About Video

This audio-recording deals with the heart sounds and various murmurs, wherein audiovisual technology has been used to appreciate the subtle nuances of cardiac auscultation. The art and skill of cardiac auscultation, has been traditionally passed down from expert teachers in medical colleges to gullible students. However, competence in this field of expertise remains extremely variable, largely because it cannot be quantified by objective parameters. In this module of learning, digital audiovisual technology has been used which will enable the amateur cardiologist to appreciate subtle nuances of auscultation. Auscultation of the heart begins with appreciation of the two normal heart sounds namely first heart sound (S1) and second heart sound (S2). Together, the S1 and S2 produce a rhythm that sounds like “lub-dub lub-dub lub-dub”. The S1 is produced by closure of the mitral valve followed by the tricuspid valve, at the onset of ventricular systole. The intensity of S1 depends upon the distance between the mitral leaflets at the onset of systole, which in turn, depends on the diastolic filling time. When the diastolic filling time is short, the distance between the mitral leaflets is long and they snap together loudly. Causes of a loud S1 are mitral stenosis, tachycardia and a short PR interval. When the diastolic filling time is long, the distance between the mitral leaflets is short and they snap together softly. Causes of a soft S1 are mitral regurgitation, bradycardia and a long PR interval. The mitral and tricuspid components of S1 are usually inseparable. Splitting of S1 occurs when the tricuspid component is delayed. Causes of a split S1 are right bundle branch block and Ebstein anomaly. The intensity of S1 is variable if the diastolic period varies from beat-to-beat. Causes of a variable S1 are atrial fibrillation and atrioventricular dissociation. The S2 is normally split and produced by closure of the aortic valve followed by the pulmonary valve, at the end of ventricular systole. The intensity of the aortic component (A2) and pulmonary component (P2) of S2 depends upon the rate of deceleration of retrograde flow. The A2 is loud in systemic hypertension and in aneurysmal dilatation of the aorta, while it is soft in calcific aortic stenosis and absent in aortic atresia. The P2 is loud in pulmonary hypertension and in dilatation of the pulmonary artery, while it is soft in pulmonary stenosis and absent in pulmonary atresia. The S2 is normally split with closure of the aortic valve being followed by the closure of the pulmonary valve, at the end of ventricular systole. The splitting of S2 is better appreciated during inspiration because increase in venous return delays the pulmonary component or P2. Wide splitting of S2 is observed in right bundle branch block (delayed right ventricular activation), pulmonary stenosis (prolonged right ventricular ejection) and in mitral regurgitation (short left ventricular ejection time). Reverse or paradoxical splitting of S2 is where A2 follows P2. In that case, the splitting narrows down in inspiration when P2 is delayed. Reverse splitting of S2 is observed in left bundle branch block (delayed left ventricular activation), aortic stenosis (prolonged left ventricular ejection) and in aortic valve regurgitation (long left ventricular ejection time). Pacing of the right ventricle by an external pacemaker or pre-excitation by an accessory bypass tract also cause reverse splitting of S2. Wide and fixed splitting of S2 that does not widen further during inspiration occurs in atrial septal defect. The shunt abolishes the effect of respiration on atrial filling. Fixed splitting of S2 also occurs in right ventricular dysfunction. This is because inspiration cannot augment ventricular filling any further. The third heart sound (S3) is a soft sound that follows S2. It is produced by a sudden halt in diastolic ventricular filling and coincides with the “y” descent of the jugular pulsation. Physiological S3 is heard in high-output states, valvular regurgitation and cardiac shunt. Pathological S3 is heard in left ventricular systolic dysfunction. The pericardial knock (PK) resembles S3 but it occurs earlier and is sharper in character. It is heard in case of constrictive pericarditis. The fourth heart sound (S4) is a high-pitched sound that precedes S1. It is produced by atrial contraction and coincides with the “a” wave of the jugular venous pulse. The S4 is always pathological and indicates impaired left ventricular relaxation as in case of systemic hypertension, aortic stenosis and restrictive/hypertrophic cardiomyopathy. The opening snap (OS) is produced by sudden tensing of the anterior mitral leaflet at the end of isovolumic relaxation and beginning of ventricular filling. It is typically audible in mitral stenosis and indicates pliability of the valve. The opening snap is absent in calcific stenosis and after mitral valvotomy. A short interval between the S2 and OS indicates high left atrial pressure and severe mitral stenosis, since ventricular filling begins early after S2. The tumor plop (TP) of left atrial myxoma resembles the OS of mitral stenosis. It is produced by prolapse of the myxoma into the mitral valve orifice. An ejection click (EC) is a sharp sound that precedes the ejection systolic murmur of aortic or pulmonary valvular stenosis. It is produced by sudden halt of maximal excursion of the valve leaflets and indicates end of isovolumic contraction with onset of ejection. Presence of ejection click indicates pliability of the valve, differentiates valvular from infundibular stenosis and rules out innocent flow murmurs. In case of mitral valve prolapse, single or multiple nonejection click(s) are audible in mid-systole, indicating sudden tensing of the redundant anterior mitral leaflet. A pansystolic murmur begins with S1, spans the entire systole and ends with S2. Causes of pansystolic murmur are mitral/tricuspid regurgitation and ventricular septal defect. In mitral regurgitation (MR), the murmur stops short of S2 and is only early systolic if the MR is acute or severe, since high left atrial pressure impedes flow in late systole. Similarly in ventricular septal defect (VSD), the murmur is only early systolic if the VSD is large in size, muscular in location or associated with pulmonary arterial hypertension. An ejection mid-systolic murmur is diamond-shaped and peaks in mid-systole. Causes of an ejection murmur are aortic and pulmonary valve stenosis. In aortic stenosis (AS), the mid-systolic murmur may be preceded by an ejection click, accompanied by a palpable thrill and it radiates towards the neck. A late-systolic murmur is heard in case of mitral valve prolapse, due to late-systolic mitral regurgitation. It is preceded by a single or multiple nonejection click(s). An early-diastolic murmur just follows the S2 and stops short of S1. Causes of an early-diastolic murmur are aortic and pulmonary valve regurgitation. The early-diastolic murmur of aortic regurgitation (AR) is decrescendo in nature and it is high-pitched, soft and blowing in character. The murmur of AR is best heard over the parasternal area with the diaphragm of the stethoscope firmly pressed and the patient sitting up leaning forward. The early-diastolic murmur of pulmonary regurgitation (PR) with a loud P2 indicates pulmonary arterial hypertension. It is known as the Grahm-Steel murmur. A mid-diastolic murmur follows the opening snap and undergoes accentuation before S1. Causes of a mid-diastolic murmur are mitral and tricuspid stenosis. The length of the mid-diastolic murmur correlates with the severity of mitral stenosis (MS). Presystolic accentuation is absent in the presence of atrial fibrillation. The mid-diastolic murmur of mitral stenosis is harsh and low-pitched, rough and rumbling in character. The murmur of MS is best heard over the mitral area with the bell of the stethoscope lightly placed and the patient lying in the left-lateral position. A late-diastolic murmur occurs in case of left atrial myxoma and follows the tumor plop. The murmur changes in character with the position of the patient. Besides mitral stenosis and atrial myxoma, other causes of a mid or late diastolic murmur are mitral leaflet fluttering in case of aortic regurgitation (Austin Flint murmur) and increased diastolic flow (mitral regurgitation and ventricular septal defect). A continuous murmur occurs throughout systole, crosses the S2 and spills over into diastole. It has the same character in systole and diastole. Causes of a continuous murmur are patent ductus arteriosus (PDA), aortopulmonary window (APW), ruptured aneurysm sinus of Valsalva (SOV), arteriovenous fistula (AVF), coarctation of aorta, venous hum and mammary soufflé. The continuous murmur of PDA is maximum around the S2. It is known as machinery murmur or the Gibson’s murmur. When pulmonary hypertension develops, the murmur remains only systolic. A systolo-diastolic murmur is a combination of a systolic murmur and diastolic murmur. It has a different character in systole and diastole. Causes of a systolo-diastolic murmur are aortic stenosis with regurgitation (rheumatic heart disease), ventricular septal defect with aortic regurgitation (supracristal VSD) and atrial septal defect with mitral stenosis (Lutembacher syndrome). Other sounds that may be heard over the precordium are pericardial rub (pericarditis), mediastinal crunch (mediastinal emphysema), Means-Lerman scratch (thyrotoxicosis). The intensity and character of a murmur may change with the position of the patient, the phase of respiration and performance of certain maneuvers. Murmurs that may change with the position of the patient are those of mitral valve prolapse, atrial myxoma and bacterial endocarditis. During inspiration, increase in venous return to the right atrium increases the intensity of murmurs arising from the right side of the heart and decreases the intensity of left-sided murmurs. The reverse happens during expiration. An exception to this rule is the ejection click of pulmonary valve stenosis that reduces in intensity during the phase of inspiration. Maneuvers that reduce the size of the left ventricular cavity, reduce the intensity of most left-sided murmurs. These maneuvers are standing, Valsalva and nitroglycerine. Conversely, maneuvers that increase the size of the left ventricular cavity, increase the intensity of most left-sided murmurs. These are squatting, hand-grip and propranolol. Exceptions to this rule are the murmurs of mitral valve prolapse (MVP) and hypertrophic obstructive cardiomyopathy (HOCM) that are left-sided murmurs but become louder and longer with maneuvers that reduce the size of the left ventricular cavity. This is because reduction in the size of the left ventricular cavity, increases the degree of mitral leaflet buckling and outflow tract obstruction respectively.