Download ATRIAL PREMATURE BEATS

Instrumental methods of examination
of cardiovascular system
Department of Internal Medicine
Propedeutics and Tuberculosis
Normal ECG
The scheme of ECG interpretation
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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.
Normal ECG
Components of ECG
Determination of inner deviation of etriums and
ventricles
ECG in standard leads
ECG in amplified 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
Hypertrophies of heart
chambers
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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
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Left atrial hypertrophy:
- broad biphasic P in I,
AVL, V5-V6
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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
Left ventricular hypertrophy
Hyperthrophy of the left ventricle
Hyperthrophy of the right ventricle
Disorders of heart rrhythm:
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I. Disorders of excitation (arrhythmias):
1. Sinus arrhythmia
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2. Ectopic arrhythmias:
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sinus tachycardia,
sinus bradycardia
sinus arrhythmia
extrasystole (sinus, atrial, atrioventricular,
ventricular)
Paroxismal tachycardia (atrial, ventricular).
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
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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 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.
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SINUS BRADYCARDIA
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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
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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.
Ectopic arrhythmias
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I. Extrasystole
- atrial
- atrioventricular
- ventricular.
II. Paroxismal tachycardia
- atrial
- ventricular.
ATRIAL PREMATURE BEATS
(Atrial Extrasystoles)
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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
ATRIO-VENTRICULAR PREMATURE BEATS
(AV extrasystoles)
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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.
VENTRICULAR PREMATURE BEATS
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Ventricular premature beats are similar to atrial premature
beats in mechanism and manifestations but are much more
common. Together, they are the commonest causes of a
grossly irregular rhythm with anormal heart rate. Ectopic
impulse formation causes ventricular contraction to occur
sooner than then extexpected beat. The sound of this
contraction is audible. The pause between the ectopic
ventricular beat and the next normally occurring ventricular
beat is longer than the usual interval between 2 regular
beats. When this pause, combined with the coupling interval
(the interval between the preceding regular ventricular beat
and the ectopic beat), equals twice the cycle length of
regularly occurring ventricular beats, the pause is
compensatory, whereas the pause is not compensatory in
atrial premature beats because the sinus node is depolarized
and must start a new basic rhythm. Single premature beats
that occur after every normal beat produce bigeminy.
Exercise generally abolishes premature beats in normal
hearts, and the rhythm becomes regular.
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Premature beats have no definite significance in
the absence of coronary disease, hypertrophic
cardiomyopathy, or prolapse of the mitral valve
unless they arise early in diastole, are
frequent, occur from multiple foci, occur
with rapid ventricular rates or inruns,
interrupt the T wave (R-on-T phenomenon),
or are due to digitalis toxicity. The importance of
the R-on-T phenomenon in predicting the
likelihood of ventricular fibrillation is still being
debated. Sudden death occurs more frequently
(presumably as a result of ventricular fibrillation)
when ventricular premature beats occur in the
presence of known coronary disease,
hypertension, cardiomyopathy, and possibly
prolapsed mitral valve, but not in individuals with
no known cardiac disease even in themiddle-aged
normal population.
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а- extrasystole from the left ventricle
б- extrasystole from the right ventricle
Ventricular Extrasystoles
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Main features:
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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.
Ventricular extrasystole
Ventricular bigeminy and quadrigeminy
Dangerous extrasystoles by Lawn
Paroxismal tachycardia
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This is a group of 4 and more
extrasystoles from one focus of
excitation.
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.
PAROXYSMAL ATRIAL TACHYCARDIA
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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 170220/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.
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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
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Ventricular PT
ATRIAL FIBRILLATION
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Atrial fibrillation is the commonest chronic
arrhythmia. It occurs most frequently in rheumatic
heart disease, especially mitral stenosis, and
arteriosclerotic heart disease. It may appear
paroxysmally before becoming the established
rhythm in thyrotoxicosis and other disorders.
Infection, trauma, surgery, poisoning, or excessive
alcohol intake may cause attacks of atrial fibrillation
in patients with normal hearts. 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.
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The impulses pass through the atria at
varying speeds and are mostly blocked at
the atrioventricular node. The ventricular
response is completely irregular, ranging
from80 to 160/min in the untreated state.
Because of the varying stroke volumes
induced by the varying periods of diastolic
filling, not all ventricular beats result in
apalpable peripheral pulse. The difference
between the apical rate and pulse rate is the
"pulse deficit"; this deficit is greater when
the ventricular rate is high. Exercise
intensifies the irregularity when the heart
rate is slow. Carotid sinus massage usually
slows the ventricular response but does not
terminate the arrhythmia.
Atrial fibrillation
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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
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а- ventricular flutter
б- ventricular fibrillation
Disorders of heart conduction:
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Atrial block
Atrioventricular block:
I degree
 II degree (Mobitz I, II and III)
 III degree
Hiss bundlebranch block (right, left).
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Atrial block
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ECG signs: broad P wave
Intraatrial block
AV block
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I degree: Prolongation of PQ
II degree: Prolongation of PQ and periodical
missing of QRS,
- Mobitz I: Venkebach’s periods (gradual PQ
prolongation)
- 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 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