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1. Mechanism: The first heart sound (S1) is produced by closure of the atrioventricular (AV) valves: the mitral valve (M1 component) and tricuspid valve (T1 component) as ventricular contraction begins. If heart sounds are thought of as “lub-dub,” S1 is the “lub.” The M1 is louder than T1 and therefore the dominant component of S1. The M1 usually slightly precedes the T1.
2. Auscultation: Under normal conditions, the S1 is best audible over the apex.
1) Loud S1: Slim body type, tachycardia, short PR interval, ventricular premature beats, mitral (and tricuspid) stenosis (in patients with no significant valve calcifications).
2) Soft S1: Obesity, barrel chest, emphysema, pneumothorax, pericardial effusion, heart failure, myocardial infarction, prolonged PR interval, mitral (and tricuspid) regurgitation. Generally, this occurs because sound is muffled by water, air, or adipose tissue, or because the AV valves close less forcefully. Less forceful closure can be due to myocardial injury or more closed position at the onset of systole. Severe, heavily calcified mitral stenosis can cause a soft S1.
3) S1 of varying intensity: Mobitz type I (Wenckebach) second-degree AV block, complete heart block, atrial fibrillation, ventricular tachycardia, and frequent ventricular premature beats. It may sometimes develop in healthy individuals with significant respiratory sinus arrhythmia. Generally, this occurs due to variable positioning of the AV valves at the onset of systole.
4) S1 splitting (the first component is usually louder): Complete right bundle branch block (RBBB), premature ventricular beats, pacemakers. Splitting can reverse in the setting of left bundle branch block, pacemaker, or mitral stenosis.
1. Mechanism: The second heart sound (S2) is produced by closure of the semilunar valves: the aortic valve (A2 component) and pulmonary valve (P2 component). Due to higher left-sided cardiac pressures and lower left-sided vascular compliance, the A2 is louder and slightly precedes the P2. The components are audible as one sound on expiration and become split on inspiration due to increased venous return (referred to as physiologic splitting). Standing from sitting may also decrease venous return, thus decreasing physiologic splitting. The ideal place to listen for splitting is the left second or third intercostal space.
2. Auscultation: The S2 is best audible over the aortic valve area. A split S2 without a known clinical cause needs to be differentiated from a late systolic click (which usually has higher frequency, shorter duration, and is most pronounced over the lower left sternal border or apex) or diastolic sound.
1) Wide S2 splitting: The time between the A2 and the P2 is longer than normal and may be also more appreciable on expiration. This is caused by delayed closing of the pulmonic valve. Causes: RBBB, pulmonic stenosis, pulmonary hypertension, preexcitation with an accessory pathway in the left ventricle, left ventricular pacing, atrial septal defect (a fixed split: splitting remaining unchanged with inspiration and expiration).
2) Paradoxical S2 splitting: This occurs in states that cause the P2 to precede the A2. In such cases, as inspiration causes delay of the P2, the A2 and the P2 are closer together during inspiration and farther during expiration (where venous return is less and right ventricular systole ends earlier). Therefore, splitting of the S2 is more pronounced or perhaps only audible on expiration. Complete left bundle branch block, aortic stenosis, left ventricular outflow tract obstruction, left ventricular failure, high afterload states (eg, hypertension), preexcitation syndrome with an accessory pathway in the right ventricle, and right ventricular pacing all delay the A2 relative to the P2 and therefore may show a paradoxically split S2.
3) Loud P2: This is heard when the pulmonic component of the S2 is louder than the aortic:
a) Increased intensity P2: Pulmonary hypertension, atrial septal defect.
b) Decreased intensity A2: Aortic regurgitation, aortic stenosis, aortic calcification, mitral regurgitation, heart failure.
4) Loud A2: Most commonly found in hypertension due to increased pressure load across the aortic valve, but it can also be seen in coarctation and other aortopathies causing high ascending aortic pressure.
5) Single S2 (independent of the respiratory cycle): Absence of one of the S2 components or overlapping of the components. Causes: any of the above causes of decreased intensity of the A2, decreased P2 due to pulmonary stenosis, or conditions such as obesity, pneumothorax, pericardial effusion, emphysema, or aging that decrease sound conduction to the skin and potentially make the P2 inaudible. Pericardial effusion, pneumothorax, and obesity may cause a quiet S2.
1. Mechanism: The third heart sound (S3) is produced by abrupt deceleration of blood flow (mainly to the left ventricle) in early diastole, usually from high filling volumes. Physiologic causes: pregnancy, healthy children, and young adults. Pathologic causes: myocardial infarction, decreased ventricular contractility (increased end-diastolic volume in patients with systolic heart failure) due to any cause (see Heart Failure), or ventricular volume overload (eg, due to regurgitant valvular lesions). A right-sided S3 may be audible in right-sided heart failure and heard best along the left sternal boarder. It may increase with inspiration.
2. Auscultation: The S3 is a low-frequency sound that is best audible using the bell of a stethoscope. S3 from the left ventricle is best audible over the apex during expiration (in the left lateral decubitus position); S3 from the right ventricle is best audible over the left lower sternal border during inspiration. The S3 is louder during exercise or after elevation of the lower limbs and softer in an upright position. The S3 is often explained using the word “Kentucky,” where S1 represents “ken,” S2 represents “tuc,” and S3 represents “ky.”
1. Mechanism: The fourth heart sound (S4) is produced in late diastole during atrial contraction into a stiff, noncompliant ventricle. The S4 is typically not present in patients with atrial fibrillation because atrial contraction is absent. The S4 may be present in healthy children and adolescents, especially in young athletes. Causes of a left-sided S4 include left ventricular hypertrophy or impaired diastolic relaxation (especially infiltrative cardiomyopathies and ischemic heart disease). Causes of a right-sided S4 include right ventricular hypertrophy, pulmonary hypertension, and pulmonic stenosis.
2. Auscultation: The S4 is a low-frequency sound that is best audible using the bell of a stethoscope; other characteristics of the S4 are similar to those of the S3. Left-sided S4s are heard at the apex with the patient in the left lateral decubitus position; right-sided S4s are heard at the left sternal border and increase with inspiration. The S4 is sometimes said to sound like the world “Ten-nes-see,” where the S4 represents “ten” and S1 represents “nes.”
1. Mechanism: The pericardial knock, produced in early ventricular diastole, is thought to be due to sudden deceleration of ventricular filling caused by a noncompliant pericardium. It is a pathognomonic sign of constrictive pericarditis.
2. Auscultation: The pericardial knock is a high-frequency diastolic sound that is usually audible in the precordial area shortly after the S2, distinguishing it from the similarly timed S3.
1. Mechanism: The opening snap is thought to represent sudden tension of the chordae tendineae as leaflets of a stenotic mitral valve prematurely complete opening in diastole. It becomes less apparent with significant valve calcification.
2. Auscultation: A loud, short, high-frequency sound that occurs in early diastole and is best audible between the apex and the left sternal border. It can occur together with a loud S1 and diastolic murmur in mitral stenosis. The more severe the stenosis, the shorter the interval between the S2 and the opening snap. Contrasted with the S3, the opening sound is higher in pitch and usually closer to the S2. The opening snap is a pathognomonic sign of rheumatic mitral stenosis.
1. Mechanism: Systolic clicks occur during ventricular systole.
1) Early systolic (ejection) clicks are caused by ejection of blood into a dilated artery or through a stenotic valve. Causes include aortic dilation (hypertension, connective tissue disorder, bicuspid aortic valve, atherosclerosis), dilation of the main pulmonary artery (pulmonary hypertension), bicuspid aortic valve, aortic stenosis, and pulmonic stenosis.
2) Midsystolic and late systolic clicks are caused by sudden tension of stretched chordae tendineae and ballooning of the cusps of the AV valves. The most frequent cause is mitral valve prolapse.
2. Auscultation: Short high-frequency sounds. Early systolic (ejection) clicks occur before or with carotid upstroke. They are best audible at the upper sternal border and apex. Right-sided (pulmonic) ejection clicks may decrease with inspiration. Midsystolic and late systolic clicks occur after carotid upstroke and are best audible over the apex. Reduced preload causes the click to appear earlier, while increased preload causes the click to appear later in the S2.