X hits on this document

PDF document

Common Congenital Heart Lesions - page 15 / 126

322 views

0 shares

0 downloads

0 comments

15 / 126

15 of 126

Regurgitant Semilunar Valve Disease Aortic Regurgitation (AR)

Clinical Presentation:

  • Dyspnea on exertion (CHF)

  • Fatigue

  • Decreased exercise tolerance

  • Uncomfortable sensation of a forceful heartbeat associated with high pulse pressure

  • Chest pain (occasionally)

Physical Exam: Typical findings:

  • o

    Auscultation:

    • “blowing” early diastolic decrescendo murmur heard along left sternal border (heard best after patient exhales while leaning forward)

        • In severe AR, can sometimes hear a low-frequency mid-diastolic rumbling sound at the cardiac apex (called the Austin Flint murmur) – thought to reflect turbulent blood flow across the mitral valve during diastole due to downward displacement of the mitral anterior leaflet by the stream of the AR. Austin Flint murmur distinguishable from the murmur of MS by absence of an opening snap or presystolic accentuation of the murmur.

      • o

        Blood Pressure: HALLMARK of AR is wide pulse pressure (PP = systolic – diastolic; normal = 30-40 mmHg; wide > 40 mmHg) because a larger stroke volume produces a larger pulse pressure at any given aortic compliance

      • o

        Pulse: bounding pulses (strong, forceful pulses)

      • o

        Carotids: Depending on severity of the AR, might see bifid contour of the tall part of the carotid pulse and have a smaller contoured notch

      • o

        Palpation: hyperdynamic LV impulse (due to volume overload and eccentric hypertrophy)

  • Note:

    • o

      Acute Aortic Regurgitation: have no opportunity to dilate the LV, so it is relatively non-compliant and have a dramatic rise in pressure.

      • o

        Chronic Aortic Regurgitation: see wide pulse pressure, hyperdynamic apical impulse

        • Onset of symptoms in a chronic AR patient is usually an indication of the development of LV contractile dysfunction and the prognosis worsens once LV decompensation takes place.

Etiology:

  • Abnormalities of the aortic leaflets: (that lead to stiffening and/or incomplete closure of the aortic valve)

    • o

      Rheumatic: 25% of patients with rheumatic heart disease will develop AR

      • o

        Endocarditis: freely multiplying organisms make and enlarge vegetations that lead to leaflet complications oCongenital (e.g. bicuspid valve)

  • Dilataion of the aortic root:

      • o

        Aortic aneurysm/dissection: aortic aneurysm is ballooning of the aorta; when aorta enlarges and stretches, it becomes prone to an aortic dissection, which is a separation or tear in the lining of the artery that allows blood to flow between the inner and outer walls of the vessel yet remains contained in the aorta.

      • o

        Marfan syndrome: Think tall, thin people with spindly fingers. From an autosomal dominant connective tissue disease that appears in 4-6 of every 100,000 people. Marfan's syndrome causes deformations and defects in several body systems, most notably the ocular, skeletal, and cardiovascular (at least 90 percent of people with the Marfan syndrome will have heart involvement).

      • o

        Also Annulo-aortic actasia and Syphilis: no details about these w/ respect to AR in book or lectures

Document info
Document views322
Page views322
Page last viewedWed Dec 07 22:26:09 UTC 2016
Pages126
Paragraphs5002
Words33792

Comments