Transcript Disorder of heart rhythm

Disorder of heart rhythm
Ph.D., MD, Assistant Professor
Potikha N.Ya
ETIOLOGY
Functional violations and
influences
- ANS activity changes
- Physical load
- Body’s t0 change (fever; hyperthermia,
-
hypothermia)
Hormone’s blood concentration changes
Intracranial pressure increase
Infection (flu, typhoid)
breathing (in children)
ETIOLOGY
Organic factors
- inflammation of myocardium (infection ,
uninfection )
- myocardium dystrophy (hypoxia,
ischemia, amiloidosis)
- myocardium necrosis
ETIOLOGY
Toxic influences
- alcohol
- medicines (beta-adrenoblockers)
- catecholamines
- glucocorticoids
- bacterial toxins
- phosphororganic substances
ETIOLOGY
Hormone balance violation
-
Hyperthyroidism
Hypothyroidism
suprarenal glands hyperfunction
suprarenal glands hypofunction
ETIOLOGY
Ions imbalance
- changes of K, Na, Ca, Mg, Cl
cardiomyocytes concentration
(because long time using diuretics,
uncontrolled using mineral water)
Organism more sensitive to К+
deficit than to АТP one
ETIOLOGY
Mechanical influences
- catheter using (for diagnosis and for
treatment)
- operation
- chest trauma
PATHOGENESIS
(pathological condition of the heart)
Injury of conductive system
different parts
No electrical homogenous of
myocardium
No electrical functional stable of
myocardium (violation of MRP)
PATHOGENESIS
(ARRHYTHMIAS THEORIES)
Electricity of injury
(No electrical homogenous of myocardium)
Zone of injury
membrane is partly depolarized
(MRP = 0 mV or +20 mV)
Normal tissue
membrane is completely depolarized
(MRP = -90 mV)
potential difference appears between both these zones
and ectopic driver activates
PATHOGENESIS
(ARRHYTHMIAS THEORIES)
Ectopic rhythm driver activation
(electrical functional unstable myocardium )
Subthreshold oscillations : unstable MRP
causes low amplitude fluctuation, which can cause early
depolarization (hypoxia, K+ deficit, heart distention)
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ТМПП
ТМПД
ТМПП
PATHOGENESIS
(ARRHYTHMIAS THEORIES)
Ectopic rhythm driver activation
(electrical functional unstable myocardium )
Overthreshold oscillations : appears at
retardation or at breaking of repolarization (MAP cann’t
be transformed in to MRP and new action potential
arrears and as a result - ectopic rhythm)
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ТМПП
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PATHOGENESIS
(ARRHYTHMIAS THEORIES)
“Re-entry”
Gist: repeat or multiple impulses enter in some
area of conductive system of the heart or in
contractile myocardium
Condition:
• There are 2 conductive ways, which are separated
functionally or structurally
• There is block of impulses transmission thought the one
conductive way
• Impulses transmission is possible only in reverse route
ARRHYTHMIAS CLASSIFICATION
Automatism violations
Conduction violations
Combined violations (automatism,
conduction and excitability)
Automatism violation
*Nomotopic
(gist – violation of impulses formation in
sinus node)
1. Sinus tachycardia
2. Sinus bradycardia
3. Sinus arrhythmia (respiratory)
*Heterotopic rhythms
(gist – dominance of ectopic area
activity)
1. Tardy ectopic rhythm (vicarious, passive)
2. Unparoxismal tachycardia
3. Migration of supraventricular rhythm driver
Nomotopic Automatism violation
Sinus tachycardia
Reasons: physical load, emotional stress, heart
failure, myocardium ischemia or infarction,
myocardium dystrophy
ECG: sinus rhythm, HR 90-180 /min,
R-R duration<0,60 c
Nomotopic Automatism violation
Sinus bradycardia
Reasons: n. Vagus high activity (sportsmen,
flu, typhoid), intracranial pressure increase
(results from irritation of n.Vagus nucleas)
ECG: sinus rhythm, HR 59-40 /min,
R-R duration>1,0 с
sec
sec
Nomotopic Automatism violation
Sinus (respiratory) arrhythmia
Reasons: breathing (in children), after grip,
neurocirculative dystone
ECG: sinus rhythm, difference between the
shortest R-R and longest R-R >0,15 sec
s
s
s
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Heterotopic rhythms
Tardy ectopic rhythm (vicarious, passive)
Source: atrium, AV node,
ventricle
Meaning: protection of
the heart at long time
asystole (at SA node
arrest)
Kinds:
-atrial
-аtrial- ventricular
- Ventricular
(HR <40/min)
Heterotopic rhythms
Unparoxismal tachycardia
Source:
atrium, AV node , ventricle
ECG:
-HR 90-130/min
- progressive beginning and
finishing
- regular ventricle rhythm
Heterotopic rhythms
Migration of supraventricular rhythm driver
Gradual removal of rhythm driver
from SA node to AV node
ECG:
P wave configuration violation
Change of P-Q duration
Arrhythmia
Conduction violations
heart block
- Sinus atrial
- (or SA node arrest)
- Atrial
- Atrial-ventricular
- ventricular
pre-excitation
syndrome
1. WPW syndrome
2. CLC syndrome
Conduction violations
Sinus atrial block (arrest)
Violation of impulses transmission from SA-node to
atriums (most often - noncomplete)
ECG : PQRST complex is absent
compensatory pause is equal 2 (R-R)
Some time 3-4 PQRST complexes fall out and tardy ectopic
rhythm (vicarious, passive) appears
Conduction violations
Atrial block
Violation of impulses transmission through the atrium
conductive system
ECG : Р duration >0,11 sec, Р - deformed
Conduction violations
АV-block
Violation of impulses transmission through
the AV node
1 degree
2 degree: Mobitz type I, Mobitz type II, type III (high
degree AV block)
3 degree (complete AV block )
Conduction violations
АV-block
ECG :
PQ>0,2 sec
1 degree
Conduction violations
АV-block
2 degree
* Mobitz type I (Venkebah) - Progressive increase of PQ duration
(Venkebah’s pariods) with after fall out QRST
* Mobitz type II - PQ are prolonged or N but their length is constant
QRST fall out (periodicity is 2:1, some time 3:1, 4:1)
* type III (high degree AV block) - QRST fall out (periodicity is 2:1, 3:1,
4:1)
bradycardia (tardy ectopic rhythm arrears)
Symptoms: dizziness, unconsciousness
Conduction violations
АV-block
2 degree
Conduction violations
АV-block
3 degree (complete)
* Absolute stop impulses conduction from atriums to ventricles
* Independent excitation and contraction of the atriums and
ventricles
ECG : Р amount > QRS amount, P waves and QRS complexes appear
independently, some time Р are masked by QRS or T and that
causes their deformation
Conduction violations
АV block
Stokes-Adams’s syndrome
Reasons:
- long time asystole (more than 10-20 seс) (occures at
transition of АV-block 2 degree type III into complete
АV-block
- long time asystole at АV-block 3 degree (complete)
- long time asystole at ventricles fibrillation because
АV-block 3 degree
Signs: unconsciousness, convulsions
(because:
decreased heart output and brain hypoxia)
Prognosis: at every attack patient can die
Conduction violations
ventricle block
Violation of impulses conduction in ventricle
conductive system
Giss’s bundle branches block
* block of 1 branche
* block of 2 branches
* block of 3 branches
* local intraventricle block
ECG : QRS deformation
Conduction violations
Pre-excitation syndrome
WPW (Wolff-Parkinson-White) syndrome
Reason:
additional Kent’s bungle (impulses don’t travel through the AV
node but through Kent’s brunch)
ECG : PQ<0,12 sec, QRS is deformed and wide because Δ-wave, ST
и T are localesed dyscordly, pre-excitation of the ventricles
wave
Conduction violations
Pre-excitation syndrome
CLC (Clerk-Levy-Critesco) syndrome
(syndrome of short PQ)
Reason:
additional Jaims’s bungle (impulses came to ventricles
earlier than through the AV node)
ECG : PQ<0,12 sec, QRS unchanged
Conduction violations
Pre-excitation syndrome
Complications
Pre-excitation of any area in ventricle
Y
Formation of electrical unstable myocardium
Y
“Re-entry” mechanism activation
Y
Ectopic driver appearens
Y
extrasistole
paroxysmal tachycardia
ventricle flutter (ventricular tachycardia)
Arrhythmias in the result of combined
violations (automatism, conduction and excitability)
Extrasistole
Paroxysmal tachycardia
Atrium flutter
Atrium fibrillation
Ventricle flutter (ventricular tachycardia)
Ventricle fibrillation
Extrasistole
extraordinary systole in the result of
ectopic pacemaker activation
Reason:
*
*
Membrane’s high oscillative activity
“re-entry” mechanism
Types, ECG signs:
- atrial (Р deformed)
- atrial-ventricular (Р appears after QRS)
- ventricular (no Р before QRS, QRS deformation,
complete compensatory pouse)
Extrasistole
ECG signs:
Р deformation
(atrial)
Extrasistole
(AV)
ECG signs: Р appears after QRS
Extrasistole
(ventricular)
ECG signs: no Р before QRS, deformation of QRS,
complete compensatory pause
Paroxysmal tachycardia
Attack of the heart contractions
(140-250/min), which sudden onset and
offset at regular rhythm
Mechanisms:- “re-entry”, ectopic driver activation
Types, ECG signs :
- atrial (Р deformed)
- atrial-ventricular (Р appears after QRS)
- ventricular (no Р before QRS, QRS is deformed and
wide)
Duration – from some seconds to some minutes
Paroxysmal tachycardia
(ventricle)
Atrium flutter
rapid and regular atrial contructions with a rate from 240 to 450/min
Mechanisms: re-entry, ectopic driver activation
ECG : regular and rapid F-waves (sawtooth pattern), QRS unchanged
Atrium fibrillation
rapid and unregular atrial contructions
with frequency 350-700/min
Mechanisms: re-entry, ectopic driver activation
ECG : unregular and rapid f-waves (sawtooth
pattern), complexes QRS appear irregular
Ventricle flutter and fibrillation fibrillation
Flutter – frequent (200-300/min) regular excitation and contraction of the
ventricles because impulses from ectopic driver circulates constantly (“reentry”)
ECG : no P, QRS is wide
Fibrillation – frequent (200-500/min), inregular and haotic excitation
and contraction of cardiomyocyte’s separated groups in ventricles
(finally ventricles don’t contract)
ECG : changed shape and amplitude of the waves without any intervals
Thank you for attention !