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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
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
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
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 infants nares (warn the parents first)
INSPECTION:
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.):
Polands anomaly (unilateral absence of pectoralis major/minor) Harrisons 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
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)
Found w/ the fingertips with the patient upright Note interspace location, relation to the midclavicular/anterior axillary line, amplitude compared to RV impulse
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....)
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)
Left and right infraclavicular areas Left anterior axillary line R and L axillae R and L interscapular areas of back (for pulmonary/aortic collaterals)
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
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.):
Increased S1:
Increased cardiac output Increased A-V valve flow velocity (acquired mitral stenosis, but not congenital MS)
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
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):
Reversed splitting
LBBB WPW Paced beats PVCs 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
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):
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 Ebsteins anomaly myocarditis
S4 Associations (cont.):
Click:
Usually pathologic Snappy, high pitched sound usually in early systole Due to vibrations in the artery distal to a stenotic valve
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)
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 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 Dont let murmurs distract you from the rest of the exam!!
Various combinations used for all normal and abnormal heart sounds
General descriptors:
Timing within the phase Duration within the phase Character/quality Location of maximum intensity on the precordium Radiation of murmur
MANEUVERS
Routine positions-
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
Apex of the heart falls toward the chest wall Brings out mitral valve and aortic valve murmurs
Jugular vein compression/turning the head can abolish venous hum Lying the patient perfectly flat is the most reliable method of quieting the hum. Compression of the subclavian artery or shoulder extension can abolish supraclavicular bruit
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)
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
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.):
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
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
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:
Skin:
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/PVCs) 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:
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:
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
Grade I-III intensity No thrills associated at any area of precordium Only minimal transmission Not harsh Brief duration (usually early to mid-systole)
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 PAs, etc. Better heard in children due to their thinner chest walls with greater proximity of stethoscope to vessel
Most common innocent murmur of childhood Needs maneuvers normal ECG to differentiate from subAS, HOCM, VSD
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
Charactervibratory, groaning, musical, buzzing, squeaking, guitar-string twanging, cooing dove Variationloudest supine, after exercise, with fever, anemia, or excitement Disappears or localizes to LLSB when upright
Age rangeuncommon in infancy, commonly age 2 to 6 years, rare in teens Etiologyunknown, may be associated with LV ejection Similar murmur seen with LV false tendons (but does not tend to diminish as much when upright)
Need to differentiate from ASD, PS, subAS, VSD, and true/organic PPS
Variationlouder when supine, fever, exercise, anemia Age rangemost commonly age 8-14 years, but early childhood to young adults Etiologynormal ejection vibrations into MPA
Need to differentiate from valvar PS, ASD, true/organic PPS, and ToF
LocationLUSB RadiationLMSB, bilateral axillae, midback, approximately same intensity over entire precordium Timingearly to mid-systole
Age rangenewborns, especially premies. May last 3 6 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
Need to differentiate from supravalvar or valvar AS, CoA, bicuspid AoV Bruit is French for noise
Intensitygrade I-III, ?IV (may have a faint localized thrill) Pitchmid-pitched Charactermay be slightly harsh
Variationdecreased intensity with hyperextension of shoulders; louder with anxiety, anemia, or trained athletes w/ resting bradycardia Age rangechildren and young adults Etiologyunknown, ? 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
Locationanterior neck to midinfraclavicular area, R side > L side Radiationmay go to LMSB Timingcontinuous with diastolic accentuation Intensitygrade I-III Pitchmid to low
Charactersoft, whispering, roaring, or blowing, distant-sounding Variationdisappears when supine, with head turn AWAY from the side listened to, with gentle manual compression of jugular venous return w/ fingers, or w/ Valsalva
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)
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
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)
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
Age rangerare (hopefully!) in pediatric population Etiologyincreased blood flow to the relatively smaller mammary blood vessels