Term 5 - PathoPhysio > VALVULAR HEART DISEASES 3 > Flashcards

Flashcards in VALVULAR HEART DISEASES 3 Deck (10):

Mitral Regurgitation (MR)


  • Mitral valve prolapse is now probably the most common cause, followed by coronary artery disease
  • MR may be acute or chronic or congenital:
  • Acute causes:
    • Ruptured chordae tendineae as in infective endocarditis; Trauma; Acute rheumatic fever -Ruptured or dysfunctional papillary muscles as in Ischemia; Myocardial infarction;Myocardial abscess -Perforated leaflet as in infective endocarditis
  • Chronic causes:
    • Inflammatory as in Rheumatic heart disease and Collagen vascular disease -Infection as in Infective endocarditis -Degenerative as in Myxomatous degeneration of the valve leaflets; Calcification of the mitral annulus -Rupture or dysfunction of the chordae tendineae or papillary muscles as in Infective endocarditis; Trauma; Acute rheumatic fever; Myocardial infarction


Pathophysiology of acute MR:

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Pathophysiology of chronic MR:

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MR: Hemodynamic changes

  • An incompetent (leaky) mitral valve allows blood to regurgitate from LV to LA during ventricular systole 
  • An elevated left atrial volume and pressure during ventricular systole 
  • Left ventricular volume and also pressure increase during ventricular diastole 
  • There is no pressure gradient between LA and LV throughout during ventricular filling 
  • Systolic murmur appears

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Symptoms of MR:

  • The presentation of MR depends on how quickly valvular incompetence develops
  • Patients with chronic mitral regurgitation develop symptoms gradually over time
  • Common complaints in chronic MR include: Dyspnea, easy fatigability, and palpitations Dyspnea - due to pulmonary edema Fatigue - due to decreased forward blood flow to the peripheral tissues Palpitations - due to atrial fibrillation
  • Common complaints in acute MR include: symptoms of left heart failure - shortness of breath, orthopnea, and shock


Physical Examination in MR:

  1. Laterally displaced and Hyperdynamic Apical Impulse:
    • Reason for lateral displacement - The compensatory increase in left ventricular volume and wall thickness Reason for hyperdynamic - The ventricle now has a low-pressure chamber (LA) into which to eject blood When mitral regurgitation develops suddenly, the apical impulse is not displaced or hyperdynamic, because the LV has not had enough time for compensatory volume increases to occur
  2. Holosystolic (pansystolic) Murmur:
    • Regurgitant flow into the LA produces a high-pitched murmur that is heard throughout systole
    • The murmur begins with S1, continues to the S2
    • Murmur is of constant intensity throughout systole
    • Unlike the murmur of AS, there is no variation in the intensity of the murmur as the heart rate changes
    • The murmur does not change in intensity with respiration
    • It is heard best at the apex and radiates to the axilla
  3. Muffled S1 and S2:
    • The murmur often obscures the first and second heart sounds
  4. Loud S3:
    • A third heart sound is heard in a patient with severe MR or if heart failure is present


Mitral Valve Prolapse (MVP)

  • Other terms: Floppy valve, Barlow’s
  • Etiology
    • Congenital
    • Marfan’s syndrome
    • Rheumatic heart disease
    • Sequelae of MI
  • Pathophysiology
    • Valve leaflet has redundant tissue
    • Extra tissue balloons into LA, click sound


  • Mitral Valve Prolapse
  • Clinical Presentation

  • Asymptomatic
  • Symptomatic
    • Palpitations
    • Arrhythmias
    • Atypical Chest Pain

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MVP-Physical Exam/Diagnosis

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Physiologic maneuvers in the differential diagnosis of heart murmurs:

  1. Respiration:
    • Right-sided murmurs typically increase with inspiration, while left-sided murmurs generally are louder during expiration (“RILE”)
  2. Valsalva maneuver:
    • Most murmurs decrease in length and intensity during the Valsalva maneuver Two exceptions are - the systolic murmurs of hypertrophic cardiomyopathy (HCM) & mitral valve prolapse (MVP) – they become louder
  3. Handgrip (isometric exercise):
    • Murmurs of MR , AR and VSD increase with handgrip due to increase in afterload on LV
  4. Transient arterial occlusion:
    • Transient external compression of both arms by bilateral cuff inflation to 20 mmHg greater than peak systolic pressure augments the murmurs of MR, AR and VSD (due to increase in afterload on LV) This maneuver does not affect the murmurs due to other causes
  5. Positional changes:
    • i) Standing - Most murmurs diminish with standing due to reduced preload. Exceptions: the murmur of HCM & MVP become louder ii) Passive leg raising - Most murmurs become louder, while the murmurs of HCM and MVP typically soften and may disappear due to increased preload