Transcript THE PHYSICAL EXAMINATION IN CARDIOLOGY

THE PHYSICAL
EXAMINATION IN
CARDIOLOGY AND
INNOCENT MURMURS
Cardiac physical examination can
be amongst the most diagnostic if
done correctly and carefully

Knowledge of cardiac physiology and
auscultation techniques/maneuvers can
often determine a diagnosis, or help to form
a strong differential diagnosis
Physical examination-
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Evaluating signs throughout the body for
evidence of hemodynamic sufficiency or
insufficiency
More difficult to assess in infants and
children
Exam findings should be often easier to
hear in cooperative younger children and in
adolescents than in adults
GENERAL EXAMINATION
GUIDELINES
The patient:
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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
Should be calm and quiet
The stethoscope:
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Should be your 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
The stethoscope (cont.):
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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
The environment:
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Should be quiet (patient, family, clinic
attendants, exam room, surrounding areas)
– May briefly disconnect ventilator or occlude
suction devices
– Brief bilateral occlusion of infant’s nares (warn
the parents first)
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Should be well lit
INSPECTION:
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Chest observation gives clues to
cardiopulmonary disease
Can be insensitive
INSPECTION (cont.):
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Asymmetry can indicate RVE
Increased A-P chest diameter indicates
chronic air trapping/hyperinflation
Pectus deformities--usually no significant
cardiopulmonary consequences
Kyphoscoliosis--can have cardiopulmonary
effect
INSPECTION (cont.):
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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
Apical Impulse:
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Visualization to assess ventricular
size/thickness
Normally distinct and located at 4ICS
at/inside the midclavicular line
Apical Impulse (abnormal):
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Hyperdynamic impulse in normal location:
think increased cardiac output or LVH
Hyperdynamic and downward/leftwardly
displaced: think LVE
Indistinct impulse associated with RVH
Precordial heave is seen with RVE
PALPATION:
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Sometimes overlooked and not always
helpful
Use the most sensitive portion of the hand
Lay the heel of R hand at left sternal border
with fingertips pointing to left axilla
RV impulse:
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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)
LV/apical impulse (PMI):
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Found w/ the fingertips with the patient
upright
Note interspace location, relation to the
midclavicular/anterior axillary line,
amplitude compared to RV impulse
LV/apical impulse (abnormal):
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Strong impulse is due to increased cardiac
output or LVH
Downward/leftward displacement--LVE
(with or without LVH)
Thrills:
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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
PERCUSSION:
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Usually not performed for cardiac borders,
but for lung fields
Should be done in the upright position (even
infants can be held upright....)
AUSCULTATION: the bread
and butter of the business
Where to listen:
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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)
Where to listen (cont.):
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Left and right infraclavicular areas
Left anterior axillary line
R and L axillae
R and L interscapular areas of back (for
pulmonary/aortic collaterals)
Where to Listen (Other sites):
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Lungs
Cranium (temples/orbits/fontanelle)
Liver
Neck (carotid area)
Abdomen
Lumbar/abdominal region over renal area
Mouth/trachea with respiration
Femoral artery
How to listen:
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Have a system, e.g. method of inching
Listen systematically: S1, S2, systolic
sounds, systolic murmurs, diastolic sounds,
diastolic murmurs
Normal heart sounds
S1:
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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
S1 (cont.):
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If split heard better at the apex, may
actually be S4 or ejection click
Tends to be more low-pitched and long as
compared to S2
Differentiate S1 from S2 by palpating
carotid pulse:
 S1 comes before and S2 comes after carotid
upstroke
Decreased S1:
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Slowed ventricular ejection rate/volume
Mitral insufficiency
Increased chest wall thickness
Pericardial effusion
Hypothyroidism
Decreased S1 (cont.):
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Cardiomyopathy
LBBB
Shock
Aortic insufficiency
First degree AV block
Other Abnormal S1 (cont.):
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Increased S1:
 Increased cardiac output
 Increased A-V valve flow velocity (acquired
mitral stenosis, but not congenital MS)
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Wide splitting of S1:
 RBBB (at tricuspid area)
 PVC’s
 VT
S2:
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From closure vibrations of aortic and
pulmonary valves
Often ignored, but it can tell much
Divided into A2 and P2 (aortic and
pulmonary closure sounds)
Best heard at LMSB/2LICS
Higher pitched than S1--better heard with
diaphragm
S2 splitting (normal):
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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
S2 splitting (normal, cont.):
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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
S2 splitting (abnormal):
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Persistent expiratory splitting
 ASD
 RBBB
 Mild valvar PS
 Idiopathic dilation of the PA
 WPW
S2 splitting (abnormal, cont.):
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Widely fixed splitting
 ASD
 RBBB
S2 splitting (abnormal, cont.):
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Wide /mobile splitting
 Mild PS
 RVOTO
 Large VSD or PDA
 Idiopathic PA dilation
 Severe MR
 RBBB
 PVC’s
S2 splitting (abnormal, cont.):
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Reversed splitting
 LBBB
 WPW
 Paced beats
 PVC’s
 AS
 PDA
 LV failure
Single S2:
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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
Extra heart sounds
S3 (gallop):
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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
S3 (cont.):
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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
S3 (abnormal):
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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
S4 (gallop):
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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
S4 (cont.):
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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
S4 Associations:
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CHF!!!
HCM
severe systemic HTN
pulmonary HTN
Ebstein’s anomaly
myocarditis
S4 Associations (cont.):
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Tricuspid atresia
CHB
TAPVR
CoA
AS w/ severe LV disease
Kawasaki’s disease
Click:
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Usually pathologic
Snappy, high pitched sound usually in early
systole
Due to vibrations in the artery distal to a
stenotic valve
Can be associated with:
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Valvar aortic stenosis or pulmonary stenosis
Truncus arteriosus
Pulmonary atresia/VSD
Bicuspid aortic valve
Mitral valve prolapse (mid-systolic click)
Ebstein’s anomaly (can have multiple
clicks)
Does NOT occur w/ supravalvar
or subvalvar AS, or calcific
valvar AS.
Whoop (sometimes called a
honk):
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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
Friction rub:
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Creaking sound heard with pericardial
inflammation
Classically has 3 components; can have
fewer than 3 components
Changes with position, louder with
inspiration
Murmur:
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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!!
Cardiac exam and murmur
general descriptors:
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Various combinations used for all normal
and abnormal heart sounds
General descriptors:
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Heart sound splitting
Grade/intensity
Phase
Shape
Pitch
General descriptors (cont.):
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Timing within the phase
Duration within the phase
Character/quality
Location of maximum intensity on the
precordium
Radiation of murmur
MANEUVERS
Routine positions-
Supine and standing or sitting examinations
should be performed on all patients
Other physical maneuvers
Squatting:
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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
Sudden standing:
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Decreased afterload, decreased venous
return and stroke volume, increased heart
rate, increased SVR):
Accentuates the murmur and S4 of subAS,
MVP, and HOCM
Left lateral decubitus positioning
or leaning forward
in an upright position:
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Apex of the heart falls toward the chest wall
Brings out mitral valve and aortic valve
murmurs
Some maneuvers for innocent
murmurs (more later):
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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
Other maneuvers:
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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)
Other maneuvers (cont.):
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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
THE REST OF THE BODY-don’t forget it!!
Vital signs:
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Temperature
Respiratory rate
Heart rate
Blood pressure
Oxygen saturations
Weight and height
Lungs:
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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)
Lungs (cont.):
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Possible signs of increased pulmonary
blood flow
 Tachypnea
 Dyspnea
 Retractions
 Flaring
 Grunting
 Panting
Edema:
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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)
Edema (cont.):
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Locations:
 Periorbital
 Scrotal
 Pre-sacral
 Hand/foot area
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Nonpitting pedal/hand edema or
lymphedema in a newborn: think Turner’s
or Noonan’s syndrome
Liver:
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Measure at midclavicular line where it
crosses the 9th costal cartilage
Can be right-sided (situs solitus), left-sided
(situs inversus), or midline (situs
ambiguous--measured subxiphoid)
Liver (cont.):
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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
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Use warm, gentle hands
Liver--abnormal:
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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
Spleen:
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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
Infective endocarditis:
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Splenomegaly
New/changing murmur
Fever
Positive blood cultures
Neurologic changes
Peripheral signs of embolic phenomena
Ascites:
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Severe right or right AND left sided CHF-from Fontan anastomosis, dilated
cardiomyopathy
Nutrition/muscle mass:
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Wasting (systemic, bitemporal)--from poor
nutrition/high metabolic demand (CHF)
Skin:
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Sweating and pallor (diaphoresis) -associated with increased adrenergic tone
Cyanosis of the mucus
membranes:
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Central--from > 3g reduced Hb in the
arterial blood due to cardiac or pulmonary
shunting
Acrocyanosis--from low cardiac output
Differential cyanosis
Arterial Pulses:
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Assess for rate, rhythm, volume, character
Evaluate radial, brachial, femoral, pedal
(dorsalis pedis or posterior tibialis) pulses
Also palmar and plantar pulses in newborns
Congenital absence of dorsalis pedis in 10%
of population
Simultaneous evaluation of both radial
pulses and R radial plus a femoral pulse
Rate:
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Bradycardic (conditioning, heart block,
digoxin toxicity)
Normal
Tachycardic (CHF, excitement, fever,
anemia, arrhythmia)
Rhythm:
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Regular
Irregular (can be sinus arrhythmia with
respiratory variation or PAC/PVC’s)
Regularly irregular
Irregularly irregular (arrhythmia)
Volume:
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Bounding/water hammer (pulse pressure
>30 mmHg in infant, >50 mmHg in child)
Full
Normal
Thready
 low output states: shock, severe CHF, large
VSD or PDA
 L sided obstruction: AS, aortic atresia, HLHS
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Absent
Character:
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Normal
Alternans
Bisferiens
Paradoxus
Clubbing:
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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
OTHER SYSTEMS
Facial features of certain
syndromes, chromosomal
anomalies, and associations
important to recognize:
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Anomalies of the eyes and lens, nose, ears,
mandible/maxilla, tongue, dentition and
gingiva, asymmetry of the facial
musculature, etc.
CNS:
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Developmental delay
Seizures
Certain personality traits associated with
these findings (usually not in isolation)
Extremities:
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Abnormal palmar creases
Polydactyly
Arachnodactyly
Thumb/radial anomalies
Phocomelia
Pseudohypertrophy
Nail anomalies
GI tract:
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T-E fistula
Omphalocele
Imperforate anus
Diaphragmatic hernia
Esophageal or duodenal atresia
GU tract:
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Renal anomalies
Bladder anomalies
Gonadal dysgenesis
External genitalia anomalies
Nephrocalcinosis
Skeleton:
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Scoliosis
Sternal anomalies
Tall or short stature
Hypermobility of the joints
Fused/hemi/absent/butterfly vertebrae
Caudal regression
Skin:
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Poor wound healing
Increased elasticity
Lentigines/nevi
Hemangiomata
Petechiae
Fragility/bruisability
Cafe’ au lait spots
Endocrine anomalies:
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Hypercalcemia
Hypocalcemia
Hyper or hypothyroidism
Hypogonadism
Renal tubular acidosis
INNOCENT MURMURS
INNOCENT MURMURS:
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Also known as flow, benign, normal,
nonpathologic, 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
General “Rules” of Innocent
Murmurs:
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Grade I-III intensity
No thrills associated at any area of
precordium
Only minimal transmission
Not harsh
Brief duration (usually early to mid-systole)
More General “Rules” of
Innocent Murmurs:
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Never solely diastolic
Never loudest at the RUSB/R base
No clicks
Normal S2
Occur at areas of mismatch of
normal blood flow volumes with
decreasing vessel caliber size
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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
Having more than one innocent
murmur in a patient is normal,
too!
Vibratory Systolic Murmur
(Still’s Murmur):
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Most common innocent murmur of
childhood
Needs maneuvers  normal ECG to
differentiate from subAS, HOCM, VSD
Still’s Murmur (Characteristics):
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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
Still’s Murmur (Characteristics,
cont.):
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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
Still’s Murmur (Characteristics,
cont.):
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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)
Innocent Pulmonary Systolic
Murmur:
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Need to differentiate from ASD, PS, subAS,
VSD, and true/organic PPS
Innocent Pulmonary Systolic
Murmur (Characteristics):
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Location—LUSB
Radiation—possible to hear at LMSB
Timing—early to mid-systole with peak in
mid-systole
Innocent Pulmonary Systolic
Murmur (Characteristics, cont.):
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Intensity—grade I-III
Pitch—mid to high-pitched
Character—soft, blowing, somewhat
grating, diamond-shaped
Innocent Pulmonary Systolic
Murmur (Characteristics, cont.):
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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
Physiologic Peripheral
Pulmonic Stenosis (PPS):

Need to differentiate from valvar PS, ASD,
true/organic PPS, and ToF
Physiologic PPS
(Characteristics):
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Location—LUSB
Radiation—LMSB, bilateral axillae, midback, approximately same intensity over
entire precordium
Timing—early to mid-systole
Physiologic PPS
(Characteristics, cont.):
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Intensity—grade I-II
Pitch—high-pitched
Character—blowing, not harsh, diamondshaped
Variation—none
Physiologic PPS
(Characteristics, cont.):
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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
Supraclavicular or
Brachiocephalic Systolic Murmur
(Carotid Bruit):
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
Need to differentiate from supravalvar or
valvar AS, CoA, bicuspid AoV
Bruit is French for “noise”
Carotid Bruit (Characteristics):
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Location—suprasternal notch,
supraclavicular areas
Radiation—carotids, below clavicles
Timing—early to mid-systole
Carotid Bruit (Characteristics,
cont.):
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Intensity—grade I-III, ?IV (may have a
faint localized thrill)
Pitch—mid-pitched
Character—may be slightly harsh
Carotid Bruit (Characteristics,
cont.):
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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
Venous Hum:
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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
Venous Hum (Characteristics):
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Location—anterior neck to midinfraclavicular area, R side > L side
Radiation—may go to LMSB
Timing—continuous with diastolic
accentuation
Intensity—grade I-III
Pitch—mid to low
Venous Hum (Characteristics,
cont.):
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
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
Venous Hum (Characteristics,
cont.):

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
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”
Mammary Souffle
(Characteristics):



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)
Mammary Souffle
(Characteristics, cont.):




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
Mammary Souffle
(Characteristics, cont.):


Age range—rare (hopefully!) in pediatric
population
Etiology—increased blood flow to the
relatively smaller mammary blood vessels