By Elliot Chesler M.D. (Rand.) F.R.C.P. (Edin.) F.A.C.C. (auth.)
Clinical Cardiology, fifth version provides an authoritative and analytical method of scientific cardiology. the writer describes intimately the bedside talents of heritage taking and actual exam. A complete account of the pathology, common background, and remedy of either congenital and bought center sickness is given for either the grownup and pediatric age groups.This precious reference quantity is designed for scientific scholars, interns, citizens and fellows in cardiology in addition to experts in inner medicine.
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Extra info for Clinical Cardiology
With expiration, right ventricular filling is diminished and P2 moves closer to the first heart sound as the duration of right ventricular systole diminishes (Fig. 6). Respiratory changes in left ventricular volume lags a few beats behind that of the right. During inspiration, there is an increase in the pulmonary vascular capacitance leading to pooling of blood in the lungs and a decreased left atrial pressure. This leads to ® diminished left ventricular stroke volume and left ventricular ejection time, thus shortening the interval from the first heart sound to A2.
Tricuspid opening long A2-0S interval. Contrariwise, tachycar- 34 3. Auscultation dia or a high cardiac ouput raises the left atrial pressure and thus shortens the A2-0S interval in the presence of relatively mild mitral stenosis. In atrial fibrillation this interval varies according to the preceding RR interval. As the RR interval shortens, so does the A2-0S interval. This is related to the fact that long diastolic filling periods reduce left atrial pressure and therefore shorten the A2-0S interval.
The murmur softens with amyl nitrite inhalation and becomes louder after phenylephrine. It is a result of prolapsing of the mitral leaflets (particularly the posterior) in late systole at the time when the pressure in the left ventricle is falling off and when the gradient between the left ventricle and left atrium is decreasing. Maximal billowing of the posterior leaflet occurs in late systole and coincides with the late systolic click, when the chordae are maximally stretched. Generally speaking, the degree of regurgitation is of no hemodynamic importance, but there may be a tendency for progressive elongation of the chordae, leading to their eventual rupture with severe mitral insufficiency.