Increase preload.

Maintain/increase afterload – this may seem counterintuitive because the stenotic valve is already increasing the afterload. However, coronary perfusion pressure (above the stenotic lesion) relies on that added pressure.

Use an alpha-1 agonist (eg. phenylephrine) – to keep pressures adequate without an increased HR.

Avoid spinal anesthesia – due to sympathectomy (reduced SVR and hypotension). Epidural anesthesia CAN be done – but relies heavily on the anesthesia provider’s judgement

Keep HR at a conservative high – typically between 70-80. Bradycardia AND tachycardia will lead to reduced cardiac output. Beta blockers for tachycardia. If bradycardic, use atropine, glycopyrrolate, or ephedrine.

Maintain contractility.

sync to the R wave – If cardioversion is required for tachycardia.

Maintain atrial kick – These patients rely heavily on this for adequate stroke volume so avoid at all costs loss of this function (junctional rhythms or A-fib).

Early auscultation – will help an early diagnosis and treatment, but more importantly, will help shape the anesthetic plan if the patient is presently undiagnosed. Symptoms typically do not manifest until the disease process is severe. Therefore, always listen for this murmur – especially in the elderly, and before giving spinal anesthesia. The murmur is high pitched “diamond shaped” crescendo-decrescendo ejection murmur heard best at the right upper sternal border which radiates to the neck and carotid arteries.

The aortic valve becomes stenosed. This causes a backup of blood, which leads to increased pressures in the left ventricle. This load of pressure forces the ventricle to compensate by getting bigger (as most muscles do to an increased load). In the medical world they will say that the muscle is building “in parallel,” meaning the muscle is simply getting thicker rather than wider. This is called concentric hypertrophy. This increased thickness then requires more oxygen and, at the same time, is creating a greater compression on the arteries that would supply it – a double-whammy. If uncorrected (typically by a valve replacement), this will continue until the patient’s heart can no longer support the pressure. The weakening heart will no longer be able to support the cardiac output it needs, leading to syncopy, angina, and dyspnea (the SAD triad of aortic stenosis). These symptoms begin to show when the valve orifice is < 0.8 cm2. The normal orifice is 2.5-3.5 cm2. The pressure-volume loop will be heightened.