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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- 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, midback, 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, diamondshaped 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 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.): 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
