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 Phase 4

Phases of the cardiac action potential Phase 0 – rapid depolarization phase - Na+

channels Phase 1 – K+ and Cl- channels Phase 2 – „plateau“ - Ca2+ channels Phase 3 – rapid repolarisation - K+ channels Phase 4 – resting potential (diastole) - K+

channels, 3Na+-2K+-ATPase, Ca2+-ATPase, 3Na+-1Ca2+-exchager

SA node action potential

Phase 4

spontaneous diastolic depolarisation

Ca2+ channels

ECG

P wave – atrial depolarisationPR segment – delay in the AV nodeQRS complex – ventricular depolarisationT 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 afterdepolarizationNew depolarization appears in phase 4 of previous action potential but sooner than normalCause: 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+, Ca2+ ) 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) 1st degree

2nd degree

– type 1 (Mobitz I, Wenckenbach)

– type 2 (Mobitz II)

3rd degree

Left bundle branch block

Right bundle branch block

Wolff-Parkinson-White syndrome