Severe Aortic Stenosis and a Perforated Viscus: The Anaesthetic Dilemma

The core physiology. In severe aortic stenosis the left ventricle cannot increase stroke volume across a fixed orifice. Cardiac output therefore becomes critically dependent on heart rate (to a point), preload, afterload and sinus rhythm. In addition, the hypertrophied ventricle has high myocardial oxygen demand and poor subendocardial perfusion, so hypotension is rapidly followed by ischaemia and arrest. Classic precipitants of decompensation are hypovolaemia, tachycardia, loss of sinus rhythm and a fall in systemic vascular resistance - all of which anaesthesia and sepsis produce.

Implications for preparation:

• Correct hypovolaemia cautiously but adequately: these patients need preload. Sepsis has caused vasodilatation and third-space loss; give fluid in measured aliquots while watching blood pressure and stroke volume.
• Preserve afterload. Do not be seduced into deep vasodilatation; a noradrenaline or phenylephrine infusion started early and titrated is preferable to large fluid boluses alone.
• Avoid tachycardia. Keep the rate controlled; a rate around 60–70 with adequate diastolic filling time is ideal.

Her drugs:

• Continue bisoprolol. Abrupt beta-blockade withdrawal in a patient with a hypertrophied ventricle produces rebound tachycardia and ischaemia. Give it with a sip of water; do not omit it.
• Withhold lisinopril on the day of emergency surgery. ACE inhibition blunts the compensatory vasoconstrictor response to vasodilating anaesthetic agents and increases the risk of refractory hypotension during and after induction. Given she has already taken it, anticipate a more vasoplegic induction and start vasopressor support earlier.

Spinal anaesthesia alone is the wrong choice here. Sympathectomy from a neuraxial block causes a rapid fall in systemic vascular resistance, which in severe aortic stenosis cannot be compensated by an increase in stroke volume - effectively an acute afterload-loss arrest. The block also spreads unpredictably in a septic, elderly patient and cannot easily be extended for a full laparotomy. A high block would also impair respiratory function.

General anaesthesia with a carefully controlled induction is the safer route. A combined technique with a low-dose epidural or spinal for postoperative analgesia can be considered, but only after the patient is stabilised, and it must not be used to produce the main surgical anaesthetic.

Induction and maintenance:

• Optimise first: fluid challenge to a responsive state, vasopressor infusion running before induction, adequate preoxygenation, arterial line before induction, and full monitoring including a cardiac output monitor if available.
• Induction: a slow, titrated agent that preserves vascular tone - for example etomidate or a low-dose opioid plus a small dose of propofol, with phenylephrine drawn up. Avoid ketamine-induced tachycardia if the rate is already high.
• Maintenance: volatile agent at low concentration with a background opioid and muscle relaxant, aiming for normocapnia, normothermia and a heart rate of 60–80. Treat hypotension promptly with vasopressor and rate control before reaching for more fluid.
• Postoperative destination: critical care with invasive monitoring; anticipate a prolonged vasopressor requirement, acute kidney injury from the combination of sepsis and low cardiac output, and atrial fibrillation, which she will tolerate very poorly.
• Analgesia: thoracic epidural may be helpful if coagulation is normal, but if there is any doubt use multimodal systemic analgesia with local anaesthetic wound catheters, since an epidural-induced hypotensive episode in this patient is difficult to rescue.

Framing. This is not a choice between a safe operation and a risky one; it is a choice between a very high-risk operation and an almost certain death from faecal peritonitis. Untreated perforation carries a mortality approaching 100%, so the operation, however hazardous, is the option with the better expected outcome - but the risk must be honestly stated: mortality in the region of 20–40% or higher given severe aortic stenosis, sepsis and renal impairment, with a significant chance of prolonged critical care and dependency even on survival.

I would explain in plain terms:

• The hole in the bowel will not heal without surgery.
• Her heart valve makes the anaesthetic dangerous, mainly because her heart cannot compensate for the blood pressure changes that sepsis and anaesthesia cause.
• We would plan for a damage-control approach: the shortest possible operation to control the contamination, critical care, and a second look only if she improves.

Factors that would push me towards comfort-focused care:

• Pre-existing severe frailty, dependency in activities of daily living, or significant cognitive impairment;
• Patient-expressed wishes to avoid prolonged life-support, or a valid advance decision;
• Multiorgan failure already established at presentation (vasopressor-dependent with lactate >5, anuria, coagulopathy) where the chance of meaningful recovery is very low;
• A technically uncontrollable source with no realistic chance of restoring gastrointestinal continuity.

The decision belongs to the patient if she has capacity - she is drowsy, so treat reversible causes, involve the family as advocates, and document clearly. The surgical and anaesthetic teams should agree a shared plan and a ceiling of care before induction, rather than discovering disagreement in theatre.