Download Arrhythmias.25.Feb.2011

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the work of artificial intelligence, which forms the content of this project

Document related concepts
no text concepts found
Transcript
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
Internodal
pathways
Left
bundle
branch
Right
bundle
branch
Purkinje
fibers
The effect of autonomic nervous system
sympathetic
parasympathetic
heart rate (chronotropic)
b1 increases
decreases
contractility (inotropic)
b1 increases
decreases
conduction in AV node
(dromotropic)
b1 increases
decreases
increases
decreases
excitability (bathmotropic)
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 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
threshold membrane potential
Faster spontaneous depolarization
(catecholamines)
More rapid slope of spontaneous depolarization
(SA) or resting potential (e.g. ventricular cells)
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
Triggerd activity
Characterization: abnormal phase of repolarization in the previous
impuls leads to earlier new depolarization
2 types:
Early afterdepolarization


New depolarization appears in phase 3 of
previous action potential
Cause: slower repolarization – e.g. because of
hypokaliemia
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+, 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
Related documents