Cardiac Physical Exam and Innocent Murmurs Presentation

7/31/2019 Cardiac Physical Exam and Innocent Murmurs Presentation

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THE PHYSICAL

EXAMINATION INCARDIOLOGY AND

INNOCENT MURMURS

Jeff Boris, Lt Col, USAF, MC

Pediatric Cardiologist


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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


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GENERAL EXAMINATION

GUIDELINES


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The patient:

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


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The stethoscope:

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


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The stethoscope (cont.):

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


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The environment:

Should be quiet (patient, family, clinic

attendants, exam room, surrounding areas)

May briefly disconnect ventilator or occludesuction devices

Brief bilateral occlusion of infants nares (warn

the parents first) Should be well lit


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INSPECTION:

Chest observation gives clues to

cardiopulmonary disease

Can be insensitive


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INSPECTION (cont.):

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


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INSPECTION (cont.):

Polands anomaly (unilateral absence of

pectoralis major/minor)

Harrisons grooves seen in the lower chest

Pulsations/rocking seen with large shunts,

MR, or AI


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Apical Impulse:

Visualization to assess ventricular

size/thickness

Normally distinct and located at 4ICS

at/inside the midclavicular line


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Apical Impulse (abnormal):

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


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PALPATION:

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


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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)


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LV/apical impulse (PMI):

Found w/ the fingertips with the patient

upright

Note interspace location, relation to the

midclavicular/anterior axillary line,

amplitude compared to RV impulse


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LV/apical impulse (abnormal):

Strong impulse is due to increased cardiac

output or LVH

Downward/leftward displacement--LVE(with or without LVH)


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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


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PERCUSSION:

Usually not performed for cardiac borders,

but for lung fields

Should be done in the upright position (eveninfants can be held upright....)


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AUSCULTATION: the bread

and butter of the business


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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)


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Where to listen (cont.):

Left and right infraclavicular areas

Left anterior axillary line

R and L axillae

R and L interscapular areas of back (for

pulmonary/aortic collaterals)


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Where to Listen (Other sites):

Lungs

Cranium (temples/orbits/fontanelle)

Liver

Neck (carotid area)

Abdomen

Lumbar/abdominal region over renal area Mouth/trachea with respiration

Femoral artery


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How to listen:

Have a system, e.g. method of inching

Listen systematically: S1, S2, systolic

sounds, systolic murmurs, diastolic sounds,diastolic murmurs


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Normal heart sounds


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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


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S1 (cont.):

If split heard better at the apex, mayactually be S4 or ejection click

Tends to be more low-pitched and long ascompared to S2

Differentiate S1 from S2 by palpatingcarotid pulse:

S1 comes before and S2 comes after carotidupstroke


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Decreased S1:

Slowed ventricular ejection rate/volume

Mitral insufficiency

Increased chest wall thickness

Pericardial effusion

Hypothyroidism


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Decreased S1 (cont.):

Cardiomyopathy

LBBB

Shock

Aortic insufficiency

First degree AV block


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Other Abnormal S1 (cont.):

Increased S1:

Increased cardiac output

Increased A-V valve flow velocity (acquiredmitral stenosis, but not congenital MS)

Wide splitting of S1:

RBBB (at tricuspid area)

PVCs

VT


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S2:

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


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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


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S2 splitting (normal, cont.):

Respiratory variation causes splitting on

inspiration: pulmonary vascular resistance

When supine, slight splitting can occur inexpiration

When upright, S2 usually becomes single

with expiration


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S2 splitting (abnormal):

Persistent expiratory splitting

ASD

RBBB

Mild valvar PS

Idiopathic dilation of the PA

WPW


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S2 splitting (abnormal, cont.):

Widely fixed splitting

ASD

RBBB


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Wide /mobile splitting

Mild PS

RVOTO

Large VSD or PDA

Idiopathic PA dilation

Severe MR RBBB

PVCs


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Reversed splitting

LBBB

WPW

Paced beats

PVCs

AS PDA

LV failure


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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


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Extra heart sounds


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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


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S3 (cont.):

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


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S3 (abnormal):

Seen with Kawasakis disease--disappears

after treatment

If prolonged/high pitched/louder: can be a diastolic flow rumble indicating

increased flow volume from atrium to ventricle


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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


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S4 (cont.):

Better heard at the apex or LLSB in the

supine or left lateral decubitus position

Occurs separate from S3 or as summationgallop (single intense diastolic sound) with

S3


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S4 Associations:

CHF!!!

HCM

severe systemic HTN

pulmonary HTN

Ebsteins anomaly

myocarditis


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S4 Associations (cont.):

Tricuspid atresia

CHB

TAPVR

CoA

AS w/ severe LV disease

Kawasakis disease


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Click:

Usually pathologic

Snappy, high pitched sound usually in early

systole

Due to vibrations in the artery distal to a

stenotic valve


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Can be associated with:

Valvar aortic stenosis or pulmonary stenosis

Truncus arteriosus

Pulmonary atresia/VSD

Bicuspid aortic valve

Mitral valve prolapse (mid-systolic click)

Ebsteins anomaly (can have multiple

clicks)


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Does NOT occur w/ supravalvar

or subvalvar AS, or calcific

valvar AS.


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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/ VSDs closing w/ an aneurysm,

subAS, rarely TR

Some whoops evolve to become systolicmurmurs


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Friction rub:

Creaking sound heard with pericardial

inflammation

Classically has 3 components; can havefewer than 3 components

Changes with position, louder with

inspiration


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Murmur:

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 Dont let murmurs distract you from the rest

of the exam!!


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Cardiac exam and murmur

general descriptors:

Various combinations used for all normaland abnormal heart sounds


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General descriptors:

Heart sound splitting

Grade/intensity

Phase

Shape

Pitch


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General descriptors (cont.):

Timing within the phase

Duration within the phase

Character/quality

Location of maximum intensity on the

precordium

Radiation of murmur


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MANEUVERS


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Routine positions--

Supine and standing or sitting examinations

should be performed on all patients


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Other physical maneuvers


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Squatting:

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


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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

Left lateral decubitus positioning


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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


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Some maneuvers for innocent

murmurs (more later): Jugular vein compression/turning the head

can abolish venous hum

Lying the patient perfectly flat is the mostreliable method of quieting the hum.

Compression of the subclavian artery or

shoulder extension can abolishsupraclavicular bruit


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Other maneuvers (cont.):

Isometric handgrips

Valsalva (straining) maneuver--forced

expiration against a closed glottis after fullinspiration for at least 10 seconds

Chemical maneuvers--rarely, if ever,

performed today due to better imagingtechniques


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THE REST OF THE BODY--

dont forget it!!


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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)


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Lungs (cont.):

Possible signs of increased pulmonary

blood flow

Tachypnea Dyspnea

Retractions

Flaring Grunting

Panting


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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)


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Edema (cont.):

Locations:

Periorbital

Scrotal Pre-sacral

Hand/foot area

Nonpitting pedal/hand edema orlymphedema in a newborn: think Turners

or Noonans syndrome


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Liver:

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)


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Liver (cont.):

Measurements:

2-3 cm below the RCM in the infant

2 cm below the RCM from 1-3 years of age1 cm below the RCM from 4-5 years of age

Use warm, gentle hands


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Liver--abnormal:

Hepatomegaly caused by systemic venous

congestion

Right-sided CHF: liver enlarges, becomesfirm, 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


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Infective endocarditis:

Splenomegaly

New/changing murmur

Fever

Positive blood cultures

Neurologic changes

Peripheral signs of embolic phenomena


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Ascites:

Severe right or right AND left sided CHF--

from Fontan anastomosis, dilatedcardiomyopathy


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Nutrition/muscle mass:

Wasting (systemic, bitemporal)--from poor

nutrition/high metabolic demand (CHF)


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Skin:

Sweating and pallor (diaphoresis) --

associated with increased adrenergic tone


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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


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Arterial Pulses:

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


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Rate:

Bradycardic (conditioning, heart block,

digoxin toxicity)

Normal Tachycardic (CHF, excitement, fever,

anemia, arrhythmia)


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Rhythm:

Regular

Irregular (can be sinus arrhythmia with

respiratory variation or PAC/PVCs) Regularly irregular

Irregularly irregular (arrhythmia)

V l


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Volume:

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

Absent


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Character:

Normal

Alternans

Bisferiens

Paradoxus


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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 ofhypoxemia, can disappear with anemia


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OTHER SYSTEMS

Facial features of certain


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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 facialmusculature, etc.


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GI tract:

T-E fistula

Omphalocele

Imperforate anus

Diaphragmatic hernia

Esophageal or duodenal atresia


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GU tract:

Renal anomalies

Bladder anomalies

Gonadal dysgenesis

External genitalia anomalies

Nephrocalcinosis


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Skeleton:

Scoliosis

Sternal anomalies

Tall or short stature

Hypermobility of the joints

Fused/hemi/absent/butterfly vertebrae

Caudal regression


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Skin:

Poor wound healing

Increased elasticity

Lentigines/nevi

Hemangiomata

Petechiae

Fragility/bruisability

Cafe au lait spots


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Endocrine anomalies:

Hypercalcemia

Hypocalcemia

Hyper or hypothyroidism

Hypogonadism

Renal tubular acidosis


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INNOCENT MURMURS


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INNOCENT MURMURS:

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


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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)

More General Rules of


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More General Rules of

Innocent Murmurs:

Never solely diastolic

Never loudest at the RUSB/R base

No clicks

Normal S2


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Occur at areas of mismatch of

normal blood flow volumes withdecreasing vessel caliber size

e.g. LVOT, RVOT, branch PAs, etc.

Better heard in children due to their thinner

chest walls with greater proximity ofstethoscope to vessel


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Having more than one innocent

murmur in a patient is normal,

too!


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Stills Murmur (Characteristics):

Locationmax at LLSB

Radiationmay radiate to LMSB, apex,

and R-L base (hockey-stick distribution),although may not completely radiate

Timingmid-systole

Intensitygrade I-II Pitchmid to low

Stills Murmur (Characteristics


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Still s Murmur (Characteristics,

cont.): Charactervibratory, groaning, musical,

buzzing, squeaking, guitar-string

twanging, cooing dove Variationloudest supine, after exercise,

with fever, anemia, or excitement

Disappears or localizes to LLSB whenupright

Stills Murmur (Characteristics


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Still s Murmur (Characteristics,

cont.): Age rangeuncommon in infancy,

commonly age 2 to 6 years, rare in teens

Etiologyunknown, may be associatedwith LV ejection

Similar murmur seen with LV false tendons

(but does not tend to diminish as muchwhen upright)

Innocent Pulmonary Systolic


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Murmur:

Need to differentiate from ASD, PS, subAS,

VSD, and true/organic PPS



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Murmur (Characteristics): LocationLUSB

Radiationpossible to hear at LMSB

Timingearly to mid-systole with peak inmid-systole



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Murmur (Characteristics, cont.): Intensitygrade I-III

Pitchmid to high-pitched

Charactersoft, blowing, somewhatgrating, diamond-shaped



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Murmur (Characteristics, cont.): Variationlouder when supine, fever,

exercise, anemia

Age rangemost commonly age 8-14years, but early childhood to young adults

Etiologynormal ejection vibrations into

MPA

Physiologic Peripheral


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Physiologic Peripheral

Pulmonic Stenosis (PPS):

Need to differentiate from valvar PS, ASD,

true/organic PPS, and ToF

Physiologic PPS


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Physiologic PPS

(Characteristics):

LocationLUSB

RadiationLMSB, bilateral axillae, mid-back, approximately same intensity over

entire precordium

Timingearly to mid-systole

Physiologic PPS


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Physiologic PPS

(Characteristics, cont.): Intensitygrade I-II

Pitchhigh-pitched

Characterblowing, not harsh, diamond-shaped

Variationnone

Physiologic PPS


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(Characteristics, cont.):

Age rangenewborns, especially premies.

May last 36 months but not longer

(requires further eval if persistent)

Etiologysmall relative size of branch PA

bifurcation to MPA at birth with acute angle

turbulence and relative obstruction

Supraclavicular or


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Brachiocephalic Systolic Murmur

(Carotid Bruit):

Need to differentiate from supravalvar or

valvar AS, CoA, bicuspid AoV Bruitis French for noise


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Carotid Bruit (Characteristics):

Locationsuprasternal notch,

supraclavicular areas

Radiationcarotids, below clavicles Timingearly to mid-systole


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Carotid Bruit (Characteristics


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Carotid Bruit (Characteristics,

cont.): Variationdecreased intensity with

hyperextension of shoulders; louder with

anxiety, anemia, or trained athletes w/resting bradycardia

Age rangechildren and young adults

Etiologyunknown, ? turbulence at takeoffof carotid or brachiocephalic vessels


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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


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Venous Hum (Characteristics):

Locationanterior neck to mid-

infraclavicular area, R side > L side

Radiationmay go to LMSB Timingcontinuous with diastolic

accentuation

Intensitygrade I-III Pitchmid to low

Venous Hum (Characteristics,


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cont.):

Charactersoft, whispering, roaring, or

blowing, distant-sounding

Variationdisappears when supine, withhead turn AWAY from the side listened to,

with gentle manual compression of jugular

venous return w/ fingers, or w/ Valsalva



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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)

Etiologyturbulence in jugular and

subclavian venous return meeting in SVC

M S ffl


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Mammary Souffle:

Occurs in certain circumstances of breast

development/activity and disappear

otherwise Differentiate from PDA, AVM, or AS/AI

Souffleis French for breath

Mammary Souffle


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Mammary Souffle

(Characteristics):

Locationheard over/just above breasts in

late pregnancy or in lactating women

Radiationnone Timingmay be systolic only, systole with

diastolic spill-over, or continuous with late

systolic accentuation (most common)

Mammary Souffle


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Mammary Souffle

(Characteristics, cont.):

Intensitygrade I-III

Pitchmid to high

Characterblowing or breath-like Variationobliterated by increased

stethoscope pressure or compressing the

tissue on both sides of the stethoscope


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Cardiac Physical Exam and Innocent Murmurs Presentation