Arrhythmias CUE CARDS

Question 1

How are arrhythmias classified?

Answer 1

> Location (atria, ventricle)

> Rate (brady-, tachy-)

Question 2

What different options for managing arrhythmias?

Answer 2

> Anti-arrhythmic agents
> Electrical cardioversion
> Ablation
> Pacemakers
> Implantable Cardioverter Defibrillators

Question 3

What is Bradyarrythmia?

Answer 3

> Atrioventricular (AV) block [missing QRS and T waves]
First degree block: impulses delayed in the AV node but reaches the ventricles
Second Degree Block: some atrial impulses don’t reach ventricles
Third Degree Block: no impulses reach ventricles

Question 4

What are the causes Bradyarrythmia?

When should it be treated and what should it be treated with?

Answer 4

> Causes include: drug (beta blockers, verapamil, diltiazem, digoxin, amiodarone) and hypothyroidism
Treat only if symptomatic with pacemaker

Question 5

What are ventricular tacyarrhythmias?

When is it most common?

What symptoms does it cause?

Answer 5

> Any rhythm faster than 100 beats per minute
Heart beating so fast: lose cardiac output (CO) leading to collapse

> Most common following an MI

> Causes symptoms based on drop in CO (syncope, palpitations, dyspnea)

Question 6

How are ventricular tachyarrhythmias managed?

Answer 6

> Emergency management (acute): cardioversion, lignocaine/amiodarone/sotalol (IV bolus or infusion)

> Chronic management: (implantable cardiverter defibrillator and possible amiodarone/sotalol/flecainide/atenolol or metoprolol)

Question 7

In ventricular tacharrhythmias, why do drugs that are used chronically play a limited role?

Answer 7

Drugs used in chronic management may play a limited role as sudden episodes of VT can result in death

Question 8

What is Torsades de Pointes?

Answer 8

> Ventricular tachycardia in which the QRS axis is constantly shifting, often in patients with QT prolongation

Question 9

What is the cause of Torsades de Pointes?

Answer 9

> Caused by drugs
Drug interactions: if you combine CYP3A4 substrate with CYP3A4 inhibitor, you see increase in concentration of CYP3A4 substrate, precipitating QT prolongation

Question 10

What is AF?

Answer 10

> Characterised by abnormal impulse in atria leading to fibrillating atria, then disordered impulse conduction to ventricles, resulting in rapid ventricular rate
Usually presents with irregular ventricular rate 160-180bpm
ECG changes depend upon AV conduction (P wave absent)

Question 11

What is AF associated with?

Answer 11

> Hypertension
> Valvular heart disease
> Diabetes mellitus
> Coronary artery disease
> Heart Failure

Question 12

What is AF triggered by?

Answer 12

> Thyrotoxicosis
Alcohol
Caffeine
Exercise

Question 13

What are the Classifications of AF?

Answer 13

> Paroxysmal AF: Episodes that spontaneously terminate or are cardoverted within 7 days; may recur

> Persistent AF: Episodes that last >7 days and don’t self terminate

> Long-standing Persistent AF: Continuous AF lasting for >1 year

> Permanent AF: applies when a decision has been made jointly by patient and physician to accept presence of AF and stop further attempts to restore or maintain sinus rhythm

Question 14

What two risks are associated with AF?

Answer 14

> Atrial remodelling: not so worried in older group of patients, younger group may need to consider

> Thromboembolic stroke: atria not emptying blood properly (because it’s fibrillating rather than contracting) - blood pools in atria causing blood clots to form - blood clots embolise - break off - goes into ventricle - up into brain

Question 15

What are the 2 Treatment Objectives in AF?

Answer 15

> Symptom Control: convert to sinus rhythm, control ventricular rate

> Thromboembolic prevention

Question 16

What is the difference between Rate vs. Rhythm Control?

Answer 16

> Rate: slowing of ventricular rate only, not concerned with atrial functioning

> Rhythm: attempting to convert the patient into normal sinus rhythm, stop atria from fibrillating and put them back into synchronised cardiac rhythm

Question 17

How is rate vs rhythm determined?

Answer 17

> Paroxysmal: Rhythm

> Permanent: Rate

Question 18

Try rhythm control first for patients with persistent AF who?

Answer 18

> Symptomatic
Younger
Presenting for the first time with lone AF
Secondary to a treated or corrected precipitant
With congestive heart failure
Physically active patients

Question 19

Try rate control first for patients with persistent AF who?

Answer 19

> Over 65
With coronary artery disease
With contraindications to antiarrhythmic drugs

Question 20

How is rhythm control managed?

Answer 20

> Direct current cardioversion (may be acute due to hemodynamic instability or non-urgent): sotalol, amiodarone, flecainide

> Pharmacological conversion: sotalol, amiodarone, flecainide, may also be used prior to direct current cardioversion

> Radiofrequency ablation of aberrant pathways

Question 21

Between Amiodarone, Sotalol, Flecainide; which drug has the most benefit in the recurrence of AF?

Answer 21

> Tendency for amiodarone to be more effective and flecainide also
Sotalol less effective

Question 22

What is the tolerability of amiodarone, sotalol and flecainide?

Discuss patient selection of flecainide

Answer 22

> Amiodarone less tolerated compared to sotalol and flecainide
Flecainide use needs to be carefully selected. Needs to be restricted to those who aren’t at risk of arryhthmias

Question 23

Is there a benefit in using rhythm control over rate control and vice versa?

Answer 23

> From a theoretical point of view, it would be better to convert a patient back to sinus rhythm rather than simply control ventricular rate

> In reality, we are limited by the efficacy and toxicity of the drugs that we use to achieve this

> Therefore, there is no clear benefit to restoring sinus rhythm with drugs, versus simply controlling ventricular rate

Question 24

Discuss amiodarone hyperthyroidism

Answer 24

> In patients who are iodine deficient, iodine allows synthesis of thyroid hormones causing hyperthyroidism
Patients go from being asymptomatic to becoming symptomatic hyperthyroidism
Unmasking underlying condition (treat as for underlying thyroid disorder)
Cytotoxic effect of amiodarone causes thyroiditis: corticosteroids may be used for treatment

Question 25

Discuss amiodarone hypothyroidism

Answer 25

> In patients with pre existing but asymptomatic and undiagnosed hypothyroidism, the additional iodine results in reduced thyroid hormone synthesis
Patient becomes symptomatic
Treat as for hypothyroidism

Question 26

What is pill-in-the-pocket in the context of AF?

Answer 26

> Patients with infrequent symptomatic paroxysmal AF

> Administration of a stat dose when patient symptomatic (flecainide and may see beta blockers being used)

Question 27

What is an advantage of using pill-in-the-pocket?

Answer 27

Avoids treated patients in a chronic way with drugs with unpleasant side-effects

Question 28

What careful patient selection is needed in pill-in-the-pocket?

How should this be tested?

Answer 28

> Patients with a low risk of proarrhythmia
No structural heart disease, normal LVF, systolic BP > 100, no vascular diease, no IHD
Able to understand how to, when to, take the medication
Administer a test dose under ECG monitoring

Question 29

What is CHA2DS2-VASc?

What is a disadvantage of using CHADS2?

Answer 29

> Calculating someones risk to go on to have a stroke

> May underestimate risk in some patients

Question 30

Discuss Estimating Stroke risk based on CHA2DS2-VA score and Treatment of TE prevention?

Answer 30

> Score = 0: OAC or antiplatelets not recommended (low risk, don’t need therapy to prevent stroke. Risk of bleeding would outweigh potential benefits)

> Score = 1: Consider OAC

> Score = 2: OAC recommended (assess for contraindications, consider patients values and preferences, correct reversible bleeding factors)

Question 31

Discuss the use of Aspirin in Patients at low risk of stroke instead of Warfarin (previous recommendation)

Answer 31

> Previously, there was a recommendation in patients at low risk of stroke to use aspirin instead of warfain
Bleeding risk of aspirin is lower (low risk of stroke, can’t justify bleeding risk of warfarin - aspirin used as alternative, not as effective)
Recommendation has gone away but still may see in practice

Question 32

What is HASBLED?

Answer 32

Used to assess bleeding risk

Question 33

Discuss the benefits and risks of warfarin in TE prevention

Answer 33

> Benefits: protecting against ischaemic stroke (below INR of 2, efficacy wears off very quicky - INR of 1.5 = stroke risk much more significant than INR of 2)

> Risks: significant increase in risk of bleeding above 3

Question 34

Compare warfarin and DOACs in TE prevention

Answer 34

> Risk of significant bleeding of the DOACs may be lower than that of warfarin (apixaban) or similar (dabigatran and rivaroxaban)
DOACs appear to be associated with a lower risk of intra-cranial haemorrhage
If a patient does have a bleed while taking DOACs, it’s very difficult/impossible to reverse the effect, unlike warfarin, which can be reversed by giving vitamin K, fresh frozen plasma or clotting factor concentrate
Dabigatran reversal now possible

Question 35

Why are there complex instructions with verapamil and dabigatran?

“with verapamil, dabigatran dose does not need alteration. However, if adding verapamil to dabigatran, or starting both drugs together on the same day, dabigatran must be given 2 hrs before verapamil for the first 3 days to avoid drug interaction”

Answer 35

> Because verapamil is an inhibitor of Pgp, but is also an inducer of Pgp (in short term = you see inhibition of Pgp only, after a few days = you see increase in production of Pgp as a result of induction)

> If you give at the same time, you see verapamil inhibiting absorption of the efflux of dabigatran etexilate via Pgp, you would see increased absorption and therefore increased concentration