Arrhythmias Flashcards
What should be the only pathway for electrical activity to pass between the atria and ventricles?
AV node
What is an arrhythmia?
An irregular heart beat
What are the two main classes of arrhythmia?
- Supraventricular (SVT)
- Ventricular (VT)
These classifications are based on the origin of the arrhythmia
What does “supraventricular” confer about the location of the arryhtmia’s origin?
It is above the ventricles and within the atria, SA node, AV node or His origin
Name 3 tachycardic SVT arrhythmias
- Atrial fibrillation
- Atrial flutter
- Ectopic atrial tachycardia
Name 2 bradycardic SVT arrhythmias
- Sinus bradycardia
- Sinus pauses
What are AV node arryhthmias due to?
Re-entrant rhythms
e.g. AVN re-entrant tachycardia (SVT arrhythmia)
Where and why do ventricular arrhythmias arise?
Arise in ventricles due to ectopic beats from latent pacemakers
What is supraventricular paroxysmal tachycardia?
A re-entrant tacycardia
This comes and goes spontaneously
Wolf-Parkinson-White syndrome involves which type of arrhythmia?
Paroxysmal supraventicular tachycardia
What are the three types of venticular arrythmias?
- Ventricular tachycardia
- Ventricular fibrillation
- Asystole - the heart fails to beat
What are ectopic beats
Beats arising from outwith the SA node
Which factors may promote tachycardia and ectopic beats?
- Hyperthermia
- Hypoxia
- Hypercapnia
- Cardiac dilatation
- Hypokalaemia (prolongs repolarisation)
Which factors may induce bradycardia and heart block?
- Hypothermia
- Hyperkalaemia
What are afterdepolarisations?
Depolarisations occurring, for various reasons, within phase 2 of the myocitic action potential
They may induce a second heart beat
Afterdepolarisations are associated with use of which drug and why?
Digoxin
It leads to a calcium overload in cells making contractions easier
Deficiency of which element will potentiall lead to afterdepolarisations and why?
Potassium
Hypokalaemia leads to afterdepolarisations because a lack of potassium means cells cannot depolarise as easy since potassium is used for depoalrisation
What is the name of the accessory pathway utilised in WPW syndrome?
The bundle of Kent
How is sinus tachycardia treated?
Beta blockers
What is micro re-entry?
This is when the AV nodal re-entrant tachycardia circuit uses the circuit within the AVN
Micro re-entry is most common in which type of person?
Young woman
Acutely, how are SVT arrhythmias treated?
Increase vagal tone via:
- Valsalva manouvre
- Carotid sinus massage
How are SVTs treated long term to slow the conduction in the AVN?
- Adenosine
- Verapamil
Problematic accessory tracts are treated by what?
Radiofrequency abalation
What is first degree AV block?
There is no block
The PR interval is increased
There is no treatment
What are the two types of second degree heart block?
- Mobitz type I
- Mobitz type II
Describe Mobitz type I
PR interval gradually increases until a QRS comple does not occur
The cycle then resets
Describe Mobitz type II
The is pathological and usually involves a ratio of P waves to QRS complexes since only some P waves can get through
Common ratios are 2:1 and 3:1
What is third degree heart block?
No potentials from the SA node will make it through the AV node so there is no coordination between atrial and ventricular coordination
What is the treatment for third degree heart block?
Ventricular pacing
How do ventricular arrythmias present on ECG?
Wide QRS
How can ventricular tachycardia often be identified on ECG?
- Wide QRS
- No P waves (present, yet not visible)
- Large T wave opposite to QRS deflection
This is for monomorphic VT which involves just one circuit so all the beats are the same
What is polymorphic VT and how does it present on ECG?
This happens all over the ventricles so there are numerous circuits leading to completely irregular patterns
Give an example of polymorphic VT
Torsades de Pointes
How can VT be treated acutely, and why is this treatment useful?
Adenosine
It can aid the diagnosis depending on its effect as it has a short half life
When a VT is unstable, how is it treated?
Direct current cardioversion (DCCV)
If VT is stable, how is it treated?
Anti-arrhythmic drugs
How is VT treated long term?
- Re-vascularisation to correct ischaemia
- No anti-arrhythmic drugs as these worsen outcomes long-term
- Cardioverter defibrillation use if life threatening
- VT catheter ablation
- Beta blockers
What is ventricular fibrillation?
Ventricular activity is chaotic and leads to the heart losing its ability to function as a pump
How is ventricular fibrillation treated?
- Defibrillation
- CPR
What is the most serious potential consequence of atrial fibrillation?
Stroke
Which 3 main categories can atrial fibrillation be classified under?
- Paroxysmal - episodes terminate spontaneously last < 48 hours
- Persistent - episodes are not self terminating - last > 48 hours
- Permanent - continuous AF which cannot be cardioverted, or attempts to do so may be inappropriate
The first detected episode of AF is often also described as a form
What are the symptoms of AF?
- Palpitations
- Dyspnoea
- Chest pain
- Pre-syncope (dizziness) or syncope
- Fatigue
What are the sign(s) for AF?
An irregularly irregular pulse
What is used for diagnosis of AF and why?
ECG
Other conditions can give an irreguarly irregular pulse such as ventricular ectopics
What are the two components of AF management?
- Rate/rhythm control
- Reducing stroke risk (anticoagulation)
How do rate and rhythm control vary?
- Rate - accepts there will be an irregular pulse, yet aims to slow down the pulse
- Rhythm - attempts to return the patient to normal sinus rhythm (cardioversion)
Which two methods can be used for cardioversion?
- Drugs
- Synchronised DC electrical shocks
What is used for first line in AF to control the rate?
Either:
- Beta blocker
- Rate limiting calcium channel blocker (diltiazem)
Assuming first line rate control treatment fails for AF, what is second line?
Combination therapy using any 2 of the following drugs:
- Beta blocker
- Diltiazem
- Digoxin
What is a normal rate for atrial fibrillation?
Can be >300bpm
In theory, in atrial fibrillation, the ventricular contraction rate should match the atrial rate since there is nothing wrong with the conduction pathway in this sense.
Why is it that this doesn’t happen when atrial contraction rates get very high?
The AV node cannot conduct impulses at this rate and this is the rate limiting factor for ventricular contraction
Why is it dangerous when patients switch from AF to sinus rhythm?
There is high risk of an embolism being pushed out the atria when they contract properly
This can lead to stroke
Before attempting cardioversion, what must be confirmed about the patient’s disease or pharmacological status?
They have had symptoms for less than 48 hours
or
Have been anticoagulated prior to cardioversion
This is to avoid the risks of stoke via embolism release
What is the scoring strategy used to determine the most appropriate anticoagulation strategy depending on the patient’s risk of stroke?
CHA2DS2-VASc
Which invasive procedure can allow for sinus rhythm in AF to be restored?
Catheter abalation of atrial focus
(or surgery)
What treatment is given, or considered, when a patient has the following CHA2DS2-VASc scores:
a) 0
b) 1 (female)
c) 1 (male)
d) 2
a) None
b) None
c) Consider anticoagulation
d) Offer anticoagulation rather than consider
What are the components of CHA2DS2-VASc?
C - Congestive heart failure (points = 1)
H - Hypertension (points = 1)
A2 - Age >= 75 (points = 2); age 65-74 (points = 1)
D - Diabetes (points = 1)
S2 - Prior stroke or TIA (points = 2)
V - Vascular disease (points = 1)
S - Sex - female (points = 1)
If AF has an onself of <48 hours how may a patient be cardioverted?
Electrical - DC cardioversion
Pharmacologically - Amiodarone (structure heart disease), flecainide or amiodarone (without structural disease)
If it is confirmed the onset of AF was under 48 hours, what should be done after cardioversion in such patients?
Nothing
Further anticoagulants are unnecessary
(they are already anticoagulated by heparin for example, before cardioversion)
If the patient has had AF for >48 hours what should be done before cardioversion?
The patient must be anticoagulated for at least 3 weeks beforehand
If the patient has had AF for >48 hours what cardioversion technique is recommended?
Electrical cardioversion
Patients should then be anticoagulated for at least 4 weeks
What is the main drug used for pharmaclogical cardioversion of atrial fibrillation?
Amiodarone
(or flecainide, if no evidence of structural heart disease)
Following a stroke or TIA, what is the anticoagulant of choice?
Warfarin
In acute stroke patients, why is anticoagulation therapy delayed?
Risk of haemorrhage
When would digoxin be the preffered agen to control rate in patients with AF?
If the patient has coexistent heart failure
(otherwise, beta blocker or calcium channel blockers are used)
Which agents can maintain sinus rhythm in patients with a history of AF?
- Amiodarone
- Flecainide
- Sotalol
What is lone AF?
AF in the absence of underlying heart disease
Possibly genetic
What is the gold standard for terminating AF via cardioversion?
Electrical cardioversion
This is more effective than the pharmacological option
In AF, where is the ectopic focus commonly located?
Ostia of pulmonary veins
Where does ventricular tachycardia originate?
Ventricular ectopic focus
What are the two main types of VT?
Monomorphic VT - Mostly caused by MI (all waves are the same on ECG)
Polymorphic VT - all waves on ECG are different as there are many areas producing ectopic beats
Give a common example of polymorphic VT
Torsades de pointes
How is VT managed if the patient has low systolic BP (<90mmHg), chest pain, heart failure or heart rate >150bpm?
Immediate cardioversion
If antiarrhythmic drugs fail for VT management what must be used?
Electrical cardioversion
Syncronised DC shocks
Which drugs will be used in VT?
- Amiodarone
- Lidocaine
Which drug is strictly not used to treat VT?
Verapamil
If drug therapy fails what can de done for patients with VT?
- Implantable cardioverter-defibrillator (ICD) - particularly useful for patients with LV dysfunction
- EPS - electrophysiological study
Name some drugs that can induce a long QT interval
- Amiodarone
- Sotalol
- Class 1a antiarrhythmic drugs
What are some causes for a long QT interval?
- Hypokalaemia
- Hypocalcaemia
- Acute MI
- Myocarditis
Which sign on an ECG is distinctive of Torsades de pointes?
Long QT interval
(may also deteriorate into VF)
How is long QT interval treated?
Magnesium sulphate (IV)
What causes Wolff-Parkinson-White syndrome?
Accessory pathway (bundle of Kent) between atria and ventricles
(can be left or right sided)
Which type of arrhythmia is associated with WPW syndrome?
Atrioventricular re-entry tachycardia (AVRT)
What are possible ECG features for WPW syndrome?
- Short PR
- Delta waves
- Left/right axis deviation depending on side of accessory pathway
How is type A (left sided - by far the most common) differentiated with type B (right sided) WPW syndrome?
There is a dominant R wave in V1 in type A that is not present in type B
What is the management for WPW syndrome?
Radiofrequency ablation of the accessory pathway
Sotalol, amiodarone or flecainide
When treating WPW syndrome, which drug should be avoided if there is coexistent AF?
Sotalol
(may increase transmission through accessory pathway by prolonging AV refractory period)
What are cannon A waves and where are they seen?
Visible pulsations in the JVP
What causes cannon A waves?
Particular associated with third degree heart block, when atria and ventricles contract simultaneously
A large pressure is pushed against the AV valves which radiated back up the jugular vein
This is also associated with pulmonary hypertension
What defines first degree heart block?
Lengthened PR interval
(PR > 0.2 seconds)
