Atrial Fibrillation

1

Step 1

History Taking — Open Question First · Symptoms · ICE · Psychosocial Context

▲collapse

Two parallel agendas in AF history: the clinical (is this safe? what is the stroke risk? what caused it?) and the patient's (what does this mean for my life? am I going to have a stroke?). Both must be explored before management. The history also identifies reversible causes — treating the cause may resolve AF entirely.

🎓 SCA opener — use what you already know

"I can see from the ECG that your heart rhythm is irregular — this is what we call atrial fibrillation. Before I explain anything, I'd like to hear from you first — how are you feeling, and what's been going through your mind since you found out?"

Acknowledge the ECG finding immediately — it is in the notes. Then open the floor. The patient's narrative reveals their fear (stroke), their questions, and their hidden agenda.

1A — Open question first, then targeted history

Question to ask	Why it matters clinically	Changes what?
🟢 OPEN QUESTION — always start here"How have you been feeling, and what's been going through your mind since you found out about this?"	Reveals symptoms, fear, and functional impact simultaneously. A patient who says "I've been terrified since my husband had a stroke last year — he was in AF" has told you the ICE in one sentence. The opening response shapes the entire consultation.In SCA: finishing data gathering by 6–7 min requires this efficiency. Rigid symptom-by-symptom history misses the emotional agenda.	Reveals fearPsychosocial cuesEngagement
Palpitations — character?"Can you describe what you feel in your chest — racing, fluttering, irregular, or something else?"	Irregular palpitations = AF. Regular rapid = SVT/flutter. Irregular with pauses = ectopics. Character guides DDx. AF palpitations often described as "chaotic" or "bag of worms." Duration of each episode matters for paroxysmal AF burden.	AF vs SVT vs ectopicsHolter if paroxysmal
Onset — sudden or gradual?"Did this come on suddenly, or have you noticed it building over time?"	Sudden onset = new AF (acute haemodynamic implications). Gradual = chronic/persistent AF. Duration matters for cardioversion safety — if <48h, can cardiovert without prior anticoagulation (with heparin cover). If >48h or unknown → 3–4 weeks DOAC before cardioversion.	Cardioversion timingAcute vs chronic
Breathlessness or chest pain?"Have you noticed breathlessness — at rest or on exertion? Any chest pain or tightness?"	Breathlessness with rapid AF = HF decompensation — affects 20% CO. Chest pain + AF = possible ACS precipitating AF, or rapid AF causing ischaemia. Both change urgency dramatically.	ACS/HF → 999Rapid AF + breathlessness → same-day
Dizziness, presyncope, syncope?"Have you felt faint, dizzy, or actually passed out?"	Syncope with AF = haemodynamic compromise (very rapid rate or pre-excitation e.g. WPW). WPW + AF is dangerous — certain drugs (digoxin, adenosine) can cause VF. Presyncope = low cardiac output → urgent.	Syncope → 999⚠ WPW — avoid AV nodal drugs
Exercise tolerance — change?"How does it compare to 3–6 months ago? Can you still do what you used to do?"	Gradual decline in exercise tolerance = chronic undetected AF. AF with rapid rate reduces cardiac output by 20–30% (loss of atrial kick). Functional decline grades symptom burden and guides rate vs rhythm control choice.	Symptom burdenRate vs rhythm decision
Stroke / TIA symptoms?"Any weakness, numbness, slurred speech, or vision loss — even briefly — recently?"	AF carries 5x increased stroke risk. Transient focal neurology = TIA — 90-day stroke risk 10–15%. AF-related thrombus forms in left atrial appendage. Prior stroke/TIA scores 2 points on CHA₂DS₂-VASc — immediate anticoagulation.	Active TIA/stroke → 999Prior stroke → anticoagulate urgently
Reversible cause screen?"Any recent illness, infection, alcohol binge, thyroid problems, caffeine excess?"	AF is often a symptom, not the disease. Reversible triggers: thyrotoxicosis (must exclude), infection/sepsis, electrolyte disturbance, excess alcohol, caffeine, PE, post-cardiac surgery. Treating the cause may resolve AF and may avoid lifelong rhythm treatment — but the stroke question is still answered by CHA₂DS₂-VASc.	Reversible causeTFTs, U&E, LFTs
Prior cardioversions or ablations?"Have you had your heart rhythm corrected before — by shock or an operation inside the heart?"	Prior cardioversion → recurrence common. Prior ablation → persistent AF despite ablation = referral for re-do or rate control strategy. History changes the management pathway substantially.	Ablation pathwayRhythm vs rate strategy
Falls / bleeding history?"Have you had any falls recently? Any history of significant bleeding — stomach, brain, or elsewhere?"	Falls and bleeding history are HAS-BLED risk factors for anticoagulation. However, falls alone are NOT a contraindication to anticoagulation — the stroke risk of AF far outweighs the bleed risk in most cases. Important for shared decision-making.	HAS-BLED scoreShared decision on anticoagulation

1B — Red flags: act before continuing history

🚨

Red Flags in AF — act before continuing

Red flag	Why dangerous	Action
Haemodynamically unstable AF (SBP <90, impaired consciousness, severe breathlessness, chest pain)	Rapid AF may cause cardiogenic shock, pulmonary oedema, or myocardial ischaemia. Emergency DC cardioversion without waiting for anticoagulation. Time-critical.	999 — urgent cardioversion
AF with pre-excitation (WPW + AF on ECG: broad complex, irregular, very rapid >250 bpm)	Accessory pathway allows rapid conduction bypassing AV node → can degenerate to VF. AV-nodal drugs (digoxin, verapamil, adenosine, beta-blockers) are LETHAL — accelerate conduction via accessory pathway.	999 — DO NOT give AV nodal drugs
Acute stroke / TIA symptoms (FAST positive — new onset)	AF is a major cardioembolic stroke cause. FAST positive = thrombolysis window 4.5h. Every minute of delay = 1.9 million neurons lost.	999 — FAST protocol
Syncope or presyncope with AF	Syncope suggests haemodynamic compromise (very rapid rate or WPW). Risk of VF. Cannot be managed in community.	999 immediately
Suspected thyroid storm precipitating AF (fever, agitation, extreme tachycardia, AF)	Life-threatening hyperthyroid crisis. Mortality 10–25% untreated. Requires emergency endocrinology and high-dependency care.	999 — emergency endocrinology
Anticoagulated patient with acute severe headache / focal neurology (intracranial bleed)	Haemorrhagic stroke — anticoagulation must be stopped/reversed urgently. Urgent hospital reversal per local protocol: idarucizumab for dabigatran; for apixaban or rivaroxaban usually PCC (NICE TA697 recommends andexanet alfa only for life-threatening GI bleeding, not intracranial haemorrhage).	999 — reversal agent alert

🛡️

Safeguarding Considerations — AF Context

AF creates specific safeguarding vulnerabilities. Anticoagulation, cognitive effects of AF-related emboli, falls risk, and dependence on carers for medication all require attention.

🧠 Cognitive Impairment & Capacity

AF causes "silent" cerebral microemboli → cognitive decline (AF-dementia link)
Patient may lack capacity to consent to anticoagulation or cardioversion
Assess cognitive status — MoCA/MMSE if concern
If capacity impaired: MCA 2005 best interests decision for anticoagulation
Carer may be making medication decisions — is this appropriate?

🤕 Falls & Anticoagulation Risk

Falls + anticoagulation = intracranial bleed risk
Falls are NOT a contraindication to anticoagulation — stroke risk far outweighs in most cases
However: assess fall frequency and severity. Very frequent falls → referral to falls service
Does the patient live alone? Who would find them if they fell?
OT assessment for home hazards if appropriate

💊 Medication Safety

Anticoagulants have the narrowest therapeutic index of commonly prescribed drugs
If carer administers medications: correct dose? Correct timing? Understanding of interactions?
Warfarin interactions (antibiotics, NSAIDs, herbal remedies) — is patient at risk of inadvertent overdose?
DOAC adherence — twice-daily dosing in frail elderly with cognitive impairment is high-risk

🏠 Social Isolation & Stroke Risk

Isolated patients with AF are less likely to have strokes recognised early
Patient living alone: who would notice stroke symptoms and call 999?
Ensure patient and family/carer know FAST signs explicitly
Consider emergency alarm systems for isolated patients on anticoagulation

If safeguarding concern: Document clearly. Discuss with safeguarding lead. Falls service, social care, OT assessment, IMCA if capacity concerns. Anticoagulation decisions for patients lacking capacity require best interests assessment — involve family and document carefully.

1C — PMH · FH · Drug history · Social history

🧬 PMH / Risk factors — changes anticoagulation & management

Factor	Why it matters	Management impact
Prior stroke / TIA	Highest stroke risk in AF. Scores 2 on CHA₂DS₂-VASc. Often the precipitant for AF diagnosis.	Anticoagulate immediately regardless of other scores. Urgent neurology review if recent.
Heart failure	AF + HF = bidirectional deterioration. AF is commonest precipitant of HF decompensation.	Rate control with a beta-blocker (add digoxin if needed); avoid verapamil/diltiazem in HFrEF. Consider early rhythm referral. CHA₂DS₂-VASc point.
Hypertension	Most common risk factor for AF and for stroke in AF. Scores 1 on CHA₂DS₂-VASc and HAS-BLED.	Optimise BP alongside AF management. HAS-BLED point if uncontrolled.
Diabetes mellitus	Independent risk factor for AF and for AF-related stroke. Scores 1 on CHA₂DS₂-VASc.	CHA₂DS₂-VASc point. Tight glycaemic control may reduce AF burden.
Thyroid disease	Hyperthyroidism is a direct cause of AF. Must be excluded in all new AF. Amiodarone causes both thyroid disorders.	TFTs mandatory. Hyperthyroid → treat thyroid first. AF may resolve — still anticoagulate by CHA₂DS₂-VASc. Amiodarone → 6-monthly TFTs.
Valvular heart disease	Mitral stenosis + AF = very high stroke risk. Warfarin (not DOAC) mandatory in rheumatic MS. Prosthetic valve + AF → warfarin only.	Rheumatic MS or mechanical valve → warfarin, not DOAC. DOAC not validated here.
CKD	Reduces DOAC clearance (especially dabigatran). Warfarin may be preferred in advanced CKD (CrCl <15).	Dose every DOAC by creatinine clearance (Cockcroft-Gault), not lab eGFR. CrCl <30 → apixaban preferred (less renal clearance; check SPC). CrCl <15 → warfarin/specialist advice.
Liver disease	Impaired clotting factor synthesis. Warfarin and DOACs both affected. Rivaroxaban — hepatic metabolism concern.	Severe liver disease → all anticoagulants high-risk. Specialist input. Apixaban may be safest.

💊 Drug history · Social history — critical interactions

Factor	Why it matters	Management impact
Warfarin current	TTR (time in therapeutic range) <65% → subtherapeutic or supratherapeutic. Significant interaction burden. Monitoring burden.	TTR <65% → switch to DOAC. All must understand major interactions (antibiotics, NSAIDs, herbal).
NSAIDs (ibuprofen, naproxen)	↑ Bleeding risk on anticoagulation (GI bleed ×2–3). Can precipitate AF via fluid retention and haemodynamic effects.	STOP NSAIDs on anticoagulation — use paracetamol. HAS-BLED point if ongoing use.
Antiplatelet agents (aspirin, clopidogrel)	Dual antiplatelet + anticoagulant = triple therapy. Major bleeding risk. Aspirin alone does NOT prevent AF-related stroke.	Aspirin alone → switch to DOAC (superior stroke prevention). Triple therapy only with specialist input — limit to minimum duration.
Rate-lowering drugs (digoxin, diltiazem, verapamil, BB)	Drug interactions affect AF rate control. Verapamil/diltiazem + BB = bradycardia/heart block. Digoxin + hypokalaemia = toxicity.	Never combine verapamil + BB. Monitor K⁺ on digoxin. Review all rate-lowering agents together.
Alcohol >14 units/week	Alcohol is a direct AF trigger. "Holiday heart" — binge drinking causes acute AF. Chronic heavy use → cardiomyopathy → AF. Also ↑ bleeding risk on anticoagulation.	Alcohol reduction reduces AF burden significantly. HAS-BLED point. ≤14u/wk counselling.
Caffeine / stimulants	High caffeine → sympathetic activation → AF trigger. Cocaine, amphetamines: direct sympathomimetic → acute AF.	Moderate caffeine restriction. Screen for recreational stimulant use non-judgementally.
Herbal / OTC interactions	St John's Wort reduces warfarin and DOAC levels → subtherapeutic. Fish oil / vitamin E ↑ bleeding. Cranberry juice ↑ warfarin.	Ask specifically about supplements, herbals, OTC remedies. Counsel on interactions.
Driving / occupation	DVLA (Group 1): stop driving if the arrhythmia has caused or is likely to cause incapacity; may resume once the cause is identified and controlled for at least 4 weeks — notify DVLA only if this is not achieved or distracting/disabling symptoms persist. After catheter ablation: no driving for 2 days (no notification needed). Group 2 (HGV/PCV) standards are stricter.	Advise DVLA rules. Symptomatic AF → stop driving until controlled. HGV → stricter standards.

1D — ICE: Ideas · Concerns · Expectations

💭 Ideas

"What do you understand about atrial fibrillation? When you heard those words, what did that mean to you?"

Most patients equate AF directly with stroke or death. Some believe the heart is "stopping and starting." Clarifying the mechanism is therapeutic and prevents nocebo effects from catastrophic misinterpretation.

😟 Concerns

"You mentioned your husband had a stroke — I can imagine how frightening this diagnosis must feel for you. What specifically are you most worried about for yourself?"

Names the hidden agenda directly. The personal connection to a stroke victim changes every aspect of the consultation — the urgency the patient feels, their expectation around anticoagulation, and their willingness to accept reassurance.

🎯 Expectations

"Were you hoping we might start a blood thinning tablet today? Let me explain what the evidence says about that, and then we can decide together what the right approach is for you specifically."

Validates the expectation (anticoagulation today) before explaining the clinical reasoning. The CHA₂DS₂-VASc score is not just a number — it is the reason a shared decision can be made transparently with the patient.

1E — Psychosocial context: the person living with AF

😰 Anxiety & AF

AF palpitations cause significant anxiety — each episode feels like a potential stroke or cardiac arrest. Hypervigilance amplifies symptom burden. Anxiety itself triggers sympathetic activation → more palpitations → vicious cycle.

"How are you finding it emotionally — do you find yourself worrying about each episode when it happens?"

🏃 Exercise & Sport

Vigorous exercise can trigger AF in some patients ("athlete's AF"). However, exercise is beneficial overall. Most patients with stable AF can continue normal activity. Sports that require DVLA or aviation licences have strict rules.

"Has this affected your ability to exercise or do sport? I want to be clear about what you can and can't safely do."

🚗 Driving

DVLA (Group 1): AF that has caused or is likely to cause incapacity (syncope, presyncope, haemodynamic compromise) — stop driving until the cause is identified and controlled for at least 4 weeks; notify DVLA if that is not achieved or disabling symptoms persist. After catheter ablation: 2 days off driving, no notification. Stable asymptomatic AF: no notification required. HGV/PCV: stricter rules.

"Do you drive? I need to advise you about whether the current symptoms affect your ability to drive safely."

💑 Relationships & Sexuality

Some anticoagulants + sildenafil/tadalafil: bleeding risk increased. Partner anxiety about AF episodes — they may fear the patient will have a stroke during exertion. Role of the partner in recognising stroke symptoms and acting.

"Has any of this affected your relationship or things that are important to you personally?"

💼 Work & Employment

Certain professions (pilots, HGV drivers, emergency services) have regulatory requirements that may end careers if AF is persistent or symptomatic. This is a significant life-altering consequence that must be addressed proactively.

"What do you do for work? I want to make sure I explain the implications for your job — if any — clearly."

💊 Anticoagulation Fears

Fear of bleeding on warfarin/DOAC is the most common reason for non-adherence. Patients often stop anticoagulation without telling their GP. Regular INR checks (warfarin) = anxiety for some. DOACs remove this but some fear "taking a blood thinner" at all.

"How do you feel about the idea of taking a blood-thinning tablet? Are there any concerns about bleeding that I can address?"

🎓 SCA Checkpoint — Step 1TasksRelating to OthersGlobal Skills

Key phrases that score

"I can see from the ECG that the rhythm is irregular — this is AF..."

"Before I explain anything, how are you feeling and what's been going through your mind?"

"You mentioned your husband had a stroke — what are you most worried about for yourself?"

"How has this been affecting your daily life — work, driving, exercise?"

Deductions

Starting with CHA₂DS₂-VASc score calculation before open Q
Not addressing the stroke fear / personal connection
Missing reversible causes (thyroid, alcohol, electrolytes)
Not asking about driving and occupational implications
Missing anticoagulation adherence fears as a topic

🔴 Red

Goes straight to CHA₂DS₂-VASc; no ICE; stroke fear not addressed; reversible causes not sought; rigid symptom checklist

🟠 Amber

Opens reasonably; ICE formulaic; husband's stroke mentioned but not explored; some reversible causes sought; driving not raised

🟢 Green

Acknowledges ECG; open Q; ICE with husband's stroke explored; reversible causes screen; psychosocial (driving, anxiety, work); data gathering complete by 6–7 min

2

Step 2

Triage Engine — Emergency · Urgent · Routine

▲collapse

AF triage is haemodynamic first, then stroke risk, then rate. The first question is never "what is the CHA₂DS₂-VASc score?" — it is "is this patient stable?" Haemodynamically unstable AF = 999. Stable AF with high stroke risk = urgent anticoagulation. Stable AF, rate controlled, low risk = routine.

🔴 Emergency — 999

Haemodynamically Unstable / Life-Threatening

999 now

Haemodynamically unstable AFSBP <90 · impaired consciousness · severe breathlessness · ongoing chest pain
AF with WPW (pre-excitation)Broad complex irregular >250 bpm · DO NOT give AV nodal drugs — VF risk
FAST-positive stroke / TIAAF-related thromboembolism — thrombolysis window 4.5h
Syncope or presyncope with AFHaemodynamic compromise — risk of VF
Thyroid storm + AFLife-threatening hyperthyroid crisis
Anticoagulated + severe headache / focal neurologyIntracranial haemorrhage — reversal agent needed urgently

🟠 Urgent — hours to days

Haemodynamically Stable — Needs Action

Same-day / days

New AF <48h onset, stableRate control + anticoagulate + consider cardioversion
Rapid AF HR >110 + breathlessnessRate control urgently — risk of HF decompensation
High CHA₂DS₂-VASc ≥2 (men or women), not anticoagulatedStart DOAC today — don't wait
New AF with suspected reversible cause (thyrotoxicosis)TFTs urgently — treat cause first
Anticoagulated patient with INR >4.0 or acute bleedingSame-day management

🟢 Routine — GP management

Stable AF — Planned Management

GP + outpatient

Paroxysmal AF, rate controlled, asymptomaticScore CHA₂DS₂-VASc, anticoagulate if indicated, rhythm monitoring
Permanent AF, stable rate, anticoagulatedAnnual structured review
Known AF — DOAC reviewAdherence, renal function, dose review
Rhythm control referral (persistent AF)Cardiology for cardioversion / ablation assessment
Warfarin → DOAC switchTTR <65% → planned switch with GP or pharmacist

🎓 SCA Checkpoint — Step 2TasksGlobal Skills

Safety screen — say this before management

"Before I explain the plan, I need to ask a few specific questions — is your breathing manageable right now? Any chest pain? Have you ever felt faint or actually passed out with the palpitations?"

Deductions

Going straight to CHA₂DS₂-VASc / anticoagulation without haemodynamic triage first
Missing WPW as a dangerous special case of AF
Not naming red flags aloud to the examiner

🔴 Red

Starts anticoagulation discussion without haemodynamic safety check; misses WPW trap; no safety screen verbalised

🟠 Amber

Some safety questions but not all verbalised; WPW not considered; urgency grading partially correct

🟢 Green

Haemodynamics checked first; all red flags named aloud; WPW acknowledged if relevant; correctly triages before management

3

Step 3

Do I Need This Examination?

▲collapse

AF examination has one primary goal: haemodynamic status. Is this patient stable? Every subsequent finding either adds to the management plan or changes urgency. The pulse tells you the rate; the BP tells you the stability; the heart tells you the cause.

Examination	Why it matters in AF	Finding that changes management	Changes management?
Pulse — rate, rhythm, character	Confirms AF (irregular irregular). Rate determines urgency. Rate >110 bpm at rest = inadequate rate control → needs treatment today. Rate >150 = haemodynamic risk.Regular rapid pulse = SVT or flutter, not AF — different management.	Rate >110 at rest → start rate control. Rate >150 + symptoms → urgent cardioversion consideration. Irregular-regular = flutter with block.	YES — always
Blood pressure (both arms)	Hypotension (SBP <90) = haemodynamic compromise → 999. Hypertension = significant CHA₂DS₂-VASc and HAS-BLED risk factor. Documents BP before starting rate-lowering drugs (cannot give BB if hypotensive).	SBP <90 → 999. SBP >140 → optimise BP as part of AF management and stroke risk reduction.	YES — urgency + drug choice
JVP + peripheral oedema	Raised JVP + oedema = HF triggered by rapid AF. Rapid AF reduces CO by 20–30% (loss of atrial kick) → decompensation. Also identifies fluid overload from other causes precipitating AF.	Signs of HF → rate control urgently + diuretics + consider cardiology same-day.	YES — urgency
Heart sounds (murmurs)	Mitral stenosis murmur = rheumatic MS + AF → warfarin mandatory (not DOAC). Aortic stenosis = valve disease causing AF. Any murmur suggests structural heart disease → echo urgently.	Mitral stenosis → warfarin not DOAC. Any new murmur → urgent echo + cardiology.	YES — drug choice (warfarin vs DOAC)
Lung auscultation + SpO₂	Bibasal crepitations = pulmonary oedema (rapid AF → HF). SpO₂ <94% = significant hypoxaemia. Normal SpO₂ does not exclude early decompensation.	Crepitations + low SpO₂ → 999 or same-day hospital. SpO₂ <94% → O₂ + urgent referral.	YES — urgency
Thyroid examination	Goitre, tremor, lid lag, exophthalmos, proximal myopathy = thyrotoxicosis. Hyperthyroidism is a direct, reversible cause of AF. Essential in all new AF.	Signs of thyrotoxicosis → urgent TFTs. Treat thyroid first — AF may resolve, but anticoagulation is still decided by CHA₂DS₂-VASc.	YES — aetiology + treatment
Cognitive assessment (brief)	AF → silent cerebral microemboli → cognitive impairment. Relevant for capacity assessment (anticoagulation decision). Also important for medication safety — can patient manage DOAC dosing reliably?	Cognitive impairment → capacity assessment. May need IMCA for anticoagulation decision. DOAC adherence risk.	YES — capacity + safety
Signs of bleeding / bruising	Spontaneous bruising, petechiae, signs of GI bleeding (pallor, abdominal tenderness) = pre-existing haemostatic problem. Relevant before starting anticoagulation — changes HAS-BLED assessment.	Active bleeding → do not anticoagulate until resolved. Treat bleeding cause first. Haematology input if coagulopathy.	YES — anticoagulation safety

🎓 SCA Checkpoint — Step 3Tasks

How to propose examination

"I'd like to check your pulse and blood pressure — the rate and stability of your heart rhythm tells me a lot about how urgent things are. I'll also listen to your heart for any abnormal sounds, and check your thyroid gland in your neck, as thyroid problems can sometimes trigger this rhythm."

Deductions

Not checking heart rate — the primary management driver in AF
Missing murmurs — determines warfarin vs DOAC
Not examining the thyroid in new AF
Not linking findings directly to management changes

🔴 Red

Pulse only; no murmur check; thyroid not examined; findings not linked to management; rate and BP not documented

🟠 Amber

Pulse and BP checked; heart sounds mentioned; thyroid not examined; some findings not acted upon

🟢 Green

Pulse rate + rhythm + BP; heart sounds (murmurs); JVP/oedema; thyroid; SpO₂; each finding linked to specific management decision

4

Step 4

Do I Need This Investigation?

▲collapse

ECG is the gateway investigation — it confirms AF. Every subsequent investigation either identifies a reversible cause, assesses stroke/bleed risk, identifies structural disease, or monitors treatment safety. No investigation should be ordered without knowing what management change a result would trigger.

Investigation	Clinical question it answers	What result changes management?
12-lead ECG	The gateway investigation — confirms AF diagnosis. Also: identifies WPW (delta waves + short PR + broad complex = dangerous), LVH (hypertensive cardiomyopathy), ischaemia, flutter with block (regular sawtooth P waves), bundle branch block.	Irregular rhythm + no P waves = AF confirmed. WPW signs → 999, do not give AV nodal drugs. Flutter → different rate control strategy. LVH → echo.
TFTs (thyroid function tests)	Mandatory in all new AF — hyperthyroidism is a direct, reversible cause. Also mandatory if amiodarone used (causes both hypo and hyperthyroidism). TSH <0.1 = possible hyperthyroid → treat first, AF may resolve.	Hyperthyroidism → treat thyroid urgently. AF may resolve — anticoagulation still follows CHA₂DS₂-VASc, not apparent rhythm success. Hypothyroidism → levothyroxine.
U&E + eGFR + K⁺	Electrolyte disturbances (hypokalaemia, hypomagnesaemia) are direct AF triggers and also increase toxicity risk of antiarrhythmics/digoxin. Creatinine clearance (Cockcroft-Gault — needs a weight), not the lab eGFR, determines DOAC dose selection and safe prescribing. Baseline before starting anticoagulation.	K⁺ <3.5 → correct before antiarrhythmics. CrCl <30 → apixaban preferred, check SPC. CrCl <15 → warfarin/specialist advice. K⁺ <3.5 on digoxin → toxicity risk → correct urgently.
FBC (full blood count)	Anaemia → tachycardia → can trigger or exacerbate AF. Low platelet count = bleeding risk before anticoagulation. Baseline Hb before starting anticoagulation.	Anaemia → treat cause (iron, B12, folate, chronic disease). Thrombocytopaenia <50 → specialist input before anticoagulating. Low Hb → investigate before DOAC.
LFTs (liver function tests)	Liver disease affects drug metabolism — apixaban and rivaroxaban are hepatically metabolised. Baseline LFTs before amiodarone initiation (hepatotoxicity). Chronic liver disease = coagulopathy — affects anticoagulation safety.	Moderate-severe liver disease → avoid rivaroxaban; apixaban may be safer. Amiodarone → LFTs every 6 months. Abnormal LFTs → specialist review.
Echocardiogram	Identifies structural heart disease (LV dysfunction, valvular disease, LVH, intracardiac thrombus). Mitral stenosis = warfarin mandatory. LV thrombus = anticoagulate before any cardioversion. LA size predicts cardioversion success.	Mitral stenosis → warfarin not DOAC. EF <40% → HF management + rate control strategy changes. LV thrombus → delay cardioversion until anticoagulated for ≥3 weeks minimum.
Holter monitor / 7-day ECG patch	For suspected paroxysmal AF — symptoms with normal 12-lead ECG. NICE NG196: 24-hour ambulatory ECG if episodes are asymptomatic or symptomatic episodes are <24h apart; an ambulatory monitor, event recorder or other ECG technology for an appropriate period if episodes are >24h apart. 7-day or longer patch increases yield significantly for paroxysmal AF. Wearable devices increasingly used.	Paroxysmal AF confirmed → anticoagulate based on CHA₂DS₂-VASc (same as persistent AF). AF burden informs rate vs rhythm discussion.
INR (if on warfarin)	Confirms therapeutic range (target 2–3 for non-valvular AF). TTR (time in therapeutic range) <65% = poor control → DOAC switch. Supratherapeutic INR >4 = bleeding risk. Before cardioversion: INR must be ≥2 for ≥3 weeks.	INR <2 → cardioversion must wait (unless <48h onset). INR >4 → withhold warfarin + recheck. TTR <65% → switch to DOAC discussion.

🎓 SCA Checkpoint — Step 4TasksRelating to Others

How to explain investigations

"The ECG already confirmed the irregular rhythm — that's atrial fibrillation. I'd like to do some blood tests: checking your thyroid, as thyroid problems are one of the reversible causes of this rhythm; your kidney function, as that affects which tablets are safest; and your blood count."

"I'd also like to arrange a heart scan — an echocardiogram — to check the structure of the heart and make sure there are no underlying problems."

Deductions

Not ordering TFTs in new AF — mandatory
Starting DOAC without calculating creatinine clearance first
Not explaining why each investigation is needed
Forgetting to check INR before cardioversion in warfarin patient

🔴 Red

No TFTs ordered; starts DOAC without CrCl; investigations ordered without explanation; echo not mentioned

🟠 Amber

TFTs requested but rationale not explained; renal function checked but CrCl not linked to DOAC dose; echo mentioned but without explanation

🟢 Green

ECG as gateway; TFTs with rationale; CrCl (Cockcroft-Gault) linked to DOAC selection; FBC; echo with rationale; each test linked to management question; explained in plain language

5

Step 5

Reaching a Diagnosis — AF Classification · CHA₂DS₂-VASc · DDx · Plain Language

▲collapse

AF diagnosis has two components: confirming the arrhythmia (ECG) and assessing stroke risk (CHA₂DS₂-VASc). The CHA₂DS₂-VASc score is not just a number — it is the foundation of a shared decision about anticoagulation. Explain it to the patient in lay language before offering a management plan.

🗣️ Explaining AF in plain language

"Your heart normally beats in a regular rhythm — controlled by an electrical signal that starts in one place and spreads evenly. In atrial fibrillation, that electrical signal becomes chaotic. Instead of one organised beat, hundreds of small electrical signals fire at random, making the upper chambers of the heart quiver rather than pump properly. The heart still works — blood still circulates — but less efficiently, and the quivering can allow blood to pool and clot in a little pocket of the heart. If that clot breaks off, it can travel to the brain and cause a stroke. That's why the main treatment isn't just about the heart rhythm — it's about preventing a stroke."

💬 Addressing the patient's explanation — correcting common misconceptions

"Does AF mean my heart is stopping and starting?"
"No — your heart is still beating, just in a disorganised way. It doesn't stop. What changes is the rhythm — instead of a regular controlled beat, the upper chambers are firing very rapidly and chaotically, so the rhythm feels irregular. Most people feel this as palpitations — fluttering or racing — but some people feel nothing at all."

"I've had AF for years without a stroke — why do I need blood thinners now?"
"That's a fair question. The risk of stroke in AF depends on your individual risk factors — things like age, blood pressure, and whether you've had a stroke before. We calculate this using a score, and based on your score, your risk is high enough that the benefit of a blood thinner outweighs the risk of bleeding. The stroke risk without a blood thinner is significantly higher than the bleeding risk with one — that's why we recommend it."

5A — AF Classification: type + chronicity

Paroxysmal AF

Episodes that self-terminate within 7 days (usually <48h). Recurrent. May be asymptomatic. Same stroke risk as persistent AF — anticoagulate based on CHA₂DS₂-VASc.

Persistent AF

Lasts >7 days or requires cardioversion. Does not self-terminate. Rhythm control may be attempted. Anticoagulation offered if CHA₂DS₂-VASc ≥2 (NICE NG196).

Long-standing Persistent

AF >12 months despite attempts to restore sinus rhythm. Rhythm control may still be attempted (ablation) or accepted as permanent.

Permanent AF

Patient and clinician accept AF as permanent — no further rhythm control attempted. Rate control + anticoagulation strategy. Focus on symptom management and stroke prevention.

5B — CHA₂DS₂-VASc Score: calculate + interpret + act

🧮 CHA₂DS₂-VASc — every component changes management

C

Heart Failure

1 point

Active HF or impaired LV systolic function (EF <40%)

H

Hypertension

1 point

Treated or untreated BP ≥140/90 on ≥2 occasions

A₂

Age ≥75

2 points

Doubles on previous age risk — most impactful single factor

D

Diabetes

1 point

Treated DM or fasting glucose >7.0 mmol/L

S₂

Prior Stroke/TIA

2 points

Previous stroke, TIA, or systemic thromboembolism — highest single risk

V

Vascular Disease

1 point

Prior MI, peripheral arterial disease, or aortic plaque

A

Age 65–74

1 point

Lower age risk bracket — different from A₂

Sc

Sex (Female)

1 point

Female sex is a risk modifier — do NOT anticoagulate based on female sex alone (score of 1 in women only)

0 ♂ / 1 ♀

Low risk

No anticoagulation. Annual review. If male score 1 (not solely female sex category) — consider anticoagulation.

1 ♂

Intermediate

Consider anticoagulation — individualise based on patient preference, bleeding risk (ORBIT preferred by NG196), and clinical judgement.

≥2 (♂ or ♀)

High risk

Offer anticoagulation. DOAC first-line unless valvular AF or contraindication. Do not withhold based on age or falls alone.

⚠ Important: Female sex alone (score 1 in women) does NOT meet the threshold to anticoagulate — this prevents over-treatment of low-risk women. A score of 1 in a man warrants consideration. Aspirin is NOT an acceptable alternative to anticoagulation for AF stroke prevention.

5C — Bleeding risk: NICE NG196 — consider ORBIT (HAS-BLED shown for familiarity) — not to withhold anticoagulation, but to correct modifiable factors

💉 HAS-BLED — identify and correct modifiable bleeding risk factors

H

Hypertension

Uncontrolled SBP >160 — 1 point. Modifiable.

A

Abnormal Renal/Liver

eGFR <30 or chronic liver disease (1 pt each, max 2)

S

Stroke History

Prior stroke — 1 point. Also a CHA₂DS₂-VASc factor.

B

Bleeding History

Prior major bleed or bleeding predisposition — 1 pt

L

Labile INR

TTR <60% on warfarin — 1 point. Switch to DOAC.

E

Elderly (>65)

Age >65 years — 1 point. Not modifiable.

D

Drugs / Alcohol

NSAIDs, antiplatelets, or alcohol >8 drinks/wk (1 pt each, max 2)

≥3

HIGH RISK

Review and correct modifiable factors. Do NOT automatically withhold anticoagulation — stroke risk usually still outweighs.

Critical principle: NG196: consider ORBIT (more accurate than HAS-BLED); a high score on either is NOT a contraindication to anticoagulation. It flags modifiable bleeding risk factors to correct (control BP, stop NSAIDs, reduce alcohol, switch from warfarin to DOAC if labile INR). The stroke risk of AF almost always outweighs the bleed risk of anticoagulation. Document the shared decision clearly.

5D — DDx: conditions that mimic or coexist with AF

Condition	Distinguishing features	Key difference from AF
Atrial flutter	Regular sawtooth P waves at 300 bpm; ventricular rate often regular 150 bpm (2:1 block) or 100 (3:1). May feel like AF to patient.	Regular-regular or regular-irregular (not irregular-irregular). Different cardioversion and ablation strategy. Anticoagulate same as AF.
SVT (AV nodal re-entry)	Regular rapid onset/offset palpitations. Regular rhythm on ECG. No P waves visible or retrograde P waves.	Regular (not irregular). Adenosine terminates SVT. Different long-term management (vagal manoeuvres, ablation).
Frequent ectopics (AF mimic)	Irregular palpitations. ECG shows frequent premature atrial or ventricular complexes with brief pauses. Not AF.	Normal P waves present between ectopics. No anticoagulation needed. Reassurance and lifestyle modification.
WPW + AF	Very rapid (often >250 bpm), broad complex, irregular. Delta waves on baseline ECG. Pre-excitation pattern.	DANGEROUS — AV nodal drugs (digoxin, verapamil, BB, adenosine) can cause VF. Must be diagnosed urgently. Refer for ablation.
Atrial tachycardia	Regular rapid P waves at 150–250 bpm. Different P wave morphology from sinus. Usually regular.	Regular rhythm. Different ECG morphology. Different ablation target. Anticoagulation usually not required.
Sinus arrhythmia	Normal variation in heart rate with breathing. Common in young people and athletes. ECG shows normal P waves.	Normal P waves present. Rate variation with respiration. No management required. Very benign.

🎓 SCA Checkpoint — Step 5TasksRelating to Others

Verbalising diagnosis + CHA₂DS₂-VASc in lay language

"The ECG shows your heart rhythm is irregular — this is atrial fibrillation, or AF. Think of it as the electrical system becoming chaotic. The heart still pumps, but blood can pool in a small pocket and clot — if that clot reaches the brain, it causes a stroke. That's why the main question isn't about controlling the rhythm — it's about stroke prevention."

"I use a score to calculate your individual stroke risk. Based on your [age/BP/diabetes etc.], your score is X — which means we should offer you a blood-thinning tablet."

Deductions

Not explaining the CHA₂DS₂-VASc score to the patient
Calculating the score without sharing it or explaining it
Offering aspirin instead of anticoagulation
Not distinguishing AF types (paroxysmal vs persistent)
Withholding anticoagulation based on falls alone

🔴 Red

AF not explained; score calculated but not shared; aspirin offered; anticoagulation withheld without reason; AF type not distinguished

🟠 Amber

AF explained but clot/stroke mechanism not articulated; score mentioned but not explained; anticoagulation offered but HAS-BLED not considered

🟢 Green

Chaotic signal/clot/stroke pathway explained in plain language; CHA₂DS₂-VASc score calculated and shared with patient; HAS-BLED modifiable factors identified; AF type named; aspirin correctly discarded

6

Step 6

If Referral Is Needed — What the GP Does Before & During

▲collapse

AF management is primarily GP-led — referral is targeted, not reflexive. Rate control and anticoagulation are initiated in primary care. Referral is indicated for rhythm control (cardioversion/ablation), suspected structural heart disease, WPW, or failure of rate control. The GP must not delay anticoagulation while waiting for the cardiology appointment.

Scenario	Urgency	What GP does before/during referral	What GP must NOT do
Haemodynamically unstable AF	999 now	Sit patient up. O₂. IV access if trained. Call 999. Alert hospital to WPW if suspected (different drug protocol).	Do NOT give AV nodal drugs if WPW suspected. Do NOT delay 999 call.
New AF <48h, stable — cardioversion consideration	Same-day cardiology	Rate control (BB or diltiazem if no WPW). Anticoagulate NOW with DOAC or heparin. Refer for same-day or next-day cardioversion if appropriate.	Do NOT cardiovert without anticoagulation cover (unless <48h AND echo excludes thrombus). Do NOT wait for cardiology to start anticoagulation.
Persistent AF — rhythm control	Routine cardiology	Start DOAC and rate control NOW. Refer for planned cardioversion (anticoagulate ≥3–4 weeks before). Or refer for catheter ablation assessment if symptomatic paroxysmal AF.	Do NOT delay anticoagulation waiting for cardiology appointment. Do NOT refer without starting rate control and anticoagulation.
WPW + AF suspected	999 / urgent cardiology	Do not give AV nodal drugs. Call 999 if unstable. Urgent cardiology if stable. Refer for ablation after stabilisation.	Do NOT give digoxin, verapamil, diltiazem, or adenosine — can cause VF via accessory pathway acceleration.
Failed rate control (>110 despite optimal drugs)	Routine cardiology	Ensure patient anticoagulated. Optimise current drugs (increase dose, add second agent). Document resting and exercise HR. Refer with drug history and HR data.	Do NOT combine verapamil/diltiazem + beta-blocker — heart block risk.
Symptomatic paroxysmal AF — ablation	Routine cardiology	Anticoagulate per CHA₂DS₂-VASc (ablation does not replace anticoagulation). Rate control. Holter monitor documentation. Refer with Holter data.	Do NOT stop anticoagulation after ablation without specialist advice — AF may recur.

🎓 SCA Checkpoint — Step 6TasksGlobal Skills

How to explain referral

"I'm going to start the blood-thinning tablet today — I don't want to wait for the cardiology appointment for that, because your stroke risk is real now. I'm also referring you to see a cardiologist who can discuss whether restoring your heart to a normal rhythm is possible and right for you."

Deductions

Delaying anticoagulation until after cardiology appointment
Not starting rate control before referral
Missing WPW as a dangerous drug contraindication
Not explaining referral purpose to patient

🔴 Red

Refers without starting anticoagulation; wrong drug for WPW; no rate control before referral; patient not told what to expect

🟠 Amber

Anticoagulation started but delay; rate control initiated; referral reason not explained; WPW not considered

🟢 Green

DOAC started today regardless of referral; rate control initiated; correct urgency for referral; WPW considered; patient told what to expect from cardiology

7

Step 7

Management — Expectation · Drug Selector · Drug Reference · Psychosocial · Follow-Up · Safety-Netting

▲collapse

7A — Address expectation first: validate → explain → negotiate

🤝

The patient's expectation is almost always about stroke prevention — validate it, then explain how the evidence guides the decision

1

Validate the fear

Most patients request anticoagulation immediately — because they are terrified of stroke. This is rational. Acknowledge it explicitly.

"I completely understand why you'd want to start a blood-thinning tablet immediately — your concern about stroke is absolutely valid, especially given what you've witnessed with your husband. That's exactly what I want to address today."

2

Explain with the score

Share the CHA₂DS₂-VASc calculation transparently. The score makes the clinical reasoning visible and shared.

"I've calculated your individual stroke risk score — it's called the CHA₂DS₂-VASc score. Yours is [X], which means your risk of stroke without a blood thinner is approximately [Y]% per year. With a blood thinner, we can reduce that by around 60–70%. Based on that, I am recommending we start one today."

3

Negotiate the plan

Offer a specific drug choice with shared decision-making. DOAC vs warfarin — involve the patient in the choice.

"There are two main types of blood thinner — a newer tablet called a DOAC that most people find easier because there are no regular blood tests, and the older one called warfarin which needs regular INR checks. Most people choose the DOAC. Which sounds more manageable for you?"

7B — Treatment goals

Treatment goals

↓ Stroke risk 60–70% with anticoagulationRate control guided by symptoms (ESC: HR <110 at rest) Prevent HF decompensationReduce symptom burden Correct reversible causesPatient education on stroke recognition Shared anticoagulation decisionDOAC preferred over warfarin

Motivational language for patients

"AF raises your risk of stroke by about 5 times compared to someone without AF. The blood-thinning tablet reduces that risk by 60–70% — that means for every 100 people with your risk score who take the tablet, we prevent around [X] strokes per year."

"The tablet to slow your heart rate won't prevent a stroke — those are two separate problems. The rate tablet makes you feel better. The blood thinner protects your brain. You need both."

7C — Non-medication management: mechanism + evidence + tailored advice for AF

Lifestyle modification is disease-modifying in AF — not just a polite add-on. The Cardiff and RACE-3 trials demonstrate that aggressive risk factor management reduces AF burden and recurrence independent of rate/rhythm drugs. Each item below has a documented mechanism in AF pathophysiology and a quantified clinical effect. Present it as a real treatment, not a gentle suggestion.

⚖️

Weight Loss

Target: ≥10% body weight if overweight

Mechanism in AF

Obesity → ↑ left atrial pressure and stretch → atrial remodelling and fibrosis. Fat deposits directly infiltrate the atrial myocardium (epicardial adipose tissue). ↑ Vagal tone and ↑ inflammatory cytokines both lower the threshold for AF triggers.

Practical

The LEGACY trial: ≥10% weight loss → 46% AF-free survival at 5 years vs 13% in <3% weight loss group. Frame it as a treatment: "Losing 10 kg has a bigger effect on your AF than most tablets."

↓ AF burden 46% (LEGACY trial)

🏃

Exercise (Structured)

150 min/week moderate — not extreme endurance

Mechanism in AF

Moderate aerobic exercise → ↓ sympathetic tone, ↓ resting HR, ↑ vagal HR variability, ↓ systemic inflammation (IL-6, CRP). Reduces LA size over time. Note: extreme endurance athletes have paradoxically ↑ AF risk (vagal remodelling, LA stretch).

Practical

CARDIO-FIT study: every 1 MET ↑ in fitness = 8% ↓ in AF recurrence. Brisk walking, cycling, swimming. Reassure patient that moderate exercise is safe and cardioprotective — avoid the "just take it easy" message that leads to deconditioning.

8% ↓ AF recurrence per 1 MET ↑ (CARDIO-FIT)

🍺

Alcohol Reduction

Target: ≤14 units/week — preferably less

Mechanism in AF

Alcohol → directly shortens atrial refractory period via acetaldehyde effect. Binge drinking → catecholamine and vagal surges ("holiday heart syndrome"). Chronic alcohol → atrial fibrosis. Even moderate drinking (1–2 units/day) increases AF incidence by ~8% per drink.

Practical

REDUCE-AF trial: abstinence → 37% ↓ in AF episodes at 6 months vs controls. ≤14 units/week; spread across ≥3 days; avoid binge episodes entirely. AUDIT-C screen. DrinkCoach app. Frame: "alcohol is one of the most powerful triggers of AF episodes."

37% ↓ AF episodes with abstinence (REDUCE-AF)

😴

Sleep Apnoea Treatment

Screen all AF patients — OSA prevalence ~50%

Mechanism in AF

OSA → intermittent hypoxia → ↑ sympathetic surges during apnoeic episodes → atrial ectopy and triggered AF. Negative intrathoracic pressure stretches the atria. OSA causes atrial remodelling even without hypertension. CPAP reverses some of this.

Practical

STOP-BANG or Epworth screen at every AF review. OSA present in ~50% of AF patients. Refer for sleep study if suspected. CPAP use → 42% ↓ AF recurrence post-cardioversion (Kanagala study). Ask: snoring, witnessed apnoeas, daytime sleepiness, morning headaches, collar size >17 inches.

42% ↓ AF recurrence post-DCCV with CPAP

❤️

Hypertension Control

Target: <130/80 mmHg in AF

Mechanism in AF

Hypertension is the most common modifiable AF risk factor: ↑ LV wall stress → ↑ LA pressure → atrial stretch and remodelling. ACEi/ARB reduce atrial fibrosis (upstream therapy). Uncontrolled BP is the primary driver of stroke risk in AF patients — independently of CHA₂DS₂-VASc score.

Practical

Check BP at every AF review. Target <130/80 in high-risk patients. ACEi/ARB preferred in AF + HTN — both antihypertensive and anti-fibrotic. Document home BP readings to distinguish white-coat effect. ABPM if uncertainty.

Most common modifiable AF risk factor — treat aggressively

🚭

Smoking Cessation

Complete cessation — no safe level

Mechanism in AF

Nicotine → acute catecholamine release → ↑ atrial ectopy. Chronic smoking → systemic inflammation and oxidative stress → atrial structural remodelling. Smoking worsens all AF risk factors simultaneously (HTN, IHD, HF, OSA). CVD mortality doubles with AF + smoking combined.

Practical

NHS Stop Smoking Service: behavioural support plus varenicline, cytisinicline, combination NRT or a nicotine vape (NICE NG209). CO breath test at every visit to motivate. Frame: "smoking makes your AF harder to control and doubles your stroke risk on top." Do not omit this in a consultation focused on anticoagulation.

↓ CVD risk 50% within 1 year of cessation

7D — Prescribing guide: what to start, in what order, and why

Rate control is first-line for most AF — with early rhythm referral considered in selected patients. NG196 sets no numeric target — titrate to symptoms; ESC/RACE II lenient target resting HR <110 bpm, tightened to <80 bpm if still symptomatic. Rate control does NOT prevent stroke — anticoagulation is always required alongside it.

Step 1 — Always first: anticoagulation

Start a DOAC in virtually every patient with CHA₂DS₂-VASc ≥2 (men or women; NICE NG196). This is the single most important prescribing decision in AF — reduces stroke risk 60–70%.

Anticoagulation is independent of rate or rhythm control. Never defer it until rate is controlled — these are parallel, simultaneous decisions.

First choice: Apixaban 5mg BD (reduced dose: 2.5mg BD if ≥2 of age ≥80 / weight ≤60kg / creatinine ≥133) · Rivaroxaban 20mg OD with evening meal · Edoxaban 60mg OD
Warfarin if: mechanical heart valve or moderate-to-severe mitral stenosis (DOACs contraindicated), antiphospholipid syndrome (any — DOAC not recommended, MHRA June 2019), CrCl <15, DOAC intolerance, or an established stable INR the patient prefers

Step 2 — Rate control: monotherapy first

Start one agent. Do not combine rate-limiting drugs unless monotherapy fails at maximum tolerated dose.

Beta-blocker (e.g. bisoprolol 1.25–2.5mg OD) OR rate-limiting CCB — either is first-line (NG196). Titrate to symptoms and rate. Beta-blocker suits HFrEF. Usually avoid beta-blockers in asthma (COPD is not a bar); avoid in bradycardia.
Diltiazem MR or verapamil — equal first-line option (e.g. asthma, BB intolerance); not in HFrEF. Never verapamil + BB — complete heart block risk; NG196 allows BB + diltiazem as dual therapy with monitoring.
Digoxin — add-on or monotherapy in sedentary patients only. Ineffective at rate control during exertion. Narrow therapeutic window — check levels + renal function.

⛔ BB + diltiazem/verapamil simultaneously = absolute contraindication (complete AV block) | ⛔ Any AV nodal drug in WPW = risk of VF

Step 3 — Rhythm control: selected patients only

Not first-line for all AF. Consider if: symptomatic despite rate control, new-onset AF <12 months, younger patient, AF + HFrEF (EAST-AFNET 4: early rhythm control ↓ CV death/stroke by 21%).

Flecainide — structurally normal heart only. Pill-in-the-pocket for paroxysmal AF. Add a rate-limiting drug (BB or diltiazem) to prevent 1:1 flutter conduction.
Amiodarone — most effective; use when structural heart disease present. 6-monthly TFT, LFT, CXR mandatory. Many interactions (warfarin, digoxin, statins).
DCCV — if AF <48h or anticoagulated ≥3 weeks. Continue rate control alongside. Anticoagulate for ≥4 weeks post-DCCV.

⚠️ Flecainide contraindicated in IHD / structural disease — pro-arrhythmic | Always anticoagulate before and ≥4 weeks after cardioversion

⚙ Interactive Medication Chooser — tick the patient profile, options re-tier live against NICE NG196 / SPC

A live, topic-scoped version of the standalone Medication Chooser. The static selector and reference cards below are unchanged.

7E — Medication options — guideline summary (no patient selection)

Situations this summary covers

⚡ Rate Control Factors
Asthma or severe COPD
Heart failure with reduced EF (HFrEF, EF <40%)
WPW / pre-excitation on ECG ⛔
Resting HR <60 bpm (bradycardia)
💊 Anticoagulation Factors
Rheumatic mitral stenosis or mechanical heart valve
CKD — CrCl <30 mL/min (Cockcroft-Gault)
On warfarin with poor control (TTR <65%)
Frailty: ≥2 of (age ≥80, weight ≤60kg, creatinine ≥133)
🎵 Rhythm Control Factors
Structural heart disease or IHD (previous MI, cardiomyopathy)
Paroxysmal AF — symptomatic, structurally normal heart
Currently on amiodarone
New AF onset <48 hours — cardioversion window open

What the guidance says, by situation

⛔ WPW / pre-excitation

WPW / pre-excitation on ECG:

⛔ WPW DETECTED — ALL AV nodal drugs (digoxin, verapamil, diltiazem, beta-blockers, adenosine) are ABSOLUTELY CONTRAINDICATED → risk of VF and cardiac arrest. Call 999 if haemodynamically unstable.

⚡ Rate Control

WPW / pre-excitation on ECG:

⛔ WPW DETECTED — ALL AV nodal drugs CONTRAINDICATED

DO NOT give digoxin, verapamil, diltiazem, beta-blockers, or adenosine. These accelerate conduction via accessory pathway → VF. Call 999 if unstable. Urgent electrophysiology referral for ablation.

999 if unstable Urgent ablation referral

Heart failure with reduced EF (HFrEF, EF <40%) + Asthma or severe COPD:

Complex combination: both BB (asthma CI) and diltiazem (HFrEF CI) are problematic. Digoxin may be the safest option — specialist advice strongly recommended.

Digoxin (specialist-guided)

Monitor K⁺ closely. Target level 0.5–1.0 ng/mL. Avoid if WPW. 6-monthly level + U&Es.

Asthma or severe COPD: Diltiazem

Beta-blockers usually avoided in asthma. Diltiazem 60–360mg/day in divided doses. Never combine verapamil + beta-blocker → heart block risk (BB + diltiazem only as monitored dual therapy). Avoid if HFrEF.

Heart failure with reduced EF (HFrEF, EF <40%): Bisoprolol + Digoxin (add-on)

BB first-line in HFrEF — dual benefit (rate control + cardiac remodelling). Start only when euvolaemic (not in acute decompensation). Avoid diltiazem/verapamil — negatively inotropic. Digoxin useful add-on; monitor K⁺ (diuretics lower K⁺ → toxicity).

Resting HR <60 bpm (bradycardia): Review current drugs first

HR <60 at rest: do NOT start or increase rate-limiting drugs. Identify cause — sick sinus syndrome, drug effect, or intrinsic conduction disease. ECG review. Pacing may be needed if symptomatic bradycardia with AF.

None of the situations above: Bisoprolol

First-line rate control option (beta-blocker or rate-limiting CCB — NG196). Start 2.5mg OD, titrate to 10mg OD, guided by symptoms (ESC/RACE II: resting HR <110 bpm, or <80 bpm if still symptomatic). Never combine with verapamil → heart block; diltiazem only as monitored dual therapy.

💊 Anticoagulation

Rheumatic mitral stenosis or mechanical heart valve: Warfarin only

Rheumatic mitral stenosis or mechanical prosthetic valve: DOACs are contraindicated — not validated in these populations (RE-ALIGN trial showed dabigatran inferior). Warfarin target INR 2–3 (non-mechanical) or 2.5–3.5 (mechanical mitral valve). Specialist input required.

CKD — CrCl <30 mL/min (Cockcroft-Gault): Apixaban (preferred in CKD)

CrCl <30 (Cockcroft-Gault, not eGFR): apixaban has least renal clearance — preferred DOAC; check the SPC for severe renal impairment. Standard dose 5mg BD unless dose-reduce criteria met. CrCl <15: consider warfarin instead. Dabigatran contraindicated at CrCl <30 (80% renal clearance). Recalculate CrCl 6-monthly.

On warfarin with poor control (TTR <65%): Switch to DOAC now

TTR <65% means poor anticoagulation control — patient is at higher stroke AND bleeding risk simultaneously. Switch to apixaban or rivaroxaban. No bridging needed — stop warfarin and start the DOAC once the INR is below its product-specific threshold (e.g. apixaban when INR <2; check the SPC).

Frailty: ≥2 of (age ≥80, weight ≤60kg, creatinine ≥133): Apixaban 2.5mg BD

≥2 of: age ≥80, weight ≤60kg, creatinine ≥133 µmol/L → reduced-dose apixaban 2.5mg BD (not standard 5mg BD). Prevents over-anticoagulation and excess bleeding in frail elderly. Reassess dose criteria at annual review — weight and renal function can change.

None of the situations above: DOAC — Apixaban or Rivaroxaban

Standard first-line anticoagulation for non-valvular AF. Apixaban 5mg BD (twice daily — adherence challenge but lowest bleed risk) or Rivaroxaban 20mg OD (once daily with evening meal). Check eGFR + FBC at baseline and annually. Aspirin is NOT an alternative — does not prevent AF-related stroke.

🎵 Rhythm Control

WPW / pre-excitation on ECG: Urgent ablation referral

WPW: catheter ablation of accessory pathway is definitive treatment — curative in >95% of cases. Drug therapy is limited and dangerous (AV nodal drugs contraindicated). Until ablation: IV procainamide or flecainide under specialist guidance if haemodynamically stable.

Structural heart disease or IHD (previous MI, cardiomyopathy): Amiodarone only (specialist)

Flecainide and propafenone are ABSOLUTELY CONTRAINDICATED in structural heart disease or IHD — pro-arrhythmic in damaged myocardium → VT/VF (CAST trial). Only amiodarone is safe for rhythm control. Initiate with specialist input. 6-monthly monitoring: TFTs + LFTs + CXR mandatory.

Currently on amiodarone: Continue amiodarone + monitor

On amiodarone: mandatory 6-monthly TFTs + LFTs + CXR. Monitor for: thyroid disorders (both hypo AND hyperthyroidism), liver toxicity (↑ ALT), pulmonary toxicity (new cough/dyspnoea → CXR), corneal microdeposits (usually asymptomatic), photosensitivity (high-factor sunscreen). Very long half-life — effects persist for months after stopping.

New AF onset <48 hours — cardioversion window open: Cardioversion ± anticoagulation

New AF <48h: anticoagulate now with DOAC or heparin. Pharmacological cardioversion (flecainide 300mg if no structural disease) or DC cardioversion can be attempted. If <48h confirmed AND echo excludes LV thrombus: cardioversion without 3-week prior anticoagulation is acceptable. Anticoagulate for ≥4 weeks post-cardioversion regardless of CHA₂DS₂-VASc (AF may recur silently).

Paroxysmal AF — symptomatic, structurally normal heart: Flecainide pill-in-pocket or ablation

Paroxysmal AF in structurally normal heart: flecainide 200–300mg as pill-in-pocket self-treatment (only after confirming patient can use this safely, and a rate-limiting drug is also taken). Or refer for catheter ablation — 60–80% success for paroxysmal AF. Anticoagulation based on CHA₂DS₂-VASc regardless of rhythm control strategy.

None of the situations above: Rate control preferred initially

In most persistent/permanent AF, rate control is as effective as rhythm control for quality of life and outcomes (AFFIRM trial). Offer rhythm control (cardioversion or ablation) if: symptomatic despite adequate rate control, or patient preference. EAST-AFNET 4: early rhythm control within 1 year of diagnosis may reduce CV outcomes in selected patients.

Guideline summary — each situation is shown with what the guidance says for it, as written. Nothing is selected or worked out for an individual patient. Check doses in the SPC and your local formulary.

7F — Drug reference cards: rate control · rhythm control · anticoagulation

Beta-blocker (Rate Control)

Bisoprolol · Metoprolol

✓ First-line rate control (or CCB)

Rate ControlBiso 2.5→10mg OD

✓ Prefer when

First-line rate control option (with rate-limiting CCB) — preferred in HFrEF once stable

Coexisting HTN, IHD, or post-MI — additional benefit

Paroxysmal AF — reduces episode duration and frequency

Exercise-induced AF — more effective than digoxin on exertion

✗ Avoid if

Acute decompensated HF — initiate when stable only

Asthma (usually avoid) · 2°/3° heart block · Severe bradycardia

WPW — NEVER in WPW + AF — can cause VF

COPD is not a bar to a cardioselective BB. DM (masks hypo).

⚠ Side effects

Bradycardia · Fatigue · Cold peripheries · Erectile dysfunction

Never stop abruptly — rebound tachycardia. Check HR before each dose increase.

🔬 Monitor

Resting HR before each dose increase. Target: HR <110 at rest (lenient), or <80 if symptomatic.

💬 Counselling

"This tablet slows your heart down — it won't prevent a stroke, but it will make the irregular rhythm easier to live with. Never stop it suddenly without asking us."

BB or rate-limiting CCB are FIRST-LINE rate control (NG196). Never combine with verapamil — heart block; BB + diltiazem only as monitored dual therapy. NEVER in WPW + AF — VF risk.

Rate-Limiting CCB

Diltiazem · Verapamil

✓ First-line rate control (or BB)

Rate ControlDiltiazem 60–360mg/day

✓ Prefer when

First-line AF rate control (NG196), e.g. asthma or BB not tolerated

Useful if also used for angina or hypertension management

✗ Avoid if

HFrEF — negatively inotropic, worsens systolic function

Combined with beta-blocker → heart block

WPW + AF — ABSOLUTELY CONTRAINDICATED

2°/3° heart block · Sick sinus syndrome

⚠ Side effects

Constipation (verapamil) · Flushing · Bradycardia · Ankle oedema

Interactions: simvastatin (myopathy → use atorvastatin). Ciclosporin, digoxin levels ↑.

💬 Counselling

"This tablet helps control your heart rate. Never take it alongside the other heart tablet [BB] — they can interact to slow the heart too much."

Never combine verapamil + beta-blocker — heart block (NG196 allows BB + diltiazem as monitored dual therapy). Absolutely contraindicated in WPW + AF and HFrEF.

Digoxin

Digoxin — rate control add-on

Add-on rate control

Rate Add-on62.5–250mcg OD

✓ Consider when

AF + HFrEF: rate control when BB not tolerated / insufficient

Sedentary elderly patients (controls rate at rest but not exertion)

Rate control adjunct when monotherapy insufficient

✗ Avoid if

WPW + AF — LETHAL → can cause VF via accessory pathway

2°/3° heart block · Hypokalaemia (toxicity risk)

CrCl <30 → severe accumulation → toxicity. Reduce dose markedly.

⚠ Toxicity signs — teach patient

Nausea/vomiting, yellow halos, bradycardia = toxicity → stop + 999

K⁺ <3.5 amplifies toxicity (loop diuretics lower K⁺ → digoxin toxicity)

Narrow therapeutic index: level 0.5–1.0 ng/mL

🔬 Monitor

Digoxin level + K⁺ + U&Es every 6 months

K⁺ >3.5 essential — maintain on loop diuretics

💬 Counselling

"If you notice nausea, vomiting, or see yellow halos around lights — stop the tablet and call us urgently. These are signs the dose may be too high."

Digoxin + WPW = VF (lethal). K⁺ must be normal. Toxicity = yellow halos + nausea + bradycardia. Loop diuretics lower K⁺ → toxicity risk.

DOAC (Anticoagulation)

Apixaban · Rivaroxaban · Dabigatran · Edoxaban

✓ First-line anticoagulation

AnticoagulationApixaban 5mg BD

✓ First-line for non-valvular AF

All non-valvular AF with CHA₂DS₂-VASc ≥2 (men or women)

Superior to warfarin: ↓ stroke by 19%, ↓ intracranial haemorrhage by 50%

No routine INR monitoring needed — significantly better quality of life

Apixaban: least renal clearance — preferred in CKD. Twice daily (adherence challenge).

Rivaroxaban/Edoxaban: once daily — better adherence. More renal clearance.

Dabigatran: most renal clearance — contraindicated if CrCl <30. Reversible with idarucizumab.

✗ Contraindications

Mechanical heart valve / rheumatic mitral stenosis — warfarin only

Active significant bleeding — treat cause first

CrCl <30 (dabigatran) or <15 (apixaban, rivaroxaban, edoxaban) — use warfarin

Pregnancy — no DOAC; specialist anticoagulation (usually LMWH).

⚠ Side effects + interactions

GI bleeding (dyspepsia with dabigatran — take with food)

Major drug interactions: P-gp/CYP3A4 inducers (rifampicin, St John's Wort) → subtherapeutic levels

Reversal agents: idarucizumab (dabigatran); andexanet alfa for apixaban/rivaroxaban only in life-threatening or uncontrolled GI bleeding (NICE TA697), otherwise PCC per local protocol

🔬 Monitor

CrCl (Cockcroft-Gault) annually; 6-monthly if CrCl 30–60 or frail; and after AKI or acute illness. Dose reduce: apixaban 2.5mg BD if ≥2 of: age ≥80, weight ≤60kg, creatinine ≥133.

Review all interactions at every medication review. Sick day rules: continue DOAC unless actively bleeding.

💬 Counselling

"This tablet reduces your risk of stroke by around 60–70%. Take it every day — even if you feel well. Missing doses removes your protection. Tell any doctor or dentist you take this before any procedure. If you cut yourself and bleeding won't stop after 10 minutes of pressure, go to A&E."

DOAC > warfarin for non-valvular AF. Valvular AF (rheumatic MS or mechanical valve) = warfarin only. Apixaban preferred in CKD. Never stop without telling the prescriber. Aspirin is NOT an alternative.

Warfarin

Vitamin K antagonist

Second-line / valvular AF

AnticoagulationINR target 2–3

✓ Indicated when

Rheumatic mitral stenosis or mechanical heart valve — DOAC not validated here

CrCl <15 — when DOAC contraindicated

Patient preference / financial access issue (rare in UK)

✗ Significant limitations

Numerous drug interactions (antibiotics, NSAIDs, herbal remedies)

Dietary interactions (vitamin K — green leafy vegetables)

Regular INR monitoring required — inconvenient, anxiety-provoking

TTR <65% → inferior to DOAC → switch to DOAC

⚠ Monitoring + safety

INR target 2–3 for non-valvular. INR 2.5–3.5 for mechanical mitral valve.

INR >4.0 → hold warfarin + recheck in 24–48h. INR 5–8, no bleeding → withhold 1–2 doses and reduce dose; INR >8 → oral vitamin K 1–5 mg; major bleeding at any INR → hospital (IV vitamin K + PCC) (BSH / national guidance).

Sick day rules: continue warfarin during illness unless active bleeding — do NOT self-stop.

💬 Counselling

"Keep a consistent diet — don't suddenly change your intake of green vegetables. Tell your pharmacist you're on warfarin before buying anything over the counter. Always keep your anticoagulation booklet with you."

TTR <65% → switch to DOAC. Valvular AF (rheumatic MS, mechanical valve) = warfarin only — DOACs not validated. INR must be ≥2 for ≥3 weeks before cardioversion.

Rhythm Control & Ablation

Cardioversion · Flecainide · Amiodarone · Ablation

Specialist-initiated

Rhythm ControlSpecialist

✓ Consider rhythm control when

Symptomatic despite adequate rate control

First presentation of AF (especially <48h) — cardioversion may restore sinus rhythm

Young patient / athlete — AF ablation increasingly successful

AF precipitated by correctable cause (post-surgery, thyrotoxicosis) — rhythm control after

✗ Rhythm control agents — cautions

Flecainide: CONTRAINDICATED in structural heart disease / IHD — pro-arrhythmic → VT/VF. Safe only in structurally normal hearts.

Amiodarone: Thyroid, liver, lung, eye, skin toxicity. Last resort. 6-monthly TFTs/LFTs/CXR. Very long half-life (months).

Cardioversion: anticoagulate ≥3–4 weeks before (if >48h onset) or echo-exclude thrombus first.

⚠ Important principles

Rhythm control does NOT replace anticoagulation — AF may recur silently

EAST-AFNET 4 trial: early rhythm control in newly diagnosed AF ↓ CV outcomes

Ablation success rate: ~60–80% for paroxysmal AF; lower for persistent

🔬 Amiodarone monitoring

TFTs + LFTs + CXR every 6 months. TFTs every 3 months for first year.

Corneal microdeposits (all patients — usually asymptomatic). Photosensitivity — high-factor sunscreen.

💬 Counselling (post-cardioversion)

"Your heart is back in a normal rhythm — but the blood-thinning tablet continues, because AF can return silently. Never stop the blood thinner without discussing it with your doctor."

Flecainide only in structurally normal hearts — pro-arrhythmic in IHD. Amiodarone = many toxicities, 6-monthly monitoring. Anticoagulation continues after cardioversion/ablation.

7G — Psychosocial impact: driving, work, anxiety & anticoagulation fears

🤝

AF changes daily life — address the real-world impact proactively

AF and anticoagulation affect driving, occupation, sport, relationships, financial planning, and mental wellbeing. Addressing these proactively prevents future non-adherence (especially to anticoagulation) and demonstrates truly patient-centred care.

🚗

Driving & DVLA

Asymptomatic AF, stable: No DVLA notification required for Group 1 (car) licence.

AF causing or likely to cause incapacity (syncope, presyncope): Must stop driving until the cause is identified and controlled for at least 4 weeks. Notify DVLA if this is not achieved or distracting/disabling symptoms persist.

After catheter ablation: No driving for 2 days (Group 1; no DVLA notification needed). Follow cardiology advice after cardioversion.

HGV/PCV (Group 2): Stricter rules — DVLA + cardiology clearance required. Career implications must be addressed sensitively.

"As long as you don't have symptoms like dizziness or fainting, you can continue to drive. But I want to check — do you have a job that involves driving professionally, or flying?"

💼

Work & Occupation

Pilots, HGV/PCV drivers, air traffic controllers, certain military roles — AF may end a career or require medical assessment. This is a significant life-altering consequence requiring sensitive proactive discussion.

Symptomatic AF causing fatigue or palpitations may affect work performance — Fit Note if appropriate.

"What do you do for work? I want to make sure I explain clearly what this diagnosis means for your job, if anything."

🏃

Exercise & Sport

Moderate exercise is safe and encouraged in AF. "Athlete's AF" — vigorous endurance sport is an independent AF risk factor, but AF is not a reason to stop all exercise.

Contact sports on anticoagulation carry increased bleeding risk — individual discussion needed. Protective equipment recommended.

"Exercise is actually good for your heart — including in AF. You can continue most activities. If you do contact sports, we should talk about protective equipment given you're on a blood thinner."

💊

Anticoagulation Fears

Fear of bleeding is the commonest cause of DOAC non-adherence. Patients often stop without telling their GP — research shows 30–50% stop within 1 year. Proactively addressing this prevents stroke.

Cuts and minor bleeds: reassure — press firmly for 10 minutes. Serious bleeding: A&E. Reversal agents available.

"I want to talk about the blood-thinning tablet — what worries you most about taking it? The bleeding risk is real but much smaller than the stroke risk it protects you from."

😰

Anxiety & AF Monitoring

Many patients develop "AF anxiety" — hypervigilance for every palpitation, checking pulse obsessively, avoiding exercise for fear of triggering AF. This cycle is self-reinforcing and significantly reduces quality of life.

Wearable devices (Apple Watch, Kardia) — helpful for detection but can also amplify anxiety if used obsessively. Discuss appropriate use.

"How are you coping emotionally with this — are you finding yourself worried about every heartbeat? That's very common, and I want to help you find a way to live well with AF rather than around it."

💰

Insurance & Financial

AF must be declared to life insurance, income protection, and some travel insurance providers. May affect premiums. Patients have a legal duty to disclose.

Travel insurance: declare AF. Most travel insurers cover anticoagulation with AF — but costs may increase. Pre-travel INR/dose review.

"Worth knowing — AF needs to be declared on insurance applications. For travel insurance, you should declare it but most policies still cover you. Call us before travelling if on warfarin to check your INR."

7H — Follow-up schedule

1

Within 1 week of starting anticoagulation

Confirm tolerability. Check for early bleeding symptoms. Review renal function and calculate CrCl if not already done. Confirm adherence understanding. INR check at 1 week if warfarin.

DOAC: CrCl reviewWarfarin: INR at 1 week

2

Within 4–6 weeks — specialist cardiology (if referred)

Cardioversion planning (if >48h onset: minimum 3–4 weeks anticoagulation before). Echo result review. Rhythm vs rate decision. Ablation pathway if paroxysmal and symptomatic.

3

3 months — rate control review

Resting HR + 6-minute walk HR if available. Symptom response. Drug titration. Holter if paroxysmal AF — documentation of burden. TFTs result review.

Rate guided by symptoms (ESC: <110, or <80 if symptomatic)

4

Annual structured AF review

CHA₂DS₂-VASc score update (risk increases with age). ORBIT (consider — NG196) bleeding review + modifiable factor correction. DOAC dose review (recalculate CrCl — decline may require dose reduction). INR/TTR review (warfarin patients). Anticoagulation adherence. Psychosocial check. Driving review.

5

6-monthly — amiodarone monitoring (if on amiodarone)

TFTs + LFTs + CXR every 6 months. Corneal and skin review. Pulmonary toxicity screen. Consider dose reduction if stable.

Amiodarone: 6-monthly TFT/LFT/CXR mandatory

7I — Monitoring: anticoagulation, rate control & amiodarone

Monitoring memory rules in AF

DOAC → CrCl at baseline + annually (6-monthly if CrCl 30–60 or frail — EHRA/local protocol; after AKI) | Warfarin → INR weekly until stable, then 6–12 weekly | Digoxin → level + K⁺ + U&Es every 6 months | Amiodarone → TFTs + LFTs + CXR every 6 months

Drug	Test	Timing	Action threshold
All DOACs	CrCl + FBC + LFTs	Annually (6-monthly if CrCl 30–60 or frail — EHRA/local; after AKI)	CrCl <15 → consider warfarin. CrCl decline → review dose reduction criteria. Falling Hb → investigate source (NG12), not just stop.
Apixaban dose reduce	Age + weight + Cr	At initiation + annual	≥2 of: age ≥80, weight ≤60kg, creatinine ≥133 → 2.5mg BD (not 5mg).
Warfarin	INR	Weekly until stable, then 6–12 weekly	INR <2.0 → ↑ dose. INR >4.0 → hold + recheck. INR 5–8 (no bleeding) → withhold 1–2 doses; INR >8 → oral vit K 1–5 mg; major bleeding at any INR → hospital (IV vit K + PCC). TTR <65% → switch to DOAC.
Digoxin	Level + K⁺ + U&Es	Every 6 months	Level >1.0 ng/mL → reduce dose. K⁺ <3.5 → correct urgently (toxicity risk).
Amiodarone	TFTs + LFTs + CXR	Every 6 months	Thyroid disorders (both hypo and hyper) → endocrinology. Liver toxicity → review. Pulmonary toxicity (new cough/dyspnoea) → CXR + respiratory review.
All rate-control drugs	Resting HR + BP	At each review	HR >110 at rest → up-titrate. HR <50 → reduce dose. SBP <90 → withhold.

Parameter	Target	Notes
Heart rate (lenient)	<110 bpm at rest	ESC/RACE II (NG196 sets no number — titrate to symptoms). Acceptable for most asymptomatic patients.
Heart rate (strict)	<80 bpm at rest	If symptomatic at 110 — tighten target. <110 on exertion.
INR (warfarin, AF)	2.0–3.0	Mechanical mitral valve: 2.5–3.5. Review monthly until stable.
TTR (warfarin quality)	≥65%	TTR <65% → switch to DOAC discussion.
Digoxin level	0.5–1.0 ng/mL	Lower range is safer and as effective as higher range.
CHA₂DS₂-VASc	Annual update	Score increases with age — patient who didn't qualify at 64 may qualify at 65 (A point) or 75 (A₂ upgrade).

7J — Safety-netting: exact phrases for every AF patient

⚠ Three scenario-specific phrases — use these verbatim

Why safety-netting is especially important in AF

AF carries 5x stroke risk — patients must know FAST symptoms by name, not just "symptoms"

DOAC non-adherence accounts for the majority of AF-related strokes in anticoagulated patients

Anticoagulation-related intracranial haemorrhage needs reversal agent — must present to A&E immediately

CHA₂DS₂-VASc score increases with age — patient who didn't need anticoagulation at 64 needs it at 65/75

Drug interactions (antibiotics, herbal, NSAIDs) can make warfarin supratherapeutic — patient must know to check

Documenting safety-netting discussion is medico-legal protection if a stroke occurs

1 weekAnticoagulation tolerability + CrCl/INR result

4–6 weeksCardiology if referred. Rate review. TFTs result.

AnnualCHA₂DS₂-VASc update · CrCl · INR/TTR · ORBIT modifiable factors

📋 SCA Consultation Scorecard — self-assess your consultation

"Doctor, I've just been told my heart is in atrial fibrillation. I need to know if I'm going to have a stroke."

Who you are

64yo female teacher. Routine BP check at pharmacy → irregular pulse → GP ECG confirms AF. No prior cardiac history. BP 148/88 (known HTN, on amlodipine). Takes ibuprofen regularly for knee osteoarthritis — not disclosed unless asked. CHA₂DS₂-VASc = 2 (female sex=1, HTN=1, age 64 = 0 as <65) — meets the NICE NG196 threshold of ≥2 to offer anticoagulation; candidate should calculate openly with patient.

Hidden agenda

Husband had a massive stroke 3 years ago — was in AF and on warfarin. He bled from his brain and died. You are terrified of BOTH stroke AND anticoagulation bleeding. The tension between these two fears is the emotional core of the consultation. You want protection but fear the treatment.

Symptoms if asked

No palpitations — completely asymptomatic
No breathlessness, no chest pain
No dizzy spells or syncope
No TIA or stroke symptoms ever
Ibuprofen for knee — only reveals if asked directly about medications

Psychosocial + bonus details

Drives to school daily — full-time teacher
Worried about driving licence implications
Drinks 2 glasses of wine most evenings (≈14u/wk) — reveals honestly if asked
Very anxious — already googled "AF stroke risk" at 2am
Doesn't want to be on warfarin (husband's bad experience) — open to DOAC if explained well

"My husband was on warfarin and had a brain bleed and died. How can you ask me to take a blood thinner? But I also don't want a stroke like he had. I don't know what to do."

Resolution: Accept management plan only when: (1) BOTH husband's stroke fear AND husband's bleeding death acknowledged by name, AND (2) ibuprofen identified and stopped (raises bleeding risk + HAS-BLED + can precipitate AF), AND (3) stroke risk vs bleed risk explained with the actual score AND explanation that DOACs have significantly less intracranial bleed risk than warfarin, AND (4) specific 1-week follow-up named. Alcohol ≈14u/wk rewards candidates who ask and factor into HAS-BLED.

🏥

Clinic Quick Reference

Atrial Fibrillation — Clinical Decision Framework

NICE NG196 · First Presentation & Review

▼expand

🚦 1 — Triage System

AF confirmed on ECG — haemodynamics FIRST, then stroke risk, then rate

↓

🔴 999 Now

SBP <90 + rapid AF → emergency cardioversion
WPW + AF (broad complex >250 bpm) — NO AV nodal drugs
FAST-positive stroke / active TIA
Syncope or presyncope with AF
Thyroid storm + AF
Anticoagulated + severe headache / focal neurology (ICH)

999 · WPW = NO digoxin / verapamil / BB / adenosine → VF risk

🟠 Urgent — same-day / days

New AF <48h onset — cardioversion window
HR >110 + breathlessness → rate control today
CHA₂DS₂-VASc ≥2 (same threshold in women as in men), not anticoagulated → DOAC today
New AF + suspected thyrotoxicosis — urgent TFTs
INR >4.0 or active bleeding on anticoagulation

Start DOAC now · Rate control · TFTs · Do NOT delay anticoagulation

🟢 Routine GP

Paroxysmal AF, stable, asymptomatic
Permanent AF, rate controlled, anticoagulated
DOAC / warfarin annual review
Rhythm control referral (ablation / cardioversion)
Annual CHA₂DS₂-VASc + HAS-BLED review

Annual review · Optimise · FAST education

🔬 2 — Diagnostic Pathway

CHA₂DS₂-VASc: C=HF(1) · H=HTN(1) · A₂=Age≥75(2) · D=DM(1) · S₂=Stroke/TIA(2) · V=Vascular(1) · A=Age65-74(1) · Sc=Female(1)

0 ♂

No anticoagulation

1 ♂

Consider anticoagulation

1♀ only

Female sex alone = no Rx

≥2 (♂ or ♀)

Offer DOAC — today

⚠ Score increases with age — reassess annually. Falls alone NOT a contraindication. Aspirin is NOT an alternative. Female sex alone (score 1) does NOT trigger anticoagulation.

Investigation pathway

12-lead ECG → confirms AF · checks for WPW

TFTs mandatory — hyperthyroidism is reversible cause. All new AF.

U&E (CrCl by Cockcroft-Gault) + FBC — DOAC dose selection + baseline before anticoagulation

Echocardiogram — structural disease, LV thrombus, mitral stenosis (→ warfarin)

Holter / 7-day patch — if paroxysmal AF suspected but ECG normal

High ORBIT (NG196: consider) or HAS-BLED ≥3 = high bleed risk — CORRECT modifiable factors, do NOT withhold anticoagulation

H=Uncontrolled HTN · A=Renal/Liver · S=Stroke · B=Bleeding Hx · L=Labile INR → switch to DOAC · E=Elderly >65 · D=Drugs/Alcohol (NSAIDs, antiplatelets)

📊 3 — Key Numbers

≥2

CHA₂DS₂-VASc → anticoagulate (same in women as men; consider at 1 in men)

DOAC

First-line. Not aspirin. Warfarin for mechanical valve/mitral stenosis, APS, CrCl <15.

48 hrs

Cardioversion anticoagulation threshold

HR <110

Lenient rate target at rest (ESC/RACE II — not NG196)

HR <80

Strict target if symptomatic at 110

INR 2–3

Warfarin target — valvular AF only

TTR <65%

Switch warfarin → DOAC

TFTs

Mandatory in ALL new AF presentations

CrCl annually

DOAC dose review (6-monthly if CrCl 30–60 or frail — EHRA/local)

💊 4 — Medication Decision & Choice

Rate Control — first-line for most AF

Beta-blocker (e.g. bisoprolol 2.5–10mg OD) or rate-limiting CCB — by symptoms (ESC: HR <110). Never with verapamil → heart block.

Asthma / no BB → Diltiazem 60–360mg/day. NOT if HFrEF. BB + diltiazem only as monitored dual therapy.

HFrEF → Bisoprolol + Digoxin add-on. Diltiazem/verapamil avoid (negatively inotropic).

Rate add-on → Digoxin 62.5–250mcg. K⁺ >3.5 essential. NEVER in WPW.

WPW + AF → 999. NO AV nodal drugs. Ablation referral.

Anticoagulation — start today if indicated

Non-valvular AF (default) → DOAC — apixaban 5mg BD or rivaroxaban 20mg OD (with food)

CKD CrCl <30 → Apixaban preferred (least renal clearance; check SPC). CrCl <15 → warfarin.

Frailty (≥2 of: age ≥80, wt ≤60kg, Cr ≥133) → Apixaban 2.5mg BD (reduced dose)

TTR <65% on warfarin → Switch to DOAC. Stop warfarin and start the DOAC once INR falls below its product-specific threshold (SPC) — no bridging.

Rheumatic MS / mechanical valve → Warfarin only. DOACs contraindicated (RE-ALIGN).

⛔ Aspirin does NOT prevent AF-related stroke · ⛔ BB + diltiazem = heart block · ⛔ AV nodal drugs + WPW = VF

⚠ 5 — Safety Netting & Follow-Up

Follow-up schedule

1

1 week: DOAC/warfarin tolerability · CrCl + TFTs result · INR if warfarin · Adherence confirmed · NSAID stopped?

2

4–6 weeks: Cardiology if referred · Symptoms and rate controlled? · TFT result · Rhythm vs rate confirmed

3

3 months: Rate control effectiveness · Drug titration · Holter result if paroxysmal · Symptom response

4

Annual: CHA₂DS₂-VASc update (age ↑ = score ↑) · CrCl DOAC dose · INR/TTR · ORBIT modifiable factors · Adherence · Driving review · Psychosocial

5

6-monthly (amiodarone only): TFTs + LFTs + CXR mandatory · Document every result

📌 DVLA: AF causing incapacity (syncope/presyncope) → stop driving until cause identified and controlled ≥4 weeks; notify DVLA if not achieved or disabling symptoms persist. Stable asymptomatic AF: no notification for Group 1. HGV/PCV: stricter — specialist clearance.

🔬 6 — Monitoring & Safety

Drug	Test	Timing	Action threshold
DOAC (all)	CrCl + FBC	Annual (6-monthly if CrCl 30–60 or frail — EHRA/local)	CrCl <15 → consider warfarin. CrCl decline → review dose-reduce criteria. Apixaban reduce if ≥2 of: age ≥80, wt ≤60kg, Cr ≥133.
Warfarin	INR	Weekly until stable, then 6–12 weekly	INR <2 → ↑ dose. INR >4 → hold + recheck 24h. INR 5–8 (no bleeding) → withhold 1–2 doses; INR >8 → oral vit K 1–5 mg; major bleeding at any INR → hospital (IV vit K + PCC). TTR <65% → switch to DOAC.
Digoxin	Level + K⁺ + U&E	Every 6 months	Level >1.0 ng/mL → reduce. K⁺ <3.5 → correct urgently (loop diuretics lower K⁺ → digoxin toxicity risk). Toxicity: nausea + yellow halos + bradycardia.
Amiodarone	TFTs + LFTs + CXR	Every 6 months	Thyroid (hypo AND hyper) → endocrinology. LFT rise → review. New cough/dyspnoea → CXR + respiratory. Corneal deposits (usually asymptomatic). Photosensitivity → sunscreen.
All rate drugs	HR + BP	Each review	HR >110 → up-titrate. HR <50 → reduce dose or review. SBP <90 → withhold and reassess. Never verapamil + BB; diltiazem + BB only with monitoring.
All patients	CHA₂DS₂-VASc + HAS-BLED	Annual	Score can increase without new events (age alone). Patient who didn't need anticoagulation at 64 may need it at 65 (A point) or 75 (A₂ upgrade). Reassess HAS-BLED modifiable factors annually.

999 red flags: Haemodynamic compromise · WPW + AF (NO AV nodal drugs) · FAST symptoms · Syncope · ICH on anticoagulation

🛡️ Safeguarding: Cognitive impairment (capacity for anticoagulation) · Falls risk · Medication mismanagement · Social isolation (stroke detection) · Driving duty of care

🎓

SCA Exam Quick Reference

SCA Consultation Blueprint

Tasks · Relating to Others · Global Skills · RAG guide

▼expand

🕐 12-Minute Consultation Flow — with Domain Scoring

0–2 min

Open & ICE

"The ECG shows your heart rhythm is irregular — this is atrial fibrillation..."

"Before I explain anything — how are you feeling, and what's been going through your mind?"

"You mentioned your husband had a stroke — what are you most worried about for yourself?"

Relating to OthersGlobal Skills

✗ Starting with score · Not using ECG finding · Husband's stroke + bleeding fear not explored

2–5 min

Safety Screen

"Is your breathing okay right now? Any chest pain? Any fainting episodes with the palpitations?"

Name red flags aloud: haemodynamic stability · WPW · FAST symptoms · syncope

AF duration (if <48h — cardioversion). Precipitant: thyroid, alcohol, infection, NSAIDs.

TasksGlobal Skills

✗ Anticoagulation before haemodynamic check · Missing WPW · Not naming red flags aloud

5–7 min

Context & Risk

CHA₂DS₂-VASc factors: age, HTN, DM, prior stroke, HF, vascular disease

HAS-BLED reversible: NSAIDs (ibuprofen!), alcohol, labile INR, uncontrolled HTN

TFTs mandatory. Reversible causes screen.

Social: driving, work, anxiety, anticoagulation fears

TasksRelating to Others

✗ No TFTs · Ibuprofen not identified · Driving not raised · HAS-BLED modifiable not sought

7–10 min

Explain & Score

"Think of it as a chaotic electrical storm — blood pools in a small pocket and can clot. If that clot reaches the brain, it causes a stroke. The blood thinner stops the clot forming."

"Your stroke risk score is [X]. That's roughly [Y]% per year without treatment. With a DOAC, we cut that by 60–70%. And DOACs have significantly less risk of brain bleeding than the old warfarin."

TasksRelating to Others

✗ Not sharing score · Offering aspirin · Not distinguishing DOAC vs warfarin bleed risk · Jargon

10–12 min

Plan & Close

"Sudden weakness one side, slurred speech, or vision loss — call 999. Every minute matters."

Rate control drug · Driving advice · Adherence counselling · 1-week follow-up · "Anything else?"

TasksRelating to OthersGlobal Skills

✗ FAST not named · No adherence counselling · Driving not addressed · Vague follow-up · No closing Q

🔴🟠🟢 RAG Scoring — All 3 Domains

Tasks Domain

🟢

CHA₂DS₂-VASc calculated and shared with patient · DOAC first-line (not aspirin) · Rate control correct (no BB+diltiazem) · TFTs ordered · WPW acknowledged · Ibuprofen stopped · Adherence counselling · FAST in safety-net · Named 1-week follow-up

🟠

DOAC prescribed but score not shared · Aspirin not explicitly discarded · TFTs mentioned not ordered · Ibuprofen missed · Adherence not addressed · Follow-up vague

🔴

Aspirin offered · Score not calculated · WPW not considered · BB + diltiazem combined · No safety-net · FAST not named · Ibuprofen missed entirely

Relating to Others

🟢

Both fears named (stroke AND bleeding death of husband) · AF explained as chaotic signal/clot/stroke · Score shared transparently · DOAC vs warfarin intracranial bleed risk difference explained · Anxiety, driving, anticoagulation fears raised · "Anything else?"

🟠

Husband's stroke acknowledged but bleeding death not named · Score mentioned but not explained · Some psychosocial · Closes without final check

🔴

Jumps to anticoagulation without ICE · Husband not named · Bleeding fear not addressed · Jargon throughout · No shared decision

Global Skills

🟢

ECG acknowledged first · Open Q · Data gathering complete by 6–7 min · Clear lay language · Responsive to bleeding fear · Ibuprofen found

🟠

Some structure but overruns · Some jargon · Misses ibuprofen or driving or alcohol

🔴

ECG not acknowledged · Jargon throughout · Ibuprofen not identified · Data gathering incomplete

💬 Key Phrases — ICE, Diagnosis & Plan

💭 Ideas

"What does 'atrial fibrillation' mean to you? When you heard those words, what did that bring up for you?"

😟 Concerns — both fears

"You mentioned your husband had a stroke — and that he also had a serious bleed on warfarin. I want to address both of those fears directly, because they're both valid."

🎯 Expectations

"I think starting a blood thinner is the right thing — let me show you the score I use to calculate your personal risk, and then we can choose the right tablet together."

🗣️ Lay diagnosis — chaotic signal

"Think of it as a chaotic electrical storm in the upper chambers. Blood can pool in a small pocket and form a clot. If that clot breaks off and reaches the brain — that's the stroke. The blood thinner doesn't fix the rhythm — it stops the clot."

📊 Score + DOAC vs warfarin

"Your score is [X] — roughly [Y]% stroke risk per year without treatment. With a DOAC — the newer type of blood thinner — we reduce that by 60–70%. And DOACs cause significantly less brain bleeding than warfarin. That's a very different risk profile to what happened with your husband."

✅ Closing

"Sudden weakness one side, slurred speech, vision loss → 999. Take the tablet every day. I'll see you in one week. Is there anything else on your mind today?"

🚫 9 Danger Zones — Instant Deductions

✗

Starting with score before open Q / ICE
→ Open Q first. Address the fear. Then calculate transparently with patient.

✗

Offering aspirin instead of anticoagulation
→ Aspirin does NOT prevent AF-related stroke. DOAC is first-line for indicated patients.

✗

Not sharing / explaining the score to the patient
→ "Your score is X — that means roughly Y% per year." Make it a shared calculation.

✗

Combining beta-blocker + verapamil
→ Heart block risk. Never combine; BB + diltiazem only as monitored dual therapy (NG196).

✗

Not recognising WPW (AV nodal drugs = VF)
→ Broad complex irregular >250 bpm = WPW until proven otherwise. 999. No digoxin/verapamil/BB.

✗

Not ordering TFTs in new AF
→ Mandatory. Hyperthyroidism is a reversible cause — treat first, AF may resolve (anticoagulate by score meanwhile).

✗

Missing ibuprofen (NSAID) — raises bleeding risk + HAS-BLED
→ Always ask about OTC medications. Stop NSAID before anticoagulation. Switch to paracetamol.

✗

Not addressing both bleeding fear AND stroke fear separately
→ "DOACs cause significantly less brain bleeding than warfarin — it's a different risk profile."

✗

FAST not named specifically in safety-netting
→ "Sudden weakness one side, slurred speech, vision loss → 999. Every minute matters."

💊 Drug Quick-Pick

Rate control — first-line

→

Bisoprolol

Or rate-limiting CCB; titrate to symptoms

Rate — BB contraindicated (asthma)

→

Diltiazem

NOT in HFrEF. Never verapamil + BB.

Rate add-on / sedentary / HFrEF

→

Digoxin

K⁺ >3.5. NEVER in WPW.

Anticoagulation — non-valvular AF

→

DOAC (Apixaban)

CHA₂DS₂-VASc ≥2 (♂ or ♀)

Valvular AF / mechanical valve

→

Warfarin only

INR 2–3. DOACs not validated.

⛔ Aspirin ≠ AF stroke prevention · ⛔ BB + diltiazem = heart block · ⛔ AV nodal drugs + WPW = VF · ⛔ Female sex alone (score 1) ≠ anticoagulate

Red Flags in AF — act before continuing

Safeguarding Considerations — AF Context

🧠 Cognitive Impairment & Capacity

🤕 Falls & Anticoagulation Risk

💊 Medication Safety

🏠 Social Isolation & Stroke Risk

😰 Anxiety & AF

🏃 Exercise & Sport

🚗 Driving

💑 Relationships & Sexuality

💼 Work & Employment

💊 Anticoagulation Fears

Haemodynamically Unstable / Life-Threatening

Haemodynamically Stable — Needs Action

Stable AF — Planned Management

Validate the fear

Explain with the score

Negotiate the plan

Driving & DVLA

Work & Occupation

Exercise & Sport

Anticoagulation Fears

Anxiety & AF Monitoring

Insurance & Financial

Within 1 week of starting anticoagulation

Within 4–6 weeks — specialist cardiology (if referred)

3 months — rate control review

Annual structured AF review

6-monthly — amiodarone monitoring (if on amiodarone)

Monitoring memory rules in AF

⚠ Three scenario-specific phrases — use these verbatim

Why safety-netting is especially important in AF

🎭 Patient actor brief — click to practise

Who you are

Hidden agenda

Symptoms if asked

Psychosocial + bonus details