Heart murmur pathophysiology

Heart murmur Microchapters
Home
Patient Information
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
History and Symptoms
Physical Examination
Laboratory Findings
Echocardiography
Treatment
Medical Therapy
Case Studies
Case #1
Heart murmur pathophysiology On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Heart murmur pathophysiology All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Heart murmur pathophysiology
CDC on Heart murmur pathophysiology
Heart murmur pathophysiology in the news
Blogs on Heart murmur pathophysiology
Directions to Hospitals Treating Heart murmur
Risk calculators and risk factors for Heart murmur pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor(s)-in-Chief: Nuha Al-Howthi, MD[2]

Overview

Turbulent flow is responsible for most murmurs. Turbulent flow occurs when the velocity of blood flow becomes critically high because of a high volume of flow, the flow goes through an irregular or narrow area, the flow empties into a dilated vessel or chamber, or if the flow goes backward through an incompetent valve, septal defect, or patent ductus arteriosus. Frequently, a combination of these factors is operative. The sounds most commonly originate from the abnormal movement of blood across valves and between cardiac chambers. When this occurs, turbulence results, which produces vibrations in the chambers of the heart or outflow vessels that are detected as Murmurs.

summery of pathophysiology

	pathophysiology
aortic stenosis	There is a progressive narrowing of the valve. When the aortic valve area decreased by at least half, there will be a change in the antegrade velocity at the level of the aortic valve and also at the subvalvular (below the aortic valve) or supravalvular (above the aortic valve) levels. this will lead to chronic pressure overload in the left ventricle. chronic pressure caused by aortic stenosis lead to a slow compensatory mechanisms, the most prominent one is ventricular hypertrophy that leads to diastolic dysfunction and systolic dysfunction. Summary of the pathophysiology of aortic stenosis: Pathophysiology of aortic stenosis
aortic regurgitation	Aortic insufficiency develop when the pressure in the left ventricle falls below the pressure in the aorta,leading to volume overload of the left ventricle. In acute aortic insufficiency: Sudden decrease in stroke volume and increase in left ventricular end diastolic volume causing decrease cardiac output and reflex tachycardia, which eventually lead to profound hypotension and cardiogenic shock. pulmonary edema develops in severe cases due to the rapidly rising in the left ventricular end diastolic pressure which equalizes with the aortic end-diastolic pressure leading to back flow of blood. In chronic aortic insufficiency: there is compensation for increased left ventricular end diastolic volume by progressive left ventricular dilatation and left ventricular hypertrophy, which maintains normal wall stress. Overtime, when the left ventricular hypertrophy fails to keep up with chronic volume overload, the left ventricle decompensate causing reduction in the left ventricular wall compliance with resultant congestive heart failure.
mitral stenosis	Mitral stenosis (MS) is most commonly secondary to acute rheumatic fever. Generally, the initial valvulitis is associated with valvular regurgitation then over the years, the commissures fuse and the valves thicken and calcify. Usually, the rate of decrement in the valve area is about 0.1 cm2/year once mitral stenosis is present. When the cross sectional area is about 2 cm2 called Mild Mitral Stenosis. When the cross sectional area goes below 2 cm2: there will be impediment to the flow of blood into the left ventricle, creating a pressure gradient that increased by increases in the heart rate or cardiac output. The atrial kick is required to fill the left ventricle with blood when the valve is so tight and the gradient is so high. When the heart rate goes above a certain point, the diastolic filling period is insufficient to fill the ventricle with blood and pressure builds up in the left atrium, leading to pulmonary congestion. When the mitral valve area goes less than 1 cm2: the pressure gradient across the mitral valve will be 20 mm Hg and the left atrial pressure about 25 mm Hg. This left atrial pressure causes an elevated pulmonary capillary wedge pressure, congestive heart failure and pulmonary edema. The pressure overload of the left atrium will cause the left atrium to increase in size. make it more prone to develop atrial fibrillation. When atrial fibrillation develops, the atrial kick is lost.
mitral regurgitation	Acute Mitral Regurgitation Develop when there is sudden disruption of one or more of the components of the mitral valve, such as leaflet perforation, rupture of a chordae tendineae, or rupture of the papillary muscle. In the acute setting, the total stroke volume is increased, but the forward cardiac output into the aorta is decreased because a proportion of the blood is going backward into the left atrium. Pulmonary congestion and hypoxia occur in acute MR causes a sudden volume overload of both the left atrium and the left ventricle. Chronic Compensated mitral regurgitation: Develops slowly and the left ventricle develops eccentric hypertrophy to reduce the wall stress associated with the rise in total stroke volume. In the left atrium, the chronic volume overload causes left atrial enlargement, allowing the filling pressure in the left atrium to decrease and reduces the pulmonary capillary wedge pressure. Chronic decompensated mitral regurgitation: In this phase, the ventricular myocardium is no longer able to contract adequately to compensate for the volume overload of MR, and the stroke volume of the left ventricle begins to decrease. The reduced stroke volume causes a decrease in the forward cardiac output and an increase in the end-systolic volume. The increased left ventricular end-systolic volume in turn causes increased left ventricular end diastolic pressures and increased pulmonary capillary wedge pressures. As the wedge pressure rises, the patient may develop symptoms of congestive heart failure such as dyspnea, PND and orthopnea and signs of congestive heart failure including rales.