10

10 CASE 10


A 58-year-old woman comes to her primary care physician complaining of shortness of breath and difficulty sleeping at night, especially while lying down. She complains of coughing at night that awakens her.


The patient first reports having symptoms 3 days ago. The symptoms do not appear to be worsening. She has a history of mitral valve prolapse in the past, but this has not been symptomatic.



PHYSICAL EXAMINATION



VS: T 37°C, P 80/min, R 15/min, BP 100/70 mm Hg, BMI 24

PE: The patient has a systolic murmur that is heard best at the apex of the heart. The intensity of the murmur is constant throughout systole. The patient has rales during inspiration bilaterally in the base of the lung. There is no sign of peripheral edema.


LABORATORY STUDIES



ECG: Normal, including no displacement of the ST segment

Plasma analysis: CK-MB normal.

Echocardiogram: Left atrial enlargement.


DIAGNOSIS


Mitral valve regurgitation



PATHOPHYSIOLOGY OF KEY SYMPTOMS


The mitral valve usually closes and isolates the left atrium from the left ventricle during ventricular systole. In patients with mitral valve regurgitation the high pressures generated during left ventricular systole lead to the ejection of blood into the aorta (normal) as well as the backward flow of blood from the left ventricle into the left atrium (abnormal). Retrograde blood flow through the mitral valve is turbulent and can be heard as a systolic murmur (see Fig. 9-1, p.30 in Case 9).


The intensity of the murmur is fairly constant (holosystolic), reflecting the significant pressure gradient across mitral valve during ventricular systole. In addition, the timing of the murmur extends throughout the interval between the first and second heart sounds (pansystolic), because the pressure gradient exists during this entire interval. These characteristics distinguish the murmur of the mitral valve regurgitation from that of the other systolic murmur, aortic stenosis.


Mitral valve regurgitation can occur after rupture of the chordae tendineae or papillary muscles. The initiating event can be a myocardial infarction, infective endocarditis, trauma, or, in this case, degeneration of the valvular tissue in patients with mitral valve prolapse.


Normal functioning of the cardiac valves is essential to the pumping ability of the heart. Normally, the left ventricular and diastolic volume is about 150 mL and 60% of this volume is ejected into the aorta during ventricular systole (60% ejection fraction) and 40% remains in the left ventricle as the end-systolic left ventricular volume. In this patient, blood in the left ventricle at the end of diastole can (1) be pumped into the aorta, (2) be pumped retrograde back into the left atrium, or (3) remain in the left ventricle. The ejection fraction is reduced because of the retrograde flow of blood through the mitral valve. In addition, the left atrium now has two sources of filling: the normal filling of blood flowing from the pulmonary vein and the retrograde filling of blood flowing from the left ventricle during ventricular systole. Consequently, the left atrium is enlarged and left atrial pressures are elevated (Fig. 10-1).


image

FIGURE 10–1 Mitral regurgitation causes characteristic giant v waves on the left atrial (LA) pressure monitor. LV, Left ventricle.

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Jul 4, 2016 | Posted by in PHYSIOLOGY | Comments Off on 10

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