Rapid atrial fibrillation in a patient with severe aortic stenosis presenting for emergency surgery
A 79-year-old woman (weight 52 kg) presents at 22:00 with a displaced distal radius fracture requiring manipulation under anaesthesia. She has severe aortic stenosis (echo 3 months ago: valve area 0.8 cm2, mean gradient 42 mmHg, EF 55%) and permanent atrial fibrillation. She takes apixaban (last dose yesterday morning), bisoprolol, furosemide and atorvastatin. On assessment she is breathless at rest, HR 138 irregular, BP 98/60, SpO2 93% on room air, JVP elevated, bibasal crackles, cool peripheries. ECG shows AF at 140 with no acute ischaemic changes. Hb 102, platelets 140, INR 1.1, potassium 4.1, creatinine 130 micromol/L. The orthopaedic team wants to proceed to theatre immediately.
1. Outline your assessment and immediate management priorities before any anaesthetic, and justify why the fracture is not the most urgent problem.
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This is a patient with severe aortic stenosis in fast AF with clinical decompensation: breathlessness at rest, hypoxia, hypotension, raised JVP, crackles and cool peripheries indicate pulmonary oedema and low cardiac output. The fixed outflow obstruction means the left ventricle cannot increase stroke volume to compensate for loss of atrial contribution and shortened filling time; tachycardia is therefore poorly tolerated and can precipitate cardiogenic shock. The fracture is not the most urgent problem because a delay of a few hours for medical optimisation carries far less risk than inducing anaesthesia in an decompensated, rate-uncontrolled patient with severe AS. Priorities: (1) controlled rate reduction, using cautious intravenous bisoprolol or, if haemodynamically borderline, amiodarone, with continuous ECG and invasive blood pressure monitoring; avoid agents that drop afterload abruptly; (2) treat congestion with intravenous furosemide and consider non-invasive ventilation for hypoxia; (3) correct triggers: check for infection, anaemia (transfuse if Hb falls further and symptomatic, given fixed output), electrolytes and thyroid; (4) involve cardiology and ICU; (5) assess anticoagulation reversal need only if neuraxial or major bleeding risk, and note apixaban was given yesterday, which is relevant if a regional block is planned. A manipulation under anaesthesia can usually be done with a haematoma block or a carefully titrated general anaesthetic once rate and congestion are improving, ideally within 12 to 24 hours rather than immediately.
2. If surgery proceeds after optimisation, describe your anaesthetic plan and the haemodynamic principles you would apply.
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Principles: maintain sinus rhythm if possible, but if AF persists keep rate controlled; preserve preload and afterload; avoid tachycardia and avoid vasodilation. Severe AS means the ventricle is preload-dependent and intolerant of afterload reduction, so spinal anaesthesia with a high block is risky. My preference for a brief procedure is a general anaesthetic with careful titration, or an awake haematoma block with sedation if the patient can lie flat and is cooperative. Plan: invasive arterial line before induction; large-bore access; consider cardiac output monitoring. Induction with a slowly titrated agent (e.g. etomidate or cautious propofol) plus opioid, maintaining systemic vascular resistance with phenylephrine ready or running; avoid drugs that cause tachycardia (e.g. ketamine, pancuronium, atropine unless bradycardic). Ventilate to normocapnia and avoid high PEEP that reduces venous return. Maintain rate with short-acting beta-blockade if AF becomes rapid, but be ready for hypotension. Postoperative: high-dependency care, continue rate control, monitor for pulmonary oedema, and ensure early cardiology follow-up for consideration of aortic valve intervention, since this presentation predicts a poor outcome without definitive treatment. Document a shared decision with the patient and team about the risks of proceeding versus delaying.