What is an abnormal heart sound that is most commonly a sign of defective heart valves?

Auscultation

Heart sounds are generated by contraction of the heart and flow across different parts of it. First and second heart sounds are the result of closing of atrioventricular and semilunar valves. It is recommended to listen to the heart sounds from the least intensity focus of the sounds, is right lower sternal border and inching space to reach to the apex, where the sounds are the strongest.

When you report the heart sounds, it is advised to start with this order: heart sounds including S1, S2, S3, S4, additional sounds such as ejection or nonejection click, tumor PLOP, pericardial sound, pacemaker sounds, and murmurs. You have to point out the intensity duration, radiation, quality, and timing of the murmur.

Auscultation

Heart sounds are generated by contraction of the heart and flow across different parts of it. The first and second heart sounds are the result of closing of the atrioventricular and semilunar valves. It is recommended to listen to the heart sounds from the least intense focus of the sounds (i.e., the right lower sternal border and inching space to reach to the apex where the sounds are the strongest).3,4

It is recommended when listening to the heart sound to start from the focus that has the least intensity of the sounds (right lower sternal border) and then go to other points inch by inch.

Muffled heart sounds.

The heart sounds can be dampened, or muffled, when attenuated by structures between the stethoscope and the heart. While blood transmits vibrations generated by the heart very well, other fluids, tissues, air, and bone attenuate cardiac vibrations. Body habitus and age can affect the acoustics of the heart sounds. Large depositions of adipose tissue, thick skin, and thick musculature can attenuate heart sounds. Fluid between the stethoscope and the heart, such as subcutaneous edema, pleural effusion, and pericardial effusion, can muffle heart sounds. Gas accumulation, associated with subcutaneous emphysema, pneumothorax, and pneumopericardium, can muffle heart sounds. Similarly, abnormal soft tissue structures or solidification of tissues, such as cutaneous or subcutaneous masses, pulmonary masses, pneumonia, pulmonary edema, pulmonary abscesses or granulomas, and pulmonary hemorrhage can lead to attenuation of heart sounds.

Heart Sounds.

Heart sounds can be heard by auscultation of the heart through the chest wall with a stethoscope. Heart sounds generally reflect the closing of the heart valves and include normal and abnormal sounds. The first heart sound (S1) is the sound heard with the closing of the mitral and tricuspid valves and is best heard with placement of the diaphragm of the stethoscope at the apex of the heart. The second heart sound (S2) represents aortic and pulmonic valve closures and is best auscultated with the diaphragm of the stethoscope at the second intercostal space. S1 precedes S2, and together these compose the “lub-dub” sounds.

The third heart sound (S3) may be normal (physiological) or abnormal (pathological). A physiological S3 is sometimes heard in children and young adults, but an S3 in a person over 30 years of age is generally pathological and is commonly present in older patients with heart failure. The pathological S3 is often an early sign of heart failure. If present, the S3 heart sound occurs immediately after the S2, coinciding with the period of rapid ventricular filling, and is a soft and low frequency sound that is best heard with the bell of the stethoscope lightly rested over the chest wall.29 Despite findings that interrater agreement on the presence of an S3 heart sound is low to moderate, and that its sensitivity and specificity for the presence of heart failure are also only fair to good (sensitivity 51%, specificity 90% for patients with heart failure),33 the presence of abnormal heart sounds along with JVD is associated with increased heart failure hospitalization, heart failure deaths, and death from all causes in patients with heart failure.30

The fourth heart sound (S4) is an abnormal heart sound that can be heard immediately before S1 and indicates increased resistance to ventricular filling due to high atrial pressure or increased ventricular thickness. The presence of an S4 may indicate myocardial infarction or shock.

Origins of the Heart Sounds

Normal heart sounds originate from vibrations of heart valves when they close and from heart chambers when they fill or contract rapidly. The amount of pressure that forces the valve closure influences the intensity of a heart sound. Other mechanical factors such as valve stiffness, thickness, and excursion have less effect on sound intensity.

Cardiac murmurs are the direct result of blood-flow turbulence. The amount of turbulence and consequently the intensity of a cardiac murmur is directly proportional to both the pressure difference or gradient across a narrowing or defect and the blood flow or volume moving across the site.

As sound radiates from its source, sound intensity diminishes with the square of the distance. Consequently, heart sounds should be loudest near the point of origin. However, other factors influence this relationship. Sound passage through the body is affected by the transmission characteristics of the tissues. Fat has a more pronounced dampening effect on higher frequencies than does more dense tissue such as bone. If the difference in tissue density is significant—for example, between the heart and lungs—more sound energy is lost. Only the loudest sounds may be heard when lung tissue is positioned between the heart and chest wall.

In contrast to intensity, the frequency of a cardiac murmur is proportional to pressure difference or gradient across a narrowing alone.

I Characteristics of Heart Sounds and Murmurs

Different heart sounds and murmurs are distinguished by four characteristics: (1) timing (i.e., systolic or diastolic), (2) intensity (i.e., loud or soft), (3) duration (i.e., long or short), and (4) pitch (i.e., low or high frequency). A fifth characteristic, the sound’s quality, is also sometimes included in descriptions of sounds (e.g., it may be described as “musical,” a “whoop,” or a “honk”). Almost all heart sounds contain a mixture of frequencies (i.e., they are not musical in the acoustical sense, but instead are “noise,” like the static of a radio tuned between stations). Therefore the descriptors low frequency and high frequency do not indicate that a sound has a pure musical tone of a certain low or high pitch but instead that the bulk of the sound’s energy is within the low or high range.

Although the human ear can hear sounds with frequencies from 20 to 20,000 cycles per second (Hz), the principal frequencies of heart sounds and murmurs are at the lower end of this range, from 20 to 500 Hz.1,2 Therefore low-frequency sounds are those whose dominant frequencies are less than 100 Hz, such as third and fourth heart sounds and the diastolic murmur of mitral stenosis. These sounds are usually difficult to hear because the human ear perceives lower frequencies relatively less well than higher frequencies. The murmur containing the highest frequency sound is aortic regurgitation, whose dominant frequencies are approximately 400 Hz. The principal frequencies of other sounds and murmurs are between 100 and 400 Hz.

Heart Sounds

The heart sounds should be assessed in both the right and left chests, including auscultation anteriorly, posteriorly, and in both axillae. A practitioner may diagnose dextrocardia when the heart sounds are louder in the right chest even though they are audible in the left chest. The precordium should be interrogated in a stepwise fashion, encompassing the five important areas: (1) right upper sternal border (RUSB), (2) left upper sternal border (LUSB), (3) left midsternal border (LMSB), (4) left lower sternal border (LLSB), and (5) left-sided apical region (LVap).

Any irregularity of the heart rate should be noted, with particular attention to variation with breathing (sinus arrhythmia). If the patient is old enough to hold his or her breath, irregularity secondary to sinus arrhythmia should disappear with a breath hold. Auscultation of the neck, skull, and liver areas may identify arteriovenous malformations in these areas or carotid bruits and venous hums.

Much information is obtained from the heart sounds. The first heart sound (S1) represents closure of the tricuspid and mitral valves at the onset of systole and is best heard at the apex. The component parts may be appreciated separately (called splitting of a heart sound) at the LLSB in older children and adolescents with slower heart rates, with the mitral component normally first. On occasion, the splitting will be very noticeable, and sometimes the sound is mistakenly interpreted as a click. S1 will be single in patients with an atretic atrioventricular (AV) valve or tachycardia. A loud S1 occurs with increased flow across the mitral valve from large left-to-right shunts, such as a large VSD or patent ductus arteriosus, or moderate to severe mitral regurgitation, and is best heard at the apex. When there is increased flow across the tricuspid valve, as in a large atrial septal defect (ASD) or tricuspid regurgitation, the accentuated first sound is best heard at the LLSB. Accentuation of the S1 occurs with marked mitral or tricuspid stenosis. With a short PR interval, as in Wolff-Parkinson-White (WPW) syndrome, and with increased cardiac output, the S1 is increased. A soft first heart sound is present in congestive heart failure or with prolonged atrioventricular (AV) conduction.

The second heart sounds are best heard in the second and third left intercostal spaces. The second heart sound (S2) represents closure of the aortic (A2) and pulmonary (P2) valves at the end of systole, in that order. An accurate assessment of the quality of this heart sound is critical in a thorough cardiac examination. Under normal circumstances, systemic vascular resistance (SVR) is higher than pulmonary vascular resistance (PVR), allowing slightly longer systolic ejection time into the pulmonary bed. As a result, the aortic valve closes before the pulmonary valve (A2P2). This splitting of S2 also varies with the respiratory cycle. During inspiration, increased central venous return to the right heart takes longer to cross the right ventricular outflow tract. Closure of the pulmonary valve is delayed compared to the ejection time in expiration; thus, the aortic and pulmonic components of S2 are more readily separated from each other in inspiration. This variability in the timing of A2 and P2 with the respiratory cycle is termed physiologic splitting. If this variability is not appreciated beyond infancy or at slower heart rates, an abnormality of the cardiopulmonary system must be suspected.

The intensity of the components of the second heart sound reflects not only the pressure in the respective vessels, but also their position within the thorax and the thickness of the chest wall. In d-transposition of the great arteries (d-TGA), for example, the second heart sound is “single” because the posterior pulmonic component cannot be heard. Likewise, in TOF, the soft pulmonic component from a stenotic valve may not be audible. A loud pulmonic component or an apparent single S2 may signal the presence of pulmonary artery hypertension if heard beyond the neonatal period when pulmonary resistance may normally be elevated (Table 1-2).

Physiologic splitting of S2 occurs only when PVR is normal, so any abnormality of PVR will alter this physiologic effect. The higher the PVR caused by a large leftto-right shunt or pulmonary vascular disease, the shorter the pulmonary ejection time. P2 will occur closer to A2 and, although they are still separate from each other, the splitting is termed narrow. When PVR is equal to or greater than SVR, closure of A2 and P2 will be nearly simultaneous, resulting in an audible “single” S2. This is a sign of severe pulmonary hypertension. Alternatively, the splitting of S2 will be accentuated (“widened”) under certain circumstances. When the right heart is volume-loaded from a left-to-right shunt at the atrial level, the physiologic variation between A2 and P2 is lost as the stroke volume is increased, both in inspiration and expiration. Another situation in which S2 shows “fixed splitting” is in the presence of a complete right bundle branch block. This intraventricular conduction delay causes a slight prolongation of right ventricular ejection time, so P2 is always delayed compared to normal.

A third heart sound (S3) may normally be present in infants because it occurs at the peak of ventricular inflow into a compliant ventricle. As the ventricle ages, the velocity of ventricular filling diminishes and S3 cannot be heard. S3 is best heard at the cardiac apex or the LLSB. It becomes more prominent when there is increased volume of ventricular inflow (as is seen in lesions with left-to-right shunts causing increased pulmonary blood flow), valvar regurgitation, and high cardiac output (as is seen with anemia). The physiologic low-pitched S3 sound that can occur in well children and adolescents takes on the intonation of “Kentucky.” Referring to an S3 as a gallop generally connotes other findings consistent with congestive heart failure. A gallop is a lower-pitched sound that occurs in diastole, during the ventricular filling phase, and is best heard with the bell of the stethoscope.

A fourth heart sound (S4) occurs during atrial contraction and is associated with a limitation of ventricular distensibility. It has been associated with cardiomyopathy and hypertension and is more common in adults, again heard best at the apex or the LLSB. In the adult population, S4 gallops are pathologic and signify the presence of a noncompliant ventricle, occurring immediately before S1. Occasionally, in children with congestive heart failure, the same situation applies.

Other heart sounds may be present. Clicks are sounds made by the opening of abnormal valves. The most common clicks occur in systole and are related to abnormalities of the aortic, pulmonic, and mitral valves. Ejection clicks occur early in systole, immediately after S1, and represent the opening of a structurally abnormal aortic or pulmonary valve, which is usually bicuspid. Pulmonic ejection clicks are best heard at the LUSB and aortic clicks at the LLSB. Clicks with onset midway between S1 and S2 occur in mitral valve prolapse as the closed, myxomatous valve billows backwards toward the left atrium in mid to late systole. Tricuspid valve abnormalities occur less commonly, but additional heart sounds may be heard in Ebstein's anomaly of the tricuspid valve, probably due to motion of the redundant leaflets and to atrial hypertension.

I Introduction

Abnormal prosthetic heart sounds may be the only clue explaining the patient’s dyspnea, syncope, or chest pain. To recognize these abnormal sounds simply and quickly, the clinician must first understand the normal prosthetic heart sounds. This section focuses on rigid mechanical valves, such as caged-ball valves (Starr-Edwards),† single tilting-disc valves (Björk-Shiley, Medtronic-Hall), and bileaflet tilting-disc valves (St. Jude Medical).21-23

Examination

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Heart sounds

S1 and S2 are often diminished due to poor cardiac contractility.

S3 (also known as “gallop”) is present in 15%–20% of patients with an AMI.

S4 is frequently found in patients with long‐standing hypertension or cardiac dysfunction.

New murmur is worrisome and can indicate papillary muscle rupture, MVP, or ventricular septal defect.

If friction rub is present, pericarditis should be considered.

Lung

If lungs are clear in the setting of chest discomfort, consider right ventricular MI.

If rales are present, CHF may be present.

If breath sounds are unequal or unilaterally absent, pneumonia and pneumothorax should be considered.

Vascular system

Carotid bruits may indicate atherosclerotic disease.

If unequal radial and femoral pulses are present, thoracic aortic or abdominal aortic dissection, respectively, should be considered.

Jugular venous distention (JVD) after deep inspiration may indicate right‐sided MI.

Skin

The skin of a patient with chest discomfort will likely be diaphoretic.

A sympathomimetic response may occur in conjunction with a variety of conditions, including pain and hypotension.

Abdomen

A pulsatile mass or aortic bruit suggests abdominal aortic aneurysm.

Hepatojugular reflux may indicate CHF.

Extremities

Dependent edema may indicate the presence of CHF.

Rectum

Rule out active gastrointestinal (GI) tract bleeding; this can exacerbate tenuous CAD, causing ischemia. Active GI tract bleeding also must be ruled out before lytics and heparin are administered.

Malodorous, black tarry stool strongly suggests an active GI tract bleed. Heme‐positive brown stool may be indicative of an active GI tract bleed.

Digital stethoscope

Hearing the heart sounds is an integral part of cardiology and is now possible remotely as well. Studies have shown that the digital stethoscope may be more sensitive than the conventional stethoscope.261 Using it for remote hearing makes it a valuable tool in telecardiology. Digital stethoscopes (Fig. 5) are compact electronic stethoscopes combining a high-resolution visual display with traditional auscultation. Using the device, medical professionals can perform dynamic remote auscultation. In addition, the visual waveforms presented in the format of the classical phonocardiogram can be transmitted to the specialist at the remote end for analysis and validation.