Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5835_Библиотеки_им_академика_М_И_Перельмана.pdf
11.2 Origin of Heart Sounds
The heart, although a single organ, can be considered as two pumps that propel
blood through two different circuits. The right atrium receives venous blood from
the head, chest, and arms via the large vein called the superior vena cava and
receives blood from the abdomen, pelvic region, and legs via the inferior vena cava.
Blood then passes through the tricuspid valve to the right ventricle, which propels it
through the pulmonary artery to the lungs. In the lungs venous blood comes in con-
tact with inhaled air, picks up oxygen, and loses carbon dioxide. Oxygenated blood
is returned to the left atrium through the pulmonary veins. Valves in the heart allow
blood to flow in one direction only and help maintain the pressure required to pump
the blood. The cross-sectional view of a human heart is shown in Figure 11.2.
Alternating contractions and relaxation of the myocardium causes the heart to
pump; the sound it makes is called the heartbeat. These contractions are stimulated
by electrical impulses from a natural pacemaker, the sinoatrial (SA) node located in
the muscle of the right atrium. An impulse from the SA node causes the two atria to
contract, forcing blood into the ventricles. Contraction of the ventricles is controlled
by impulses from the atrioventricular (AV) node located at the junction of the two
atria. Following contraction, the ventricles relax, and pressure within them falls.
284 Diagnosis of Heart by Phonocardiography
0
−1
−0.5
0.2 0.4 0.6 0.8
1
1.2 1.4 1.6 1.8
0
0.5
1
Abnormal
Time sec.
Normalized voltage
0
−1
−0.5
0.2 0.4 0.6 0.8
1
1.2 1.4 1.6 1.8
0
0.5
1
Normal
Normalized voltage
(a) (b)
Figure 11.1 (a) Phonocardiograph and (b) a sample phonocardiogram.
Right Left
Right
ventricle
Inferior
vena cava
Right
atrium
Tricuspid
valve
Pulmonary
valve
Right
pulmonary
veins
Superior
vena cava
Apex
Septum
Left ventricle
Mitral valve
Aortic
valve
Left atrium
Left
pulmonary
veins
Aorta
Pulmonary
artery
Figure 11.2 The cross-sectional view of a human heart.
Blood again flows into the atria and an impulse from the SA node starts the cycle
over again. The conduction system of the human heart is shown in Figure 11.3. This
process is called the cardiac cycle, which is comprised of a relaxation (diastole) and
a contraction (systole).
Diastole is the longer of the two phases and it allows the heart to rest between
contractions. The average adult rate is 70 beats per minute at rest. The rate
increases temporarily during exercise, emotional excitement, and fever and
decreases during sleep. The rhythmical noises accompanying a heartbeat are called
heart sounds. Normally, two distinct sounds are heard through the stethoscope: a
low, slightly prolonged sound that occurs at the beginning of ventricular contrac-
tion, or systole, and a sharper, higher-pitched “dup” (the second sound) at the end
of systole. Occasionally audible in normal hearts is a third soft, low-pitched sound
coinciding with early diastole. A fourth sound, also occurring during diastole, is
revealed by graphic methods but is usually inaudible in normal subjects. Heart mur-
murs may be readily heard by a physician as soft swishing or hissing sounds that fol-
low the normal sounds of heart action. Murmurs may indicate that blood is leaking
through an imperfectly closed valve and may signal the presence of a serious heart
problem.
11.2.1 Auscultatory Areas
Events related to the heart valves are best heard not over their anatomic locations,
but in the auscultatory areas bearing their names. It is now commonly accepted that
the externally recorded heart sounds are not caused by valve leaflet movements per
se, as earlier believed, but by vibrations of the whole cardiovascular system trig-
gered by pressure gradients. The cardiohemic system may be compared to a
fluid-filled balloon, which, when stimulated at any location, vibrates as a whole.
Externally, however, heart sound components are best heard at certain locations on
the chest individually, and this localization has led to the concept of secondary
11.2 Origin of Heart Sounds 285
SA node
Left
atrium
Right
atrium
Right
ventricle
Left
ventricle
AV node
The pathways
Figure 11.3 Conduction system of a human heart.
sources on the chest related to the well-known auscultatory areas: the mitral, aortic,
pulmonary, and tricuspid areas. The standard auscultatory areas are shown in Fig-
ure 11.4. The mitral area is near the apex of the heart. The aortic area is to the right
of the sternum, in the second right intercostal space. The tricuspid area is in the
fourth intercostal space near the right sternal border. The pulmonary area lies at the
left parasternal line in the second or third left intercostal space.
11.2.2 Rate and Rhythm
Identification of cardiac rate and rhythm is an important aspect of the cardiac exam-
ination. Depending on the patient’s heart rate, normal is 60 to 100 beats per minute
(bpm), bradycardia is <60 bpm, tachycardia is >100 bpm, and the rhythm is regular
or irregular. If it is irregular, try to identify the pattern; for example, do early beats
appear on a more or less regular basis (regularly irregular rhythm) or are they totally
irregular (irregularly irregular rhythm)?
With the rate and rhythm known,you cannarrow yourdifferential diagnosis list
considerably: A regular rhythm with tachycardia is consistent with sinus tachycar-
286 Diagnosis of Heart by Phonocardiography
Aortic Area—located in the second intercostal space at the right sternal margin.
The systolic murmurs of Aortic Stenosis and Increased Aortic Valve Flow.
Pulmonic Area—located in the second intercostal space at the left sternal border.
The systolic murmur of Pulmonic Stenosis and the diastolic murmur of Pulmonic
Regurgitation.
Tricuspid Area—located at the lower left sternal border (LLSB). The diastolic mur-
mur of Tricuspid Stenosis.
Mitral Area—located about the apex beat, which is usually in the fifth intercostal
space. It is also called the apical, or the left ventricular area. The systolic murmur of
Mitral Regurgitation and the diastolic murmurs of Mitral Stenosis and Increased Val
-
vular Flow.
Figure 11.4 Ausculatory areas.
dia, atrial or nodal (supraventricular) tachycardia, atrial flutter with a regular ven-
tricular response, and ventricular tachycardia. A regular rhythm with a normal rate
is consistent with either a normal sinus rhythm or atrial flutter with a regular ven-
tricular response. A regular rhythm with bradycardia is often seen with sinus
bradycardia, second-degree heart block, and complete heart block. A normal rate
with a regularly irregular rhythm is consistent with sinus arrhythmia, ventricular
premature contractions, and atrial or nodal (supraventricular) premature contrac-
tions. A normal rate with an irregularly irregular rhythm is seen in patients with
atrial fibrillation and atrial flutter with varying block. Ofcourse, almost any combi-
nation of heart rate and rhythm may occur in those patients with a malfunctioning
electronic pacemaker. Don’t forget to add this to your differential diagnosis list
when appropriate.
11.2.3 Normal Heart Sounds
11.2.3.1 First Heart Sound (S1)
The normal first heart sound (S1) is traditionally thought to arise from mitral (M1)
followed by tricuspid (T1) valve closure. Because the intensity of S1 depends on the
velocity of the blood and resultant force of closure of the AV valves, factors that
increase the force and velocity of ventricular pressure rise tend to increase the inten-
sity of S1. The position of the AV valves at the onset of systole also affects S1 inten-
sity. If ventricular contraction occurs against a wide-open valve, the LV leaflets
attain a higher velocity (thus louder S1) than if the valve were partially closed.
S1 is normally loudest at the apex. Exercise and excitement increase the force
and velocity of ventricular contraction and thus S1 intensity. Bradycardia is associ-
ated with an apparent softening of S1, since the AV valves are already closed at the
onset of ventricular contraction. Splitting of S1, which may occur in normal
patients, is best heard over the left lower sternal border.
11.2.3.2 Second Heart Sound (S2)
A normal second heart sound (S2) is produced by the pressure changes and vibra-
tion of valves and contiguous structures induced by motion of the aortic and pul-
monic leaflets toward their respective ventricles. The normal first component is
aortic and referred to as A2; the second is pulmonic (P2).
The A2 is heard best in the aortic area, but is also heard well in the mitral and
pulmonic areas. P2 is usually heard only in the pulmonic area and at Erb’s point.
Normally, P2 is softer than the preceding A2, and this difference in intensity
increases with age. Exercise increases the intensity of both A2 and P2. Deep inspira-
tion tends to increase P2 intensity.
Inspiratory separation ofS2 into two audible components, A2 and P2, is present
throughout life, except in the newborn. Splitting is primarily due to delay in P2.
During expiration, P2 occurs at nearly the same time as A2. Splitting of S2 is best
heard in the third left intercostal space, or in the pulmonic area toward the end of
inspiration, with the patient in the supine position.
Recognition of the first and second heart sounds can be made easier by follow
-
ing these hints: Because systole (the time of ventricular contraction) is usually
11.2 Origin of Heart Sounds 287
shorter than diastole (the time of ventricular relaxation), there is a longer pause
between S2 and S1 than between S1 and S2. S1 is of longer duration and of lower
pitch; S2 is of shorter duration and of higher pitch. S1 is usually best heard at the
apex; S2 is usually best appreciated in the aortic and pulmonic areas. The presence
of tachycardia or bradycardia may change these relationships. In the patient, palpa-
tion of the apical impulse or the carotid pulse will assist in identification of S1,
because S1 occurs slightly before these events.
11.2.3.3 Third Heart Sound (S3)
The physiologic third heart sound (S3) is a low-pitched vibration occurring in early
diastole during the time of rapid ventricular filling. The S3 sound is produced by the
abrupt transmission of forces to the chest wall when the blood mass enters the right
ventricle. The S3 sound is commonly heard in children and adolescents and in some
young adults. Whenheard after the age of 30, it is called a gallop sound, and is a sign
of pathology, such as left ventricular failure.
The physiologic S3 occurs just after A2 and is best heard at the apex with a
patient in the left semilateral position. S3 normally disappears completely when the
patient sits or stands or performs any maneuver that lowers heart rate. Conversely,
factors that increase heart rate, such as exercise, tend toaccentuate aphysiologic S3.
11.2.3.4 Fourth Heart Sound (S4)
The physiologic fourthheart sound(S4) is a very soft, low-pitched noise occurring in
late diastole, just before S1. S4 generation is related to the ventricular filling by atrial
systole. Vigorous atrial contraction produces rapid acceleration of blood mass.
Associated with this event are vibrations in the left ventricle wall and mitral appara-
tus, which are heard as the S4.
A physiologic S4 may be heard in infants, small children, and adults over the age
of 50. It is usually heard only at the apex with the patient placed in the left
semilateral position. A physiologic S4 is poorly transmitted and is rarely accompa-
nied by a shock (when the S4 can be felt as well as heard). Wide transmission of a
loud S4 associated with a shock is pathologic and is referred to as an S4 gallop.
As in the case of S3, maneuvers that increase the force and frequency of ventricu-
lar contraction will accentuate S4. Conversely, maneuvers associated with cardiac
slowing will diminish S4 intensity.
11.2.4 Abnormal Heart Sounds
11.2.4.1 Abnormal S1
An abnormally accentuated S1 is most often associated with mitral stenosis. Other
conditions associated with a loud S1 are left-to-right shunts, hyperkinetic circula-
tory states (such as in anemia, thyrotoxicosis, and fever), accelerated AV conduc-
tion, and tricuspid stenosis.
An abnormally diminished S1 is associated with mitral and tricuspid stenosis,
moderate or severe aortic regurgitation, delay in AV conduction, and diseases that
reduce the force and velocity of ventricular contraction (acute myocardial infarc
-
288 Diagnosis of Heart by Phonocardiography
tion, cardiomyopathies, congestive heart failure, and acute myocarditis). A dimin-
ished S1 may also be found in patients with either pulmonary emphysema or very
heavy upper body musculature.
A variable S1 is seen in those conditions that vary the velocity of AV valve clo-
sure and/or the relationship between atrial and ventricular systole: ventricular
tachycardia, complete AV block, artificial ventricular pacemakers, junctional
tachycardia with AV dissociation, and atrial fibrillation.
An abnormal S1 may be heard in the presence of complete right bundle branch
block, premature ventricular contractions, Ebstein’s anomaly (where tricuspid
valve excursion is wide and closure is delayed), ventricular tachycardia, or with arti-
ficial pacing.
11.2.4.2 Abnormal S2
An accentuated S2 is seen with diastolic hypertension, systolic hypertension in the
elderly, coarctation of the aorta, dilation of the aorta (as in syphilitic aortitis,
Morphan’s syndrome, and chronic severe hypertension), and advanced atheroscle-
rosis of the aorta. Pulmonary hypertension (from left-to-right shunts, pulmonary
thromboembolism, pulmonary emphysema, left ventricular failure, and mitral ste-
nosis) is also associated with an accentuated S2.
A diminished S2 is seen in elderly patients with aortic stenosis, pulmonary
emphysema, and pulmonic stenosis. Abnormal splitting of S2 (splitting other than
that normally observed during inspiration) is associated with delayed electrical acti-
vation of the right ventricle (as in complete right bundle branch block and prema-
ture ventricular beats, and with left ventricular pacemakers), prolonged right
ventricular or shortened left ventricular ejection time (as in valvular or infundibular
pulmonic stenosis, mitral regurgitation, and ventricular septal defects), and altered
impedance of the pulmonary vascular bed (massive pulmonary embolism).
Wide and fixed splitting of S2 (i.e., splitting of S2 that does not vary with respi-
ration) is found in patients with large atrial septal defects, severe pulmonary steno-
sis, and right ventricular failure.
Paradoxical splitting of S2 (when splitting increases with expiration) is usually
due to a delayed A2. This delay in A2 may be due to electrical conduction disorders
(complete left bundle branch block, right ventricle premature contractions, and ven-
tricular tachycardia) or mechanical disorders (severe valvular aortic stenosis, left
ventricular outflow obstruction, hypertrophic cardiomyopathy, coronary artery
disease, myocarditis, and congestive cardiomyopathy).
11.2.5 Murmur Classifications
Figure 11.5 discusses the various types of murmurs found in the heart.
11.2.5.1 Murmur Mechanisms
Figure 11.6 explains the mechanisms by which heart murmurs are caused.
11.2 Origin of Heart Sounds 289
290 Diagnosis of Heart by Phonocardiography
Early Systolic Murmur—begins with S1 and ends before or about the middle of
systole.
Mid Systolic Murmur—begins after S1 and ends before S2.
Late Systolic Murmur—begins at about the middle of systole and ends at the
time of S2.
Holosystolic Murmur—begins with S1 and ends with, or continues somewhat
beyond, S2.
Early Diastolic Murmur—begins with S2.
Mid Diastolic Murmur—begins after S2.
Late Diastolic Murmur—occurs immediately prior to S1.
Continuous Murmur—has both systolic and diastolic components.
Crescendo—the loudness of the murmur increases progressively. The systolic
component of a patent ductus arteriosus murmur is of this type.
Decrescendo—the loudness of the murmur deceases progressively. The murmurs
of aortic and pulmonic regurgitation are examples of this type.
Crescendo-Decrescendo—the loudness of the murmur increases and then
decreases. This configuration is typical of systolic ejection murmurs.
Plateau—the loudness of the murmur remains relatively constant. Holosystolic
murmurs are representative of this type.
Figure 11.5 Murmurs in the heart.
11.2.7 Gallop Sounds
The term gallop sounds refers to the cadence of S1 and S2 along with either an S3 or
an S4, or their summation. This nomenclature arose because the trio of sounds sim-
ulates the cadence of a galloping horse, especially when the heart rate approaches
100 bpm. Gallop sounds are by definition diastolic events. The S3 or ventricular
gallop occurs early in diastole, whereas the S4 or atrial gallop occurs inlate diastole,
just before the first heart sound (S1).
When both S3 and S4 gallops are present with a slow to moderate heart rate,
one hears a quadruple rhythm. With faster heart rates, the S3 and S4 gallops
become fused with each other in middiastole to produce a summation gallop. The
term gallop sounds generally refers to the pathological third and fourth heart
sounds, whereas the terms S3 and S4 usually refer to the normal, physiologic third
and fourth heart sounds.
Repeating the word Kentucky can mimic the S3, or ventricular gallop, which
occurs shortly after S2. Unlike the normal or physiologic S3, the S3 gallop may be
palpable. In addition, standing diminishes the normal S3 intensity, but has no effect
11.2 Origin of Heart Sounds 291
Increased blood flow through a normal structure may produce murmurs. An
example is an aortic systolic murmur associated with anemia.
Flow into a dialated chamber will result in vortex formation and a murmur.
In comparison with the dilation, the normal vessel is relatively constricted.
For example, when the aorta is dilated and the aortic valve is of normal size,
a relative constriction exists, and a murmur is produced.
A regurgitant stream passing the edge of an incompetent valve causes it to
vibrate. A murmur is produced in the same manner that a note is created in a
reed instrument.
Projections into a blood stream, such as a roughened valve or an
arteriosclerotic projection into a vessel, represent wake-forming obstructions
that may produce murmurs.
Blood flowing past a partial obstruction, as in aortic stenosis, results in a peri-
odic fluctuation in the blood. Vortices from a wake downstream from the
obstruction. A vortex can be thought of as a small amount of blood having a
whirling motion and tending to form a partial vacuum in the center that
draws blood toward it. The pressure variations in the wake occur when blood
from other areas fills the space occupied by the vortex just prior to its being
shed. These pressure fluctuations (murmur sounds) in the blood are transmit-
ted to and through the heart, vascular structures, and adjacent tissues.
Shunting of blood out of a high-pressure chamber through an abnormal pas-
sage, such as a ventricular septal defect or patent ductus arteriosus, may pro-
duce murmurs. The pitch of these murmurs increases with the velocity of
blood. High-pressure gradients, and thus high blood velocities, produce mur-
murs of pitch higher than those associated with low-pressure gradients.
Figure 11.6 Murmur mechanisms.
on an S3 gallop. The main causes of an S3 gallop include left and right ventricular
diastolic overloading and reduced left and right ventricular compliance.
The left ventricular S3 gallop (LV S3G) is best heard at the cardiac apex, and
with the patient in the left lateral recumbent position. Having the patient exercise
and/or hold his or her breath in expiration also accentuates the LV S3G. The right
ventricular S3 gallop (RV S3G) is best heard at the left lower sternal border, and is
not heard at the apex. Inspiration tends to increase the intensity of an RV S3G.
Repeating the word Tennessee can mimic the S4, or atrial gallop, which occurs
just prior to S1. A normal or physiologic S4 is rarely heard except in young children
and the elderly, and is almost never palpable (as is an S4 gallop). Causes of the S4
gallop include reduced end-diastolic compliance, right ventricular systolic and dia-
stolic overloading, and left ventricular diastolic overloading.
The left ventricular S4 gallop (LV S4G) is best heard at the cardiac apex,
although it is often widely transmitted. The gallop may be accentuated by placing
the patient in the left lateral recumbent position, or by having the patient exercise, or
hold his or her breath in expiration.
The right ventricular S4 gallop (RV S4G) is best heard at the left lower sternal
border, and is not heard at the apex. Rapid, deep inspiration and exercise tends to
accentuate an RV S4G.
11.2.8 Clicks
Systolic clicks are usually referred to as either ejection or nonejection, depending
mainly on when they occur during systole.
Ejection clicks occur early in systole at the time blood is being ejected from the
left ventricle into the aorta or from the right ventricle into the pulmonary artery.
Ejection clicks are usually associated with abnormalities of the semilunar valves or
great vessels. When associated with either left or right ventricular outflow tract
obstruction, ejection clicks indicate that the lesion is valvular in location.
Nonejection clicks occur in mid to late systole. They are usually the result of
either mitral (mitral clicks) or tricuspid (tricuspid clicks) valve prolapse. By far, the
most common cause of a nonejection click is mitral valve prolapse, especially of the
posterior mitral leaflet.
Aortic ejection clicks are high-pitched sounds that occur in early systole. Inten-
sity is not affected by respiration or patient position. Left-sided valvular ejection
sounds are heard best in the aortic area and are not widely transmitted. The ejection
click of aortic stenosis is heard best in the mitral area but is widely transmitted. Aor-
tic ejection clicks are seen in congenital and rheumatic valvular aortic stenosis with a
deformed but flexible aortic valve. Conditions associated with obstruction of the
aorta, such as systemic hypertension and coarctation of the aorta, are also
associated with aortic ejection clicks.
Pulmonic ejection clicks, like aortic ejection clicks, are high-pitched sounds of
early systole. Unlike the aortic click, the pulmonic ejection click is heard best in the
pulmonic area and is rarely transmitted. The pulmonic ejection click is the only right
heart sound that decreases in intensity during inspiration. Pulmonic ejection clicks
are often associated with mild to moderate valvular pulmonic stenosis, dilation of
the pulmonary artery (as seen in pulmonary hypertension),and tetralogyof Fallot.
292 Diagnosis of Heart by Phonocardiography
Nonejection clicks are high-frequency sounds of mid to late systole. Clicks asso-
ciated with mitral valve prolapse (mitral clicks) are heard best in the mitral area and
usually are not widely transmitted. Those associated with tricuspid valve prolapse
(tricuspid clicks) are best appreciated along the left lower sternal border. Mitral and
tricuspid clicks are sometimes only heard with the patient standing. In this position,
the ventricles are smaller and the degree of prolapse of both mitral and tricuspid
valves is increased. Having the patient exercise or move to a position other than
standing usually diminishes the intensity of both mitral and tricuspid clicks.
11.2.9 Opening Snaps
11.2.9.1 Tricuspid Valve Opening Snap
In etiology an opening snap of the tricuspid valve is classically heard in cases of
tricuspid stenosis and also has been reported in conditions associated with increased
blood flow across the tricuspid valve, as in large atrial septal defects (ASDs).
The auscultatory characteristics of the tricuspid valve opening snap (TVOS)
resemble those of the mitral valve opening snap (MVOS; discussed next). However,
the TVOS is louder at the left lower sternal border or over the xiphoid area. Addi-
tionally, the loudness of the TVOS usually increases markedly during inspiration,
whereas the MVOS is often louder on expiration. The interval between the first
component of S2 (A2) and the TVOS tends to be longer than the interval between
A2 and the MVOS.
11.2.9.2 Mitral Valve Opening Snap
In etiology when an elevated left atrial pressure forces the mitral valve to open rap-
idly to its point of maximal excursion, an opening snap is produced. The opening
snap is related to the abrupt halting of the rapid opening motion of the AV valve,
and to vibrations of the AV apparatus and the intracavitary blood mass at the end of
isovolumetric relaxation of the ventricles.
Mitral stenosis is the most common cause of an opening snap of the mitral
valve. Other, relatively rare, causes of an MVOS are endocardial fibroelastosis, ven-
tricular septal defect (VSD), second- and third-degree AV block, tricuspid atresia
associated with a large ASD, patent ductus arteriosus, and hyperthyroidism. The
common element inthese conditions isincreased bloodflow across themitral valve.
With auscultatory characteristics the opening snap of the mitral valve has a
quality similar to the normal heart sounds and is often confused with a splitting S2.
The brief, sharp, rather snapping sound is heard shortly after the A2 component of
S2.
The MVOS is heard best midway between the pulmonic and mitral areas. When
loud, it is widely transmitted over the entire precordium. Optimum audibility is
often achieved by turning the patient to the left lateral position. Standing tends to
lower the left atrial pressure and thus increase the A2–OS interval.
A soft OS may be intensified after exercise that increases atrial pressure. The
A2–OS interval is not altered during different phases of respiration; however, the
MVOS is usually loudest on expiration.
11.2 Origin of Heart Sounds 293