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Cardiac Physical Exam and Innocent Murmurs Presentation.pdf
1. Dr J P Soni
• Nodal officer Pediatric Cardiology
• Dr S N Medical College, Jodhpur
THE PHYSICAL EXAMINATION
IN CARDIOVASCULAR SYSTEM
THE PHYSICAL EXAMINATION
IN CARDIOVASCULAR SYSTEM
3. DEFENITION
• Arterial pulse - Rhythmic distension of arterial
wall felt along peripheral artery with each
effective left ventricular contraction during
cardiac cycle is.
• It is caused by pressure changes in aorta.
• Systolic ejection of blood from left ventricle to
aorta, cause expansion of aorta and then recoil,
setting up pressure wave or pulse.
• Pulse wave travels faster than blood with
velocity of 5-8m/sec( Blood flow at velocity of
0.5msec.
4. Normal Pulse
– The normal central aortic pulse wave is characterized by a
fairly rapid rise (Anacrotic limb) to a somewhat rounded
peak, the anacrotic shoulder, present on the ascending limb,
occurs at the time of peak rate of aortic flow just before
maximum pressure is reached.
– The less steep descending limb(catacrotic limb) is
interrupted by a sharp downward deflection, coincide with
reflux of blood back into aota, called incisura - dicrotic
notch & dicrotic wave coincide with aortic valve closure.
– The pulse pressure is about 30-40 mmHg.
5. Anacrotic limb
Catacrotic limb
Dicrotic wave – due to return of
same blood by closing semilunar valve
P – LV contraction
“t” – Elastic recoil of aorta
“n” – Regurgitation of blood
back form aorta to LV
6. Normal Pulse
– As the pulse wave is
transmitted peripherally,
the initial upstrokes
becomes steeper, the
anacrotic shoulder becomes
less apparent, and the
incisura is replaced by the
smoother dicrotic notch.
7. Method of study
• Arterial pulse is studied by Palpation of superficial arteries
of the body.
• E.g. Radial, brachial, femoral, carotid, dorsalis pedis etc.
• While palpating radial pulse middle three fingers are used.
• Middle finger is used for compression, volume & rate
assessment of pulse.
• Ring finger is used to study the condition of vessel wall.
• Also palmar and plantar pulses in newborns
8. Peripheral Pulses
Radial pulse
• At wrist , lateral to flexor
carpi radialis tendon ,
place your three middle
fingers over the radial
pulse
Simultaneous evaluation of both
radial pulses and a femoral pulse
9. The Carotids
• The patient lies down with the head of the bed elevated 30 degrees
• Carotid pulsations is visible just medial to sternomastoid.
• Use your left thumb for right carotid pulse & vice versa.
• Place the left thumb on the right carotid A. in the lower third of the
neck at the level of the cricoid cartilage, Place tip of thumb b/w larynx
& ant.border of sternocleidomastoid - just inside the medial border of
the sternomastoid and press posteriorly
• Never press both carotids at same time
10. Brachial pulse
• Use your thumb ( rt
thumb for rt.arm & vice
versa ) with your fingers
cupped round the back of
the elbow.
• Brachial pulse – felt in
front of the elbow just
medial to tendon of
biceps.
11. Femoral Pulse
• Is felt at groin just
below inguinal
ligament midway b/w
ant.sup.iliac.spine &
symphysis pubis.
12. Popliteal Pulse
• Knee to be flexed 40
deg. Heel resting on
bed
• Place fingers over
lower part of
popliteal fossa &
fingers are moved
sideways to feel
pulsation of
Popliteal.A against
post.aspect of tibial
condyles.
13. Posterior Tibial Pulse
• Felt just behind medial
malleolus , midway b/w
medial malleolus & tendo
achillis.
14. Dorsalis Pedis Pulse
• Felt just lateral to tendon
of ext.hallucis longus.
Congenital absence of dorsalis
pedis in 10% of population
16. Rate:
Heart rate / minute; count for one full minute.
Indicate true rate of ventricular contraction.
Normal
Bradycardic (conditioning, heart block, digoxin
toxicity)
Tachycardic (CHF, excitement, fever, anemia,
arrhythmia)
17. Rate
• Count the pulse for 1 min / at least 30 sec
• Normal : AGE RATE/MIN
0-1 DAY 94-155(122)
1-3 DAY 90-166(122)
3-7 DAY 106-182(128)
7-30 DAY 106-182(149)
1-3 MNTHS 120-179(149)
3-6MTHS 105-185(141)
6-12MTHS 108- 169(131)
1-3Y 89-152 (!!9)
3-5Y 73-137(109)
5-8YRS 65-133(100)
8-12YRS 62-130(91)
12-16 60-120(80)
18. Sinus Tachycardia
• Physiological : infants
children
anxiety , emotion
• Pathological : Tachyarrhythmia- SVT, VT
High output states
▪ Drugs – atropine
nifedipine
caffiene, nicotine
19. High Output States
• Anaemia
• Pyrexia
• Beri beri
• Thyrotoxicosis
• Pheochromocytoma
• AV fistula
24. Pulsus Parvus
Parvus = small, weak pulse rise slowly and Has
late systolic phase.
Aortic stenosis
Mitral stenosis
Hypovolemia
25. Collapsing Pulse or
Water hammer Pulse
(Corrigan Pulse)
It is characterized by rapid upstroke and down stroke
Of pulse wave, no dichrotic notch .
PDA, Aorto-pulmonary window
AR
Arterio-venous fistula
Rupture of sinus of Valsalva.
Severe Mitral regurgitation
26. Bisferiens Pulse
• TWO systolic peaks ,
• the percussion & tidal waves
separated by distinct
midsystolic dip.
• Detected more rapidly by
palpating carotid artery.
• AS+AR
27. Pulsus Paradoxus
• Exaggerated reduction in
strength of arterial pulse
during normal inspiration due
to exaggerated insp fall in
sys.pressure (> 10 mm)
• >20mm Hg – detected by
palpating brachial Artery
• If Milder fall – measuring BP
will give clue of this pulse
28. Pulsus Paradoxus
• Venous return normally increases with inspiration
• Despite this, BP normally decreases by up to 8
mm Hg on inspiration
• This paradoxical response is due to:
– Increased pulmonary capacitance
– Increased negative intra-thoracic pressure with
inspiration and
– The phase lag between right and left sided events
29. How to measure Pulsus
Paradoxus
• Pulsus paradoxus is an exaggerated inspiratory fall
in BP
– Ask the subject to breath normally
– Auscultate Korotkoff’s sounds as the BP cuff is slowly
lowered and Timewith respiration simultaneously
– Mark pulse when BP sounds which are heard only in
expiration
– Mark pulse, when BP sounds are heard both in
expiration & inspiration. Korotkoff’s sounds seem to
double at this point.
– The measured difference gives clue to pulsus paradoxus
35. Dicrotic Pulse
• 2 peaks .
• 2nd peak is in diastole after S2.
• Normally a small wave that follows aortic valve closure
( dicrotic notch ) is exaggerated
• Due to very low stroke vol & per. Resistance.
• LVF
36. Volume:
Indicate amplitude of the pulse, depends upon stroke
volume, elasticity of vessel wall & peripheral resistance.
This measures amount of blood flowing with every heart
beat.
Normal
Bounding/water hammer (pulse pressure >30 mmHg in
infant, >50 mmHg in child)
Thready
− low output states: shock, severe CHF, large VSD or PDA
− L sided obstruction: AS, aortic atresia, HLHS
Absent
37. Radio – femoral Delay
• Usually 2 radial pulses come simultaneously &
femoral comes 5msec before ipsilateral radial
pulse.
• Delay in femoral pulse – obstruction of aorta –
coarctation
38. Vessel Wall Thickness
• Assess the state of medium sized arteries which
are palpable.
• Method: palpate radial artery with middle 3
fingers.
Occlude proximally & with index finger
empty artery by pressing out blood distally.
Applying pressure on either side – roll the
artery over underlying bone using middle finger.
39. Condition of vessel wall
• Sufficient pressure should be exerted on the
artery to abolish pulsation in vessel.
• Artery should be rolled beneath the finger against
underlying bone.
• Arterial wall cannot be felt, soft in young.
• It become tortuous, easily palpable & whip cord
• Like in old age due to arteriosclerosis.
40. Pulse Deficit
• Diff b/w heart rate & pulse rate , when
counted simultaneously for one minute.
Features Atrial fibrillation Ectopics
Pulse deficit > 10 / min < 10 / min
On exertion Persists/increase Decrease
rhythm Irregularly
irregular
Regularly
irregular
41. Blood Pressure
▪ Definition: the force exerted by the blood against the
blood vessel wall. The highest pressure in the cycle is
the systolic blood pressure and the lowest is the
diastolic.
▪ BP = Heart Rate x Total Peripheral Resistance*
* blood volume, viscosity, vessel elasticity sympathetic
activity, kidney function
42. How to take the measurement
• Palpate the location of the brachial artery
• Position the arm cuff over the brachial artery
80% of circumference 80% of arm length
43. How to take the measurement
• Palpate the location of the brachial artery
• Position the arm cuff over the brachial artery
• Obtain an estimated systolic pressure by palpation prior
to auscultation
• Inflate cuff to 30 mmHg above the estimated systolic BP
• Deflate the cuff slowly, 2-3 mmHg/second
• Note the first of 2 regular beats as systolic pressure.
• Use Kortokoff V (last sound heard as the diastolic
pressure)
• Continue deflation for 10 mmHg past last sound to
assure sound is not a skipped beat
• Record as an even number and to the nearest 2 mmHg
(round upward)
44. Cuff Sizes
Cuff Name Bladder
Width
Bladder
Length
Mid Arm
Circumference
Child 8 21 16 to <22cm
Small arm 10 24 22 to <27cm
Average arm 13 30 27 to<33cm
Large arm 16 38 33 to <41cm
Extra Large 17 43 41 to <52cm
Based on AHA Guidelines
49. Why Internal Jugular Vein?
• IJV has a direct course to RA.
• IJV is anatomically closer to RA.
• IJV has no valves( Valves in EJV prevent
transmission of RA pressure)
• Vasoconstriction Secondary to hypotension
( in CCF) can make EJV small and barely
visible.
50. Why Right Internal Jugular Vein?
• Right jugular veins
extend in an
almost straight line
to superior vena
cava, thus
favouring
transmission of the
haemodynamic
changes from the
right atrium.
R L
51. Why Right Internal Jugular Vein?
R L
• The left
innominate vein
is not in a straight
line and may be
kinked or
compressed
between Aortic
Arch and
sternum, by a
dilated aorta, or
by an aneurysm.
52. What is Normal JVP
• The normal JVP
reflects phasic
pressure changes
in the right
atrium -
• It consists of
three positive
waves a,c,v.
And
two negative
troughs x,y.
53. How to distinguish JVP- Carotid
pulsatation
• Simultaneous palpation of the left carotid artery aids
the examiner in relating the venous pulsations to the
timing of the cardiac cycle.
Venous pulsation Arterial pulsation
Best seen Best palpable
Lateral medial
Have Upper limit No upper limit
Sinuous
55. The centre of the right atrium is 5 cm below the angle of louis in
any position. At 45 degree angle of louis and supraclavicular
fossa comes in one plane. Thus JVP pulsatation above the 5cm
will be visible at 45 degree only.
58. Normal JVP Waveform
• a wave - atrial systole
• x descent – onset of
atrial relaxation
• c wave - small positive
notch in the 'x' descent
due to bulging of the AV
ring into the atria in
ventricular contraction
or due carotid pulsatation
• x' (prime) descent !!!
– occurs during systole due to
RV contraction pulling down
the TV valve ring “descent of
the base”
– a measure of RV contractility
• v wave - after the x' descent
- slow positive wave due to
right atrial filling from venous
return
• y descent - rapid emptying
of the RA into RV due to TV
opening
61. • Venous distension due to RA contraction
Retrograde blood flow into SVC and IJV
• Synchronous with S1, Follow P of ECG
• Precede Carotid pulse
a WAVE
62. • The x descent: is due to
X Atrial relaxation
X` Descent of the floor of the right atrium
during right ventricular systole.
Begins during systole and ends before S2
• The c wave:
Occurs simultaneously with the carotid pulse
Artifact by Carotid pulsation
Bulging of TV into RA during ICP
63. v WAVE
• Rising right atrial pressure when blood flows into the right
atrium during ventricular systole when the tricuspid valve is
shut.
• Synchronous with Carotid pulse
• Begins in early systole, Peaks after S2 and ends in early
diastole
64. y DESCENT
• The decline in right atrial pressure when the tricuspid valve
reopens
• Following the bottom of the y descent and before beginning of
the a wave is a period of relatively slow filling of the ventricle,
the diastases period, a wave termed the h wave.
65. • The x descent occurs just prior to the second heart sound (
during systole), while the y descent occurs after the second heart
sound (during diastole).
• Normally X descent is more prominent than Y descent. Y
descent is only sometimes seen during diastole. Descents are
better seen than positive waves.
• The a wave occurs just before the first sound or carotid pulse
and has a sharp rise and fall.
• The v wave occurs just after the arterial pulse and has a slower
undulating pattern.
• The c wave is never seen normally.
Identifying Wave Forms
72. Tricuspid regurgitation
• Absent X Decsent
• CV/ Regurgitant Wave
• Has a rounded contour
and a sustained peak
• Followed by a rapid deep
Y descent
• Amplitude of V increases
with inspiration.
• Cause subtle motion of
ear lobe with each heart
beat
c
73. “a” wave equal to “v” wave
ASD
Prominent X descent
followed by a large V
wave
M Configuration
Indicates a large L-R
shunt
With PAH A wave
becomes more
prominent
If L JVP > R JVP
indicates associated
PAPVC
76. Constrictive pericarditis.
• M shaped contour
• Prominent X and Y descent (FRIEDREICH`SIGN)
• Y descent is prominent as ventricular filling is
unimpeded during early diastole.
• This is interrupted by a rapid raise in pressure as the
filling is impeded by constricting Pericardium
• The Ventriclar pressure curve exhibit Square Root sign
77.
78. The Abdomino-jugular Reflux:
Technique and Hemodynamic
Correlates
Abdominal pressure of 35mm Hg applied with rolled up
manometer
Patient instructed to breath normally
JVP estimated 12 seconds after compression
79. Abdomino-jugular reflux
• Is positive when JVP increase after 10 sec of abdominal
pressure followed by a rapid drop in pressure of 4 cm on
release of compression.
• Most common cause of a positive test is RHF
• Positive test in: Borderline elevation of JVP
Silent TR
Latent RHF
• False positive: Fluid overload
• False Negative: SVC/IVC obstruction
Budd Chiari syndrome
• Positive Test imply SVC and IVC are patent
80. Specific JVP patterns
Condition Pattern
Normal waveform X' deeper than Y
Post CABG X' shallower, now = Y
Atrial fibrillation CV wave
Tricuspid regurgitation CV wave
Complete heart block Irregular cannon A waves
Tamponade JVP brisk X' > Y
Constriction JVP brisk X' & Y descents
X' less exaggerated than Y
RV infarction JVP –low amplitude
81. The patient:
Male Should have their shirt(s) off, or wear
an examination gown
Females nine years old and older should
wear a gown with the opening in the front
CVS examination Should be in calm and
quiet room.
84. PALPATION
Lay a prewarmed hand very gently on the chest, remembering the
heart may not be in its normal position. With the tips of the right first
and second fingers, depress the thorax just left of the
xiphoid process The fingertips are now lying on the right ventricle. A
faint impulse is allowable, but if the heart is enlarged, a definite
forceful movement will be present
85. INSPECTION & PALPATION:
Asymmetry can indicate RVE
Kyphoscoliosis--can have cardiopulmonary
effect
Poland’s anomaly (unilateral absence of
pectoralis major/minor)
Harrison’s grooves seen in the lower chest
Pulsations/rocking seen with large shunts,
MR, or AI
86. PALPATION:
Use the most sensitive portion of the hand
Lay the heel of R hand at left sternal border
with fingertips pointing to left axilla
87. Apical Impulse:
It is lower most, outer most, definite cardiac
pulsation, felt in
3rd ICS medial to left mid-clavicular line in new
born.
4th ICS medial to left mid-clavicular line in infant
5th ICS medial to left mid-clavicular line in Adult.
This apical area corresponds with mitral area & is
due impact of left ventricle. .
It help in assessment of ventricular size /
thickness.
88. LV apical impulse (PMI):
Found with fingertips with the patient
upright
One should always note interspace location,
relation to the midclavicular /anterior
axillary line, amplitude compared to RV
impulse
89. Relation
Apex beat
&
Trachea
TRACHEA
Apex beat
Should be in Inside to midclavicular
line
Outside to midclavicular line
Central Normal
position
AR,AS, Sys. hypertension
Right Rt lung collapse Rt side pl. effusion or
pneumothorax
Left Right side pl. effusion
or pneumothorax
Lt lung collapse
90. LV apical impulse :
Strong impulse is due to increased cardiac
output or LVH
Downward/leftward displacement--LVE
(with or without LVH)
91. Apical Impulse :
Hyper-dynamic : Forceful but illsustained
Hyper-dynamic impulse in normal location:
think increased cardiac output or LVH
Hyper-dynamic and downward/left wardly
displaced: think LVE
Indistinct impulse associated with RVH
Precordial heave is seen with RVE
92. Apical Impulse :
Heaving : Forceful and sustained
Tapping : Normal apex beat
93. Left para-sternal heave
RV impulse:
Felt at the LSB--usually slight
RVH (without RVE)--parasternal tap
(sharply localized, quickly rising)
RVE (with or without RVH)--parasternal
lift (diffuse, gradually rising)
94. Thrills:
Palpation of a loud murmur
Found in the precordial, suprasternal, or
carotid artery area
If low intensity murmur, probably just a
pulsation and NOT a thrill
95. 95
Percussion
• Aim:to determine the size and
shape of the heart .
• Absolute dullness: contain no gas
Relative dullness : real size
96. 96
Maneuver Of Percussion
• Patient should be in erect position –the
pleximeter is vertical with the
intercostal space
• Patient should be in the recumbent
position –the pleximeter is parallel with
the inter-costal space
97. • It is done for detection of-
Pericardial effusion- with shifting
dullness
Cardiac enlargement
99. The stethoscope:
Should be own!!!
Should have a separate bell and diaphragm
Bell allows in all sounds
Diaphragm lets in middle and high
frequency sounds, attenuates low pitched
sounds
100. The stethoscope :
Bell should be used relatively lightly (avoid
diaphragm effect)
Diaphragm should be small enough to fit on
the chest of the patient
Should have tubing which is short (16-18
inches)
Should have earpieces that are comfortable
and snug
101. Auscultation
• Use the diaphragm for high pitched sounds and
murmurs
• Use the bell for low pitched sounds and murmurs
102. Where to listen:
Apex/5LICS (mitral area)
Left lower sternal border/4LICS (tricuspid
and secondary aortic area)
Right middle sternal border/2RICS (aortic
area)
Left middle sternal border/2LICS
(pulmonary area)
103. Auscultation
1. Position the patient supine with the head of the table slightly
elevated.
2. Always examine from the patient's right side. A quiet room is
essential.
3. Listen with the diaphragm at the right 2nd intercostal near the
sternum (aortic area).
4. Listen with the diaphragm at the left 2nd intercostal near the
sternum (pulmonic area).
5. Listen with the diaphragm at the left 3rd, 4th, and 5th
interspaces near the sternum (tricuspid area).
104. 6. Listen with the diaphragm at the apex (mitral area).
7 Listen with the bell at the apex.
8. Listen with the bell at the left 4th and 5th inter-costal
near the sternum.
9. Have the patient roll on their left side.
➢ Listen with the bell at the apex.
➢ This position brings out S3 and mitral murmurs.
105. 10 Have the patient sit up, lean forward, and hold
their breath in exhalation.
➢ Listen with the diaphragm at the left 3rd and
4th inter-costal near the sternum.
➢ This position brings out aortic murmurs.
11. Record S1, S2.
12. Auscultate the carotid arteries.
106. Other site for auscultation
Lungs
Cranium (temples/orbits/fontanelle)
Liver
Neck (carotid area)
Abdomen
Lumbar/abdominal region over renal area
Mouth/trachea with respiration
Femoral artery
107. How to listen:
Have a system, e.g. method of inching
Listen systematically: S1, S2, S3, S4
Murmur
systolic sounds, systolic murmurs,
diastolic sounds, diastolic murmurs
109. S1:
May be due to acceleration/deceleration
phenomena in the LV near the A-V valves
Best heard at the apex and LLSB
Often sounds single unless slow heart rate
Differentiate S1 from S2 by palpating carotid
pulse:
− S1 comes before and S2 comes after carotid upstroke
111. Decreased S1 :
Cardiomyopathy
LBBB
Shock
Aortic insufficiency
First degree AV block
112. Other Abnormal S1 :
Increased S1:
− Increased cardiac output
− Increased A-V valve flow velocity (acquired
mitral stenosis, but not congenital MS)
Wide splitting of S1:
− RBBB (at tricuspid area)
− PVC’s
− VT
113. S2:
From closure vibrations of aortic and
pulmonary valves
Divided into A2 and P2 (aortic and
pulmonary closure sounds)
Best heard at LMSB/2LICS
Higher pitched than S1--better heard with
diaphragm
114. S2 splitting (normal):
Normally split due to different impedance
of systemic and pulmonary vascular beds
Audible split with > 20 msec difference
Split in 2/3 of newborns by 16 hrs. of age,
80% by 48 hours
Harder to discern in heart rates > 100 bpm
115. S2 splitting (normal):
Respiratory variation causes splitting on
inspiration: pulmonary vascular resistance
When supine, slight splitting can occur in
expiration
When upright, S2 usually becomes single
with expiration
116. S2 splitting (abnormal):
Persistent expiratory splitting
− ASD
− RBBB
− Mild valvar PS
− Idiopathic dilation of the PA
− WPW
117. S2 splitting (abnormal):
Widely fixed splitting
− ASD
− RBBB
Wide & varible splitting
− Mild PS
− RVOTO
− Large VSD or PDA
− Idiopathic PA dilation
− Severe MR
− RBBB
− PVC’s
119. Single S2:
Single S2 occurs with greater impedance to
pulmonary flow, P2 closer to A2
Single and loud (A2): TGA, extreme ToF, truncus
arteriosus
Single and loud (P2): pulmonary HTN!!
Single and soft: typical ToF
Loud (not single) A2: CoA or AI
121. S3 (gallop):
Usually physiologic
Low pitched sound, occurs with rapid filling
of ventricles in early diastole
Due to sudden intrinsic limitation of
longitudinal expansion of ventricular wall
Makes Ken-tuck-y rhythm on auscultation
122. S3 :
Best heard with patient supine or in left
lateral decubitus
Increased by exercise, abdominal pressure,
or lifting legs
LV S3 heard at apex and RV S3 heard at
LLSB
123. S3 (abnormal):
Seen with Kawasaki’s disease--disappears
after treatment
If prolonged/high pitched/louder:
− can be a diastolic flow rumble indicating
increased flow volume from atrium to ventricle
124. S4 (gallop):
Nearly always pathologic
Can be normal in elderly or athletes
Low pitched sound in late diastole
Due to elevated LVEDP (poor compliance)
causing vibrations in stiff ventricular
myocardium as it fills
Makes “Ten-nes-see” rhythm
125. S4 :
Better heard at the apex or LLSB in the
supine or left lateral decubitus position
Occurs separate from S3 or as summation
gallop (single intense diastolic sound) with
S3
128. What is a Murmur?
Murmur is the Sounds made by turbulence in
the heart or blood stream
Can be benign (innocent, flow, functional) or
pathologic
Murmurs are the leading cause for referral for
further evaluation
Don’t let murmurs distract you from the rest of
the exam!!
• .
129. Basics of murmur
1. When does it occur - systole or diastole
2. Where is it loudest - A, P, T, M
130. Describing a heart murmur
When does it occur - systole or diastole
1. Timing
– murmurs are longer than heart sounds
– HS can distinguished by simultaneous palpation of the
carotid arterial pulse
systolic, diastolic, continuousI.
Systolic Murmurs:
1. Aortic stenosis - ejection type
2. Mitral regurgitation - holosystolic
3. Mitral valve prolapse - late systole
II. Diastolic Murmurs:
1. Aortic regurgitation - early diastole
2. Mitral stenosis - mid to late diastole
132. Describing a heart murmur
–Where is it loudest ?
Location of maximum intensity is
determined by the site where the
murmur originates e.g.
Aortic
Pulmonary
Tricuspid
Mitral listening areas
133. Describing a heart murmur :
4. Radiation
– reflects the intensity of the murmur and the direction of
blood flow
5. Intensity
– graded on a 6 point scale
• Grade 1 = very faint
• Grade 2 = quiet but heard immediately
• Grade 3 = moderately loud
• Grade 4 = loud
• Grade 5 = heard with stethoscope partly off the chest
• Grade 6 = no stethoscope needed
*Note: Thrills are assoc. with murmurs of grades 4 - 6
134. Describing a heart murmur :
6. Pitch
– high, medium, low
7. Quality
– blowing, harsh, rumbling, and musical
8. Others:
i. Variation with respiration
• Right sided murmurs change more than left sided
ii. Variation with position of the patient
iii. Variation with special maneuvers
• Valsalva/Standing => Murmurs decrease in length and intensity
EXCEPT: Hypertrophic cardiomyopathy and Mitral valve prolapse
135. Systolic Murmurs
Derived from increased turbulence associated with:
1. Increased flow across normal SL valve or into a dilated great
vessel
2. Flow across an abnormal SL valve or narrowed ventricular
outflow tract - e.g. aortic stenosis
3. Flow across an incompetent AV valve - e.g. mitral regurg.
4. Flow across the interventricular septum
136. Early Systolic murmurs
1. Acute severe mitral regurgitation
– decrescendo murmur
– best heard at apical impulse
– Caused by:
i. Papillary muscle rupture
ii. Infective endocarditis
iii. Rupture of the chordae tendineae
iv. Blunt chest wall trauma
2. Congenital, small muscular septal defect
3. Tricuspid regurg. with normal PA pressures
137. Mid-systolic (ejection) murmurs
• Are the most common kind of heart murmur
• Are usually crescendo-decrescendo
• They may be:
1. Innocent
• common in children and young adults
2. Physiologic
• can be detected in hyperdynamic states
• e.g. anemia, pregnancy, fever, and hyperthyroidism
3. Pathologic
• are secondary to structural CV abnormalities
• e.g. Aortic stenosis, Hypertrophic cardiomyopathy, Pulmonic
stenosis
138. Pansystolic (Holosystolic)
Murmurs
• Are pathologic
• Murmur begins immediately with S1 and continues up to
S2
1. Mitral valve regurgitation
– Loudest at the left ventricular apex
– Radiation reflects the direction of the regurgitant jet
i. To the base of the heart = anterosuperior jet (flail posterior
leaflet)
ii. To the axilla and back = posterior jet (flail anterior leaflet
– Also usually associated with a systolic thrill, a soft S3, and a short
diastolic rumbling (best heard in left lateral decubitus
2. Tricuspid valve regurgitation
3. Ventricular septal defect
139. Diastolic Murmurs
• Almost always indicate heart disease
• Two basic types:
• 2. Rumbling diastolic murmurs in mid- or late
diastole suggest stenosis of an AV valve e.g. mitral stenosis
• Two components:
1. Middiastolic - during rapid ventricular filling
2. Presystolic - during atrial contraction; therefore, it disappears if
atrial fibrillation develops
• Is low-pitched and best heard over the apex (w/ the bell)
• Little or no radiation
• Murmur begins after an Opening Snap; S1 is accentuated
140.
141.
142. Diastolic Murmurs
2. Early decrescendo diastolic murmurs
– signify regurgitant flow through an imcompetent semilunar valve
• e.g. Aortic regurgitation
• Best heard in the 2nd ICS at the left sternal edge
• High pitched, decrescendo
• Blowing quality => may be mistaken for breath sounds
• Radiation:
i. Left sternal border = assoc. with primary valvular pathology;
ii. Right sternal edge = assoc. w/ primary aortic root pathology
• Other associated murmurs:
i. Midsystolic murmur
ii. Austin Flint murmur
143. Continuous Murmurs
• Begin in systole, peak near s2, and continue into all or part of diastole.
1. Cervical venous hum
– Audible in kids; can be abolished by compression over the IJV
2. Mammary souffle
– Represents augmented arterial flow through engorged breasts
– Becomes audible during late 3rd trimester and lactation
3. Patent Ductus Arteriosus
– Has a harsh, machinery-like quality
4. Pericardial friction rub
– Has scratchy, scraping quality
147. Increases afterload/systemic vascular
resistance, initially increased venous return,
increased stroke volume, decreased HR
Reduces the murmur of AS w/ HCM
Increases the murmur of MR
Squatting:
148. Sudden standing:
Decreased afterload, decreased venous
return and stroke volume, increased heart
rate, increased SVR):
Accentuates the murmur and S4 of subAS,
MVP, and HOCM
149. Left lateral decubitus
positioning or leaning forward
in an upright position:
Apex of the heart falls toward the chest wall
Brings out mitral valve and aortic valve
murmurs
150. Summary
A. Presystolic murmur
– Mitral/Tricuspid stenosis
B. Mitral/Tricuspid regurg.
C. Aortic ejection murmur
D. Pulmonic stenosis (spilling
through S20
E. Aortic/Pulm. diastolic
murmur
F. Mitral stenosis w/ Opening
snap
G. Mid-diastolic inflow murmur
H. Continuous murmur of PDA
151. Whoop (sometimes called a
honk):
Loud, variable intensity, musical sound
heard at the apex in late systole
Classically associated w/ MVP and MR
Seen w/ VSD’s closing w/ an aneurysm,
subAS, rarely TR
Some whoops evolve to become systolic
murmurs
152. Friction rub:
Creaking sound heard with pericardial
inflammation
Classically has 3 components; can have
fewer than 3 components
Changes with position, louder with
inspiration
154. INNOCENT MURMURS:
Also known as flow, benign, normal, non-
pathologic, functional, inorganic, or
physiologic
Occur in up to 77% of neonates, 66% of
children, and can be increased to up to 90%
with exercise or using phonocardiography
155. General “Rules” of Innocent
Murmurs:
Grade I-III intensity
No thrills associated at any area of
precordium
Only minimal transmission
Not harsh
Brief duration (usually early to mid-systole)
156. More General “Rules” of
Innocent Murmurs:
Never solely diastolic
Never loudest at the RUSB/R base
No clicks
Normal S2
157. Occur at areas of mismatch of
normal blood flow volumes with
decreasing vessel caliber size
e.g. LVOT, RVOT, branch PA’s, etc.
Better heard in children due to their thinner
chest walls with greater proximity of
stethoscope to vessel
158. Having more than one innocent
murmur in a patient is normal,
too!
159. Some maneuvers for innocent
murmurs :
Jugular vein compression/turning the head
can abolish venous hum
Lying the patient perfectly flat is the most
reliable method of quieting the hum.
Compression of the subclavian artery or
shoulder extension can abolish
supraclavicular bruit
160. Other maneuvers:
Transient arterial occlusion
Breath-holding in end-expiration in the
upright position or leaning forward
Deep breath inspiration in upright position
Lower extremity elevation (passive) while
lying down
Exercise (running in place)
161. Other maneuvers :
Isometric handgrips
Valsalva (straining) maneuver--forced
expiration against a closed glottis after full
inspiration for at least 10 seconds
Chemical maneuvers--rarely, if ever,
performed today due to better imaging
techniques
162. Vibratory Systolic Murmur
(Still’s Murmur):
Most common innocent murmur of
childhood
Needs maneuvers normal ECG to
differentiate from sub AS, HOCM, VSD
163. Still’s Murmur (Characteristics):
Location—max at LLSB
Radiation—may radiate to LMSB, apex,
and R-L base (“hockey-stick” distribution),
although may not completely radiate
Timing—mid-systole
Intensity—grade I-II
Pitch—mid to low
164. Still’s Murmur :
Character—vibratory, groaning, musical,
buzzing, squeaking, “guitar-string
twanging,” “cooing dove”
Variation—loudest supine, after exercise,
with fever, anemia, or excitement
Disappears or localizes to LLSB when
upright
165. Still’s Murmur :
Age range—uncommon in infancy,
commonly age 2 to 6 years, rare in teens
Etiology—unknown, may be associated
with LV ejection
Similar murmur seen with LV false tendons
(but does not tend to diminish as much
when upright)
169. Innocent Pulmonary Systolic
Murmur :
Variation—louder when supine, fever,
exercise, anemia
Age range—most commonly age 8-14
years, but early childhood to young adults
Etiology—normal ejection vibrations into
MPA
173. Physiologic PPS :
Age range—newborns, especially premies.
May last 3 – 6 months but not longer
(requires further eval if persistent)
Etiology—small relative size of branch PA
bifurcation to MPA at birth with acute angle
→ turbulence and relative obstruction
175. Carotid Bruit :
Location—suprasternal notch,
supraclavicular areas
Radiation—carotids, below clavicles
Timing—early to mid-systole
176. Carotid Bruit :
Intensity—grade I-III, ?IV (may have a
faint localized thrill)
Pitch—mid-pitched
Character—may be slightly harsh
177. Carotid Bruit :
Variation—decreased intensity with
hyperextension of shoulders; louder with
anxiety, anemia, or trained athletes w/
resting bradycardia
Age range—children and young adults
Etiology—unknown, ? turbulence at takeoff
of carotid or brachiocephalic vessels
178. Venous Hum:
Most common continuous innocent
murmur, and probably the second most
common innocent murmur
Need to differentiate from AS/AI, AVM,
anomalous left coronary artery arising from
the PA, or PDA if L-sided
179. Venous Hum:
Location—anterior neck to mid-
infraclavicular area, R side > L side
Radiation—may go to LMSB
Timing—continuous with diastolic
accentuation
Intensity—grade I-III
Pitch—mid to low
180. Venous Hum:
Character—soft, whispering, roaring, or
blowing, distant-sounding
Variation—disappears when supine, with
head turn AWAY from the side listened to,
with gentle manual compression of jugular
venous return w/ fingers, or w/ Valsalva
181. Venous Hum :
Age range
– pre-school through grade school age (very
common)
– adol. to young adults (rarely heard, can be seen
w/ increased blood flow states e.g. anemia,
pregnancy, thyrotoxicosis)
Etiology—turbulence in jugular and
subclavian venous return meeting in SVC
182. Mammary Souffle:
Occurs in certain circumstances of breast
development/activity and disappear
otherwise
Differentiate from PDA, AVM, or AS/AI
Souffle is French for “breath”
183. Mammary Souffle:
Location—heard over/just above breasts in
late pregnancy or in lactating women
Radiation—none
Timing—may be systolic only, systole with
diastolic spill-over, or continuous with late
systolic accentuation (most common)
184. Mammary Souffle:
Intensity—grade I-III
Pitch—mid to high
Character—blowing or breath-like
Variation—obliterated by increased
stethoscope pressure or compressing the
tissue on both sides of the stethoscope
185. Mammary Souffle :
Age range—rare (hopefully!) in pediatric
population
Etiology—increased blood flow to the
relatively smaller mammary blood vessels
190. NYHA Class Symptoms
I
Cardiac disease, but no symptoms and no limitation in ordinary physical
activity, e.g. shortness of breath when walking, climbing stairs etc.
II
Mild symptoms (mild shortness of breath and/or angina) and slight
limitation during ordinary activity.
III
Marked limitation in activity due to symptoms, even during less-than-
ordinary activity, e.g. walking short distances (20–100 m).
Comfortable only at rest.
IV
Severe limitations. Experiences symptoms even while at rest. Mostly
bedbound patients.
191. Lungs:
Pulmonary congestion probably nonexistent
in infants (more manifest by tachypnea or
retractions)
Cardiac asthma: fine crackles heard in
older children associated w/ CHF (coarse
crackles indicate a pneumonia)
193. Edema:
Caused by systemic venous congestion
Seen more in older children and adults
(little evidence of this in infants)
More often seen in renal- or liver-induced
hypoproteinemia (esp. if marked)
194. Edema :
Locations:
− Periorbital
− Scrotal
− Pre-sacral
− Hand/foot area
Non pitting pedal/hand edema or lymph
edema in a newborn: think Turner’s or
Noonan’s syndrome
195. Liver:
Measure at mid-clavicular line where it
crosses the 9th costal cartilage
Can be right-sided (situs solitus), left-sided
(situs inversus), or midline (situs
ambiguous--measured subxiphoid)
196. Liver :
Measurements:
– 2-3 cm below the RCM in the infant
– 2 cm below the RCM from 1-3 years of age
– 1 cm below the RCM from 4-5 years of age
Use warm, gentle hands
197. Liver--abnormal:
Hepatomegaly caused by systemic venous
congestion
Right-sided CHF: liver enlarges, becomes
firm, loses distinct edge
Pulsatile liver: tricuspid regurgitation or
other cause of elevated R sided pressures
Hard liver may be more serious than large,
soft liver
198. Spleen:
Normally felt in newborns under the LCM
Significant enlargement can indicate
TORCH infection with an associated
cardiac lesion
Isolated splenomegaly is usually not seen
w/ CHF
202. Skin:
Sweating and pallor (diaphoresis) --
associated with increased adrenergic tone
203. Cyanosis of the mucus
membranes:
Central--from > 3g reduced Hb in the
arterial blood due to cardiac or pulmonary
shunting
Acrocyanosis--from low cardiac output
Differential cyanosis
204. Clubbing:
Thickening of tissues at the base of
the nails
Due to capillary engorgement
associated with chronic hypoxemia
and polycythemia.
Seen in cyanotic congenital heart
disease and pulmonary disease
Can reverse after improvement of
hypoxemia, can disappear with
anemia
206. Facial features of certain
syndromes, chromosomal
anomalies, and associations
important to recognize:
Anomalies of the eyes and lens, nose, ears,
mandible/maxilla, tongue, dentition and
gingiva, asymmetry of the facial
musculature, etc.
207. CNS:
Developmental delay
Seizures
Certain personality traits associated with
these findings (usually not in isolation)
