Auscultation
1. Become comfortable with your stethescope.
2. Engage the diaphragm of your stethescope and place it firmly over the 2nd right
intercostal space, the region of the aortic valve. Then move it to the other side of the
sternum and listen in the 2nd left intercostal space, the location of the pulmonic valve.
Move down along the sternum and listen position the diaphragm over the 4th
intercostal space, left midclavicular line to examine the mitral area. These locations
are rough approximations and are generally determined by visual estimation.
1
3. In each area, listen specifically for S1 and then S2. S1 will be loudest over the
left 4th intercostal space (mitral/tricuspid valve areas) and S2 along the 2nd R and L
intercostal spaces (aortic/pulomonic valve regions).
4. Note that the time between S1 and S2 is shorter then that between S2 and S1.
This should help you to decide which sound is produced by the closure of the
mitral/tricuspid and which by the aortic/pulmonic valves and therefore when systole
and diastole occur.
5. Compare the relative intensities of S1 and S2 in these different areas.
6. In younger patients, you should also be able to detect physiologic splitting of S2.
That is, S2 is made up of 2 components, aortic (A2) and pulmonic (P2) valve closure.
On inspiration, venous return to the heart is augmented and pulmonic valve closure
is delayed, allowing you to hear first A2 and then P2. On expiration, the two sounds
occur closer together and are detected as a single S2. Ask the patient to take a deep
breath and hold it, giving you a bit more time to identify this phenomenon. The two
components of S1 (mitral and tricuspid valve closure) occur so close together that
splitting is not appreciated.
7. You may find it helpful to tap out S1 and S2 with your fingers as you listen,
accentuating the location of systole and diastole and lending a visual component to
this exercise. While most clinicians begin asucultation in the aortic area and then
move across the precordium, it may actually make more sense to begin laterally and
then progress towards the right and up as this follows the direction of blood flow. Try
both ways and see which feels more comfortable.
8. Listen for extra heart sounds. While present in normal subjects up to the ages of
20-30, they represent pathology in older patients. An S3 is most commonly
associated with left ventricular failure and is caused by blood from the left atrium
slamming into an already overfilled ventricle during early diastolic filling. The S4 is a
sound created by blood trying to enter a stiff, non-compliant left ventricle during atrial
contraction. It's most frequently associated with left ventricular hypertrophy that is the
result of long standing hypertension.
2
9. Either sound can be detected by gently laying the bell of the stethoscope over the
apex of the left ventricle (roughly at the 4th intercostal space, mid-clavicular line) and
listening for low pitched "extra sounds" that either follow S2 or precede S1. These
sounds are quite soft, so it may take a while before you're able to detect them.
Type
Inspiration
Expiration
Cause
Normal or physiologic
Wide, fixed splitting
Atrial septal defect
Wide split, varies with
inspiration
Pulmonary stenosis,
RBBB
Paradoxical splitting
Hypertrophic
cardiomyopathy
3
Listening for Extra Heart Sounds
Positioning the patient on their left side while you listen may improve the yield of
this exam. The presence of both an S3 and S4 simultaneously is referred to as a
summation gallop.
Murmurs
These are sounds that occur durin g systole or diastole as a result of turbulent
blood flow. Traditionally, students are taught that auscultation is performed over the
4 areas of the precordium that roughly correspond to the "location" of the 4 valves of
the heart.
Valves are not strictly located in these areas nor are the sounds created by
valvular pathology restricted to those spaces. So, while it might be OK to listen in
only 4 places when conducting the normal exam, it is actually quite helpful to listen in
many more when any abnormal sounds are detected.
If you hear a murmur, ask yourself:
a. Does it occur during systole or diastole?
b. What is the quality of the sound? It sometimes helps to draw a pictoral
representation of the sound.
c. What is the quantity of the sound? The rating system for murmurs is as follows:

1/6? Can only be heard with careful listening

2/6? Readily audible as soon as the stethescope is applied to the chest

3/6? Louder then 2/6

4/6? As loud as 3/6 but accompanied by a thrill

5/6? Audible even when only the edge of the stethescope touches the chest

6/6? Audible to the naked ear
Most murmurs are between 1/6 and 3/6. Louder generally indicates greater
pathology.
Intensity of Murmur
Grade 1
just audible with a good stethoscope in a quiet room
4
Grade 2
quiet but readily audible with a stethoscope
Grade 3
easily heard with a stethoscope
Grade 4
a loud, obvious murmur with a palpable thrill
Grade 5
very loud, heard only over the pericardium but elsewhere in the body
Grade 6
heard with stethoscope off chest
d. What is the relationship of the murmur to S1 and S2?
e. What happens when you march your stethescope from the 2nd RICS (the aortic
area) out towards the axilla (the mitral area)? Where is it loudest and in what
directions does it radiate? By moving in small increments you will be more likely to
detect changes in the character of a particular murmur and thus have a better
chance of determining which valve is affected and by what type of lesion.
Auscultation over the carotid arteries: In the absence of murmurs suggestive of
aortic valvular disease, you can listen for carotid bruits (sounds created by turbulent
flow within the blood vessel) at this point in the exam. Place the diaphragm gently
over each carotid and listen for a soft, high pitched "shshing" sound. It's helpful if the
patient can hold their breath as you listen so that you are not distracted by
transmitted tracheal sounds.
The meaning of a bruit remains somewhat controversial. I was taught that bruits
represented turbulent flow associated with intrinsic atherosclerotic disease and that
the disappearance of a bruit which was previously present was a sign that the lesion
was progressing. However, a number of studies provide evidence that
atherosclerotic disease is frequently absent when a bruit is present as well as the
reverse situation.
This is actually of clinical importance because recent data suggest that it may be
beneficial to surgically repair carotid disease in patients who have significant
stenosis yet have not experienced any symptoms. Thus, it is becoming increasingly
important to determine the best way of identifying asymptomatic carotid artery
disease... and carotid auscultation may, in fact, not be the mechanism of choice.
Identifying the Most Common Murmurs:
1. Systolic Murmurs: In the adult population, these generally represent either aortic
stenosis or mitral regurgitation. To distinguish between them, remember the
following: Murmurs of Aortic Stenosis (AS):
5
Tend to be loudest along the upper sternal borders and get softer as you move
down and out towards the axilla. There is, however, a phenomenon referred to at the
Gallavardin Effect which can cause murmurs of AS to sound as loud towards the
axilla as they do over the aortic region. When this occurs, the shape of the sound
should be similar in both regions, helping you to distinguish it from MR.
Have a growling, harsh quality (i.e. get louder and then softer also referred to as a
crescendo decrescendo, systolic ejection, or diamond shaped murmur). When the
stenosis becomes more severe, the point at which the murmur is loudest occurs later
in systole, as it takes longer to generate the higher ventricular pressure required to
push blood through the tight orifice.
Are better heard when the patient sits up and exhales.
Are heard in the carotid arteries and over the right clavicle. Radiation to the
clavicle can be appreciated by simply resting the diaphragm on the right clavicle. To
assess for transmission to the carotids, have the patient hold their breath while you
listen over each artery using the diaphragm of your stethescope. Carotid bruits can
be confused with the radiating murmur of aortic stenosis. In general, carotid bruits
are softer. Also, murmurs associated with aortic pathology should be audible in both
carotids and get louder as you move down the vessel, towards the chest. In settings
where carotid pathology coexists with aortic stenosis, a loud transmitted murmur
associated with a valvular lesion may overwhelm any sound caused by intrinsic
carotid disease, masking it completely.
Carotid upstrokes refer to the quantity and timing of blood flow into the carotids
from the left ventricle. They can be affected by aortic stenosis and must be assessed
whenever you hear a murmur that could be consistent with AS. This is done by
placing your fingers on the carotid artery as described above while you
simultaneously listen over the chest.
There should be no delay between the onset of the murmur, which marks the
beginning of systole, and when you feel the pulsation in the carotid. In the setting of
critical aortic stenosis, small amounts of blood will be ejected into the carotid and
there will be a lag between when you hear the murmur and feel the impulse. This is
referred to as diminished and delayed upstrokes, as opposed to the full and prompt
inflow which occurs in the absence of disease. Mild or moderate stenosis does not
alter the character of carotid in-flow.
Sub-Aortic stenosis is a relatively rare condition where the obstruction of flow
from the left ventricle into the aorta is caused by an in-growth of septal tissue in the
6
region below the aortic valve known as the aortic outflow tract. It causes a
crescendo-decrescendo murmur that sounds just like aortic stenosis.
As opposed to AS, however, the murmur is louder along the left lower sternal
border and out towards the apex. This makes anatomic sense as the obstruction is
located near this region. It also does not radiate loudly to the carotids as the point of
obstruction is further from these vessels in comparison with the aortic valve. You
may also be able to palpate a bisferiens pulse in the carotid artery.
Furthermore, the murmur will get softer if the ventricle is filled with more blood as
filling pushes the abnormal septum away from the opposite wall, decreasing the
amount of obstruction. Conversely, it gets louder if filling is decreased. This
phenomenon can actually be detected on physical exam and is a useful way of
distinguishing between AS and sub-aortic obstruction. Ask the patient to valsalva
while you listen. This decreases venous return and makes the murmur louder (and
will have the opposite effect on a murmur of AS). Then, again while listening, squat
down with the patient. This maneuver increases venous return, causing the murmur
to become softer. Standing will cause the opposite to occur. You need to listen for 20
seconds or so after each change in position to really appreciate any difference.
Because the degree of obstruction can vary with ventricular filling, sub-aortic
stenosis is referred to as a dynamic outflow tract obstruction. In aortic stenosis, the
degree of obstruction that exists at any given point in time is fixed.
Murmurs of Mitral Regurgitation (MR):
Sound the same throughout systole.
Generally do not have the harsh quality associated with aortic stenosis. In fact,
they sound a bit like the "shshing" noise produced when you pucker your lips and
blow through clenched teeth.
Get louder as you move your stethescope towards the axilla.
Will get even louder if you roll the patient onto their left side while keeping your
stethescope over the mitral area of the chest wall and listening as they move. This
maneuver brings the chamber receiving the regurgitant volume, the left atrium,
closer to your stethescope, accentuating the murmur.
Get louder if afterload is suddenly increased, which can be accomplished by
having the patient close their hands tightly. MR is also affected by the volume of
blood returning to the heart. Squatting increases venous return, causing a louder
7
sound. Standing decreases venous return, thereby diminishing the intensity of the
murmur.
Holosystolic
Midsystolic
S1
S1
S2
S1
S1
S2
itral regurgitation co-exist, which can be difficult to sort out on exam. Moving your
stethescope back and forth between the mitral and aortic areas will allow for direct
comparison, which may help you decide if more then one type of lesion is present or
if the quality of the murmur is the same in both locations, changing only in intensity.
2. Diastolic Murmurs
Tend to be softer and therefore much more difficult to hear then those occurring
during systole. This makes physiologic sense as diastolic murmurs are not
8
generated by high pressure ventricular contractions. In adults they may represent
either aortic regurgitation or mitral stenosis, neither of which is too common. While
systolic murmurs are often obvious, you will probably not be able to detect diastolic
murmurs on your own until you have had them pointed out by a more experienced
examiner.
Aortic Regurgitation (AR):
Is best heard along the left para-sternal border, as this is the direction of the
regurgitant flow.
Becomes softer towards the end of diastole (a.k.a. decrescendo).
Can be accentuated by having the patient sit up, lean forward and exhale while
you listen.
Occasionally accompanies aortic stenosis, so listen carefully for regurgitation in
patients with AS.
Will cause the carotid upstrokes to feel extraordinarily full as significant
regurgitation increases ventricular pre-load, resulting in ejection of an augmented
stroke volume. AI can also produce a double peaked pulsation in the carotids known
as a bisferiens pulse, which is quite difficult to appreciate. Feeling your own carotid
impulse at the same time that you're palpating the patient's may accentuate this
finding. In cases of co-existent AS and AI, a bisferiens pulse suggests that the AI is
the dominant problem. It may also be present with sub-aortic stenosis (see above),
helping to distinguish it from AS.
Mitral Stenosis (MS):
Heard best towards the axilla.
9
Can be accentuated by having the patient role onto their left side while you
listen with the bell of your sthethescope.
Associated with a soft, low pitched sound preceding the murmur, called the
opening snap. This is the noise caused by the calcified valve "snapping" open. It can,
however, be pretty hard to detect.
Auscultation, an ordered approach:
Try to focus on each sound individually and in a systematic fashion.
Ask yourself: Do I hear S1? Do I hear S2? What is their relative intensities in
each of the major valvular areas? Is S2 split physiologically? Are there extra sounds
before S1or after S2 (i.e. an S4 or S3)? Is there a murmur during systole? Is there a
murmur during diastole? If a murmur is present, how loud is it? What is its character?
Where does it radiate? Are there any maneuvers which affect its intensity?
Remember that these sounds are created by mechanical events in the heart.
As you listen, remind yourself what is happening to produce each of them. By linking
auscultatory findings with physiology, you can build a case in your mind for a
particular lesion.
A few final comments about auscultation:
Pulmonic valve murmurs are rare in the adult population and, even when
present, are difficult to hear due to the relatively low pressures generated by the right
side of the heart.
Tricuspid regurgitation (TR) is relatively common, most frequently associated
with elevated left sided pressures which are then transmitted to the right side of the
heart. In this setting, both mitral and tricuspid regurgitation often co-exist. The
murmur of MR is generally louder then that of TR, again due to the higher pressures
on the left side of the heart. It can therefore be difficult to sort out if there is
co-existent TR when MR is present. Try to listen along both the low left and right
sternal borders and compare this to the mitral area. Move your stethoscope slowly
across the precordium and note if there is any change in the character/intensity of
the murmur. TR murmurs are also accentuated by inhalation, which increases
venous return and therefore flow across the valve.
Patients with COPD (emphysema) often have very soft heart sounds. Air
trapping and subsequent lung hyperinflation results in a posterior-inferior rotation of
10
the heart away from the chest wall and causes the interposition of lung between the
chest wall and heart. In this setting, heart sounds can be accentuated by having the
patient lean forward and fully exhale prior to listening. Furthermore, in any patient
with particularly "noisy" breath sounds, it may be helpful to ask them to hold their
breath while you examine the heart.
Rubs: These are uncommon sounds produced when the parietal and visceral
pericardium become inflamed, generating a creaky-scratchy noise as they rub
together. The classic rub is actually made up of three sounds, associated with atrial
contraction, ventricular contraction, and ventricular filling. In reality, its rare to hear all
3 components (more commonly, 2 are apparent). They can be accentuated by
listening when the patient sits up, leans forward and exhales, bringing the two layers
in closer communication. I feel compelled to mention this finding only because a
common short hand for reporting the results of the cardiac exam comments on the
absence of "Gallops, murmurs, or rubs," implying that rubs are a frequent finding.
If a patient has an abnormal heart sound due to a structural defect that has
been quantified by echocardiography, make sure that you compare your findings to
those identified during the study.
Don't get frustrated! Auscultation is a difficult skill to "master" and we are all
continually refining our techniques. Take your time. Make sure the room is quiet. Be
patient. Ask for help frequently. Read about particular murmurs and their
pathophysiology when you encounter them. A number of the more subtle findings
can be very difficult to identify when the patient is tachycardic, a not uncommon
scenario as this is one of the compensatory mechanisms for dealing with the
dysfunction that has generated these findings in the first place. Re-examination after
the patient has made clinical improvement may be more revealing.
In general, many of the above techniques are not used when examining every
patient. If the exam is normal, it would be neither efficient nor revealing to put a
patient through all of these maneuvers.
The symptoms and signs of common diseases in circulation system
Content of this part
11






Mitral
stenosis
Mitral
insufficiency(mitral
regurgitation)
Aortic
stenosis
Aortic
insufficiency(Aortic
regurgitation)
Pericardial effusion
Heart failure
MITRAL
STENOSIS
Etiology
MITRAL
STENOSIS
MITRAL
STENOSIS
pathophysiology
MITRAL
STENOSIS
MITRAL
STENOSIS
Symptoms





Dyspnea on exertion
Paroxysmal nocturnal dyspnea
Orthopnea
Pulmonary edema.
Haemoptysis (bronchial vein rupture,
pulmonary embolism).
MITRAL
bronchitis, left veutrieular failure,
STENOSIS
signs
 Inspection:
 Mitral face (malar flush)
 cyanosis
 the cardiac apex beat displace laterally
 may be left parasternal heave of right ventricular hypertrophy.
MITRAL
STENOSIS
signs
Palpation: There may be a diastolic thrill in cardiac apex.
Percussion:
the shape of heart border will like a pear
MITRAL
STENOSIS
signs
Auscultation:
12




MITRAL INSUFFICIENCY
（mitral regurgitation)
Etiology
MITRAL INSUFFICIENCY
Floppy (prolepsing) mitral valve leaflets
Ischaemic papillary muscle dysfunction
Severe left ventricular failure with dilatation of the mitral ring.
Rarely. cardiomyopathy, congenital mal formation (Marfan's syndrome),
infective endocarditis and rupture of the chordae tendinae.
MITRAL INSUFFICIENCY
MITRAL INSUFFICIENCY
pathophysiology
Chronic mitral insufficiency
Acute mitral insufficiency
MITRAL INSUFFICIENCY
pathophysiology
MITRAL INSUFFICIENCY
pathophysiology
Chronic mitral insufficiency
MITRAL INSUFFICIENCY
pathophysiology
Acute MR
MITRAL INSUFFICIENCY
symptoms
 Progressive dyspnoea develops as a result of pulmonary congestion and
this is followed by right heart failure.
 Fatigue and palpitation are common.
 hemoptysis are uncommon compared with mitral stenosis.
MITRAL INSUFFICIENCY
signs
 Inspection:


the cardiac apex beat displace to left and downward.
A parasternal heave may be present and due to systolic expansion of the
left atrium (rather than from right ventricular hypertrophy)
13
MITRAL INSUFFICIENCY
signs
 Palpation
 tapping cardiac impulse
 systolic thrill in cardiac apex
 Percussion
the cardiac dullness border displace to left
and downward
MITRAL INSUFFICIENCY
signs
 Auscultation:
 The mitral first sound is soft
 There is an apical pansystolic murmur, it is a harsh ,blowing sound,
radiating to the left axilla, the intensity usually exceed 3 grade, sometimes
with a thrill.
Aortic
stenosis
 Under 60 years; rheumatic or congenital.
 60--75 years: calcified congenital bicuspid valve, more common in men.
 Over 75 years: degenerative calcification, more common in the old patients
(women).
Aortic
stenosis
Aortic
stenosis
Aortic
stenosis
Pathophysiology




Aortic
stenosis
Pathophysiology
Aortic
stenosis
symptoms
In the early phase, there may be no symptoms
Angina , syncope (which may be due to the low cardiac output)
Dyspnoea for left ventricular failure occurred
Sudden death
Aortic
stenosis
14
signs
 Inspection:
the cardiac apex beat displace laterally and downward.
 Palpation:

Left ventricular hypertrophy (sustained and heaving apex beat)
 An aortic systolic thrill in right second intercostals spaces and radiating to
the carotid arteries
Aortic
stenosis
signs
 Percussion:
In the early phase of aortic stenosis, the cardiac border is normal or the
cardiac dullness border displace slightly to left and downward
Aortic
stenosis
signs
Auscultation:

A2 will be quite or absent

An
aortic
systolic ejection murmur maximal in the right
second intercostals space,it is a coarse ,blowing sound;The intensity
is more than 3 grade and radiating to neck.
Aortic
(Aortic
insufficiency
regurgitation)
etiology
Aortic
insufficiency
Aortic
insufficiency
Aortic
insufficiency
pathophysiology
AI
Aortic
insufficiency
pathophysiology
AI
Aortic
insufficiency
symptoms
Aortic
insufficiency
signs
 Inspection:
the cardiac apex beat can displace to left
and downward

carotid artery impulse strongly

15

head nodding with pulse---de musset`s sign
Aortic
insufficiency
signs
 Palpition



thrusting apical pulse
water hammer pulse
capillary pulsation in nail beds---Quincke`s
Aortic
sign
insufficiency
signs
 The wide pulse pressure and high stroke volume produce several signs, all
based on this same pathophysiology.
These signs include :
 water hammer pulse or collapsing pulse
 capillary pulsation in nail beds---Quincke`s
sign
 head nodding with pulse---de musset`s sign
 Femoral bruit(`pistol shot`)
 Duroziez's sign (both systolic and
diastolic bruits over the femoral artery
when it is compressed by the bell of thestethoscope)
Aortic
insufficiency
signs
 Percussion:
the cardiac border like a “boot”or the cardiac dullness border displace
slightly to left and downward
Aortic
insufficiency
signs
 Auscultation:
 The classic murmur of aortic regurgitation is a diastolic blowing murmur
heard along the left sternal border, leaning forward
 Austin flint murmur( there is usually also a systolic flow murmur in the apex.
This murmur producing is dur to mitral valve be affected with flutter of the
anterior leaflet and premature closure,if the AI is severe)
16


Femoral bruit(`pistol shot`)
Duroziez's sign
Pericardial effusion
Pericardial effusion
pathophysiology
 The pericardial space in humans normally contains between 30 and 50 ml of
fluid.
 Pericardial effusion may develop as a response to injury of the parietal
pericardium with all cases of acute pericarditis.
 if the accumulation of fluid causes increased intrapericardial pressure,
result in cardiac compression, and the symptoms of cardiac tamponade
will develop.
Pericardial effusion
Pericardial effusion
pathophysiology
 The development of increased intrapericardial pressure secondary to
pericardial effusion depends on several factors:
 (1) the absolute volume of the effusion,
(2) the rate of fluid accumulation,
(3) the physical characteristics of the pericardium itself .
If additional fluid accumulates slowly, the pericardium stretches: the
pericardial sac can accommodate up to 2 liters without elevation of
intrapericardial pressure.
If additional fluid is rapidly added to a volume exceeding about 150 to 200
ml, a marked rise of intrapericardial pressure occurs.
.




Pericardial effusion
symptoms
Oppressive dull ache or pressure in the chest
Cough due to bronchial or tracheal compression
Dyspnea due to lung compression
edema
17
Pericardial effusion
signs
 Inspection:
the cardiac apical pulse decrease or disappear
 Palpition:
the cardiac apical pulse decrease or disappear
paradoxical pulse
 Percussion:
 the cardiac border displace to both side(right and left), the shape of
cardiac border can change followed the position;

when upright position,the width of cardiac apex dullness will be increase;
decubitus position, the width of cardiac base dullness will be increase
Pericardial effusion
signs
 Auscultation:
Pericardial Friction sound, when the amount of effusion increase, the rub
can be quiet. the heart sounds may become quieter.
Heart Failure
pathophysiology
 the heart is unable to pump the blood sufficient to meet the demond of the
body.
 Clinical manifestation are congestive of circulatory system and the
insufficient supply blood for organs, so we also defined it as congestive
Heart failure (CHF).
 There are many reason to develop the HF, the deteriorating cardiac function
is primarily due to two major mechanism:
Heart Failure
pathophysiology

impairment of myocardial contractile force: MI, cardiomyopathy,
myocarditis.

mechanical abnormality : valvular heart diseases, various congenital heart
disease.

Expect the primary etiology, Some inducible
reasons can promote the
development of HF, for example: infection, arrhythmia, rapid fluid
18
transfusion or intake more sodium.
Heart Failure
Symptoms
 left ventricular HF

dyspnea
exertional dyspnea
paroxysmal nocturnal dyspnea, PND
dyspnea occurs even at rest
Orthopnea

Fatigue

nocturia, diaphoresis, cough, hemoptysis.
Heart Failure
Symptoms
 Right ventricular HF
 abdominal distention,
 oliguria，
 no appetite
 and even nausea and vomiting.
Heart Failure
signs
Left ventricular HF
The signs of LVF due to the pulmonary congestion
 Inspection:
Common physical findings of LVF include tachycardia, tachypnea, cool
skin, diaphoresis, cyanosis, the patient have to keep sitting position.
Heart Failure
signs
 Palpition:
 On precardial palpation, the apical impulse is felt to be englarged, and it is
displaced to the left.
 The pulse alternans can be detect in the patient with severe LVF.
 Percussion:
the signs of cardiomegaly,
Heart Failure
signs
 Auscultation:
 The heart rate increased, there may be
diastolic gallop rhythm on
precordia.
19












The intensity of second heart sound on the area of pulmonary valve is
louder.
Moist rales and wheezing in the chest.
Heart Failure
signs
Right ventricular HF
The signs of RVF due to the systemic criculation congestion
Inspection:
RVF is manifested by elevated venous pressure.
Engorgement of neck veins, cyanosis, edema of the extremities.
Some patients appeared jaundice.
Heart Failure
signs
Palpition:
There may be hepatomegaly with tenderness, edema of the extremities.
In some patients, anasarca may be obversed( generalized massive edema
involving all parts of the body including chest wall, and even face.
Heart Failure
signs
Percussion:
There may be signs of ascites and pleural effusion.( this was not
characteristic sign of RVF
Auscultation:
There may be a pansystolic murmur of functional tricuspid insufficiency as a
result of dilatation of tricuspid valve ring.
http://depts.washington.edu/physdx/heart/tech1.html
20