Murmurs are abnormal heart sounds that are heard using a stethoscope. 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 (aorta or pulmonary artery) that are detected as audible, low frequency sounds. Murmurs are distinct from the normal heart sounds that represent the closure of semilunar and atrioventricular valves during the cardiac cycle .
Murmurs can be divided into two general classifications related to origin: those caused by valve defects and those caused by
interchamber defects that permit an abnormal flow of blood between cardiac chambers. In order to understand the pathophysiology of murmurs, it is first necessary to understand the physical factors governing the flow of blood (i.e.,
hemodynamics ), the basic anatomy of the heart, and the sequence of events that occurs as the heart contracts and relaxes (i.e., cardiac cycle).
Murmurs can also be separated into systolic and diastolic murmurs . The former occurs during ventricular contraction ( systole) and the latter occur during ventricular filling (diastole).
Functional Cardiac Murmurs
Functional murmurs (also called physiologic murmurs) can occur in the absence of valvular pathology. An example would be an aortic systolic ejection murmur caused by a high cardiac output state. Very high flow velocities in the aorta can lead to turbulent flow which will result in a murmurs during the ejection phase of the cardiac cycle. Examples of this include high cardiac outputs in trained athletes and high output states during anemia. Another example is pregnancy where the elevated resting cardiac output can result in physiologic ejection murmurs during rest.
Ventricular Septal Defect
In the normal development of the heart, the interventricular foramen closes off to form the membranous part of the interventricular septum. Failure of this structure to close produces a ventricular septal defect that permits shunting of blood from the left to the right ventricle (left-to-right ventricular shunt) during systole. The shunt is left-to-right because left ventricular pressure greatly exceeds right ventricular pressure during systole. For example, right ventricular systolic pressure might be 25 mmHg when left ventricular systolic pressure may be 120 mmHg or higher. This leads to a large
pressure gradient across the opening in the septum so that blood flows from the left to right ventricle during systole. The flow of blood across this shunt produces a characteristic holosystolic murmur (i.e., between S 1 and S 2 ). Often, the murmur is louder with smaller defects because of increased turbulence .
There can be serious consequences to ventricular septal defects. The shunting of blood increases right ventricular volume and its output by the Frank-Starling mechanism . This increased output can lead to pulmonary hypertension. Furthermore, the increased pulmonary flow leads to left atrial enlargement and increased left ventricular
preload and stroke volume by the Frank-Starling mechanism. Over time, these hemodynamic changes can lead to symptoms of congestive heart failure and dyspnea.
Cardiac Valve Disease
What are heart valves and what is their function?Valves within the heart separate the right atrium and ventricle (tricuspid valve), the left atrium and ventricle (mitral valve), the right ventricle and the pulmonary artery (pulmonic valve), and the left ventricle and aorta (aortic valve) (click here to see cardiac anatomy diagram). The valves ensure that blood flows in a single pathway through the heart by opening and closing in a particular time sequence during the cardiac cycle . Normal valves permit blood to flow in only one direction, for example, from the right atrium into the right ventricle. When heart valves become diseased or damaged, they may not fully open or close. This can seriously impair cardiac function by causing blood to leak backwards into cardiac chambers or by requiring heart chambers to contract more forcefully to move blood across a narrowed valve.
What causes valve dysfunction?
Disease (bacterial, viral) and inflammation
Congenital heart defects
Ischemic heart disease
Cardiac hypertrophy or dilation
as occurs in heart failure
Ruptured chordae tendineae
A chronic disease process is responsible for defective valves in most older individuals. Sometimes, the disease results from a triggering event many years earlier, such as rheumatic fever. Bacterial infection, viral infection and inflammation of valves (infective endocarditis) can produce changes in valve structure and function. Normally, valve leaflets are very thin and flexible, but they can become thickened and rigid in response to a disease processes. When this occurs, the valve leaflets may not be able to fully open or completely close. Valve disease found in younger individuals is usually due to a congenital defect in the embryologic development of the heart. Valve dysfunction can occur secondarily to other cardiac diseases, such as coronary artery disease, cardiac hypertrophy and cardiac dilation. If coronary artery disease progresses to the point where papillary muscles become hypoxic or infarcted, then the impaired contractile function of these muscles can lead to a leaky tricuspid or mitral valve. Cardiac hypertrophy or dilation, by altering cardiac chamber structure and dimensions, can lead to valve dysfunction. Finally, valve dysfunction can also occur if the chordae tendineae that connect the valve leaflet to the papillary muscle rupture.
How are valve defects classified?
There are two general types of cardiac valve defects: stenosis and insufficiency. Some patients, however, may have a combination of stenosis and insufficiency. Valvular
stenosis results from a narrowing of the valve orifice (reduced cross-sectional area of the opened valve) that is usually caused by a thickening and increased rigidity of the valve leaflets, often accompanied by calcification. When this occurs, the valve does not open completely as blood flows across it, thereby resulting in a high resistance to flow and the development of a large pressure gradient across the valve when blood is flowing through the valve. In other words, pressure increases in the chamber proximal to the valve and decreases in the chamber or artery distal to the valve.
Valvular insufficiency occurs when the valve leaflets do not completely seal when the valve is closed. This causes regurgitation of blood (backward flow of blood) into the proximal chamber. For example, in aortic valve insufficiency blood regurgitates from the aorta into the left ventricle after ventricular ejection.
What are the clinical symptoms of defective valves?
Valvular stenosis and insufficiency can have serious cardiac consequences, and produce the following clinical symptoms:
Shortness of breath (dyspnea )
Fatigue
Reduced exercise capacity
Light headedness or fainting (syncope)
Heart failure
Pulmonary hypertension
Pulmonary/systemic edema
Chest pain (angina)
Arrhythmias
Blood clots (thromboembolism) which can cause stroke
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