Auscultation of the heart is accomplished by use of a stethoscope with dual chest pieces. The diaphragm is ideal for high-frequency sounds, whereas the bell aids in auscultation of low-frequency sounds. When one is listening for low-frequency tones, the bell should be placed gen- tly on the skin with minimal pressure applied. If the bell is applied more firmly, the skin will stretch and higher-frequency sounds will be heard (as when using the diaphragm). Auscultation should ideally be performed in a quiet setting with the patient’s chest exposed and the examiner best positioned to the right of the patient. Four major areas of auscultation are evaluated, starting at the apex and moving toward the base of the heart. The mitral valve is best heard at the apex or location of the PMI. Tricuspid valve events are appreciated in or around the left fourth intercostal space adjacent to the sternum. The pulmonary valve is best evaluated in the second left intercostal space.
The aortic valve is assessed in the second right intercostal space. These areas should be evaluated from apex to base using the diaphragm and then evaluated again with the bell. Auscultation of the back, the axillae, the right side of the chest, and the supraclavicular areas should also be done. Having the patient perform maneuvers such as leaning forward,
19 CHAPTER 3 Evaluation of the Patient With Cardiovascular Disease
exhaling, standing, squatting, and performing a Valsalva maneuver may help to accentuate certain heart sounds (Table 3.4).
Normal Heart Sounds
All heart sounds should be described according to their quality, inten- sity, and frequency. There are two primary heart sounds heard during auscultation: S1 and S2. These are high-frequency sounds caused by closure of the valves. S1 occurs with the onset of ventricular systole and is caused by closure of the mitral and tricuspid valves. S2 is caused by closure of the aortic and pulmonic valves and marks the beginning of ventricular diastole. All other heart sounds are timed based on these two sounds.
S1 has two components, the first of which (M1) is usually louder, heard best at the apex, and caused by closure of the mitral valve. The second component (T1), which is softer and thought to be related to closure of the tricuspid valve, is heard best at the lower left sternal bor- der. Although there can be two components, S1 is typically heard as a single sound. S2 also has two components, which typically can be easily distinguished. A2, the component caused by closure of the aortic valve, is usually louder and heard earlier and is best heard at the right upper
sternal border. P2, caused by closure of the pulmonic valve, is recognized best over the left second intercostal space. With expiration, a normal S2 is perceived as a single sound. With inspiration, however, venous return to the right heart is augmented, and the increased capacitance of the pul- monary vascular bed results in a delay in pulmonic valve closure. A slight decline in pulmonary venous return to the left ventricle leads to earlier aortic valve closure. Therefore, physiologic splitting of S2, with A2 pre- ceding P2 during inspiration, is a normal finding.
Additional heart sounds can at times be heard in normal individ- uals. A third heart sound can sometimes be heard in healthy children and young adults. This is referred to as a physiologic S3, which is rarely heard after the age of 40 years in a normal individual. A fourth heart sound is caused by forceful atrial contraction into a noncompliant ventricle; it is rarely audible in normal young patients but is relatively common in older individuals.
Murmurs are auditory vibrations generated by high flow across a normal valve or normal flow across an abnormal valve or structure.
Murmurs that occur early in systole and are soft and brief in duration are not typically pathologic and are termed innocent murmurs. These usually are caused by flow across normal left ventricular or right ven- tricular outflow tracts and are found in children and young adults.
Some systolic murmurs may be associated with high-flow states such as fever, anemia, thyroid disease, and pregnancy and are not innocent, although they are not typically associated with structural heart disease.
They are called physiologic murmurs because of their association with altered physiologic states. All diastolic murmurs are pathologic.
Abnormal Heart Sounds
Abnormalities in S1 and S2 are related to either intensity (Table 3.5) or respiratory splitting (Table 3.6). S1 is accentuated with tachycardia and with short PR intervals, whereas it is softer in the setting of a long PR interval. S1 varies in intensity if the relationship between atrial and ventricular systole varies. In those patients with atrial fibrillation, atrial filling and emptying is not consistent because of the variable HR lead- ing to beat-to-beat changes in the intensity of S1. This also can occur with heart block or AV dissociation. In early mitral stenosis, S1 is often accentuated, but with severe stenosis, there is decreased leaflet excursion and S1 is diminished in intensity or altogether absent (Figs. 3.3 and 3.4).
As previously mentioned, splitting of S1 is not frequently heard. However, it is more apparent in conditions that delay closure of the tricuspid valve, including right bundle branch block and Ebstein’s anomaly (Audio Clip 3.1, Ebstein Abnormalities).
TABLE 3.4
Effects of Physiologic Maneuvers on Auscultatory Events
Maneuver
Major Physiologic Effects
Useful Auscultatory Changes
Respiration ↑ Venous return
with inspiration ↑ Right heart murmurs and gallops with inspiration;
splitting of S2 (see Fig. 3.3) Valsalva (initial ↑ BP,
phase I; followed by ↓ BP, phase II)
↓ BP, ↓ venous return,
↓ LV size (phase II) ↑ HCM
↓ AS, MR
MVP click earlier in systole;
murmur prolongs Standing ↓ Venous return
↓ LV size ↑ HCM
↓ AS, MR
MVP click earlier in systole;
murmur prolongs Squatting ↑ Venous return
↑ Systemic vascular resistance
↑ LV size
↑ AS, MR, AI
↓ HCM
MVP click delayed;
murmur shortens Isometric exercise
(e.g., handgrip) ↑ Arterial pressure
↑ Cardiac output ↑ Gallops
↑ MR, AI, MS
↓ AS, HCM Post PVC or
prolonged ↑ Ventricular filling ↑ AS
R-R interval ↑ Contractility Little change in MR Amyl nitrate ↓ Arterial pressure
↑ Cardiac output
↓ LV size
↑ HCM, AS, MS
↓ AI, MR, Austin Flint murmur
MVP click earlier in systole;
murmur prolongs Phenylephrine ↑ Arterial pressure
↑ Cardiac output
↓ LV size
↑ MR, AI
↓ AS, HCM MVP click delayed;
murmur shortens
↑, Increased intensity; ↓, decreased intensity;
AI, aortic insufficiency; AS, aortic stenosis; BP, blood pressure; HCM, hypertrophic cardiomyopathy; LV, left ventricle; MR, mitral regurgi- tation; MS, mitral stenosis; MVP, mitral valve prolapse; PVC, prema- ture ventricular contraction; R-R, interval between the R waves on an electrocardiogram.
TABLE 3.5
Abnormal Intensity of Heart Sounds
S1 A2 P2
Loud Short PR interval Mitral stenosis with
pliable valve
Systemic hypertension Aortic dilation Coarctation of the aorta
Pulmonary hypertension Thin chest wall Soft Long PR interval
Mitral regurgitation Poor left ventricular
function Mitral stenosis with
rigid valve Thick chest wall
Calcific aortic stenosis Aortic regurgitation
Valvular or subvalvular pulmonic stenosis
Varying Atrial fibrillation Heart block
— —
A2, Component of second heart sound caused by closure of aortic valve;
P2, component of second heart sound caused by closure of pulmonic valve; S1, first heart sound.
S2 can be accentuated in the presence of hypertension, when the aortic component will be louder, or in pulmonary hypertension, when the pulmonic component will be enhanced. In the setting of severe aortic or pulmonic stenosis, leaflet excursion of the respective valves is reduced and the intensity of S2 is significantly diminished. It may become absent altogether if the accompanying murmur obscures what remains of S2.
There are several patterns of abnormal splitting of S2. S2 can remain single throughout respiration if either A2 or P2 is not present or if they occur simultaneously. A2 can be absent, as previously mentioned, with severe aortic stenosis. P2 can be absent with a number of congen- ital abnormalities of the pulmonic valve. Splitting may be persistent throughout the respiratory cycle if A2 occurs early or if P2 is delayed, as in the presence of right bundle branch block. In that case, splitting is always present but the interval between A2 and P2 varies somewhat.
In fixed splitting, the interval between A2 and P2 is consistently wide and unaffected by respiration. This finding is observed in the presence of an ostium secundum atrial septal defect or right ventricular failure.
Paradoxical splitting of S2 occurs when P2 precedes A2. This leads to splitting with expiration and a single S2 with inspiration. It is com- monly found in situations of delayed electrical activation of the left ventricle, as in patients with left bundle branch block or right ventric- ular pacing. It can also be seen with prolonged mechanical contraction of the left ventricle, as in patients with aortic stenosis or hypertrophic cardiomyopathy.
The third heart sound, S3, is a low-pitched sound heard best at the apex in mid diastole. Because it is low pitched, it is best recognized with use of the bell on the stethoscope. As stated previously, S3 can be physi- ologic in children but is pathologic in older individuals and often asso- ciated with underlying cardiac disease. An S3 occurs during the rapid filling phase of diastole and is thought to indicate a sudden limitation of the expansion of the left ventricle. This can be seen in cases of vol- ume overload or tachycardia. Maneuvers that increase venous return accentuate an S3, whereas those that reduce venous return diminish the intensity. The fourth heart sound, S4, is also a low-frequency sound, but in contrast to S3, it is heard in late diastole, just before S1. The S4 gallop occurs as a result of active ejection of blood into a noncompli- ant left ventricle. Therefore, when atrial contraction is absent, such as in atrial fibrillation, an S4 cannot be heard. This heart sound is also best recognized with the use of a bell at the apex. It can be heard in patients with left ventricular hypertrophy, acute myocardial infarction,
or hyperdynamic left ventricle. At times, an S3 and an S4 can be heard in the same patient. In tachycardic states, the two sounds can fuse in mid diastole to form a summation gallop.
S3 and S4 gallops are heard in mid diastole and late diastole, respec- tively. There are other abnormal sounds that can be heard during systole and early diastole. Ejection sounds are typically heard in early systole and involve the aortic and pulmonic valves. These are high-fre- quency sounds that can be heard with a diaphragm shortly after S1.
TABLE 3.6
Abnormal Splitting of S
2Single S2
Widely Split S2 With Normal Respiratory Variation
Fixed Split S2
Paradoxically Split S2 Pulmonic
stenosis Systemic
hypertension Coronary artery
disease Any condition
that can lead to paradoxical splitting of S2
Right bundle branch block Left ventricular pacing Pulmonic stenosis Pulmonary
embolism Idiopathic dilation of
the pulmonary artery Mitral regurgitation Ventricular septal
defect
Atrial septal defect Severe right
ventricular dysfunction
Left bundle branch block Right ventricular
pacing Angina, myocardial
infarction Aortic stenosis Hypertrophic
cardiomyopathy Aortic
regurgitation S2, Second heart sound.
S1
S1
S1
S1
S1
S1
S1
S1
S1
S1
S1
S1
S1
S2
A P
A
A
A
A
A P
P
P
P
P S2
S2
S2 S3-4
S2
S4
Loud S1
Loud S2
S2
S2
S2 S3
S3 gallop
S4 gallop
Summation gallop
Expiration
Inspiration
Expiration
Inspiration
Expiration
Inspiration
First heart sound
Second heart sound
Expiration
Inspiration
Physiologic splitting
Fixed splitting
Paradoxical splitting Abnormally wide but physiologic splitting ECG
Fig. 3.3 Abnormal heart sounds can be related to abnormal intensity, abnormal presence of a gallop rhythm, or abnormal splitting of the sec- ond heart sound (S2) with respiration. A2, Component of S2 caused by closure of aortic valve; ECG, electrocardiogram; P2, component of S2 caused by closure of pulmonic valve.
21 CHAPTER 3 Evaluation of the Patient With Cardiovascular Disease
Ejection sounds are caused by the opening of abnormal valves to their full extent, such as with a bicuspid aortic valve or congenital pulmonic stenosis. They are frequently followed by a typical ejection murmur of aortic or pulmonic stenosis. Ejection sounds can also be heard with systemic or pulmonary hypertension, in which case the exact mecha- nism is not clear.
Midsystolic to late systolic sounds are called ejection clicks. They are most commonly associated with mitral valve prolapse. They are also high pitched and easily auscultated with the diaphragm. The click occurs because of maximal displacement of the prolapsed mitral leaflet into the left atrium and resultant tensing of chordae and redundant leaflets (Audio Clip 3.2, Mitral Valve Prolapse). The click is usually followed by a typical murmur of mitral regurgitation. Any maneuver that decreases venous return will cause the click to occur earlier in systole, whereas increasing ventricular volume will delay the click (see Table 3.4).
The opening of abnormal mitral or tricuspid valves can be heard in early diastole. This opening snap is most frequently associated with rheumatic mitral stenosis. It is heard if the valve leaflets remain pliable and is generated when the leaflets abruptly dome during diastole. The frequency, intensity, and timing of the click have diagnostic signifi- cance. For example, the shorter the interval between S2 and the open- ing snap, the more severe the degree of mitral stenosis, because this is a reflection of higher left atrial pressure. The pericardial knock of constrictive pericarditis and tumor plop generated by an atrial myxoma also occur in early diastole and may be confused with an opening snap.
They can typically be differentiated from an S3 gallop because they are higher-frequency sounds.
Murmurs
Murmurs are a series of auditory vibrations generated by either abnor- mal blood flow across a normal cardiac structure or normal flow across an abnormal cardiac structure, both of which result in turbulent flow.
These sounds are longer than individual heart sounds and should be described on the basis of their location, frequency, intensity, qual- ity, duration, shape, and timing in the cardiac cycle. The intensity of a given murmur is typically graded on a scale of 1 to 6 (Table 3.7).
Murmurs of grade 4 or higher are associated with palpable thrills. The intensity or loudness of a murmur does not necessarily correlate with the severity of disease. For example, a murmur can be quite harsh when it is associated with a moderate degree of aortic stenosis. If stenosis is critical, however, the flow across the valve is diminished and the mur- mur becomes rather quiet. In the presence of a large atrial septal defect, flow is almost silent, whereas flow through a small ventricular septal defect is typically associated with a loud murmur.
The frequency of a murmur can be high or low; higher-frequency murmurs are more correlated with high velocity of flow at the site of turbulence. It is also important to notice the configuration or shape of a murmur, such as crescendo, crescendo-decrescendo, decrescendo, or plateau (Fig. 3.5). The quality of a murmur (e.g., harsh, blowing, rumbling) and the pattern of radiation are also helpful in diagnosis.
Physical maneuvers can sometimes help clarify the nature of a particu- lar murmur (see Table 3.4).
Murmurs can be divided into three different categories (Table 3.8).
Systolic murmurs begin with or after S1 and end with or before S2. Diastolic murmurs begin with or after S2 and end with or before S1. Continuous murmurs begin in systole and continue through diastole.
Murmurs can result from abnormalities on the left or right side of the heart or in the great vessels. Right-sided murmurs become louder with inspiration because of increased venous return. This can help differentiate them from left-sided murmurs, which are unaffected by respiration.
Systolic murmurs should be further differentiated based on tim- ing (i.e., early systolic, midsystolic, late systolic, and holosystolic mur- murs). Early systolic murmurs begin with S1, are decrescendo, and end typically before mid systole. Ventricular septal defects and acute mitral regurgitation may lead to early systolic murmurs. Midsystolic murmurs begin after S1 and end before S2, often in a crescendo- decrescendo shape. They are typically caused by obstruction to left ventricular outflow, accelerated flow through the aortic or pulmonic valve, or enlargement of the aortic root or pulmonary trunk. Aortic stenosis, when less than severe in degree, causes a midsystolic murmur that may be harsh and may radiate to the carotids. Pulmonic stenosis leads to a similar murmur that does not radiate to the carotid arteries but may change with inspiration. The murmur of hypertrophic car- diomyopathy may be mistaken for aortic stenosis; however, it does not radiate to the carotids and becomes exaggerated with diminished venous return. Innocent or benign murmurs may also occur as a result of aortic valve sclerosis, vibrations of a left ventricular false tendon, or vibration of normal pulmonary leaflets. They are generally less First
heart sound
(S1)
Second heart sound
(S2) S4 S1
M1
M1 TT11 AA22 PP22
S2 S3
ES C OS
Fig. 3.4 The relationship of extra heart sounds to the normal first (S1) and second (S2) heart sounds. S1 is composed of the mitral (M1) and tricuspid (T1) closing sounds, although it is frequently perceived as a single sound.
S2 is composed of the aortic (A2) and pulmonic (P2) closing sounds, which are usually easily distinguished. A fourth heart sound (S4) is soft and low pitched and precedes S1. A pulmonic or aortic ejection sound (ES) occurs shortly after S1. The systolic click (C) of mitral valve prolapse may be heard in mid systole or late systole. The opening snap (OS) of mitral stenosis is high pitched and occurs shortly after S2. A tumor plop or peri- cardial knock occurs at the same time and can be confused with an OS or an S3, which is lower in pitch and occurs slightly later.
TABLE 3.7
Grading System for Intensity of Murmurs
Grade Description
1 Barely audible murmur
2 Murmur of medium intensity
3 Loud murmur, no thrill
4 Loud murmur with thrill
5 Very loud murmur; stethoscope must be on the chest to hear it; may be heard posteriorly
6 Murmur audible with stethoscope off the chest
S1
S1 S2
S1 S2
S1
Diastolic rumbling murmur of mitral stenosis
Decrescendo diastolic murmur Systolic
ejection murmur Holosystolic regurgitant
murmur S1
E LV
LA
MVO
OS
S2 S1 E
Fig. 3.5 Abnormal sounds and murmurs associated with valvular dysfunction displayed simultaneously with left atrial (LA), left ventricular (LV), and aortic pressure tracings. The shaded areas represent pressure gradients across the aortic valve during systole or across mitral valve during diastole; they are characteristic of aortic stenosis and mitral stenosis, respectively. AVO, Aortic valve opening; E, ejection click of the aortic valve; MVO, mitral valve opening; OS, opening snap of the mitral valve; S1, first heart sound; S2, second heart sound.
TABLE 3.8
Classification of Heart Murmurs
Class Description Characteristic Lesions
Systolic
Ejection Begins in early systole; may extend to mid or late systole Crescendo-decrescendo pattern
Often harsh in quality
Begins after S1 and ends before S2
Valvular, supravalvular, and subvalvular aortic stenoses Hypertrophic cardiomyopathy
Pulmonic stenosis
Aortic or pulmonary artery dilation Malformed but nonobstructive aortic valve
↑ Transvalvular flow (e.g., aortic regurgitation, hyperkinetic states, atrial septal defect, physiologic flow murmur)
Holosystolic Extends throughout systolea Relatively uniform in intensity
Mitral regurgitation Tricuspid regurgitation Ventricular septal defect Late Variable onset and duration, often preceded by a nonejection click Mitral valve prolapse Diastolic
Early Begins with A2 or P2
Decrescendo pattern with variable duration Often high pitched, blowing
Aortic regurgitation Pulmonic regurgitation Mid Begins after S2, often after an opening snap
Low-pitched rumble heard best with bell of stethoscope Louder with exercise and left lateral position
Loudest in early diastole
Mitral stenosis Tricuspid stenosis
↑ Flow across atrioventricular valves (e.g., mitral regurgitation, tricuspid regurgitation, atrial septal defect)
Late Presystolic accentuation of mid-diastolic murmur Mitral stenosis
Tricuspid stenosis Continuous
Systolic and diastolic components
“Machinery murmurs”
Patent ductus arteriosus Coronary atrioventricular fistula
Ruptured sinus of Valsalva aneurysm into right atrium or ventricle Mammary soufflé
Venous hum
A2, Component of S2 caused by closure of aortic valve; P2, component of S2 caused by closure of pulmonic valve; S1, first heart sound; S2, second heart sound.
aEncompasses both S1 and S2.