Mechanisms of cardiac arrhythmias Flashcards
What causes cardiac arrhythmia?
they result from disturbances in impulse formation or impulse conduction (or both) Some mechs: -altered automaticity -re-entry of excitation -triggered activity
What is altered automaticity?
normal pacemaker gone haywire
e.g. tachycardia or bradycardia
What are some possible causes of tachycardia?
- NE (sympathetics)
- stimulants
- ischemia- current of injury
- ventricular aneurysm (stretching)- open stretch activ channels
- sick sinus syndrom
- fever
- hyperthyroidism (enhance latent pacemakers)
- hypokalemia (membr less permeable to K so less flows out = more positive max diastolic potential)
How would you see tachycardia on an EKG?
- sinus tachy: normal just faster
- premature atrial contraction
- premature ventricular contraction
- atrila or ventricular tachycardia: one of them is faster
- supraventricular tachycardia: both too fast, pacemaker coming somewhere from the atria
What could cause bradycardia arrhythmias?
- drugs: antiarrhytmics, beta blockers (block NE), Ca antagonist, digitalis
- anesthetics
- IM/ischemia
- sick sinus syndrome
- aging: fibrosis- lose pacemaker cells
How does digitalis work?
it increases the rate of contraction so it stimulates the vagus to slow down heart rate
overall: decrease oxygen requirement
What are the requirements for re-entry of excitation?
can occur anywhere in the heart! most common cause of dysrhythmias
- geometry: need to have a loop
- slow or delayed conduction
- unidirectional conduction block
Explain re-entry of excitation
the impulse enters the damaged area which has a more + RMP aka less Na channels available so the impulse is slower
by the time it comes out, the surrounding tissue is ready for another impulse so goes for it
What could cause re-entry of excitation?
ischemia
IM
congenital bypass tracks
What is Wolf-Parkinson-White syndrome?
Patients have a bypass track connecting the RA to RV
-similar histologically to parking cells so rapid conduction and long refractory period
When the impulse comes, it goes through fast bypass and stimulates that part of ventricle
goes through normal path and stimulates the rest
result: prolonged QRS cuz the heart is not contracting all at once
How would you see re-entry of excitation on an EKG?
you would get
- premature atrial or ventricular beats
- supraventricular tachycardia
- atrial flutter: reentry aroudn the atria
- atrial or ventricular fibrillation: chaotic!
What is triggered activity?
can occur in both atrial and ventricular tissues
abnormal!!!!!!!!
spontaneous beats are trigged at inappropriate time =.=
Explain delayed afterdepolarizations (DAD)
why?
digitalis toxicity
elevated catecholamines (NE/Epi)
fast HR
Mech: elevated intracell [Ca]
-taken by the SR and released abnormally after AP ended
taken out of the cell by the exchanger- (1 Ca out, 3 Na in –> net inward current) -> depolarizing
–caused delayed afterdepolarization: if amplitude high enough, can cause an AP for heart
*can generate single early beat or multiple beats (tachy)
How would see an DAD on an EKG?
premature atrial (PAC) or ventricular (PVC) contractions atrial or ventricular tachycardias
What is an early afterdepolarization (EAD)?
spontaneous beat on the RRP of the previous beat
-dev during final phase of repolarization
hit threshold at slower rate
can generate single (R on T) or repetitive triggered AP (tachy)
due to prolongation of AP duration
@ slower HR
mech? not sure but probly abnormal re-activation of slow inward Ca current
can contribute to prolonged Q-T syndrome (prolongs AP)
causes:
acidosis (e.g. ischemia), hypokalemia (lengthen AP), quinidine (antiarrythmic), bradycardia
