Background
Cardiovascular diseases remain the leading cause of morbidity and mortality worldwide. Following a detailed medical history, physical examination plays a key role in the evaluation of the cardiovascular system, with cardiac auscultation being a fundamental component. Although it requires proper training and is subject to interobserver variability, auscultation provides critical early clues in patient assessment and serves as a cost-effective method for detecting various heart conditions.
Heart sounds are primarily generated by the opening and closing of heart valves, blood flow through valve orifices, filling of the ventricles, and friction between cardiac surfaces. During auscultation, attention should be given to specific anatomical areas including the cardiac apex, the aortic area located in the second right or third left intercostal space, the pulmonary area in the second left intercostal space, and the tricuspid area around the fourth and fifth left intercostal spaces. Additionally, sounds may radiate to other regions such as the carotid arteries, the left axilla, the interscapular area, and the base of the heart, which should also be assessed.
The examination should be performed with the patient in different positions including supine, left lateral decubitus, and sitting while leaning forward. In each position, clinicians should systematically listen for the first and second heart sounds (S1 and S2), physiological splitting, respiratory variations, and any abnormal sounds during systole and diastole. Dynamic maneuvers such as standing, performing the Valsalva maneuver, squatting, and hand grip can aid in evaluating certain murmurs, though their use has decreased with the growing reliance on echocardiography.
Accurate interpretation of heart sounds also depends on identifying the phase of the cardiac cycle in which they occur. This can be achieved by simultaneously palpating the carotid artery, as the upstroke of the carotid pulse corresponds to ventricular systole. Recent advancements have introduced tools such as murmur recognition systems, artificial intelligence models, heart sound classifiers, and digital stethoscopes to enhance the accuracy of auscultation. These technologies aim to overcome limitations such as background noise and user variability and are increasingly being integrated into wearable devices and computer-aided diagnostic systems for more reliable heart sound analysis.
2.Types of Heart sounds
Systolic Heart Sounds
Systolic heart sounds primarily include the first heart sound (S1) and systolic clicks.
The first heart sound (S1), along with the second heart sound (S2) which occurs during diastole forms the characteristic “lub-dub” of the cardiac cycle. S1 occurs just after systole begins and is mainly produced by the closure of the mitral valve, with contributions from the tricuspid valve. It typically has a high frequency and may be split. In mitral stenosis, S1 is usually accentuated. In contrast, S1 can be diminished or absent in mitral regurgitation due to leaflet sclerosis or rigidity. However, in cases of mitral regurgitation caused by myxomatous changes or underlying ventricular dysfunction (such as papillary muscle dysfunction or ventricular dilation), S1 may still be clearly audible. When first-degree atrioventricular block is present, S1 is often reduced or absent because the mitral and tricuspid valves begin closing slowly before ventricular systole begins.
Systolic clicks occur exclusively during systole and are recognized by their shorter duration and higher pitch compared to S1 and S2. Their timing within systole can vary depending on hemodynamic conditions, and they may be single or multiple.
In congenital aortic or pulmonary stenosis, early systolic clicks are believed to arise from abnormal ventricular wall tension. These clicks typically appear near the onset of systole (just after S1) and do not vary with changes in preload or afterload. Similar early systolic clicks can be heard in severe pulmonary hypertension.
In mitral valve prolapse or tricuspid valve prolapse, clicks usually occur in mid-to-late systole and are thought to result from abnormal stress on elongated chordae tendineae or redundant valve leaflets. When associated with myxomatous degeneration, clicks may appear at any time during systole. Their timing shifts depending on ventricular volume: during reduced filling (e.g., standing or performing a Valsalva maneuver), clicks move closer to S1; with increased filling (e.g., lying down), they shift toward S2, especially in mitral valve prolapse. These clicks can vary significantly between examinations, sometimes even disappearing entirely for unclear reasons.
Diastolic Heart Sounds
Diastolic heart sounds include the second (S2), third (S3), and fourth (S4) heart sounds, as well as diastolic knocks and mitral valve-related sounds.
In contrast to systolic sounds, diastolic sounds are generally lower in pitch, softer, and longer in duration. Except for S2, most diastolic sounds in adults are considered abnormal. However, an S3 can be a normal variant in individuals under 40 years old or during pregnancy.
The second heart sound (S2) marks the onset of diastole and results from the closure of the aortic (A2) and pulmonic (P2) valves. Normally, A2 precedes P2, and during inspiration, increased venous return to the right heart delays P2, leading to physiologic splitting of S2. This type of splitting typically becomes audible only on inspiration.
In some conditions, such as pulmonic valve stenosis or complete right bundle branch block, P2 is further delayed, causing a widely split S2 that still varies with breathing. However, in atrial septal defect of the secundum type, P2 is delayed regardless of respiration, producing a fixed wide split of S2. In contrast, ventricular septal defects with normal right ventricular volume do not produce fixed splitting.
When aortic valve closure is delayed, as seen in aortic stenosis or left bundle branch block, a reversed or paradoxical splitting of S2 can occur. In this case, the split is heard during expiration and disappears with inspiration because the delayed A2 coincides with P2.
A single S2 may be noted in cases where the aortic valve is severely stenotic, regurgitant, or absent, or in congenital anomalies like truncus arteriosus, where only one outflow valve is present.
The third heart sound (S3) occurs during early diastole, specifically during the passive filling phase of the ventricles. It is typically associated with a dilated and noncompliant ventricle, and in adults, it often signals significant ventricular dysfunction. However, in children, and occasionally up to the age of 40, S3 may be a normal finding. It can also be physiologically present in pregnancy. The right-sided S3 is best heard when the patient is supine and during inspiration, as the negative intrathoracic pressure increases right ventricular filling volume. In contrast, the left-sided S3 is more clearly heard during expiration, especially when the patient is in the left lateral decubitus position, as the heart comes closer to the chest wall.
The fourth heart sound (S4) is produced late in diastole due to atrial contraction forcing blood into a stiff or noncompliant ventricle. Like S3, S4 is also low-pitched and heard best with the bell of the stethoscope. During inspiration, the intensity of right ventricular S4 increases, while left ventricular S4 becomes softer. S4 is generally more frequently detected than S3 and is most often associated with diastolic dysfunction. It is absent in atrial fibrillation, since the atria are not contracting, but is commonly present during myocardial ischemia or immediately after a myocardial infarction. Unlike S3, which may be benign in some cases, S4 is always considered abnormal.
In patients with significant systolic dysfunction, S3 may occur either alone or in combination with S4. Conversely, isolated S4 is typically seen in those with diastolic dysfunction.
A summation gallop is heard when both S3 and S4 are present and merge due to tachycardia, which shortens the diastolic interval. In such cases, both sounds may be so close together that they become indistinguishable. When prominent, these sounds may be palpable at the cardiac apex, particularly when the patient lies in the left lateral decubitus position.
A diastolic knock is a distinct sound that also occurs during early diastole, roughly at the same timing as S3. Unlike S3, it is a loud, abrupt thudding sound and is not accompanied by S4. This sound typically suggests a sudden halt in ventricular filling due to a noncompliant and constricted pericardium, such as in constrictive pericarditis.
An opening snap (OS) may also be heard in early diastole, especially in the setting of mitral stenosis, and less commonly in tricuspid stenosis. The mitral opening snap is a brief, high-pitched sound, best heard using the diaphragm of the stethoscope. It is typically heard soon after the pulmonic component of the second heart sound (S2). The shorter the interval between S2 and the OS, the more severe the mitral stenosis, reflecting a higher left atrial pressure. The intensity of the snap is influenced by the flexibility of the valve leaflets-it tends to be loud when the valve is still pliable but becomes softer and may eventually disappear as the valve becomes fibrotic or calcified. Although the OS may sometimes be heard at the apex, it is more commonly best heard or exclusively detected at the lower left sternal border.
Ejection systolic sounds
Ejection systolic sounds occur during the early phase of ventricular systole. These sounds are typically high-pitched and are best heard using the diaphragm of the stethoscope. They may originate from either valvular or vascular sources.
Valvular ejection sounds
These are commonly heard in individuals with abnormalities of the aortic or pulmonary valves. These sounds are present shortly after the first heart sound (S1). The aortic ejection sound is usually best heard at the apex or in the aortic area and is often associated with bicuspid aortic valves or aortic regurgitation. When the aortic valve is pliable, the ejection click is louder in intensity. As calcification of the valve increases, the intensity of the ejection click diminishes. In cases of severe calcific aortic stenosis, the ejection click may be absent. Similarly, the ejection sound is typically not heard in subvalvular or supravalvular aortic stenosis. If an aortic ejection sound is present without other signs of aortic stenosis, it strongly suggests the presence of a bicuspid aortic valve.
The pulmonary ejection sound is most commonly associated with pulmonary valve stenosis and is best heard in the pulmonary area. Unlike most sounds originating from the right side of the heart, the intensity of this sound decreases with inspiration. This phenomenon is thought to occur because inspiration allows increased venous return from the right atrium, which may partially open the pulmonary valve during diastole. As a result, the valve opens more gradually during systole, leading to a reduction in sound intensity.
Vascular ejection sounds:
These are generated in the aorta or pulmonary artery. Aortic vascular ejection sounds are associated with conditions such as aortic sclerosis with a tortuous aortic root, systemic hypertension, ascending aortic aneurysm, and aortic root dilatation. These sounds are usually heard in the aortic area and are not typically transmitted to the apex. Pulmonary vascular ejection sounds are related to pulmonary hypertension or pulmonary artery dilation and are best heard at the second or third left intercostal space.
Nonejection systolic clicks:
These are associated with mitral valve prolapse or tricuspid valve prolapse, with mitral valve prolapse being more commonly observed. This click is a high-pitched systolic sound that follows S1 and is heard best at the apex in cases of mitral valve prolapse or in the tricuspid area for tricuspid valve prolapse. The timing between S1 and the prolapse click varies depending on the volume status of the ventricle, as the prolapse occurs when the ventricle reaches a particular volume.
When the end-diastolic volume is increased, such as in the presence of bradycardia, when lying in the supine position, or during handgrip or squatting, the interval between S1 and the click is prolonged. When the end-diastolic volume is reduced, as may occur with tachycardia, upon standing, or during the Valsalva maneuver, the S1-to-click interval becomes shorter. These variations in timing help differentiate prolapse clicks from other systolic sounds.
Approach to Cardiac Murmurs
The timing of a murmur in the cardiac cycle provides important diagnostic information and is typically related to the underlying cause. For instance, systolic and diastolic murmurs are usually linked to different valvular abnormalities. Specific features heard during auscultation, such as the location, intensity, quality, and radiation of the murmur, help identify the valve involved.
Several physical maneuvers, including inspiration, the Valsalva maneuver, handgrip, squatting, and amyl nitrate inhalation, can influence cardiac dynamics. These maneuvers modify preload, afterload, or intrathoracic pressure, which can help differentiate among the various types of murmurs.
All patients who present with a heart murmur should be evaluated using a chest X-ray and an electrocardiogram. Echocardiography is essential for confirming the diagnosis, assessing the severity of the condition, and monitoring changes over time. When significant valvular disease is suspected, referral to a cardiologist is often appropriate for further evaluation and management.
Systolic Murmurs
Systolic murmurs can be either physiological or pathological in nature. Based on their timing within systole, they may occur early, in mid-systole, in late systole, or may extend throughout systole as holosystolic murmurs. These murmurs are generally categorized into three types: ejection, regurgitant, and shunt murmurs.
Ejection murmurs:
These result from turbulent forward blood flow through narrowed or irregular valves or outflow tracts, as seen in conditions such as aortic stenosis or pulmonic stenosis. These murmurs most often occur during mid-systole and have a crescendo-decrescendo pattern, meaning they gradually increase in intensity before fading. The severity of the obstruction determines the murmur’s characteristics: more severe narrowing leads to a longer crescendo phase and a shorter decrescendo.
Some systolic ejection murmurs do not indicate significant structural abnormalities and are termed innocent or functional murmurs. These are especially common in healthy infants and children, where mildly turbulent blood flow creates soft, benign murmurs. A well-known example is the Still murmur, a vibratory systolic sound believed to arise from the vibration of the mitral valve’s chordae tendineae. In older adults, similar murmurs may be heard due to age-related stiffening of valves or arteries.
Pregnant women frequently develop soft ejection murmurs at the second intercostal space adjacent to the sternum. These murmurs are attributed to the physiological increase in blood volume and cardiac output, which raises blood flow velocity through otherwise normal cardiac structures. When pregnancy is complicated by significant anemia, the intensity of these murmurs can increase. It is important to distinguish these murmurs from the mammary souffle, a sound caused by increased blood flow through the breast vasculature.
Regurgitant murmurs:
These are produced by backward blood flow, such as that seen in mitral or tricuspid regurgitation. Ventricular septal defects can create similar murmur patterns. These murmurs typically extend across the entire systole, producing a holosystolic sound. Their loudness is influenced by the pressure and volume of the regurgitated blood: high-velocity, low-volume regurgitation produces louder murmurs, while high-volume regurgitation may result in softer sounds.
Late systolic murmurs:
Sometimes preceded by a click, are most associated with mitral valve prolapse or dysfunction of the papillary muscles.
Shunt murmurs:
These arise either directly at the site of abnormal connections, such as a patent ductus arteriosus or a ventricular septal defect, or indirectly from hemodynamic changes elsewhere, such as increased flow through the pulmonic valve caused by a left-to-right atrial septal defect. Murmurs resulting from atrial septal shunts themselves are rarely audible.
To accurately classify the type and timing of a murmur, bedside maneuvers such as inspiration, Valsalva, squatting, and handgrip are often employed, as these can influence the flow dynamics and enhance diagnostic clarity.
Diastolic Murmurs
Diastolic murmurs are always considered pathological. They are usually classified based on their timing within diastole and may be early, mid, or late diastolic. Early diastolic murmurs most often arise from aortic regurgitation or pulmonic regurgitation. Murmurs occurring during the mid or early-to-mid portion of diastole typically result from mitral stenosis or tricuspid stenosis. When a patient is in normal sinus rhythm, a murmur heard in the late diastolic phase may indicate rheumatic involvement of the mitral valve.
In some cases, murmurs originating from mitral or tricuspid valves are caused by atrial tumors or intracardiac thrombi. These murmurs can be inconsistent and may vary with changes in the patient’s body position or even between different physical examinations. This variability is due to the shifting position of the intracardiac mass, which influences the flow of blood across the affected valve.
Continuous Murmurs
Continuous murmurs extend through both systole and diastole and are considered abnormal. They typically indicate the presence of a shunt that allows blood to flow during the entire cardiac cycle, which is why the murmur remains audible even after the second heart sound. These murmurs can arise from a variety of structural cardiac abnormalities, many of which are associated with findings of right or left ventricular hypertrophy. In some cases, they may produce a palpable thrill. As pulmonary artery resistance increases in shunt-related conditions, the intensity of the diastolic portion of the murmur tends to diminish. Eventually, if pulmonary and systemic vascular resistances become equal, the murmur may no longer be detectable.
In cases of patent ductus arteriosus, the murmur is typically loudest at the second intercostal space beneath the medial end of the left clavicle. When the condition involves an aortopulmonary window, the murmur is heard centrally at the level of the third intercostal space. Murmurs originating from systemic arteriovenous fistulas are best auscultated directly over the site of the lesion. Those due to pulmonary arteriovenous fistulas or stenosis of a branch of the pulmonary artery tend to have a more diffuse quality and may be heard across the chest.
Physiological conditions that increase circulatory volume, such as pregnancy, anemia, or hyperthyroidism, may lead to a continuous venous hum. This hum is commonly heard in the right supraclavicular area and is also frequently present in healthy children. A related sound, known as mammary souffle, results from increased blood flow in a dilated internal mammary artery. It can be mistaken for a cardiac murmur. Mammary souffle is usually best heard over the breast area near the second or third intercostal space on either side of the chest and, while often considered continuous, it is generally more prominent during systole.
Technique
Step 1: Prepare the Environment
Begin by ensuring that the examination takes place in a quiet, comfortable environment to avoid missing subtle heart sounds. Ask the patient to remove any clothing covering the chest to allow for full access. It is also advisable to warm the stethoscope diaphragm or bell before placing it on the patient’s skin, as a cold instrument can cause the patient to tense up, potentially interfering with sound transmission.
Step 2: Position the Patient
Proper positioning is essential for accurate auscultation. Start with the patient lying supine, which is the standard position for initial examination. To enhance certain heart sounds, ask the patient to shift positions as needed. The left lateral decubitus position where the patient lies on their left side is particularly useful for auscultating low-pitched sounds at the apex of the heart, such as the third and fourth heart sounds (S3, S4) and murmurs of mitral stenosis. Sitting the patient up and having them lean slightly forward is effective for better hearing aortic valve sounds, especially in conditions like aortic regurgitation.
Step 3: Select the Correct Stethoscope Side
Using the stethoscope correctly is crucial for detecting the full range of heart sounds. The diaphragm is best for high-pitched sounds, including the first (S1) and second (S2) heart sounds, as well as murmurs of aortic and mitral regurgitation and pericardial friction rubs. Firm pressure should be applied when using the diaphragm. The bell of the stethoscope, on the other hand, is designed to pick up low-pitched sounds such as S3, S4, and the murmur of mitral stenosis. It should be used with light pressure to avoid inadvertently converting it into a diaphragm and thereby missing low-frequency sounds.
Step 4: Identify Auscultatory Areas
Auscultation should follow a systematic approach to cover all major heart valve areas. Begin at the aortic area, located at the second right intercostal space near the sternum. Next, move to the pulmonic area at the second left intercostal space. Then proceed downward to the tricuspid area, found at the lower left sternal border, around the fourth or fifth intercostal space. Finally, auscultate the mitral area at the apex of the heart, typically the fifth left intercostal space at the midclavicular line. Using a consistent Z-pattern or reverse “L” can help ensure that no important areas are missed.
Step 5: Listen Carefully
At each of the auscultatory sites, listen over several cardiac cycles to thoroughly evaluate the heart sounds. Focus on identifying the normal heart sounds (S1 and S2), their intensity and timing, as well as any abnormal or extra sounds such as splitting of S2, S3, S4, clicks, or opening snaps. Also assess for murmurs, paying attention to their timing (systolic or diastolic), location, intensity (grade), pitch (high or low), and whether they radiate to other areas (e.g., to the neck in aortic stenosis or the axilla in mitral regurgitation).
Step 6: Use Respiratory and Positional Variations
Respiration can influence certain heart sounds, so it’s helpful to auscultate while the patient breathes normally and then while holding their breath. This can help diminish extraneous lung sounds and clarify underlying cardiac sounds. Additionally, some heart murmurs and abnormal sounds may change in intensity during inspiration versus expiration, which can aid in localizing whether the issue is right-sided or left-sided.
Step 7: Perform Special Maneuvers (If Needed)
To further evaluate murmurs, specific bedside maneuvers can be employed. Deep inspiration typically accentuates right-sided murmurs due to increased venous return, while expiration enhances left-sided murmurs. Having the patient squat increases venous return and preload, making murmurs of aortic stenosis more pronounced. Conversely, standing or performing the Valsalva maneuver decreases venous return and preload, which can amplify murmurs associated with hypertrophic cardiomyopathy. The handgrip maneuver increases systemic vascular resistance (afterload), thereby intensifying murmurs such as mitral regurgitation. These maneuvers are especially helpful in differentiating between similar-sounding murmurs.
