Disorders of heart rhythm

D.D., Professor Denefil Olha Volodymyrivna

 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)

- myocardial dystrophy (hypoxia,

ischemia, amyloidosis)

- myocardial necrosis
 ETIOLOGY

Toxic influences

- alcohol
- medicines (beta-adrenoblockers)
- catecholamine
- glucocorticoids
- bacterial toxins
- phosphor organic substances
D.D., Professor
Denefil O.V.
 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 Normal tissue

membrane is partly depolarized membrane is completely depolarized
(MRP = 0 mV or +20 mV) (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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 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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 PATHOGENESIS
(ARRHYTHMIAS THEORIES)

“Re-entry”
Nature: 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 (violation of impulses formation in

sinus node)
1. Sinus tachycardia
2. Sinus bradycardia
3. Sinus arrhythmia (respiratory)
*Heterotopic rhythms (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
 Nomotopic Automatism violation
Sinus (respiratory) arrhythmia
Reasons:
breathing (in
children), after
viruses infections,
neurocirculative
dystonia
ECG: sinus rhythm,
difference
between the
shortest R-R and
longest R-R >0,15
sec
 Heterotopic rhythms
Tardy (slowly) 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
accelerated ectopic rhythm
Unparoxismal tachycardia
Source:
atrium, AV node , ventricle
ECG:
-HR 90-130/min
- progressive beginning and
finishing
- regular ventricle rhythm
 Heterotopic rhythms
Migration of supraventricular pacemaker
Gradual removal
of pacemaker
from SA node to
AV node
ECG:
P wave
configuration
violation Change
of P-Q duration
Arrhythmia
 Conduction violations
heart block pre-excitation
ventricular
- Sinus atrial syndrome
- (or SA node arrest)

1. WPW syndrome
- Intra Atrial
(Kent bundle)

- Atrial-ventricular
2. CLC syndrome
(James bundle)
- ventricular
 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 (two waved)
 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 1 degree

ECG :
PQ>0,2 sec
 Conduction violations
АV-block 2 degree
* Mobitz type I (period of 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
Complete AV block
 Conduction violations
АV block
Stokes-Adams’s syndrome
Reasons:
- long time asystole (more than 10-20 seс) (occurs 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
Giss’s bundle left branche
block
 Conduction violations
Pre-excitation syndrome
WPW (Wolff-Parkinson-White) syndrome
Reason: additional Kent’s bungle (impulses don’t transmit 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 localized dyscordly, pre-excitation of the ventricles

wave
WPW (Wolff-Parkinson-
White) syndrome
 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 (atrial)

ECG signs:
Р deformation
 Extrasistole (from AV node)

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)
Paroxysmal tachycardia
(ventricle)
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 contractions
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
Flutter – frequent (200-300/min) regular excitation and contraction of the
ventricles because impulses from ectopic driver circulates constantly (“re-
entry”)
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
Premature Ventricular
Contractions
Premature Atrial Contractions
Junctional rhythms

Accelerated junctional rhythms

Thank you for attention !