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25. im Arrhytmias and their consequences deaae539f11521d123bf68536f89ee19

Normally, heart work depends on normal automatism (conditions of driver
sino-atrial node), excitability, conductive heart system condition and contractive
myocardium properties:
Arrhythmia is the condition, which is characterized by the violation of such
heart physiological properties, as automatism, conduction of impulses through
conductive ways, contractive myocardium properties by the violation of heart
ability to learning of excitation rhythm, by the violation of frequency, rhythm or
coordination of heart beats.
Etiology of heart rhythm disorder
The rhythm violations arise under the influence of different pathological
agents, which can be divided on such groups:
1) Functional violations and influences, for example: violation of vegetative
nerves system condition (sympathetic or parasympathetic link hyperactivity),
physical work, physical overload, body temperature changes, the increase of
intracranium pressure, respiration (especially in children);
2) Organic injury of myocardium, for example: inflammation of myocardium (as
the result of infection), the myocardium dystrophy (in the result of hypoxia,
ischemia or amiloidosis), necrosis of myocardium;
3) Influences of toxic substances on the myocardium (alcohol, drugs, big dose
adrenalin and noradrenalin, glucocorticoids, bacterial toxins, phosphororganic
4) Hormone balance disorder (hyperthyroidism, hypothyroidism, hyperfunction of
supranephral glands);
5) Violation of intracellular or extracellular ions balance (changes of sodium,
potassium, calcium, magnesium and chlorine concentration);
6) Mechanical influences on the heart (catheter using for the diagnosis and
treatment heart diseases, operation on the heart, chest trauma).
Pathogenesis of heart rhythm disorder
Ability to automatic impulses formation depends on pacemaker cells activity
of the sinoatrial node, in which spontaneous slow depolarization of cells membrane
takes place during diastole. As the result, action membrane potential arises after
achievement of some critical level (threshold level critical potential).
Impulses generation depends on maximum diastolic potential of these cells,
on maximum diastolic potential measure, after which action membrane potential
arises, and on speed of slow diastolic depolarization. The decrease of the threshold
level maximum diastolic potential SA node p-cells or/and slow diastolic
depolarization speed increase stimulates of the sinus tachycardia appearance at
body temperature increase, in the result of sympathetic stimulation or withdrawal
of vagal tone. On the contrary, decrease of speed slow spontaneous diastolic
hyperpolarization in diastole causes the sinus bradycardia. Tone oscillations of n.
Vagus at breathing time can induce the sinus respiratory arrhythmia (increase of
hear beats during the inspiration). Respiratory arrhythmia in norm is in children,
but now very often can be observed in adult.
Own automatism of lower part conductive heart system can appear in
pathological conditions (arises so-called heterotopic or ectopic rhythm driver).
That condition is the result of the automatism sinoatrial node ability decrement, so
generation of the impulses arises in another myocardium conductive parts, new
ectopic automatism driver appears. Beginning such automatism driver is the result
damage of the different part conductive system, or electrical heterogeneous of
myocardiocytes, or electrical unstable of myocardiocytes (especially in fourth
phase action potential during formation of the resting membrane potential). In that
cases extraordinary heart contractive or only ventricles arises (extrasystole).
There are three mechanisms of the new ectopic rhythm driver appearance.
1. Appearance of the injured electricity in myocardium. It is the result of
electrical heterogeneous myocardiocytes. So, between the uninjured myocardium
(membrane charge is -90 mV – membrane resting potential) and injured one
(membrane is partly or totally depolarized, membrane charge, for example, is 0
mV or +20 mV) arises difference of the potential and it is the reason of the ectopic
rhythm beginning.
2. Ectopic rhythm driver activation. It is the result of electrical unstability
myocardiocytes and beginning in one case of the subthreshold level oscillations
(unstable low amplitude oscillations of the resting membrane potential) and in
other one - the beginning of overthreshold level oscillations (at the retardation or
breaking of repolarization).
3. Re-entry mechanism. Under normal conditions, an electrical impulse is
conducted through the heart in an orderly, sequential manner. The electrical
impulse then dies out and does not reenter adjacent tissue because that tissue has
already been depolarized and is refractory to immediate stimulation. However,
under certain abnormal conditions, an impulse can reenter an area of myocardium
that was previously depolarized and depolarize it again. There three conditions are
the necessary for this mechanism beginning: 1 – two conductive ways are the
functionally or anatomically disconnected; 2 – some conductive way is blocked; 3
– the antegrade conductive way is blocked, but the retrograde one is preserved. So,
in that condition impulse (or impulses) travels numerous through some area of
conductive system and returns through another pathway to the reactivated
Classification of heart rhythm disorders
The classification of heart arrhythmia types is based on the main heart
properties violations.
1. Automatism violations. There are two groups of arrhythmias, which arise
in the result of sinus-atrium node functional state violation. The first group is
named nomotopic automatism violation and includes sinus tachycardia, sinus
bradycardia and sinus arrhythmia. The second group is named heterotopic
automatism violation and includes atrium-ventricular rhythm and idioventricular
2. Conduction violations. There are two groups. The first group conduction
violation unites block: sinus one, atrium one, atrium-ventricular one, ventricle one.
The second group includes Wolf-Parkinson-White syndrome (pre-excitations
3. Arrhythmias in the result of combined heart properties violations
(automatism, conduction and excitability). This group unites extrasystole,
paroxysmal tachycardia, atria flutter, ventricle flutter, atria fibrillation, and
ventricle fibrillation.
Automatism violations
Nomotopic (sinus node) rhythms.
1. Sinus tachycardia refers to a rapid heart rate (> 100 to 180 beats per
minute) that has the origin in the SA node. The main reasons are physical or
emotional stress, myocardial ischemia or infarction, myocardial dystrophy,
congestive heart failure, fever, hyperthyroidism, pharmacological agents (atropine,
isoproterenol, adrenalin), compensatory response to decreased cardiac output. ECG
sings: all waves have normal configuration and priority, P wave and PR interval
(0.12 to 0.20 second) precedes each QRS complex (sinus rhythm), all R-R are
Sinus tachycardia
2. Sinus bradycardia describes a slow heart rate (< 60 to 40 beats per
minute) that has the origin in the SA node. It may be normal in trained athletes
who maintain a large stroke volume, during sleep; in pathological condition after
influenza or typhoid, intracranium pressure rise, irritation of the n. Vagus
nucleases, may be an indicator of poor prognosis in patient with acute myocardial
infarction that is associated with hypotension. ECG sings: all waves have normal
configuration and priority, normal P wave and PR interval precedes each QRS
complex (sinus rhythm), all R-R are lengthened. This arrhythmia may cause heart
output decrease and leads to cerebral or coronary blood flow insufficiency, in that
condition ectopic pacemaker could be activated.
Sinus bradycardia
3. Sinus (respiratory) arrhythmia is characterized by gradually lengthening
(at expiration) and shortening (at inspiration) R-R intervals and is the result of
intrathoracic pressure changes during respiration. It is the normal for the children
and can occur in adult after influenza, at neurocirculative dystone, hypertension,
congestive heart failure, diabetes mellitus. ECG sings: sinus rhythm, difference of
all R-R is more than 0.15 second (at norm difference of all R-R is less than 0,15
Sinus (respiratory) arrhythmia
Heterotopic rhythms. They are the result of ectopic automatism driver activation
that is localized out SA node (for example, in atrium, in AV-node or in ventricle)
because SA node failure (reasons - digitalis toxicity, myocardial infarction, acute
myocarditis, excessive vagal tone, hyper- or hypokalemia).
1. Tardy ectopic rhythm (vicarious, passive) arises at the SA node arrest. ECG
sings: heart beats not more 60 per minute. If ectopic pacemaker is localized in
atrium on ECG inverted P wave is observed before QRS. If ectopic pacemaker is
localized in AV node on ECG inverted P wave is observed after normal QRS, or
hidden in QRS (atrial-ventricular rhythm). If ectopic pacemaker is localized in
ventricle heart rate is less then 40 per minute, QRS is deformed (wide, distorted), it
is so called idioventricular rhythm.
2. Unparoxismal tachycardia begins and ends gradually, heart rate is 90 –
130/min. Ectopic driver may be localized in atrium, in AV node or in ventricle. So,
complex PQRST has sings of nonsinus rhythm (alteration of configuration,
duration and succession waves)
3. Migration of supraventricular rhythm driver is characterized by the gradual
removal of rhythm driver from SA node to AV one. ECG sings: violation of P
wave configuration and lasting, dysrtythmia.
Conduction violations
Conduction violations include two groups of arrhythmias: heart block and preexcitation syndrome and has the results from abnormality impulse conduction.
Causes of heart block are conductive ways damage (myocardial infarction,
myocarditis, cardiosclerosis, heart failure, coronary heart disease, vagal tone).
Conduction block can arise in the AV nodal fibers, in bungle of His, in the
Purkinje conduction system, between SA node and atrium, inside atrium.
1. Sinoatrial block has such sings: impulses are not transmitted out the SA
node, so on ECG waves P, QRS, and T are absent, pause is equal 2 (R-R). Some
time occurs sinus arrest and on ECG no 3 or 4 (sequence) cardiac complex, it may
result irregular pulse, prolonged period of asystole.
Second-degree sinoatrial block
2. Atrial block ECG sings: P waves are deformed and their duration is more
than 0.11 second.
3. Atrium-ventricular block has three degree.
First-degree AV block is characterized only by the prolonged P-Q interval
(< 0.2 second) in the result of retardation impulses conduction from atria to
ventricles through AV node. Isolated first-degree AV block is never symptomatic.
First-degree AV block
Second-degree AV block is divided into two types. Type-first (Mobitz
type I or Wenkebach phenomenon) is characterized by progressive lengthening
of the PQ interval until an impulse is blocked, one cardiac cycle falls and then the
cycle repeats again. After the fall of ventricle contraction Р-Q interval is restored,
gradually becoming longer with each heart contraction. R-R are different, rhythm
is irregular and there are more P waves than QRS complexes
Type-first (Mobitz type I)
Type II (Mobitz type II) is usually associated with organic cardiac disease. It
is the intermittent block of atrial impulses conduction with a constant PR interval
(normal or long), but QRS complexes fall more frequently, may be such
correlations: 2:1; 3:1; 4:1. This type is complicated by cardiac output decrease.
Type II (Mobitz type II)
Third-degree AV block, or complete AV block, occurs when the
conduction link between the atria and ventricles is lost. The atria continue to beat
at a normal rate and the ventricles develop their own rate, which normally is slow
(30-40/min, idioventricular rhythm). The atria and ventricles rates are regular but
dissociated (on ECG P waves and QRS complexes occur independently, count of P
waves more than QRG. It causes periods of syncope, known as a Stokes-Adams
attack (sings: asystole more than 10-20 sec, a decrease of cardiac output,
insensibility, convulsions, is possible death).
Third-degree AV block
4. Ventricle block. Interruption of impulse conduction through the bundle
branches is called bundle branch block. These blocks usually do not cause
alterations in the rhythm of the heartbeat. Bundle branch block interrupts the
normal progression of depolarization, causing the ventricles to depolarize one after
the other because the impulses must travel through muscle tissue rather than
through the specialized conductive tissue. It cause the QRS deformation, it is wide
(normal is 0.08 to 0.12 second) and distorted. The left bundle branch bifurcates
into left anterior and posterior fascicles. An interruption of one of these fascicles is
referred to as a hemiblock. Their ECG sings are very difference, but the main sing
is QRS complex deformation.
The left bundle branch block
Pre-excitation or Wolff-Parkinson-White (WPW) syndrome exists when
atrial impulses are transmitted directly to the ventricles through shortcut
conduction pathways. The impulses do not travel through the AV node but through
accessory brunch (bungle of Kent). This connects the conduction system of the
atria to either ventricle, bypassing the AV node. Impulses go down the accessory
pathways and return by the normal conduction system to set up a re-entry system,
it can cause supraventricular tachycardia. The ECG is characterized by a short P-R
(less than 0.12 sec), a slurred upstoke on the QRS (delta wave), a wide QRS (more
than 0.10 sec), secondary ST and T waves are changed (repolarization is altered).
characterized by a short PR interval without a delta wave. These syndromes are
dangerous because may cause electricity unstabilized myocardium, activation of
ectopic driver and extrasistoles or paroxysmal ventricular tachycardia beginning.
Arrhythmias in the result of combined heart properties violations
Combined heart properties violations include disorders of automatism,
conduction and irritability.
Extrasystole is the extraordinary systole in the result of ectopic pacemaker
activation. New pacemaker (out sinus node) causes beginning excitation wave,
which spreads in altered direction. Dependency on cell localization, where the
extraordinary impulse is formed, distinguishes such types of extrasystole: sinus,
atrial, atria-ventricular and ventricular.
Sinus extrasystole or premature atrial contraction is a beat initiated by an
ectopic atrial focus that appears early in the cycle (before the next expected sinus
beat). An excitation wave is usually conducted through the ventricular pathway in
the normal manner not changes the shape of the QRS. A pause will follow the beat,
and the SA node will start a new cycle. Atrial extrasystole is the result of ectopic
pacemaker activation in different parts of atria. It is characterized by Р wave
distortion (depressed, dysphasic, negative) because excitation wave goes
retrograde, by partial compensatory pause.
Sinus extrasystole
Atrio-ventricular extrasystole is observed at beginning ectopic pacemaker in
AV node (top and middle part). Excitation wave spreads in two directions: in
ventricles — in normal, in atria – in retrograde. So, Р wave is negative and
indicates or after normal QRS complex or can be coincide with QRS.
Atrio-ventricular extrasystole
Ventricular extrasystole or premature ventricular contraction (it is caused by
a ventricular ectopic pacemaker) is more dangerous than sinus or atrial because
violates the pumping action of the heart. After such extrasystole the ventricle
usually is not able to repolarise sufficiently to respond to the next impulse that
arises in the SA node (compensatory pause arises), diastolic volume is usually
insufficient for ejection of blood. On the ECG: extrasystole complex is registered
early in the cycle, is not usually preceded by P wave, QRS is distorted and wide,
large looping ST segment opposite in direction to that of the QRS, full
compensatory pause (interval between the R waves before and after the
extrasystole complex is twice that of the normal R-R).
Ventricular extrasystole
Paroxysmal tachycardia. Extraordinary contractions can arise one by one or
by groups. Paroxysmal tachycardia develops in case of numerous extrasystoles,
with a rapid heart rate (in measure 140-250 beats per min, averaging about 170),
which sudden onset and offset and couses physiological rhythm break. Duration of
paroxysm can be different – from (some) seconds to (some) minutes, after that it
similarly suddenly ends and adjusts normal rhythm.
Atrial paroxysmal tachycardia is mostly observed. The patient frequently
complains of a sudden pounding or fluttering in the chest associated with weakness
or breathlessness. The fast rate stresses then heart and increases its need for
oxygen. The tachycardia may also diminish cardiac output because of shortened
ventricular filling tame. The heart is beating so rapidly that the ventricle doesn’t
have time to fill completely, each beat pumps out less blood. If this tachycardia
persists, the usual treatment is stimulation of the n.Vagus by carotid sinus or eyes
massage, which slows the heart rate. Since this can produce dangerous slowing or
cardiac arrest, the patient should be monitored.
Atrial flutter is a rapid and regular atrial ectopic tachycardia, with a rate that
ranges from 240 to 450 beats per minute. There two types of atrial flutter.
Type I flutter is the result of re-entry mechanism in the right atrium and the
rate frequency may be 240-350/min.
The mechanism of type II is unknown. The atrial rate ranges between 350
and 450 beats in minute. On the ECG are defined regular and rapid F-waves
(sawtooth pattern). Not all of the impulses are conduced, so the ventricular rate is
usually slower. Because the impulses are coming so rapidly, the AV node cannot
accept and conduct each one and ventricle response may be regular or irregular
(some degree of block occurs at the node).
Atrial fibrillation is the result of chaotic current flow within the atria. When the
atrial cells cannot repolarize in time for the next incoming stimulus, the ectopic
current is rejected by the refractory cells and sent in another direction. On ECG:
atrial electrical activity is disorganized and indicated by f-waves with frequency
350-700/min. Conduction through the AV node is disorganized, so complexes
QRS appear irregular; the peripheral pulse is grossly irregular, and a pulse deficit
can be observed.
Ventricle flutter (ventricular tachycardia) is the result of ventricle frequency
excitement by permanently circulation impulses (re-entry mechanism). A rate
usually is 150-200/min. On ECG: rate is fast, QRS is wide, and P waves may
sometime be visible in the complex QRS. It is very dangerous arrhythmia because
it leads to reduced cardiac output, and many times, to ventricular fibrillation.
Ventricle flutter
In ventricular fibrillation, the ventricle quivers but doesn’t contract, so there is
no cardiac output, and there are no palpable or audible pulses. The classic ECG
pattern of ventricular fibrillation is that of gross disorganization without
identifiable waveforms or intervals (frequency 200-500/min).
Ventricular fibrillation
Preventing more serious arrhythmias often involves drug therapy, electrical
stimulation, or surgical intervention. The correction of very dangerous arrhythmias
can involve the use of an electronic pacemaker, cardioversion, or defibrillation.
Electrical interventions can be used in emergency and elective situations. A
pacemaker is an electronic device that delivers an electrical stimulus to the heart. It
is used to initiate heartbeats in situations when the normal pacemaker of the heart
is defective or in complete heart block in which the rate of cardiac contraction and
consequent cardiac output is inadequate to perfuse vital tissue. Overdrive pacing is
used to treat recurrent ventricular tachycardia, atrial flutter. A pacemaker may be
used as a temporary or a permanent measure.
Defibrillation and synchronized cardioversion are two reliable methods for
treating ventricular tachycardia and fibrillation.
The discharge of electrical energy that is synchronized with the R wave of
the ECG is referred to as synchronized cardioversion, and unsynchronized
discharge is known as defibrillation. The goal of both these techniques is to
provide an electrical pulse to the heart in such a way as to completely depolarize
the heart during passage of the current. This electrical current interrupts the
disorganized impulses, allowing the SA node to regain control of the heart.
Defibrillation depolarizes all of the myocardial cells simultaneously and allows the
SA node to resume normal conduction.