Description- The mitral valve, normally consists of two leaflets (bicuspid valve) that open during ventricular diastole and close during systole. During systole, the mitral valve closes and prevents the backflow of blood from the left ventricle (LV) to the left atrium (LA). Closure of the valve helps maintain LV diastolic pressure and volume and thus systemic and coronary perfusion pressure.
- Mitral regurgitation (MR) is the presence of a backflow leak through the valvular apparatus during systole.
- Ranges in severity from trace, mild, moderate, to severe. Severity is classified by the amount of regurgitant volume, regurgitant orifice area size, and regurgitant fraction by echocardiography.
- Acute MR is the sudden onset of symptoms usually due to an acute event such as myocardial infarction and valvular apparatus trauma or disruption.
- Chronic MR has a gradual onset and may be sustained for many years and may be compensated or uncompensated.
EpidemiologyIncidence
- Rheumatic heart disease is the most common cause of MR world-wide; mitral valve prolapse is the most common cause in the US (accounts for 45%).
- Mean age of rheumatic MR is 36 years old.
- Following a myocardial infarction, 20–30% of patients develop MR.
Prevalence
- Mitral valve prolapse is present in ~4% of the population
- Under 20 years of age, males > females
- Males >50 years of age have more severe disease
Morbidity
- Acute MR has a higher rate of morbidity and mortality due to the pathophysiology. Acute congestive heart failure (CHF) and cardiogenic shock may occur. Operative mortality is near 80%.
- Chronic MR may be asymptomatic for years. Chronic severe MR will lead to eventual decompensation with diastolic and systolic dysfunction and CHF.
- Surgical management becomes the common end point to both acute and chronic MR.
- Global and regional left atrial (LA) functions are altered in patients with chronic MR secondary to myxomatous mitral valve disease (1) [C].
- Left ventricular dysfunction may be present with MR and may be underestimated in severe MR. The decreased after load on the LV with backward flow through the mitral valve gives the false appearance of normal function. In severe MR, a low LV ejection fraction carries a very poor prognosis.
Mortality
- MR due to flail leaflets and LA diameter of >55 mm is associated with increased mortality under medical management (2) [B].
- Mild MR is an independent predictor of post-MI mortality.
- Atrial fibrillation was identified by multivariate logistic regression analysis as a predictor of in-hospital death after non-cardiac surgery; OR 11.579 (3) [B].
Etiology/Risk FactorsMay be associated with any condition that alters mitral valve closure. Organic, also known as intrinsic valve disease, may be due to myxomatous changes, rheumatic heart disease, mitral valve prolapse, or calcific valve disease. Functional MR results from a non-valvular disease such as dilated cardiomyopathy, causing incomplete closure of the mitral valve.
Physiology/Pathophysiology- Acute MR is often due to ruptured chordae or papillary muscle resulting in an acute increase in LV diastolic volume, LA volume, LV ejection fraction (EF), and aortic systolic pressure. Acute fulminant CHF may ensue and is marked by a decrease in contractility and EF. Mitral valve prolapse and tissue diseases (e.g., rheumatic heart disease, myxomatous disease) may present with an acute phase that is often milder in onset and leads to chronic MR.
- Chronic MR has a more insidious onset and may take months to years to become symptomatic. Eccentric left ventricular hypertrophy, atrial enlargement, and increased heart rate compensate for the extra volume of regurgitation; ejection fraction is maintained and symptoms typically do not appear without exertion or positional changes. As regurgitant volume and MR worsen over time, the left ventricle decompensates. The ventricle becomes too enlarged and the increased wall stress and decreased myocardial perfusion lead to diminishing EF and CHF, end organ hypoperfusion, decreased coronary perfusion pressure, increased myocardial oxygen demand, and cardiogenic shock. In addition, increases in LA pressure lead to pulmonary congestion and eventually chronic decompensated CHF with right ventricular failure. LA enlargement leads to atrial fibrillation which diminishes forward flow and increases the risk of thrombus formation. Sympathetic stimulation increases systemic vascular resistance to maintain pressure but worsens MR. 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.
- Maintain high-normal sinus rhythm to minimize regurgitant time and excessive left ventricular filling.
- Systemic vascular resistance may be 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.
- Decrease pulmonary hypertension by avoiding increased pulmonary vascular resistance from hypoxia, hypercapnia, acidosis, and pulmonary vasoconstrictors.
- Maintain contractility with inotropes if unresponsive to volume and afterload changes.
Symptoms- Shortness of breath
- Fatigue
- Dyspnea on exertion
- Palpitations
- Orthopnea
- 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 work up for diastolic or systolic CHF.
- May be discovered early after detailed physical exam and heart auscultation of murmur.
- Usually classified by echocardiographic measurement of color Doppler flow across the valve.
Signs/Physical Exam
- Systolic murmur
- Signs of congestive heart failure
- Endocarditis
- Cyanosis
- Medical management of angina, CHF, diabetes, hypertension, and hyperlipidemia, if associated.
- Balloon mitral valvuloplasty or valve replacement.
- Previous treatment of infective endocarditis.
- Anticoagulation or ablation for atrial fibrillation.
- Antihypertensives including calcium channel blockers and avoiding beta-blocker bradycardia.
- Anti-anginals including nitrovasodilators.
- Heart failure treatments including digoxin, ACEI/ARB, and diuretics.
- Statin therapy if indicated.
Diagnostic Tests & InterpretationLabs/Studies
- Basic metabolic profile: Monitoring electrolytes and the kidney function.
- Complete blood count: Monitoring for preoperative infection and hematocrit and platelet counts adequate for surgery.
- Basic coagulation studies: Evaluation of liver function and adequate levels for surgery.
- Electrocardiogram: Diagnosis of arrhythmia and ischemic changes.
- Chest X-ray: Cardiopulmonary status
- CT scan for evaluation of aorta.
- Echocardiogram: Diagnosis and classification of disease severity and ventricular function.
Concomitant Organ Dysfunction - Concomitant mitral stenosis or aortic valve disease in rheumatic heart disease
- Ischemic cardiomyopathy or hypertrophic cardiomyopathy
- Hypertension
- Pulmonary hypertension, congestion, and pleural effusion
- Renal insufficiency
Circumstances to delay/Conditions - Severe decompensated symptomatic MR with decreased left ventricular function for non-cardiac surgery
- Recent MI or stroke
- Sepsis or infection
- Unrelated end organ failure
Severe mitral regurgitation criteria:
- >60 mL regurgitant volume
- >50% regurgitant volume
- Effective regurgitant orifice area >0.4 cm2
- Color Doppler vena contracta >0.7 cm
- Pulmonary vein flow reversal on ventricular systole
- Severe LA enlargement
- MR jet ‘V’ wave and PCWP cannon "V" wave
Depends on surgical procedure and severity of underlying disease.
Medications/Lab Studies/Consults Standard postoperative fluid and electrolyte management and related laboratory studies.
ComplicationsPerioperative arrhythmia