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1. Mitral Regurgitation Dr Rati Prabha 1

2. Posterior PM is supplied by PDA of RCA Anterior PM: LAD by diagonal & CX by marginal branches 2

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5. Classification 1 o MR: disease of mitral leaflets- II & IIIa 2 o MR: Ds of LV or annulus-I & IIIb Ischemic: Functional(non-ischemic) 5

6. Congenital MR Mitral valve prolapse : Marfan syndrome, Ehler-Danlos syndrome, osteogenesis imperfecta , dominant cutis laxa   Isolated cleft of the anterior mitral valve leaflet Double orifice mitral valve: with AV septal defect Ebstein's malformation of the mitral valve 6

7. Pathophysiology Afterload (resistance to LV emptying) is reduced. For same EDV,: ESV↓, EF↑, but forward SV↓. LAP increased In chronic MR, there is ↑EDV d/t eccentric Hypertrophy, and ESV & forward SV returns to N. LA enlarges, and LAP falls In chronic decompensated MR, due to myocardial dysfunction, ESV ↑, EF↓ and FSV↓. LAP ↑ Eccentric HYP. In MR is due to development of new sarcomeres in series. 7

8. SYMPTOMS 8

9. Pts with mild to mod. isolated MR are generally asymptomatic . Chronic severe MR: Fatigue , exertional dyspnea , and orthopnea : due to reduced forward stroke volume and increased PAP Palpitations : AF due to atrial enlargement Right sided HF : painful hepatic congestion, ankle edema , distended neck veins, ascites , and secondary TR in pts with pul HTN Acute pulmonary edema : acute Severe MR 9

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12. PHYSICAL FINDINGS Carotid arterial upstroke is sharp and low volume in severe MR  The cardiac impulse is brisk and hyperdynamic displaced to the left and downward . 12

13. Auscultation Soft S1, Wide splitting of S2:Shortening of LV ejection & early closure of Aortic V. P2 louder than A2 in Pul HTN S3 due to rapid filling of LV 13

14. Holosystolic murmur: commences immediately after the soft S  1  and continues beyond and may obscure the A  2 Loudest at apex usually constant in intensity(even in AF) Other systolic murmurs like AS are variable blowing, high-pitched May radiate to axilla , L infrascapular area Radiation to aortic area/sternum may occur with abnormalities of posterior leafleat ( eg MVP) May cause systolic thrill 14

15. Silent MR Severe MR caused by LV dilation, acute myocardial infarction, or paraprosthetic valvular regurgitation, or in those who have marked emphysema, obesity, chest deformity, or a prosthetic heart valve, the systolic murmur may be barely audible or even absent 15

16. VSD : Murmur is usually loudest at the sternal border rather than the apex and is often accompanied by a parasternal , rather than an apical thrill TR : usually heard best along the left sternal border, is augmented during inspiration, and is accompanied by a prominent  v  wave and  y descent in the jugular venous pulse. 16

17. ECHO assess the mechanism of the MR and its hemodynamic severity LV function Associated valvular abnormalities 17

18. leaflet structure and function, chordal integrity, LA and LV size, annular calcification, and regional and global LV systolic function Enlargement of the left atrium and left ventricle, with increased systolic motion of both chambers.  18

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22. Pulsed wave Doppler of the pulmonary vein flow. The top panel shows the normal pattern, forward in systole and diastole. The middle panel shows blunting of the systolic flow, associated with increasing degrees of mitral regurgitation. The bottom panel shows the typical pattern of systolic reversal seen in severe MR. Note the nonlaminar aspect of the flow in the reversed S wave, caused by severe MR 22

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24.  Made at the level of the chordae from endocardial edge to endocardial edge in systole A measurement greater than 40 mm defines LV dilatation. End diastolic diameter > 55 is defined as LV dilation 24

25. ECG Left Atrial enlargement Atrial fibrillation LV hypertrophy 25

26. CXR left atrial enlargement convexity or straightening of the left atrial appendage just below the main pulmonary artery (along left heart border) double density sign : the right side of the enlarged left atrium pushes into the adjacent lung and creates an addition contour superimposed over the right heart elevation of the left main bronchus and splaying of the carina upper zone venous enlargement due to pulmonary venous hypertension left ventricular enlargement  is also eventually present due to volume overload 26

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28. Medical Treatment Anticoagulation in patients with AF Vasodilators in acute MR ACE inhibitors, B blockers and Biventricular pacing for chronic MR Diuretics and digoxin if in HF Avoid isometric forms of exercise 28

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30. Surgical Management Early surgical management is recommended before LV dysfunction becomes severe or irreversible Performed before the ejection fraction is less than 60% or before the left ventricle is unable to contract to an end-systolic dimension of 45 mm (normal <40 mm) or end diastolic dimension > 55 mm MV repair is preferred to replacement as it preserves LV geometry and avoids prosthesis insertion 30

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32. Anaesthetic goals Preload is increased. Afterload is decreased . Goal is mild tachycardia, vasodilation . Avoid myocardial depression . Monitor the magnitude of regurgitant flow with a pulmonary artery catheter (size of the V wave) and/or echocardiography 32

33. Post op LV Dysfunction Left ventricular dysfunction: With mitral competence restored, the low-pressure outlet for left ventricular ejection is removed. The enlarged LV must then eject entirely into the aorta At the same time, the preload augmentation inherent to MR is removed The systolic performance of the LV often declines after surgical correction of MR inotropic and vasodilator therapy and, if necessary, intraaortic balloon pump augmentation 33

34. RV dysfunction in post CBP period may require T/T with dobutamine , isoproterenol , and milrinone 34

35. Thank you 35