University

ofGalway.ie
Our Case
• You are the medical student attached to the stroke service. You are with the team on the ward round when

you go to see a 70 year old lady who was admitted 4 days ago with an acute right sided weakness and some

expressive dysphasia. She was diagnosed with an acute ischemic stroke and successfully underwent
thrombolysis on the night of her admission. She is has been recovering on the ward since and apart from

some minor residual expressive dysphasia, has been doing well.

 70 year old female

Past medical history Medications (NKDA)

§ Eltroxin 100mcg in the morning

Social history
§ Hypothyroidism
§ Chronic Obstructive pulmonary disease § Ultibro Breezhaler 85/43mcg once a day (indacaterol/glycopyrronium) § Retired, lives at home
§ Aspirin 75mg once a day
with sister
§ Hypertension
§ Ramipril 2.5mg once a day § She is normally fully
§ Hypercholesterolemia
§ Bisoprolol 5mg once day
independent and
§ Ischemic heart disease (2 stents to the LAD 3 years ago) mobilises with a stick
§ Atorvastatin 20mg once day
§ Heart failure with reduced ejection fraction
§ Bumetanide 1mg once a day
§ Current smoker – with
60 pack year hx
§ Lumbar disc degeneration § Combivent nebulisers 4 times a day (salbutamol/ipratropium)
§Drinks one glass of
§ Ibuprofen 400mg three times a day (started 2 weeks ago for lower
back pain) whiskey per night
 On examination
General inspection à Looks well. Sitting out reading paper.
Feels “fine” – no chest pain, palpitations or SOB.

Mild ejection Good air entry SNT • RR 18

systolic murmur - bilaterally BS+ • SpO2 95% RA
no radiation • BP 146/84
• HR 82 (irregularly
irregular)
Peripheral: No evidence of pitting oedema, no calf pain/swelling
• T 37.0

On the ward round the consultant asks you to palpate the patients radial pulse. You note that it feels irregularly irregular. You estimate
the rate to be 82 beats per minute. You suspect she may be in atrial fibrillation.
Question - Provide three potential differentials for an irregularly irregular pulse
 Atrial fibrillation

Multifocal atrial tachycardia

Differential for
irregularly
irregular pulse Premature Atrial Complexes or
Premature Ventricular Complexes
Atrial flutter with variable block
Looking at Mary’s history, what potential risk factors for atrial fibrillation can you
identify from her history?
Modifiable vs non modifiable

Smoking
COPD

Afib often precipitated/provoked by:

• Infection
• Heart failure
• PE
 Describe the findings on the ECG provided. Comment
on all of the following
• NB – remember history will be the most helpful
• Rate
• Rhythm
• Axis
• P waves
• QRS complexes
• T waves
• PR interval
• ST segment
• Overall diagnostic impression
•Anything additional
You compare this to her admission ECG and note that her ECG on admission showed normal sinus rhythm at a rate of 80 beats
per minute.
What is atrial fibrillation
You confirm that Mary is in atrial fibrillation. Given that his ECG was normal on admission, how
would you classify this Mary’s atrial fibrillation?
 What is Atrial
Fibrillation?
• A supra ventricular tachyarrhythmia
uncoordinated atrial electrical activation
and consequently ineffective atrial
contraction.
• Electrocardiographic characteristics of AF
include:
• Irregularly irregular R-R intervals
• Absence of distinct repeated P waves; and
• Irregular atrial activations

• Pathogenesis is now thought to involve an

interaction between initiating triggers, often
in the form of rapidly firing ectopic foci
located inside one or more pulmonary veins,
and an abnormal atrial tissue substrate
capable of maintaining the arrhythmia.
Classification of A Fib (ESC)
AF pattern Description

First diagnosed (often AF which has not been diagnosed before – irrespective of symptoms/severity
incorrectly called ‘new
onset’)
Paroxysmal AF that terminates, either spontaneously or with intervention within 7 days
(<7 days)
Persistent AF that is continuously sustained beyond 7 days, including episodes that are
(>7 days) terminated by cardioversion (drugs or DC cardioversion) after 7 days or more
Long standing Continuous AF >12 months duration when still pursuing a rhythm control strategy
persistent
Permanent AF that is accepted by the patient and physician, that no further attempts will be
made to restore sinus rhythm. This term should not be used in the contact of
rhythm control with anti arrhythmic drug therapy or ablation.
What initial investigations would you request in order to investigate his atrial fibrillation? Justify each investigation
12 lead ECG – essential to diagnose atrial fibrillation
 Investigations

Labs Radiology
Bedside investigations
• FBC - WCC elevated in infection, Hb and platelets • CXR - ?evidence of infection (precipitant of afib)
• 12 Lead ECG or evidence of heart failure
needed if you’re starting a NOAC.
• Blood pressure • Renal profile - ?CKD. Electrolytes can precipitate
Other
arrhythmias. Also will need to know renal function for
anticoagulation • Trans-Thoracic echo
• CRP - Infection can precipitate a fib • Trans oesophageal echo if considering
cardioversion
• TFTs - Hyperthyroidism can cause a fib • Coronary Angiography
• BNP - if evidence of heart failure • Sleep studies (if you suspect sleep apnea)
Mary’s feels well and she asks if things could be left “well enough alone”?
What are the potential complications of atrial fibrillation if left unmanaged?
 Figure 4 Clinical
presentation of AF and
AF-related outcomes

©ESC
©ESC

www.escardio.org/guidelines 2020 ESC Guidelines for the diagnosis and management of atrial fibrillation
(European Heart Journal 2020-doi/10.1093/eurheartj/ehaa612)
What scoring system is used to predict a
patient’s stroke risk in atrial fibrillation?

Calculate Mary’s score and stroke risk

CHA2DS2 - VASc
• Hypertension - +1
• Age - + 2
• Vascular disease - + 1
• Previous Stroke, TIA, or Thromboembolism - +2

• Total score - 6
What is the HASBLED score? What is Mary’s HASBLED score?
HAS-BLED - 4 (Stroke, Elderly, NSAID, Aspirin)
Table 9 factors for bleeding with OAC and antiplatelet therapy
Non-modifiable Potentially modifiable Modifiable Biomarkers
Age >65 years Extreme frailty ± Hypertension/elevate SBP GDF-15
Previous major bleeding excessive risk of Concomitant Cystatin C
Severe renal impairment (on fallsa antiplatelet/NSAID / CKD-EPI
dialysis or renal transplant) Anaemia Excessive alcohol intake cTnT-hs
Severe hepatic dysfunction Reduced platelet Non-adherence to OAC Von Willebrand
(cirrhosis) count or function Hazardous hobbies / factor (+ other
Malignancy Renal impairment occupations coagulation
Genetic factors (e.g., CYP 2C9 with CrCl <60 mL/min Bridging therapy with markers)
polymorphisms) VKA management heparin
Previous stroke, small-vessel strategyb INR control (target 2.0–
disease, etc. 3.0), target TTR >70%c
Diabetes mellitus Appropriate choice of OAC
Cognitive impairment/dementia and correct dosingd

©ESC
aWalking aids; appropriate footwear; home review to remove trip hazards; neurological assessment where appropriate. bIncreased INR monitoring, dedicated OAC
clinicals, self-monitoring/self-management, educational/behavioural interventions. cFor patients receiving VKA treatment. dDose adaptation based on patient’s age, body
weight, and serum creatinine level.

www.escardio.org/guidelines 2020 ESC Guidelines for the diagnosis and management of atrial fibrillation
(European Heart Journal 2020-doi/10.1093/eurheartj/ehaa612)

HAS BLED is a tool to help identify potential modifiable risk factors

Would you anticoagulate Mary?
Justify your answer
CHA2DS2VASc
Anticoagulation should be
considered in all, if:
• CHA2DS2VASc ≥1 in males
• CHA2DS2VASc ≥2 in females

• If a patient is deemed to be at low

stroke risk then you should
reassess them in 4-6 months as
score can change
When looking up your answers you come across 2 different classes of
anticoagulant used in the management of atrial fibrillation: Vitamin K
antagonists and Direct Oral Anticoagulants (DOAC)
With respect to these two drug groups, what are their:
(i) Mechanism of action
(ii) 2 potential advantages
(iii) 2 potential disadvantages
(iv) Monitoring required
Oral
anticoagulation
o NOAC/DOAC (Novel oral anticoagulant
vs Direct oral anticoagulant)
Oral
anticoagulation

o Know the MOA of

each class of drug
Warfarin –Vit K Antagonist
o Some patients may be on warfarin for afib which
was started before DOAC’s came to market
o MOA: no synthesis or activation of Protein C, S,
Factor 2, 7, 9, 10.
o Target INR in atrial fibrillation is between 2-3 with a o Advantages
time in therapeutic range of >70%
o oral administration
o DOACs are preferred in AF, except for 3 indications o Antidote available (vit K)
below: o No contraindication in renal failure
oMechanical heart valve
oModerate/severe mitral stenosis –so called o Disadvantages:
‘valvular afib’ o Bleeding
oCKD/dialysis patients à Creatinine clearance o Narrow therapeutic range
<15ml/min o Multiple drug/drug interactions
o Requires INR monitoring
If a patient has severe mitral stenosis, would this change your
anticoagulant choice?
In a patient who cannot take oral anticoagulation long term,
what non-pharmacological options are there for stroke
prevention?
Watchman device (PROTECT AF and
PREVAIL)
• LAA is non inferior to VKA treatment as
per these 2 trials
In relation to the management of atrial fibrillation, what is
meant by the following terms?

(i) Rate control

(ii) Rhythm Control

Do you know any non-pharmacologic methods of doing this?

Treatment
Rate Control
o Pharmacological strategy
o Non-pharmacological strategy

Rhythm Control - cardioversion

o Pharmacological cardioversion
o Electrical cardioversion
Rate control - pharmacological strategy
o Rate control alone is often sufficient to reduce symptoms related to atrial fibrillation. Optimal heart
rate in AF is unclear
o Beta-blockers (e.g bisoprolol, metoprolol): are often first-line rate-controlling agents, good agents for
acute rate control. CI in severe asthma, severe allergy, recent cocaine use
o Non-dihydropyridine calcium channel blockers (NDCC): verapamil and diltiazem provide good rate
control and can improve AF-related symptoms compared with beta-blockers. First line in those with a CI
to beta blocker. Contraindicated in heart failure (EF <40%), cardiogenic shock, allergy
o Digoxin – inhibits Na/K ATPase pump – increasing contractile force of heart and reduces heart rate.
Can be used in addition to BB
o Amiodarone - Only if the others can’t be used or don’t work. Can inadvertently cardiovert a patient!
Careful if the patient has a fib of >48 hours duration. NB side effects
Amiodarone Digoxin
Rate control – non-
pharmacological
strategy
o Ablation of the AV node and
implantation of a pacemaker
o Radiofrequency ablation is performed by
burning the AV node and stopping the
transmission of atrial impulses to the
ventricles. The pacemaker then takes
over
o Pacemaker dependent for life – limited
to patients who cannot be managed with
rate control/rhythm control.

o What are the potential complications of

pacemaker insertion?
Indications for PPM
o Sick sinus syndrome
o Symptomatic sinus bradycardia
o Tachy-brady Syndrome
o AF with sinus node dysfunction
o Complete AV block (3rd degree HB)
o Chronotropic incompetence
o Cardiac Resynchronisation Therapy – with
biventricular pacing
Rhythm control - Cardioversion
o Uses a combination of approaches including including cardioversion, antiarrhythmic medication, and
catheter ablation, along with an adequate rate control, anticoagulation therapy.
o The primary indication for rhythm control is to reduce AF-related symptoms and improve QoL
o AF progression is associated with a decrease in QoL and, with time, becomes irreversible or less amenable
to treatment (e.g left atrial dilation)
o Important to assess factors that favour rhythm control
o Younger age
o First episode of AF
o Tachycardia induced cardiomyopathy
o Normal/moderately increased LAVI on echo (left atrial volume index)
o Few co-morbidities
o AF precipitated by temporary event (acute illness)
o Rate control difficult to achieve
o Patient choice
Rhythm control – pharmacological strategy
o Pharmacological cardioversion to sinus rhythm is an elective procedure indicated in
haemodynamically stable patients only.
o A ‘wait-and-watch’ strategy (usually for <24 h) may be considered in patients with recent-onset AF as a
non-inferior alternative to early cardioversion. The following medications may be used:
o Flecainide (IV/PO): indicated in patients without significant LV hypertrophy (LVH), LV systolic
dysfunction, or ischaemic heart disease, results in prompt (3-5 hours), safe restoration of sinus rhythm
in >50% of patients. Side effects – hypotension, can precipitate A flutter with 1:1 conduction
o Amiodarone (IV): mainly used in patients with heart failure. 44% will restore SR (8- 12 hours to several
days). Side effects – QT prolongation, hypotension, phlebitis when given IV.
 “Pill in the Pocket”
o In selected outpatients with rare paroxysmal AF episodes
o A self-administered oral dose of flecainide may be preferred (permitting
an earlier conversion), provided that the drug safety and efficacy has
previously been established in the hospital setting.
o An atrioventricular node-blocking drug (e.g. metoprolol) should be
instituted in patients treated with class flecainide to avoid
transformation to AFL with 1:1 conduction.
o Atrial flutter with 1:1 conduction is associated with severe
haemodynamic instability and progression to ventricular fibrillation
o Instructions for patients is to take metoprolol, and then 30 mins later
can take Anti arrhythmic drug.
Rhythm control – electrical cardioversion
o Pre-treatment with AADs can improve the efficacy of elective electrical cardioversion
o Factors associated with an increased risk for AF recurrence after elective cardioversion include
older age, female sex, previous DCCV, renal impairment, structural heart disease, large left atrial
volume, heart failure.
o Direct current cardioversion synchronized shocks (70-120 J) – can increase the J if necessary
o DCCV can be performed safely in sedated patients treated with IV midazolam and/or propofol
o Pads positioned in the AP position is more effective
o Skin burns may occasionally be observed following this
o Post procedural bradycardia can be observed
o Can you cardiovert any patient, at any time?
When considering if a patient is suitable for rhythm control,
why is the time of onset of atrial fibrillation important?
o Haemodynamically unstable ? DCCV
o “Unstable” – signs of shock, acute heart failure,
chest pain/ischaemic on ECG, Syncope
o If stable à next step is to determine if they
could have a LAA thrombus
o Already on therapeutic DOAC? DCCV
o If No then start doac
o AF < 48 hours – then DCCV
o AF > 48hours – then TOE before DCCV
AF Catheter Ablation
(Pulmonary Vein
Isolation)
o Generally second line after
failure of or intolerance to anti-
arrhythmic drug therapy
o A lot of patients will require more
than 1 procedure to achieve
symptom control
o Works better in younger patients,
without structural heart disease –
up to 80% success rate in non
recurrence of AF in selected
patients
Mary made great progress with the multidisciplinary team and is finally ready to go home.
During her admission she was commenced on Apixaban 5mg twice a day by the consultant.
Before her discharge the consultant has asked the intern to make sure that Mary is aware of
her apixaban dosing and side effects. You follow the intern to listen to her discussion with
Mary.
 Counselling a patient for a DOAC
o Indication for treatment doses: Prevention of stroke and systemic embolism in adult patients with non-valvular AF (NVAF)
o Advantages (vs. warfarin): fixed dose, INR monitoring not required, more stable anticoagulation control if taken reliably,
favourable major bleeding profile overall, lower incidence of intracranial haemorrhage, less drug/diet interactions, easier to
manage around surgery/procedures
o Disadvantages (vs. warfarin):not appropriate for all pts (e.g extremes of body weight, renal impairment), some monitoring still
required (eg renal function)
o Seek medical attention: Bloody /black tarry stools, coughing/vomiting up blood, bloody urine, nose bleeds (lasting for > 5-
10mins or if pt does not usually suffer from nose bleeds), severe or spontaneous bruising, unusual headaches, excessive vaginal
bleeding, cuts that take longer than 5 minutes to stop bleeding, blood shot eye.
o Seek immediate medical attention: involved in major trauma, significant blow to the head or are unable to stop bleeding
oSurgical procedures (including dental treatment) and hospital admission: patient must inform healthcare professional that they
are taking DOAC
oContraception, à Women should not become pregnant nor breast feed whilst taking DOAC. Reliable contraception is required.
oMonitoring is required – although not as frequently as warfarin à renal function 3-6 monthly, FBC.