Mitral regurgitation

Mitral regurgitation develops due to incomplete closure of the left atrioventricular valve during systole. As a result, the blood is regurgitated from the left ventricle to the left atrium.

Mitral regurgitation may be organic and functional. Organic regurgitation arises as a result of rheumatic endocarditis. Connective tissue develops in the cusps of the mitral valve, which then contracts to shorten the cusps and the tendons. The edges of the affected valve do not meet during systole and part of the blood is regurgitated through the slit into the left atrium from the ventricle during its contraction.

In functional (relative) regurgitation the mitral valve is not altered but the orifice, which it has to close, is enlarged and the cusps fail to close it completely. Functional incompetence of the mitral valve may develop because of dilatation of the left ventricle (in myocarditis, myocardial dystrophy, or cardiosclerosis) and weakening of the circular muscle fibres that form the ring round the atrioventricular orifice. Affection of papillary muscles may also cause functional mitral regurgitation. Functional regurgitation thus depends on dysfunction of the muscles responsible for the closure of the valve.

Etiology

• rheumatic fever;

• bacterial endocarditis;

• atherosclerosis;

• congenital heart defects;

• mitral valve prolaps;

• perforation, rupture of the mitral valve, trauma of mitral cusps.

Disorders of hemodynamics

Disorders of hemodynamic occur because the bicuspid valve fail to close adequately and during systole of the left ventricle part of blood is regurgitated into the left atrium where added to the normal blood amount delivered from the pulmonary veins. This mitral regurgitation produces volume overload of the left atrium. Pressure in the left atrium increases (in normal 5-7 mm Hg), the atrium becomes hypertrophied. During diastole the amount of blood that is delivered into the left ventricle from the overfilled left atrium exceeds normal. The left ventricle has to perform excess work and become hypertrophied. In late stages of the disease, when the contractile power of the myocardium of the left ventricle weakens, diastolic pressure in it increases and this in turn increases significantly pressure in the left atrium, consequently overfills pulmonary veins, and develops hypertension in the lesser circulation and reflective contraction of the arterioles in the lesser circulation. The raised atrial and pulmonary venous pressure leads to pulmonary edema. Together with the spasm in the arterioles pressure in the pulmonary artery increases significantly. The right ventricle can therefore be hypertrophied. In case of progression of disease, the right ventricle is dilated and tricuspid regurgitation occurs.

Clinical features

Clinical features appear when near 10 ml of blood returns from the left ventricle into the left atrium. Most patients have no complaints for a long time and feel like healthy people. Than congestion in the lesser circulation develops, patient feels fatigue, exhaustion, palpitations of the heart, cough, exertional and nocturnal dyspnea.

Objective examination. The patient's condition is from satisfactory to grave. Consciousness is clear. Posture is active. In case of development of heart failure with congestion in lesser circulation the posture is active with restriction due to the dyspnea. In late stage may be forced posture - orthopnea. Acrocyanosis is determined.

Examination of respiratory system. Intermediate percussion sound, decreased vesicular breathing and fine bubbling rales, even crepitation are revealed over the low lobes of lungs due to the congestion as a signs of raised pulmonary capillary pressure and chronic pulmonary congestion.

Examination of cardiovascular system. In inspection of heart region the diffuse apex beat is determined, displaced to the left in V, sometimes VI intercostals space.

During palpation: the apex beat is diffuse, intensified and resistant due to hypertrophy of the left ventricle.

In percussion reveals displacement of the upper border of the relative cardiac dullness upward, left border to the left. In the late stage of disease the right border of relative cardiac dullness is displaced to the right due to hypertrophy of the right ventricle. The configuration of the heart becomes mitral with indistinct waist of the heart.

In auscultation reveals decreased first heart sound at the apex because the mitral valves never closed completely. In the late stage, when the blood pressure rises in the lesser circulation, the second heart sound is accentuated and may be splitted over the pulmonary trunk. Blood pressure does not change in compensated mitral incompetence. The characteristic sign of the mitral regurgitation: blowing, decreasing murmur, which is heard at the heart apex it synchronous with the first heart sound. Murmur arises during systole when the stream of blood passes a narrow slit leading from the left ventricle to the left atrium. Murmur can be transmitted in the left axillary region and along the left edge of the sternum, it becomes more intensive after physical exertion, in lying position on the left side during deep expiration.

Complications of mitral regurgitation, acute pulmonary edema, atrial fibrillation/flutter very rare, chronic left ventricular and atrial failure, chronic right ventricular heart failure and chronic total ventricular heart failure.