Arrhythmias Flashcards
Arrhythmias - history?
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
AF - history?
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
Patient with syncope - on antiarrythmic drug (e.g. Flecainide, Sotalol) - one possible diagnosis?
Possible proarrythmia - maybe 1C drugs/Sotalol started because of paroxysmal AF - may have precipitated bradyarrythmia in patient with Sick sinus syndrome
Patient with known WPW presenting with new onset AF or Atrial flutter. What is the risk? Mx? Which agents must you avoid?
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…!
CHADS2VASC score?
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)
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?
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
How would you distinguish between VT from SVT with aberrant conduction? (what makes VT more likely)? (6)
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
What is electrophysiology study (EPS)?
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)
AF - associated conditions and underlying aetiology? (10)
Acute: triggers - electrolytes, anaemia, infection, hypoxia, thyroid
Chronic: HTN, IHD, Obesity / OSA, MV disease, PE
Recent abdominal / thoracic surgery, Alcohol, WPW, ASD
AF - what are you looking for in TTE? (5)
MV disease / other valvular abnormalities
IHD - RWMA
Hypertensive changes - chamer size / thickness, diastolic dysfunciton
Cardiomyopathy (e.g. ETOH)
What are the prophylactic drug of choice for paroxysmal AF? (3)
Sotalol
Amiodarone
Flecainide (IC) - if the structure of the heart is normal
AF - choice of rate-controlling agents are: beta-blockers, CCBs and digoxin. What is the goal of therapy other than rate control?
To prevent or reverse LV impairment caused by tachycardia-induced cardiomyopathy
Would you DC cardiovert this patient with AF?
There is risk of embolism if AF ≥48 hours
- TOE cardioversion (to rule out left atrial appendage thrombus or slow contrast flow suggesting turbulence)
- Anticoagulate for 1 month - cardiovert - further 1 month of anticoagulation
What is your approach to cardioverting this patient with new onset AF? (<48 hours)
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)
- DC cardioversion
Successful cardioversion of new-onset AF <48h. Would you recommend life-long anticoagulation despite patient is in SR?
Based on CHADS2VASC. Anticoagulate as usual (unless score is 0 in men, 1 in women, in which case no-anticoagulation is reasonable)
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)
Rheumatic heart disease
Valvular disease
Prosthetic valve
Severe LV dysfunction
Heart failure
Diabetes
Previous TE
What is your approach to cardioverting this patient with AF >48 hours (or duration is unknown), with respect to anticoagulation?
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
Tx option for intractable, symptomatic AF despite rate-control and previously cardioversion hasn’t been successful? What is the success-rate?
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%
Complications of PVI? (4) What is the incidence of major complications?
Complete Heart block (hence often ablation + PPM)
Cardiac perforation - pericardial tamponade
Pulmonary Vein stenosis
Fistula (atrio-oesophageal)
Risk 3-5%
When would you dose reduce Rivaroxaban & Dabigatran?
If CrCl 30-49
Rivaroxaban: 15mg OD (usual = 20mg OD)
Dabigatran: 110mg BD (usual = 150mg BD)
When would you dose reduce Apixaban to 2.5mg BD?
If ≥2 of below
Age >75
Weight < 60kg
Cr >130
AF - situations where you cannot use NOAC? (2)
Any valve replacement
Mitral stenosis
What are the options for anticoagulated patient for AF who presents with ACS?
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
Patient on dialysis or severe CKD eGFR <30) - would you anticoagulate?
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.
