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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) 100 80 60 40 20 0 1 11 21 31 41 51 -20 -40 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) 100 80 60 40 20 0 1 11 21 31 41 51 -20 -40 ТМПП ТМПД ТМПП 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 s 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 !