Severe aortic stenosis in an elderly woman with a hip fracture
An 82-year-old woman is brought to the emergency department after a mechanical fall, with a displaced left femoral neck fracture. She has severe aortic stenosis: valve area 0.7 cm2, mean gradient 46 mmHg, peak velocity 4.2 m/s, ejection fraction 58%, and two episodes of exertional syncope in the past year. The local TAVR waiting list means she cannot be assessed for at least six weeks. She takes aspirin 75 mg and atorvastatin. Blood pressure is 118/70 mmHg, heart rate 62 beats/min in sinus rhythm, and SpO2 is 96% on 2 L/min nasal cannula. Auscultation reveals a harsh ejection systolic murmur radiating to the carotids. Troponin is mildly raised at 32 ng/L with a flat repeat. She is in severe pain, and the orthopaedic team wants to operate within 24 hours. She weighs 48 kg.
1. Discuss the choice between general, neuraxial and combined anaesthetic techniques with reference to the pathophysiology of severe aortic stenosis.
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In severe aortic stenosis the left ventricle is concentrically hypertrophied and stiff, with a fixed outflow obstruction. Stroke volume is critically dependent on preload (the atrium must contract against a stiff ventricle, so sinus rhythm matters), on an adequate systemic vascular resistance to perfuse the coronaries, and on a controlled heart rate; tachycardia both shortens diastolic coronary filling and increases oxygen demand, and any abrupt fall in afterload produces a fall in stroke volume that cannot be compensated by increasing output across the fixed valve. Hypotension is therefore poorly tolerated and readily precipitates ischaemia, arrhythmia and cardiac arrest.
A high neuraxial block causing abrupt sympathectomy is the most dangerous option. A carefully titrated technique is acceptable: either a low-dose spinal (1.5-2.0 mL of 0.5% hyperbaric bupivacaine) or, better, a continuous spinal or epidural catheter titrated in small increments, combined with a fascia iliaca block for analgesia and to reduce opioid requirements. General anaesthesia with an arterial line allows precise control but induction agents cause vasodilatation and myocardial depression, and volatile agents reduce systemic resistance.
In practice, a combined approach is attractive: fascia iliaca block for positioning and postoperative analgesia, then either light general anaesthesia with careful titration or a graded neuraxial technique, with an arterial line placed before induction. The technique matters less than the discipline of maintaining sinus rhythm, preload and vascular tone.
2. What haemodynamic targets and pharmacological strategy would you use, and how would you treat a sudden fall in blood pressure after induction?
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Targets: heart rate 60-80 beats/min in sinus rhythm, avoiding rates above 90; systolic pressure within 10-20% of her baseline of 118 mmHg, with a mean arterial pressure of at least 65-70 mmHg; adequate preload without fluid overload, since her stiff ventricle will not tolerate rapid large boluses and is prone to pulmonary oedema.
Preparation: invasive arterial monitoring before induction, and a phenylephrine infusion of 0.3-0.5 mcg/kg/min started before induction, or norepinephrine 0.03-0.05 mcg/kg/min, so that vasodilatation from the induction agent is pre-empted rather than chased.
Sudden hypotension after induction:
- Stop or reduce the volatile agent and any drug causing vasodilatation, and exclude a mechanical cause such as hypovolaemia or anaphylaxis.
- Give a small phenylephrine bolus of 50-100 mcg and increase the infusion. Phenylephrine is first-line because it raises systemic resistance without tachycardia.
- If hypotension is accompanied by bradycardia, use ephedrine 3-6 mg or glycopyrrolate 0.2 mg to restore rate and contractility; if the rhythm is a new bradyarrhythmia or asystole, atropine is appropriate.
- Give a cautious 250 mL crystalloid bolus and reassess; then consider low-dose epinephrine if pressure remains inadequate.
- Look for ischaemia or arrhythmia on the monitor and treat accordingly. Avoid pure vasodilators and avoid nitrous oxide in a patient with poor ventricular compliance.
3. What are the consequences of delaying surgery for valve intervention, and how would you counsel the team?
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Hip fracture surgery delayed beyond 48 hours is associated with increased mortality, pneumonia, pressure ulcers, delirium and loss of mobility. In a patient with severe symptomatic aortic stenosis, however, non-cardiac surgery carries a substantial perioperative cardiac risk, and the two risks pull in opposite directions.
The key distinction is between decompensated and compensated disease. She has a mildly raised but flat troponin and no rest pain, syncope at exertion only, and is currently haemodynamically stable, so there is no indication for urgent valve intervention before surgery. A six-week wait for TAVR assessment is not a reasonable reason to keep an 82-year-old immobile in traction.
My counsel would be: proceed with surgery within 24-48 hours under a carefully planned technique, with a cardiac anaesthetist, arterial line, critical care bed booked, and blood products cross-matched. Correct anaemia and dehydration preoperatively, continue aspirin, do not start a beta-blocker de novo on the day of surgery because of the risk of bradycardia and hypotension, and treat pain promptly with a fascia iliaca block. Meanwhile refer to cardiology for expedited TAVR assessment, and agree in advance with the team that if she becomes decompensated (pulmonary oedema, refractory angina, hypotension) before surgery, balloon aortic valvuloplasty could be considered as a bridge.