Arrhythmias Flashcards
what is a cardiac arrhythmias?
disturbances to heart rate, or rhythm
what 2 things may cause arrhythmias?
Changees in;
1) impulse formation
2) impulse conduction
how are arrhythmias described? (2)
1) rate
- bradycardia
- tachycardia
2) site of origin
- supra-ventricular (atria & AV node)
- ventricular
alterations in impulse formation can involve what 2 things?
1) changes in auto-maticity
2) triggered activity
abnormalities in impulse conduction arise from what 3 things?
1) re-entry
2) conduction block
3) accessory tracts
what components of the cardiac conduction system demonstrate a spontaneous phase 4 depolarisation & automaticity?
all components of cardiac conduction
what is the fastest pacemaker in the heart?
SA node (usually 70-80BP M)
what is SA nodes pacemaker ability to be dominate over other ‘latent’ pacemakers known as?
Overdrive suppression
what does the SA node need to discharge in order to exert normal control of rate & rhythm?
= must discharge action potentials at higher, regular frequency than any other structures in the heart
what 2 things may altered automaticity be?
1) physiological
2) patho-physiological
what does pathophysiology mean in the setting of altered automaticity?
when the function of the SA node, as the normal pacemaker, is taken over by another ‘latent pacemaker’ as the result of overdrive suppression
when might SA node lose its overdrive suppression occurs? (2)
1) if SA node firing frequency is pathologically low
2) if conduction of impulse from SA node is impaired
what is an escape beast?
a impulse that is generated by a latent pacemaker
what is an escape rhythm?
= series of ectopic beats
- a run of impulses generated by latent pacemakers
when else might the SA node lose its overdrive suppression?
- if the latent pacemaker fires at an intrinsic rate faster than the SA node rate (even if SA node is functioning normally)
what sort of beats do latent pacemakers initiate?
what do the beasts generate?
= an ECTOPIC BEAT
= ECTOPIC RHYTHM
- ectopic meaning abnormal place or position
when may ectopic rhythms result?
1) ischaemia
2) hypokalaemia
3) increased sympathetic activity
4) fibre stretch
5) others
when else might the SA node lose its overdrive suppression?
in response to tissue damage
- i.e. post myocardial infarction
Yes or No.
can non-pacemaker cells, when partially depolarised, assume spontaneous activity?
Yes
what is after-depolarisations (AD)?
when a normal action potential triggers ABNORMAL oscillations in membrane potentials that occur during or after re-polarisation
If the ADs is of a sufficient amplitude to reach threshold what would it cause?
premature action potentials & beats
what 2 things can after-depolariisation be?
1) early after-depolarisation (EADs)
2) delayed after-depolarisation (DADs)
what might a repeated after-depolarisation cause?
sustained arrhythmia
when would the EADS occur?
during the inciting action potential within;
1) phase 2 - AD mediated Ca2+ channels
2) phase 3 - AD mediated by Na+ channels
when are EADS most likely to occur?
when heart rate is slow
where are after-depolarisations likely tot occur?
Purkinje fibres
what are EADS associated with?
- prolongation of action potential
- drugs prolonging the QT interval
what drug can prolong the QT interval?
sotalol
when would the DADs occur?
after complete re-polarisation
what can cause DADs?
1) large increase in [Ca2+]
= excessive [Ca2+] resulting in;
- oscillatory release of Ca2+ from SR
- transient inward current occurring in phase 4
when are DADs most likely to occur?
when heart rate is fast
how are DADs increased and decreased by?
Increased
= prolongation of duration of action potential by drugs
Decreased
= shortening of duration of action potential by drugs
when else may DADs bee triggered?
1) by drugs that increase Ca2+, e.g. catecholamines
2) or release, from SR, digoxin
RECAP;
- what 3 things can cause defects in impulse conduction?
1) re-entry
2) conduction block
3) accessory blocks
what is re-entry?
when an action potential goes through one area of the myocardium that then re-enters that area of the myocardium and re-activates it in a way that is separate to the SA node
what is re-entry - textbook definition?
= self sustaining electrical circuit stimulating an area of myocardium repeated/rapidly
what does the re-entrant circuit require?
1) unidirectional block
- anterograde conduction prohibited
- retrograde conduction allowed
2) slowed retrograde conduction velocity
if the conduction goes in the wrong direction, what is it called?
retrograde direction
what is the conduction block ‘done’ through?
AV node
what 2 things can a conduction block be?
1) partial (incomplete)
2) complete
if there is a partial conduction block, what happens?
give an example…
= slowed conduction
e.g. First degree AV block
in a partial conduction block and slowed conduction does the tissue conduct all impulses?
yes - tissue conducts all impulses but just more slowly than usual
in an intermittent block, party of the partial block, does the tissue conducts all impulses?
give an example..
no - the tissue conducts only some impulses but not others.
e.g. Second degree AV block
what are the 2 types of intermittent blocks?
1) Mobitz type I
2) mobitz hype II
what happens to the PR interval in Mobitz type I?
PR interval increases from cycle two cycle until AV node fails & ventricular beat is missed
what happens to the PR interval inn Mobitz type II?
PR interval is constant but with every nth = ventricular de-polarisation is missing
in a complete block, are any impulses conducted through he affected area?
give an example…
= no impulses are conducted through the affected area
= third degree AV node
describe how the atria & ventricles beat in a complete conduction?
atria & ventricles beat independently
wha is the ventricular pacemaker now?
Purkinje fibres
- fire slowly & unreliably
= bradycardia & low cardiac output
what are accessory tract pathways?
when some individuals possess electrical pathways in parallel to the AV node
what is a common accessory tract pathway?
bundle of kent
Are impulse conduced through a bundle of Kent faster or slower than if they were conducted by AV node?
Faser
what do ventricles do to set up the conduction for a re-entratn loop predisposing to tachyarrhytmias?
- ventricles receive impulses from both normal & accessory pathways
what do anti-arrhythmic drugs generally do?
inhibit specific ions channels (or activate/block specific receptors) with the intention of suppressing abnormal electrical activity
how are anti-arrhythmic drugs classified?
by their effect on cardiac action potential
how are anti-arrhythmic drugs classified according to the Vaughn Williams classification?
Four classes;
I, II, III & IV
Class one can be sub-divided into Ia, Ib & Ic
Yes or No.
are all anti-arrhythmic agents selective blockers of Na+, K+ or Ca2+ channels?
No - some block more than one channel type
an example of drug blocking more than 1 channel type.
amiodarone
what do class IA, IB & IC drugs target? give examples of each
voltage activation Na+ channels
Class IA = Disopyramide
Class IB = Lignocaine
Class IC = Flecainide
what do class II drugs do? give an example?
= B-adrenoceptor (as antagonist)
e.g. metoprolol
what do class III drugs do? give an example?
= voltage activated K+ channels
e.g. amiodarone
what do class IV drugs do? give an example?
= voltage activated Ca2+ channels
e.g. verapamil
what do class IA drugs do?
associate & dissociate from Na+ channels at a moderate rate.
- slow rate of rise of AP & prolong refractory period
what do class IB drugs do?
associate with and dissociate from NA+ channels at a rapid rate.
- prevents premature beats
what do class IC drugs do?
associate with and dissociate from Na+ channels at a slow rate.
- depress conduction
what do class II drugs do?
decrease rate of de-polarisation in SA and AV nodes
what do class III drugs do?
prolong AP duration increasing refractory period
what do class IV drugs do?
slow conduction in SA and AV nodes
- decreasing force of cardiac contraction
Class I ages block Na+ channels. In times when there is a high frequency firing, what state are the Na+ channels most likely to be in?
= open & inactivated states
when do class I agents bind preferentially?
bind to targeting areas of the myocardium in which firing FREQUENCY IS HIGHEST (thus when channels are open) in a use-dependent manner without preventing hear form beating at normal frequencies.
when do class I agents dissociate from the Na+ channels?
when it is in the resting stage.
Therefore, what happens too the class I agents performance if heart rate increases?
- less time for unblocking
- more time for blocking
= steady state block increases, particularly for agents with slow dissociation rates
describe what happens in people with ischaemic myocardium?
- myocytes are partially depolarised & action potential is of longer duration thus;
= inactivated state of Na+ channel is available to Na+ channel blockers for longer period
= rathe of channel recovery from blocked is decreased
what feature of Na+ channel blockers allows them to act preferentially on ischaemic tissue and block arrhythmogenic focus at its source?
higher affinity of Na+ channel blockers for open & inactivated states of channel
what classes of drugs are used if the arrhythmia is atrial based?
Class IC & III
what classes of drugs are used if arrhythmia is ventricle based?
Class IA, IB, II
what drugs are used if arrhythmia is AV node based?
- adenosine
- digoxin
Classes II, IV
what drugs are used in atria & ventricles and AV accessory pathways?
- amiodarone
- sotalol
- classes IA, IC
what are the 3 drugs that could be used in supra ventricular arrhythmias?
1) adenosine
2) digoxin
3) verapamil
how does adenosine work?
activates A1 - adenosine receptors coupled to Gi/O
- opens ACh sensitive K+ channels
- hyperpolarizes the AV node, suppressing impulse conduction
- used to terminate paroxysmal supra-ventricular tachycardia caused by re-entry involving AV node, SA node or arial tissue
how does digoxin work?
simulates vagal activity
- slows conduction & prolongs refractory period in AV & bundle of His
- treats atrial fibrillation
- chaotic re-entrant impulse conduction through atrium
how does verapamil work?
blocks L-type volage activation Ca2+ channels
- Slows conduction and prolongs refractory period in AV node and bundle of His
- Used to treat atrial flutter and fibrillation– chaotic re-entrant impulse conduction through the atria that may be conducted via the AV node to the ventricles
Largely replaced by adenosine for acute treatment, still used for prophylaxis
what is a side effect of high does verapamil?
may cause heart block
when should verapamil be used with great caution?
in combination with other drugs that have a negative ionotropic effect
what drugs is used to treat ventricle arrhythmias?
Lignocaine
what does Lignocaine do?
rapid block of voltage activated Na+ channels
- Blocks inactivated channels with little effect on open channels
- Due to rapid unblocking primarily affects Na+ channels in areas of the myocardium that discharge action potentials at high rate (e.g. an ischaemic zone)
how should lignocaine be administered?
IV
what 4 drugs can be used to treat atrial & ventricular arrhythmias?
1) diso-pyramide & procainamide
2) flecainide
3) propanolol and atenolol
4) amiodarone and sotolol
how does disopyramide and procainamide work?
moderate the rate of block & unblock of voltage activated Na+ channels
how should disopyramide and procainimide be administered and why?
Disopyramide = orally
- prevent recurrent ventricular arrhythmias
Procainamide = IV
- treat ventricular arrhythmias following MI
what does flecainide do?
slows rate of block & unblock of voltage activated Na+ channels
- Strongly depresses conduction in the myocardium and reduces contractility
when is flecainide mainly used?
for prophylaxis of paroxysmal atrial fibrillation
what sort of isotropic action does flecainide have?
negative inotropic action
what do propranolol and atenolol do?
control SVT by suppressing impulse conduction through AV node
- suppress excessive sympathetic drive that may trigger VT
what do amiodarone and sotolol do?
slows re-polarisation of AP by block of voltage activated K+ channels & hence increases action potential duration & effective refractory period
- suppress re-enttry
what may some of the side effects of long term use of amiodarone be?
- pulmonary fibrosis
- thyroid disorders
- photosensitivity reactions
- peripheral neuropathy
