbances:

Defeat
myocardium of any etiology:
coronary artery atherosclerosis,
myocarditis, dilated and hypertrophic
cardiomyopathies, heart defects, sugar
diabetes, thyroid disease,
menopause, amyloidosis, sarcoidosis,
hemochromatosis, myocardial hypertrophy
with arterial hypertension and
chronic pulmonary heart intoxication
(alcohol, nicotine, medicinal
preparations, industrial substances
(mercury, arsenic, cobalt, chlorine and
organophosphorus compounds), closed
heart injuries, involutive processes
with aging.

Defeat
SU and congenital conduction system
and acquired genes, for example,
SSSU, sclerosis and calcification of fibrous
heart skeleton and primary
sclerodegenerative lesion
conduction system of the heart with development
AV– and intraventricular blockade,
additional pathways
(e.g., syndromes of WPW, CLC).

Prolapse
heart valves.

Tumors
hearts (myxomas, etc.).

disease
pericardium: pericarditis, pleuropericardial
adhesions, metastases to the pericardium, etc.

Electrolyte
disturbances (impaired potassium balance,
calcium, sodium, magnesium).

Mechanical
heart irritation (catheterization,
angiography, heart surgery).

Reflex
influences from internal organs
when swallowing, straining, changing
body position, etc.

Violations
nervous regulation of the heart (syndrome
vegetative dystonia, organic
CNS lesions).

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stress (with the development of hyperadrenalinemia,
hypokalemia, stress-ischemia).

Idiopathic
cardiac abnormalities
rhythm (etiology unknown).

Examination
heart rhythm patient
includes interrogation, clinical
and instrumental research methods.
It aims to identify the causes.
the development of arrhythmias, those adverse
factors that may contribute
their progression in the future, accurate
determination of the types of arrhythmias, diagnosis
state of the heart (valvular apparatus,
size of heart chambers, wall thickness,
contractility).

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patient questioning pay attention
on anamnestic data: first
the appearance of discomfort in the area
heart and related phenomena;
diagnosis (if it was carried out)
objective disorders of the cardiovascular
systems and other organs and systems,
which could entail
development of heart rhythm disturbances;

previous treatment and
its effectiveness; development dynamics
symptoms until treatment
patient to the doctor. It’s very important to find out
did the patient have bad habits
production hazards which
he suffered diseases, and also know
family history. Identification of complaints
the patient matters a lot so
like heart rhythm disturbances often
accompanied by the appearance of unpleasant
sensations. They are determined by the type
rhythm disturbances, degree of hemodynamic
disorders, the nature of the underlying
disease.

Most
frequent complaints
patients with arrhythmias are unpleasant
sensations in the heart: palpitations
(sensations of rhythmic or irregular
palpitations), interruptions, feelings of fading
and “stopping” the heart, pain of various
character or sense of contraction, feeling
heaviness in the chest, etc. Sensations may
have different durations and
frequency, develop suddenly or
gradually, periodically or without
a certain pattern.

But
in addition, there may be a sharp weakness,
headache, dizziness, nausea,
syncopal states what is
hemodynamic development indicator
violations. With a decrease in contractile
left heart abilities are noted
shortness of breath, cough, suffocation. Appearance or
heart failure progression
with arrhythmias are prognostically
unfavorable.

Violations
heart rate in many cases
accompanied by a feeling of fear and
anxiety. In some patients, arrhythmias occur
asymptomatic.

Clinical
studies reveal:
the patient’s condition may be different
(satisfactory to severe) in
depending on the type of violation and the source
condition of the patient. Possible lethargy,
loss of consciousness (fainting), manifestations
hypoxic encephalopathy up to
coma Autonomic Nervous Disorders
systems manifest as anxiety,
disturbing behavior, discoloration
skin, sweating, polyuria, bowel movements
etc.

The color of the skin may be pale,
and hyperemic, especially with
the presence of arterial hypertension,
cyanotic in heart failure.
With left ventricular heart
insufficiency revealed changes
during physical examination of the system
respiratory system – weakening of the vesicular
breathing or hard breathing, wet
noisy wheezing, sometimes combined with
dry wheezing.

It can be determined
emphasis II tone on the pulmonary artery.
Cardiovascular Examination
systems often detect frequency changes
heart rate (heart rate) and frequency
heart rate – increase or decrease,
violation of the rhythm of heart sounds and
pulse waves. Volume changes
tones, for example, different volume I
atrial fibrillation (MA) tones
increased I tone in ventricular
extrasystole, weakening it with
paroxysmal supraventricular
tachycardia (PNT).

Filling reduction
heart rate is determined by vascular
deficiency, with MA often occurs
pulse shortage. Often observed
changes Blood pressure – hypo– or hypertension.
With right ventricular heart
failure – liver enlargement
and her soreness. With a decrease in renal
blood flow – oliguria. May also
thromboembolic syndrome develop.

Instrumental
research methods.
Electrocardiography remains leading
method in recognition of violations
heart rate. Used as
simultaneous research and more
continuous: for 3 minutes, 1 and
24 hours. For example, in patients with coronary artery disease
ventricular extrasystoles on the usual
ECGs are detected in 5% of cases, with a 3-minute
registration – in 14%, at 1 – hour – at
38% of patients, within 24 hours –
85% of patients.

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Daily Holter
ECG monitoring provides
research in various conditions (at
loads, in a dream, while eating and
etc.), which allows to identify provocative
factors in the development of arrhythmias. Holter
monitoring allows you to give
qualitative and quantitative assessment
heart rhythm disturbances.

Samples with
dosed physical activity
used to clarify the diagnosis of coronary heart disease,
identify the relationship of rhythm disturbances
with angina pectoris and with physical exertion,
assessment of the effectiveness of the therapy,
as well as arrhythmogenic action
medications. With insufficient
ECG efficacy studies for
diagnose
premature arousal syndrome
ventricles, for diagnosis
cures
transit or permanent SSSU
transesophageal ECG is used.

Causes of the disease

Atrial fibrillation is one of the most common types of arrhythmias. A healthy heart contracts at a rate of 60-90 beats per minute. Heart rate is monitored by a pulse sent by the sinus node. In AF, many impulses arrive at the heart muscle at the same time, which causes the atria to contract with a frequency of up to 700 beats per minute. With such a reduction in muscle tissue, blood cannot enter the ventricles, from where it is distributed to the arteries and tissues.

Atrial fibrillation on the ECG is manifested in the form of rhythm disturbances and heart rate. Diagnosis includes several examination methods.

The causes of this common pathology can be many:

  1. Myocardial infarction. With a heart attack, the myocardial blood supply ceases, as a result of which part of the muscle tissue dies and is replaced by scar tissue. Complications of this pathology depend on the severity of the patient’s condition and the amount of damaged tissue. Angina pectoris and atrial fibrillation are some of the most common consequences of a heart attack.
  2. Cardiosclerosis With cardiosclerosis, necrotic processes in the myocardium occur for various reasons that are difficult to determine. The essence of this disease is that scar tissue grows in muscle and reduces the contractility of the heart. Atrial fibrillation can be both a sign and a consequence of cardiosclerosis.
  3. Hypertension With increased blood pressure, the load on the heart and blood vessels becomes greater, which leads to complications such as tachycardia, angina pectoris and atrial fibrillation.
  4. Thyrotoxicosis. Thyroid hormones regulate the work of all internal organs, including the heart. If the level of hormones is pathologically high, then the contractility of the heart muscle increases.

In addition to the reasons, there are provocative factors, such as stress, bad habits, prolonged use of drugs that affect the cardiovascular system, alcohol abuse, a sedentary lifestyle and obesity, diabetes mellitus.

AF can manifest itself in different ways: in the form of seizures or be constant. Manifestations of the disease largely depend on the stage and severity of its course.

Mild forms of the disease can be asymptomatic. In other cases, the patient feels an attack of tachycardia, a strong, painful heartbeat, chest pain, general weakness, dizziness, fainting, shortness of breath, a feeling of a sharp lack of air, panic fear.

An attack of AF can last quite a long time and not disappear without medical intervention. In some cases, uncontrolled urination is also observed.

The following types of atrial fibrillation are distinguished:

  • By the duration of the manifestations. Paroxysmal AF lasts from 2 days to a week. It can take place on its own or after drug treatment. Persistent AF is accompanied by longer seizures (more than a week), the disease requires treatment. Chronic atrial fibrillation lasts constantly, and the heart rate cannot be restored.
  • By type of arrhythmia. There are flickering and atrial flutter. When blinking, the pulse is distributed unevenly across the myocardium, causing the fibers of the heart muscle to contract quickly and randomly. At the same time, ventricular contractions will be unproductive. During flutter, the contraction of the fibers proceeds more slowly, therefore this form of AF is considered easier, but the pumping function of the heart is still impaired.
  • The largest heart rate. There are tachysystolic arrhythmias (heart rate of more than 90 beats per minute), normosystolic (heart rate does not increase much, from 60 to 100 beats per minute), bradysystolic (heart rate is reduced, does not reach 60 beats per minute).

In some cases, AF is detected by chance during the examination, although the patient did not feel any characteristic symptoms. One of the clear signs of atrial fibrillation is the private pulse. In the case when the heart rate is so large that it exceeds the pulse, it may not be detected at all.

Atrial fibrillation refers to severe pathologies, it has a significant cause of the appearance, which must be treated together with the arrhythmia itself.

Among the causes of the disease can be noted:

  • dysfunctions in the endocrine system;
  • atherosclerotic changes in the vessels;
  • cardiovascular failure;
  • disturbances in the body’s water-salt balance;
  • cardiosclerosis;
  • violations of acid-base balance;
  • congenital or acquired heart defects;
  • cardiomyopathy;
  • hypertension;
  • neoplasms of the heart;
  • kidney failure;
  • surgical interventions on the heart and blood vessels;
  • myocarditis.

Often the disease is a consequence of coronary heart disease. Myocardial areas lacking nutrition and oxygen can occur both in the ventricles and in the atria. With extensive ischemia, atrial fibrillation develops faster and has a more pronounced clinic.

Arterial hypertension is in second place after coronary heart disease among the factors in the development of atrial fibrillation. With prolonged hypertension, the left ventricle does not function well during diastole. In addition, his myocardium increases, which contributes to left ventricular hypertrophy and the occurrence of atrial fibrillation. In addition, other equally important internal and external causes of the development of flickering arrhythmia are distinguished.

Associated with the condition of the heart and its functioning. Generally represented by the following diseases:

  • heart defects (acquired and congenital), in which there is an expansion (dilatation) of the atria;
  • cardiomyopathies (hypertrophic, and more often dilated);
  • infective endocarditis;
  • constrictive pericarditis;
  • myocardial dystrophy, which developed against a background of alcoholism and hormonal disorders (during menopause);
  • myxoma of the left atrium;
  • mitral valve prolapse, in which hypertrophy of the left atrium is observed;
  • primary amyloidosis of the heart, developed after 70 years.

Structural changes in the heart are a common cause of atrial fibrillation

They are much smaller than internal ones. Atrial fibrillation is most often triggered by pulmonary diseases that contribute to the development of chronic pulmonary heart disease.

The cause may be hemochromatosis, which is manifested by diabetes mellitus and pigmentation. With thyrotoxicosis, atrial arrhythmia also occurs. In some athletes, MA is observed against the background of an increased load on the heart.

If the patient cannot identify external or internal causes of the development of pathology, then the idiopathic form of atrial fibrillation is diagnosed.

Frequent ventricular extrasystole as bigeminia


paired extrasystoles – if in a row
two extrasystoles are recorded (pr.
– pirouette, spindle-shaped, “dance
around the point, “torsades
de
pointes
– two extrasystolic cardiac
cycles follow one after another,
multidirectional);


group (salvo) extrasystole
or short paroxysm of tachycardia –
if three or more follow in a row
extrasystole;

The following clinical forms of atrial fibrillation are distinguished.

  1. Paroxysmal supraventricular tachycardia – signs of the disease are observed for 7 days.
  2. Persistent atrial fibrillation – the duration of the disease is more than 7 days.
  3. Permanent form – the clinical picture can be more or less pronounced, but practically without attenuation of the process.

The severity of the clinic contributes to the division of the pathological process according to the severity of the course into four classes;

  • the first is characterized by the absence of signs;
  • second, some symptoms may be observed, but there are no complications and the usual way of life of a person is practically not broken.
  • the third – the clinical picture is pronounced, complications appear.
  • fourth, the patient is given disability due to severe complications and loss of capacity for work.

In the development of atrial fibrillation, it is also customary to distinguish two main forms.

Atrial fibrillation, or fibrillation. The mechanism of development is the previously mentioned ri-entri, in which there is a frequent and irregular contraction of the atria and ventricles. The latter in the diastole can be filled with blood, but because of their chaotic work, they are not able to make a normal discharge of blood. In severe cases, atrial fibrillation passes into ventricular fibrillation, which can subsequently cause cardiac arrest.

Atrial flutter is a rhythmic form of disturbance in cardiac activity, in which the atria are reduced to 400 beats per minute, and the ventricles to 200 beats / min. Atria almost never relaxes in the diastole, therefore, almost no blood enters the ventricles, which does not allow for normal blood circulation throughout the body.

Sometimes in one patient, there may be an alternation of flutter and atrial fibrillation. This is due to the great similarity of the mechanisms of occurrence of these two pathological conditions.

ECG with the proximal form of av-blockade of the III degree

Far
atrioventricular block
II degree or incomplete atrioventricular
high degree blockade – characterized
a high degree of violation of AV conduction,
loss of every second sinus
pulse or conducted 1 of 3, 1 of 4, 1 of
5 sine pulses (conductivity
respectively 2 1, 3: 1, 4: 1, etc.).

It
leads to severe bradycardia, amid
which may cause the disorder
consciousness (dizziness, loss of consciousness
and etc.). Severe ventricular bradycardia
promotes the formation of substitute
(slipping) contractions and rhythms.
Atrioventricular block II degree
Type III can occur as in
proximal and distal
form of atrial ventricular dysfunction
conductivity, respectively, complexes
can QRS may be unchanged
(at proximal) and deformed
(with distal blockade).

Blockade
III degree
or complete, transverse atrioventricular
blockade: characterized by complete
cessation of sinus
pulses from the atria to the ventricles,
in the result of bringing the atria and ventricles
excited and contracted independently
apart from each other. Ventricular driver
rhythm is in the atrioventricular
connection in the stem of the beam
His or in the ventricles or legs of the bundle
Gisa.

ECG-
signs: number
ventricular contractions reduced to
40-30 and less per minute, P waves are recorded
with a pace of 60-80 per minute; sinus teeth
P have no connection with QRS complexes;
QRS complexes
may be normal or deformed
and widened; P waves can be recorded
at various times systole and diastole
ventricles layered
QRS complex or T wave
and warp them.

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atriventricular blockade II and III
degree, especially distal form
complete atrioventricular block,
ventricular asystole may develop
up to 10-20 sec, which leads to hemodynamic
impairment
volume of circulating cut and hypoxia
brain, the patient eventually loses
consciousness, convulsive develops
syndrome. Such attacks are called
attacks of Morgagni-Adams-Stokes.

Combination
complete atrioventricular block with
atrial fibrillation or flutter
called Frederick’s syndrome.
Frederick’s syndrome indicates the presence of
severe organic diseases
sclerotic hearts
inflammatory or degenerative
processes in the myocardium (chronic
Ischemic heart disease,
acute myocardial infarction
cardiomyopathies, myocarditis).

1.
Absence on an ECG
teeth
P, instead of which waves are recorded
atrial fibrillation (f) or atrial flutter (F).

2.
Ventricular rhythm of non-sinus origin
(ectopic: nodular or idioventricular).

3.
R – R intervals are constant (correct
rhythm).

4.
The number of ventricular contractions is not
exceeds 40-60 per minute.

Syndrome
Frederic (a combination of fibrillation
atria and complete AV block)

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10. What are the ECG signs of atrial extrasystoles.

Sinoatrial
blockade (sinoauricular)
– is
violation of electrical
pulse from the sinus node to the atria.

Sinoatrial
blockade occurs
with inflammatory and degenerative
changes in atria in the area
CA site (with rheumatic heart disease, myocarditis,
atherosclerotic cardiosclerosis,
acute myocardial infarction), in the treatment
cardiac glycosides, quinidine,
morphine, with increasing tone of the wandering
a nerve.

Sinoatrial
blockade I
degree
manifested by delayed formation
pulses in the sinus node or slow
their conduct to the atria. This blockade
cannot be detected by ECG,
since excitation is not reflected on the ECG
sinus node.

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sinoatrial blockade II
degree
part of the pulses from the sinus node is not
comes to the atria, which leads to
prolapse of the atria and
ventricles.

1)
partial sinoauricular block II
grade I
type or partial sinoauricular
blockade II
degrees with periodicals Samoilov-Wenckebach;

2)
partial sinoauricular block II
grade II
type or Mobitz type.

Sinus
increase in heart rate is called tachycardia
90 to 140 per minute when stored
correct sinus rhythm.

Sinus
tachycardia due to increased
automatism of the main pacemaker
– Sinoatrial node (CA node). CA node
regularly produces electrical
pulses with a frequency of 90 to 140 per min.,
which are carried out in the usual way by
atria and ventricles.

ECG signs:
correct alternation of P waves and
QRS-T complex,
characteristic for sinus rhythm,
R-R interval not more than 0,75 seconds; with severe tachycardia
– oblique depression of the S-T segment no more than 1 mm, increase
the amplitude of the teeth T and P, stratification of the tooth
P on the T wave of the previous cycle.

In healthy
people sinus tachycardia occurs
during physical exertion or emotional
voltage. Sinus tachycardia also
happens with thyrotoxicosis, anemia,
myocarditis, heart failure,
vascular insufficiency (collapse),
aortic valve insufficiency, with
ischemia and dystrophic changes in
CA site, various infections, toxic
effects on the CA site, increase
body temperature.

Sinus
bradycardia is called a decrease
Heart rate up to 59–40
per minute while maintaining the correct
sinus rhythm.

Sinus
bradycardia due to a decrease
automatism of the CA node.

ECG signs:
the correct alternation of the tooth of the Ri complex
QRST
in all
cycles characteristic of sinus rhythm,
with a frequency of 59-40 per min., RR interval
more than 1 sec With severe bradycardia
the amplitude of the P wave can decrease
and several
increase duration
P-Q interval
(R)
(up to 0,21-0.22 s).

Among
healthy people sinus bradycardia
especially observed in athletes,
with increasing tone of the vagus nerve.
Sinus bradycardia occurs in acute
myocarditis, myxedema, with some
infections (flu, typhoid fever, infectious
hepatitis), with uremia, with exposure
medications (cardiac
glycosides, opium, pilocarpine), with
myocardial infarction (with depression
automatism of the CA site due to ischemia),
increased intracranial pressure
(irritation of the center of the vagus nerve).

Atrial
extrasystole: premature cardiac
P-QRST cycle;
tooth P
extrasystolic cycle in shape
different from P waves previous
non-extrasystolic cycles; interval
P-q
atrial extrasystoles may be
shortened, normal or elongated;
QRST
extrasystoles is no different from
non-extrasystolic; compensatory
the pause is incomplete.

Atrioventricular
extrasystoles may be pre-excited
atria, simultaneous excitation
atria and ventricles, with prior
excitation of the ventricles.

Atrioventricular
extrasystole with pre-excitation
atria:
P-QRST premature cardiac cycle;
extrasystolic tooth P negative,
preceded by QRST;
PQ interval
shortened QRST complex
no different from non-extrasystolic;
compensatory pause incomplete.

Atrioventricular
extrasystole with simultaneous
excitation of the atria and ventricles:
premature heart cycle
represented by the QRST complex;
tooth P is absent; extrasystolic
QRST complex
no different from non-extrasystolic;
compensatory pause incomplete; in
individual cases of the QRST complex
can be moderately deformed so
how the P wave of extrasystoles is layered
on extrasystolic QRS complex.

Atrioventricular
extrasystole with
previous ventricular excitation:
premature heart cycle
represented by the P – QRST complex;
tooth P
negative, does not precede the complex
QRS,
and is located after the QRS complex
on the S – T segment;
extrasystolic QRS complex
no different from non-extrasystolic;
compensatory pause incomplete.

Ventricular
extrasystole is premature
impulse of the heart
from different parts of the conductive system
ventricles. Ventricular extrasystole
characterized by the appearance on the ECG
premature extraordinary
altered ventricular complex
QRST,
significant deformation and expansion
extrasystolic complex QRST,
ST segment location
and T wave extrasystoles discordantly
the direction of the main tooth of the complex
QRS,
lack of tooth P
before ventricular extrasystole,
the presence of a full compensatory pause.

On
localization of the source of excitation
ventricular extrasystole may be
right- and left ventricular. Wherein
first that ventricle is excited in
which arose extrasystolic
momentum and then belatedly occurs
depolarization of the other ventricle.
Therefore, right ventricular extrasystole
resembles a single complex with
blockade of the left leg of the bundle of His, and
left ventricular – blockade of the right
branch bundle legs

Right ventricular
extrasystole: premature cardiac
the cycle is represented by the QRST complex,
which is significantly different from
non-extrasystolic (duration
QRS
more than 0,11 sec); S wave
in leads V1,
V2,
III, aVF
deep and wide; R wave
in leads V5, V6,
I, aVL
tall and wide;

Left ventricular
extrasystole: premature cardiac
the cycle is represented by the QRST complex,
which is significantly different in form
from non-extrasystolic (complex
QRS
for a duration of more than 0,11 sec); R wave
in leads V1,
V2,
III, aVF
tall and wide, S wave
in leads V5,
V6,
I, aVL
deep and wide;

ST segment
in leads V5,
V6,
I, aVL
above the contour, and the T wave
positive in these leads; interval
internal deviation in assignments
V1,
V2
over 0,03 sec; ST segment
in leads V1,
V2,
III, aVF
below the contour and the T wave
negative in these leads; tooth
P
is absent; compensatory pause
complete.

Paroxysmal
tachycardia

it’s suddenly starting and suddenly
increasing seizure
heart rate from
140 to 250 per minute while maintaining the correct
regular rhythm. Attack
paroxysmal tachycardia continues
usually from a few
seconds to several hours, less often longer.

Paroxysmal
tachycardia is supraventricular,
supraventricular (due to
frequent ectopic pulses,
outgoing from the atria, the AV connection)
or ventricular (ectopic
impulses
come from the ventricles).

Supraventricular
paroxysmal tachycardia

Paroxysmal
ventricular tachycardia, registered
moment of restoration of sinus rhythm
after administration of aymalin.

important
sign of paroxysmal tachycardia
is conservation
throughout paroxysm correct
rhythm which
does not change after physical
stress, emotional stress,
with deep breathing or
after atropine injection, unlike
sinus tachycardia.

1)
suddenly
beginning
and suddenly ending
heart attack
up to 140-250 per minute while maintaining the correct
rhythm the number of cardiac complexes is three
and more;

в
cases where ectopic
impulses
come from the atria, the presence of
in front of every ventricular complex
QRS
reduced
deformed, biphasic or
negative P wave; in cases where
ectopic
impulses
come from the AV connection, in the leads
II,
III,
aVF
negative teeth are recorded
P located behind QRS complexes
or merging with them and not registering
on an ECG;

в
cases where ectopic
impulses
come from the atria
atrioventricular deterioration is observed
developmental conductivity
atrioventricular block
I
degrees (lengthening the PQ interval)
more than 0,2 s
or II
degree
с
periodic
loss of individual
complexes.

normal
unchanged ventricular complexes
QRS,
QRS-like registered
before paroxysmal
tachycardia.

Atrial
tachycardia (automatic or reciprocal
intraatrial). The right rhythm.
Atrial rhythm 140-200
min Non-sinus teeth P. Carotid massage
sinus causes a slowdown in AV conduction,
but does not eliminate arrhythmia.

Paroxysmal
AV nodal reciprocal tachycardia.
Supraventricular tachycardia with narrow
QRS complexes. Heart rate 150–220
min, P wave is usually layered on
QRS complex or immediately following
him. Starts and stops abruptly.
Carotid sinus massage slows down
Heart rate and often stops paroxysm.

2)
deformation and expansion of the QRS complex
more than 0,12 sec
discordant segment arrangement
ST
and T wave;

3)
availability
atrioventricular dissociation, i.e.
complete dissociation of the rhythm frequency
ventricles (QRS complex
and normal
atrial rhythm (P wave)
occasionally
registering single normal
unchanged QRST complexes
sinus origin (“captured”
ventricular contraction).

Symptoms of pathology

Clinical manifestations of the pathology largely depend on hemodynamic and heart rate disorders. Patients complain mainly about shortness of breath, abnormalities in the functioning of the organ, which mainly occur even with the slightest physical activity. Less commonly, patients feel dull and aching pain behind the sternum.

When listening to patients, abnormal heart contractions with a disturbed rhythm, a different tonality, which depends on the duration of the diastole, are noted. The previous brief pause provokes the first loud tone, and the second either weakens significantly or completely disappears. Atrial fibrillation does not produce hypertension or hypotension, the pulse remains rhythmic, but with a tachysystolic form, the pulse lags behind heart rate.

The clinic of the disease is primarily determined by its form of development. If this is paroxysmal atrial fibrillation, then vivid characteristic symptoms are observed:

  • palpitations sharply quickens;
  • there is an attack of suffocation;
  • not enough air;
  • it becomes difficult to inhale and exhale;
  • weakness and trembling appear throughout the body;
  • urination increases;
  • sweating increases;
  • arms and legs become cold;
  • the patient may panic.

Heart rate is the main criterion for the condition of the patient. The more beats per minute, the worse the patient will feel. In some cases, due to acute heart failure, arrhythmogenic collapse develops when a person loses consciousness due to poor blood supply to the brain.

Before the appearance of a pronounced clinic, for a long time, small chest pains, shortness of breath, feeling of lightheadedness can be observed. Such signs can be considered precursors of atrial fibrillation.

Pathology can manifest itself in the form of small seizures, which at first are either not felt at all or are perceived as temporary discomfort. The lack of treatment for arrhythmias in the early stages affects the decrease in working capacity and the appearance of complications in the form of angina pectoris, shortness of breath, swelling of the extremities, enlarged liver, and problem breathing. Appointed timely treatment of atrial fibrillation will help to avoid premature myocardial wear.

Diagnosis of atrial fibrillation

During an external examination of the patient, pallor of the skin and mucous membranes, cyanosis near the nose and mouth, and an excited state are determined. Counting the heart rate will indicate tachycardia, and an irregular heartbeat, with possible pulsation in the area of ​​large arteries, will tell you about the direction of making the correct diagnosis.

The next stage is electrocardiography, which is available at almost all levels of hospitalization of patients. The first cardiogram can be done in an ambulance or when a patient visits a clinic.

The main manifestations of atrial fibrillation on an electrocardiogram:

  • the P wave does not appear, indicating a lack of sinus rhythm;
  • different intervals are visible between the ventricular complexes, which confirms the irregularity of heart contractions;
  • teeth can be large-wave (indicate flutter) or small-wave (indicate atrial fibrillation).

Examination of the 12-lead ECG helps determine acute atrial fibrillation. Paroxysmal attacks of atrial fibrillation are detected by Holter monitoring, when ECG and blood pressure are monitored throughout the day.

Additional methods for diagnosing atrial fibrillation:

  • Echocardiography (echocardioscopy) along with an ultrasound of the heart are prescribed for suspected insufficiency of the left ventricle. The methods allow you to visually see organic disturbances and make the most accurate calculation of the ejection fraction.
  • Transesophageal examination with an electrocardiograph – used in case of unproven atrial fibrillation using ECG and Holter monitoring. During the study, an attack of arrhythmia is provoked, which is determined on the cardiogram.
  • X-ray examination is indicated for the appointment of patients with paroxysmal and permanent forms. In the first embodiment, it is effective in cases of suspected pulmonary embolism – pulmonary embolism, in the second – to assess congestive pulmonary events that developed due to chronic heart failure.
  • Biochemistry and a general blood test – is prescribed to determine hormonal indicators and markers of a disease such as cardiomyopathy.
Detonic  What is arrhythmia or ventricular tachycardia such as pirouette

In typical cases, the diagnosis of atrial fibrillation is made on the basis of complaints received, data from an external examination, a patient survey and an electrocardiographic study.

Treatment and possible complications of pathology

If the disease is asymptomatic, there is no need for medical treatment. Enough preventative measures and regular monitoring. In this case, atrial fibrillation can pass without treatment and complications.

AF treatment includes:

  1. Preparations for the prevention of thrombosis. Blood clots are dangerous because they can come off and clog a vital artery. With atrial fibrillation, blood thinners are prescribed. As a rule, these are Aspirin and Heparin. However, they must be taken with caution due to the high risk of side effects in the form of bleeding.
  2. Drugs for normalizing heart rate. These medications help to normalize heart rate and normalize the rhythm. These include Propafenone and Amiodarone. The drug begins within an hour after administration.
  3. Beta blockers. These drugs reduce heart rate to the desired level, as well as normalize blood pressure. They help significantly extend the life of patients who have already developed a complication in the form of heart failure. However, bronchial asthma is a contraindication to taking, since beta-blockers can trigger bronchospasm.

If medication does not help, the doctor will recommend a pacemaker, which with the help of electrical impulses will affect the atria and ventricles, causing them to contract at the right rhythm.

In acute cases, first aid should be provided. For this, an ambulance team is called, and before her arrival the patient is laid horizontally. If they took antiarrhythmic drugs, they need to be drunk at the dose indicated by the doctor. After the team has established a preliminary diagnosis of atrial fibrillation, hospitalization is carried out.

Indications for hospitalization:

  • Paroxysmal arrhythmia detected for the first time.
  • The attack lasted up to seven days, which threatens the development of pulmonary embolism.
  • Paroxysm was not stopped at the prehospital stage.
  • A permanent form is determined, against which heart failure has developed.
  • During the attack, complications appeared in the form of a stroke, heart attack, pulmonary edema, acute heart failure.

In the hospital, the causes of the pathology are clarified, and the form of flicker is specified. Further, the treatment tactics depend on the final diagnosis, confirmed by additional research methods and analyzes.

Used drugs that reduce heart rate and restore the sinus node. If necessary, cardioversion is used, which is primarily indicated for acute left ventricular failure. Successful restoration of sinus rhythm prevents the development of pulmonary embolism. After the patient is prescribed antiarrhythmic drugs.

Electrocardioversion – treatment of atrial fibrillation with the help of electric current, used to restore sinus rhythm. It is carried out in emergency and planned cases involving a defibrillator and anesthesia. Emergency electrocardioversion is used for paroxysms lasting up to 2 days and arrhythmic collapse.

Contraindications to electrocardioversion:

  • long-standing arrhythmia (more than 2 years);
  • severe heart failure with a chronic course;
  • untreated thyrotoxicosis;
  • a stroke or heart attack in the patient’s history;
  • in the cavity of the heart, thromboembolic formations are determined on an echo cardioscope.

Occasionally, persistent atrial fibrillation is not amenable to medical treatment and cannot be treated by electrocardioversion due to contraindications. In such cases, it is transferred to a permanent form with further treatment according to the protocol of this disease.

Patients with this form of the disease are treated with cardiac glycosides and beta blockers. The first group of drugs includes egilok, coronar, concor. The second is digoxin. With the help of drug therapy, the heart rate is reduced.

With all forms of atrial fibrillation, anticoagulants and antiplatelet agents are indicated. Especially in the presence of high risks of pulmonary embolism. The standard dose of aspirin in cases not at risk of thromboembolism is 325 mg / day.

It is used in the case of heart defects and other diseases when antiarrhythmic drugs are not perceived by patients or their effectiveness is manifested.

    Radiofrequency ablation (RFA) is a low-traumatic operation performed to cauterize atrial sites in which a circulating pulse is detected. To do this, use a radio sensor located on the electrode, introduced through the femoral artery. Intervention is carried out under anesthesia and control of X-ray television. The operation is performed a small amount of time and is cons >

The relief of attacks of paroxysmal MA is carried out using intravenous administration of the following drugs:

  • Novocainamide 10%, is administered in saline at a dose of 5 or 10 ml. The drug can dramatically lower blood pressure, therefore, it is prescribed, as a rule, with mesatone.
  • Asparkam or pananginum in a dose of 10 ml.
  • Strofantin 0,025% is used in a dose of 1 ml for drip administration to physical. mortar or for inkjet.
  • Cordarone at a dose of 5 mg / kg is administered dropwise or very slowly on 5% glucose.

A polarizing mixture of glucose, insulin and potassium solution. In diabetes mellitus, the glucose-insulin mixture is replaced with saline.

Of the anticoagulants and antiplatelet agents, the following are most often used:

  • Cardiomagnyl at a dose of 100 mg, once, at lunch.
  • Warfarin is taken once a day at a dose of 2,5-5 mg.
  • Clopidogrel at a dose of 75 mg, once, at lunch.

The listed drugs are taken under strict control of the coagulation system parameter.

If a flickering cardiac arrhythmia is diagnosed and what the doctor explained in detail, then not only medicines, but also folk remedies for treating the disease can be used. In particular, it is recommended to coordinate with the attending doctor and take:

  • Shredded yarrow grass, from which tincture is prepared and taken in small quantities for no more than a month.
  • Walnuts are chopped and taken together with honey before meals. The course of treatment is at least a month.
  • Dill seeds are poured with boiling water and infused, after the broth is filtered and taken before meals, one-third of a glass.
  • Soothing decoctions and infusions of valerian, hawthorn, lemon balm will help calm the nervous system, strengthen the cardiovascular system.

It is strongly not recommended to treat acute paroxysm with alternative drugs!

Dietary nutrition is an important factor in the treatment of atrial fibrillation. The disease can progress with frequent consumption of fried, fatty foods, smoked foods and butter. Excessive vinegar, salt, sugar, and spices negatively affect the cardiac activity. Therefore, the diet needs to be built sparing, rich in vitamins, minerals, heart-healthy components (linseed oil, grapefruit, apples, fish, mushrooms, cereals, beans and beans).

Cardiogram Procedure

The process of taking an electrocardiogram is painless and non-invasive, and the availability of this research method is wide: an electrocardiograph can be found in any hospital.

ECG removal is the correct placement of the electrodes. In this case, it is important for the patient to observe a number of recommendations before the study, so as not to accidentally affect its results.

  • overeating is prohibited before the procedure;
  • 12 hours before the procedure, it is recommended not to smoke;
  • alcohol is prohibited before the procedure;
  • before the procedure, it is necessary to exclude for a while the intake of certain drugs that may affect the results, but this can only be done after consulting a doctor, self-medication withdrawal is unacceptable;
  • you can’t get carried away on the eve of hard physical work or undergo severe stress;
  • coffee is also prohibited on the eve of the procedure.

Failure to comply with these simple recommendations will reduce the entire value of the study to naught, since most of these factors provoke the appearance on the ECG in the best case of signs of tachycardia, and sometimes other pathologies.

When the patient is ready, he is asked to strip to the waist, as well as to free his legs from the tissue at least until the middle of the lower leg. That is why the study is recommended to wear light and loose clothing, which is easy to take off.

After undressing, the patient lies down on the couch. Now his main task is to lie still and wait until the study is over.

In the meantime, a nurse or doctor will lubricate the electrode application area with a special gel that improves adhesion to the skin and install electrodes. During the study, the patient needs to lie still, so it is recommended to immediately take a comfortable pose.

The study does not last long, and upon its completion the patient is given results, the deciphering of which is performed by the attending physician.

Complications of atrial fibrillation

Heart arrhythmia can be constant, in which flickering is present for a long time (from seven days or more, and in some patients, periods of about one year are recorded), as well as paroxysmal, when paroxysms are diagnosed – attacks lasting less than seven days, after which the heart rhythm spontaneously normalizes. The chronic form of pathology lasts more than one year.

The disease is characterized by a prolonged course, which provokes various complications and hemodynamic disorders. This provokes symptoms of heart failure, worsens performance. The daily life of such patients suffers substantially.

Among patients with this pathology, a rather high mortality rate. It comes due to ventricular fibrillation and gastric arrhythmia, which is the direct cause of death.

Also, the causes of pathology are of great importance for therapy, because the treatment of the disease is complex – it is necessary to eliminate the cause and manifestations of the ailment.

Prevention of atrial fibrillation

Subject to medical recommendations, maintaining the daily regimen, adequate sleep and rest, you can significantly reduce the risk of developing atrial fibrillation and atrial flutter. The following tips will also help in the prevention of diseases:

  • quitting smoking, drinking alcoholic beverages;
  • avoidance of stressful situations and physical overstrain;
  • therapy of diseases associated with the cardiovascular system;
  • taking sedatives in case of excitement or irritability;
  • Strengthening the body with vitamin and mineral complexes suitable for heart training.

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Tatyana Jakowenko

Editor-in-chief of the Detonic online magazine, cardiologist Yakovenko-Plahotnaya Tatyana. Author of more than 950 scientific articles, including in foreign medical journals. He has been working as a cardiologist in a clinical hospital for over 12 years. He owns modern methods of diagnosis and treatment of cardiovascular diseases and implements them in his professional activities. For example, it uses methods of resuscitation of the heart, decoding of ECG, functional tests, cyclic ergometry and knows echocardiography very well.

For 10 years, she has been an active participant in numerous medical symposia and workshops for doctors - families, therapists and cardiologists. He has many publications on a healthy lifestyle, diagnosis and treatment of heart and vascular diseases.

He regularly monitors new publications of European and American cardiology journals, writes scientific articles, prepares reports at scientific conferences and participates in European cardiology congresses.

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