Full, Fast, Forward

Full – maintain preload with fluids, maintain sinus rhythm to keep LV full.  Too much fluid will worsen severe AR with increased LVEDP, mitral regurg, and pulmonary edema.

Fast – goal HR 80-100 bpm.  The slower the heart rate, the more time in diastole, the more time for regurgitation.  Too fast may easily cause ischemia even without CAD.  Ephedrine, Glycopyrrolate, low-dose epinephrine infusion

Forward – maintain contractility, reduce the afterload to promote forward flow, but remember aortic diastolic pressure is needed for coronary perfusion. Inotropic = Milrinone, dobutamine, low-dose epi infusion. To reduce afterload consider analgesia/anesthetic depth, CCBs, nitroprusside, hydralazine.

Safely Reduce SVR – If SVR is high, Propofol and volatile agents favorably decrease SVR, but high doses can cause dangerous cardiac depression. Use an adjunct to blunt the sympathetic reflex when intubating.  

Smooth Emergence – Gradual/smooth emergence to avoid increases in SVR

Neuraxial Anesthesia – Neuraxial anesthesia can typically be performed in patients with moderate AR, but is generally avoided in those with severe AR. In either case, arterial lines are recommended prior to neuraxial anesthesia. Furthermore, pre-neuraxial fluid administration and neuraxial drugs are recommended to be administered carefully to avoid worsening of hemodynamics and symptoms related to AR.

Arterial lines – As stated above, A-lines should be employed for neuraxial anesthesia. Otherwise, A-lines are typically reserved for patients symptomatic or confirmed to have a significantly reduced EF.

Diagnostics – AR causes a diastolic murmur at the left sternal border, a pulsus bisferiens on the a-line, and large V-waves from the LA. Color doppler vena contracta width severity is 0.3-0.6 cm for moderate, and greater than 0.6cm is considered severe.

Pathophysiology – Inadequate closure of the aortic valve during diastole allows blood to regurgitate into the ventricle. This blood overloads the volume of the left ventricle. This causes increases in end-diastolic wall tension, which over time, will cause eccentric hypertrophy. Eccentric hypertrophy (ventricular stretching or chamber enlargement) leads to the heart being unable to effectively eject the blood needed to supply adequate perfusion. Furthermore, much of the blood that should fill the left ventricle (from the left atrium) is unable to move forward, which causes a “back-up” of blood to the lungs and right side of the heart.

Types – Type I involves annular dilation or cusp perforation, Type II involves excessive/flail leaflet motion, and Type III involves restricted leaflet motion.

Severity – in the moderate stage 30-55% of the blood ejected from the left ventricle is regurgitant (regurgitant fraction). RA is considered to be severe when then regurgitant volume is greater than 60%.

Chronic AR – Chronic AR/AI causes overload of the LV, and subsequently the LV can’t receive the volume that should be delivered by the left atrium. This overload, with time, causes eccentric LVH (high ventricular compliance) and low diastolic aortic pressure, all of which leads to ischemia, even in the absence of CAD. Chronic AR can take 20 years or more to develop.

Symptoms – symptoms will typically do not occur until the moderate stage (30-55% regurgitant fraction). Symptoms start with breathing issues such as exertional dyspnea, nocturnal dyspnea, or orthopnea. Rapid decline is often seen after these symptoms appear. Late symptoms include increased LVEDP, decreased ejection fraction, and pulmonary edema. Systemic vascular resistance (SVR) will increase to perfuse the organs, but will ultimately worsen AR.

Etiology – Rheumatic fever is the primary cause worldwide, but in the United States it is usually a congenital or degenerative cause, such as a bicuspid valve, annulus dilation from syphilis, rheumatoid and psoriatic arthritis, ankylosing spondylitis, Marfan, Ehlers-Danlos, or lupus

Acute AR/AI – has a higher mortality because the ventricle has not adapted to the overload in volume. This form is far less common, and typically related to trauma, aortic dissection, and infective endocarditis. Symptoms are pulmonary edema, ↓BP, and weakness.
This type calls for emergent surgery.