Chapter V Thorax

Chapter V Thorax
D. Heart and blood vessels
Heart Part II
by Dr. Zhuo-ren Lu
IV. Auscultation
A. A routine procedure of auscultation includes heart
rate, rhythm, cardiac sound, extra heart sound,
cardiac murmur and pericardial friction sound.
1. Auscultatory valve area
(1) The mitral valve area is in the 5th left intercostal
space, 1 or 2 cm medial to the midclavicular line or
the apical impulse area particularly in pathological
(2) The pulmonary valve area is in the second left
intercostal space just lateral to the sternum.
(3) The aortic area is located in the second right
intercostal space just lateral to the sternum.
(4) The second aortic area is in the 3rd or 4th left
intercostal space lateral to the sternum.
(5) The tricuspid valve area is located at the left or
right side of the junction of the xiphoid process and
the sternum.
The routine procedure of auscultation is
recommended as counterclockwise direction: apex
 pulmonary valve area  aortic valve area 
second aortic valve area  tricuspid valve area.
2. Heart rate (HR) and rhythm
The heart rate normally varies with age, sex and
physical activity. In adults, it usually varies from
60 to 100 beats per minutes. The rate is increased
(tachycardia) in severe anemia, high fever,
hyperthyroidism, heart failure and various types
of arrhythmia.
The HR above 160 beats/min indicates that the
supraventricular tachycardia.
The heart rate may be decreased (bradycardia) in
increased intracranial pressure, obstructive
jaundice, syncopy, complete heart block, and
most cases of sick sinus syndrome.
l There may be a pulse deficit (HR  pulse rate) in
atrial fibrillation(Af), which constitutes a grossly
irregular rhythm and extremely variable in heart
Normally, the rhythm of the heart beat is regular or
slight irregular during respiration with no clinical
importance, and any deviation from this regularity
is termed arrhythmia.
The most common cause of the arrhythmia is
premature contraction (extrasystole). It may occur as
the result of excessive smoking or alcoholic intake,
and also in some organic heart diseases.
In bigeminal beats it is coupled or occurs in pair,
with the second beat usually being weaker. In
trigeminal beats, there is a pause after every third
3. Heart sounds
(1) The first heart sound (S1 )
l It is mainly produced by closure of both
the mitral and tricuspid valves. The mitral
valve closure precedes slightly that of the
tricuspid valve.
S1 is synchronous with the apical
impulse and corresponds with the onset of
ventricular systole.
(2) The second heart sound (S2 )
It is produced by closure of both the
aortic and pulmonary valves. Normally,
aortic valve closure precedes pulmonary
valve does.
l Normally, P2  A2 in children and young
persons, P2  A2 in old persons, and P2  A2
in mid-age persons.
The differentiation between S1 and S2:
There is a longer pause between S2 and the
subsequent S1 (diastole) than between S1 and S2
S2 is usually clearly audible in the pulmonary
valve area.
S2 is higher in frequency and shorter in duration
than S1.
It may identify S1 by synchronous palpation at
the apex or over the carotid artery.
(3) The third heart sound (S3) (S3)
Being low in both frequency and intensity, it is
best heard with the bell of the stethoscope.
It occurs during the phase of early diastolic
filling after S2. This sound is heard in most
children and some adults.
(4) The fourth heart sound (S4)
Like the third sound, S4 is also low in
frequency and intensity, and is best heard at the
apex. The sound occurs late in diastole and is
related to atrial contraction. It is rarely heard
under normal condition.
A. Changes of intensity
(1) All heart sounds
In some patients with pulmonary emphysema
or a very muscular chest wall, all heart sounds
may be distant.
(2) S1
The principal factor responsible for the
intensity of is the position of the atrioventricular
valve at the onset of ventricular contraction.
A loud S1 may be heard in mitral stenosis
because less filling from left atrium to left
ventricle and then the mitral valve in a lower
l Tachycardia, anemia, fever, exercise, and
hyperthyroidism may be associated with an
intensity of S1.
l A lower S1 may be caused by the illness of
(3) S2
l S2 becomes louder with hypertension or
pulmonary artery hypertension.
l A decrease in intensity of S2 over the
aortic and/or pulmonary valve area may be
caused by the damaged integrity and
activity of the related semilunar valve.
B. Splitting of heart sounds
(1) A widely splitting of S1 at the apex suggests
commonly the possibility of right boundle branch
block because the second component of S1 delays.
(2) Splitting of S2 is of great practical importance. It
is the results of the marked asynchrony between the
aortic valve and pulmonary valve closure. Because
of the normal increase in venous return to the right
side of the heart on inspiration, the right ventricle
requires a slight longer period to empty itself.
Normal splitting: in pulmonary valve stenosis and
pulmonary artery hypertension and CRBBB, the
splitting of S2 is clearly audible with inspiration.
Fixed splitting: in ASD, there is a wide fixed split of
S2 over the pulmonary valve area with little or no
change in the degree of splitting during either phase
of respiration.
Paradoxical splitting: in CLBBB, the order of valve
closure may be reversed. On expiration, pulmonary
closure occurs first and is followed by aortic valve
closure. During inspiration the pulmonary valve
closure is normal delayed, with increased filling on
the right side of the heart, and the two components
then move closer together on inspiration.
C. Extra heart sounds
Diastolic extra heart sounds: gallop rhythm
(ventricular gallop, atrial gallop, summation
gallop), opening snap, pericardial knock
Systolic extra heart sounds: systolic ejection
sounds and ejection clicks
(1) Gallop rhythm
The term refers to that
condition in which three and occasionally four
heart sounds are spaced to audibly resemble
the canter of a horse.
The protodiastolic (ventricular gallop) is a brief lowpitched sound, usually heard near the end of the
first third of diastole.
It is the pathologic counterpart of the third heart
sound and occurs at the time of rapid diastolic
ventricular filling. The ventricular gallop sound is
produced by an overdistension of the ventricle in the
rapid filling phase of diastole, associated with an
increase in ventricular diastolic volume and pressure.
Ventricular gallop is usually heard at the apex in
ventricular failure from any cause.
Presystolic (atrial gallop)
l It is associated with systolic overloading of
ventricles where the ventricular diastolic pressure
is elevated, namely, in systemic or pulmonary
hypertension and in aortic or pulmonary stenosis.
l The atrial gallop may also occur wherever the
distensibility of the ventricle is impaired, such as MI,
hypertension, and myocardiopathy.
l It may even precede the signs of left ventricular
The atrial gallop sound is low-pitched, of short
duration, and is best heard when the bell of the
stethoscope is applied lightly to the chest wall.
Quadruple rhythm
When both the ventricular and atrial gallop sounds
are present, this results in a quadruple rhythm.
Summation gallop
If both the ventricular and atrial gallop sounds are
present and the heart rate increases, the diastolic
interval shortens and the extra sounds come closer
together. They may actually fuse, resulting in a
summation gallop.
(2) Opening snap
The opening snap occurs soon after S2 and is
produced by opening of the atrioventricular valves.
l In mitral stenosis, the valve forms a restrictive
diaphragm, which bulges into the left atrium
during systole and then springs into the left
ventricle when atrial pressure suddenly exceeds
ventricular diastolic pressure.
l This sound is brief in duration and higher in pitch
than other gallop sounds.
l It is heard best in the left 3rd and 4th parasternal
areas with the patient in left lateral position.
(3) Pericardial knock
In the presence of constrictive pericarditis, at
times an extra sound is heard in diastole
occurring shortly after S2.
It occurs earlier in diastole than the ventricular
gallop does. Pericardial knock is higher in
frequency and transmitted widely than opening
It is heard best in the apex or the left lower
parasternal area.
(4) Systolic ejection sounds and ejection clicks
Pulmonary ejection clicks may occur in stenosis of
the pulmonary valve, in pulmonary hypertension,
and in that situation where the pulmonary artery is
dilated. They are best heard over the pulmonary
auscultatory valve area.
 Aortic ejection clicks occur in stenosis of the aortic
valve, aortic regurgitation, aneurysm of the
ascending aorta, and hypertension with dilatation of
the aorta. They are heard over the base of the heart
as well as at the apex.
Some middle and late systolic clicks occur just
prior to or during a late systolic murmur. The
systolic click is probably related to the prolapsed
mitral valve with longer chordae or exuberant
leaflets. Following the termination of the prolapse,
the late murmur is a reflection of late systolic
mitral regurgitation. It is referred to as mitral
valve prolapse syndrome (middle and late systolic
clicks - late systolic mitral regurgitation).
4. Cardiac murmurs
Cardiac murmurs are abnormal sounds
produced by vibrations within the heart
itself or in the walls of the large arteries.
Murmurs are definitely longer in
duration than heart sound, and are clearly
audible with different qualities.
A. Mechanism of production
1. Increasing the rate or velocity of blood flow
2. Decrease in the diameter of a heart valve or a
constriction in one of the major arteries
3. Valve insufficiency
4. The abnormal communication between the right
and left sides of chambers
5. By inserting a taut membrane (vegetation,
ruptured chordae)
6. By a sudden increase in the diameter of a major
vessel (aneurysm).
B. Characterization of murmurs
(1) Location
The described location of a murmur is the site
of precordium where it is audible most
significantly. Murmurs of valvular origin are
auscultatory valve areas.
(2) Timing
Systole and diastole may be divided into
three parts: early, middle, and late. Murmur
may occur one part of systole or diastole, but at
times may persist throughout systole.
Certain systolic murmurs are produced by
insufficiency of the mitral and tricuspid valves or
by stenosis of the aortic and pulmonary valves.
Most diastolic murmurs are the results of
stenosis of the mitral and tricuspid valves or
insufficiency of aortic and pulmonary valves.
The most common lesions encountered are
mitral stenosis, mitral and aortic insufficiency.
(3) Quality
On occasion the quality of cardiac murmurs may
be of assistance in arriving at a more accurate
l A blowing systolic murmur is often produced in
mitral or tricuspid insufficiency and atrial or
ventricular septal defect.
l The mid- and late diastolic murmurs caused by
mitral stenosis increase in intensity and assume a
rumbling quality.
l High-pitched blowing murmurs may resemble
the sound of a whistle and at times are musical in
character (vegetation or ruptured chordae).
(4) Intensity
l A grade I murmur is barely audible.
A grade II murmur is usually readily heard
and slight louder than grade I.
l Grade III and IV murmurs are quite loud.
l Grade IV is often accompanied by a thrill.
l Grade V is even more pronounced, and also
accompanied by a thrill.
l A grade VI murmur is so loud that even it may
be heard with the stethoscope just removed from
the chest wall.
Grade I and II are frequently
encountered in persons without organic
heart disease, whereas those of grade III
intensity or louder seldom occur in a
normal heart.
In clinic, diastolic murmurs are not
graded because most of them occur in
organic heart diseases.
(5) Transmission
Some murmurs are transmitted with or in the
direction of the bloodstream by which they are
l The murmur of aortic regurgitation may be
heard distinctly down along the left border of the
sternum and over the apex.
l The murmur caused by aortic stenosis may be
audible over the carotid arteries.
L The murmur of mitral regurgitation may
transmit with the direction to left axilla.
C. Classification of murmurs
(1) Systolic murmurs
Ejection murmurs is short in duration. They
begin after S1, attain a peak in early or middle
systole, and terminate before S2.
Examples of systolic ejection murmurs are those
in aortic stenosis and pulmonary stenosis,
including the vast majority of so-called
functional murmurs.
Pansystolic murmurs It is of longer duration than
the ejection murmur and usually obscures S1 and
Mitral pansystolic murmurs are high-pitched,
blowing in character, and frequently radiate toward
the left axilla. Pansystolic murmurs are usually
associated with mitral regurgitation, tricuspid
regurgitation and VSD.
Murmurs that originate on the right side of the
heart frequently increase in intensity during the
course of inspiration. This fact may assist in
differentiating tricuspid from mitral regurgitation
and also in distinquishing between pulmonary and
aortic ejection murmurs.
Functional systolic murmur is commonly
heard in children and young adults without any
structural abnormality or recognizable heart
It is characteristically soft, blowing or ejection in
quality, early, short, limited area, slight in intense
(grade I or II), and variable.
It is usually heard best at the pulmonary valve area
and apex. Functional murmur varies with
position and respiration.
(2) Diastolic murmurs
Regurgitant diastolic murmur is early in onset,
beginning immediately after S2, is longer in
duration, and is pandiastolic in nature.
l The murmur of aortic regurgitation is highpitched, sighing or splashing in character, and
transmitted along the left lower sternal border or
the direction to the apex.
l Regurgitant diastolic murmur also may occur
in pulmonary regurgitation.
Ventricular filling murmurs
are low-pitched diastolic murmurs. In true
mitral stenosis there is a definite delay in
emptying of the left atrium.
Austin Flint murmur
Relative stenosis of the mitral or tricuspid valve
may occur in mitral regurgitation, aortic
regurgitation, and in some cases of congenital
heart disease with left-to-right shunt. This
murmur is less intense and shorter in duration
than its organic counterpart. The nonobstructed mitral valve with higher position
becomes relatively stenotic with respect to
accommodating this large volume of blood.
Graham Steell murmur
A soft diastolic murmur may be heard
over the pulmonary auscultatory valve
the relative
regurgitation of the pulmonary valve
owing to the dilatation of pulmonary artery
when mitral stenosis exists.
(3) Continuous murmurs
The prototype of a continuous murmur is
the Gibson murmur of patent ductus
arteriousus. It is heard maximally under
the left clavicle.
5. Pericardial friction rub
l This to-and-fro rubbing be heard over the entire
precordial region or a very small area.
It may be heard in both phases of the cardiac
cycle. Pericardial friction rub is unaffected by
respiration and is thus differentiated from a pleural
friction rub.
l It is also increased as pressing the stethoscope
firmly against the patient’s chest wall.
l A rub may be readily heard at one moment and
be absent several minutes later.
The intensity of the rub is usually increased
when the subject is sitting upright and leaning

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