CARDTAC DYSRHYTHMIAS

The older term ‘arrhythmia’ should better be replaced by thenew term ‘dysrhythmia’ for obvious reasons. Cardiac  dysrhythmia includes all conditions where the cardiac rate and rhythm are altered or there is defect in the conductive system. Dysrhythmias in relation to rate and rhythm mayhave its origin in the SA node, atrium, AV junction or in
the ventricle Mechanisms of production of dysrhythmia Bradycardia and tachycardia may arise from abnormalities of automaticity arising out of a single cell and disturbances of conduction arising out of interactions between cells. Thus accelerated automaticity, triggered activity and a re-entry phenomenon are main mechanisms for dysrhythmogenesis A. Accelerated automaticity
In this mechanism in the SA node an abnormal pacemaker impulse competes with the normal pacemaker function. This
is seen in sinus tachycardia, escape rhythms and accelerated junctional rhythms. B. Triggered activity Here the oscillations of transmembrane potential develop at
the end of action potential which is due to myocardial injury At times when these oscillations reach the threshold potential
dysrhythmnia is produced. This is usually seen in atrial tachycardia after digitalis toxicity and ventricular dysrhythmias in long QT syndrome C. Re-entry Phenomenon In recent years His bundle electrocardiography has revolutionized our understanding of various types of cardiac dysrhythmias. In fact, it is believed now-a-days that many of the arthythmias occur as a result of re-entry phenomenon. The term re-entry means that the original stimulus re-enters in site of origin which may be located in SA node, Atria, AV node, bundle of His and Purkinje system.

SINUS BRADYCARDIA
When the heart rate is less than 60 beats per minute it is called
sinus bradycardia
Causes
Physiogical
1. During deep sleep.
2. Athletes.
Pathological
1. Viral infection.
2. Obstructive jaundice.
3. Hypothyroidism
4. Carotid sinus syncope.
5. Increased intracranial tension.
6. Sick sinus syndrome.
7. Hypothermia.
8. Myocardial infarction.
9. Gram negative sepsis.
10. Vasovagal fainting attack.
11. Some cases of severe anemia.
12. Aortic stenosis.
13. Mallory Weiss syndrome. Boerhaave’s syndrome
15. Drugs: Digitalis, Betablocker, Calcium Antagonists
(Verapamil, Diltiazem), Amiodarone, Cimetidine, Clonidine.
16. Giant left atrium.concepts in diagnosis and therapy. SUPRAVENTRICULAR TACHYCARDIA
These are of following types:
1. Paroxysmal atrial tachycardia.
2. Re-entrant atrial tachycardia which includes atrial fibrillation and flutter
3. Atrioventricular nodal re-entrant tachycardia (AVNRT) utilising concealed bypass tract. This includes WPW syndrome
4. Multifocal or chaotic atrial tachycardia.
5. AV junctional tachycardia which may be paroxysmal and non-paraxysmal

Wandering Pacemaker in the Sinus node Here there is passive transfer of the predominant pacemakerfocus from the SA-node to another latent pacemaker havingthe next highest automaticity in the atrial musculature or inthe AV junctional tissue. In the ECG there may be a cyclical increase in the R-R interval, gradually shortening PR intervaland change in P-wave configuration. Persistent increased vagal tone may be responsible for it.

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