Welcome to the Heart Sounds on the go with iPod website. Here one will be able to listen to the five most common heart sounds, plus have the added benefit of downloading the sound files, and take them with you on one's iPod or other MP3 device (Palm, cell phone) for later review. Click on each heart sound title to load the sound on your computer, or right-click the name to save the file to your computer. Two studies: Mastering cardiac murmurs: the power of repetition. Chest 2004;126:470-5 The power of repetition in mastering cardiac auscultation. Amer J Med     2006;119:73-5 Have demonstrated repetion is key in the masterization of cardiac auscultation. Too often today's upcoming young physicians are losing their cardiac auscultation abilities, and now with the files below, created by Michael J. Barrett, M.D., F.A.C.C., of the Temple University School of Medicine, one can stay current with cardiac auscultation.

	Mitral Regurgitation Mitral regurgitation can be divided into the following 3 stages: acute, chronic compensated, and chronic decompensated. In the acute stage, which usually occurs with a spontaneous chordae tendineae rupture secondary to myocardial infarction, there is a sudden volume overload on an unprepared left ventricle and left atrium. The volume overload on the left ventricle increases left ventricular stroke work. Increased left ventricular filling pressures, combined with the transfer of blood from the left ventricle to the left atrium during systole, results in elevated left atrial pressures. This increased pressure is transmitted to the lungs resulting in acute pulmonary edema and dyspnea. If the patient tolerates the acute phase, the chronic compensated phase begins. The chronic compensated phase results in eccentric left ventricular hypertrophy. The combination of increased preload and hypertrophy produces increased end-diastolic volumes, which, over time, result in left ventricular muscle dysfunction. This muscle dysfunction impairs the emptying of the ventricle during systole. Therefore, regurgitant volume and left atrial pressures increase, leading to pulmonary congestion.

Aortic Stenosis When the aortic valve becomes stenotic, resistance to systolic ejection occurs and a systolic pressure gradient develops between the left ventricle and the aorta. Stenotic aortic valves have a decreased aperture that leads to a progressive increase in left ventricular systolic pressure. This leads to pressure overload in the left ventricle, which, over time, causes an increase in ventricular wall thickness (ie, concentric hypertrophy). At this stage, the chamber is not dilated and ventricular function is preserved, although diastolic compliance may be affected. Eventually, however, the left ventricle dilates. This, coupled with a decrease in compliance, is associated with an increase in left ventricular end-diastolic pressure, which is increased further by a rise in atrial systolic pressure. A sustained pressure overload eventually leads to myocardial decompensation. The contractility of the myocardium diminishes, which leads to a decrease in cardiac output. The elevated left ventricular end-diastolic pressure causes a corresponding increase in pulmonary capillary arterial pressures and a decrease in ejection fraction and cardiac output. Ultimately, congestive heart failure (CHF) develops.

	Innocent Systolic Murmur Those murmurs that occur in the absence of structural cardiac disease are said to be 'innocent'. They have been variously described as functional, benign, innocuous or physiologic murmurs. Innocent Murmurs of Childhood Systolic murmurs Vibratory Still's murmur Pulmonary flow murmur Peripheral pulmonary arterial stenosis murmur Supraclavicular or brachiocephalic systolic murmur Aortic systolic murmur Continuous murmurs Venous hum Mammary arterial soufflé

Aortic Regurgitation Incompetent closure of the aortic valve can result from intrinsic disease of the cusp, diseases of the aorta, or trauma. Aortic regurgitation may be a chronic disease process or it may occur acutely, presenting as heart failure. The most common cause of chronic aortic regurgitation used to be rheumatic heart disease, but presently it is most commonly bacterial endocarditis. In developed countries, it is caused by dilatation of the ascending aorta (eg, aortic root disease, aortoannular ectasia). Diastolic reflux through the aortic valve can lead to left ventricular volume overload. The severity of the aortic regurgitation is dependent on the diastolic valve area, the diastolic pressure gradient between the aorta and left ventricle, and the duration of diastole. An increase in systolic stroke volume and low diastolic aortic pressure produces an increased pulse pressure.

Mitral Stenosis The normal area of the mitral valve orifice is 4-6 cm2, which effectively creates a common chamber between the left atrium and the left ventricle in diastole. In early diastole, a small and brief pressure gradient is present, but, during most of the filling period, the pressures in the 2 chambers are equal. Narrowing of the valve area to less than 2.5 cm2 impedes the free flow of blood and causes a build up of left atrial pressure (LAP) to promote normal transmitral flow volume. Critical mitral stenosis occurs when the opening is reduced to 1 cm2. At this stage, a LAP of 25 mm Hg is required to maintain a normal cardiac output. With progressive stenosis, critical flow restriction reduces left ventricular output. The increase in LAP also enlarges the left atrium and raises pulmonary venous and capillary pressures. The resulting pulmonary congestion and reduced cardiac output can mimic primary left ventricular failure, but left ventricular contractility is normal in most cases of mitral stenosis. As the disease evolves, chronic elevation of LAP eventually leads to pulmonary hypertension, tricuspid and pulmonary valve incompetence, and secondary right heart failure.