Rapid high frequency fluttering of anterior mitral valve leaflets during systole on 2D ECHO is characteristically seen with
Correct Answer: Aortic regurgitation
Description: Ans. d (Aortic regurgitation) (Ref. Harrison 17th/p. 1477)Harrison 12th/p. 1477The extent and velocity of wall motion are normal or even supernormal, until myocardial contractility declines. A rapid, high-frequency fluttering of the anterior mitral leaflet produced by the impact of the regurgitant jet is a characteristic finding. The echocardiogram is also useful in determining the cause of AR, by detecting dilatation of the aortic annulus and root or aortic dissection.AORTIC REGURGITATIONEtiology# In approximately two-thirds of patients with valvular AR, the disease is rheumatic in origin.# AR represents the most frequent serious lesion in patients surviving nonpenetrating cardiac injuries.Pathophysiology# In patients with wide-open (free) AR, the volume of regurgitant flow may equal the effective forward stroke volume.# In contrast to MR, in which a fraction of the LV stroke volume is delivered into the low-pressure LA, in AR the entire LV stroke volume is ejected into a high-pressure zone, the aorta.# Considerable thickening of the LV wall also occurs with chronic AR and Myocardial ischemia may occur.C/f# M>F# In patients with acute severe AR, as may occur in infective endocarditis, aortic dissection, or trauma, pulmonary edema and/or cardiogenic shock may develop rapidly.# Chronic severe AR may develop.Physical Findings# UNCOMMON SIGNS OF AORTIC REGURGITATION INCLUDE;- Large-volume, 'collapsing' pulse also known as:1. Watson's water hammer pulse Q2. Corrigan's pulse (rapid upstroke and collapse of the carotid artery pulse). Corrigan's pulse: A rapidly rising "water-hammer" pulse, which collapses suddenly as arterial pressure falls rapidly during late systole and diastole.3. Quincke's pulse: Capillary pulsations, an alternate flushing and paling of the skin at the root of the nail while pressure is applied to the tip of the nail.4. Traube's sign: A booming "pistol-shot" sound heard over the femoral arteries.5. Duroziez's sign: a to-and-fro murmur audible if the femoral artery is lightly compressed with a stethoscope.6. de Musset's sign: jarring of the entire body and the bobbing motion of the head with each systole.7. Hill's sign: a > 20 mm Hg diff in popliteal and brachial systolic cuff pressures, seen in chronic severe AI.8. Lighthouse sign (blanching & flushing of forehead)9. Landolfi's sign (alternating constriction & dilatation of pupil)10. Becker's sign (pulsations of retinal vessels)11. Muller's sign (pulsations of uvula)12. Mayen's sign (diastolic drop of BP>15 mm Hg with arm raised)13. Rosenbach's sign (pulsatile liver)14. Gerhardt's sign (enlarged spleen)15. Lincoln sign (pulsatile popliteal)16. Sherman sign (dorsalis pedis pulse is quickly located & unexpectedly prominent in age>75 yr)17. Ashrafian sign (Pulsatile pseudo-proptosis).In many patients with pure AR or with combined AS and AR, the carotid arterial pulse is bisferiens, i.e., with two systolic waves separated by a troughsAuscultation# In patients with severe AR, the aortic valve closure sound (A2) is usually absent.# An S3 and systolic ejection sound are frequently audible, and occasionally an S4 also may be heard.# The murmur of chronic AR is typically a high-pitched, blowing, decrescendo diastolic murmur, heard best in the third intercostal space along the left sternal border.# "Cooing" or musical diastolic murmurs suggest eversion of an aortic cusp vibrating in the regurgitant stream.# A mid-systolic ejection murmur is frequently audible in isolated AR. It is generally heard best at the base of the heart and is transmitted along the carotid vessels.# A third murmur frequently heard in patients with severe AR is the Austin Flint murmur, a soft, low-pitched, rumbling mid-diastolic murmur. It is probably produced by the diastolic displacement of the anterior leaflet of the mitral valve by the AR stream but does not appear to be associated with hemodynamically significant mitral obstruction.# The auscultatory features of AR are intensified by strenuous handgrip, which augments systemic resistance.ECG# In patients with chronic severe AR, the ECG signs of LV hypertrophy become manifest.# In addition, these patients frequently exhibit ST-segment depression and T-wave inversion in leads I, aVL, V5, and V6 ("LV strain").# Left axis deviation and/or QRS prolongation denote diffuse myocardial disease, generally associated with patchy fibrosis, and usually signify a poor prognosis.Echocardiogram# The extent and velocity of wall motion are normal or even supernormal, until myocardial contractility declines.# A rapid, high-frequency fluttering of the anterior mitral leaflet produced by the impact of the regurgitant jet is a characteristic finding.0# Color flow Doppler echocardiographic imaging is very sensitive in the detection of AR, and Doppler echocardiography is helpful in assessing its severity.# With severe AR, the central jet width exceeds 65% of the left ventricular outflow tract, the regurgitant volume is 60 ml/ beat, the regurgitant fraction is 50%, and there is diastolic flow reversal in the proximal descending thoracic aorta.Chest X-RayIn chronic severe AR, the apex is displaced downward and to the left in the frontal projection. In the left anterior oblique and lateral projections, the LV is displaced posteriorly and encroaches on the spine.Aortic Regurgitation: TreatmentAcute Aortic RegurgitationPatients with acute severe AR may respond to intravenous diuretics and vasodilators (such as sodium nitroprusside), but stabilization is usually short-lived and operation is indicated urgently. Intra aortic balloon counterpulsation is contraindicated. Beta-blockers are also best avoided. Surgery is the treatment of choice.Chronic Aortic RegurgitationEarly symptoms of dyspnea and effort intolerance respond to treatment with diuretics, and vasodilators (ACE inhibitors, dihydropyridine calcium channel blockers, or hydralazine) may be useful as well. Surgery can then be performed in more controlled circumstances. Expert consensus is strong regarding the need to control systolic blood pressure (goal <140 mmHg) in patients with chronic AR, and vasodilators are an excellent first choice as antihypertensive agents. Beta blockers may be useful to retard the rate of aortic root enlargement in young patients with Marfan syndrome and aortic root dilatation with no or only mild AR. Patients with severe AR should avoid isometric exercises.
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