Division of Pediatric Cardiology Dr S N Medical College, Jodhpur

1. • Dr J P Soni
THE PHYSICAL EXAMINATION
IN CARDIOVASCULAR SYSTEM
THE PHYSICAL EXAMINATION
IN CARDIOVASCULAR SYSTEM

2. Cardiovascular system Examination

3. Arterial Pulses:
◆ It is the pressure wave which travels along
the walls of arteries when blood is ejected from
left ventricle into aorta during systole.
• when this pressure wave travels along walls
of arteries → expansion of art. Walls → palpated
as arterial pulse.
• The velocity of pressure pulse wave is 15 time >
than velocity of blood in aorta
• It is 100 times > than velocity of blood flow in
peripheral arteries.

4. VELOCITY OF PRESSURE PULSE WAVE
IN DIFF. ARTERIES
• Aorta 4m/sec
• Large arteries 8m/sec
• Peripheral arteries 16m/sec

5. ◆ The transmission of pressure pulse wave is
independent and much faster than the velocity of
blood flow.
•
◆ Normally Art. Pulse ends in arterioles→ there are
no capillary pulsations .
◆ No pulsations in vein except jugular vein.
◆ The amplitude of arterial pulse depends on pulse
pressure.

6. DEFENITION
• Arterial pulse - Rhythmic distension of arterial
wall felt along peripheral artery with each
effective left ventricular contraction during
cardiac cycle is.

7. Pulsation
• 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.

8. Pulse pressure:
It is the difference between diastolic and systolic
B.P:
It depends on:
• Stoke volume
• Elasticity of arteries
• Character of ejection of blood from left
venrtical.

9. 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.

10. 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

11. 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.

12. 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

13. 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

14. 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

15. 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.

16. Femoral Pulse
• Is felt at groin just
below inguinal
ligament midway b/w
ant.sup.iliac.spine &
symphysis pubis.

17. 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.

18. Posterior Tibial Pulse
• Felt just behind medial
malleolus, midway b/w
medial malleolus & tendo
achillis.

19. Dorsalis Pedis Pulse
• Felt just lateral to tendon
of ext.hallucis longus.
Congenital absence of dorsalis
pedis in 10% of population

20. Arterial Pulses Evaluation:
Assess arterial pulse for
 rate
 rhythm
 volume
 character
 Vessel wall
 Radio-femoral relationship,
 pulse deficit.

21. 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)

22. 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)

23. Sinus Tachycardia
• Physiological : infants
children
anxiety , emotion
• Pathological : Tachyarrhythmia- SVT, VT
High output states
▪ Drugs – atropine
nifedipine
caffiene, nicotine

24. High Output States
• Anaemia
• Pyrexia
• Beri beri
• Thyrotoxicosis
• Pheochromocytoma
• AV fistula

25. Sinus Bradycardia
• Physiological : Atheletes, sleep
• Pathological : severe hypoxia
hypothermia
sick sinus syn
myxoedema
obs.jaundice
raised ICT
▪ Drugs : beta blockers, verapamil, diltiazem

26. Relative Bradycardia
• Typhoid
• Pt on beta blocker
• CNS infection with raised ICT

27. Rhythm:
 Regular
 Irregular (can be sinus arrhythmia with respiratory
variation or PAC/PVC’s)
 Regularly irregular – extra systole
 Irregularly irregular (arrhythmia) Atrial fibrillation

28. • CATACROTIC PULSE: Normal arterial pulse:
1. Percussion waves, P - Produced by ejected blood in arterial
system
2. Tidal wave, T - Generated along arterial wall
3. Dicrotic notch and dicrotic wave – in downstroke of pulse, d/t
elastic recoil of vessel
*wavy pattern is not felt in health since it is obliterated by normal
vascular tone

29. CHARACTER OF ARTERIAL PULSE
- Pulsus Bigeminus
- Pulsus altenunans
- Anacrotic Pulse
- Pulsus Parvs et Tardus
- Bounding pulse
- Pulsus Bisferinens
- Dicrotic Pulse
- Pulsus Paradoxus
- Thready Pulse
- Waterhammer Pulse

30. Pulsus Bigeminus Coupling of the pulses
waves in pairs
Followed by a pause
Alternate premature beats
AV block
Sinoatrial block with Vent.
Escape
Pulsus bigeminus
is a cardiovascular phenomenon characterized by groups of
two heartbeats close together followed by a longer pause. The
second pulse is weaker than the first beat. The smaller beat is
palpated as either a missing or an extra beat, and on EKG resembles a
PVC. These PVCs appearing every other beat are also called
extrasystoles.

31. Pulsus Alternans
• Alternating strong &
weak pulse.
• Palpation of radial,
femoral, brachial pulses
• Palpation by light
pressure, breath held in
mid expiration
• Better – recording BP,
when sys.pressure
alternates by >20mm
Pulsus Alternans Strong and weak beat occurring
alternately
LVF
Toxic myocarditis
Paroxysmal Tachycardias
Following Premature beat

32. PULSES IN AORTIC STENOSIS
Increased resistance to left ventricular ejection due to fixed obstruction
reduces the stroke volume, prolongs left ventricular total ejection time,
and retards the rate of initial stroke output into the aorta and distal
arterial system.
**Characteristics:
--Anacrotic character (anacrotic pulse): gives the impression of
interruption of the upstroke of the carotid pulse. Aortic stenosis is likely
to be hemodynamically significant when the anacrotic notch is felt
immediately after the onset of the upstroke. When an anacrotic notch
occurs very early on the ascending limb of the arterial pulse, it can be
appreciated in the radial pulse and suggests moderate to severe aortic
stenosis.

33. • **--Delayed upstroke of the ascending limb (pulsus tardus): delayed peak and slower
upstroke of the carotid pulse. The delay can be appreciated by simultaneous palpation of the
carotid pulse and auscultation of the interval between S1 and S2 (duration of systole).
Normally the peak of the carotid pulse occurs closer to S1; in the presence of severe aortic
stenosis, it is usually closer to S2. In the presence of fixed outflow obstruction, the central
aortic pulse demonstrates a progressively slower rise of the ascending limb, a lower anacrotic
shoulder, and a peak closer to the incisura as the severity of obstruction increases.
• --Small amplitude (pulsus parvus): The amplitude of the pulse decreases with a diminished
stroke volume.
• --Shudder (thrill) on the ascending limb: is frequently palpable on the ascending limb of
the pulse.
• ** The usual changes in the carotid pulse due to aortic stenosis are modified in this situation,
particularly the amplitude.

34. Anacrotic Pulse
Two upbeats, in systole
Pulse is typically small slow rising with delayed peak.
Aortic stenosis
Pulse/ Characteristic Examples
Anacrotic Pulse Slow rising
Twice beating
Both waves felt in systole
Aortic Stenosis

35. Pulsus Parvus
Parvus = small, weak pulse rise slowly and Has
late systolic phase.
Aortic stenosis
Mitral stenosis
Hypovolemia
Pulsus Parvus et
Tardus
Slow rising
Anacrotic wave not felt
Aortic Stenosis

36. Pulsus Tardus
• Delayed systolic peak resulting from
obstruction of lt.ven.ejection
• Fixed LV obs – Valvular AS

37. Pulsus Parvus et
Tardus
• Small vol pulse with delayed systolic peak
• Severe AS

38. Collapsing or hammer Pulse (Corrigan)
It is characterized by rapid upstroke and down stroke
Of pulse wave, no dichrotic notch w
PDA, Aorto-pulmonary window
AR
Arterio-venous fistula
Rupture of sinus of valsulva.
Severe Mitral regurgitation
Waterhammer
Pulse(Corrigan’s Pulse)
High volume pulse
Sharp rise
Ill-sustained
Sharp fall
Pulse pressure is at least 60mmHg
Aortic Regurgitation

39. Bisferiens Pulse
• 2 systolic peaks ,the
percussion & tidal waves
separated by distinct
midsystolic dip.
• Detected more rapidly by
palpating carotid artery.
• AS+AR
Pulsus Bisferiens Rapid rising
Twice beating
Both waves felt in systole
Idiopathic Hypertrophic
Subaortic Stenosis(jerky pulse)
Severe AR with mild AS
HOCM

40. 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.a.
• Milder fall – measuring BP
Pulsus Paradoxus SBP fall more than 10mmHg
during inspiration (exaggeration
of normal)
Does not happen if thoracic
cage is immobile
SVC Obstruction
Lung conditions(Asthma,
emphysema, airway
obstruction)
Pericardial effusion
Constrictive pericarditis
Severe CCF
Reversed Bernheim sign

41. 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

42. 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. Time respiration simultaneously
– Mark when BP sounds are heard only in expiration
– Mark when BP sounds are heard both in expiration &
inspiration. Korotkoff’s sounds seem to double at this
point.
– The difference is the measured pulsus paradoxus

43. Pulsus Paradoxus
An exaggerated drop in SBP (>10mmHg) with inspiration

44. Pulsus Paradoxus
• Cardiac tamponade,
• Constrictive pericarditis,
• severe airway obs ,
• SVC obstruction

45. Reverse Pulsus
Paradoxus
Peripheral arterial systolic and
diasdolic pulses pressure
increase on inspiration, while
heart sounds remain audible
Patient on Continuos airway
pressure on mechanical
ventilator
Idiopathic hypertrophic
subaotic stenosis
Isorhyrthmic ventricular
rhyrhtm
Reversed Pulsus Paradoxus

46. 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
Dicrotic Pulse Twice beating
First wave in systole, second wave in
diastole
(seen when PR and DP is low)
Felt due to hypotonia of vessel wall
Fever (e.g. typhoid fever)
Endotoxic shock
CCF
Cardiac Tamponade
Following open heart surgery

47. 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

48. Radio – femoral Delay
• Usually 2 radial pulses come simultaneously &
femoral comes 5msec before ipsilateral radial
pulse.
• Delay in femoral pulse – obstruction of aorta –
coarctation

49. 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.

50. 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.

51. Pulse Apex Deficit
• Diff b/w heart rate & pulse rate , when
counted simultaneously for one minute.
• Diff b/w AF & Ectopics
Features Atrial fibrillation Ectopics
Pulse deficit > 10 / min < 10 / min
On exertion Persists/increase Decrease
rhythm Irregularly
irregular
Regularly
irregular

52. 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

53. How to take the measurement
• Palpate the location of the brachial artery
• Position the arm cuff over the brachial artery
40% of circumference 80 -100 % of circumference

54. 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)

55. 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

56. Equipment
• Aneroid
• Ocillometric
• Hybrid
• Mercury (used only for accuracy
check in MI)

59. Jugular Venous
Pressure
• Which vein to inspect for - JVP ?
Internal/External jugular vein

60. 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.

61. 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.

62. Why Right Internal Jugular Vein?
• 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.

63. 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.

64. 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

65. JVP Inspection

66. 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.

67. ---------------------------------------------------------
---------------------------------------------------------
Angle of louis
• Usually JVP is less than 8 cm water that is
< 3 cm above level of sternal angle.

69. 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

70. A-
Atrial contraction C- Tricuspid closure
• V-
f

72. • 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

73. • 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

74. 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

75. 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.

76. • 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

77. Abnormalities of jugular venous
pulse
A. Low jugular venous pressure
1. Hypovolaemia.

78. B. Elevated jugular venous pressure
1. Intravascular volume overload conditions
Right ventricular infarction
Left heart failure
Myocardial infarction.
Valvular Heart Disease
Cardiomyopathy
2. Constrictive pericarditis.
3. Pericardial effusion with tamponade

79. Elevated “a” wave
Increased Resistance to
RV Filling.
Tricuspid stenosis
R Heart Failure
PS
PAH

80. Cannon “a” wave
• Atrial-
ventricular
Dissociation
(atria contract against
a closed tricuspid
valve)
Complete heart block
VPC
Ventricular
tachycardia
Ventricular pacing
Junctional rhythm
Junctional
tachycardia.

81. Absent “a” wave
• 1. Atrial fibrillation

82. Elevated “v” wave
1. Tricuspid regurgitation.
2. Right ventricular failure.
3. Restrictive cardiomyopathy.
4. Cor Pulmonale

83. 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

84. “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

85. 1. Cardiac tamponade.
2. Constrictive Pericarditis
3. RVMI
4. Restrictive Cardiomyopathy
5. Atrial septal defect
Prominent “x” descent
Blunted “x” descent
1. Tricuspid regurgitation.
2. Right atrial ischaemia

86. Prominent “y” descent
1. Constrictive pericarditis.
2. Tricuspid regurgitation.
3. Atrial septal defect.
1. Cardiac tamponade.
2. Right ventricular infarction
3. Restrictive Cardiomyopathy
Absent “y” descent
Slow “y” descent
1. Tricuspid stenosis.
2. Right atrial myxoma.

87. 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

89. The Abdomino-jugular Test:
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

90. 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

91. 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

92. 2000’S
Pulse Oximetry saturation
Pulse oximetry – right upper limb and lower
limb, three time at interval of 60 minutes

94. Central cyanosis
•noted in the trunk, tongue, mucous membranes
•due to reduced oxygen saturation
Peripheral cyanosis
•noted in the hands and feet, around mouth due to reduced local blood flow
The cyanosis usually correspond to oxygen saturation of 70-80%.
Therefore mild desaturation may clinically be missed.

95. Differential cyanosis
1. pink upper,
blue lower
CoA, IAA, Pulm Htn
Blue lower
Pink Upper Pink Upper

96. blue upper and pink lower limb
d-TGA with pulm Htn
*indicates serious underlying
cardiac
Deep Blue upper
Less blue

97. Pulse Oximetry
•Easy to use, harmless when done correctly
•Accuracy of 2% in the range of 70 to 100%
•Consider for CHD’s when Sat <94% at 24 hours of age
•Should be obtained prior to discharge from nursery
= Policy for newborn’s - Measure sat in foot
If <95%, gets evaluation

98. 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.

99. 99
Inspection & Palpation
1 Pre-cardial projection and
excavation
2 Apical impulse
3 Abnormal pulsations of
precardium

100. Precordium -Inspection
Palpation• Apex beat
– Location
– Character
• Heaving
• Thrusting
• Double
• Tapping
• Paradoxical
• Left parasternal heave
• Thrills (palpable
murmurs)
– Systolic
– Diastolic
• Palpable P2
(pulmonary
hypertension)
• Pacemaker box

101. 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

102. 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

103. 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

105. 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.

106. 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

107. LV apical impulse :
 Strong impulse is due to increased cardiac
output or LVH
 Downward/leftward displacement--LVE
(with or without LVH)

108. 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

109. Apical Impulse :
 Normal S1 is not palpable
 Tapping : Normal apex beat, S1 palpable
 Heaving : Forceful and sustained
 Hyperdynamic : Forceful but not sustained

110. 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)

111. 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

112. 112
Percussion
• Aim:to determine the size and
shape of the heart .
• Absolute dullness: contain no gas
Relative dullness : real size

113. 113
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

114. AUSCULTATION:

115. 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

116. 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

117. Auscultation
• Use the diaphragm for high pitched sounds and
murmurs
• Use the bell for low pitched sounds and murmurs

118. 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)

119. 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).

120. 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.
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.

121. 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

122. 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

123. Normal heart sounds

124. 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

125. Decreased S1:
 Slowed ventricular ejection rate/volume
 Mitral insufficiency
 Increased chest wall thickness
 Pericardial effusion
 Hypothyroidism

126. Decreased S1 :
 Cardiomyopathy
 LBBB
 Shock
 Aortic insufficiency
 First degree AV block

127. 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

128. 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

129. 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

130. 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

131. S2 splitting (abnormal):
 Persistent expiratory splitting
− ASD
− RBBB
− Mild valvar PS
− Idiopathic dilation of the PA
− WPW

132. 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

133. S2 splitting (abnormal):
 Reversed splitting
− LBBB
− WPW
− Paced beats
− PVC’s
− AS
− PDA
− LV failure

134. 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

135. Normal Sounds Heart sound
S1 S2
Event Due closure of AV Due to closure of
semilunar valve
Pitch Lower Higher
Duration Longer Shorter
Point of maximal
intensity
At cardiac Apex Base of the heart
Location in cardiac cycle At the end of the long
pause
At the beginning of the
long pause
S3 ventricular gallop S4 atrial gallop
Event Due rapid ventricular
filling
Due Atrial contraction
Timing During early diastole During late diastole
Feature May be normal,
physiological
Always abnormal
Suggest Can be sign of systolic
ventricular failure
Can be sign of diastolic
ventricular failure
Ventricle is compliant Ventricle noncompliant
HEART SOUND

136. S1 abnormalities
Decreased S1 Loud S1 Split Reverse split
MR, TR MS,TS RBBB Ectopic beats
Absent if Av
calcified
High output
state
Pul.
Hypertension
S2 abnormalities
Decreased S2 Loud S2 Single S2
Loud A2 Loud P2 Absent A2 Absent P2
AS, PS
CALCIFIED
SEMILUNAR
VALVE
Hypertension,
Aortic
aneurysm
Dilated aorta
ASD, PDA,
VSD
AS PS,TOF, TGA
S2 Splitting
Wide & fixed Wide &
variable
Narrow Narrow
splitting
ASD, MR VSD, RBBB SEVERE AS &
PS
AS, HOCM

138. Extra heart sounds

139. 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

140. 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

141. 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

142. 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

143. 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

144. S4 Associations:
 CHF!!!
 HCM
 severe systemic HTN
 pulmonary HTN
 Ebstein’s anomaly
 myocarditis

145. S4 Associations:
 Tricuspid atresia
 CHB
 TAPVR
 CoA
 AS w/ severe LV disease
 Kawasaki’s disease

146. 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!!
• .

147. Basics of murmur
1. When does it occur - systole or diastole
2. Where is it loudest - A, P, T, M

148. 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

149. Shape of Murmurs
Systolic Murmurs
• Aortic stenosis
• Mitral insufficiency
• Mitral valve prolapse
• Tricuspid insufficiency
Diastolic Murmurs
• Aortic insufficiency
• Mitral stenosis
S1 S2 S1
2. Shape : crescendo (grows louder), decrescendo,
crescendo-decrescendo, plateau

150. 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

151. 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

152. 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

153. 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

154. 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

155. Midsystolic (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

156. 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

157. 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

160. 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

161. 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

162. MANEUVERS

163. Routine positions--
 Supine and standing or sitting examinations
should be performed on all patients

164. Other physical maneuvers

165.  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:

166. 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

167. 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

168. 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

169. 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

170. Friction rub:
 Creaking sound heard with pericardial
inflammation
 Classically has 3 components; can have
fewer than 3 components
 Changes with position, louder with
inspiration

171. INNOCENT MURMURS

172. 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

173. 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)

174. More General “Rules” of
Innocent Murmurs:
 Never solely diastolic
 Never loudest at the RUSB/R base
 No clicks
 Normal S2

175. 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

176. Having more than one innocent
murmur in a patient is normal,
too!

177. 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

178. 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)

179. 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

180. Vibratory Systolic Murmur
(Still’s Murmur):
 Most common innocent murmur of
childhood
 Needs maneuvers  normal ECG to
differentiate from sub AS, HOCM, VSD

181. 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

182. 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

183. 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)

184. Innocent Pulmonary Systolic
Murmur:
 Need to differentiate from ASD, PS, subAS,
VSD, and true/organic PPS

185. Innocent Pulmonary Systolic
Murmur :
 Location—LUSB
 Radiation—possible to hear at LMSB
 Timing—early to mid-systole with peak in
mid-systole

186. Innocent Pulmonary Systolic
Murmur :
 Intensity—grade I-III
 Pitch—mid to high-pitched
 Character—soft, blowing, somewhat
grating, diamond-shaped

187. 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

188. Physiologic Peripheral
Pulmonic Stenosis (PPS):
 Need to differentiate from valvar PS, ASD,
true/organic PPS, and ToF

189. Physiologic PPS :
 Location—LUSB
 Radiation—LMSB, bilateral axillae, mid-
back, approximately same intensity over
entire precordium
 Timing—early to mid-systole

190. Physiologic PPS :
 Intensity—grade I-II
 Pitch—high-pitched
 Character—blowing, not harsh, diamond-
shaped
 Variation—none

191. 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

192. Supraclavicular or
Brachiocephalic Systolic Murmur
(Carotid Bruit):
 Need to differentiate from supravalvar or
valvar AS, CoA, bicuspid AoV
 Bruit is French for “noise”

193. Carotid Bruit :
 Location—suprasternal notch,
supraclavicular areas
 Radiation—carotids, below clavicles
 Timing—early to mid-systole

194. Carotid Bruit :
 Intensity—grade I-III, ?IV (may have a
faint localized thrill)
 Pitch—mid-pitched
 Character—may be slightly harsh

195. 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

196. 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

197. 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

198. 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

199. 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

200. 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”

201. 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)

202. 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

203. Mammary Souffle :
 Age range—rare (hopefully!) in pediatric
population
 Etiology—increased blood flow to the
relatively smaller mammary blood vessels

205. don’t forget it!!
THE REST OF THE BODY--

206. Vital signs:
 Temperature
 Respiratory rate
 Weight and height

208. 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.

209. 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)

210. Lungs :
 Possible signs of increased pulmonary
blood flow
− Tachypnea
− Dyspnea
− Retractions
− Flaring
− Grunting
− Panting

211. 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)

212. 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

213. 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)

214. 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

215. 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

216. 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

217. Infective endocarditis:
 Splenomegaly
 New/changing murmur
 Fever
 Positive blood cultures
 Neurologic changes
 Peripheral signs of embolic phenomena

218. Ascites:
 Severe right or right AND left sided CHF--
from Fontan anastomosis, dilated
cardiomyopathy

219. Nutrition/muscle mass:
 Wasting (systemic, bitemporal)--from poor
nutrition/high metabolic demand (CHF)

220. Skin:
 Sweating and pallor (diaphoresis) --
associated with increased adrenergic tone

221. 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

222. 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

223. OTHER SYSTEMS

224. 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.

225. CNS:
 Developmental delay
 Seizures
 Certain personality traits associated with
these findings (usually not in isolation)

226. Extremities:
 Abnormal palmar creases
 Polydactyly
 Arachnodactyly
 Thumb/radial anomalies
 Phocomelia
 Pseudohypertrophy
 Nail anomalies