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This article focuses on the practical use of the stethoscope. The art of the cardiac physical examination includes skillful auscultation. The article provides the author's personal approach to the patient for the purpose of best hearing, recognizing, and interpreting heart sounds and murmurs. It should be used as a brief introduction to the art of auscultation. This article also attempts to illustrate heart sounds and murmurs by using words and letters to phonate the sounds, and by presenting practical clinical examples where auscultation clearly influences cardiac diagnosis and treatment. The clinical sections attempt to go beyond what is available in standard textbooks by providing information and stethoscope techniques that are valuable and useful at the bedside.
THIS article focuses on the practical use of the stethoscope. The art of the cardiac physical examination includes skillful auscultation. Even in an era of advanced easily available technological bedside diagnostic techniques such as echocardiography, there is still an important role for the hands-on approach to the patient for the purpose of evaluating and reassessing cardiac status. Knowing the cardiac history, monitoring the pulse and blood pressure, and listening to the heart and lungs are integral parts of nursing care. Proper use of the stethoscope is still relevant and important to patient care. This article provides the author's personal approach to the patient for the purpose of best hearing, recognizing, and interpreting heart sounds and murmurs. It should be used as a brief introduction to the art of auscultation. Although there are many excellent audiovisual aids to auscultation, the cardiac examination should be honed and mastered at the bedside. This article also attempts to illustrate heart sounds and murmurs by using words and letters to phonate the sounds, and by presenting practical clinical examples where auscultation clearly influences cardiac diagnosis and treatment. We begin by discussing proper stethoscope selection and use.
It has been stated that proper auscultation of the heart depends less on what is around the ears and more on what is between the ears. Nevertheless, there are certain easily recognized features that make a stethoscope more capable of transmitting heart sounds to the ears.
The cardiac stethoscope requires both a bell and a diaphragm to transmit the full spectrum of heart sounds. The difference between the two is that the bell allows low-frequency sounds. The diaphragm filters those out when necessary. Both are used as needed to allow detection of all auditory aspects of heart sounds and murmurs.
There are cardiac stethoscopes that do not have a bell. The bell effect is created by light pressure on a specially designed stethoscope diaphragm. When the stethoscope was first invented, there was no diaphragm, just a bell. The diaphragm effect could still be created by firm pressure on the skin to stretch it, resulting in a makeshift temporary diaphragm. We still use this bell-push technique in every patient. Examples for using the bell and the diaphragm appropriately are presented in subsequent sections.
Electronic stethoscopes can change filter frequency settings to toggle between bell and diaphragm modes. New electronic stethoscopes with ambient noise reduction such as the Littmann Model 3000 (Fig 1) reduce distracting ambient noise through noise cancellation rather than just filtering, so the heart sounds remain unaffected and can actually be selectively amplified.
Tubing should be kept comfortably short (to better hear high-pitched heart sound components). The tubing should remain long enough to allow a comfortable listening posture. This is determined to some degree by the listener's height, arm length, ability to bend the lower back, and degree of personal willingness to lean over patients from the right side.
Because of the anatomy of the ear canal, the angle of direction of earpieces is very important. The external ear canal travels toward the eardrum at an anterior angle. A good stethoscope has angled earpieces to allow easy adjustment of this angle to permit forward tilting to align with the external ear canal and to create a complete seal that excludes ambient noise. A good habit to try to optimize this angle at the onset of auscultation consists of moving the head up and down in an exploratory manner while listening for improved audibility of heart sounds. Carrying a stethoscope around by stuffing it into a laboratory coat pocket may change and misalign this critical angle.
Earpieces should feel comfortable. The fit should be snug without causing discomfort when used for prolonged periods of time. An earpiece can be too large, allowing ambient noise to enter. It can also be too small, too soft, or applied with too great a pressure-making it rest too deeply in the ear canal, with the earpiece aperture partly or even completely occluded. A common mistake is to choose earpieces that are too small and enter too far. The ear canal should be occluded, not invaded. Larger, looser-fitting earpieces can be made to fit more snugly during auscultation, if needed, by pressing the arms of the stethoscope together with the free hand. Listening from the right side of the patient keeps the stethoscope in a relatively straight line from the ears to the chest.
The stethoscope is a medical tool. As such, it should be kept clean and regularly disinfected to prevent spreading infection from patient to patient. Earpieces should be periodically inspected for cracks and for earwax accumulation. Tubing should also be visually inspected for cracks on a routine basis. Leaks in the tubing due to cracks can also be detected by blowing into one earpiece while the other is obstructed. The absence of leaks can be further sought by abruptly breaking the seal of the stethoscope bell with the skin during routine auscultation. Rapid removal of the bell should elicit a pressure sensation in the ear when the tubing is intact.
As a rule, the bell is held lightly, and the diaphragm is pressed firmly against the skin of the chest wall. The examiner should become adept at applying the stethoscope bell with as little pressure as possible. The pressure should be no more than what is required to create a seal to exclude ambient noise. This enhances the faint low-frequency vibrations from ventricular and atrial gallops. As already mentioned, firm pressure with the bell makes the stethoscope behave like a diaphragm by stretching the skin and making it filter heart sounds in the way a rigid diaphragm does-by damping vibrations. The high-pitched murmurs of aortic regurgitation and some cases of mitral regurgitation are better heard with the use of the diaphragm to filter out the low-frequency components of other distracting heart sounds. The diaphragm is pressed very firmly against the skin for this purpose.
The room should be made as quiet as possible. Ambient noise must be minimized. High ambient noise levels and intermittent loud sounds from speech or electronic equipment interfere significantly with auscultation. Faint sounds are masked by louder sounds. The loud sound does not even have to coincide with the faint sound. The ear instinctively tunes to the louder sound and ignores the fainter sound. Proper auscultation technique requires listening to one thing at a time. Faint sounds require concentration. They should be listened to (without loud distractors) for as long as necessary. This allows the ear to become attuned to the full intensity of that particular sound level. Sometimes it also helps to close one's eyes. Auscultation cannot be a hurried examination. The period of time necessary for proper examination will (hopefully) progressively decrease with experience. Electronic stethoscopes with ambient noise reduction are also available. They may dramatically improve the diagnostic yield of an auscultatory examination in a noisy environment such as a moving ambulance, or a busy emergency department.
The patient is usually approached from the right side and the cardiac examination always begins with proper positioning of the patient. The patient should be positioned, and the examination bed or table should be adjusted to allow sequential examination of the patient in the sitting, recumbent, and left lateral decubitus positions. Sitting positions include upright, reclining back at an approximately 45 degree angle, and any other angle that optimizes neck vein inspection. Additional patient positions during advanced dynamic auscultation may include standing and squatting, face down on the bed, and leaning forward while standing or sitting. Both the examiner and the patient must be comfortable. Room temperature should be appropriate for the patient's state of dress. The patient should be properly gowned so that the skin of the chest wall can be reached by the examiner without having to fumble with the patient's clothing. Proper auscultation should not be done through clothing. The stethoscope should be applied directly on the skin. Lighting should be available to cast tangential shadows on the skin of the right side of the neck so that internal and external jugular veins can be inspected while simultaneously listening to the heart.
Inspection of the patient should precede auscultation since there are many visual clues to the presence, extent, and nature of heart disease. Once auscultation begins, it may be useful to close the eyes temporarily to improve auditory concentration. During the rest of the time the eyes should be trained on the right side of the neck where the jugular venous pulsations are best seen.
Inspection of the jugular venous pulsations helps in the timing of heart sounds and murmurs. In the normal patient the most prominent jugular venous upstroke is the A wave. The A wave is produced by right atrial contraction and becomes visible just before the first heart sound is heard with the stethoscope.
Venous neck pulsations must be differentiated from arterial pulsations. Venous pulses are weak, not palpable. Venous pulses are obliterated by pressure at the base of the neck, altered by changes in body position, and affected by respiration and by pressure on the abdomen (hepatojugular reflux).
The carotid upstroke should be used to time systole and to characterize the pulse as normal, weak and delayed, bounding, shuddering, or multicomponent.1
Palpation of the right carotid arterial pulse should also be performed from the patient's right side. It can be done comfortably by using the examiner's left thumb when the left hand is free. When the right hand is free, the left carotid pulse is palpated with the examiner's right index and middle fingers. The carotid upstroke is felt after one hears the first heart sound and before one hears the second heart sound. It is a good method to time systole. The radial artery should not be used to time the cardiac cycle during auscultation because there is a delay before the pulse arrives at the radial artery. In the intensive care unit, electrocardiographic monitoring equipment may be set to sound a beep to mark the QRS of the patient. This beep is also a marker of systole and should be audible simultaneously with the carotid upstroke.
The normal carotid pulse is felt in systole, after the first heart sound is heard, and before the second heart sound is heard. A weak and delayed (parvus-et-tardus) pulse is palpated in patients with aortic stenosis. There may also be a palpable shudder (called a thrill) in the pulse of these patients. A bounding pulse is felt in hypertension, aortic regurgitation, or patent ductus arteriosus. A 2-component systolic pulse is called a bisferiens pulse.
A triple-sensory (not for the southpaw) approach to the patient consists of visual information from the neck, auditory information from the stethoscope, and tactile (palpation) input from the free hand which is not holding the stethoscope. To place the stethoscope on the chest at the point of maximal impulse, one would find the impulse with the right hand, hold the stethoscope with the left hand, and place it directly over the impulse felt with the right hand. Once the stethoscope is properly positioned with the left hand over the palpating right hand-it is possible to change the stethoscope from left hand to right hand. The right hand can then vary the pressure exerted by the stethoscope and further fine-tune the position of the already properly positioned chest piece. The eyes of the examiner continue to observe the venous neck pulsations throughout this entire process.
Auscultation should be systematic, with a consistent approach from patient to patient. One goal of the experienced examiner (while remaining methodical) is to identify memorable auscultatory features that are unique to the patient (much the same way that one recognizes the voice of a long-lost acquaintance on the phone).
A systematic approach requires that heart sounds should be identified first and murmurs should initially be ignored. The number of heart sounds per cardiac cycle is readily determined. Triple rhythms (more than 2 heart sounds per cycle) are thus identified early in the cardiac assessment. Respiratory splitting of the second heart sound, heard at the upper left sternal border, is also identified and characterized early in the examination.
The listening sequence can begin at the point of maximal impulse at the cardiac apex, or at the upper right sternal border. The stethoscope is then walked up and down the left sternal border. The neck, clavicles, and other parts of the chest are also an integral part of the auscultatory examination. Sometimes the heart sounds are distant and difficult to hear but are still transmitted to the bones. Listening with the diaphragm over the right clavicle may be very rewarding in such cases. An amplifying electronic stethoscope is also quite useful in such cases.
Hearing should be selectively tuned for one auscultatory feature at a time. The rationale is the same as when listening to an orchestra playing. After an initial overall impression of sound, it is necessary to selectively tune in to an individual instrument to truly appreciate it.
Distant, faint heart sounds may be heard better by asking the patient to exhale. It should be kept in mind, however, that held expiration affects some auscultatory findings. Deep inspiration followed by slow deliberate exhalation may slow the heart rate briefly, prolonging the cardiac cycle and thus providing more time to listen to a particular murmur. Some subtle auscultatory findings such as rubs, gallops, and rumbles are transient and may only be heard briefly during a few cardiac cycles immediately after turning the patient on his or her left side.
Patients with barrel chests due to lung disease can be positioned semi-sitting and the stethoscope can be applied in the subxiphoid region. An electronic stethoscope with ambient noise reduction may dramatically improve tone and clarity of heart sounds in a noisy environment.
The first and second heart sounds actually sound quite different. The first sound is longer and lower pitched. The second sound is shorter and higher pitched. The loudness of heart sounds changes with location. The second heart sound is louder at the base (upper right and left sternal borders). The first heart sound is louder at the apex. This phenomenon is made most obvious by putting the patient in the left lateral decubitus position, finding the point of maximal impulse, putting the diaphragm there, and then comparing the relative loudness of the first and second heart sounds by alternatively listening back and forth between the apex and the base.
At slow heart rates, systole is noticeably shorter than diastole. Consequently, the second heart sound follows the shorter pause, while the first heart sound follows the longer pause.
The first heart sound (S1) marks the end of diastole and the beginning of systole. It is heard at the time that the mitral and tricuspid valves are closing.2 The systolic carotid upstroke becomes palpable after (never before) S1 is heard. S1 is produced predominantly by mitral leaflet closure (M1). valve closure (contributing to S1-making it M1T1) can be heard best at the lower left sternal border. Tricuspid closure closely follows the mitral component. This combined first heart sound is slightly longer in comparison to the shorter and sharper second heart sound. In other words, S1 is longer and also lower pitched compared to S2. S1 may sound single, or closely spilt (reduplicated). The degree of reduplication of S1 does not change with respiration.
The examiner should become proficient in distinguishing S1 from S2 and in recognizing changes in loudness of S1. The intensity of S1 is affected by the atrioventricular (AV) conduction interval. Patients with short AV intervals have a loud first heart sound. This is illustrated in patients with the short PR interval of Wolff-Parkinson-White syndrome. In a patient with a short PR interval, the first heart sound is loud owing to the short time interval between maximal mitral leaflet opening (after the P wave) and mitral leaflet closure (after the QRS). S1 is also loud in mitral stenosis.
S1 is soft in patients with a long PR interval and delayed atrioventricular conduction. S1 is produced when ventricular pressure rises rapidly during systole, exceeding the respective atrial pressures, and closing the AV valves. In patients with heart failure, S1 may be soft or inaudible owing to a slower rate of ventricular pressure rise in systole. In patients with left heart failure, S1 may be inaudible where it is usually heard the best-at the apex. In such patients a simple stethoscope maneuver may be very rewarding. The diaphragm is pressed firmly at the apex while paying attention to the intensity of S1. It is then pressed firmly at the left lower sternal border, again selectively listening to S1. This alternating placement of the stethoscope is repeated as many times as necessary. In the normal patient, S1 will be louder at the apex (the so-called mitral area). In this same normal patient, at the left lower sternal border (the so-called tricuspid area) S1 may be reduplicated (closely split mitral and tricuspid components), slightly longer (owing to the presence of both mitral and tricuspid components), but not louder. If S1 is louder, or only present at the left lower sternal border, the inference is that the mitral component of the first heart sound is decreased and the examiner is mainly hearing the tricuspid component of S1.
The intensity of S1 is variable in patients with atrial fibrillation, and in those with a variable PR interval such as complete heart block and Wenckebach second-degree heart block. Although the intensity of the first heart sound varies to some degree in most patients with atrial fibrillation, it may be difficult to ascertain that this indeed is the case with rapid "irregularly irregular" heart sounds. The following technique for eliciting variable intensity of heart sounds should be practiced and honed in patients with atrial fibrillation and a slow ventricular response. It also works well in patients with complete heart block since the ventricular rate is usually slow. This approach for detecting variable intensity of the first heart sound consists of sliding the stethoscope away from the area of maximal intensity to the point where the first heart sound is completely inaudible. The extreme of "variable intensity" is "audible S1 alternating with inaudible S1" and is a good way to start learning to recognize variable intensity of heart sounds. It is easier to detect a first heart sound that actually disappears completely and returns intermittently. The examiner should progressively distance the stethoscope from S1 so that it becomes fainter and fainter and eventually becomes inaudible. In patients with variable intensity, there will be a spot along this stethoscope path where S1 "comes in and out" during different cardiac cycles. Once the ear is trained, it will become easy to detect more subtle variations in the intensity of heart sounds.
For the author, the auscultatory anchor-point to auscultation is actually the second, rather than the first, heart sound. This is done by identifying the second heart sound and "anchoring" the timing of everything else to this sound. Our reasons for using and teaching this approach are explained below.
The second heart sound has been called the key to heart disease.3 For us, it is also the key to beginning the auscultatory examination. The aortic component of the second heart sound originates from aortic valve closure. In the normal patient it is easily heard and identified at the upper left sternal border. Furthermore, it is widely transmitted and is usually audible in all the important auscultatory areas of the chest and neck. The second heart sound is sharper and shorter than the first heart sound and can become easily recognizable with practice. Phonating the first and second heart sounds as "lub" and "dup," respectively, illustrates that difference.
The beginning "stethoscopist" should become thoroughly familiar with the second heart sound by listening to as many different patients as possible. As mentioned, in addition to "sharper and shorter," the second heart sound is widely transmitted across the chest and should be listened to at the upper right sternal border, upper left sternal border, lower left sternal border, and in the apical left lateral chest area.
At the upper right sternal border, the second heart sound is usually louder than else on the chest and it is single. It is single there, because at the upper right sternal border, all one hears is aortic valve closure. The aortic valve is very close to the stethoscope, which is why the second heart sound is louder there than anywhere else on the chest.
At the upper left sternal border, the second heart sound may be split. This may be mimicked by saying the word "butter" (the splitting is the "ter" in butter). The splitting is called reduplication. The second heart sound is reduplicated at the upper left sternal border because in addition to aortic valve closure, one may also hear pulmonic valve closure. At the upper left sternal border-the pulmonic valve is very close to the stethoscope.
The lower left sternal border and the apical left lateral chest area are best for transmitted tricuspid and mitral valve closure sounds, respectively. Fortunately, the aortic component of the second heart sound (A2) is heard there as well. Thus, one can usually hear both the first and second heart sounds at the lower left sternal border and at the apical left lateral chest area.
The third heart sound, also called S3 gallop, ventricular gallop, or protodiastolic gallop, is a low-frequency sound that is best heard with the bell of the stethoscope held lightly against the skin. It is frequently present in healthy children and healthy young adults, and may be referred to in these cases as a physiologic S3. The physiologic S3 disappears by age 30 at the latest. The finding of an S3 in older adults is usually ominous and is typically associated with decompensated systolic heart failure.4 It may disappear after medical treatment. An S3 may be heard without heart failure in patients with diastolic volume overload. This may be due to hemodynamically significant mitral regurgitation. Congenital heart defects that cause left to right shunts may give rise to an S3 owing to torrential early diastolic blood flow into the left ventricle. For example, patent ductus arteriosus, atrial septal defect, and large ventricular septal defects can all have an S3 in addition to their other auscultatory features.
Loud early diastolic sounds are not gallops.5 The stenotic mitral valve opens with a loud sound early after S2. This is the opening snap (OS) of mitral stenosis. As mitral stenosis progresses, left atrial pressure rises and the opening snap moves closer to S2. In other words, the S2-OS interval gets shorter with worsening mitral stenosis. There may be an identical-to-the-ear, loud, early diastolic sound in patients with a left atrial myxoma. This pedunculated large tumor abruptly stops short (restrained by the stalk) in early diastole on its path toward the mitral orifice, creating a halting sound that is called a tumor plop.
Finally, patients with constrictive pericarditis due to thickened or calcified pericardium may develop an early to middiastolic sound owing to abrupt cessation of ventricular filling. This is termed a pericardial knock.
An echocardiogram can easily allow distinction between a snap and a plop. The thick, hockey-stick-shaped stenotic mitral valve is easily distinguished from a large left atrial tumor using echocardiography. On the other hand, pericardial constriction should be sought by searching for physical signs in addition to ordering imaging studies such as echocardiograms, chest computed tomographic scans, and cardiac magnetic resonance imaging. Patients with constrictive pericarditis may exhibit dramatic abnormalities in jugular venous pulsations, the pericardial knock may change in loudness with standing and squatting (louder on squatting), and there may be systolic retraction of the apical impulse.
The fourth heart sound is also called an S4 gallop, atrial gallop, or presystolic gallop. It requires active late diastolic left atrial contraction. The priming booster-pump action of left atrial contraction may cause an audible low-frequency sound in clinical situations with diastolic dysfunction. The S4 sound is caused by tensing of the left ventricular myocardium and mitral valve apparatus. Important clinical examples include uncontrolled hypertension and acute myocardial infarction. An S4 may also be present in aortic stenosis, hypertrophic cardiomyopathy, and acute mitral regurgitation.
The S4 should be searched for intentionally. Otherwise it may be overlooked even by an experienced examiner. An S4 is best heard with the bell of the stethoscope held lightly against the skin.6 Forceful pressure may obliterate it. Increasing and decreasing the bell pressure during auscultation can help differentiate an S4 followed by S1 from S1 followed by an ejection sound. Both S1 and ejection sounds have high-frequency components that remain audible even when the bell is pressed down. An S4 will become muffled or will completely disappear when the skin is stretched by pushing down on the bell. Some very-low-frequency components of S4 may be palpable at the apex without being audible. The search for an S4 should therefore combine palpation with auscultation. By looking at one's fingers as they palpate the precordium, it may also be possible to see the S4. So an S4 can be heard, felt, and seen in some patients. Owing to the loss of atrial contraction, the S4 disappears with onset of atrial fibrillation. Having the patient cough several times may elicit a previously inaudible gallop.
A right ventricular S4 may be found in conditions with right ventricular diastolic dysfunction. Important clinical examples are pulmonary hypertension and pulmonic valve stenosis. Two important clues help distinguish a right-sided S4: location and respiratory variation. A right-sided S4 is best heard at the left lower sternal border rather than at the apex. A right-sided S4 gets louder on inspiration. A left-sided S4 does not change during respiration but may get fainter on inspiration because of an increase in interposed lung tissue between the stethoscope and the left ventricle.
Murmurs should always be evaluated after the heart sounds. The carotid upstroke or the apical impulse should be used to time the murmurs to decide if they are systolic or diastolic. Systolic murmurs can be simplified into 2 broad categories: ejection quality or not.7 The systolic ejection murmur (SEM) is over diagnosed in patient progress notes. To be ejection quality, the murmur should get progressively louder, reach a peak, and then get progressively softer. Murmurs can be further described as harsh, blowing, or musical.
The loudness of murmurs can be consistently classified by using the following grading system. Grade 1/6 murmurs are barely audible even by experienced examiners under ideal listening conditions. They have been referred to as the "absence of silence." Grade 2/6 murmurs are soft, audible with selective concentration, but may not be immediately apparent during a casual examination. Grade 3/6 murmurs are unmistakable. They are immediately audible on applying the stethoscope, but there is no palpable thrill. The presence of a palpable thrill makes the murmur a grade 4/6 murmur or greater. Grades 5 and 6 are rare. If the stethoscope can be partly lifted off the chest, and the already loud murmur remains audible, the murmur is grade 5/6. Grade 6/6 murmurs are audible with the stethoscope held off the chest. To get transmitted through the air to the stethoscope, these rare 6/6 murmurs can be harsh with low frequencies, which may give them a sound much like the buzzing of a bee, or the clearing of a throat.
A new systolic murmur in the course of acute myocardial infarction may be due to a newly ruptured mitral papillary muscle, or it may be due to ventricular septal rupture. A mitral regurgitation jet directed into the posteriorly located left atrium is highly unlikely to create a palpable anterior precordial thrill along with the murmur. Conversely, the jet of blood traveling from the high pressure posteriorly located left ventricle, through a ruptured ventricular septum into the anteriorly located lower-pressure right ventricle is quite likely to be both palpable and audible (grade 4/6) at the anterior precordium. Simply placing the hand on the chest (to feel for the presence or absence of a thrill) may help distinguish one murmur from the other.
Murmurs in children and adolescents may indicate congenital or acquired heart disease. More often they are innocent murmurs.8 Seven of 10 school-age children can have innocent murmurs on careful auscultation.9 Flow in the pulmonary artery may be audible as a musical vibratory still's murmur.
A systolic-diastolic venous hum is a common normal physiological murmur in children, rare in adults.10 It is due to the torrential downward rush of blood from the jugular veins into the superior vena cava. It may rarely be loud and roaring, with a palpable thrill. It is usually best heard on the right side of the neck, just over the clavicle with the patient sitting. It decreases or disappears when the patient assumes the recumbent position. When the venous hum is also audible at the right sternal border, over the sternum itself, or on the left sternal border, it can be mistaken for the murmur of a patent ductus arteriosus, or for a to-and-fro bellows-like aortic stenosis/regurgitation murmur. As opposed to aortic and ductal murmurs, the venous hum can be dramatically altered by certain maneuvers. It can be obliterated by pressure over the jugular vein above the point of maximal murmur, and can be made to decrease or disappear by changing from the sitting to the supine position. Turning the head to the left will increase the loudness of a right supraclavicular venous hum.
Other innocent murmurs are the supraclavicular bruit, mammary souffle, and cardiorespiratory murmur.
Patients with aortic stenosis invariably have a murmur. The typical murmur of aortic stenosis is systolic, ejection quality (also referred to as crescendo-decrescendo). Ejection murmurs start out soft, get progressively louder as blood flow accelerates across the stenotic valve, and, after reaching a peak intensity, become progressively softer. As the severity of stenosis worsens, the murmur reaches its peak later in systole (Fig. 2).
Patients with bicuspid aortic valves have a loud, early systolic ejection click prior to the onset of the systolic murmur.11 Early systolic ejection clicks should be distinguished from split first heart sounds. ejection sounds are loud and can be phonated as "lubTUK [horizontal ellipsis] dup"(S1TUK [horizontal ellipsis] S2). The "TUK" of aortic ejection occurs later than the tricuspid component of the first heart sound (T1). The aortic ejection click TUK is louder, more widely transmitted, and may be loudest in the mitral area (in spite of its aortic origin). This aortic ejection click does not vary with respiration. Patients with pulmonic stenosis may also have an ejection click. The ejection click of pulmonic stenosis decreases with inspiration, and the intensity of the pulmonic ejection click can vary dramatically during the respiratory cycle.
As the left ventricle becomes hypertrophied, stiff, and noncompliant owing to the aortic valve obstruction, the patient may develop an audible atrial gallop (S4).12 The presence of an atrial gallop in a young patient with aortic stenosis suggests that aortic stenosis is hemodynamically significant. Older patients may have atrial gallops with milder degrees of aortic stenosis because the left ventricle is noncompliant for other reasons-such as coexisting hypertension, or simply just due to the aging process. Conversely, the absence of an atrial gallop at any age makes severe aortic stenosis unlikely.
Left ventricular ejection time may also become progressively prolonged by severe aortic stenosis. The resulting delayed closure of the stenotic aortic valve is manifested on auscultation as paradoxical splitting of the second heart sound. The unaffected P2 is audible earlier than the delayed A2 in expiration. The second heart sound is split on expiration and becomes single on inspiration. This is the opposite of the normal inspiratory splitting of the second heart sound, hence the term paradoxical splitting.
The intensity of A2 decreases with worsening aortic stenosis. When the aortic leaflets become immobile, A2 becomes completely inaudible. The examiner only hears a second heart sound (P2) in the pulmonic area. To demonstrate this, the stethoscope is applied to the upper left and upper right sternal borders in alternating fashion. The second heart sound, in this case, is only heard at the upper left sternal border (pulmonic area). Since A2 is gone, the second heart sound also remains single and does not split with respiration.
While listening to the murmur of aortic stenosis, the patient may have premature ventricular contractions. The listener should compare the loudness of the murmur from beat to beat. The murmur that immediately follows the compensatory pause will be much louder than the previous and subsequent murmurs.
The auscultatory hallmark of aortic regurgitation is a high-pitched, blowing early diastolic murmur. Hearing this subtle murmur in a critical care setting may dramatically influence diagnosis and treatment. A patient with chest pain may undergo transesophageal echocardiography instead of coronary. This murmur begins with the second heart sound, but may quickly taper and fade away. Patients with aortic regurgitation often have a systolic murmur as well. The sometimes loud but nondiagnostic systolic high-flow murmur may distract the inexperienced listener from the subtle but diagnostic diastolic murmur. The examiner may be able to hear the diastolic murmur by having the patient sit, lean forward, exhale, and hold his or her breath. The diaphragm of the stethoscope should be pressed very hard while listening for this murmur on both sides of the upper sternal border.13
Patients with isolated aortic regurgitation may have an obvious systolic flow murmur with a subtle diastolic murmur. The flow murmur may get mistakenly dismissed as a functional innocent murmur if the listener does not hear the diastolic murmur, which is never functional (Fig. 3). Patients with both aortic regurgitation and aortic stenosis may have a harsh systolic murmur along with the diastolic blowing murmur. This combined systolic-diastolic murmur sounds like a bellows and has been called a to-and-fro murmur. The listener should also analyze the heart sounds. A decreased M1 may be due to premature closure of the mitral valve by the jet of acute severe aortic regurgitation. A loud A2 is evidence against a calcified immobile stenotic aortic valve. An ejection click provides evidence for a bicuspid aortic valve. Patients with worsening chronic severe aortic regurgitation may actually develop a decrease in the duration and loudness of their diastolic murmurs. At the same time they may exhibit many prominent physical findings owing to their bounding arterial pulses. The eponyms of these physical findings are listed below.
Corrigan's pulse: prominent pulsations of the carotid arteries
Bisferiens pulse: double systolic arterial impulse-the so-called twice-beating heart
De Musset's sign: head nodding with each heartbeat
Duroziez's sign: systolic and diastolic femoral artery bruit
Hill's sign: accentuated leg systolic pressure with greater than 40 mmHg difference from the brachial artery systolic pressure
Muller's sign: pulsation of the uvula with each heartbeat
Palmar click: palpable systolic flushing of the palms
Quincke's pulse: cyclic reddening and blanching of the nail capillaries
Traube's sign: loud "pistol shot" sound heard over the femoral artery
Water hammer pulse: brisk femoral pulsation similar to that felt with a water hammer-a Victorian toy. The water hammer was a glass tube filled partly with water or mercury in a vacuum. The water or mercury produced a slapping impact when the glass tube was turned over.
One reason for stressing these physical findings in an article on auscultation is that the diastolic murmurs of aortic regurgitation and of pulmonic regurgitation sound the same, but only the murmur of aortic regurgitation will be accompanied by the above physical findings.
The murmur of mitral regurgitation is plateau-shaped. It does not get louder and softer like an ejection murmur. When it is holosystolic, it begins in early systole and remains uniform until it ends with S2. The murmur is typically heard well at the apex and may extend to the left axillary region. Unlike the murmur of aortic stenosis, it does not radiate to the neck. Mitral regurgitation can be present in clinical entities such as mitral valve prolapse, inferior myocardial infarction, dilated cardiomyopathy, and hypertrophic cardiomyopathy.
An alternate name for mitral valve prolapse is a name that describes the auscultatory findings: click-murmur syndrome. In turn, the click of mitral valve prolapse has an alternate name that describes it by what it is not: nonejection click. The term nonejection refers to the timing. Mitral valve prolapse was not described until 1963. Mid-to-late systolic clicks were thought to be extracardiac until Barlow's description of the intracardiac mid-to-late systolic buckling of the mitral valve into the left atrium. This negative name may be thought to imply (wrongly) that a mid-to-late systolic nonejection click is also a noncardiac click.
Ejection clicks have already been discussed. They closely follow the first heart sound and may be the best clinical clue to the presence of a bicuspid aortic valve. In contrast, the nonejection clicks of mitral valve prolapse occur later in systole. The timing of the phonic for the mitral prolapse click (ki) sounds like "look it up"-luh (S1) [horizontal ellipsis] pause [horizontal ellipsis] ki (in mid-to-late systole) [horizontal ellipsis] pause [horizontal ellipsis] tup (S2). The midsystolic click (produced by the prolapsing mitral valve) may be followed by a murmur of mitral regurgitation. Attention to the location of the murmur helps identify the prolapsing leaflet. The mitral regurgitation jet in mitral valve prolapse is directed away from the culprit leaflet. Posterior mitral leaflet prolapse will direct the mitral regurgitation jet to the anterior portion of the left atrium. The murmur in this case of posterior mitral leaflet prolapse will be heard best at the base of the heart at the upper left sternal border. In contrast, the murmur of anterior mitral leaflet prolapse is directed toward the posterior portion of the left atrium. Consequently, the examiner may be surprised by a murmur below the left scapula in patients with anterior mitral leaflet prolapse. Since the heart sounds may not be transmitted to the back along with the murmur, the unsuspecting or inexperienced examiner may dismiss this murmur as breath sounds. The distinction between anterior and posterior leaflet prolapse is clinically important. The operation to repair posterior mitral leaflet prolapse is technically less challenging.
The murmur and click of mitral valve prolapse are dramatically altered by standing and squatting. Standing brings the click closer to S1 and may make it easier to hear separately from S1 and S2. Squatting moves the click closer to S2 but, more importantly for the examiner, increases the loudness of the late systolic murmur.14
Hypertrophic cardiomyopathy is a leading cause of sudden death in the young athlete, so it is important to recognize this murmur. As opposed to the fixed gradient of valvular aortic stenosis, patients with hypertrophic cardiomyopathy have murmurs that are altered in a unique manner by changes in cardiac hemodynamics. A sequence of serial hemodynamic events can occur as outflow to the aorta from the left ventricle becomes hampered by localized ventricular septal hypertrophy below the aortic valve. Left-ventricular ejection is followed by outflow obstruction. This may be followed by mitral regurgitation, which serves to depressurize the outflow obstruction. The sequence of ejection, obstruction, regurgitation can also explain the behavior of murmurs that can be heard in this entity. The left ventricle begins to eject in systole, which may give rise to an ejection murmur. In auscultation terms, the examiner can clearly distinguish the first heart sound as a separate sound before the murmur begins. The hypertrophy of the interventricular septum can create a dynamic gradient in the left-ventricular outflow, making the murmur respond dramatically to dynamic auscultation. Having the patient squat during auscultation will decrease the loudness of the murmur. When the patient stands back up from the squatting position, the murmur becomes much louder. In the squatting position, there is increased venous return to the heart, which increases the left ventricular volume and reduces the degree of outflow obstruction. On standing back up, the left-ventricular volume decreases because of the decreased venous return and also because of the usually increased heart rate. The dynamic nature of the murmur is also exemplified by performing a Valsalva maneuver. In hypertrophic cardiomyopathy, "bearing down" and closing the glottis will increase the intrathoracic pressure and decrease left ventricular volume-increasing the loudness of the murmur.
Acute inferior myocardial infarction can be accompanied by acute mitral regurgitation. In contrast to chronic mitral regurgitation, acute regurgitation into a noncompliant left atrium may create auscultatory evidence of that fact. A loud S4 suggests a forceful atrial contraction. A loud P2 indicates pulmonary hypertension. The murmur of acute mitral regurgitation may be lower pitched ("rumbling") than the typical high-pitched ("blowing") murmur of chronic mitral regurgitation.
In the clinical practice of medicine it is rare for a physical finding alone to make a definitive diagnosis.15 The presence of a pericardial rub on auscultation is sufficient to make the diagnosis of pericarditis. A patient with new-onset chest pain and a pericardial rub on auscultation will not get whisked to the catheterization laboratory from the emergency department, and may get an echocardiogram instead. Pericardial rubs are easy to diagnose when they have all 3 components-two components are heard in diastole and one is heard in systole. A classic 3-component rub can be phonated as "cha-cha-cha." Rubs have been compared to the creaking leather of a new saddle, or the crunching sound made by stepping on fresh dry snow. A rub may sound superficial to the examiner-as if it is originating "halfway up the stethoscope." Rubs may sometimes sound musical, like the sound of a wet finger sliding over glass, and unfortunately may consequently get mistaken for murmurs. Some rubs sound like sandpaper; hence the term friction rub. To us, the term friction rub belongs in the Department of Redundancy Department. Pericardial rubs are notoriously evanescent; so they should be sought "repeatedly and often." Post-open heart surgery and dialysis patients are quite likely to develop transient rubs while in the hospital.
A 3-component rub can be mimicked by holding the diaphragm of the stethoscope in the clenched hand and delivering 3 quick scratches to the outside surface of that hand while listening with the stethoscope (Fig 4).
Heart sounds can be illustrated by using familiar sounds or words to mimic their nature and timing. Figure 5 shows the timing of the nonejection click of mitral valve prolapse. The click is relatively loud and sharp, so the consonant "k" is employed. The timing of the S1, midsystolic click, and S2 sequence is remarkably similar to the phrase "look it up." In contrast, the timing of an ejection click in cases of bicuspid aortic valve is approximated by saying "lutuk" quickly (because the delay between S1 and the ejection click is much shorter). The timing of S4 followed by S1 is no different, but there is no click. Gallops rarely sound sharp, so no consonant is used. Instead, "luh" illustrates the muffled thud of the typical S4. "Luh lub" said quickly accomplishes this purpose. Finally, the last "ta" of the Spanish word "patata" is used to illustrate the timing of the middiastolic S3 gallop. The words "Tennessee" and "Kentucky" have also been used to illustrate the timing of S4 and S3 respectively.
In summary, the goal of this article is to present practical information on the use of the stethoscope. Phonics are presented to clarify the differences in the timing of different heart sounds. This is neither a comprehensive, nor a balanced, presentation. The focus is on selected practical aspects. The section on choosing and using a stethoscope is extensive because it is difficult to find in the current literature. The clinical sections attempt to go beyond what is available in standard textbooks by providing information and stethoscope techniques that are valuable and useful at the bedside.
1. O'Rourke MF. The arterial pulse in health and disease. Am Heart J. 1971;82(5):687-702. [Context Link]
2. Laniado S, Yellin EL, Miller H, Frater RW. Temporal relation of the first heart sound to closure of the mitral valve. Circulation. 1973;47(5):1006-1014. [Context Link]
3. Leatham A. The second heart sound, key to auscultation of the heart. Acta Cardiol. 1964;19:395. [Context Link]
4. Timmis AJ. The third heart sound. Br Med J (Clin Res Ed). 1987;294(6568):326-327. [Context Link]
5. Martinez-Lopez JI. Sounds of the heart in diastole. Am J Cardiol. 1974;34(5):594-601. [Context Link]
6. Bethell HJ, Nixon PG. Understanding the atrial sound. Br Heart J. 1973;35(3):229-235. [Context Link]
7. Leatham A. Splitting of heart sounds and a classification of systolic murmurs. Circulation. 1957;16(3):417-421. [Context Link]
8. Weaver WF, Walker GH. Innocent cardiovascular murmurs in the adult. Circulation. 1964;29:702-707. [Context Link]
9. Fogel DH. The innocent systolic murmur in children: a clinical study of its incidence and characteristics. Am Heart J. 1960;59:844-855. [Context Link]
10. Fowler NO, Gause R. The cervical venous hum. Am Heart J. 1964;67:135-136. [Context Link]
11. Waider W, Craige E. First heart sound and ejection sounds. Echocardiographic and phonocardiographic correlation with valvular events. Am J Cardiol. 1975;35(3):346-356. [Context Link]
12. Wood P. Aortic stenosis. Am J Cardiol. 1958;1(5): 553-571. [Context Link]
13. Dressler W, Rubin R. Complex shape and variability of the diastolic murmur of aortic regurgitation. Am J Cardiol. 1966;18(4):616-621. [Context Link]
14. Devereux RB, Perloff JK, Reichek N, Josephson ME. Mitral valve prolapse. Circulation. 1976;54(1):3-14. [Context Link]
15. Spodick DH. Pericardial rub. Prospective, multiple observer investigation of pericardial friction in 100 patients. Am J Cardiol. 1975;35(3):357-362. [Context Link]
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