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Mitral stenosis

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Mitral stenosis

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Mitral stenosis

  1. 1. Mitral Stenosis for beginners Pratap Sagar Tiwari Pic ref: http://int-prop.lf2.cuni.cz/foto/016/pic00026.jpg
  2. 2. Uptodate 20.3
  3. 3. Mitral stenosis • MS is characterized by obstruction to left ventricular inflow at the level of MV due to structural abnormality of the MV apparatus.1 • MS is due to thickening and immobility of the mitral valve leaflets. • The normal MVO has a CSA of 4-6 cm2. 1. Carabello, B. A. (2005). "Modern Management of Mitral Stenosis". Circulation 112 (3): 432–7
  4. 4. Etiology • Rheumatic heart disease • Congenital MS • Mitral annular calcification (particularly in patients with ESRD). • Conditions that simulate MS: IE with large vegetation, LA myxoma, ball valve thrombus, and cor triatriatum. • Less common causes: malignant carcinoid disease, SLE, RA, mucopolysaccharidoses, Fabry disease, Whipple disease, and methysergide therapy.
  5. 5. Rheumatic mitral stenosis • In RMS, the MVO is slowly diminished by progressive fibrosis, calcification of the valve leaflets. • The flow of blood from LA to LV is restricted and LAP rises, leading to pulmonary venous congestion and breathlessness. • There is dilatation and hypertrophy of the LA, and left ventricular filling becomes more dependent on left atrial contraction. • Note: The association of atrial septal defect with rheumatic mitral stenosis is called Lutembacher syndrome.
  6. 6. Pathophysiology LAE Atrial Fibrillation ↑LAP precipitate pul edema  Acute dyspnea ↓Ventricular fillingThromboembolism Palpitation Stroke Hoarseness :due to compression of the LRLN by a dilated LA or pulmonary artery (Ortner syndrome) High pressure ruptures Pulmonary vessels :hemoptysis
  7. 7. Pulmonary Hypertension Backward transmission of the elevated left atrial pressure ↑ Pulmonary artery pressure ↑RAP & development of right sided heart failure RV hypertrophy & enlargement Hepatomegaly & Pulsatile liver Tricuspid regurgitation JVD Parasternal heave Prominent v wave Prominent a wave TR Peripheral edema Loud P2, later becomes palpable
  8. 8. Pathophysiology: MS Fatigue/Dyspnea/ ↓Functional capacity ↓ MVA Pul congestionAFib ↑ LAP ↑ LAP transmitted to pulmonary venous system LA enlargement (compensation to attempt to lower LAP) ↑ LAP, LAE LA remodelling LA clot Exertional Dyspnea /Pul edema ↑PVR ,PHTN RV pressure overload RVH RV dilates & fails With significant obstruction to flow from PVR & MS CO ↓ (first with exercise then at rest)
  9. 9. History • Generally asymptomatic at rest during the early stage. However, factors that ↑ HR such as fever, severe anemia, thyrotoxicosis, exercise, and Afib dyspnea. • Systemic embolization may lead to stroke, renal failure, or MI. • Hoarseness :compression of the LRLN against the pulmonary artery by the enlarged LA. Also, compression of bronchi by the enlarged LA can cause persistent cough. Cough also occurs due to pul congestion • Hemoptysis may occur. • Palpitation • Chest pain (due to pul hypertension) • Oedema / Ascites (Right heart failure) • Pregnant women with mild MS may become symptomatic during their 2nd trim (↑in blood vol ).
  10. 10. Physical examination • Presence of mitral facies (pinkish-purple patches on the cheeks) indicate chronic severe MS (reduced CO & vasoconstriction). JVD may be seen. • In pt with sinus rhythm, a prominent a wave :↑ RA pressure from pul HTN & RVfailure. • A prominent v wave :is seen with TR.
  11. 11. Palpation • The arterial pulses are reduced in volume due to the decreased SV. • Pulses may be irregular in Afib. • Tapping apex beat that is not displaced. • Left parasternal heave - presence of RVH due to pulmonary HTN • A P2 may be palpable in the 2LICS.
  12. 12. Parasternal Heave • Grade 1 : visible but not palpable • Grade 2 : Visible & palpable and obliterable • Grade 3: Visible & palpable but not obliterable
  13. 13. Cardiac auscultation: Heart sounds • The S1 is accentuated because of a wide closing excursion of the mitral leaflets. • The degree of loudness of the S1 depends on the pliability of the MV. • The intensity of the S1 ↓ as the valve becomes more fibrotic, calcified, and thickened. • The S2 is initially normal but, with the development of PHTN, P2 becomes ↑ in intensity .
  14. 14. Cardiac auscultation: Opening snap • An OS of the MV is heard at the apex when the leaflets are still mobile . • The OS is due to the abrupt halt in leaflet motion in early diastole. • Note: The OS following S2 may be mistaken for a split S2 (OS is best appreciated at the apex, not the base. ) • As the MS progresses and LAP is ↑, the OS occurs earlier after S2 or A2. Thus, the shorter the A2-OS interval, the more severe the MS.
  15. 15. Cardiac auscultation: murmur • low-pitched diastolic rumble that is most prominent at the apex. • Although the intensity of the diastolic murmur does not correlate with the severity of the stenosis, the duration of the murmur is helpful since it reflects the transvalvular gradient and the duration of blood flow across the valve. • The ↑ in atrial pressure after atrial contraction, results in an increase in the loudness of the murmur, termed "presystolic accentuation" .
  16. 16. MS: • The diastolic murmur and OS are diminished with inspiration, but augmented with expiration (in contrast to TS). With inspiration, the A2-OS interval widens . • Increasing venous return, eg, by lying the patient down and lifting the legs, augments the gradient; as a result, the diastolic murmur lengthens while the A2-OS intervals shorten. (Similar changes are seen in response to exercise.) • In contrast, reducing venous return with amyl nitrate, the Valsalva maneuver, or standing after squatting shortens the murmur and lengthens the A2-OS interval.
  17. 17. MS: murmur • On auscultation of mitral area of the heart, s1 is short ,sharp and accentuated and s2 is normal. • Opening snap is heard just after s2. • There is low pitched, mid –diastolic, rumbling murmur with presystolic accentuation of Grade 4 intensity in the mitral area without any radiation. • The murmur is best heard at cardiac apex with bell of steths ,in left lateral position ,at the height of expiration and after doing mild exercise.
  18. 18. MDM: D/D • It is not Carey coombs murmur (occurs in active rheumatic vulvulitis and oedema of MV cusps gives rise to soft MDM) because there is absence of loud s1, OS and diastolic thrill. • It is not Austin flint murmur (which is a functional low pitch mid diastolic murmur in pt with AI in which murmur is produced as the regurgitant jet flow hits the anterior mitral leaflets) because in AFM, the presystolic component is absent, there is no thrill, and S1 is not loud. And there is no OS. Moreover in AFM of AI ,there are features of LVH and peripheral signs of AI which is not present in this case. • It is not MDM of TS ,because the murmur of TS would be best heard in LSB and increases at the height of inspiration.
  19. 19. CXR
  20. 20. CXR • Backward displacement of esophagus by enlarged LA(in lat view) • Enlarged LA , Double shadow due to enlarged LA • Straightening of left heart border • Splaying of carina (The left main bronchus is lifted up by the enlarged LA) • Prominent upper zone pulmonary veins (Inverted moustache sign / Antler’s horn sign / Cephalisation pulmonary of blood flow) • Kerley B lines (indicating fluid collection in the interlobular septa)
  21. 21. Management • Patients with minor symptoms should be treated medically. • Intervention by balloon valvuloplasty, mitral valvotomy or MVR should be considered if the patient remains symptomatic despite medical Rx or if PHTN develops. • Anticoagulation :to reduce the risk of systemic embolism, • Ventricular rate control (digoxin, β-blockers CCB) in AFib • Diuretic therapy to control pulmonary congestion. • Antibiotic prophylaxis against infective endocarditis is no longer routinely recommended.
  22. 22. End of slides

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