Eight o'clock ward round, day two after a coronary artery bypass, and the monitor shows atrial fibrillation at a hundred and fifty. Calum's answer is amiodarone — and that is the single most common wrong answer on the unit. Not because amiodarone is wrong, but because of where it sits in the order. This is atrial fibrillation on the cardiothoracic intensive care unit, top to bottom. And it matters beyond the bedside: in a recent Fellowship paper it was the worst-performing question on the whole exam, with a pass rate of about 43 per cent. The examiners were specific about where candidates fell down — the management, and the anaesthetic for elective DC cardioversion. The bit everyone assumes is easy. We start with how common it is — about a third of patients after coronary surgery, up to half after valve or combined procedures, peaking on days two and three — and why it isn't benign. Then a framework you can use on a ward round: substrate and trigger. The substrate is atrial; the triggers are catecholamines, pain, hypovolaemia, hypoxia, anaemia, electrolytes and the inflammatory response to bypass. Almost every trigger is something you can change. Then the four strands of management — rhythm, rate, recurrence and thromboembolism — and the step that comes before all of them. Correct the physiology first: potassium, magnesium, pain, volume; exclude tamponade and pneumothorax with a scan and a film, not a glance at the drain; look for sepsis; and check for a misplaced epicardial pacing wire irritating the atrium. Only then a drug. Amiodarone as the workhorse — why it acts on both rhythm and rate, and why the slow loading dose is a safety feature rather than fussiness in a shocked post-cardiotomy patient. Then the drugs we avoid, and the specific reason for each: digoxin, verapamil and diltiazem, flecainide and the lesson of the CAST trial, beta-blockers (and why esmolol if you must), and adenosine as a diagnostic rather than a treatment. Plus the Vaughan Williams classification in ninety seconds, and when an unstable patient needs a synchronised shock rather than a drug. Anticoagulation next: our local position on new-onset post-operative AF and the reasoning behind it, anticoagulant mechanisms and reversal agents, the case for and against the direct oral anticoagulants, and neuraxial timings. Then a trap specific to cardiac surgery — andexanet alfa can look exactly like heparin resistance on bypass, which is why you tell the perfusionist before you reverse, not afterwards. We finish with the section the examiners said was done worst — the anaesthetic for a DC cardioversion list, including what to avoid and the bailout you set up before the first patient — and the long-term options for rhythm, rate and stroke prevention. Chapters (00:00) Cold open — AF at 150, and the commonest wrong answer(00:50) Why this was the worst-answered exam question(01:20) Incidence, and why it isn't benign(02:10) Substrate and trigger(02:40) Causes of AF in general(03:30) The four strands of management(03:50) Correct the physiology first(04:20) The misplaced pacing wire(04:50) Amiodarone, and why the slow load matters(06:30) The drugs we avoid — and why(08:00) The Vaughan Williams classification(08:50) The unstable patient(09:20) Anticoagulation: our local position(10:00) Mechanisms and reversal(11:00) For and against the DOACs(11:30) Neuraxial timings(11:50) Reversal before bypass — andexanet and apparent heparin resistance(13:10) Anaesthesia for DC cardioversion(14:30) Long-term rhythm, rate and stroke prevention(15:10) Wrap-up Key takeaways Post-operative AF affects about a third of patients after CABG and up to half after valve or combined surgery, peaking on days two to three — often self-terminating, but not benignThink substrate (atrial trauma, inflammation, stretch, fibrosis, a large left atrium) and trigger (catecholamines, pain, hypovolaemia, hypoxia, anaemia, electrolytes, the inflammatory response)Four strands of management: restore rhythm, control rate, prevent recurrence, prevent thromboembolismCorrect the physiology first: K⁺ 4.5–5.5, Mg²⁺ above 1.0, treat pain and hypovolaemia, exclude tamponade and pneumothorax, look for sepsis, and check the pacing wiresAmiodarone 300 mg over 20–60 minutes (never as a rapid bolus), centrally where possible, then 600–900 mg over 24 hours — rapid loading causes negative inotropy and vasodilationDigoxin is not an acute agent; verapamil and diltiazem are negatively inotropic; flecainide is contraindicated in structural heart disease and ischaemia (the CAST lesson); esmolol if you must beta-block; adenosine is diagnostic, not therapeuticAdverse features — shock, syncope, myocardial ischaemia, heart failure — mean synchronised DC cardioversion, not a drug; know the Resuscitation Council adult tachycardia algorithmKnow anticoagulants by mechanism, because reversal follows mechanismReversing a DOAC before bypass? Tell the surgeon and the ...
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