Arrhythmias

Question 1

Arrhythmias - history?

Answer 1

P: regular/irregular/syncope/dizziness/terminated by Valsalva (SVT)

What was it? NSVT? Sustained VT (or VF) was the patient conscious or unconscious on presentation?

R: FH of sudden death (LQTS, Brigada, HOCM), pro-arrhythmic (flecainide, sotalol)

I: 24h Holter, Loop recorder, EPS (looking for inducible arrythmias, e.g. VT - very memorable), TTE, Angiogram (for VT/VF), cardiac biopsy? (RV dysplasia), MRI (sarcoid, RV dysplasia, amyloid)

Complications: if was ablated - heart block or cardiac rupture

M: Adenosine (patient remembers it well!), Valsalva?, EPS (inducible VT may mean DC cardioversion), Catheter ablation, AICD, PPM

C: any AICD firing off, current symptoms, follow-up

Question 2

AF - history?

Answer 2

P: palpitations, angina, SOB, collapse, dizziness

R: HTN, IHD, Thyroid, MV disease, ETOH, PE, OSA, WPW, ASD

** CHADS2VASC score

C: stroke/TIA, CCF. Complications of drugs (bleeding, IPF…etc)

M: anticoaulation, medications

C: well/poorly controlled rate/rhythm

Question 3

Patient with syncope - on antiarrythmic drug (e.g. Flecainide, Sotalol) - one possible diagnosis?

Answer 3

Possible proarrythmia - maybe 1C drugs/Sotalol started because of paroxysmal AF - may have precipitated bradyarrythmia in patient with Sick sinus syndrome

Question 4

Patient with known WPW presenting with new onset AF or Atrial flutter. What is the risk? Mx? Which agents must you avoid?

Answer 4

These patients are at risk of sudden death/syncope as very rapid ventricular rates may occur - if the accessory pathway can conduct at high rates

Treat as usual, if unstable, cardioversion.

NEVER verapamil, adenosine, digoxin.

These agents enhance conduction via accessory pathways while blocking the AV node…!

Question 5

CHADS2VASC score?

Answer 5

CCF (1)

HTN (1)

Age (1 if ≥65)

Diabetes (1)

Stroke/TIA/VTE (2)

Vascular disease (1) - PVD, MI, Aortic plaque

Age (+1 if ≥ 75)

Sex (1 for female)

Question 6

For PPM… what does it mean by

Single chamber, Double chamber

Atrial (A) sensing, ventricular (V) pacing

Atrial pacing, ventricular sensing

Atrial and Ventricular pacing

(So where would you see the pacing spike (s) in ECG?

Answer 6

Single chamber PM (RA) = for sinus node dysfunction with normal AV. Rare.

Single chamber PM (RV) = to generate reliable CO in patients with slow AF.

Dual chamber PM (RA+RV) = to allow for physiological delay between atrial

and ventricular conduction.

• Atrial (A) sensing, ventricular (V) pacing = spike before QRS
• Atrial pacing, ventricular sensing = spike before P
• Atrial and Ventricular pacing = spikes before P and another one before QRS

Question 7

How would you distinguish between VT from SVT with aberrant conduction? (what makes VT more likely)? (6)

Answer 7

Concordance (either +ve or -ve throughout the pre-cordial leads

AV dissociation (where P marches through QRS complexes)

Widened QRS (>0.14 if RBBB, >0.16 if LBBB)

Known ischaemic heart disease (broad complex tachy in IHD is usually VT - in 95%)

Changes in QRS morphology from pre-existing BBB

Left-axis deviation

Question 8

What is electrophysiology study (EPS)?

Answer 8

EPS is a catheter based technique used to identify and treat precise location of cardiac arrhythmia.

It assesses inducibility of atrial or ventricular arrhythmias - both before and after treatment - indeed, it is now used in conjunction with catheter ablation (accessory pathways, AV node, regions around 4 pulmonary veins for AF)

Question 9

AF - associated conditions and underlying aetiology? (10)

Answer 9

Acute: triggers - electrolytes, anaemia, infection, hypoxia, thyroid

Chronic: HTN, IHD, Obesity / OSA, MV disease, PE

Recent abdominal / thoracic surgery, Alcohol, WPW, ASD

Question 10

AF - what are you looking for in TTE? (5)

Answer 10

MV disease / other valvular abnormalities

IHD - RWMA

Hypertensive changes - chamer size / thickness, diastolic dysfunciton

Cardiomyopathy (e.g. ETOH)

Question 11

What are the prophylactic drug of choice for paroxysmal AF? (3)

Answer 11

Sotalol

Amiodarone

Flecainide (IC) - if the structure of the heart is normal

Question 12

AF - choice of rate-controlling agents are: beta-blockers, CCBs and digoxin. What is the goal of therapy other than rate control?

Answer 12

To prevent or reverse LV impairment caused by tachycardia-induced cardiomyopathy

Question 13

Would you DC cardiovert this patient with AF?

Answer 13

There is risk of embolism if AF ≥48 hours

1. TOE cardioversion (to rule out left atrial appendage thrombus or slow contrast flow suggesting turbulence)
2. Anticoagulate for 1 month - cardiovert - further 1 month of anticoagulation

Question 14

What is your approach to cardioverting this patient with new onset AF? (<48 hours)

Answer 14

Anticoagulation

• Overall embolic risk is very low. However, in many cases, we cannot accurately define onset of AF. If the onset of AF is not convincingly within the last 48 hours, Mx is same as >48h.
• In high-risk patient (e.g. prior TE, valve disease…etc), anticoagulate for 4-weeks before attempting cardioversion
• Even in low-risk patients, if Chads2vasc ≥1, anticoagulate if cardioversion will take place <48h (if NOAC used, wait 6h before cardioversion, or use clexane/Heparin)
• If significant bleeding risk - individualised risk assessment
• Continue anticoagulation for 4 weeks (given risk of recurrence) even in low-risk patient

Rhythm / rate control

• Rate control then wait for spontaneous reversion
• Chemical cardioversion with fleicanide or class III (Amiodarone/Sotalol)
• 3. DC cardioversion

Question 15

Successful cardioversion of new-onset AF <48h. Would you recommend life-long anticoagulation despite patient is in SR?

Answer 15

Based on CHADS2VASC. Anticoagulate as usual (unless score is 0 in men, 1 in women, in which case no-anticoagulation is reasonable)

Question 16

In which patients must you anticoagulate for 4 weeks before attempting the cardioversion, even if the AF onset is definitely within last 48 hours? (7)

Answer 16

Rheumatic heart disease

Valvular disease

Prosthetic valve

Severe LV dysfunction

Heart failure

Diabetes

Previous TE

Question 17

What is your approach to cardioverting this patient with AF >48 hours (or duration is unknown), with respect to anticoagulation?

Answer 17

NOAC or Warfarin (NOAC preferred, 1B) for 4 weeks then cardioversion

If patient has strong preference to not delay cardioversion, or risk of bleeding with anti-coagulation, or can’t tolerate AF despite rate control → consider TOE cardioversion

Question 18

Tx option for intractable, symptomatic AF despite rate-control and previously cardioversion hasn’t been successful? What is the success-rate?

Answer 18

Pulmonary Vein Isolation (catheter ablation or surgical) - where Radiofrequency is used to isolate the 2 pairs of PV in LA (as almost all AF starts from here) - but the procedure is complicated and time-consuming (4-6 hours) & success rate only 60%

Question 19

Complications of PVI? (4) What is the incidence of major complications?

Answer 19

Complete Heart block (hence often ablation + PPM)

Cardiac perforation - pericardial tamponade

Pulmonary Vein stenosis

Fistula (atrio-oesophageal)

Risk 3-5%

Question 20

When would you dose reduce Rivaroxaban & Dabigatran?

Answer 20

If CrCl 30-49

Rivaroxaban: 15mg OD (usual = 20mg OD)

Dabigatran: 110mg BD (usual = 150mg BD)

Question 21

When would you dose reduce Apixaban to 2.5mg BD?

Answer 21

If ≥2 of below

Age >75

Weight < 60kg

Cr >130

Question 22

AF - situations where you cannot use NOAC? (2)

Answer 22

Any valve replacement

Mitral stenosis

Question 23

What are the options for anticoagulated patient for AF who presents with ACS?

Answer 23

Controversial and no definitive trials, and the balance between bleeding and thrombotic risk must be weighted.

Options are:

Anticoagulation + Clopidogrel 1-6 months then anticoagulant alone

Just anticoagulant

DAPT without anticoagulation

Just Clopidogrel

BMS

Question 24

Patient on dialysis or severe CKD eGFR <30) - would you anticoagulate?

Answer 24

They have both increased risk of bleeding and thrombotic risk.

No clear evidence that anticoagulation with warfarin is beneficial.

The decision must be individualised.

For example,

a young dialysis patient who has already had a stroke may benefit from treatment

whereas an older patient with difficult-to-control hypertension and previous haemorrhagic problems may not.

Question 25

Anticoagulation based on CHADS2VASC? (3)

Answer 25

If ≥2 → should anticoagulate (1A)

For 0 in male, 1 in female → no anticoagulation (2C)

For 1 in male → individualsed approach. Reasonable with either.

Question 26

Amiodarone side effects?

Answer 26

It works by prolonging AP duration. Side effects are BITCH and peripheral neuropathy

Block (heart block / Bradycarmia)

ILD

Thyroid (hyper/hypo)

Cutaneous (skin photosensitivity) / Corneal deposits

Hepatotoxicity

Question 27

AF rhythm control (non-Pharm)?

Answer 27

PVI

MAZE procedure (surgical at time of valve replacement or CABG)

Question 28

Risk of Sotalol?

Answer 28

Especially in elderly with renal impairment - prolonged QT and torsades. Think of this when patients describes dizziness/syncope

Question 29

When cardioverting new onset AF with flecainide, you must give metoprolol or other betsa blockers together. Why?→

Answer 29

Because occasionally flecainide can organise AF into atrial flutter wtih 1:1 conduction (300bpm VF). BB is needed to prevent this from happening.

Question 30

Does Rhythm control for AF reduce the risk of stroke?

Answer 30

No evidence, hence should not be used as reason to cease anticoagulation.

Question 31

CASTLE-AF trial?

Answer 31

Ablation vs. rate control vs. medication-based rhythm control - in patients with associated LV dysfunction.

There is mortality benefit for Ablation - so something to consider

Question 32

ECG interpretation - system?