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Common Congenital Heart Lesions - page 19 / 126

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Regurgitant Atrioventricular Valve Disease Mitral Regurgitation (MR)

Clinical Presentation: (most common valvular disease on a daily basis in clinics)

  • Patients w/ acute MR usually present with symptoms of pulmonary edema (fluid accumulation and swelling in the lungs), such as: severe dyspnea, anxiety while struggling to breathe, tachycardia, cold & clammy skin (due to peripheral vasoconstriction from inc. sympathetic outflow), tachypnea, coughing “frothy” sputum, lung base rales.

  • The symptoms of chronic MR are due to low cardiac output. Symptoms: fatigue and weakness on exertion.

  • Patients w/ severe MR or those who develop LV contractile dysfunction may complain of: dyspnea, orthopnea (inability to breathe easily unless one is sitting up or standing), paroxysmal nocturnal dyspnea (awakening suddenly during the night feeling short of breath) – these patients may also have symptoms of right heart failure (increased abdominal girth, peripheral edema).

Physical Exam:

  • Typical findings:

    • o

      Auscultation: widely split S2 and apical holosystolic murmur (radiates to axilla) – note that some more rare subtypes of MR have alternate best-auscultation areas that can be confused with an Aortic Stenosis murmur.

      • o

        2 exceptions to holo-systolic murmur: 1/ Acute Severe MR = early systolic, 2/ mild MR = late systolic

      • o

        To insure that the murmur is due to MR, have patient clench fists. As systemic vascular resistance rises, severity of the MR murmur will intensify.

      • o

        Can also note the effect of varying cardiac cycle length (in pt w/ A. fib or freq premature beats) on the murmur: MR murmur does not vary significantly, but AS murmur intensifies after long cycles.

      • o

        Auscultation also commonly reveals an S3, reflecting increased volume returning to the LV in early diastole.

      • o

        Palpation: often reveals a laterally displaced apical impulse due to LV enlargement.

Etiology:

  • MR may result from structural abnormalities of the mitral annulus, valve leaflets, chordae tendinae, or papillary muscles (all these structures must act in a coordinated fashion for normal closure to take place). oMyxomatous degeneration of the valve is called mitral valve prolapse (see next outline). oIschemic heart disease can harm the papillary muscles. oInfective endocarditis can cause leaflet perforation or chordae rupture. oCan have primary rupture of the chordae – gives acute, severe valve incompetence. oRheumatic fever can cause MR if shortening of chordae and retraction of leaflets occurs. oHypertrophic cardiomyopathy (HCM) causes abnormal motion in the anterior mitral leaflet, causing MR in 50% of HCM patients.

oMarked LV enlargement results in MR due to either 1/ spatial separation of papillary muscles or 2/ mitral annulus stretching to a larger diameter. oCalcification of the annulus can come with normal aging (common w/ HTN or aortic stenosis).

Pathophysiology:

  • In MR, part of the LV stroke volume is ejected backward into the LA. Thus, the forward cardiac output (CO) is less than the LV’s total output.

  • Direct consequences of MR: oElevation of LA volume and pressure oReduction of forward CO into the aorta oVolume-related stress on the LV when regurgitated volume returns to the LV in diastole along with the normal pulmonary venous return

  • According to Frank-Starling, inc LV volume Æ inc myofiber stretch and inc stroke volume w/ each contraction.

  • Severity of MR and ratio of forward/backward flow determined by 5 factors:

    • 1.

      size of mitral orifice during regurgitation

    • 2.

      systolic pressure gradient between the LV and the LA

    • 3.

      systemic vascular resistance opposing forward LV blood flow

    • 4.

      LA compliance

    • 5.

      duration of regurgitation with each systolic contraction oalso see inc in pulmonary artery and right heart pressures to push flow forward through heart

Pathophysiology continued below…

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