Mitral regurgitation Flashcards

1
Q

Definition?

A

Backflow of blood through the mitral valve due to insufficient closure caused by aberrations to the valve, chordae tendineae, papillary muscles of annulus.

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2
Q

RF?

A
  • Mitral valve prolapse
  • Rheumatic heart disease
  • Infective endocarditis
  • Trauma
  • MI
  • Congenital heart disease/IHD
  • Hypertrophic cardiomyopathy
  • Anorectic/dopaminergic drugs
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3
Q

ddx?

A

• ACS-STE/STD raised cardiac enzymes
• Infective endocarditis-Blood cultures are positive in infective endocarditis. An FBC may show anaemia, raised neutrophils, and raised ESR or C-reactive protein. Echo shows vegetations
• Mitral stenosis-rumbling mid-diastolic murmur, malar flush low pulse and loud S1 with opening snap and apex beat normal
• Aortic stenosis-slow rising pulse heaving apex LV heave, ejection systolic murmur radiates to carotids and clicks
• Aortic or pulmonic valve disease-clicks right or left of sternum
Atrial myxoma- constitutional symptoms, diastolic murmur

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4
Q

aetiology?

A
  • Degenerative mitral valve disease
  • Rheumatic fever
  • Infective endocarditis
  • Ischaemia-MI
  • CAD-papillary muscle involvement
  • Dilated cardiomyopathy
  • Acute dysfunction
  • Chronic
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5
Q

CP-acute?

A
• RF
• Dyspnoea
• LHF symptoms-pulmonary oedema
• Cardiogenic shock
• Palpitations
• Soft decrescendo murmur
• No murmur in severe regurgitation with LV systolic dysfunction or hypotension
S8 heart sound
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6
Q

CP chronic?

A
• Dyspnoea on exertion
• Fatigue
• Palpitations
• LHF 
• Lateral displacement of apical impulse
• Quiet S1 sound
• S8 heart sound
• S4 sound if functional
• Low exercise tolerance
• Low extremity oedema
• Holosystolic murmur-high-pitched blowing-radiates to left axilla and heart over apex
Increased intensity by increasing preload or afterload
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7
Q

Pathophysiology?

A

Anterior and p leaflet-bt LA and LV
Systole-closes-ejected via aortic valve into aorta
Doesn’t close all way
• Bicuspid valve-opens to allow flow into ventricles
• Diastole-open so fills ventricle with blood-
• Systole-can’t close-blood ejected into left atrium-can travel back into pulmonary system via pulomnary veins-oedema
• Pulomnary hypertension-cor pulmonale
• AF-stasis of blood
• Acute-sudden
• S1-AV close so full ventricles start contracting
• Bt-contraction-blood through A and P valves into aorta and pulmonary arteries
• S2-AP valves close so atria fill and AV valves open soon after to allow filling again
• Less closing of mitral valve-less S1 sound
• RF-autoantibodies-valve cells-inflammation and calcification
• MI-Chordae tendonae or papillary muscles cause dysfunction or rupture

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8
Q

pathophysiology of CP?

A
  • Acute MR→ ↑ LVend-diastolic volume→ rapid↑ LAand pulmonary pressure → pulmonary venous congestion →pulmonary edema
  • Chronic (compensated) MR: progressive dilation of the LV (viaeccentric hypertrophy)→↑ volumecapacity of the LV(preloadandafterloadreturn to normal values) →↑ end-diastolicvolume → maintains↑strokevolume (normal EF)
  • Chronic (decompensated) MR:progressiveLV enlargementandmyocardialdysfunction→↓strokevolume →↑ end-systolicandend-diastolicvolume →↑ LVandLA pressure→ pulmonary congestion, possible acutepulmonary edema,pulmonary hypertension, and rightheartstrain
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9
Q

Investigations first line?

A
• CVS exam-see CP for findings
• Transthoracic echo-
	• severity, mech, filial , LV size, left atrial size, others, RV systolic pressure
• ECG
Arrhythmias previous MI
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10
Q

Investigations second line?

A
  • Flow convergence method or proximal isovelocity SA
    • Location of increases in velocity and can estimate size of jet or opening
  • Colour Doppler flow-
    • Small central jet <4 cm^2 or <20% of the left atrial area is considered mild.
    • Vena contracta width <0.3 cm is considered mild; >0.7 cm is considered severe.
  • Transoesophageal echo-
    • Grading and detection of pulmonary hypertension
  • Left heart catheterisation-
    • CAD or pulmonary hypertension
  • Cardiac MRI
    • Poor ventricular function and calcification
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11
Q

Management acute?

A

• Emergency surgery
• Regurgitation can be corrected by repairing the abnormal valve leaflet or repairing or replacing the supporting valve structures. A prosthetic ring can be inserted to reshape the valve.
• Preop diuretics-furosemide-reduces afterload
• Intra-aortic balloon counter-pulsation
The intra-aortic balloon pump consists of a cylindrical balloon that sits in the aorta and actively deflates in systole, increasing forward blood flow by reducing afterload, and actively inflates in diastole, increasing blood flow to the coronary arteries. The balloon is inflated with helium by a computer-controlled, ECG-linked mechanism.

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12
Q

management if asymptomatic and high EF?

A

ACEi, Betablockers

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13
Q

management if asymptomatic and low EF?

A

• Surgical repair
Regurgitation can be corrected by repairing the abnormal valve leaflet or repairing or replacing the supporting valve structures. A prosthetic ring can be inserted to reshape the valve.

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14
Q

management if symptomatic?

A

LV ejection fraction 30% or more
• Surgery and medical treatment
• M-ACEi, Beta blockers and diuretics

left ventricular ejection fraction <30%
• First line: ACEi, beta blockers, diuretics,
Second line: Intra-aortic balloon counter-pulsation

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15
Q

prognosis?

A
  • Low risk of reoperation
  • Variable-depends on lesions or annulus size
  • Severe-LV dysfucntion in 6-10 yrs
  • Need dental or op AB prophylaxis
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16
Q

complications?

A
• Atrial fibrillation
• Pulmonary hypertension
• Post-operative stroke
• Prosthesis stenosis
• LV dysfunction and CHF
• Recurrent MR or perivalvular regurgitation after valve replacement
• Prosthesis dysfunction 
endocarditis