Arrhythmias and Anti-arrhythmics Flashcards
How long does it typically take for an AP to propagate from the AVN to myocytes?
0.2s
What is the funny current?
current activated by hyperpolarisation
sends K out and Na in
causes depolarisation
Upon sufficient depolarisation in the SAN, which calcium current activates?
ICaT
Which calcium current generates the AP upstroke in the SAN?
ICaL
What is the Calcium Clock?
- the spontaneous release of calcium from from areas of the SR just below the cell membrane
- contribute to the initiation of the upstroke of the AP in the SAN
What K currents are involved with the repolarisation in the SAN?
IKir and IKs and IKach
What is the role of ICNX at RMP in the SAN?
3Na in for Ca out…depolarising influence - reverses at peak of AP
How is the membrane potential stabilised in the Ventricular myocytes during diastole?
Kir
Which sodium channels mediate the upstroke in the ventricular AP?
Nav1.5
what is the notch in the ventricular AP caused by?
simultaneous inactivation of N and opening of rapid activating K channels
What does the P wave in the ECG symbolise?
atrial depolarisation
What does the QRS complex in the ECG symbolised?
rapid ventricular depolarisation
What does the T wave represent in the ECG?
ventricular repolarisation
How is current transmitted between cardiac muscle cells?
gap junctions
What would be considered a normal cardiac electrical vector direction?
5o’clock (anything between 3-7o’clock)
When measuring the ECG, which vector provides the best recording method?
RA ->LL
How long should a p-wave last?
0.08-0.15s
How long should the Q-T interval be?
~300ms
Why is the P wave an upward deflection?
the current is moving in the direction of the recording electrode
Why is the Q a downward deflection?
L->R depolarisation of the intraventricular septum moving towards 7/8 o’clock away from recording electrode
Why is the R an upward deflection?
ventricles depolarise towards the recording electrode
Why is the T wave an upward deflection?
repolarisation from out to in
2 negs make a positive so upstroke
Which other feature do some individuals have on their ECG?
a U wave (purkinje fibre repolarisation)
What are the potential disruptions to electrical function of the heart?
defects in impulse formation - altered automaticity
defects in impulse conduction - re-entrant arrhythmias
what usually controls automaticity in the heart?
ANS
what can happen in altered automaticity?
a latent pacemaker subverts the SAN function and overdrive suppression is lost
When may altered automaticity occur?
- if the firing frequency of the SAN is low or conduction is impaired
- if the latent pacemaker fires at a rate faster than the SAN
What may occur if the SAN firing frequency is low?
escape beats - latent pacemaker forms the impulse
escape rhythms - series of escape beats
What may occur if the latent pacemaker fires faster than the SAN?
ectopic beats
ectopic rhythm
What make cause an ectopic rhythm?
ischemia, hypokalaemia, fibre stretch
What is triggered activity?
afterdepolarisations triggered by a normal AP
EAD or DAD
When does an EAD occur?
Phase 2 terminal plateau
Phase 3 repolarisation
What causes EAD during phase 2?
Ca Channels
What causes EAD during phase 3?
Na channels
What are EADs associated with?
prolongation of the AP
When does a DAD occur?
after a complete repolarisation
What is a DAD associated with?
Ca overload, provoked by catecholamines, digoxin and HF
What is a DAD caused by?
a transient inward Na Current
What can several ectopic rhythms lead to?
VF
How is VF different to tachycardia?
VF doesnt allow blood to be pumped from the ventricles
What can sustained EADs lead to?
torsades de pointes - twisting of the QRS complexes
What are re-entry arrhythmias?
self-sustaining electrical stimulations that stimulate an area of myocardium repeatedly and rapidly
What is required for a re-entrant circuit?
unidirectional block and slow retrograde conduction velocity
What are the potential types of conduction block?
Partial
Intermittent
Complete
What happens in partial block?
the tissue conducts all impulses however more slowly than usual - first degree block
What are the forms of intermittent block?
Mobitz type I
Mobitz type 2
What happens in mobitz type I?
PR interval gradually increases from cycle to cycle until a beat is missed
What happens in mobitz type II?
PR interval normal but every ‘n’ th beat is missed
What happens in complete block?
no impulses are conducted through the affected area and the atria and ventricles beat independently
bradycardia and low CO are signs
What can happen with accessory tract pathways?
pathways that bypass the AVN and set up conditions for re-entrant loops - Wolf-Parkinson-White Syndrom
What is a common accessory pathway?
Bundle of Kent
What system is used to classify anti-arrhythmics?
Vaugn-Williams Classification
Which drugs do not fit into the V-W classification
adenosine and digoxin
What describes Class 1A?
Na channel affected
associate and dissociate at a moderate rate
slow the rise of the AP and prolong the refractory period
Give an example of a class I A drug
disopyramide
How is class IB descibed?
Na channel
associate and dissociate at a rapid rate
prevents premature beats
binds preferentially to inactive state
What is the advantage of Class IB?
doesn’t affect normal myocardium
How is class IC described?
Na channel
slow association and dissociation
Give an example of class IB?
lignocaine
Give an example of class IC?
flecainide
What do class II drugs target?
b-adrenoceptors
antagonists
How do Class II drugs act?
to decrease the rate of depolarisation in SA and AV nodes
How do Class III drugs act?
prolong the AP increasing the refractory period
How do Class IV drugs act?
slow conduction in SAN or AVN decreasing force of contraction
Which ion channels do Class III drugs affect?
Kv
Which ion channels do Class IV drugs affect?
Ca
Give an example of a class III drug
Amiodarone
Give an example of a class IV drug
Verapamil
Where do classI drugs primarily act?
the muscle not the nodes
How do class I agents block Nav channels?
by use-dependent block
What mechanism do class I agents block the Na channels?
stabilising the inactive state
When do class I agents dissociate from Na channels?
in the resting state
What are the differences in how class I A B and C affect the AP?
A - moderately blocks and prolongs the repolarisation
B - mildly blocks and shortens repolarisation
C - markedly blocks but not much effect on repolarisation
Which drugs are using to control the rate of SVT in the atria?
Class IC and III
Which drugs are used to target the ventricles?
Class IA, IB and II
Which drugs target the rhythm of the SVT in the AVN?
Class II, Class IV, digoxin and adenosine
Which drugs target the atria, ventricles and accessory pathways?
Amiodarone, Class IA, IC
