The aortic valve, normally consisting of 3 leaflets, opens during ventricular systole and closes during diastole. Valve closure prevents backflow of blood from the aorta to the left ventricle (LV) and helps maintain aortic diastolic pressure and coronary perfusion pressure.
Aortic regurgitation (AR) is the presence of a backflow leak through the valvular apparatus during diastole.
Ranges in severity from trace, mild, moderate, or severe; it is classified by the amount of regurgitant volume, regurgitant orifice area size, and pressure equalization half-time by echocardiography.
Regurgitation may be associated with any condition that alters aortic valve closure. Aortic dilation, aneurysm, dissection, and abscess are external causes of aortic valve dysfunction and account for about half of all AR cases. Rheumatic valve disease, collagen vascular diseases, connective tissue diseases (especially Marfan syndrome (1) [C]), congenital malformations, senile degeneration, and infective endocarditis are direct valvular conditions that commonly produce AR in the remainder of cases.
Acute AR is the sudden onset of backflow leak usually due to an acute event such as aortic dissection or valvular trauma.
Chronic AR has a gradual onset and may be sustained for many years.
May also accompany aortic stenosis—a narrowing of the open valvular area
Epidemiology
Incidence
Worldwide, rheumatic heart disease is the most common cause of AR.
In the US, congenital and degenerative valvular and aortic disease is most common.
Congenital bicuspid aortic valves occur in 1–2% of the US population and may contribute to AR.
Prevalence
13% in men, 8.5% in women in a Framingham study (2)
Acute AR has a higher rate of morbidity and mortality due to the underlying pathophysiology. This can result in diastolic and systolic dysfunction and eventually decompensation (CHF).
Chronic AR mortality is related to the eventual decompensation of the LV; it is more common in severe AR. Decreased ejection fraction and LV function have a poor prognosis for recovery, even after repair.
Surgical management becomes the common end point to both types of AR.
Mortality
Acute AR has a high mortality due to sudden uncompensated cardiovascular changes usually requiring immediate surgical management.
Chronic AR mortality relates to eventual decompensation of the LV and may occur at any age usually with severe AR. Decreased ejection fraction and LV function has a poor prognosis for recovery even after repair.
Yearly mortality risk relates to NYHA classification for chronic severe AR:
Male gender has a greater risk for AR with a related increased risk of hypertension, connective tissue and congenital valvular diseases, which may result in presentation at a younger age.
Severe AR is most commonly diagnosed at age 60 and above.
Physiology/Pathophysiology
Acute AR results in an acute increase in LV diastolic volume, decreased aortic diastolic pressure (forward flow), decreased coronary perfusion pressure, volume overload, and decreased diastolic function of the LV. This leads to an increase in myocardial demand, acute fulminant CHF, and cardiogenic shock. Common causes of acute AR, including aortic dissection, warrant emergent surgical repair.
Chronic AR has a more insidious onset and may take years to become symptomatic. As regurgitant volume and AR worsen over time, the LV has time to remodel with eccentric hypertrophy and dilation. The increase in diastolic volume is compensated by the enlarged LV, increased heart rate, and decreased systemic vascular resistance (SVR). Ejection fraction is maintained and may prevent symptoms without exertion or positional changes. As time passes, the ventricle becomes "too enlarged" with resultant increases in wall stress and decreases in myocardial perfusion (leads to diminished EF, CHF, and end-organ hypoperfusion). Recall Laplace's law where Tension = (Pressure × Radius)/Wall Thickness; as the radius increases, tension also increases (increases myocardial oxygen consumption). Sympathetic stimulation increases SVR to maintain pressure but worsens AR; hinders forward flow. Without timely surgical repair the heart may not be able to significantly recover.
Anesthetic GOALS/GUIDING Principles
Maintenance of cardiac output, coronary perfusion, and prevention of cardiac decompensation are the primary goals.
Normal sinus rhythm and avoidance of bradycardia to minimize regurgitant time
SVR may be mildly decreased, but should be balanced between facilitating forward flow (decreasing regurgitation) and maintaining adequate coronary and systemic perfusion pressure.
Careful fluid management and inotropic support to prevent cardiovascular overload or collapse
Diagnosis⬆⬇
Symptoms
Chronic AR may be asymptomatic for decades.
Palpitations and tachycardia
Fatigue
Dyspnea on exertion
Orthopnea
Paroxysmal nocturnal dyspnea
Angina
History
Family history of cardiac valvular disease, collagen or connective tissue disease, or congenital malformations
History of rheumatic disease or risk factors for endocarditis
Commonly diagnosed after symptomatic exercise or during workup for diastolic or systolic CHF
May be discovered early after detailed physical exam and auscultation of heart murmur
Usually classified by echocardiographic measurement of color Doppler flow across the valve
Signs/Physical Exam
Syncope
Cyanosis
Decrescendo diastolic murmur
Watson's hammer pulse (bounding pulse)
Corrigan's carotid pulse
Wide pulse pressure
Signs of CHF
Treatment History
Medical management of angina, CHF, diabetes, hypertension, and hyperlipidemia, if associated
Previous history of balloon aortic valvuloplasty or valve replacement
Previous treatment of infective endocarditis
Transesophageal echocardiography for diagnosis and risk stratification
Medications
Antihypertensives including calcium channel blockers; beta-blockers are usually not prescribed since they may cause bradycardia.
Anti-anginals including nitrovasodilators
Heart failure treatments including digoxin, ACEI/ARB, and diuretics
Statin therapy if indicated
Diagnostic Tests & Interpretation
Labs/Studies
Basic metabolic profile: Monitoring electrolytes and kidney function
CBC: Monitoring for preoperative infection and hematocrit and platelet counts adequate for surgery
CXR: Cardiopulmonary status
CT scan for evaluation of aorta
Echocardiogram: Diagnosis and classification of disease severity and ventricular function
Basic coagulation studies: Adequate levels for surgery and evaluation of liver function
CONCOMITANT ORGAN DYSFUNCTION
Dilated cardiomyopathy and diastolic dysfunction
Concomitant mitral stenosis or regurgitation in rheumatic heart disease
Pulmonary hypertension, congestion, and pleural effusion
Renal insufficiency
Hypertension
Circumstances to delay/Conditions
Unrelated end-organ failure
Recent myocardial infarction or stroke
Classifications
Severe AR criteria:
>60 mL regurgitant volume
>50% regurgitant volume
Effective regurgitant orifice area >0.3 cm2
Color Doppler Vena Contracta >0.6 cm
Regurgitant jet >60% of LVOT diameter
Aortic valve pressure half-time <250 ms
Early closure of mitral valve and LV dilation
Treatment⬆⬇
PREOPERATIVE PREPARATION
Premedications
Midazolam to prevent anxiety and increased sympathetic tone, as appropriate
Special Concerns for Informed Consent
Risk for intraoperative stroke, myocardial infarction, and death should be discussed.
INTRAOPERATIVE CARE
Choice of Anesthesia
Depends on the procedure; sedation, general (endotracheal tube or laryngeal mask airway) and regional anesthesia may be utilized.
Neuraxial techniques can result in a sympathectomy and facilitate forward flow (reduce regurgitation), but may reduce coronary perfusion pressure.
Monitors
Standard ASA monitors
Invasive monitors may be chosen based upon the severity of AR and the surgical procedure.
Induction/Airway Management
Smooth, controlled induction to maintain vital signs within normal limits
Anticholinergic medications may be administered to maintain a NSR and slightly increase the heart rate.
Maintenance
Volatile and/or intravenous anesthetics may be utilized. Reductions in SVR are desirable to facilitate forward flow; however, adequate cerebral and coronary perfusion should be ensured. Total intravenous techniques may be associated with bradycardia, particularly if utilizing high doses of remifentanil.
Fluid balance includes maintaining normal preload and hematocrit >24–30 g/dL to optimize forward flow and myocardial oxygen balance. Excessive preload may add to regurgitant volume and cause LV failure.
Extubation/Emergence
No additional concerns
Follow-Up⬆⬇
Bed Acuity
Depends on surgical procedure and severity of underlying disease
Medications/Lab Studies/Consults
Standard postoperative fluid and electrolyte management and related laboratory studies
Complications
Perioperative arrhythmia
References⬆⬇
OdiliAN, AmusaGA.Aortic aneurysm with valvular insufficiency: Is it due to Marfan syndrome or hypertension? A case report and review of literature. J Vasc Nurs. 2011;29(1):16–22.
SinghJP, EvansJC, LevyD,et al. Prevalence and clinical determinants of mitral, tricuspid, and aortic regurgitation. Am J Cardiol. 1999;83:897–902.
DujardinKS, Enriquez-SaranoM, SchaffHV, et al.Mortality and morbidity of aortic regurgitation in clinical practice: A long-term follow-up study. Circulation. 1999;99(14):1851–1857.
Van DyckMJ, WatremezC, BoodhwaniM, et al.Review articles: Transesophageal echocardiographic evaluation during aortic valve repair surgery. Anesth Analg. 2010;111:59–70.
Codes⬆⬇
ICD9
395.1 Rheumatic aortic insufficiency
424.1 Aortic valve disorders
746.4 Congenital insufficiency of aortic valve
ICD10
I35.1 Nonrheumatic aortic (valve) insufficiency
I06.1 Rheumatic aortic insufficiency
Q23.1 Congenital insufficiency of aortic valve
Clinical Pearls⬆⬇
Aortic regurgitation (AR) is most commonly an acquired disease but may be related to congenital malformations and several systemic conditions such as Marfan syndrome.
Significant signs and symptoms include shortness of breath, angina, syncope, and systolic and diastolic congestive heart failure with eccentric hypertrophy and a dilated LV.
Severity is classified by echocardiographic criteria; 60 mL or 50% regurgitant volume being severe AR.
Acute AR is life-threatening and often requires immediate surgical management.
Chronic AR requires medical or surgical management and may be asymptomatic until late stages. Symptomatic, severe AR with below normal LV EF requires urgent treatment and has poorer prognosis.