Arrhythmias. Cardiac dysrhythmia Cardiac dysrhythmia (arrhytmia) Abnormal electrical activity in the heart.

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Presentation transcript:

Arrhythmias

Cardiac dysrhythmia Cardiac dysrhythmia (arrhytmia) Abnormal electrical activity in the heart

Electrical conduction system of the heart Sinus node Internodal pathways AV node Bundle of His Right bundle branch Left bundle branch Purkinje fibers

The effect of autonomic nervous system sympathetic parasympathetic heart rate (chronotropic)  1 increases decreases contractility (inotropic)  1 increases decreases conduction in AV node  1 increases decreases (dromotropic) excitability (bathmotropic) increases decreases

Cardiac action potential

Phase 4

Phases of the cardiac action potential Phase 0 – rapid depolarization phase - Na + channels Phase 1 – K + and Cl - channels Phase 2 – „plateau“ - Ca 2+ channels Phase 3 – rapid repolarisation - K + channels Phase 4 – resting potential (diastole) - K + channels, 3Na + -2K + -ATPase, Ca 2+ -ATPase, 3Na + -1Ca 2+ -exchager

SA node action potential Phase 4 spontaneous diastolic depolarisation Ca 2+ channels

ECG P wave – atrial depolarisation PR segment – delay in the AV node QRS complex – ventricular depolarisation T wave – ventricular repolarisation

Ethiology Ischaemia, acidosis – coronary artery disease Ion disbalance – hypo-/hyperkalemia... Heart diseases – myocarditis, cardiomyopathies Autonomic nervous system dysbalance Thyroid diseases – hypo-/hyperthyreosis Toxins and drugs – caffeine, digitalis Other diseases – anaemia Genetic mutation Age

Mechanisms of arrythmias Increased automaticity –Increased normal automaticity (in SA node) –Abnormal automaticity (ectopic focus) Triggerd activity –Early afterdepolarization –Delayed afterdepolarization Reentry

Increased automaticity Increased automaticity - classification –Increased normal automaticity (in SA node) –Abnormal automaticity (ectopic focus) Automaticity –ability to generate impuls Increased normal automaticity– hyperirritability of SA node – faster activation of SA node Abnormal automaticity (ectopic focus) – hyperirritability of other myocardial cells (e.g. ventricular cells)

Mechanisms Increased resting membrane potential (ischemia – lower activity of Na/K-ATPase)  resting potential leads to earlier threshold membrane potential Decreased threshold membrane potential = earlier threshold membrane potential Faster spontaneous depolarization (catecholamines) More rapid slope of spontaneous depolarization (SA) or resting potential (e.g. ventricular cells) threshold membrane potential

Triggerd activity 2 types: Early afterdepolarization New depolarization appears in phase 3 of previous action potential Cause: slower repolarization – e.g. because of hypokaliemia Characterization: abnormal phase of repolarization in the previous impuls leads to earlier new depolarization Delayed afterdepolarization New depolarization appears in phase 4 of previous action potential but sooner than normal Cause:  intracellular Ca concentration (digitalis)

Reentry Circulation of the impulse Possible mechanisms Shorter refractory period 2 places in the heart are connected with 2 ways for impulse. In the case of blocade of one way (extra beat, scar) – impulse is conducted by one way, returns by the second one and starts circulate The way for impulse is longer than refractory period (hyperthrophy) Atrioventricular reentry impulse returns through accessory pathway (WPW syndrome)

Inherited arrhytmias Long QT syndrome Mutations (AD) of ion channels (K +, Na +, Ca 2+ ) genes Ventricular extra beats, ventricular tachycardia Unconsciousness, synkope, ventricular fibrilation, sudden death SADH – sudden arrhytmia death syndrome

Signs Electrical –Changes in the ECG Haemodynamic –Decreased preload –Decreased minute heart output Clinical –Syncope –Palpitation –Sudden cardiac death

Classification Mechanism –Disorders of impulse generation –Disorders of impulse conduction –Combined Site of origin –Supraventricular Sinus Atrial Junctional –Ventricular Rate –Tachycardia –Bradycardia

Disorders of impulse generation

Sinus arrhytmias Sinus tachycardia –rate > 100 bites/min. (normal 60 – 100bites/min.) –physiological – newborns and children, physical activity, stress –drugs – catecholamines –diseases – hyperthyreosis, anaemia... Sinus bradycardia –rate < 60 bites/min. –physiological – sportsmen –diseases – hypothyreosis...

Sinus arrhytmias Premature sinus contraction (Sinus extra beat) Sinus arrhytmia –physiological – breathing Sick sinus syndrome –inherited –coronary artery disease –hypertension –idiopathic Sinus arrest

Atrial arrhytmias Premature atrial contraction (extra beat) Atrial rhythm Atrial (supraventricular) tachycardia Atrial flutter Atrial fibrilation

Junctional arrhytmias Premature junctional contraction (extra beat) Junctional rhythm Junctional (supraventricular) tachycardia

Ventricular arrhytmias Premature ventricular contraction (extra beat) Accelerated idioventricular rhythm Ventricular tachycardia Polymorphic ventricular tachycardia Ventricular fibrilation

Disorders of impulse conduction

Heart blocks (AV blocks) 1 st degree 2 nd degree –type 1 (Mobitz I, Wenckenbach) –type 2 (Mobitz II) 3 rd degree

Left bundle branch block Right bundle branch block

Wolff-Parkinson-White syndrome