Arrhythmias Flashcards
How are arryhthmias named?
From the chamber were they originate and from the mechanism
what does the term supraventricular mean
the origin of the arrhythmia is above the ventricle, atria or AV node
What does the term ventricular mean?
The origin of the arrhythmia is in the ventricle (ventricular muscle or fascicles)
What is a ectopic beat?
a beat which originates outside of the conduction pathway and competes with the normal beat
What causes an ectopic beat to take over from sinus rhythm as the main beat?
If the ectopic beat is faster than the sinus rhythm
What is the most common mechanism of arrhythmia?
Re-entry arrhythmias
What are the symptoms of arrhythmias?
Palpitations, ”pounding heart” Shortness of breath Dizziness Loss of consciousness; ”Syncope” Faintness: “presyncope” Sudden cardiac death Angina, heart failure
what happens in defibrillation?
electrical current is delivered across the heart straight away
What happens in direct current cardioversion (DCCV)?
The electrical current waits until the QRS complex to shock the patient
If there is patient is stable and has VT what do you do?
anaesthetise them to then deliver DCCV
What is one of the benefits of ICDs over defibrillation or DCCV?
that it is not painful
what is the most common arrhytmia?
Atrial Fibrillation
What is a cardiac arrhythmia?
disturbances of heart rate, or rhythm (regularity of beats) – can be caused by changes in impulse formation, or impulse conduction
How are arrhythmias clinically described?
In terms of rate - bradycardias (HR < 60 bpm in the day < 50 bpm at night) tachycardias (HR > 100 bpm) in terms of site of origin supraventricular (atria & AV node) ventricular
What is involved in alterations in impulse formation?
- changes in automaticity
- triggered activity
What causes abnormalities in impulse conduction to arise?
re-entry
conduction block
accessory tracts
How are pacemaker potentials in the heart fired in each node?
Each node possesses automaticity and will fire a action potential if not being suppressed
The SA node (70-80 bpm) usually dominates over the latent pacemakers such as the AV node (50-60 bpm) and the Purkinje fibres (30-40 bpm) due to override suppression
For the SA node to be in control it needs to discharge action potentials at a regular frequency greater than any other structure in the heart
What drugs might cause DADs?
those which increase Ca2+ influx or Ca2+ release from the sarcoplasmic reticulum e.g. catecholamines or digoxin
What ensures that the SA node’s pacemaking it relied upon over the other latent pacemakers within the heart?
It has the highest rate and is dominant over the other latent pacemakes such as the AV node and Purkinje fibres (30-40 bpm)
- it must discharge action potentials at a regular frequency greater than any other structure within the heart
What can happen if the SA node firing is pathologically low?
there can be an escape beat initiated by a latent pacemaker - potentially give rise to an escape rhythm
What can happen id a latent pacemaker fires at an intrinsic rate faster than the SA node?
an ectopic beat or ectopic rhythm
can be a result of ischaemia, hypokalaemia, increased sympathetic activity, fibre stretch and other causes
In what way can there be loss of overdrive suppression from the AV node in response to tissue damage (MI)?
even the non-pacemaker cells when partially depolarised may assume spontaneous activity
What is an afterpolarisation?
an abnormal oscillation in action potential - if the amplitude is sufficient to reach threshold it can cause premature APs and beats
What is an early afterpolarisation EAD?
occurs during the inciting AP either in phase 2 - mediated by Ca2+ channels when Na+ channels are still inactivated or in phase 3 - mediated by Na+ channels (when partial recovery of Na+ channels from inactivation has occurred)
What are the risk factors of EADs?
- HR is slow
- occur in Purkinje fibres
- associated with prolongation of the AP and drugs prolonging the QT interval
- can lead to torsades de pointes if sustained
What is an delayed afterpolarisations (DADs)
- occur after complete repolarisation
- caused by a large increase in Ca2+
- excessive [Ca2+]i results in
oscillatory release of Ca2+ from the sarcoplasmic reticulum (SR)
a transient inward current (Iti, involving Na+-influx) that occurs in phase 4
What are the risk factors of DADs?
- when HR is fast
- increased in incidence by prolongation of the AP by drugs
- decreased in incidence by prolongation of the AP by drugs
- triggered by drugs that increase Ca2+ influx (e.g. catecholamines), or release, from the SR (e.g. digoxin)
What is re-entry?
When there is a unidirectional block anterograde conduction is prohibited and retrograde conduction is allowed
What are the different types of heart block?
1st degree - long PR interval
2nd degree - Mobitz type 1 & mobitz type 2
3rd degree - complete heart block
What is mobitz type 1?
PR interval gradually increases from cycle to cycle until AV node fails completely and a ventricular beat is missed
what is mobitz type 2?
PR interval is constant but every nth. ventricular depolarization is missing
What is the significance of conduction pathways parallel to the AV node?
A common example is the bundle of Kent
impulse through bundle of Kent is conducted more quickly than that through the AV node
ventricles receive impulses from both the normal and accessory pathways – can set up the condition for a re-entrant loop predisposing to tachyarrhythmias
What drugs would be used for treatment of atria arrhymias?
Classes 1C and III
What drugs would be used for treatment of ventricle arrhymias?
Classes 1A, 1B, II
What drugs would be used for treatment of AV node arrhymias?
Adenosine
digoxin
classes II, IV
What drugs would be used for treatment of atria and ventricles accessory pathways arrhymias?
amiodarone
sotalol
classes 1A, 1C
