THE PHYSICAL EXAMINATION IN

CARDIOLOGY AND INNOCENT MURMURS

Jeff Boris, Lt Col, USAF, MC

Pediatric Cardiologist

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--

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:

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:

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.):

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:

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) Should be well lit

INSPECTION:

Chest observation gives clues to cardiopulmonary disease

Can be insensitive

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

INSPECTION (cont.):

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:

Visualization to assess ventricular size/thickness

Normally distinct and located at 4ICS at/inside the midclavicular line

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

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

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)

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

LV/apical impulse (abnormal):

Strong impulse is due to increased cardiac output or LVH

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

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

PERCUSSION:

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:

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.):

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): 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:

Have a system, e.g. method of inching Listen systematically: S1, S2, systolic

sounds, systolic murmurs, diastolic sounds, diastolic murmurs

Normal heart sounds

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

S1 (cont.):

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:

Slowed ventricular ejection rate/volume Mitral insufficiency Increased chest wall thickness Pericardial effusion Hypothyroidism

Decreased S1 (cont.):

Cardiomyopathy LBBB Shock Aortic insufficiency First degree AV block

Other Abnormal S1 (cont.): 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

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

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

S2 splitting (normal, cont.):

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):

Persistent expiratory splitting ASD RBBB Mild valvar PS Idiopathic dilation of the PA WPW

S2 splitting (abnormal, cont.):

Widely fixed splitting ASD RBBB

S2 splitting (abnormal, cont.):

Wide /mobile splitting Mild PS RVOTO Large VSD or PDA Idiopathic PA dilation Severe MR RBBB PVC’s

S2 splitting (abnormal, cont.):

Reversed splitting LBBB WPW Paced beats PVC’s AS PDA LV failure

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

Extra heart sounds

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

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

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

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

S4 (cont.):

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:

CHF!!! HCM severe systemic HTN pulmonary HTN Ebstein’s anomaly myocarditis

S4 Associations (cont.):

Tricuspid atresia CHB TAPVR CoA AS w/ severe LV disease Kawasaki’s disease

Click:

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:

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):

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:

Creaking sound heard with pericardial inflammation

Classically has 3 components; can have fewer than 3 components

Changes with position, louder with inspiration

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

Don’t let murmurs distract you from the rest of the exam!!

Cardiac exam and murmur general descriptors:

Various combinations used for all normal and abnormal heart sounds

General descriptors:

Heart sound splitting Grade/intensity Phase Shape Pitch

General descriptors (cont.):

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:

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:

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:

Apex of the heart falls toward the chest wall Brings out mitral valve and aortic valve

murmurs

Some maneuvers for innocent murmurs (more later):

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:

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.):

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:

Temperature Respiratory rate Heart rate Blood pressure Oxygen saturations Weight and height

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)

Lungs (cont.):

Possible signs of increased pulmonary blood flow Tachypnea Dyspnea Retractions Flaring Grunting Panting

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)

Edema (cont.):

Locations: Periorbital Scrotal Pre-sacral Hand/foot area

Nonpitting pedal/hand edema or lymphedema in a newborn: think Turner’s or Noonan’s syndrome

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)

Liver (cont.):

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

Liver--abnormal:

Hepatomegaly caused by systemic venous congestion

Right-sided CHF: liver enlarges, becomes firm, loses distinct edge

Pulsatile liver: tricuspid regurgitation or other cause of elevated R sided pressures

Hard liver may be more serious than large, soft liver

Spleen:

Normally felt in newborns under the LCM Significant enlargement can indicate

TORCH infection with an associated cardiac lesion

Isolated splenomegaly is usually not seen w/ CHF

Infective endocarditis:

Splenomegaly New/changing murmur Fever Positive blood cultures Neurologic changes Peripheral signs of embolic phenomena

Ascites:

Severe right or right AND left sided CHF--from Fontan anastomosis, dilated cardiomyopathy

Nutrition/muscle mass:

Wasting (systemic, bitemporal)--from poor nutrition/high metabolic demand (CHF)

Skin:

Sweating and pallor (diaphoresis) --associated with increased adrenergic tone

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

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

Rate:

Bradycardic (conditioning, heart block, digoxin toxicity)

Normal Tachycardic (CHF, excitement, fever,

anemia, arrhythmia)

Rhythm:

Regular Irregular (can be sinus arrhythmia with

respiratory variation or PAC/PVC’s) Regularly irregular Irregularly irregular (arrhythmia)

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

Character:

Normal Alternans Bisferiens Paradoxus

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

OTHER SYSTEMS

Facial features of certain syndromes, chromosomal

anomalies, and associations important to recognize:

Anomalies of the eyes and lens, nose, ears, mandible/maxilla, tongue, dentition and gingiva, asymmetry of the facial musculature, etc.

CNS:

Developmental delay Seizures Certain personality traits associated with

these findings (usually not in isolation)

Extremities:

Abnormal palmar creases Polydactyly Arachnodactyly Thumb/radial anomalies Phocomelia Pseudohypertrophy Nail anomalies

GI tract:

T-E fistula Omphalocele Imperforate anus Diaphragmatic hernia Esophageal or duodenal atresia

GU tract:

Renal anomalies Bladder anomalies Gonadal dysgenesis External genitalia anomalies Nephrocalcinosis

Skeleton:

Scoliosis Sternal anomalies Tall or short stature Hypermobility of the joints Fused/hemi/absent/butterfly vertebrae Caudal regression

Skin:

Poor wound healing Increased elasticity Lentigines/nevi Hemangiomata Petechiae Fragility/bruisability Cafe’ au lait spots

Endocrine anomalies:

Hypercalcemia Hypocalcemia Hyper or hypothyroidism Hypogonadism Renal tubular acidosis

INNOCENT MURMURS

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 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 Innocent Murmurs:

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

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):

Most common innocent murmur of childhood

Needs maneuvers normal ECG to differentiate from subAS, HOCM, VSD

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

Still’s Murmur (Characteristics, cont.):

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.):

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:

Need to differentiate from ASD, PS, subAS, VSD, and true/organic PPS

Innocent Pulmonary Systolic Murmur (Characteristics):

Location—LUSB Radiation—possible to hear at LMSB Timing—early to mid-systole with peak in

mid-systole

Innocent Pulmonary Systolic Murmur (Characteristics, cont.):

Intensity—grade I-III Pitch—mid to high-pitched Character—soft, blowing, somewhat

grating, diamond-shaped

Innocent Pulmonary Systolic Murmur (Characteristics, cont.):

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):

Location—LUSB Radiation—LMSB, bilateral axillae, mid-

back, approximately same intensity over entire precordium

Timing—early to mid-systole

Physiologic PPS (Characteristics, cont.):

Intensity—grade I-II Pitch—high-pitched Character—blowing, not harsh, diamond-

shaped Variation—none

Physiologic PPS (Characteristics, cont.):

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):

Need to differentiate from supravalvar or valvar AS, CoA, bicuspid AoV

Bruit is French for “noise”

Carotid Bruit (Characteristics):

Location—suprasternal notch, supraclavicular areas

Radiation—carotids, below clavicles Timing—early to mid-systole

Carotid Bruit (Characteristics, cont.):

Intensity—grade I-III, ?IV (may have a faint localized thrill)

Pitch—mid-pitched Character—may be slightly harsh

Carotid Bruit (Characteristics, cont.):

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:

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):

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

Venous Hum (Characteristics, cont.):

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