CVS examination

1. Prof J P Soni
• HoD Department of Pediatric
• Division of Pediatric Cardiology
• Dr S N Medical College ; Jodhpur
CARDIOVASCULAR SYSTEM
EXAMINATION
CARDIOVASCULAR SYSTEM
EXAMINATION

2. Arterial Pulse:
◆ 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
more than velocity of blood in aorta.
• It is 100 times more than velocity of blood
flow in peripheral arteries.

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

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

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

6. 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 5-8 m/sec( Blood flow at
velocity of 0.5 m/sec.

7. 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.

8. 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.

9. 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

10. 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.

11. 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.

12. 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
a radial pulses and a femoral
pulse

13. 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

14. 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.

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

16. 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.

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

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

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

20. 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)

21. 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)

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

23. High Output States
• Anemia
• Pyrexia
• Beri beri
• Thyrotoxicosis
• Pheochromocytoma
• AV fistula

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

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

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

27. • 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 down stroke of
pulse, d/t elastic recoil of vessel
*wavy pattern is not felt in health since it is obliterated
by normal vascular tone

28. 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

29. 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.

30. 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

31. 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.

32. • **--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.

33. 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

34. 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

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

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

37. 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

38. 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

39. 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

40. 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

41. 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

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

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

44. Reverse Pulsus
Paradoxus
Peripheral arterial systolic
and diastolic 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

45. 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

46. 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

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

48. 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.

49. 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 infant &
young children.
• It become tortuous, easily palpable & whip cord
• Like in old age due to arteriosclerosis.

50. 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

51. 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

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

53. 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)

54. 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

55. Equipment
• Aneroid
• Ocillo metric
• Hybrid
• Mercury (used only for accuracy)

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

59. 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.

60. Why Right Internal Jugular Vein?
• Right jugular
veins extend in an
almost straight
line to superior
vena cava, thus
favoring
transmission of
the hemodynamic
changes from the
right atrium.

61. 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.

62. 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.

63. 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

64. JVP Inspection

65. 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.

66. ---------------------------------------------------------
---------------------------------------------------------
Angle of louis
• Usually JVP is less than 8 cm water that is
< 3 cm above level of sternal angle.

68. 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

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

71. • 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

72. • 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

73. 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

74. 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.

75. • 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

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

77. 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

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

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

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

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

82. 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

83. “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

84. 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

85. 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.

86. 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

88. 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

89. 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

90. 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

91. 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 done in calm
and quiet room.

92. 92
Inspection & Palpation
1 Pre-cordial projection and
excavation
2 Apical impulse
3 Abnormal pulsations of
precordium

93. 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

94. 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

95. 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

96. 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

97. 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.

98. 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

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

100. Apical Impulse :
 Hyper-dynamic : Forceful but ill-sustained
 Hyper-dynamic impulse in normal location:
think increased cardiac output or LVH
 Hyper-dynamic and displaced downward /left
think LVE
 Indistinct impulse associated with RVH
 Precordial heave is seen with RVE

101. Apical Impulse :
 Heaving : Forceful and sustained
 Tapping : Normal apex beat

102. 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)

103. 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

104. 104
Percussion
• Aim:to determine the size and shape
of the heart .
• Absolute dullness: contain no gas
Relative dullness : real size

105. 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

106. AUSCULTATION

107. 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

108. 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

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

110. 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)

111. 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).

112. 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.

113. 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

114. 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

115. Normal heart
sounds

116. 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

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

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

119. 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

120. 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

121. 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

122. 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

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

124. S2 splitting (abnormal):
 Widely fixed splitting
− ASD
− RBBB
 Wide & variable splitting
− Mild PS
− RVOTO
− Large VSD or PDA
− Idiopathic PA dilation
− Severe MR
− RBBB
− PVC’s

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

126. 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

127. Additional heart sounds

128. 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

129. 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

130. 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

131. 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

132. 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

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

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

135. 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!!

136. 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

137. 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

138. 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

139. 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

140. 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

141. 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

142. 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

143. Mid-systolic (ejection) murmurs
• Are the most common type 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

144. 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

145. 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

148. Diastolic Murmurs
2. Early decrescendo diastolic murmurs
– signify regurgitant flow through an incompetent 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 patholog
• Other associated murmurs:
i. Midsystolic murmur
ii. Austin Flint murmur

149. 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

150. MANEUVERS

151. Routine positions--
 CVS examination should be performed
in following position-
 Neonate and Infant in mother lap
and grown up patient in standing or
sitting position.

152. Other physical maneuvers
in
grown up children

153.  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

154. 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

155. Left lateral decubitus positioning
or leaning forward in an upright
position
 Apex of the heart falls toward the
chest wall, thus mitral valve and
aortic valve murmurs will be heard
more clearly.

156. 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

157. 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

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

159. 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

160. 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)

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

162. Occur at areas 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

163. Maneuvers which enhances
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.

164. 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)

165. Other maneuvers
 Isometric handgrips
 Valsalva (straining) maneuver--forced
expiration against a closed glottis after full
inspiration for at least 10 seconds
 Chemical maneuvers--rarely, performed
today due to availability of better imaging
techniques.

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

167. 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

168. 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

169. 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)

170. Innocent Pulmonary Systolic
Murmur
 Need to differentiate from murmur of
ASD, PS, subAS, VSD & peripheral
pulmonary stenosis

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

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

173. 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

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

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

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

177. 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

178. Supraclavicular or
Brachiocephalic Systolic
Murmur (Carotid Bruit)
 Need to differentiate from supra-
valvar or valvar AS, CoA, bicuspid
AoV
 Bruit is French word for “noise”

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

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

181. 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

182. 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

183. 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

184. 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 with fingers, or with Valsalva

185. Venous Hum
 Age range
– pre-school through grade school age (very
common)
– adolescent to young adults (rarely heard, can be
seen with increased blood flow states e.g.
anemia, pregnancy, thyrotoxicosis)
 Etiology—turbulence in jugular and
subclavian venous return meeting in SVC

186. 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”

187. 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)

188. 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

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

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

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

193. 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.

194. 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)

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

196. 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)

197. 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

198. 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)

199. 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

200. Liver
 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

201. 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
with CHF

202. Features suggestive of
infective endocarditis
 Splenomegaly
 New/changing murmur
 Fever
 Positive blood cultures
 Neurologic changes
 Peripheral signs of embolic
phenomena

203. Ascites
 Severe right or right AND left sided
CHF—
 Following Fontan anastomosis
 Dilated cardiomyopathy
 Contrictive pericarditis

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

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

206. 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

207. 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