Download cardiac arrithmia

Department faculty and hospital
therapy of medical faculty and
department internal diseases of
medical prophylactic faculty.
Cardiac arrhythmia
Docent Matchanov S.H.
• Infringements rhythm heart — One of
the most common clinical syndromes,
which is revealed not only in organic
diseases of the heart muscle (coronary
artery disease, myocardial infarction,
acquired and congenital heart disease,
cardiomyopathy, etc.), but also for
violations of neurohumoral regulation,
electrolyte shifts, toxic effects on the heart
and even healthy individuals.
Conduction system of the
heart
• Sinus tachycardia (ST) - the increase in heart rate to
100 bpm. per minute or more while maintaining the
right sinus rhythm. ST is due to increased
automaticity CA site.
• Sinus bradycardia (SB) - is slowing of heart rate
below 60 bpm. per minute while maintaining the
correct sinus rhythm. Sinus automaticity bradikradiya
due to a decrease in the SA-node.
• Sinus arrhythmia (SA) is called the wrong sinus
rhythm, characterized by periods of acceleration and
deceleration rate. Sinus arrhythmia is caused by the
formation of an irregular pulse in the SA-node, due
to: 1) the reflex changes in vagal tone in relation to
the phases of respiration, 2) spontaneous changes in
tone n.vagi out of touch with the breath, and 3)
organic damage to the CA site. Distinguish nonrespiratory and respiratory sinus arrhythmia form
Sinus tachycardia, bradycardia
and arrhythmia
Migration of supraventricular
pacemaker
• Migration of supraventricular pacemaker
is characterized by gradual, from cycle to
cycle, moving the source of rhythm from
the SA-node to the AV-connection and
back.
Extrasystoles
• Extrasystole (ES) is a premature excitation of the
heart or any of his department, due to the
extraordinary momentum that comes from the atria,
AV connections, or ventricles.
• Allodromy is a regular alternation of extrasystoles and
normal contractions: 1) bigeminy (every normal after
reduction should ES), 2) trigeminy (ES should be
after every two normal contractions), 3)
kvadrigimeniya etc.
Monotopnye ES extrasystoles originating from the
same ectopic source. Politopnye ES extrasystoles
originating from different ectopic foci. Group
(volley), the presence of beats in the ECG of three or
more consecutive premature beats.
Allorhythmic extrasystoles
Atrial extrasystoles
• Atrial extrasystoles - are preexcitation of the heart
under the influence of an extraordinary impulse of the
atria.
• ECG signs:
• 1. Premature emergence of an extraordinary wave P
'followed by a set of QRST'.
• 2. Deformation or change the polarity of the P wave
'beats.
• 3. The presence of unchanged systolic ventricular
extra set of QRST ', similar in shape to the
conventional normal QRST complexes of sinus origin
(except in cases of aberration of the complex QRS).
• 4. The presence of incomplete compensatory pause.
Extrasystoles of
AV connection
• Ectopic impulses arising in the AV connection
extends in two directions: from top to bottom on the
conduction system of the ventricles and from the
bottom up (retrograde) on the atria.
• ECG signs:
• 1. Premature extraordinary appearance on the ECG
ventricular complex unchanged QRS ', similar in
shape to the other QRS complexes of sinus origin
(except in cases of aberration of the complex).
• 2. Negative P wave 'in leads II, III and aVF after
extra-systolic complex QRS' or lack of P wave
'(through the merger of P' and QRS ').
• 3. The presence of incomplete compensatory pause.
Ventricular extrasystoles
• Ventricular premature beats (PVCs) - is the
heart preexcitation that occurs under the
influence of impulses coming from different
parts of the conducting system of the
ventricles.
• An important feature is the lack of PVCs
before extra systolic P wave QRS complex and
the presence of a full compensatory pause.
Supraventricular paroxysmal tachycardia
• Paroxysmal tachycardia (PT) - is
suddenly beginning and ending as
abruptly increased frequency of heart
attack up to 140-250 per minute, while
maintaining most of the right of a regular
rhythm.
Ventricular paroxysmal tachycardia
• Ventricular tachycardia (VT) - in most cases
it starts suddenly and as suddenly ending the
attack increased frequency of ventricular
contractions to 150-180 bpm. per minute (at
least - more than 200 bpm. in minutes or
within 100-120 bpm. per minute), usually
while retaining the correct regular heart
rhythm.
Atrial flutter
Auricular fibrillation
• Fibrillation (flicker) and atrial flutter two close to its mechanism of cardiac
arrhythmias,
which
are
often
transformed into each other in the same
patient. More frequent atrial fibrillation
(AF) or atrial fibrillation, which may be
paroxysmal or chronic
Flutter and fibrillation of ventricles
• Ventricular flutter (VF) - a frequent (up to 200-300
per minute) and rhythmic excitement and their
reduction. Fibrillation (flicker) ventricles (VF) - an
equally frequent (up to 200-500 per minute), but
random, irregular excitation and reduction of
individual muscle fibers, leading to the cessation of
ventricular systole (ventricular asystole).
• The main ECG signs of severe cardiac arrhythmias
are:
• 1. When ventricular flutter - Frequent (up to 200-300
min), regular and uniform in shape and amplitude of
the wave flutter resembling a sine curve.
• 2. Fibrillation (blink) ventricles - Frequent (up to
200-500 per minute), but irregular random waves,
which differ from each other by varying the shape
and amplitude.
Treatment
Modern methods of treating heart rhythm
disorders are divided into:
Pharmacological (use of antiarhythmic drugs);
Electrical;
Surgical;
Physical, etc.
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Drugs with antiarhythmic action is divided into
four groups according to their predominant influence
on the individual parameters PD:
Class I - sodium channel blockers ("membranestabilizing" medications), which suppress the initial
depolarization of the cardiac fibers (phase 0 TD);
Class II - b-adrenergic blockers;
Class III - blockers of potassium channels,
prolonging the duration of PD and ERP, mainly due
to the oppression of the repolarization phase of
cardiac fiber;
Class IV - Calcium channel blockers slow ("calcium
antagonists"); depress phase 0 action potential and
spontaneous diastolic depolarization in tissues with a
"slow response" (SA-node, AV connection).