Download 05_Instrumental methods of examination of cardiovascular system

Instrumental methods of
examination
of cardiovascular system
Prof. S.M. Andreychyn
• Is a method of graphic
recording of electric currents
generated in the working heart.
Electrocardiography
Conducting system
• I bipolar limb leads – right arm (R+) – left
leg (Y-).
• II bipolar limb leads – right arm (R+) – left
leg (G-).
• III bipolar limb leads – left arm (Y+) – left
leg (G-).
• Ground (black electrode on the right leg)
Bipolar limb leads
Bipolar limb leads
Ground
• aVR – the active electrode, is placed successively on the
right arm.
• aVL – the active electrode, is placed successively on the
left arm.
• aVF - the active electrode, is placed successively on the
left leg.
Unipolar limb leads
Unipolar limb leads
Bipolar and Unipolar limb leads
• V1 – right sternal border, the 4th
intercostal space.
• V2 – left sternal border, the 4th
interspace.
• V3 – left parasternal line, between the
4th and 5th interspace.
• V4 – left midclavicular line, the 5th
interspace.
• V5 – left anterior axillary line, the 5th
interspace.
• V6 – left midaxillary line, the 5th
interspace.
Chest leads
Chest leads
Normal ECG
Normal ECG
• 1. Is heart rrhythm sinus or ectopic, regular or
irregular.
• 2. Heart rate = 60/R-R (when paper speed is 50 mm/sec
R-R=N×0,02).
• 3. Amplitude of ECG voltage (amplitude of R in
standard leads ≥5 mm or their summation in I,II and III
leads ≥15 mm.
• 4. Electrical axis deviation.
• 5. Assessment of all components of ECG.
The scheme of ECG
interpretation
Normal ECG
Interval R-R
Interval P-Q Segment S-T
Segment P-Q
Interval Q-T
ECG interpretation
ECG interpretation
Determination of inner deviation of atriums and
ventricles
ECG in standard limb leads
ECG unipolar limb leads
Chest leads in norm
Causes of electrical axis deviation
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causes of right axis deviation
normal finding in children and tall thin adults
right ventricular hypertrophy
chronic lung disease even without pulmonary hypertension
anterolateral myocardial infarction
left posterior hemiblock
pulmonary embolus
Wolff-Parkinson-White syndrome - left sided accessory pathway
atrial septal defect
ventricular septal defect
causes of left axis deviation
left anterior hemiblock
Q waves of inferior myocardial infarction
artificial cardiac pacing
emphysema
hyperkalaemia
Wolff-Parkinson-White syndrome - right sided accessory pathway
tricuspid atresia
ostium primum ASD
injection of contrast into left coronary artery
Electrical axis
Hypertrophies of heart
chambers
• Left atrial hypertrophy:
• - broad biphasic P in I, AVL,
V5-V6
• Right atrial hypertrophy:
• - high acute P in III, AVF,
V1
• Right ventricular
hypertrophy:
• - high R in III, AVF, V1
• Discordant displacement of
ST segment opposite to the
lagest wave in QRS complex
• Left ventricular hypertrophy:
• - high R in I, AVL, V5-V6
• Discordant displacement of
ST segment opposite to the
lagest wave in QRS complex
• Broad QRS (more than 0,1
sec)
Right atrial hypertrophy
Left atrial hypertrophy
Hyperthrophy of the left
ventricle
Hyperthrophy of the right
ventricle
Hyperthrophy of the right ventricle
Disorders of heart rrhythm:
• I. Disorders of excitation (arrhythmias):
• 1. Sinus arrhythmia
• sinus tachycardia,
• sinus bradycardia
• sinus arrhythmia
• 2. Ectopic arrhythmias:
• extrasystole (sinus, atrial, atrioventricular, ventricular)
• Paroxismal tachycardia (atrial, ventricular).
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II. Disorders of heart conduction:
sinus, atrial,atrioventricular and ventricular blocks,
III. Combined disorders of excitation and conduction:
flutter (atrial and ventricular)
fibrillation (atrial and ventricular)
SINUS ARRHYTHMIA
• Sinus arrhythmia is a cyclic increase in normal heart rate
with inspiration and decrease with expiration. It results
from reflex changes in vagal influence on the normal
pacemaker and disappears with breath-holding or increase
of heart rate due to any cause. The arrhythmia has no
significance except in older persons, when it may be
associated with coronary artery disease.
SINUS ARRHYTHMIA
SINUS TACHYCARDIA
• Sinus tachycardia is a heart rate faster than
90 beats/min that is caused by rapid impulse formation by
the normal pacemaker secondary to fever, exercise,
emotion, anemia, shock, thyrotoxicosis, or drug effect.
The rate may reach 180/min in young persons but rarely
exceeds 160/min.
• In quick heart rate the patient feels palpitation.
SINUS BRADYCARDIA
• Sinus bradycardia is a heart rate slower than 60/min due to
increased vagal influence on the normal pacemaker. The rate
increases after exercise or administration of atropine. Slight degrees
have no significance, especially in youth, unless there is underlying
heart disease, especially coronary heart disease or acute myocardial
infarction.
• Elderly patients may develop weakness, confusion, or even syncope
with slow heart rates. Arrhythmia disappears to use ephedrine or
atropine in some patients to speed the heart rate. Rarely, artificial
pacemakers are necсessary.
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а-normal sinus rrhythm
б- sinus tachycardia
в- sinus bradycardia
г- sinus arrhythmia
• The most common mechanisms of ectopic arrhythmia are:
• 1) reentry mechanism. The depolarization wave front proceeds
antegradely through the fiber whose conduction is slowed and
returns retrogradely in a nearly fiber that had unidirectional
antegrade block.When this returning echo reaches the site of its
origin, it may then reexcite the fiber, which is now no longer
refractory.
• Alternative mechanisms are:
• 2) abnormal automaticity,
• 3) triggered activity (more rarely).
• Repetitive reentry may result paroxysmal tachycardia, if the atrial
premature beat is appropriately timed. Similarly, a single atrial
premature beat may terminate atrial tachycardia by making the
reentry pathway refractory. Recent evidence indicates that about
one-third of patients have aberrant pathways to the ventricles.
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I. Extrasystole
- atrial
- atrioventricular
- ventricular.
II. Paroxismal tachycardia
- atrial
- ventricular.
Ectopic arrhythmias
ATRIAL PREMATURE BEATS
(Atrial Extrasystoles)
• Atrial premature beats occur when an
ectopic focus in the atria fires off before the
next expected impulse from the sinus node.
Ventricular systole occurs prematurely, and
the compensatory pause following this is
only slightly longer than the normal interval
between beats. P wave is byphasic.
• ECG signs: 1) premature appearance of
cardiac complex of ECG,
• 2) non-complete compensatory pause,
• 3) P wave is biphasic or negative,
• 4) P is always recorded before QRS.
Atrial extrasystole
Atrial extrasystoly
Atrial bigeminy
• ECG signs:
• 1) premature appearance of cardiac
complex on ECG,
• 2) non-complete compensatory pause,
• 3) Depending on the location of focus
of excitation P wave occurs before
or after QRS complex or can be
superimposed on the last one.
ATRIO-VENTRICULAR PREMATURE BEATS
(AV extrasystoles)
Ventricular Extrasystoles
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premature appearance of heart complex;
P wave is abcent;
QRS complex is disfigured depending on the location of pathological focus (right or
left His bundlebranch) and broadened;
Discordant displacement of ST segment opposite to the largest wave in the QRS
complex;
complete compensatory pause.
• а- extrasystole from the left ventricle
• б- extrasystole from the right ventricle
Ventricular extrasystole
Ventricular bigeminy and
quadrigeminy
Dangerous extrasystoles by Lawn
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This is a sudden acceleration of the cardiac rhythm
ECG signs:
1) Acceleration of heart rate more than 150 per min;
2) The same shape of all cardiac complexes;
3) Sudden start and stop;
4) Equal R-R intervals.
Paroxismal tachycardia
• It occurs more often in young patients with normal hearts. Attacks begin
and end abruptly and usually last several hours. The heart rate may be
140-240/min(usually 170-220/min) and is perfectly regular, therate will
not vary more than 1-2 beats per minute.Exercise, change of position,
breath-holding, carotid sinus massage, or induced gagging or vomiting
either has no effect or promptly abolishes the attack. Patient sare
asymptomatic except for awareness of rapid heart action unless there is
underlying heart disease, especially mitral stenosis and coronary heart
disease. Inprolonged attacks with rapid rates, dyspnea or tight-ness in the
chest may be felt as palpitation, discomfort in heart region, dizziness.
PAROXYSMAL ATRIAL TACHYCARDIA
• а- atrial paroxismal tachycardia
• б- atrioventricular (nodal) tachycardia with premature excitation of
ventricles
• в- atrioventricular (nodal) tachycardia with simultaneous excitation
of ventricles and atriums
Atrial PT
Ventricular paroxismal
tachycardia
• Ventricular PT
ATRIAL FIBRILLATION
• Atrial fibrillation is the commonest chronic arrhythmia. It occurs
most frequently in rheumatic heart disease, especially mitral
stenosis, and arteriosclerotic heart disease. It is the only common
arrhythmia in which the ventricular rate is rapid and the rhythm
irregular. An ectopic atrial pacemaker fires 400-600 times per
minute.
Atrial fibrillation
ATRIAL FLUTTER
• Atrial flutter is uncommon and usually occurs inpatients with rheumatic
or coronary heart disease, cor pulmonale, or atrial septal defect or as a
result of quinidine effect on atrial fibrillation. Ectopic impulse formation
occurs at rates of 250-350, with transmission of every second, third, or
fourth impulse through the atrioventricular node to the ventricles. The
ventricular rate is usually one-half the atrial rate (2:1conduction), or
150/min. Carotid sinus massage causes sudden slowing or standstill, with
rapid return of the rate to the original level on release of pressure.When
the ventricular rate is 75 (4:1 block), exercise may cause sudden doubling
of the rate to 150 (2:1block). The first heart sound varies slightly in
intensity from beat to beat (but not when the patient is in aconstant 2:1
flutter).
Atrial flutter
Ventricular flutter and
fibrillation
Ventricular fibrillation
• а- ventricular flutter
• б- ventricular fibrillation
• Atrial block
• Atrioventricular block:
• I degree
• II degree (Mobitz I, II and III)
• III degree
Hiss bundlebranch block (right, left).
Disorders of heart
conduction:
Atrial block
• ECG signs: broad P wave
Intraatrial block
• I degree: Prolongation of PQ
• II degree: Prolongation of PQ and periodical missing of QRS,
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- Mobitz I: Venkebach’s periods (gradual PQ prolongation)
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- Mobitz II: PQ il longer but equal in all complexes,
periodical missing of QRS
• Mobitz III: long PQ, many missed QRS (more P waves on
ECG than QRS complexes but P is recorded before QRS)
• III degree or complete AV block: more P waves on ECG than
QRS complexes and P is recorded independently of QRS
AV block
AV block I degree
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Permanent prologation of PQ more than 0,20с
а- atrial form
б- nodal form
в- distal (trifascicular) form
I degree AV block
II degree AV block
III degree AV block
Left bundle branch block
(LBBB)
Left HBBB
Right HBBB
LBBB
Right bundle branch block (RBBB)
Holter ECG monitoring
Heart sonohraphy (B-mode)
B- and M-mode ultrasound of a heart
X-ray of a heart. Aortic heart configuration
Mitral heart configuration