Arrhythmias

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Arrhythmias

description

Arrhythmias. Cardiac dysrhythmia. Cardiac dysrhythmia (arrhytmia) Abnormal electrical activity in the heart. Electrical conduction system of the heart. Sinus node. AV node. Bundle of His. Left bundle branch. Internodal pathways. Right bundle branch. Purkinje fibers. - PowerPoint PPT Presentation

Transcript of Arrhythmias

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Arrhythmias

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Cardiac dysrhythmia

Cardiac dysrhythmia (arrhytmia) Abnormal electrical activity in the heart

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Electrical conduction system of the heart

Sinus node

Internodal pathways

AV node

Bundle of His

Right bundle branch

Left bundle branch

Purkinje fibers

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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

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Cardiac action potential

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Phase 4 Phase 4

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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

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SA node action potential

Phase 4

spontaneous diastolic depolarisation

Ca2+ channels

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ECG

P wave – atrial depolarisationPR segment – delay in the AV nodeQRS complex – ventricular depolarisationT wave – ventricular repolarisation

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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

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Mechanisms of arrythmias

Increased automaticity

– Increased normal automaticity (in SA node)

– Abnormal automaticity (ectopic focus)

Triggerd activity

– Early afterdepolarization

– Delayed afterdepolarization

Reentry

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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)

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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

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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)

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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)

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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

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Signs

Electrical

– Changes in the ECG Haemodynamic

– Decreased preload

– Decreased minute heart output Clinical

– Syncope

– Palpitation

– Sudden cardiac death

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Classification Mechanism

– Disorders of impulse generation– Disorders of impulse conduction– Combined

Site of origin– Supraventricular

• Sinus• Atrial• Junctional

– Ventricular Rate

– Tachycardia– Bradycardia

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Disorders of impulse generation

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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...

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Sinus arrhytmias Premature sinus contraction (Sinus extra beat) Sinus arrhytmia

– physiological – breathing Sick sinus syndrome

– inherited

– coronary artery disease

– hypertension

– idiopathic Sinus arrest

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Atrial arrhytmias Premature atrial contraction (extra beat)

Atrial rhythm Atrial (supraventricular) tachycardia Atrial flutter

Atrial fibrilation

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Junctional arrhytmias

Premature junctional contraction (extra beat) Junctional rhythm

Junctional (supraventricular) tachycardia

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Ventricular arrhytmias Premature ventricular contraction (extra beat)

Accelerated idioventricular rhythm Ventricular tachycardia

Polymorphic ventricular tachycardia Ventricular fibrilation

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Disorders of impulse conduction

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Heart blocks (AV blocks) 1st degree

2nd degree

– type 1 (Mobitz I, Wenckenbach)

– type 2 (Mobitz II)

3rd degree

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Left bundle branch block

Right bundle branch block

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Wolff-Parkinson-White syndrome