Mitral valve disease – Mitral Regurgitation Mitral valve fails to close completely, causing blood to flow back into the left atrium during ventricular systole of multiple aetiology

Anatomy of Mitral valve apparatus

45 year old women diagnosed c/o chronic mitral regurgitation posted for abdominal hysterectomy Natural history Pathophysiology Preoperative assessment Perioperative management

Clinical presentation Depends on Etiology Severity of regurgitation Left ventricular function Pulmonary hypertension Atrial fibrillation Mixed valvular lesion Coronary artery disease & Hypertension

Etiopathology Valve leaflet Rheumatic Carditis Sequlae Myxomatous Degeneration Congenital Cleft Leaflet Marfan Syndrome Infective Endocarditis HOCM Mitral valve prolapse (MVP)

Etiopathology Chordae Tendinae Rheumatic Ischemic Papillary Muscles Ischemic Annulus Calcification - elderly patients Dilatation - functional MR

Pathophysiology Regurgitation of LV SV Reduced CO & LA dilatation LA dilatation Atrial fibrillation, Clot, Reactive PHT& Right heart failure LV volume overload LVH (concentric) & LV dilatation LV failure Pulmonary edema, systemic hypotension

Assessment of severity of MR Symptoms severity Presence of PHT Physical signs of CHF ECHO

Symptoms Depends on Atrial compliance Normal compliance – pulmonary congestion symptoms Exertional dyspnea (NYHA ) Orthopnea Right heart failure symptoms ankle edema upper abdominal pain ascites Increased compliance - low cardiac output symptoms easy fatigue Palpitations (Atrial fibrillation) Embolic symptoms or past history

Ejection fraction (EF) & MR Fraction of ventricular end diastolic volume ejected EF = EDV- ESV/EDV Inspiteof LV dysfunction EF may be normal in range LA acts as low resistance pathway during systole, EF overestimates LV function LV dysfunction defined as EF< 60% (AHA Guidelines)

Echocardiographic classification of MR

Echocardiographic assessment of regurgitant lesions by color – flow Doppler GradeDescriptionCriterion 0NoneNo regurgitation into receiving chmber 1+MildRegurgitant flow limited to area near valve 2+Mild to moderateRegurgitant flow occupies up to 1/3 of LA 3+Moderate to severeRegurgitant flow occupies up to 2/3 of LA 4+SevereRegurgitant flow occupies most of receiving LA & flow reversal in pulmonary veins

Premedication Standard doses of any common agents well tolerated & desirable in normal ventricular function Poor ventricular function – doses proportional to severity of ventricular function Usual medication on the morning of surgery Supplemental O2 – PHT or pulmonary disease Antibiotic prophylaxis ? IE, ? Surgical Anticoagulation management

Monitoring Depends on LV function & procedure Full hemodymaic monitoring – if plan for afterload reduction with vasodilators Color- flow Doppler TEE quantify severity guides therapeutic interventions in severe lesions Pulmonary artery pressure monitoring

Anesthetic management objectives Tailored to severity of regurgitation jet, LV function Avoid factors exacerbating the regurgitation Bradycardia - ↑↑ LV end diastolic volume mitral annular dilatation Acute rise in SVR Excess volume expansion – dilates LV Myocardial depression Prevent & promptly treat AF

Hemodynamic goals Maintain forward systolic flow Full, Fast & Vasodilated

Preload Augment LV preload prior to induction Remember MR is dynamic Excess ventricular distension →annular dilatation → worsens MR

Heart rate & Rhythm Bradycardia detrimental ↑duration of systole→ prolongs regurgitation ↑ diastolic filling→ LV distension Sinus rhythm preferred LV filling less depends on atrial kick as compared to MS

Contractility EF underestimates LV systolic function Avoid myocardial depression How to manage hypotension? Manipulate volume & heart rate Persistent hypotension → inotropic support Dobutamine Low Dose Epinephrine Milrinone

Afterload Low SVR maximizes forward cardiac output Adequate anesthetic depth Systemic vasodilators Inodilators IABP – acute MR Alpha 1 agonists worsens MR increases SVR & reflex bradycardia Temporary use of Ephedrine bolus preferable

Pulmonary hypertension PAP & PVR elevated in acute and chronic MR Secondary RV dysfunction Avoid factors increasing PVR Hypoxia Hypercapnia Acidosis High tidal volume High PEEP

Factors affecting Mitral valve repair Acute vs chronic MR Patient’s symptom severity Left ventricular function Severity of mitral regurgitation Feasibility of successessful repair Combined valvular lesions Complications of chronic MR

Choice of agents Preserved ventricular function – most anesthetic techniques tolerated well Spinal, epidural anesthesia tolerated (avoid bradycardia) Ventricular dysfunction sensitive to volatile agents opioid based anesthetic (avoid bradycardia) pancuronium with opioids useful

Symptomatic patients NYHA 2,3 & 4 Indicated 1. Acute severe MR (class 1) 2.Absence of severe LV dysfunction(class1) 3.Severe LV dysfunction & MV repair high likely (2a) 4.Functional MR,severe LV dysfunction on maximum medical therapy includes biventricular pacing (2b) (severe LV dysfunction = EF < 30% )

Indications for Asymptomatic patients Chronic severe MR and mild to moderate LV dysfunction (class1) Chronic sever MR with normal LV function High likely successful repair (2a) New onset atrial fibrillation (2a) Pulmonary hypertension(2a) Not indicated (class 3) Normal LV function & doubt about feasibility of repair Mild or moderate MR

Mitral regurgitation complicating Pregnancy Typically well tolerated due to favorable loading conditions increased blood volume, heart rate & low SVR Increased risk of AF ECG monitoring during labor Acute AF – promptly control ventricular rate Hypercoagulability, increases risk of systemic embolism Anticoagultion New onset AF, H/o embolism & Cardioversion

Management of parturient High SVR during labor – poorly tolerated Pain, Expulsive efforts & aortic compression Prevent & treat high SVR Epidural analgesia Results in low venous return Left lateral tilt SAB tolerated by pt’s with mild to moderate MR Vasopressor of choice Chronotrophic effect of Ephedrine benefits