arrythmias Flashcards
what is an arrythmia
abnormal heart rythm
why do arrithmyas happen
interuption to normal electrical signals that coordinate contraction of heart muscle
how can the 4 cardiac arrest rhythms be classified
shockable - defib may be effective
non-shockable
cardiac arrest rhythms: shockable rhythms
ventricular tachycardia
ventricular fibrillation
cardiac arrest rhythms: non-shockable
pulseless electrical activity (all electrical activity except VF/VT, incl sinus rhythm without pulse)
asystole
tachycardia treatment summary: unstable patient
- consider up to 3 synchronised shocks
- consider consider amiodarone infusion
tachycardia treatment summary: stable patient with narrow QRS complex
AF - beta blocker or CCB
atrial flutter - beta blocker
SVT: vagal manouvers, adenosine
tachycardia treatment summary: stable patient w broad QRS
VT or unclear - amiodarone infusion
SVT w bundle branch block - treat as per normal SVT
atrial flutter
caused by a re-enterant rhythm in either atrium
electrical signal re-circulates in a self-perpetuating loop due to extra pathway
signal goes round and round without interuption
atrial flutter: atrial and ventricular bpm
atrial contraction 300bpm
signal makes way to ventricles every 2nd lap due to long AV node refractory period - 150bpm ventricular contraction
atrial flutter: ECG
‘sawtooth appearance’
p wave after p wave
atrial flutter: assoc conditions
htn
IHD
cardiomyopathy
thyrotoxicosis
atrial flutter: Mx
rate/rhythm control - beta blockers or cardioverison
treat underlying condition
radiofrequency ablation of re-enterant system
anticoagulation based on CHADVASC
supraventricular tachycardia
electrical signal re-entering atria from ventricles
- electrical signal finds way back from v to atria
- once signal back in atria it travels back through AV node –> v contraction
- self-perpetuating elec loop
SVT ECG
fast narrow QRS complex tachycardia
looks like QRS complex immediately followed by T wave
paroxysmal SVT
SVT reoccurs and remits in same patient over time
types of SVT: atrioventricular nodal re-enterant tachycardia
when the re-entry point is back through AV node
types of SVT: atrioventricular re-entarent tachycardia
when re-entry point is an accessory pathway (wolf-parkinson-white syndrome)
types of SVT: atrial tachycardia
electircal signal originates in atria somewhere other than SA node
acute management of stable pt w SVT
stepwise approach with cont. ECG monitoring
- valsalva maneouvre
- carotid sinus massage - massage carotid on one side w fingers
- adenosine
- alt to adenosine –> verapamil
- dirrect current cardioversion
adenosine
works by slowing cardiac conduction 1ry through AV nose
interupts AV node/accessory pathway during SVT and ‘resets’ back to sinus rhythm
how is adenosine given
as rapid bolus inot a large proximal cannula to ensure it reaches heart with enough impact to interupt pathway
what happens after initial adenosine administration
often cause breif period of asystole or bradycardia however it is metabolised quickly and sinus rhythm should return
when to avoid adenosine
asthma COPD heart failure heart block severe hypotension
long term management of pt w paroxysmal SVT
medication - beta blockers, CCB, amiodarone
radiofrequency ablation
wolf-parkinson white syndrome
extra elcectrical pathway connecting atria and ventricles
wolf-parkinson white syndrome: what is extra pathway often called
bundle of kent
wolf-parkinson white syndrome: definitive treatment
radiofrequency ablation of accessory pathway
wolf-parkinson white syndrome: ECG changes
short PR interval
wide QRS
delta wave - slurred upstroke on QRS
radiofrequency ablaion can be curative for certain arrythmias caused by abnormal electrical pathways, incl…
AF
atrial fluter
SVT
WPW syndrome
Torsades de pointes
type of polymorphic ventricular tachycardia
stimulate recurrent contractions withut normal repolarisation
occurs in pt w prolonged QT interval
Torsades de pointes: ECG
- QRS twist around baseline
- QRS get progressively shortet
- prolonged QT internal
prolonged QT interval
ECG finding of prolonged repolarisation after contraction
afterdepolarisations
wait longer time to repolarise causes random spontaneous depolarisation in some myocytes
abnormal depilatisations pripr to repol
clinical course of Torsades de pointes
either terminate spontaneously
progress to VT
causes of prolonged QT
long QT syndrome
medicatins: antipsychotics, citalopram, amiodarone, macrolide antibs
electrolyte disturbance - hypokalaemia, hypocalcaemia
Torsades de pointes: acute Mx
correct cause - electrolyte disturbance or meds magnesium infusion (even if have normal Mg) defibrillation if VT occurs
Torsades de pointes: longterm Mx
- avoid meds that prolong QT
- correct electrolyte disturbances
- beta blockers
- pacemaker or implantable defib
ventricular ectopics
premature ventricular beats caused by random electrical discharges from outside atria
ventricular ectopics: presentation
random, brief palpitations
ventricular ectopics: ECG
individual random, abdnormal, broad QRS complexes
ventricular ectopics: bigeminy
when V ectopics happen to frewuently that they happen after every sinus beat
ECG normal sinus beat followed by ectopic
ventricular ectopics: Mx
- check bloods for anaemia, electrolyte disturbance, thyroid disease
- reassure and no Rx if healthy
- seek advice if background heart disease or concerning features e.g. chest pain, murmur
AV node blocks
heart block
1st degree heart block
delayed atrioventricualr conduction through AV node
despite this, every atrial impulse leads to ventric contraction –> every p wave results in QRS
1st degree heart block ECG
PR interval > 0.2s
1 big square
second degree heart block
some of atrial impulses do not make it through AV nodes to ventricles
–> instances where P wave doesnt lead to QRS
several types
- mobitz T1
- mobitz T2
- 2:1 block
second degree heart block: Mobitz type 1
atrial impulses become gradually weaker until it does not pass through AV node
after failure, atrial impulses become strong again and cycle repeats
second degree heart block: Mobitz type one ECG
increasing PR interval until P wave no longer conduct –> absent QRS
second degree heart block: Mobitz type 2
there is intermitted failure of AV conduction –> missing QRS
PR interval normal
risk of asystole
second degree heart block: 2:1 block
there are 2 p waves for each QRS
every 2nd P wave is not strong enough to stimulate QRS
3rd degree heart block
complete heart block
no observable relationship between P waves and QRS
signif risk of asystole
Rx of bradycardias/AV node blocks: stable
observe
Rx of bradycardias/AV node blocks: unstable or risk of asystole
- atropine 500mcg IV
no improvement>
- atropine 500mcg IV
- other inotropes
- transcutaneous cardiac pacing
Rx of bradycardias/AV node blocks: high risk of asystole or prev asystole
- temp transvenous cardiac pacing
- permanent implantable pacemaker
atropine
antimuscarinic medication
works by inhibiting parasympathetic NS
–> pupil dilation, urinary retention, dry eyes, constipation