The aortic valve acts as the final outflow gateway of the left ventricle, ensuring unidirectional blood flow from the heart to the systemic circulation. Its proper function is central to maintaining hemodynamic stability, adequate coronary perfusion, and efficient ventricular ejection — all of which can be influenced by anesthesia. Even subtle structural or functional abnormalities can dramatically affect preload, afterload, and contractility, necessitating precise anesthetic management strategies.
Understanding the valve’s anatomy, biomechanics, and physiologic regulation enables anesthesiologists to anticipate challenges, tailor drug choices, and optimize intraoperative monitoring to maintain perfusion and cardiac stability.
Trileaflet Design:
The aortic valve comprises three semilunar cusps — right coronary, left coronary, and non-coronary — anchored to a fibrous annulus at the left ventricular outflow tract (LVOT).
Sinuses of Valsalva:
Located behind each cusp, these bulging pockets in the aortic root prevent cusp adherence to the aortic wall and facilitate smooth closure.
Coronary Ostia:
The right and left coronary arteries originate from the sinuses, ensuring perfusion during diastole.
Annulus and Commissures:
The fibrous annulus provides mechanical stability, while commissures ensure symmetric cusp attachment and balanced leaflet tension.
Sinuses of Valsalva:
During diastole, these sinuses fill and direct blood into the coronary ostia. Maintaining adequate mean arterial pressure (MAP ≥ 65 mmHg) is crucial for coronary perfusion, particularly under anesthesia when vasodilation or hypotension may occur.
Annulus and Surgical Implications:
Annular dilation (e.g., in connective tissue disorders or aortic aneurysm) may predispose to regurgitation, emphasizing the importance of tight hemodynamic control during induction and cardiopulmonary bypass.
Clinical Vignette:
During induction in an elderly patient with calcific aortic disease, an abrupt fall in blood pressure following propofol bolus can reduce coronary perfusion and precipitate ischemia. Using etomidate and pre-induction phenylephrine helps maintain stability.
Reference
Anderson RH, Mohun TJ, Spicer DE. The anatomy of the aortic root. Clin Anat. 2014;27(5):748–756.
Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA guideline for the management of patients with valvular heart disease. J Am Coll Cardiol. 2021;77(4):e25–e197.
The valve opens when left ventricular pressure exceeds aortic pressure, allowing ejection of blood with minimal resistance.
The process is passive, relying on pressure gradients rather than muscle activity.
The cusps behave like parachute flaps in a tailwind, optimizing laminar ejection flow.
Clinical Relevance:
Reduced systolic pressure gradient (e.g., due to myocardial depression or hypotension from induction agents) leads to decreased stroke volume.
Excessive afterload (from vasoconstrictors or hypertension) increases ventricular workload, worsening ischemia in patients with stenosis.
