Pathophysiology of Arrhythmias Flashcards
What are the important things to note about the conducting tissue of the heart?
- the material between the atria and ventricles on both sides are known as the AV rings and do not conduct electricity
- the only way electricity travels from atria to ventricles is through the AV node
What are the types of bradycardias?`
- sinus bradycardia
- AV block
What can cause sinus bradycardia?
- drugs (b-blockers, diltiazem)
- vagal activity
- hypothyroidism
- sinus node disease
- electrolyte abnormalities
What can cause AV block?
- vagal activity
- MI
- electrolyte abnormalities
What are the types of AV block?
- 1st degree: long PR interval
- 2nd degree Mobitz type 1: progressive lengthening of PR interval until P wave blocked and it resets
- 2nd degree Mobitz type 2: block after 2 or 3 conducted beats in regular pattern
- 3rd degree: complete AV dissociation
What are the classes of tachycardias?
- narrow complex/supraventricular tachycardias
- broad complex tachycardias/ventricular
What are the different types of narrow complex tachycardias?
- atrial tachycardias
- junctional tachycardias
- AVNRT
- AVRT
- atrial flutter
- atrial fibrillation
What are the types of broad complex tachycardias?
- SVT with rate-dependent bundle-branch block
- SVT with pre-existing bundle-branch block morphology on ECG
What are the different mechanisms of tachycardias?
- ectopic focus (tissue with pacemaker function)
- re-entry/circus movement
- fibrillation (independent wavelets of activity)
Describe circus movement
- conduction coming down through cardiac tissue meets an island of non-conducting cells
- the impulse can go one way or the other around the island
- if a critically timed ectopic beat travels down through the cardiac tissue, one of the limbs may be refractory so it can only go down one way
- by the time it has gone around the island, the limb is no longer refractory and so it can travel backwards
- this can keep going and going
What is AVNRT?
- AV nodal re-entrant tachycardia
- tachycardia where re-entry circuit is through juxtanodal material
What is AVRT?
- AV re-entrant tachycardia
- tachycardia where re-entry is through an accessory pathway
What terminates tachycardias?
adenosine
Describe Wolff-Parkinson-White Syndrome?
- pre-excitation of the ventricles
- presence of anatomical atrio-ventricular bypass tract
- shortened PR interval and wide QRS
- forms basis for circus movement and AVRT
Describe the adenosine test in narrow complex tacycardias
- bolus of adenosine given and wait for response
- if no effect: wrong diagnosis (sinus tachycardia if narrow complex, VT if broad complex)
- transient slowing with p waves: atrial flutter/tachycardia
- transient slowing without p waves: AF
- restoration of sinus rhythm: AVNRT/AVRT
What is atrial fibrillation and the symptoms of this?
- irregular narrow complex tachycardia with no p waves
symptoms:
- SOB, hypotension
- dizziness and syncope
- embolism of left atrial thrombus
in AF you would use drugs to control the HR unless what?
- the patient is symptomatic with high ventricular response rates refractory to treatment
- the patient has acute presentation with a clear precipitating cause
What are the rate control treatments for AF?
Drugs that slow AV conduction:
- diltiazem
- verapamil
- b-blockers
- digoxin
AV node ablation and permanent pacemaker
What are the rhythm control treatments of AF?
cardioversion:
- electrical DC cardioversion
- chemical (flecainide, propafanone, amiodarone)
maintenance of sinus rhythm:
- class 3 sotalol, amiodarone
- class 1c flecainide
How to distinct between VT/SVT
- if history of LV damage it will be VT
- if right bundle-branch block its SVT
How would you treat VT?
Acute:
- DC synchronised cardioversion
- amiodarone
- lignocaine
then manage underlying cause and prevent it recurring (implanted cardioverter defribrillator/anti-tachycardia pacemaker/b-blockers)
What are the mechanisms of ventricular tachycardia?
- acute LV damage (ischaemia)
- chronic LV damage (re-entry through fibrotic areas of non-conduction)
- abnormalities in Na and K channels (long QT) polymorphic
What is torsade de Pointes?
abnormal heart rhythm that can cause sudden death
What are the mechanisms of torsade de pointes?
congenital:
- ion channelopathy
- catecholaminergic polymorphic VT
- plus provocation
acquired:
- drugs that inhbit inward rectifying K channel (antihistamines/erythromycin)
- drugs that lengthen QT interval (amiodarone/sotalol)
