Valvular heart disease
Valvular heart disease: Excerpt from Handbook of Diseases
In valvular heart disease, three types of mechanical disruption can occur: stenosis, or narrowing, of the valve opening; incomplete closure of the valve; or prolapse of the valve. They can result from such disorders as endocarditis (most common), congenital defects, and inflammation, and they can lead to heart failure. (For information about causes, signs and symptoms, and diagnosis, see Forms of valvular heart disease, pages 882 to 885.)
Valvular heart disease occurs in varying forms:
❑ Mitral insufficiency. In this form, blood from the left ventricle flows back into the left atrium during systole, causing the atrium to enlarge to accommodate the backflow. As a result, the left ventricle also dilates to accommodate the increased volume of blood from the atrium and to compensate for diminishing cardiac output.
Ventricular hypertrophy and increased end-diastolic pressure result in increased pulmonary artery pressure, eventually leading to left and right ventricular failure.
❑ Mitral stenosis. Narrowing of the valve by valvular abnormalities, fibrosis, or calcification obstructs blood flow from the left atrium to the left ventricle. Consequently, left atrial volume and pressure rise and the chamber dilates.
Greater resistance to blood flow causes pulmonary hypertension, right ventricular hypertrophy, and right ventricular failure. Also, inadequate filling of the left ventricle produces low cardiac output.
❑ Mitral valve prolapse (MVP). One or both valve leaflets protrude into the left atrium. MVP syndrome is the term used when the anatomic prolapse is accompanied by signs and symptoms unrelated to the valvular abnormality.
❑ Aortic insufficiency. Blood flows back into the left ventricle during diastole, causing fluid overload in the ventricle, which dilates and hypertrophies. The excess volume causes fluid overload in the left atrium and, finally, the pulmonary system. Left ventricular failure and pulmonary edema eventually result.
❑ Aortic stenosis. Increased left ventricular pressure tries to overcome the resistance of the narrowed valvular opening. The added workload increases the demand for oxygen, and diminished cardiac output causes poor coronary artery perfusion, ischemia of the left ventricle, and left ventricular failure.
❑ Pulmonic insufficiency. Blood ejected into the pulmonary artery during systole flows back into the right ventricle during diastole, causing fluid overload in the ventricle, ventricular hypertrophy and, finally, right ventricular failure.
❑ Pulmonic stenosis. Obstructed right ventricular outflow causes right ventricular hypertrophy, eventually resulting in right ventricular failure.
❑ Tricuspid insufficiency. Blood flows back into the right atrium during systole, decreasing blood flow to the lungs and left side of the heart. Cardiac output also lessens. Fluid overload in the right side of the heart can eventually lead to right ventricular failure.
❑ Tricuspid stenosis. Obstructed blood flow from the right atrium to the right ventricle causes the right atrium to dilate and hypertrophy. Eventually, this leads to right ventricular failure and increases pressure in the vena cava.
Treatment
Therapy depends on the nature and severity of associated symptoms. For example, heart failure requires digoxin, diuretics, a sodium-restricted diet and, in acute cases, oxygen.
Other measures may include anticoagulant therapy to prevent thrombus formation around diseased or replaced valves, prophylactic antibiotics before and after surgery or dental care, and valvuloplasty. If the patient has severe signs and symptoms that can’t be managed medically, open-heart surgery using cardiopulmonary bypass for valve replacement is indicated.
Special considerations
❑ Watch closely for signs of heart failure or pulmonary edema and for adverse effects of drug therapy.
❑ Teach the patient about diet restrictions, medications, and the importance of consistent follow-up care.
❑ If the patient undergoes surgery, watch for hypotension, arrhythmias, and thrombus formation. Monitor vital signs, arterial blood gases, intake, output, daily weight, blood chemistries, chest X-rays, and pulmonary artery catheter readings.
Pictures
Book Source Details
- Book Title: Handbook of Diseases
- Author(s): Springhouse
- Year of Publication: 2003
- Copyright Details: Handbook of Diseases, Copyright © 2003 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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More About This Book:
Title: Handbook of Diseases
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2003
ISBN: 1-58255-266-5
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