Arrhythmias Flashcards
An arrhythmia is described as
- a disturbance in the rate and rhythm of the heart beat
- tacky-decreased R-R
- Brady- increased R-R
- irregular - irregular R-R intervals
Arrhythmias are caused by?
- due to changes or losses of electrical integrity
- genetic origin (ion channelopathy)
- hyperT, obesity, off target drug effects
supraventricular Arrhythmias occur?
originate higher up the conduction route than the V
* Sinus bradycardia * Sinus tachycardia * Atrial tachycardia * Atrial Fibrillation * AV block
ventricular Arrhythmias occur?
originate in the V
• Ventricular premature beats
• Ventricular tachycardia
• Ventricular fibrillation
how can they be classified by the mechanism ?
- emergence of triggered ectopic activity (automaticity)
- Delayed after depolarisations
- early after depolarisations
disturbances in conduction can occur by?
- AVN conduction block
- re-entry circuit formation
ectopic activity is usually seen at?
- the posterior left atrial wall near the region of the pulmonary vein entrance
- one or multiple sites in the heart start to generate their own electrical activity
- Spontaneous action potential generation in sites other than the SAN
DADs are
- inappropriate depolarisation during a diastolic interval
- opening of sufficient Na channels
- triggering of AP during diastolic
DADs are caused by?
- cellular overload of ca swamps SR with Ca
- phasic oscillatory phase is the release of ca from the SR via RyR2 channels
- oscillatory depolarisation inwards current via NXC channels (na Influx)
- Ca removal via NXC leading to accumulation of +1 charge due to Na influx
EADs are caused by
- reduced K efflux during repolarisation phase due to defective ion channel
- prolongation of Q-T interval
- prolongation of ADP
- prolongation of ADP allows enough time for L-T channels to recover and reactivate
what causes drug induced EADs?
- HERG channel is a depolarising channel
- drug enters and blocks channel
- prolonged repol
- one or more triggered beat
- cause torsades and de pointes
what causes AVN conduction block?
- reduced or blocked conduction through AVN
- slowing of propagation through AVN
- prolonged P-R interval
- may miss some QRS complex after P-wave
- complete lack of association between P/ QRS waves
what is re-entry circuit formation ?
is the establishment of one or multiple self sustaining circuits within the heart
- macro
- micro
- can obtain multiple in tje same LA
- can lead to unidirectional conduction block
what determines the probability of forming a re-entry circuit?
- directed related to wavelength
shorter WL = increased likelihood
ADP determines what ?
- the rate of Na channel recovery and therefore RP length
increased susceptibility to arrhythmia arises when?
- ERP is shorter
- CV is lower
a shorter ADP ?
- increases K current and decreases inward Ca current
- more rapid return to RMP
- Na channels recover quicker
- shorter RP
- increased risk of circuit
Drugs that prolong ADP work by?
- blocking VG Na channels
- fewer available Na channels requires cell to reach a higher vT
- fewer channels prolongs the ERP (APD)
- protective
- can lead to EADs
slowing CV is observed as what on an ECG?
- V conduction ,observed as increase in QRS complex duration
- atrial conduction, observed as increase in P-wave duration or P-R interval
what happens if depolarising current is reduced ?
- fewer Na channels available
- smaller charge gradient established
- due to a lower AP magnitude
= lower amplitude - increases risk of developing a re-entry circuit
the amplitude of the AP depends on?
- number of available Na channels
speed of which a return to negative RMP is controlled by?
the duration of the APD
