Aortic stenosis
Why examiners ask this
Aortic stenosis is the valve lesion where a single wrong decision, a spinal for a hip fracture, can kill the patient on the table, so it tests judgment more than knowledge. The examiner also uses it to probe physiology: why tachycardia is dangerous, why vasodilation is dangerous, why chest compressions fail. It is a reliable additional topic because the stem can hide it behind "a systolic murmur noted in the chart."
The 60-second answer
My goals are to keep the stiff, hypertrophied left ventricle full, slow and well perfused. I confirm severity from the most recent echocardiogram, a valve area of 1.0 cm2 or less, a mean gradient of 40 mmHg or more, or a jet velocity of 4 m/s or more,1 and I ask about syncope, angina and dyspnea, because symptomatic severe stenosis has a short survival and warrants a valve conversation before elective surgery.2 I place an arterial line before induction,2 I induce with etomidate or a slow titration of propofol with phenylephrine or norepinephrine running, I keep the heart rate between 60 and 80 in sinus rhythm, and I treat any fall in pressure immediately with phenylephrine because coronary perfusion of that thick ventricle depends on diastolic pressure. I avoid single-shot spinal anesthesia; a general anesthetic or a carefully titrated epidural is my choice. Defibrillator pads go on before induction, because resuscitation across a stenotic valve rarely works and access to the chest may be limited once draped.2
Decision points and the "why"
- Proceed or refer — asymptomatic severe stenosis with preserved ventricular function tolerates elective non-cardiac surgery with preparation and invasive monitoring; symptomatic severe stenosis, or a low-flow low-gradient picture with poor ventricular function, goes to the heart team for valve replacement first, and balloon valvuloplasty is only a case-by-case bridge because of restenosis and complications.2 For the valve itself, surgical replacement is preferred under 65, transfemoral TAVR over 80, and either after shared decision-making between 65 and 80.1
- Arterial line before induction — the window for treating hypotension is seconds; waiting for a cuff cycle costs coronary perfusion.
- Phenylephrine as the first vasopressor — it raises diastolic pressure without raising heart rate; ephedrine's tachycardia shortens diastolic filling of a ventricle that depends on it. Norepinephrine is my second choice when phenylephrine is not enough.
- Sinus rhythm matters — the non-compliant ventricle depends on the atrial contribution for up to 40% of filling;2 new atrial fibrillation with hypotension is an indication for synchronized cardioversion, not rate control.
- Avoid single-shot spinal — the sudden sympathectomy drops preload and afterload together, and the fixed obstruction cannot compensate by raising stroke volume. This is classic teaching rather than trial evidence; neuraxial techniques have been used safely in asymptomatic severe stenosis, so if I choose one I place the arterial line first, dose the epidural slowly in small increments, and treat hypotension immediately with norepinephrine.2
- Pulmonary artery catheter or TEE — for major surgery with large fluid shifts, TEE gives me ventricular filling and function in real time; a PA catheter overestimates filling pressures in a stiff ventricle, so I interpret the wedge accordingly.
- Monitor ischemia — subendocardial ischemia occurs with normal coronaries because wall tension is high and diastolic perfusion time is short; ST analysis in V5 and II is on from the start.
The complication they will inject
During a laparoscopic cholecystectomy the pressure falls to 70/40 with a heart rate of 130 in atrial fibrillation. I say this out loud as a spiral: loss of atrial kick, tachycardia, short diastole, hypoperfused ventricle, more arrhythmia. I ask the surgeon to desufflate, go to 100% oxygen, give phenylephrine 100–200 mcg boluses while the pads are charged, and perform synchronized cardioversion at 120–200 J biphasic if the pressure does not recover within a minute.3 I then correct what provoked it: volume, potassium, magnesium, depth of anesthesia, and surgical stimulus. If the rhythm degenerates to a pulseless state I start compressions and epinephrine, and I tell the team that compressions generate little flow across the valve, so early defibrillation and rapid return of a perfusing rhythm are the only things that work.
Pitfalls that cost points
- Choosing a spinal because "the patient is elderly and a regional technique is safer."
- Reaching for ephedrine or giving a fluid bolus alone when the problem is afterload.
- Treating the atrial fibrillation with a rate-control drug while the pressure is 70 systolic.
- Confusing aortic stenosis with hypertrophic cardiomyopathy management; both want a full, slow ventricle, but only HCM is worsened by inotropes.
- Forgetting that mitral regurgitation and aortic stenosis want opposite afterloads if both are present.
Rapid-why
Q: Why is bradycardia also dangerous? A: Stroke volume is fixed, so cardiac output is rate-dependent; below about 50 the output falls even though diastole is long.
Q: Why is nitroglycerin a poor choice for angina here? A: It drops preload and diastolic pressure, which lowers coronary perfusion of the hypertrophied ventricle and worsens the ischemia.
Q: What are the classic symptom-to-survival figures? A: Angina about 5 years, syncope about 3 years, heart failure about 2 years without valve replacement; contemporary summaries put average survival at only 1–3 years after symptom onset.4
Q: Does TAVR change the anesthetic plan afterward? A: The obstruction is gone, so I manage the patient as an elderly patient with the underlying ventricular disease, continue antiplatelet therapy, and check for a new conduction block or pacemaker.
Numbers to know
| Item | Value |
|---|---|
| Severe stenosis | Valve area ≤1.0 cm2, mean gradient ≥40 mmHg, jet velocity ≥4 m/s1 |
| Very severe stenosis | Jet velocity ≥5 m/s1 |
| Heart rate target | 60–80, sinus rhythm |
| Normal valve area | 2.5–3.5 cm2 |
| Cardioversion for unstable AF | 120–200 J biphasic, synchronized3 |
| Atrial contribution to filling | Up to 40%2 |
Links
- Preoperative cardiac evaluation for non-cardiac surgery, Hypertrophic obstructive cardiomyopathy (coming), Spinal anesthesia: dosing, spread, hypotension, Intraoperative cardiac arrest, Vasopressors and inotropes: choosing and titrating
- Atlas: Basic valvular lesions on 2D and color; The 11 TEE views
- ACC/AHA 2020 guideline for the management of valvular heart disease
Sources
- 1.2020 ACC/AHA Heart Valve Disease Guideline: Key Perspectives, Part 1 · American College of Cardiology, 2020 · acc.orgSummary of Otto CM et al., 2020 ACC/AHA valvular guideline (stage D1-D3 definitions, AVR indications, SAVR vs TAVI by age).
- 2.Anesthesia for aortic valve stenosis: Anesthesiological management of patients with aortic valve stenosis during noncardiac surgery · Die Anaesthesiologie (PubMed Central), 2024 · pmc.ncbi.nlm.nih.govBillig S et al., German-language review; atrial contribution up to 40%, arterial line and pads before induction, neuraxial evidence.
- 3.Direct-Current (DC) Cardioversion-Defibrillation · Merck Manual Professional Edition · merckmanuals.com
- 4.Aortic Stenosis · StatPearls, 2023 · statpearls.com
Facts on this page were checked against these sources on Oct 14, 2026. Guidelines change; confirm doses against current institutional protocols.