Heart sounds are the noises generated by the beating heart and the resultant flow of blood through it. Specifically, the sounds reflect the turbulence created when the heart valves snap shut. In cardiac auscultation, an examiner may use a stethoscope to listen for these unique and distinct sounds that provide important auditory data regarding the condition of the heart.
In healthy adults, there are two normal heart sounds often described as a lubb and a dub (or dup), that occur in sequence with each heartbeat. These are the first heart sound (S1) and second heart sound (S2), produced by the closing of the atrioventricular valves and semilunar valves, respectively. In addition to these normal sounds, a variety of other sounds may be present including heart murmurs, adventitious sounds, and gallop rhythms S3 and S4.
Heart murmurs are generated by turbulent flow of blood, which may occur inside or outside the heart. Murmurs may be physiological (benign) or pathological (abnormal). Abnormal murmurs can be caused by stenosis restricting the opening of a heart valve, resulting in turbulence as blood flows through it. Abnormal murmurs may also occur with valvular insufficiency (regurgitation), which allows backflow of blood when the incompetent valve closes with only partial effectiveness. Different murmurs are audible in different parts of the cardiac cycle, depending on the cause of the murmur.
Primary heart sounds
Normal heart sounds are associated with heart valves closing:
The first heart sound, or S1, forms the “lub” of “lub-dub” and is composed of components M1 (mitral valve closure) and T1 (tricuspid valve closure). Normally M1 precedes T1 slightly. It is caused by the closure of the atrioventricular valves, i.e. tricuspid and mitral (bicuspid), at the beginning of ventricular contraction, or systole. When the ventricles begin to contract, so do the papillary muscles in each ventricle. The papillary muscles are attached to the cusps or leaflets of the tricuspid and mitral valves via chordae tendineae (heart strings). When the papillary muscles contract, the chordae tendineae become tense and thereby prevent the backflow of blood into the lower pressure environment of the atria. The chordae tendinea act a bit like the strings on a parachute, and allow the leaflets of the valve to balloon up into the atria slightly, but not so much as to evert the cusp edges and allow back flow of blood. It is the pressure created from ventricular contraction that closes the valve, not the papillary muscles themselves. The contraction of the ventricle begins just prior to AV valves closing and prior to the semilunar valves opening. The sudden tensing of the chordae tendineae and the squeezing of the ventricles against closed semilunar valves, sends blood rushing back toward the atria, and the parachute-like valves catch the rush of blood in their leaflets causing the valve to snap shut. The S1 sound results from reverberation within the blood associated with the sudden block of flow reversal by the valves. If M1 occurs slightly after T1, then the patient likely has a dysfunction of conduction of the left side of the heart such as a left bundle branch blockage.
The second heart sound, or S2, forms the “dub” of “lub-dub” and is composed of components A2 (aortic valve closure) and P2 (pulmonary valve closure). Normally A2 precedes P2especially during inhalation where a split of S2 can be heard. It is caused by the closure of the semilunar valves (the aortic valve and pulmonary valve) at the end of ventricular systole and the beginning of ventricular diastole. As the left ventricle empties, its pressure falls below the pressure in the aorta. Aortic blood flow quickly reverses back toward the left ventricle, catching the pocket-like cusps of the aortic valve, and is stopped by aortic valve closure. Similarly, as the pressure in the right ventricle falls below the pressure in the pulmonary artery, the pulmonary valve closes. The S2 sound results from reverberation within the blood associated with the sudden block of flow reversal.
Splitting of S2, also known as physiological split, normally occurs during inhalation because the decrease in intrathoracic pressure increases the time needed for pulmonary pressure to exceed that of the right ventricular pressure. A widely split S2 can be associated with several different cardiovascular conditions, including right bundle branch block, pulmonary stenosis, and atrial septal defect.
Extra heart sounds
The rarer extra heart sounds form gallop rhythms and are heard in both normal and abnormal situations.
Main article: Third heart sound
Rarely, there may be a third heart sound also called a protodiastolic gallop, ventricular gallop, or informally the “Kentucky” gallop as an onomatopoeic reference to the rhythm and stress of S1 followed by S2 and S3 together (S1=Ken; S2=tuck; S3=y).
“lub-dub-ta” or “slosh-ing-in” If new, indicates heart failure or volume overload.
It occurs at the beginning of diastole after S2 and is lower in pitch than S1 or S2 as it is not of valvular origin. The third heart sound is benign in youth, some trained athletes, and sometimes in pregnancy but if it re-emerges later in life it may signal cardiac problems, such as a failing left ventricle as in dilated congestive heart failure (CHF). S3 is thought to be caused by the oscillation of blood back and forth between the walls of the ventricles initiated by blood rushing in from the atria. The reason the third heart sound does not occur until the middle third of diastole is probably that during the early part of diastole, the ventricles are not filled sufficiently to create enough tension for reverberation.
It may also be a result of tensing of the chordae tendineae during rapid filling and expansion of the ventricle. In other words, an S3 heart sound indicates increased volume of blood within the ventricle. An S3 heart sound is best heard with the bell-side of the stethoscope (used for lower frequency sounds). A left-sided S3 is best heard in the left lateral decubitus position and at the apex of the heart, which is normally located in the 5th left intercostal space at the midclavicular line. A right-sided S3 is best heard at the lower-left sternal border. The way to distinguish between a left and right-sided S3 is to observe whether it increases in intensity with inhalation or exhalation. A right-sided S3 will increase on inhalation, while a left-sided S3 will increase on exhalation.
S3 can be a normal finding in young patients but is generally pathologic over the age of 40. The most common cause of pathologic S3 is congestive heart failure.
S4 when audible in an adult is called a presystolic gallop or atrial gallop. This gallop is produced by the sound of blood being forced into a stiff or hypertrophic ventricle.
“ta-lub-dub” or “a-stiff-wall”
It is a sign of a pathologic state, usually a failing or hypertrophic left ventricle, as in systemic hypertension, severe valvular aortic stenosis, and hypertrophic cardiomyopathy. The sound occurs just after atrial contraction at the end of diastole and immediately before S1, producing a rhythm sometimes referred to as the “Tennessee” gallop where S4 represents the “Ten-” syllable. It is best heard at the cardiac apex with the patient in the left lateral decubitus position and holding his breath. The combined presence of S3 and S4 is a quadruple gallop, also known as the “Hello-Goodbye” gallop. At rapid heart rates, S3 and S4 may merge to produce a summation gallop, sometimes referred to as S7.
Atrial contraction must be present for production of an S4. It is absent in atrial fibrillation and in other rhythms in which atrial contraction does not precede ventricular contraction.
Ejection Systolic Sounds
The ejection systolic sounds are heard during the early part of ventricular systole. These sounds are generally high pitched and best audible with the diaphragm of the stethoscope. They can be valvular or vascular in origin.
Valvular ejection sounds
These are the systolic sounds that are audible in patients with defects in aortic or pulmonary valves. They are present in early systole after the S1. The aortic ejection sound is best audible at the apex or the aortic area. The pulmonary valve ejection sound is best audible at the pulmonary area.
The aortic valvular ejection sound is associated with bicuspid aortic valves and aortic regurgitation. Pliable valves generate a higher-intensity ejection click. The intensity of the ejection click decreases with increased valvular calcification. Thus, the aortic ejection click may be absent in severe calcific AS. The ejection click is also absent in supravalvular or subvalvular AS. The presence of an aortic ejection sound, in the absence of other signs of AS, strongly suggests the presence of a bicuspid aortic valve.
The pulmonary valvular ejection sound is predominantly associated with pulmonary valvular stenosis. Unlike most right-sided sounds, the ejection click of PS is decreased in intensity with inspiration. One of the proposed mechanisms is a rapid opening of the valve from the closed position with expiration, giving rise to the high-intensity sound. With inspiration, the rapid jet from the right atrium can partially open the pulmonary valve during diastole; thus, the opening of pulmonary valve with the onset of RV systole is more gradual, leading to decreased intensity of the sound.
Vascular ejection sounds
These sounds are produced at the aorta or pulmonary artery.
The aortic vascular ejection sounds are associated with aortic sclerosis with tortuous aortic root, systemic hypertension, ascending aortic aneurysm, and aortic root dilatation. This sound is usually audible at the aortic area and is not well transmitted to the apex.
The pulmonary vascular ejection sound is associated with pulmonary hypertension and pulmonary arterial dilatation. It is best audible at the left second and third intercostal area.
Nonejection systolic click
This is associated with mitral or tricuspid valve prolapse. Of the two entities, MVP is more common. Refer to the audio example below.
The nonejection systolic click is a high-pitched systolic sound that follows S1 and is heard best at the apex (MVP) or the tricuspid area (tricuspid valve prolapse) with the diaphragm of the stethoscope. The interval between S1 and the prolapse click may vary depending on the volume status of the respective ventricles, as the prolapse occurs at a specific ventricular volume. Thus, if the end-diastolic volume of the ventricle is increased, as can happen with bradycardia, in the supine position, or during hand grip or squatting, the S1 -prolapse interval is increased.
Similarly, if the end-diastolic volume is decreased, as can occur in tachycardia, upon standing up, and during the Valsalva maneuver, the S1 -click interval decreases. This time-based variation can help identify the click of mitral or tricuspid prolapse from other heart sounds.
The production of murmurs results from turbulent flow across valves. Three main factors have been attributed to cause a murmur: (1) high flow rate through normal or abnormal orifices, (2) forward flow through a constricted or irregular orifice or into a dilated vessel or chamber, and (3) backward or regurgitant flow through an incompetent valve.
When evaluating a heart murmur, it is important to know the timing of the murmur in the cardiac cycle, the location, the duration, character, configuration, radiation, aggravating maneuvers, and diminishing maneuvers.
Recognizing the periodicity of murmur helps to narrow the differential diagnoses and often guides further diagnostic evaluation. For example, all diastolic murmurs and any systolic murmur above grade 2 in severity requires further evaluation with echocardiography.The timing of the murmur is determined by palpating the carotid pulse while listening to the murmur. The carotid upstroke corresponds to the onset of systole.
The factors to focus on while evaluating a murmur are discussed briefly below.
Intensity: The intensity of the murmur depends on the volume of blood flow across the valve and the pressure gradient across which the blood flow occurs. The intensity is graded into 6 different grades, as follows:
- Grade I – Heard in a quiet room by an expert examiner
- Grade II – Heard by most examiners
- Grade III – Loud murmur without thrill
- Grade IV – Loud murmur with a thrill
- Grade V – Thrill with a very loud murmur audible with stethoscope placed lightly over the chest
- Grade VI – Thrill with a very loud murmur audible even with the stethoscope slightly away from the chest
The grade of the murmur is important, as any diastolic murmur and a systolic murmur above grade II/VI in severity warrants echocardiographic evaluation as per ACC/AHA guidelines.
Timing: Depending on when they are best heard in the cardiac cycle, the murmurs can be systolic (holosystolic, early/middle/late systolic), diastolic (early/middle/late) or continuous (ie, present in both systole and diastole).
Location: This is the area of the heart where the murmur is heard the loudest. While auscultating, one should concentrate on the apex, pulmonary area, tricuspid, and aortic areas, in addition to the axilla, base of the heart, and left fourth ICS for evidence of radiation of murmur.
As shown in Table 3, the location and timing help in determining whether the murmur is arising from the right or the left side of the heart. In addition, the position can help in locating the involved valves.
Quality/character: Different murmurs have different qualities, such as harsh, blowing, rumbling, musical, or cooing. See Table 3.
Pitch: This can be high or low pitched depending on the frequency of the murmur. The high-pitched sounds are best audible with a diaphragm and the low-pitched sounds with the bell.
Radiation: Murmurs tend to radiate to certain specific areas that are often characteristic of a particular murmur. The murmur of MR radiates to the axilla or base of the heart, depending on which leaflet is involved. In the case of AS, the murmur radiates in the direction of the jet of turbulent blood (ie, radiates to the carotids). Similarly, the aortic regurgitant murmur tends to radiate along the left sternal border.
Configuration: This corresponds to the shape of murmur intensity over time. It can be a plateau, decrescendo, crescendo-decrescendo, or crescendo murmur.
Dynamic auscultation involves certain specific maneuvers that affect the blood flow through the valves and can aid in recognition and differentiation of heart murmurs.
Inspiration: Inspiration leads to a decrease in the intrathoracic pressure with an increase in venous return to the right side of the heart. The murmurs generated from the right side of the heart increase in intensity with inspiration.
Expiration: Expiration has the opposite effect as inspiration. There is an increase in the intrathoracic pressure and a decrease in venous return to the right side of the heart. Blood in the lung is “forced” into the left heart. Hence, murmurs arising from the left side of the heart become more prominent with expiration.
Standing up: This causes a peripheral pooling of blood and a net decrease in venous return. Most murmurs are thus decreased in intensity upon standing, except that of hypertrophic obstructive cardiomyopathy (HOCM) and MVP, which become more prominent.
Squatting: Squatting causes an increase in the afterload and venous return (ie, preload). The net effect is an increase in intensity of all the murmurs, except those associated with MVP and HOCM, which become less prominent with squatting.
Straight leg raising: Passive straight leg raising increases venous return (ie, preload) and has an effect similar to brisk squatting. All murmurs increase in intensity except those of HOCM and MVP, which decrease in intensity with this maneuver.
Hand grip: Hand grip is a form of isometric exercise and increases the afterload, arterial pressure, LV volume, and LV pressure. The net effect of these changes is complex and variable. Murmurs of MR, AR, and VSD worsen with hand grip, while those of HOCM and MVP become less prominent.
Valsalva maneuver: Valsalva maneuver involves asking the patient to strain, which increases the intrathoracic pressure, thus causing a net decrease in preload. Most heart murmurs decrease in intensity with Valsalva, except those of HOCM and MVP, which become more prominent.
Amyl nitrate inhalation: Amyl nitrate is an arteriolar vasodilator and initially causes decreased afterload followed by reflex tachycardia. During the initial phase, because of reduced afterload, the murmurs of AR, MR, and VSD diminish, while those of AS are accentuated. Later on, during the tachycardic phase, the murmur of MS is accentuated.
The opening snap (OS) is a high-pitched diastolic sound produced by rapid opening of the mitral valve in MS or tricuspid valve in TS. When mitral in origin, it is best heard at the apex following the aortic sound A2, with the patient in left lateral decubitus position.
The time difference between the A2 and OS has a diagnostic implication. The closer the OS is to A2, the more severe the stenosis. The OS signifies the time moment when the left atrial pressure exceeds the LV diastolic pressure and marks the beginning of blood entry into the LV from the LA. The more severe the stenosis, the greater the LA pressure and the lesser the LA-LV early diastolic pressure gradient, leading to an early opening of the respective valve. In general, the relation between A2 and the OS depends on LV pressure at A2 closure, LA pressure at A2closure, and the rate of LV pressure decline.
The A2 -OS interval can be increased despite severe MS in patients who have systemic hypertension with an early closure of AV.
TS usually occurs in association with MS, and, as such, the findings are generally obscured by the findings of MS.
Heart and breath sounds:
Listening with skill
Listening to heart and lung sounds is a routine—but challenging—part of your patient care. Even in the best circumstances these sounds can be difficult to hear. In addition, heart sounds last slightly more than 0.10 seconds, and their pitch begins at the lowest level detectable by the human ear.1 Knowledge of technique, which I will cover here, and frequent practice will sharpen your ear.
Let’s start with preparation. Before you even place your stethoscope on your patient’s chest, you want as much quiet as possible. First, explain what you’re going to do and make sure the patient is comfortable before you begin. If a television is on in the room, turn the volume off. If there’s a lot of noise in the hallway, close the door. You may need to do this anyway to ensure privacy during the exam.
Use a stethoscope with a bell and a diaphragm. (If your stethoscope is electronic, it will have bell and diaphragm modes that you can alternate between with the press of a button.) The bell is best suited for hearing low-pitched sounds, and the diaphragm for high-pitched sounds. The ear pieces—no matter what type of stethoscope you are using—should fit snugly and align with the angle of your ear canals.
To avoid transmission of extraneous noise, be sure to remove any item you may have hung on your stethoscope. (Avoid the habit some nurses have of using their stethoscope to hang rolls of tape, tourniquets, or a hospital badge.) Then, expose the patient’s chest and place the head of the stethoscope directly on the skin instead of listening through the patient’s gown. Stand at the patient’s right side with the stethoscope tubing extended across the chest. Make sure that the tubing is not touching the chest or resting on the sheets or side rail.
You may begin auscultation at the top (base) of the heart and proceed down to the apex, or follow the reverse order, listening first at the apex and proceeding up to the base. Either approach is acceptable; what is important is that you use the same approach for the entire exam. Here, I’ll describe the base-to-apex approach.
Start with the patient supine with the head of the bed elevated 30 degrees. Auscultate all areas first with the diaphragm. To begin, place it firmly against the right side of the chest in the second intercostal space close to the sternum. Then move to the left side and listen in the same space at the left sternal border. Continue down the left sternal border, auscultating in the third and fourth intercostal spaces. Finish by auscultating the apex, which is usually found in the fifth left intercostal space just below the nipple—the midclavicular line.
Repeat the sequence, using the bell of the stethoscope. When you position the bell, use just enough pressure to create a seal between it and the skin. Exerting greater pressure than that will stretch the skin across the bell, creating a diaphragm and thereby reducing your ability to hear low-pitched sounds.
Identifying sounds in systole and diastole
At each auscultation point, concentrate first on identifying the primary heart sounds—S1and S2. These are best heard with the diaphragm. S1 coincides with closure of the mitral and tricuspid valves and the beginning of ventricular systole. It’s most intense over the apex. S1 is a lower-pitched, more pronounced sound than S2.
S2 indicates closure of the aortic and pulmonic valves and the onset of diastole. It’s best heard in the second intercostal space at the right sternal border. S2 is higher-pitched than S1 and has a clipped, closing sound.
In patients with normal heart rates, diastole is a few hundredths of a second longer than systole, making it easier to identify S2. However, diastole shortens with tachycardia, and this difference disappears, making it more difficult to distinguish between S1 and S2 in a tachycardic patient. When that’s the case, continue to auscultate and place the index finger of your free hand on the patient’s carotid artery. Lightly palpate the pulse. S1 is the sound you’ll hear at the same time you feel the pulse.4
After you’ve identified S1 and S2, shift your focus to detecting extra heart sounds. When you do hear one, note when it occurs in relation to S1 and S2. If the extra sound follows S1or S2 very closely, you may actually be hearing a splitting of that heart sound.
Remember S1 and S2 coincide with the closure of two valves, each of which produces its own sound. The closures of the mitral valve (M1) and of the tricuspid valve (T1 ) usually occur so close together that the human ear is able to detect only one sound, S1.
But a delay in tricuspid valve closure may leave enough time for the ear to hear M1 and T1separately. A split S1 is best heard in the fifth intercostal space at the left sternal border. It’s an uncommon sound, but can occur in patients with right bundle branch block.
Aortic (A2) and pulmonic (P2) valve closures produce S2. Delayed pulmonic valve closure can occur during inspiration because venous return—blood coming into the right side of the heart—increases with inspiration. This increase in volume prolongs right ventricular systole and thus delays pulmonic valve closure, producing a split S2. During expiration venous return falls, so there’s no delay in P2 closure and the split disappears. This kind of splitting is a normal or physiologic finding.
In some cases, though, a split S2 may be abnormal. A wide gap between A2 and P2 can occur with right bundle branch block. A split S2 heard during expiration is called a reverse, or paradoxical split. It’s associated with left bundle branch block, ventricular pacing, advanced left ventricular failure, and aortic stenosis. A fixed split—one heard on both inspiration and expiration—occurs with atrial septal defects (ASD). S2 heart sounds are best heard in the second and third intercostal spaces along the left sternal border.
An S3 heart sound also comes very soon after S2, occurring early in diastole as the mitral and tricuspid valves open and blood rushes into the ventricles. An S3 is normal in children and young adults, especially women and patients with a thin build. In those over 40 years of age, however, S3 is an abnormal finding indicating ventricular dysfunction. In this case blood from the atrium is trying to enter a ventricle that wasn’t completely emptied in the previous contraction.
Because it’s an early diastolic sound, S3 can be difficult to distinguish from a physiologic S2 split. However, unlike a split S2 sound, an S3 remains constant during the respiratory cycle. Its pitch is softer and best heard with the bell. An S3 heard at the apex is one of the first clinical findings in left ventricular failure. An S3 in the third to fifth intercostal spaces at the right sternal border indicates right heart failure.5
An S4 is heard just before S1, making it a late diastolic sound. It occurs when atrial contraction pumps volume into a stiff, noncompliant ventricle. You’ll most often hear an S4in a patient with a condition that causes left ventricular hypertrophy, such as hypertension or aortic stenosis. Compliance can also be affected by ischemia, so you may also hear an S4 in a patient who’s recently had an MI. You won’t hear an S4 in a patient with atrial fibrillation, however, because in this case there’s no atrial contraction.
Like S3, S4 is best heard with the bell at the apex. When you have difficulty hearing these sounds, try turning the patient toward his left side. This maneuver brings the heart closer to the anterior chest wall and thus improves sound transmission.
Listening for murmurs
Murmurs are sounds created by turbulent blood flow. They can occur at any time during the cardiac cycle. When you detect a murmur, you need to listen for a minute or more to determine its characteristics—the timing, pitch, quality, intensity, and pattern. You’ll also want to identify where you hear it the loudest and if the sound radiates to other areas.
To establish timing, focus on whether you hear the murmur continuously, during systole (after S1 and before S2) or during diastole (after S2 and before S1). When the murmur is confined to either systole or diastole, determine whether you hear it at the beginning (early), middle (mid), or end (late).
Systolic murmurs typically fall into two categories: mid-systolic and holosystolic (or pansystolic). A mid-systolic murmur begins after S1 and concludes before S2. You should notice a distinct gap between the two heart sounds and the murmur. Pay particular attention to the gap before S2. It will help you to distinguish a mid-systolic murmur from a holosystolic murmur, which is heard immediately after S1 and right up to S2 without any pauses.
Once you’ve established its timing, shift your focus to the murmur’s actual sound. Is it high-pitched, low-pitched, or somewhere in between? How would you describe its quality? Is it harsh or musical? Rumbling or blowing? What is its intensity? Do you have to really concentrate to hear a faint sound? Or do you notice the sound as soon as you put your stethoscope on the chest?
Murmurs are graded on a six-point scale. In a grade I murmur, the sound is barely audible, whatever the patient’s position. A grade II murmur is faint; a grade III is moderately loud, and a grade IV is somewhat louder and may be accompanied by a thrill. A grade V murmur is loud enough to be heard with the stethoscope held just above the chest wall. It is accompanied by thrills, as is a grade VI murmur, which is so loud that you can hear it without a stethoscope.6
Listen also for a particular pattern or shape to a murmur. Some murmurs begin softly and then become louder (crescendo). Others start out very loud and then taper off (decrescendo). You may also hear a murmur that combines the two patterns just described. It will start off softly, grow increasingly louder until it peaks, and then taper off (crescendo-decrescendo). Lastly, you may find the murmur does not change at all, making it a plateau murmur.
After you’ve established these characteristics, concentrate on the murmur’s location. Where do you hear it best? Is it most noticeable at the apex or in the second or third intercostal space? Does the sound travel or radiate to the neck, back, or axilla? The answers to each of these questions will help you hone in on the murmur’s possible cause.