Flashcards in Pathophysiology of Arrhythmias Deck (17):
what are dysrhythmias? what causes them?
-conditions where the uncoordinated sequence of electrical activity in the heart is disrupted due to:
-changes in heart cells
-changes in conduction of impulses through the heart
what are the classifications of dysrhythmia?
-Junctional (AV node)
what are the types of tachyarrhythmia?
-sustained ventricular tacharrhythmias
what are the 4 general broad categories of event?
-ectopic pacemaker activity
-delayed after depolarisation
how does heart block arise? what is usually affected?
-results from damage, usually ischaemia, to part of the conducting system
what are the 3 types of block which can occur?
-impulses slowed but make it through
-partially blocked so only some impulses make it through
-complete block hence no impulses make it through from atria to ventricles
How are the 3 types of heart block seen on an ECG trace?
1st- abnormally long PR interval
2nd- 2:1 or 3:1 describing the ratio of P waves to QRS complexes
3rd- atria depolarise at inherent rate, ventricles depolarise at inherent rate= no match up between P waves and QRS complexes
what are the subtypes of 2nd degree heart block?
Mobitz 2- most beats coordinated with constant PR interval but occasionally there is an atrial depolarisation without ventricular depolarisation
Wenkebach (Mobitz 1)- progressive lengthening of PR interval until P wave fails to produce a QRS complex then PR interval restarts and shortens back to normal
what can stimulate other areas of the heart than the SA node to develop pacemaker activity?
-damage by ischaemia, CHD, rheumatic heart disease
-increased sympathetic activity
-increased sensitivity to catecholamines
-cardiac glycoside toxicity
how does pacemaker activity arise from ischaemic damage?
causes cells to become leaky to Na and develop a funny current
how does increased sensitivity to catecholamines lead to ectopic pacemaker activity?
act on B receptors increase rate of depolarisation and cause pacemaker activity to arise from cells which are normally quiescent
what is early after depolarisation? at what stage does it occur? how is it seen on ECG?
-end of phase 2
-prolonged QT interval
-fluctuating increase in calcium permeability which can lead to setting of self sustaining depolarisations
describe the features of delayed after depolarisations.
-following every action potential some of the calcium entering phase 2 needs to be removed back into ECF by sodium calcium exchanger
-if intracellular Ca rises after depolarisations can get longer and become self perpetrating triggering an action potential
-prolonged QT interval
what is circus re-entry?
when an electrical impulse can re-stimulate a region of the heart after its refractory period has passed
how does circus re-entry arise? mention what normally should happen and what differs in circus re-entry.
-arises from an unusual direction of an impulse (usually L)
-normally impulse from SA node transmitted to branches depolarising them and then other impulses cancel one another out
-however an area of a branch could be dead so impulses can't get through and by the other time the other impulse reaches the area is repolarised
-bigger currents from tissue from other side may have enough strength to be transmitted through dead area
what is Wolf Parkinson White Syndrome? how is it seen on an ECG trace?
-additional electrical connection between atria and ventricles
-there is no AV node in the accessory connection and hence no delay for impulse to pass through hence it reaches ventricle early
-PR interval shortened QRS has early upstroke called delta wave, second part of QRS is normal since normal conduction through AV node catches up