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Kursk State Medical University

Department of Internal Diseases 1

METHODOLOGICAL RECOMMENDATIONS
FOR STUDENTS

ELECTIVE COURSE
ACTUAL PROBLEMS OF ELECTROCARDIOGRAPHY
Edited by professor L.I. Knyazeva

Kursk - 2012

: 616.12-073.97-71 (075.8)
: 54.1073

Printed by the decision of the editorialpublishing council of GBOU VPO KSMU


of Ministry of Health of Russia

Methodological recommendations for foreign students on elective course


Electrocardiography /edited by prof. L.I. Knyazeva Kursk: KSMU, 2012.
Reviewers: d.m.s., professor of the department of internal diseases 2
I.A. Sarayev.
d.m.s., professor of the department of propedeutics of internal diseases
T.A. Dronova.

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Group of authors, KSMU, 2012

AUTHORS

Knyazeva Larisa Ivanovna

Doctor of medical sciences, professor, head of the department of


internal diseases 1 of Kursk State Medical University

Knyazeva Larisa Aleksandrovna

Doctor of medical sciences, professor of the department of internal


diseases 1 of Kursk State Medical University

Borisova Natalya Aleksandrovna

Candidate of medical sciences, vice-professor of the department of


internal diseases 1 of Kursk State Medical University

Masalova Ekaterina Aleksandrovna

Candidate of medical sciences, assistant of the department of


internal diseases 1 of Kursk State Medical University

Kochinova Ekaterina Aleksandrovna

Candidate of medical sciences, assistant of the department of


internal diseases 1 of Kursk State Medical University

Contents
Chapter 1. Cardiac electrophysiology and the mechanisms of arrhythmias.
Physiological and pathological mechanisms of formation of the impulse.
physiological conduction of the cardiac impulse....................................................5
Chapter 2. P-wave: characteristic of P wave. ECG signs of P-pulmonale and Pmitrale. PQ-interval in norma and pathological PQ- interval..................................7
Chapter 3: QRS complex. Characteristic of Q-wave Characteristic of R-wave.
ECG signs of right and left ventricular hypertrophy. Characteristic of T-wave AND
QT-interval...............................................................................................................9
Chapter 4 Arrhythmias due to changes in the automacity of the sinus node.
Changes in the frequency and regularity of excitations of the sinus node (sinus
bradicardia, tachycardia, arrhythmia. arrest of the sinus node: sick sinus syndrome
.................................................................................................................................11
Chapter 5 Arrhythmias based on the mechanism of re-entry. Extrabeates. Atrial
extrasystoles. Ventricular extrasystoles Parasystole. Paroxysmal tachycardias.
Atrial paroxysmal tachycardias. Ventricular paroxysmal tachycardias.................13
Chapter 6 The Wolff-Parkinson-White syndrome. The Lown Ganong-Levine or
Clerc-Levy-Critesco syndrome..............................................................................15
Chapter 7 Block of the impulse conduction. Sino-atrial blocks. Sick sinus
syndrome. Inter-atrial blocks.................................................................................17
Chapter 8 Atrioventricular blocks: the first degree. Second degree atrioventricular
blocks: the Mobitz type I and type II. Complete atrioventricular blocks of he III
degree.....................................................................................................................19
Chapter 9 Disturbances of the intraventricular conduction. Classification of
intraventricular blocks. Left bundle branch block, subbranch blocks. Right bundle
branch block..........................................................................................................21

Chapter 10 Block of the right bundle branch and the anterior fascicular of the left
bundle branch. Block of the right bundle branch and the posterior fascicular of the
left bundle branch. Three bundle branch block.....................................................24
Chapter 11 Atrial fibrillation and flutter..............................................................25
Chapter 12 Fibrillation and flutter of the ventricles. Asystoliya..........................26
Chapter 13 Therapy of atrial fibrillation and flatter...........................................28
Chapter 14 Myocardial infarction. ECG criteria according to localization. Q and
non-Q MI...............................................................................................................30
Chapter 15 Myocardial infarction.......................................................................32
Chapter 16 True posterior MI.............................................................................33
Chapter 17 ECG signs of MI complications.......................................................35
Chapter 18 Therapy of MI..................................................................................37
Chapter 19 ECG sings of unstable coronary supply...........................................38
hapter 20. Principles of Cholter monitor..............................................................40
Chapter 21. Bases of daily monitoring of blood pressure.......................................41
Chapter 22 emergency therapy of arrhythmias..................................................43
Chapter 23 ECG sings of pericarditis..................................................................44
Chapter 24 ECG criteria of TELA.....................................................................45
LIST OF REFERENCES........................................................................................47

Chapter 1. Cardiac electrophysiology and the mechanisms of


arrhythmias. Physiological and pathological mechanisms of
formation of the impulse. physiological conduction of the cardiac
impulse
Reason: Electrocardiography is a fundamental part of cardiovascular
diseases. It is an essential tool for investigating cardiac arrhythmias and is also
useful in diagnosing cardiac disorders such as myocardial infarction. Familiarity
with the wide range of patterns seen in the electrocardiograms of normal subjects
and an understanding of the effects of non-cardiac disorders on the trace are
prerequisites to accurate interpretation. The contraction and relaxation of cardiac
muscle results from the depolarisation and repolarisation of myocardial cells.
These electrical changes are recorded via electrodes placed on the limbs and
chest wall and are transcribed on to graph paper to produce an electrocardiogram
(commonly known as an ECG).
The electrocardiogram has many uses: it may serve as an independent marker
of myocardial disease; it may reect anatomic, hemodynamic, molecular, ionic,
and drug-induced abnormalities of the heart; and it may provide information that is
essential for the proper diagnosis and therapy of many cardiac problems. In fact, it
is the most commonly used laboratory procedure for the diagnosis of heart disease.
Purpose: After studying the topic a student must:
a) have clear understanding of the ionic basis of the spontaneous electrical
activity of cardiac muscle cells
b) know the normal process of cardiac electrical excitation
c) have clear understanding of factors that control heart rate and action potential
conduction in the heart
d) know the contractile processes of cardiac muscle cells
Questions for independent work.
1. Ionic basis of the spontaneous electrical activity of cardiac muscle cells.

2. Describe how membrane potentials are created across simpered


able membranes by transmembrane ion concentration differences.
3. Characteristic of important cardiac ion channels.
4. What is defines resting potential and action potential?
5. How to define threshold potential and describe the interaction between ion
channel conditions, and membrane potential during the depolarization phase
of the action

potential?

6. How to define pacemaker potential and describe the basis for rhythmic electrical
activity of cardiac cells?
7. Describe the normal pathway of action potential conduction through the heart.
8. The relationship between electrical events of cardiac excitation and the P,
QRS, and T waves, the PR interval, and the ST segment of the electrocardiogram.
9. How diastolic potentials of pacemaker cells can be altered to produce
changes in heart rate?
10. How cardiac sympathetic and parasympathetic nerves alter heart
rate and conduction of cardiac action potentials.
11. Define the terms chronotropic and dromotropic.
12. Define and describe the excitation-contraction process.
13. Describe the influence of altered preload on the tension-producing and
shortening capabilities of cardiac muscle.
14. Define the terms contractility and inotropic state and describes the influence of
altered contractility on the tension-producing and shortening capabilities of
cardiac muscle.
15. Describe the effect of altered sympathetic neural activity on cardiac inotropic
state. The relationships between ventricular volume, muscle tension, and
intraventricular pressure.
Literature:
Lecture, Harrison.
Working plan for student during the unit.
Every student should examine patient with pathology of the heart.

Chapter 2. P-wave: characteristic of P wave. ECG signs of Ppulmonale and P-mitrale. PQ-interval in norma and pathological
PQ- interval
Reason: The sinoatrial node lies high in the wall of the right atrium and
initiates atrial depolarisation, producing the P wave on the electrocardiogram.
Although the atria are anatomically two distinct chambers, electrically they act
almost as one. They have relatively little muscle and generate a single, small P
wave. P wave amplitude rarely exceeds two and a half small squares (0.25 mV).
The duration of the P wave should not exceed three small squares (0.12 s). The
wave of depolarisation is directed inferiorly and towards the left, and thus the P
wave tends to be upright in leads I and II and inverted in lead aVR. Sinus P waves
are usually most prominently seen in leads II and V1. A negative P wave in lead I
may be due to incorrect recording of the electrocardiogram (that is, with
transposition of the left and right arm electrodes), dextrocardia, or abnormal atrial
rhythms.
After the P wave there is a brief return to the isoelectric line, resulting in the
PR segment. During this time the electrical impulse is conducted through the
atrioventricular node, the bundle of His and bundle branches, and the Purkinje
fibres. The PR interval is the time between the onset of atrial depolarisation and the
onset of ventricular depolarisation, and it is measured from the beginning of the P
wave to the first deflection of the QRS complex (see next section), whether this be
a Q wave or an R wave. The normal duration of the PR interval is three to five
small squares (0.12-0.20 s). Abnormalities of the conducting system may lead to
transmission delays, prolonging the PR interval.
This is very important to know the genesis of normal waves, segments and
complexes of ECG in normal and different pathology for diagnosis of many

diseases of CV pathology. Necessary to know electrocardiographic abnormalities.


The range of normal wave patterns must be clear for all doctors.
Timely diagnose and pathogenic treatment make possible to prevent disease
progression and treatment. That is why every physician should know main
criterias of ECG.
Purpose: After studying the topic a student must:
a) have clear understanding of normal waves of ECG
b) know the normal process of formation of all waves, complex, segments and
intervals
c) have clear understanding of ECG signs of P-wave and PQ-interval
d) know main cases of P-mitrale and P-pulmonale
e) know the ECG criteria of P-mitrale and P-pulmonale
Questions for independent work.
1. At what place of the heart is formed the stimulation?
2. What is the wave of the ECG shows atrial alternating excitation?
3. What shows PQ-interval?
4. What shows QRS complex?
5. What process begins in the myocardium after stimulation?
6. What shows ST-interval and T-wave?
7. How to measure the amplitude of the waves on the ECG?
8. How to measure the width and length of the intervals on the ECG?
9. Normal characteristic of P-wave.
10. Normal characteristic of PQ-interval.
11. ECG criteria of P-mitrale.
12. ECG criteria of P-pulmonale.
13. ECG criteria of 1 degree AV-block.
14. ECG criteria of II degree AV-block.
15. ECG criteria of II degree AV-block.

Literature:
Lecture, Harrison.
Working plan for student during the unit.
Every student should read ECG with hypertrophy of right or left atrium, I, II
or III degree AV-blocks and examine patient with these pathology.

Chapter 3: QRS complex. Characteristic of Q-wave Characteristic


of R-wave. ECG signs of right and left ventricular hypertrophy.
Characteristic of T-wave AND QT-interval
Reason: This is very important to know the genesis of normal waves,
segments and complexes of ECG in normal and different pathology for diagnosis
of many diseases of CV pathology. Necessary to know electrocardiographic
abnormalities. The range of normal wave patterns must be clear for all doctors.
The QRS complex represents the electrical forces generated by ventricular
depolarisation.With normal intraventricular conduction, depolarisation occurs in an
efficient, rapid fashion. The duration of the QRS complex is measured in the lead
with the widest complex and should not exceed two and a half small squares (0.10
s). Delays in ventricular depolarisationfor example, bundle branch blockgive
rise to abnormally wide QRS complexes (>0.12 s). The depolarisation wave travels
through the interventricular septum via the bundle of His and bundle branches and
reaches the ventricular myocardium via the Purkinje fibre network. The left side of
the septum depolarises first, and the impulse then spreads towards the right. Lead
V1 lies immediately to the right of the septum and thus registers an initial small
positive deflection (R wave) as the depolarisation wave travels towards
this lead. When the wave of septal depolarisation travels away from the recording
electrode, the first deflection inscribed is negative.

Thus small septal Q waves are often present in the lateral leads, usually
leads I, aVL, V5, and V6. These non-pathological Q waves are less than two small
squares deep and less than one small square wide, and should be < 25% of the
amplitude of the corresponding R wave.
Timely diagnose and pathogenic treatment make possible to prevent disease
progression and treatment. That is why every physician should know main
criterias of ECG.
Purpose: After studying the topic a student must:
a) have clear understanding of normal waves of ECG and analysis of QRS
complex
b) know the normal process of formation of all waves of QRS-complex
c) have clear understanding of ECG signs of Q-MI or nonQ-MI
d) know main cases of ventricular hypertrophy (left and right)
e) know the ECG criteria of ventricular hypertrophy (left and right)
f) know the characteristic of T-wave and QT-interval
Questions for independent work.
1. Analysis of the ventricular QRS complex.
2. Assessment of the ratio of waves Q, R, S in a 12-leads.
3. Measuring the amplitude and duration of the wave Q.
4. Measurement of wave amplitude R, the definition of its possible cleavage, and
the emergence of a second wave of additional R '(r').
5. Measurement of the amplitude of the wave S, broadening the definition of its
potential, serrations or splitting.
6. Analysis of segment RS-T.
7. Analysis of the T wave: to determine the polarity of the T wave,
estimate its shape and measure the amplitude of the T wave.
8. Analysis of Q-T interval.
9. ECG criteria of Q-MY.
12. ECG criteria of nonQ-MI.

Literature:
Lecture, Harrison.
Working plan for student during the unit.
Every student should read ECG with different changes of QRS complex
and examine patient with these pathology.

Chapter 4 Arrhythmias due to changes in the automacity of the sinus node.


Changes in the frequency and regularity of excitations of the sinus node (sinus
bradicardia, tachycardia, arrhythmia. arrest of the sinus node: sick sinus
syndrome

Reason: By arbitrary definition, a bradycardia is a heart rate of < 60


beats/min. A bradycardia may be a normal physiological phenomenon or result
from a cardiac or non-cardiac disorder. Sinus bradycardia is common in normal
individuals during sleep and in those with high vagal tone, such as athletes and
young healthy adults. The electrocardiogram shows a P-wave before every QRS
complex, with a normal P wave axis (that is, upright P wave in lead II). The PR
interval is at least 0.12 s. The commonest pathological cause of sinus bradycardia
is acute myocardial infarction. Sinus bradycardia is particularly associated with
inferior myocardial infarction as the inferior myocardial wall and the sinoatrial and
atrioventricular nodes are usually all supplied by the right coronary artery.
Sick sinus syndrome is the result of dysfunction of the sinoatrial node, with
impairment of its ability to generate and conduct impulses. It usually results from
idiopathic fibrosis of the node but is also associated with myocardial ischaemia,
digoxin, and cardiac surgery. The possible electrocardiographic features include
persistent sinus bradycardia, periods of sinoatrial block, sinus arrest, junctional or
ventricular escape rhythms, tachycardia-bradycardia syndrome, paroxysmal atrial
flutter, and atrial fibrillation. The commonest electrocardiographic feature is an

inappropriate, persistent, and often severe sinus bradycardia.


In adults a tachycardia is any heart rate greater than 100 beats per minute.
Supraventricular tachycardias may be divided into two distinct groups depending
on whether they arise from the atria or the atrioventricular junction. This article
will consider those arising from the atria: sinus tachycardia, atrial fibrillation, atrial
flutter, and atrial tachycardia. Tachycardias arising from re-entry circuits in the
atrioventricular junction will be considered in the next article in the series.
Purpose: After studying the topic a student must:
a) have clear understanding of changes of automatism
b) know hemodynamic changes in all arrhythmias due to abnormalities of
automatism
c) know the ECG criteria of sinus bradycardia, tachycardia
d) have clear understanding of clinical, hemodynamic changes in sick
sinus syndrome
e) know the ECG criteria in sick sinus syndrome
Questions for independent work.
1. More common pathological causes of sinus bradycardia and sinus tachycardia.
2. What typical ECG changes will be present in sinus bradycardia?
3. What is it sinus arrhythmia?
4. What typical peculiarity will be present on the ECG in sinus arrhythmia?
5. Describe ECG signs of sinus arrhythmia.
6. Describe all conditions which associated with sinoatrial node dysfunction.
7. What changes will be present on the ECG in sinus arrest?
8. What changes will be present on the ECG in junctional or ventricular
escape rhythms?
9. What changes will be present on the ECG in paroxysmal atrial flutter?
10. What changes will be present on the ECG in atrial fibrillation?
Literature:

Lecture, Harrison.
Working plan for student during the unit.
Every student should read ECG with different changes of automatism.

Chapter 5 Arrhythmias based on the mechanism of re-entry.


Extrabeates. Atrial extrasystoles. Ventricular extrasystoles
Parasystole. Paroxysmal tachycardias. Atrial paroxysmal
tachycardias. Ventricular paroxysmal tachycardias

Reason: Extrabeats very impotent variant of arrhythmias. We underline


supraventricular and ventricular extrabeats.
The QRS complex in ventricular tachycardia often has a right or left bundle
branch morphology. In general, a tachycardia originating in the left ventricle
produces a right bundle branch block pattern, whereas a tachycardia originating in
the right ventricle results in a left bundle branch block pattern. The intraventricular
septum is the focus of the arrhythmia in some patients with ischaemic heart
disease, and the resulting complexes have a left bundle branch block morphology.
Rate and rhythm In ventricular tachycardia the rate is normally 120-300
beats/minute. The rhythm is regular or almost regular (< 0.04 s beat to beat
variation), unless disturbed by the presence of capture or fusion beats (see below).
If a monomorphic broad complex tachycardia has an obviously irregular rhythm
the most likely diagnosis is atrial fibrillation with either aberrant conduction or
pre-excitation.
Ventricular arrhythmias are a broad categoryof conditions that include
premature ventricular contractions (PVCs), ventricular tachycardia, accelerated
idioventricular rhythm, torsades de pointes, ventricular flutter and fibrillation.
Premature Ventricular Contractions. Prudent medical practice dictates that therapy
for PVCs be based on the company they keep. They are common in the general

population, and if no heart disease is present, they are generally benign.


Accompanying conditions that increase catecholamine levels, as well as hypoxia,
electrolyte abnormalities, and drug toxicity, should be treated. If, however, the
PVCs occur with acute ischemic heart disease or any other organic heart disease,
they may be of greater significance.
Purpose: After studying the topic a student must:
a) have clear understanding of changes of arrhythmias
b) know hemodynamic changes in supraventricular and ventricular extrabeats
c) know the ECG criteria of supraventricular and ventricular extrabeats
d) have clear understanding of clinical, hemodynamic changes in atrial and
ventricular paroxysmal tachycardias
e) know the ECG criteria of atrial and ventricular paroxysmal tachycardia
Questions for independent work.
1. More common causes of supraventricular extrabeats.
2. More common causes of ventricular extrabeats.
3. What typical ECG changes will be present in supraventricular extrabeats ?
4. What typical ECG changes will be present in ventricular extrabeats ?
5. What hemodynamic changes will be present in supraventricular extrabeats?
6. What hemodynamic changes will be present in ventricular extrabeats?
7. What typical ECG changes will be present atrial paroxysmal tachycardia?
8. What typical ECG changes will be present in ventricular paroxysmal
tachycardia?
9. What hemodynamic changes will be present in atrial paroxysmal tachycardia?
10. What hemodynamic changes will be present in ventricular paroxysmal
tachycardia?
11. What ECG changes will be present in parasystol?
Literature:
Lecture, Harrison.

Working plan for student during the unit.


Every student should read ECG with different changes of cardiac rhythm and
must be ready for examination of patient.

Chapter 6 The Wolff-Parkinson-White syndrome. The Lown Ganong-Levine


or Clerc-Levy-Critesco syndrome

Reason: Atrioventricular re-entrant tachycardias occur as a result of an


anatomically distinct atrioventricular connection. This accessory conduction
pathway allows the atrial impulse to bypass the atrioventricular node and activate
the ventricles prematurely (ventricular pre-excitation). The presence of the
accessory pathway allows a re-entry circuit to form and paroxysmal
atrioventricular re-entrant tachycardias to occur.
Wolff-Parkinson-White syndrome. In this syndrome an accessory pathway
(the bundle of Kent) connects the atria directly to the ventricles. It results from a
failure of complete separation of the atria and ventricles during fetal development.
The pathway can be situated anywhere around the groove between the atria
and ventricles, and in 10% of cases more than one accessory pathway exists. The
accessory pathway allows the formation of a re-entry circuit, which may give rise
to either a narrow or a broad complex tachycardia, depending on whether the
atrioventricular node or the accessory pathway is used for antegrade conduction.
ECG features In sinus rhythm the atrial impulse conducts over the accessory
pathway without the delay encountered with atrioventricular nodal conduction. It is
transmitted rapidly to the ventricular myocardium, and consequently the PR
interval is short.
However, because the impulse enters non-specialised myocardium,
ventricular depolarisation progresses slowly at first, distorting the early part of the
R wave and producing the characteristic delta wave on the electrocardiogram. This

slow depolarisation is then rapidly overtaken by depolarization propagated by the


normal conduction system, and the rest of the QRS complex appears relatively
normal.
Traditionally the Wolff-Parkinson-White syndrome has been classified into
two types according to the electrocardiographic morphology of the precordial
leads. In type A, the delta wave and QRS complex are predominantly upright in the
precordial leads. The dominant R wave in lead V1 may be misinterpreted as right
bundle branch block. In type B, the delta wave and QRS complex are
predominantly negative in leads V1 and V2 and positive in the other precordial
leads, resembling left bundle branch block.
Short PR type pre-excitation (LownGanongLevine syndrome). This type of
pre-excitation described by LownGanong and Levine is evidenced by a short PR
interval without changes in QRS morphology. Usually there is not PR segment. It
is impossible to assure with a surface ECG whether it is a pre-excitation occurring
via an atrio-His path, which bypasses the AV node slow conduction area and,
therefore, does not modify the QRS complex morphology, or it is simply a
hyperconductive AV node. The association with arrhythmias and sudden death is
less frequent than in the WPW-type pre-excitation.
Purpose: After studying the topic a student must:
a) have clear understanding of changes of arrhythmias
b) know hemodynamic changes in WPW syndrome
c) know the ECG criteria of WPW syndrome
d) have clear understanding of clinical, hemodynamic changes in CLC syndrome
e) know the ECG criteria of CLC syndrome
Questions for independent work.
1. More common causes of WPW syndrome.
2. More common causes of CLC syndrome.
3. What typical ECG changes will be present in WPW syndrome?

4. What typical ECG changes will be present in CLC syndrome?


5. What hemodynamic changes will be present in WPW syndrome ?
6. What hemodynamic changes will be present in CLC syndrome?
7. What types of WPW syndrome are you know?
8. Differential diagnosis between WPW and CLC syndromes?
Literature:
Lecture, Harrison.
Working plan for student during the unit.
Every student should read ECG with different changes of cardiac rhythm and
must be ready for examination of patient.

Chapter 7 Block of the impulse conduction. Sino-atrial blocks. Sick sinus


syndrome. Inter-atrial blocks

Reason: Sino-atrial block will be completely only. Many courses may lied tj
this block. They are:

MI, cardiomyopathy, myocarditis, valvular diseases,

intoxications (hinidin, -blokers, Ca-chenal blocers and etl.), vagotonia.


Timely diagnose and pathogenic treatment make possible to prevent disease
progression and treatment. That is why every physician should know main
criterias of ECG.
Purpose: After studying the topic a student must:
f) have clear understanding of changes of arrhythmias
g) know hemodynamic changes in sino-atrial block
h) know the ECG criteria of sino-atrial block
i) have clear understanding of clinical, hemodynamic changes in sick sinus
syndrome and inter-atrial block
j) know the ECG criteria of sick sinus syndrome and inter-atrial block

Questions for independent work.


1. More common causes of sino-atrial block.
2. More common causes of sick sinus syndrome and inter-atrial block.
3. What typical ECG changes will be present in sick sinus syndrome and interatrial block ?
4. What typical ECG changes will be present in sino-atrial block ?
5. What hemodynamic changes will be present in sick sinus syndrome and interatrial block ?
6. What hemodynamic changes will be present in sino-atrial block?
Literature:
Lecture, Harrison.
Working plan for student during the unit.
Every student should read ECG with different changes of cardiac rhythm and
must be ready for examination of patient.

Chapter 8 Atrioventricular blocks: the first degree. Second degree


atrioventricular blocks: the Mobitz type I and type II. Complete
atrioventricular blocks of he III degree

Reason: Atrioventricular conduction can be delayed, intermittently blocked, or


completely blockedclassified correspondingly a first, second, or third degree
block.
First degree block. In first degree block there is a delay in conduction of the
atriimpulse to the ventricles, usually at the level of the atrioventricular node. This
results in prolongation of the PR interval to > 0.2 s. A QRS complex follows each
P wave, and PR interval remains constant.
Second degree block. In second degree block there is intermittent failure of
conduction between the atria and ventricles. Some P waves a not followed by a
QRS complex. There are three types of second degree block. Mobitz typ block
(Wenckebach phenomenon) is usually at the level of the atrioventricular node,
producing intermittent failure of transmission of the atrial impulse to the ventricles.
The initial PR interval is normal but progressively lengthens with each successive
beat until eventually atrioventricular transmission blocked completely and the P
wave is not followed by a QRS complex. The PR interval then returns to normal,
and the cyrepeats. Mobitz type II block is less common but is more likely to
produce symptoms. There is intermittent failure of conductioof P waves. The PR
interval is constant, though it may be normal or prolonged. The block is often at
the level of the bundle branches and is therefore associated with wide QRS
complexes. 2:1 atrioventricular block is difficult to classify, but is usually a
Wenckebach variant. High degree atrioventricular block, which occurs when a
QRS complex is seen only after every three, four, or more P waves, may progress
to complete third degree atrioventricular block.
Third degree block. In third degree block there is complete failure of
conduction between the atria and ventricles, with complete independence of atrial

and ventricular contractions. The P waves bear no relation to the QRS complexes
and usually proceed at a faster rate.
Purpose: After studying the topic a student must:
a) have clear understanding of changes of conduction
b) know hemodynamic changes in blocks
c) know the ECG criteria of blocks (I degree A-V block, II degree A-V block,
III degree A-V block)
d) have clear understanding of clinical, hemodynamic changes in these blocks
e) know the ECG criteria of blocks

Questions for independent work.


1. Causes of blocks.
2. Hemodynamic changes in I degree A-V block.
3. Hemodynamic changes in II degree A-V block.
4. Hemodynamic changes in III degree A-V block.
5. ECG criteria of I degree A-V block.
6. ECG criteria of II degree A-V block.
7. ECG criteria of III degree A-V block.
8. Drug therapy of blocks.
9. Indications for peismecer.
Literature:
Lecture, Harrison.
Working plan for student during the unit.
Every student should read ECG with different changes of cardiac rhythm and
must be ready for examination of patient.

Chapter 9 Disturbances of the intraventricular conduction.


Classification of intraventricular blocks. Left bundle branch block,
subbranch blocks. Right bundle branch block
Reason: Ventricular conduction disturbances or blocks can occur on the right
side or on the left side. They can affect the entire ventricle (global block)
oronlypartofit (zonal or divisional block) and the block of stimuli in all parts of the
heart may be of rst degree (partial block) when the stimulus passes through the
area but with delay, third degree (complete block) when passage of stimulus is
completely blocked, and second degree when the stimulus sometimes passes and
sometimes does not. This type of block is known as aberrancy of conduction. The
blocked area, wherever it is, is depolarised with certain delay and, in the cases of
complete global block, depolarises the latest.
Right bundle branch block. In most cases right bundle branch block has a
pathological cause though it is also seen in healthy individuals. When conduction
in the right bundle branch is blocked, depolarisation of the right ventricle is
delayed. The left ventricle depolarises in the normal way and thus the early part of
the QRS complex appears normal. The wave of depolarisation then spreads to the
right ventricle through non-specialised conducting tissue, with slow depolarisation
of the right ventricle in a left to right direction. As left ventricular depolarisation is
complete, the forces of right ventricular depolarisation are unopposed. Thus the
later part of the QRS complex is abnormal; the right precordial leads have a
prominent and late R wave, and the left precordial and limb leads have a terminal S
wave. These terminal deflections are wide and slurred. Abnormal ventricular
depolarisation is associated with secondary repolarisation changes, giving rise to

changes in the ST-T waves in the right chest leads.


Left bundle branch block is most commonly caused by coronary artery
disease, hypertensive heart disease, or dilated cardiomyopathy. It is unusual for left
bundle branch block to exist in the absence of organic disease. The left bundle
branch is supplied by both the anterior descending artery (a branch of the left
coronary artery) and the right coronary artery. Thus patients who develop left
bundle branch block generally have extensive disease. This type of block is seen in
2-4% of patients with acute myocardial infarction and is usually associated with
anterior infarction.
Functions of pacemakers. Pacemakers can pace the ventricle or the atrium, or
both sequentially. Atrial or ventricular activity can be sensed, and this sensing may
be used to trigger or inhibit pacer activity. Some pacemakers are rate adaptive. The
functions of a pacemaker are indicated by a generic code accepted by the North
American Society for Pacing and Electrophysiology and the British Pacing and
Electrophysiology Group. It is a five letter code of which only the first four letters
are used commonly. The first letter identifies the chamber paced, the second gives
the chamber sensed, the third letter indicates the response to sensing, and the
fourth identifies rate responsiveness.

AAI pacing is restricted to those patients with underlying sinus node


dysfunction but intact cardiac conduction. This mode will sense atrial activity and
inhibit pacing if the patients heart rate remains above the preset target. At lower

rates the pacer stimulates the atrium. Like all pacemakers, an AAI pacemaker can
be rate adaptive (AAIR).
VVI pacing is used in patients who do not have useful atrial function, including
those with chronic atrial fibrillation or flutter and those with silent atria. VVI
pacing tracks only ventricular activity and paces the ventricle if a QRS complex is
not sensed within a predefined interval. VVI pacing may be used as a safety net in
Dual chamber pacing has become more common as accumulated evidence shows
that sequential dual chamber pacing provides a better quality of life and improved
functional capacity for patients. In DDD mode an atrial impulse is generated if the
patients natural atrial activity fails to occur within a preset time period after the
last atrial or ventricular event. An atrial event (paced or sensed) begins the
atrioventricular interval. If a spontaneous QRS complex does not occur during the
programmed atrioventricular interval, a ventricular stimulus is generated. The
ventricular stimulus, or sensed QRS complex, initiates a refractory period of the
atrial amplifier known as the postventricular atrial refractory period. The
combination of the atrioventricular interval and the postventricular atrial refractory
period form the total atrial refractory period. The total atrial refractory period is
important because it determines the upper rate limit of the pacemaker. Patients who
are unlikely to need more than occasional pacing.
Purpose: After studying the topic a student must:
a) have clear understanding of changes of arrhythmias
b) know hemodynamic changes in blocks
c) know the ECG criteria of blocks (RBBB, LBBB, antFLBBB, postFLBBB)
d) have clear understanding of clinical, hemodynamic changes in blocks
e) know the ECG criteria of blocks
Questions for independent work.
1. Causes of blocks.

2. ECG criteria of RBBB.


3. ECG criteria of LBBB.
4. ECG criteria of anterior FLBBB.
5. ECG criteria of posterior FLBBB.
Literature:
Lecture, Harrison.
Working plan for student during the unit.
Every student should read ECG with different changes of cardiac rhythm and
must be ready for examination of patient.

Chapter 10 Block of the right bundle branch and the anterior


fascicular of the left bundle branch. Block of the right bundle
branch and the posterior fascicular of the left bundle branch. Three
bundle branch block
Reason: Global ventricular block usually shows the stimulus conduction delay
in the proximal part of the right or left branches, which is why the ventricular
block of global type is known as bundle branch block.
Timely diagnose and pathogenic treatment make possible to prevent disease
progression and treatment. That is why every physician should know main
criterias of ECG, treatment of arrhythmias and emergency therapy.
Purpose: After studying the topic a student must:
f) have clear understanding of changes of arrhythmias
g) know hemodynamic changes in blocks
h) know the ECG criteria of blocks (RBBB+antFLBBB, RBBB+postFLBBB)
i) have clear understanding of clinical, hemodynamic changes in blocks

j) know the ECG criteria of blocks


Questions for independent work.
1. Causes of blocks.
2. ECG criteria of RBBB.
3. ECG criteria of LBBB.
4. ECG criteria of anterior FLBBB.
5. ECG criteria of posterior FLBBB.
6. ECG criteria of RBBB+anterior FLBBB.
7. ECG criteria of RBBB+posterior FLBBB.
Literature:
Lecture, Harrison.
Working plan for student during the unit.
Every student should read ECG with different changes of cardiac rhythm and
should be ready for examination of patient.

Chapter 11 Atrial fibrillation and flutter


Reason: Atrial fibrillation - this is the most common sustained arrhythmia.
Overall prevalence is 1% to 1.5%, but prevalence increases with age, affecting
about 10% of people aged over 70. Causes are varied, although many cases are
idiopathic. Prognosis is related to the underlying cause; it is excellent when due to
idiopathic atrial fibrillation and relatively poor when due to ischaemic
cardiomyopathy. Atrial fibrillation is caused by multiple re-entrant circuits or
wavelets of activation sweeping around the atrial myocardium. These are often
triggered by rapid firing foci. Atrial fibrillation is seen on the electrocardiogram as
a wavy, irregular baseline made up of f (fibrillation) waves discharging at a
frequency of 350 to 600 beats/min. The amplitude of these waves varies between
leads but may be so coarse that they are mistaken for flutter waves.

Atrial flutter is due to a re-entry circuit in the right atrium with secondary
activation of the left atrium. This produces atrial contractions at a rate of about 300
beats/minseen on the electrocardiogram as flutter (F) waves. These are broad
and appear saw-toothed and are best seen in the inferior leads and in lead V1.
Purpose: After studying the topic a student must:
a) have clear understanding of changes of arrhythmias
b) know hemodynamic changes in atrial fibrillation and flutter
c) know the ECG criteria of atrial fibrillation
d) know the ECG criteria of atrial flutter
Questions for independent work.
1. More common causes of atrial fibrillation.
2. More common causes of atrial flutter.
3. What typical ECG changes will be present in atrial fibrillation?
4. What typical ECG changes will be present in atrial flutter?
5. What hemodynamic changes will be present in atrial fibrillation?
6. What hemodynamic changes will be present in atrial flutter?
7. Differential diagnosis between atrial fibrillation and flutter?
8. Therapy of atrial fibrillation and flutter.
Literature:
Lecture, Harrison.
Working plan for student during the unit.
Every student should read ECG with different changes of cardiac rhythm and
should be ready for examination of patient.

Chapter 12 Fibrillation and flutter of the ventricles. Asystoliya


Reason: Ventricular fibrillation is present when irregular undulations of

varying contour and amplitude are present. It is important to exclude asystole


when the fibrillatory waves are small in amplitude. The complications of VT are
caused by insufficient cardiac output and include death, shock, loss of
consciousness, and injury. Additional complications are associated with the
treatment of VT. Complications from antiarrhythmic drug therapy include acquired
LQTS, ventricular proarrhythmia, heart block, and organ toxicity. Complications
from implantation of a defibrillator include infection, pneumothorax, lead failure,
inappropriate shocks for supraventricular tachycardias, premature battery
depletion, and device failure.
Asystole implies the absence of any cardiac electrical activity. It results from a
failure of impulse formation in the pacemaker tissue or from a failure of
propagation to the ventricles. Ventricular and atrial asystole usually coexist.
Asystole may be structurally mediated (for example, in acute myocardial
infarction), neurally mediated (for example, in aortic stenosis), or secondary to
antiarrhythmic drugs. Electocardiographic features of asystole In asystole the
electrocardiogram shows an almost flat line. Slight undulations are present because
of baseline drift. There are several potential pitfalls in the diagnosis of asystole. A
completely flat trace indicates that a monitoring lead has become disconnected, so
check that the leads are correctly attached to the patient and the monitor. Check the
electrocardiogram gain in case it has been set at an inappropriately low level. To
eliminate the possibility of mistaking fine ventricular fibrillation for asystole,
check the trace from two perpendicular leads.
Timely diagnose and pathogenic treatment make possible to prevent disease
progression and treatment. That is why every physician should know main
criterias of ECG, treatment of arrhythmias and emergency therapy.
Purpose: After studying the topic a student must:
a) have clear understanding of changes of ventricular fibrillation and flutter
b) know hemodynamic changes in ventricular fibrillation and flutter
c) know the ECG criteria of ventricular fibrillation
d) know the ECG criteria of ventricular flutter

e) know the ECG changes in asystoliya


Questions for independent work.
1. More common causes of ventricular fibrillation .
2. More common causes of ventricular flutter .
3. What typical ECG changes will be present in ventricular fibrillation?
4. What typical ECG changes will be present in ventricular flutter?
5. What hemodynamic changes will be present in ventricular fibrillation ?
6. What hemodynamic changes will be present in ventricular flutter?
7. What ECG changes will be present in asystoliya?
8. Therapy of ventricular fibrillation and flutter.
Literature:
Lecture, Harrison.
Working plan for student during the unit.
Every student should read ECG with different changes of cardiac rhythm and
should be ready for examination of patient.

Chapter 13 Therapy of atrial fibrillation and flatter


Reason: The acute management of a patient with a ventricular
tachyarrhythmia should follow the Advanced Cardiovascular Life Support (ACLS)
guidelines. The most effective method for restoring sinus rhythm is an
unsynchronized, direct-current electrical shock to the chest. Patients with
ventricular fibrillation or pulseless VT should undergo basic cardiopulmonary
resuscitation. Although three successive shocks were recommended in the previous
ACLS guidelines, a one-shock strategy is now recommended in an attempt to
minimize the time between chest compression and shock delivery. Energy selection
for the first shock with a monophasic defibrillator should be initially 360 joules for
pulseless VT/VF and 200 joules with a biphasic defibrillator. If defibrillation does

not restore sinus rhythm, the ACLS protocol for pulseless VT/VF is followed,
which includes epinephrine (1 mg intravenously every 3 to 5 minutes) or
vasopressin (40 U intravenously once only; one dose of vasopressin may replace
either the first or second dose of epinephrine) and amiodarone (300 mg or 5 mg/kg
intravenous push with a repeat of 150 mg intravenous once only) or as a secondtier agent, lidocaine, especially in the presence of an acute coronary syndrome.
After

defibrillation,

contributing

factors

such

as

ischemia,

hypoxemia,

hypokalemia, hypomagnesemia, or extreme bradycardia should be corrected.


Patients who undergo conversion from polymorphic VT and are found to have a
long-QT interval should be treated to prevent recurrent VT. The ACLS guidelines
recommend magnesium, overdrive pacing, and isoproterenol. Intravenous
lidocaine or oral mexiletine may be considered in patients with LQT3 and torsades
de pointes.
Treatment of sustained monomorphic VT depends on the clinical status of the
patient. If the VT is not hemodynamically tolerated, immediate cardioversion is
appropriate. If the patient is hemodynamically stable, pharmacologic conversion
may be attempted. Intravenous procainamide is considered in the most recent
ACLS guidelines as reasonable for the initial treatment for hemodynamically
tolerated VT. Amiodarone should be considered if the VT is unstable, if it is
refractory to cardioversion, or if VT recurs despite other measures. Intravenous
lidocaine is considered the initial treatment for patients with stable VT occurring in
the setting of ischemia or myocardial infarction. Synchronized electrical
cardioversion should be performed if pharmacologic attempts fail. Adequate
sedation or anesthesia should precede a shock for patients who are conscious.
Overdrive pacing with a temporary transvenous pacemaker can also be used to
terminate sustained monomorphic VT, but it is rarely indicated.
Purpose: After studying the topic a student must:
a) have clear understanding of changes of arrhythmias
b) know classification of anthyarrhiphmic drugs

c) know indications and contraindications of different group


d) have clear understanding about side effects
e) know emergency therapy
Questions for independent work.
1. Principles of drug therapy.
2. Classification of anthyarrhiphmic drugs.
3. Characteristic group IA (indications and contraindications).
4. Characteristic group IB (indications and contraindications).
5. Characteristic group IC (indications and contraindications).
6. Characteristic group II (indications and contraindications).
7. Characteristic group III (indications and contraindications).
8. Characteristic group IV (indications and contraindications).
9. Indications for electrical stimulation of the heart.
Literature:
Lecture, Harrison.
Working plan for student during the unit.
Every student should read ECG with different changes of cardiac rhythm and
must be ready for examination of patient.

Chapter 14 Myocardial infarction. ECG criteria according to


localization. Q and non-Q MI
Reason: The ECG pattern of ischaemia (changes of T wave) is recorded in an
area of myocardium in which a delay of repolarisation occurs as a consequence of
decrease in blood perfusion of smaller degree than what is necessary to develop an
injury pattern, or the pattern is a consequence of ischaemia but not due to active
ischaemia (post ischaemic changes). Fromthe experimentalpoint ofview,
ischaemiamay be subepicardial, subendocardial or transmural. Fromthe clinical

point of viewonly subendocardial and transmural ischaemia exist and the latter is
considered to be equivalent to subepicardial owing to its proximity to the explorer
electrode. Experimentally, the ECG pattern of ischaemia (changes in T wave) may
be recorded in an area of the left ventricle subendocardium or subepicardium in
which, as a consequence of a decrease in blood supply (less than needed to
generate the ECG pattern of injury) or for other reasons such as cooling the area, a
delay in repolarisation in the affected zone occurs.Ifthe ischaemia is
subendocardial a higher than normal positive T wave is recorded and in the case of
subepicardial ischaemia (or in clinical practice transmural due to its proximity to
the explorer electrode) a attened or negative T wave. A vector is originated from
the zone that as a consequence of ischaemia is not yet fully repolarised and still
presents negative charges, and is directed towards the already repolarised area
presenting with positive charges (vector of ischaemia). In the case of
subendocardial ischaemia the vector of ischaemia moves away fromthe ischaemic
zone with late repolarization and originates a taller than normal T wave. If the zone
with late repolarization is subepicardial (or in clinical practice transmural), the
vector of ischaemia will explain attened or negative T wave.
Purpose: After studying the topic a student must:
a) have clear understanding of etiology of MI
b) have clear understanding of changes of ST segment
c) know changes of T-wave
d) have clear understanding of changes of Q-wave
e) know criteria of Q and non-Q-MI
Questions for independent work.
1. Ethiology of MI.
2. Pathogenesis of MI.
3. Classification of MI (according to duration).
4. Classification of MI (according to localization).
5. Morden classification of MI.

6. Laboratory diagnosis of MI.


7. ECG criteria of non-Q-MI.
8. ECG criteria of non-Q-MI.
9. Indications for thrombolysis.
Literature:
Lecture, Harrison.
Working plan for student during the unit.
Every student should read ECG with different changes of ST-segment and
T-wave, normal and pathological Q-wave and must be ready for examination
of patient.

Chapter 15 Myocardial infarction


Reason: In the clinical assessment of chest pain, electrocardiography is an
essential adjunct to the clinical history and physical examination. A rapid and
accurate diagnosis in patients with acute myocardial infarction is vital, as
expeditious reperfusion therapy can improve prognosis. The most frequently used
electrocardiographic criterion for identifying acute myocardial infarction is ST
segment elevation in two or more anatomically contiguous leads. The ST segment
elevation associated with an evolving myocardial infarction is often readily
identifiable, but a knowledge of the common pseudo infarct patterns is essential
to avoid the unnecessary use of thrombolytic treatment. In the early stages of acute
myocardial infarction the electrocardiogram may be normal or near normal; less
than half of patients with acute myocardial infarction have clear diagnostic
changes on their first trace. About 10% of patients with a proved acute myocardial
infarction (on the basis of clinical history and enzymatic markers) fail to develop
ST segment elevation or depression. In most cases, however, serial
electrocardiograms show evolving changes that tend to follow well recognised
patterns.

The earliest signs of acute myocardial infarction are subtle and include
increased T wave amplitude over the affected area. T waves become more
prominent, symmetrical, and pointed (hyperacute). Hyperacute T waves are most
evident in the anterior chest leads and are more readily visible when an old
electrocardiogram is available for comparison. These changes in T waves are
usually present for only five to 30 minutes after the onset of the infarction and are
followed by ST segment changes.
In practice, ST segment elevation is often the earliest recognized sign of acute
myocardial infarction and is usually evident within hours of the onset of
symptoms. Initially the ST segment may straighten, with loss of the ST-T wave
angle. Then the T wave becomes broad and the ST segment elevates, losing its
normal concavity. As further elevation occurs, the ST segment tends to become
convex upwards. The degree of ST segment elevation varies between subtle
changes of < 1 mm to gross elevation of > 10 mm.
Purpose: After studying the topic a student must:
a) have clear understanding of etiology of MI
b) have clear understanding of changes of ST segment
c) know changes of T-wave
d) have clear understanding of changes of Q-wave
e) know criteria of Q and non-Q-MI
Questions for independent work.
1. Etiology of MI.
2. Pathogenesis of MI.
3. Classification of MI (according to duration).
4. Classification of MI (according to localization).
5. Morden classification of MI.
6. Laboratory diagnosis of MI.
7. ECG criteria of non-Q-MI.
8. ECG criteria of non-Q-MI.

9. Indications for thrombolysis.


Literature:
Lecture, Harrison.
Working plan for student during the unit.
Every student should read ECG with different changes of ST-segment and
T-wave, normal and pathological Q-wave and must be ready for examination
of patient.

Chapter 16 True posterior MI


Reason: Posterior myocardial infarction refers to infarction of the posterobasal
wall of the left ventricle. The diagnosis is often missed as the standard 12 lead
electrocardiography does not include posterior leads. Early detection is important
as expeditious thrombolytic treatment may improve the outcome for patients with
posterior infarction. The changes of posterior myocardial infarction are seen
indirectly in the anterior precordial leads. Leads V1 to V3 face the endocardial
surface of the posterior wall of the left ventricle. As these leads record from the
opposite side of the heart instead of directly over the infarct, the changes of
posterior infarction are reversed in these leads. The R waves increase in size,
becoming broader and dominant, and are associated with ST depression and
upright T waves. This contrasts with the Q waves, ST segment elevation, and T
wave inversion seen in acute anterior myocardial infarction. Ischaemia of the
anterior wall of the left ventricle also produces ST segment depression in leads V1
to V3, and this must be differentiated from posterior myocardial infarction. The use
of posterior leads V7 to V9 will show ST segment elevation in patients with
posterior infarction. These additional leads therefore provide valuable information,
and they help in identfying the patients who may benefit from urgent reperfusion
therapy.
Resolution of changes in ST segment and T waves. As the infarct evolves, the
ST segment elevation diminishes and the T waves begin to invert. The ST segment

elevation associated with an inferior myocardial infarction may take up to two


weeks to resolve. ST segment elevation associated with anterior myocardial
infarction may persist for even longer, and if a left ventricular aneurysm develops
it may persist indefinitely. T wave inversion may also persist for many months and
occasionally remains as a permanent sign of infarction.
Typically, the depressed ST segments tend to be horizontal or downsloping.
The presence of reciprocal change is particularly useful when there is doubt about
the clinical significance of ST segment elevation.
Purpose: After studying the topic a student must:
a) have clear understanding of etiology of MI
b) have clear understanding of changes of ST segment in posterior MI
c) know changes of T-wave
d) have clear understanding of changes of Q-wave in posterior MI
e) know criteria of Q and non-Q-MI in posterior MI
Questions for independent work.
1. Etiology of in posterior MI.
2. Pathogenesis of in posterior MI.
3. Classification of MI (according to duration).
4. Classification of MI (according to localization).
5. Morden classification of MI.
6. Laboratory diagnosis of MI.
7. ECG criteria of non-Q-MI in poisterior MI.
8. ECG criteria of non-Q-MI in posterior MI.
9. Indications for thrombolysis.
Literature:
Lecture, Harrison.
Working plan for student during the unit.
Every student should read ECG with different changes of ST-segment and

T-wave, normal and pathological Q-wave in posterior MI and must be ready for
examination of patient.

Chapter 17 ECG signs of MI complications


Reason: In the clinical assessment of chest pain, electrocardiography is an
essential adjunct to the clinical history and physical examination. A rapid and
accurate diagnosis in patients with acute myocardial infarction is vital, as
expeditious reperfusion therapy can improve prognosis. The most frequently used
electrocardiographic criterion for identifying acute myocardial infarction is ST
segment elevation in two or more anatomically contiguous leads. The ST segment
elevation associated with an evolving myocardial infarction is often readily
identifiable, but a knowledge of the common pseudo infarct patterns is essential
to avoid the unnecessary use of thrombolytic treatment. In the early stages of acute
myocardial infarction the electrocardiogram may be normal or near normal; less
than half of patients with acute myocardial infarction have clear diagnostic
changes on their first trace. About 10% of patients with a proved acute myocardial
infarction (on the basis of clinical history and enzymatic markers) fail to develop
ST segment elevation or depression. In most cases, however, serial
electrocardiograms show evolving changes that tend to follow well recognised
patterns.
Timely diagnose and pathogenic treatment of MI complications make
possible to prevent disease progression and treatment. That is why every physician
should know main criterias of ECG, treatment of MI.
Purpose: After studying the topic a student must:
a) have clear understanding of etiology of MI and complications
b) have clear understanding of pathogenesis of MI complications
c) know clinical manifestation of complications
d) have clear understanding of ECG changes

Questions for independent work.


1. Etiology of complications (aneurisma of the heart, acute left failure,
arrhythmias, pericarditis, Dresler `s syndromein, recurrent MI, destruction of
IVS, thrombosis of LV in MI).
2. Pathogenesis of aneurisma of the heart, acute left failure,
arrhythmias, pericarditis, Dresler `s syndromein, recurrent MI, destruction of
IVS, thrombosis of LV in MI.
3. ECG criteria of these complications.
Literature:
Lecture, Harrison.
Working plan for student during the unit.
Every student should read ECG with complications of MI and must be
ready for examination of patient.

Chapter 18 Therapy of MI
Reason: In the clinical assessment of chest pain, electrocardiography is an
essential adjunct to the clinical history and physical examination. A rapid and
accurate diagnosis in patients with acute myocardial infarction is vital, as
expeditious reperfusion therapy can improve prognosis. The most frequently used
electrocardiographic criterion for identifying acute myocardial infarction is ST
segment elevation in two or more anatomically contiguous leads. The ST segment
elevation associated with an evolving myocardial infarction is often readily
identifiable, but a knowledge of the common pseudo infarct patterns is essential
to avoid the unnecessary use of thrombolytic treatment. In the early stages of acute
myocardial infarction the electrocardiogram may be normal or near normal; less
than half of patients with acute myocardial infarction have clear diagnostic
changes on their first trace.

Timely diagnose and pathogenic treatment of MI and complications of MI


make possible to prevent disease progression and treatment. That is why every
physician should know main criterias of ECG, treatment of MI.
Purpose: After studying the topic a student must:
a) have clear understanding of etiology of MI and complications
b) have clear understanding of pathogenesis of MI complications
c) know clinical manifestation of complications
d) have clear understanding of ECG changes
Questions for independent work.
1. Etiology of MI and complications.
2. Pathogenesis of MI and complications.
3. ECG criteria of MI and complications.
4. Indications for thrombolysis.
5. Therapy of pain syndrome.
6. Indications for nitrates.
7. Indications for -blockers.
8. Indications fot ECI.
9. Prophylacsis of ventricular fibrillation.
Literature:
Lecture, Harrison.
Working plan for student during the unit.
Every student should read ECG with MI.

Chapter 19 ECG sings of unstable coronary supply


Reason: In clinical practice electrocardiography is most often used to evaluate
patients with suspected ischemic heart disease. When interpreted in the light of the
clinical history, electrocardiograms can be invaluable in aiding selection of the
most appropriate management. Electrocardiography has limitations. A trace can

suggest, for example, that a patients heart is entirely normal when in fact he or she
has severe and widespread coronary artery disease. In addition, less than half of
patients presenting to hospital with an acute myocardial infarction will have the
typical and diagnostic electrocardiographic changes present on their initial trace,
and as many as 20% of patients will have a normal or near normal
electrocardiogram. Myocardial ischemia causes changes in the ST-T wave, but
unlike a full thickness myocardial infarction it has no direct effects on the QRS
complex (although ischemia may give rise to bundle branch blocks, which
prolongs the QRS complex). When electrocardiographic abnormalities occur in
association with chest pain but in the absence of frank infarction, they confer
prognostic significance. About 20% of patients with ST segment depression and
15% with T wave inversion will experience severe angina, myocardial infarction,
or death within 12 months of their initial presentation, compared with 10% of
patients with a normal trace. Changes in the ST segment and T waves are not
specific for ischemia; they also occur in association with several other disease
processes, such as left ventricular hypertrophy, hypokaliemia, and digoxin therapy.
Myocardial ischaemia can affect T wave morphology in a variety of ways: T
waves may become tall, flattened, inverted, or
biphasic. Tall T waves are one of the earliest changes seen in
acute myocardial infarction, most often seen in the anterior
chest leads. Isolated tall T waves in leads V1 to V3 may also be
due to ischemia of the posterior wall of the left ventricle (the
mirror image of T wave inversion).
In some patients with partial thickness ischemia the T waves show a biphasic
pattern. This occurs particularly in the anterior chest leads and is an acute
phenomenon. Biphasic T wave changes usually evolve and are often followed by
symmetrical T wave inversion. These changes occur in patients with unstable or
crescendo angina and strongly suggest myocardial ischemia.
Timely diagnose and pathogenic treatment make possible to prevent disease
progression and treatment. That is why every physician should know main

criterias of unstable coronary supply.


Purpose: After studying the topic a student must:
a) have clear understanding of etiology of unstable coronary supply
b) have clear understanding of pathogenesis unstable coronary supply
c) know clinical manifestation of unstable coronary supply
d) have clear understanding of ECG changes in unstable coronary supply
Questions for independent work.
1. Etiology of unstable coronary supply
2. Pathogenesis of unstable coronary supply.
3. ECG criteria of these complications.
4. Therapy of pain syndrome.
5. Indications for nitrates.
6. Indications for -blockers.
7. Indications fot ECI.
Literature:
Lecture, Harrison.
Working plan for student during the unit.
Every student should read ECG with unstable coronary supply and must be
ready for examination of patient.

hapter 20. Principles of Cholter monitor


Reason: The ECG pattern of ischaemia (changes of T wave) is recorded in an
area of myocardium in which a delay of repolarisation occurs as a consequence of
decrease in blood perfusion of smaller degree than what is necessary to develop an
injury pattern, or the pattern is a consequence of ischaemia but not due to active
ischaemia (post ischaemic changes). Fromthe experimentalpoint ofview,
ischaemiamay be subepicardial, subendocardial or transmural. Fromthe clinical

point of viewonly subendocardial and transmural ischaemia exist and the latter is
considered to be equivalent to subepicardial owing to its proximity to the explorer
electrode. Experimentally, the ECG pattern of ischaemia (changes in T wave) may
be recorded in an area of the left ventricle subendocardium or subepicardium in
which, as a consequence of a decrease in blood supply (less than needed to
generate the ECG pattern of injury) or for other reasons such as cooling the area, a
delay in repolarisation in the affected zone occurs.Ifthe ischaemia is
subendocardial a higher than normal positive T wave is recorded and in the case of
subepicardial ischaemia (or in clinical practice transmural due to its proximity to
the explorer electrode) a attened or negative T wave. A vector is originated from
the zone that as a consequence of ischaemia is not yet fully repolarised and still
presents negative charges, and is directed towards the already repolarised area
presenting with positive charges (vector of ischaemia). In the case of
subendocardial ischaemia the vector of ischaemia moves away fromthe ischaemic
zone with late repolarization and originates a taller than normal T wave. If the zone
with late repolarization is subepicardial (or in clinical practice transmural), the
vector of ischaemia will explain attened or negative T wave.
Purpose: After studying the topic a student must:
f) have clear understanding of etiology of MI
g) have clear understanding of changes of ST segment
h) know changes of T-wave
i) have clear understanding of changes of Q-wave
j) know criteria of Q and non-Q-MI
Questions for independent work.
1. Ethiology of MI.
2. Pathogenesis of MI.
3. Classification of MI (according to duration).
4. Classification of MI (according to localization).
5. Morden classification of MI.

6. Laboratory diagnosis of MI.


7. ECG criteria of non-Q-MI.
8. ECG criteria of non-Q-MI.
9. Indications for thrombolysis.
Literature:
Lecture, Harrison.
Working plan for student during the unit.
Every student should read ECG with different changes of ST-segment and
T-wave, normal and pathological Q-wave and must be ready for examination
of patient.

Chapter 21. Bases of daily monitoring of blood pressure


Reason: This is very important to know the genesis of normal waves,
segments and complexes of ECG in normal and different pathology for diagnosis
of many diseases of CV pathology. Necessary to know electrocardiographic
abnormalities. The range of normal wave patterns must be clear for all doctors.
The QRS complex represents the electrical forces generated by ventricular
depolarisation.With normal intraventricular conduction, depolarisation occurs in an
efficient, rapid fashion. The duration of the QRS complex is measured in the lead
with the widest complex and should not exceed two and a half small squares (0.10
s). Delays in ventricular depolarisationfor example, bundle branch blockgive
rise to abnormally wide QRS complexes (>0.12 s). The depolarisation wave travels
through the interventricular septum via the bundle of His and bundle branches and
reaches the ventricular myocardium via the Purkinje fibre network. The left side of
the septum depolarises first, and the impulse then spreads towards the right. Lead
V1 lies immediately to the right of the septum and thus registers an initial small
positive deflection (R wave) as the depolarisation wave travels towards
this lead. When the wave of septal depolarisation travels away from the recording
electrode, the first deflection inscribed is negative.

Thus small septal Q waves are often present in the lateral leads, usually
leads I, aVL, V5, and V6. These non-pathological Q waves are less than two small
squares deep and less than one small square wide, and should be < 25% of the
amplitude of the corresponding R wave.
Timely diagnose and pathogenic treatment make possible to prevent disease
progression and treatment. That is why every physician should know main
criterias of ECG.
Purpose: After studying the topic a student must:
g) have clear understanding of normal waves of ECG and analysis of QRS
complex
h) know the normal process of formation of all waves of QRS-complex
i) have clear understanding of ECG signs of Q-MI or nonQ-MI
j) know main cases of ventricular hypertrophy (left and right)
k) know the ECG criteria of ventricular hypertrophy (left and right)
l) know the characteristic of T-wave and QT-interval
Questions for independent work.
1. Analysis of the ventricular QRS complex.
2. Assessment of the ratio of waves Q, R, S in a 12-leads.
3. Measuring the amplitude and duration of the wave Q.
4. Measurement of wave amplitude R, the definition of its possible cleavage, and
the emergence of a second wave of additional R '(r').
5. Measurement of the amplitude of the wave S, broadening the definition of its
potential, serrations or splitting.
6. Analysis of segment RS-T.
7. Analysis of the T wave: to determine the polarity of the T wave,
estimate its shape and measure the amplitude of the T wave.
8. Analysis of Q-T interval.
9. ECG criteria of Q-MY.
12. ECG criteria of nonQ-MI.

Literature:
Lecture, Harrison.
Working plan for student during the unit.
Every student should read ECG with different changes of QRS complex
and examine patient with these pathology.

Chapter 22 emergency therapy of arrhythmias


Reason: The heart muscle has a tight covering that surrounds it, a lining sac
called the pericardium (peri=around +cardium=heart). This sac actually has two
layers. The visceral pericardium is only one cell layer thick and fits tightly onto the
heart muscle. The parietal pericardium is much tougher and thicker and has fibers
that tether the heart to the rib cage and diaphragm. There is a potential space
between the layers, meaning that in normal situations, it has a minimal amount of
fluid. However, should inflammation occur, it can fill with fluid. Inflammation of
the lining of the heart is called pericarditis (itis=inflammation).
Timely diagnose and pathogenic treatment make possible to prevent disease
progression and treatment. That is why every physician should know main
criterias of pericarditis.
Purpose: After studying the topic a student must:
a) have clear understanding of etiology of pericarditis
b) have clear understanding of pathogenesis pericarditis
c) know clinical manifestation of pericarditis
d) have clear understanding of ECG changes in pericarditis
Questions for independent work.
1. Etiology of arrhythmias.
2. Pathogenesis of arrhythmias .
3. ECG criteria of arrhythmias

4. Therapy of pain syndrome in arrhythmias.


5. Indications for Ca-chanal blockers.
6. Indications for -blockers.
7. Indications for pacmeccer.
Literature:
Lecture, Harrison.
Working plan for student during the unit.
Every student should read ECG with arrhythmias and must be
ready for examination of patient.

Chapter 23 ECG sings of pericarditis


Reason: The heart muscle has a tight covering that surrounds it, a lining sac
called the pericardium (peri=around +cardium=heart). This sac actually has two
layers. The visceral pericardium is only one cell layer thick and fits tightly onto the
heart muscle. The parietal pericardium is much tougher and thicker and has fibers
that tether the heart to the rib cage and diaphragm. There is a potential space
between the layers, meaning that in normal situations, it has a minimal amount of
fluid. However, should inflammation occur, it can fill with fluid. Inflammation of
the lining of the heart is called pericarditis (itis=inflammation).
Timely diagnose and pathogenic treatment make possible to prevent disease
progression and treatment. That is why every physician should know main
criterias of pericarditis.
Purpose: After studying the topic a student must:
e) have clear understanding of etiology of pericarditis
f) have clear understanding of pathogenesis pericarditis
g) know clinical manifestation of pericarditis
h) have clear understanding of ECG changes in pericarditis

Questions for independent work.


1. Etiology of pericarditis
2. Pathogenesis of pericarditis
3. ECG criteria of pericarditis.
4. Therapy of pain syndrome in pericarditis.
5. Indications for nitrates, diuretics.
6. Indications for -blockers.
7. Indications fot ECI.
Literature:
Lecture, Harrison.
Working plan for student during the unit.
Every student should read ECG with pericarditis and must be
ready for examination of patient.

Chapter 24 ECG criteria of TELA


Reason: Acute pulmonary thromboembolism is an important cause of inhospital mortality. Despite recommendations, multiple studies demonstrate
underutilization

of

adequate

prophylaxis.

The

diagnosis

of

pulmonary

thromboembolism is often difficult due to the unspecific presentation, and


treatment must be individualised appropriately for each patient on the basis of
clinical risk.
The patients condition also requires careful monitoring. Based on the most
recent guidelines of the European Society of Cardiology, this book is therefore an
useful tool for all the physicians involved in prevention, diagnosis and therapy of
pulmonary thromboembolism.
Purpose: After studying the topic a student must:
a) have clear understanding of changes of TELA

b) know hemodynamic changes in TELA


c) know the ECG criteria of TELA
d) have clear understanding of therapy in TELA
Questions for independent work.
1. More common pathological causes of TELA.
2. What typical ECG changes will be present in TELA?
3. What is it TELA?
4. What typical peculiarity will be present on the ECG TE of small ateris?
5. Ultrasound examination of the heart and typical changes in TELA.
6. X-ray changes in TELA.
7. Complications of TELA.
8. Therapy of TELA.
9. Prophelexsis of TELA.
Literature:
Lecture, Harrison.
Working plan for student during the unit.
Every student should read ECG with TELA and should be ready to do
examination of patient with TELA.

LIST OF REFERENCES
1. Clinical Medicine/Ed. by P. Kumar, M. Clark.-6-th ed.-Edinburg: Elsevier
Saunders, 2005.-1508 p.:ill.
2. Davidson's Principles and Practice of Medicine/Ed. N.R. Colledge, B.R.
Walker, S. H.

Ralston .-21st ed.-Edinburgh:Churchii

Livingstone

Elsevier,2010.-1360 p.:ill
3. Davidson's principles and Practice of Medicine/ed. by N.A. Boon, N.R.
Colledge, B.R. Walker, J.A. A.

Hunter.-20th ed.-Edinburgh: Churchill

livingstone Elsevier, 2006.-1382 p.:il.


4. Harrison's Principles of Internal Medicine/Ed. A.S. Fauci, D.L. Kasper, D.l.
Longo, E. Braunwald, S.L.

Hauser, J.L. Jameson. J. Loscalzo.-17th ed.-

New York: McGraw-Hill Medical.-2008.


5. Parker, R. General Medicine/R. Parker,

A. Sharma.-3-rd.-Edinburgh

[etc.]:Mosby Elsevier,2008.-529 p. :il .-(Crash Course)


6. =Th Parker, R. General Medicine/R. Parker, A. Sharma.-3-rd.Edinburgh [etc.]:Mosby Elsevier,2008.-529

p. :il .-(Crash Course)erapy

study guide for foreign students of medical faculty: .

/.-.:

.., .., ..; .-., , 2002.-140 .


7.

- =Teaching instructions on

fullfilling self-dependent work / Ed. L.I. Knyazeva Kursk: KSMU, 2011.- 34


p.


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