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Common Congenital Heart Lesions - page 16 / 126





16 / 126

16 of 126


  • Due to valve problems in AR, whether with the leaflet or aortic dilatation, get regurgitation of blood from aorta

back into the LV during diastole.


  • With each contraction, the LV must pump out both extra, regurgitant volume and normal volume from the LA.

  • Hemodynamic compensation due to Frank-Starling mechanism:

    • o

      increases stroke volume and maintains normal end-systolic volume

  • Severity of AR depends on:

      • 1.

        size of regurgitant aortic orifice

  • 2.

    pressure gradient across aortic valve during diastole

  • 3.

    duration of diastole

Acute vs. Chronic AR:

  • Acute AR:

    • o

      LV is normal size and relatively non-compliant

      • o

        Volume load of regurg causes LV diastolic pressure to rise

      • o

        Suddenly high diastolic pressure transmitted to LA and pulmonary circulation (can produce dyspnea and pulmonary edema)

      • o

        Usually a surgical emergency requiring Aortic Valve Replacement.

  • Chronic AR:

      • o

        LV undergoes compensation due to long-standing regurgitation.

      • o

        Get mostly LV volume overload, but also some pressure overload – so get both dilatation and some hypertrophy

      • o

        Less pressure transmitted to the LA and the pulmonary circulation

      • o

        Allowing aorta to regurgitate a large volume during diastole causes aortic (and systemic) diastolic pressure to drop substantially).

      • o

        Combo of high LV stroke volume (inc systolic pressure) and reduced aortic diastolic pressure gives a widened pulse pressure.

      • o

        Decreased aortic diastolic pressure Æ dec coronary perfusion pressure, reducing myocardial oxygen supply to the large LV…can produce angina (even without atherosclerotic coronaries)

      • o

        (Chronic) left ventricular hypertrophy results in systolic dysfunction Æ less forward CO and increase in LA and pulmonary pressures Æ patient gets symptoms of CHF

Diagnostic imaging/testing:

  • Chest X-Ray:

    • o

      Chronic AR shows an enlarged LV silhouette.

      • o

        Acute AR more likely to show pulmonary vascular congestion.

  • Echocardiography: Doppler echocardiography can identify and quantify degree of AR and can often identify the cause of the AR.

  • Cardiac Catheterization: used with contrast angiography for evaluation of LV function, quantification of the degree of AR, assessment of coexisting coronary artery diseases

Treatment: (surgical intervention not recommended till have regularly occurring symptoms and/or LV dysfunction)

  • Asymptomatic AR:

    • o

      60% of patients with asymptomatic chronic AR and normal LV contractile function will still be asymptomatic at their 10-year follow-up.

      • o

        Just need regular clinical evaluation, periodic assessment of LV function (by echo), and antibiotic prophylaxis for endocarditis.

  • Symptomatic AR with preserved LV function:

      • o

        May respond to diuretics and afterload reducing vasodilators (like ACE inhibitors).

      • o

        Ca2+ channel blocker (nifedipine) shown to reduce LV enlargement, increase LV ejection fraction, delay need for valve surgery in patients.

  • Symptomatic patients w/ severe chronic AR or asymptomatic patients w/ impaired LV contractile function:

      • o

        Need surgical valve replacement (SVR) to prevent further deterioration of LV function.

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