MINISTRY OF PUBLIC HEALTH OF UKRAINE
BUKOVINIAN STATE MEDICAL UNIVERSITY
Approval on methodological meeting
of the department of pathophisiology
Protocol №
Chief of department of the pathophysiology,
professor
Yu.Ye.Rohovyy
“___” ___________ 2008 year.
Methodological Instruction
to Practical Lesson
Мodule 2 : PATHOPHYSIOLOGY OF THE ORGANS AND SYSTEMS.
Contenting module 5. Pathophysiology of blood circulation
and respiratory system.
Theme 9: Disorders of cardiac rhythm.
Chernivtsi – 2008
1.Actuality of the theme.
The disorders of cardiac rhythm concern to complex manifestations of
pathology of heart. Its can arise in rather small damage of the conducting
system, and in some cases in structural changes. More often arrythmia arise
with infectious illnesses and intoxications as consequence of miocarditis or
dystrophy processes in cardiac muscle, and also in heart ishemic disease,
cardiosclerosis. The disorders of cardiac rhythm arise also owing to reflex
influences from various interreceptors areas (disease of liver, intestinal tract,
uterus), and also in hemodynamic disorders (arterial hypertension). Not
infrequently аrrythmia is a result of disturbance of functions central and
vegetative parts of nervous system. For example, the increase of activity
parasymphatic nervous system lead to delay of conductivity. Similar is observed
also by overdose of some medicin drugs (digitalis, quinidine, morphine). If
bradycardia is accompanied complete atrioventricular blockade, can occur
ischemia of brain with loss consciousness and occuring spasmes. Arrythmia
can be result in development of cardiac insufficiency.
2.Length of the employment – 2 hours.
3.Aim:
To khow: that ability to automatic formation of impulses depends on the
cells located in the conductive system of the heart (p-cells). A spontaneous slow
depolarization of the cellular membrane occurs in them during diastole.
Tachycardia is observed under the influence of the increased
body temperature, distension of the area of the sinoatrial
node,
sympathetic mediators; 2. In stimulation of the vagus, the impulse generation, is
slowed down as well as the heart contractions - bradycardia; 3. Fluctuations of
the - vagus tension during respiration may cause respiratory arrhythmia
(accelerate
heartbeat
on
inspiration
and
its
slowing
down-on
expiration).4.Normally respiratory arrhythmia is observed in children, rarely in
adults.
To be able: characterize arrhythmias.
To perform practical work: to analyse the mechanisms of the arrhythmias.
4. Basic level.
The name of the previous
disciplines
1.
histology
2.
biochemistry
3.
physiology
The receiving of the skills
Structure of the conducting system of heart
Main properties of heart - automatism, irritability,
conductivity, contractivity, refractory.
Mechanisms of occurrence and transfer of nervous
impulse on the conducting system of heart.
5. The advices for students.
1. 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
substances);
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).
2. 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 depolarization or/and
increase threshold level critical potential and 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
myocardiocytes.
3. 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 rhythm.
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
syndrome).
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.
4. 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 shortened.
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.
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
sec).
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.
5. 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.
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. 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 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. 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).
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.
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). Another
pre-excitation pattern is the Lown-Ganong-Levine syndrome, 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.
6. 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.
Atria-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. 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).
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.
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).
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.
5.1. Content of the theme. Etiology of heart rhythm
disorder.Pathogenesis of heart rhythm disorder. Classification of heart rhythm
disorders. Automatism violations. Conduction violations. Arrhythmias in the
result of combined heart properties violations
5.2. Control questions of the theme:
1. Etiology of heart rhythm disorder.
2. Pathogenesis of heart rhythm disorder.
3. Classification of heart rhythm disorders
4. Automatism violations
5. Conduction violations
6. Arrhythmias in the result of combined heart properties violations
5.3. Practice Examination.
Task 1. In inspection of the patient on ECG have detected: the rhythm sinus,
frequency of reductions of heart - 90/mines, РQ is shorted, slurred upstroke on QRS, (is present additional delta wave). Discordant
accommodation SТ. What is kind disorder of rhythm in the patient?
А. Sinus tachycardia В.Ventricular paroxysmal tachycardia
С. Ventricular extrasystole D. Pre excitation syndrome Е. Fibrillation
arrythmia
Task 2. In analysis of ECG in the inspected is revealed decrease of intervals R-R
duration. What is changes in activation of heart are observed in it?
А. Decrease of contractions frequency
В. Increase of contractions
frequency С. Increase of contractions force D. Decrease of contractions
force Е. Decrease of frequency contractions and force one
Task 3. In analyse of the electrocardiogram is installed: sinus rhythm, interval R-R
= 0,6 sec, situation and duration other waves and intervals are not changed.
What property of heart is infringed?
А. Automatism В. Irritability С. Conductivity D.Mastering of rhythm
Е.Contractions
Task 4. On electrocardiogram interval PQ is increase. It testifies about delay of
conducting excitation
А. From sinus node to atrials
В. Over miocardium to atrials
С. Through atrioventricular node D. Through branch of the bunch His’s
Е. Through fibres Purcenye’s
Task 5. In systola of ventricles does not arise extrasystola in reply to additional
impulse generated sinus node in conditions of pathology. It is possible to
explain the indicated fact that in the time of systola is:
А. Additional impulse does not get to ventricles
В. Myocytes of
ventricals hyperpolerised
С. In myocytes the content calcium is reduced
D Myocytes stay in state of refrectory
Е. Bond between myocytes is
blocked
Task 6. The patient after infarction of myocardium has progressing increase of
interval PQ is observed to down to fall out of ventricular complex. After
that fall out the interval PQ is restored. The most probablies violation of
cardiac rhythm in this case are:
А. Atrioventricular blockade І of degree В. Atrioventricular blockade
ІІ of degree С. Atrioventricular blockade ІІІ of degree D. Complete
atrioventricular blockade Е. Idioventricular rhythm
Real-life situations to be solved:
In the patient with neurocirculatory dystonia the frequency of cardiac
contractions is increased to 130/mines. Symptoms of organic damage of heart is
not revealed. In diagnostic vagus test (pressing on carotids sinus) the frequency of
contractions on short time has decreased, and then again has become higher.
1. How the described disorder of cardiac rhythm is named?
2. How you represent the mechanism of development of this arrythmia?
What electrophysiological processes lay in its basis?
3. Why the irritation carotid sinus has rendered normalizing influence on the
cardiac rhythm?
Literature:
1. Gozhenko A.I., Makulkin R.F., Gurcalova I.P. at al. General and clinical
pathophysiology/ Workbook for medical students and practitioners.-Odessa, 2001.
2. Gozhenko A.I., Gurcalova I.P. General and clinical pathophysiology/ Study
guide for medical students and practitioners.-Odessa, 2003. 3. Robbins
Pathologic basis of disease.-6th ed./Ramzi S.Cotnar, Vinay Kumar, Tucker
Collins.-Philadelphia, London, Toronto, Montreal, Sydney, Tokyo.-1999.