history and physical examination in cvs
TRANSCRIPT
History and Physical Examination in Cardio Vascular Systems
Prathapjai Nimboriboonporn, Pediatric cardiologist
Department of Pediatrics,Faculty of Medicine, Khon Kaen University
No conflict of interest to disclose
1. Age groups Newborns and infants
Toddlers and Preschoolers
Older Children and Adolescents
2. Post Medical and Surgical History
3. Prenatal and Birth History
4. Family History
5. Review systems, Social history
History in CVS
Newborns and infants
1. Behavior
Eating CHF; small amount gain, rapid breathing
Diaphoresis activation of sympathetic in low cardiac output
Unlabored tachypnea
2. Cyanosis
Deoxy-hemoglobin > 5 g/% (capillary level), in normal quantities of Hb; SpO2 < 85%
Difficult to recognize in anemic patient
Derived from Greek “kuaneos” meaning dark blue
Deoxyhemoglobin > 5 g/dL = SpO2 < 85% (normal quantities of Hb.)
(Difficult to recognize in anemic patient)
Central cyanosis; bluish discoloration of the skin, nail beds or
mucous membranes
Congen Cardiol Today. 2011;9:1-6.
Park's Pediatric Cardiology for Practitioners, 6th Ed.
Indian J Pediatr (November 2015) 82(11):1050–1060.
CAUSES OF CYANOSIS
Cardiac causes Non-cardiac causes
Right to left shunt lesion Intracardiac shunt
(mixing with right to left shunt)
Intrapulmonary shunt (pulmonary AVM)
RVOT obstructionParallel circulation
Respiratory: V-Q mismatch (airway, parenchyma), PPHN
Hematology: Hb abnormalities(e.g. methemoglobinemia)
Neurology: Hypoventilation
Metabolic: drugs, toxin
Cyanotic CHD Pulmonary diseases
Onset หลงั 24 -72 ชัว่โมง ทนัทีตั้งแต่แรกเกิด
เวลาร้อง อาการเขียวคล ้ามากข้ึน อาการเขียวคล ้าลดลง/ดีข้ึน
หายใจ ปกติ หรือ เร็วต้ืน หอบเหน่ือยมาก มี retraction
Murmur อาจฟังไม่ได ้murmur อาจฟังได้ innocent murmur
S2 Single Normal split
Hyperoxia อาการเขียวคล ้าไม่ดีข้ึน อาการเขียวคล ้าลดลง/ดีข้ึน
Hyperventilation อาการเขียวคล ้าไม่ดีข้ึน PPHN: อาการเขียวคล ้าลดลง/ดีข้ึน
Hyperoxia test 100% Oxygen 10 minutes
ABG (Right radial artery)
: PaO2
Hyperoxia– Hyperventilation test 100% Oxygen with PPV rate~100,
10 minutes
ABG: PaCO2 should be 25-30 mmHg
PaO2 Interpretation
<150 Cyanotic heart, severe PPHN
>150 Respiratory problems
PaO2 Interpretation
<150 Cyanotic heart
>150 severe PPHN,Respiratory problems
Central cyanosisPeripheral cyanosis
(Acrocyanosis)Differential
cyanosis
- Bluish discoloration oflips, oral mucosa, finger nail
- Bluish discoloration ofdistal part of extremities- Pink lips, oral mucosa
- Pink upper extremities- Bluish discoloration of lower extremities
- Always pathologic- Need immediateevaluation and treatment
- Usually benign- Peripheral vasoconstriction- May be from pathologiccauses (e.g. sepsis)
- Always pathologic(Congenital heart withright to left shunt across PDA)
“Cyanosis”
Right to left shunt across PDA
PPHN with PDA Interrupted aortic arch
with PDA Severe COA with PDA
Parameters Preductal > Postductal
PaO2 >10 mmHg
SpO2 >3%
99%123
75%123
preductal -
pink
Postductal
- blue89%123
Differential Cyanosis
Persistent pulmonary hypertension of newborn with PDA
Severe coarctation of aorta with PDA
Interruted aortic arch with PDA
• Pre ductal > Post ductal saturation (>3%)
• Occur when PDA is right to left flow (from PA to Ao)
Differential Cyanosis
https://www.criticalcare-sonography.com/2019/04/11/coarctation-of-the-aorta-in-a-neonate/http://www.pted.org/?id=interruptedarch1
• Post ductal > Pre ductal saturation (>3%)
• Occur when PDA flow from PA to Ao
Reverse differential Cyanosis
dTGA with PPHNwith PDA
dTGA with severeCoAwith PDA
dTGA with IAA with PDA
upper: cyanosislower: pink
https://www.facebook.com/pg/briefcardiology/photos/
Ductal dependent left sided obstruction 1st week, PDA closed; low output symptom
Left to right shunt
4-6 weeks, PVR decreases; increase left to right
shunt
ALCAPA
4-6 weeks, PVR decreases; ↓ coronary blood
flow
Time at which signs and symptoms
Newborns and infants
Toddlers and Preschoolers
1. Feeding and breathing symptoms2. Inability of physical activity3. Comparison; siblings or age mates
Older Children and Adolescents• Speak privately; drug use, sexual behavior
• Ability to tolerate exercise and physical
activity
• Orthopnea
• Paroxysmal nocturnal dyspnea
Palpitation Transient or sustained, Frequency and
duration Associated symptoms; fatigue,
shortness of breath, chest pain Circumstances (rest, exercise)
Chest painLocation/ duration
Palpitation, diaphoresis
Activity; movement, cough, breath
Exercise-induced chest pain
LVOTO, coronary abnormalities/ history
of Kawasaki syndrome
Older Children and Adolescents
Older Children and Adolescents Syncope Differential; neurogenic/ narcolepsy/ vago-vagal
or postural syncope
Postural syncope; prolonged standing, standing quickly from
sitting or supine position/ hot, n/v
Information of daily fluids intake, caffeine
Syncope without prodrome; sudden severe arrhythmia
Syncope when exercise; LVOTO, HCM
Past Medical and Surgical History
Previous hospitalization/ previous operation
Immunization status
Symptoms of poor growth
Congenital anomalies and syndromes that
associated with heart disease
Other illnesses and chronic condition
Chromosome Abnormalities
Down Syndrome (40-50%) AVSD, VSD, ASD
Trisomy 18 (95%) VSD, PDA, PS
Trisomy 13 (50-80%) VSD, PDA, Dextrocardia
Turner syndrome (45,X)(25%) CoA, BAV, ASD
Noonan syndrome (PTPN11)(85%) PS, ASD, HCM
William syndrome (7q11.23)(55-80%) Supravalvular AS, supravalvular PS
DiGeorge syndrome (22q11.2)(75-80%) Conotruncal defects
Holt-Oram syndrome (TBX5)(75%) ASD
Marfan syndrome (50%) Aortic aneurysm, MVP
Environmental factorsPregnancy related complication
Maternal GDM cardiomyopathy, Conotruncal defects
Maternal lupus congenital heart block
Congenital rubella PDA, PS
Teratogens
Alcohol, smoking ASD, VSD
Lithium Ebstein anomaly
Retinoic acid Conotruncal defects
Valproic acid ASD, VSD, AS, PA/IVS, COA
Family History
Left sided obstructive lesion (HLHS)Increase Risk of CHD in subsequent children
Syndromes associated with congenital heart
lesions• Marfan’s syndrome, Holt-Oram syndrome
• Valve abnormalities bicuspid aortic valve
• Idiopathic sudden death long QT syndrome
Vital signs
HR, RR◦ Myocardial dysfunction, pulmonary congestion, or
arrhythmia
BP◦ Both upper extremities and at least one lower
extremities
◦ Bladder of cuff 80% of circumference of the limb
◦ Width of the cuff cover at > 2/3 of the length of the extremity
◦ Korotkoff sounds
A fifth vital sign
Newborn infants◦Early mild desaturation detected may allow earlier detection of CHD
◦95% accepted as lower limit of normal
Pulse Oximetry Screening
Pulse Oxygen Saturation (SpO2)
Non-invasive and continuous assessment
of oxygenation
New generation of pulse oximeters have
improved performance during low
perfusion state
Simultaneous SpO2 from right hand and a foot (pre-ductal & post-ductal SpO2) in cyanotic infant
General appearance
Growth pattern: BW, Height, HC
General appearance, nutritional status
Dysmorphic features, color, and comfort
Cyanosis and Clubbing Child’s color (i.e., pink, cyanotic, pale)
Central cyanosis : gums and tongue
Long-standing cyanosis[>6mo] digital
clubbing
Widening and thickening of the ends of the fingers and toes
Convex fingernails
Loss of the angle between the nail and nail bed
Reddening and shininess of the terminal phalanges (early stages)
Other cause; lung disease (e.g., abscess), cirrhosis, and subacutebacterial endocarditis, familial clubbing
Clubbing fingers
Sweat on the Forehead Expression of heightened sympathetic
activity as a compensatory mechanism for
decreased cardiac output
Acanthosis Nigricans Insulin resistance (type 2 diabetes)
General appearance
CongenitalIncrease pulmonary flow (3T/2C)
◦ Transposition of great arteries◦ Truncus arteriosus◦ Total anomalous of pulmonary venous return◦ Common atrium/ common ventricle
Decrease pulmonary flow◦ Tetralogy of Fallot◦ PA/VSD, Ebstein anomaly◦ PA/IVS, Tricuspid atresia
Grown up◦ Lt Rt shunt with Eisenmenger
Central Cyanotic
Non-labored tachypnea : hypoxic respiratory drive
Grunting : producing PEEP•Pulmonary edema•Nasal flaring and intercostal and subcostal retractions •Severely distressed, the head will bob with respiratory effort
Breathing pattern
Neck Veins
Neck vein distention suggests impaired right
ventricular filling
Cannon A waves : atrial contraction against a
closed tricuspid valve
◦ Regular cannon A waves SVT or atrial flutter
◦ Irregular cannon A waves Complete heart block
o Bobbing of the head significant AR
Caused by increased carotid arterial pulsations striking the angles of the mandibles
o Lateral head movement significant TR
Regurgitant blood in SVC strikes the right mandibular angle
Neck Veins
Observation◦ Pectus excavatum ◦ Asymmetric chest wall motion
Diaphragmatic paralysis from phrenic nerve injury
Percussion ◦ Peripheral pulses, capillary refill time
Auscultation : rales or crackles, wheezing, rhonchi◦ Stridor Vascular rings or slings causing airway compression
Absent pulmonary valve with associated severe
pulmonary artery dilation
Respiratory Examination
Pectus excavatum
DDx; genetic 1/3, Marfan’s syndrome
Associated; scoliosis (15%), congenital heart
disease (1.5%), MVP
Surgical repair indication1. Transthoracic lateral diameter/
sternovertebral distance ratio > 3.52. Cosmetic
Pectus excavatum
Cardiovascular Examination
Observation
◦ Pulsations of suprasternal notch significant aortic runoff; AR
◦ Left parasternal precordial bulge RV volume load; ASD
◦ Chest wall surgical scars
Palpation, Pulses
o Diminished or weak pulses; cardiac failure or shock
o Absent or weak pulses in left arm; previous SCA flap repair COA, classical Blalock-Thomas-Taussing shunt
o Bouding pulses; aortic runoff
Cardiovascular Examination
Palpation o Regularity and quality of the pulsations, tissue
perfusion
o Thrill : vibratory sensations that represent
palpable; best felt with metacarpal heads of
the hand
Auscultation
Cardiovascular Examination
Normal S2 Semilunar valve (A,P) closure Physiologic splitting S2 during inspiration: A2 ดงักวา่และ
มาก่อน P2
ABNORMAL SECOND HEART SOUND (S2)
https://ir.uiowa.edu/cgi/viewcontent.cgi?article=1042&context=fmrc
Wide splitting of S2 occur in :
a) RV volume overload (ASD, PAPVR)b) RV outflow obstruction (PS)c) Delayed RV depolarization (RBBB)
Narrow splitting of S2 occur in:
a) PHT as the pulmonary valve closes earlier due to high PVR
b) Mild to moderate AS as the A2 is delayed
Abnormal splitting of S2
Single S2 may occur in:
a) One semilunar valve (pulmonary atresia, aortic atresia,
Truncus arteriosus)
b) Single ventricle or in large VSD with equal ventricular
pressures
c) P2 not audible (TGA, TOF, severe PS, severe AS)
Paradoxical splitting of S2 (P2 is heard before A2) occur in:
a) Severe aortic stenosis
b) Left bundle branch block
Abnormal S2
ABNORMAL SECOND HEART SOUND (S2)
Single S2Abnormal P2
intensityWidely fixed split
S2
One semilunar valve pulmonary atresia, aortic atresia, truncus arteriosusP2 not audible TGA, TOF, severe PS
Lound P2 PulmonaryhypertensionDecreased P2 severe PS, TOF
Volume overload ASD, PAPVRElectrical delay RBBB
Park's Pediatric Cardiology for Practitioners, 6th Ed.
oThird heart sound (S3) (ventricular gallop)◦ Early Diastole with rapid ventricular filling -> vibration of the
blood◦ Low-frequency sound (bell of the stethoscope) at the apex or
LLPSB◦ Normal children and young adults
o Fourth heart sounds (S4) ) (atrial gallop)◦ Late Diastole with sound of blood being force into poorly
compliant myocardium◦ Low-frequency sound, always pathologic
Pathological Heart Sounds
Heart Sounds
Clicks1. Early systolic clicks
◦ occur soon after S1 ◦ AS, PS◦ Dilated great arteries
2. Mid-systolic clicks◦ mitral valve prolapse
Diastolic opening snap (OS) is rare in children (MS)
Mid-systolic clicks in MVP
Squatting• venous return• the heart becomes larger• “C” moves toward S2
• the duration of the murmur shortens
Standing:• venous return• the heart becomes smaller• “C” moves closer to the first
heart sound (S1)• the MR murmur has an
earlier onset
JA Shaver, et al. Auscultation of the Heart. Dallas, American Heart Association, 1990, p 13. Copyright, American Heart Association
Friction Rubs
◦ Pericardial sounds (pericarditis)[sandpaper rubbed on wood] at apex
◦ Varies with the phase of the cardiac cycle◦ Louder when the patient leans forward◦ Large pericardial effusions, friction rubs can
disappear
Heart Murmurs
: Turbulent flow within the heart or blood vesselso Transmitted through the vessels, mediastinum,
chest wall to the skino Produces vibrations of the surrounding vessel
Heart murmurs 1. Intensity2. Duration3. Location4. Transmission5. Quality (harsh, vibratory)
Intensity
Grade I. Barely audible
Grade II. Soft, but easily audible
Grade III. Moderately loud murmur without a thrill
Grade IV. Loud murmur with a thrill
Grade V. Loud murmur heard with the stethoscope barely
on the chest
Grade VI. Loud murmur heard without the stethoscope
touching the chest
(A) systolic ejection mumurs
(B) S1 coincident murmurs
(C) late systolic murmurs
(D) continuous murmurs
of vascular origin
(E) continuous venous hum
(F) early diastolic murmurs
(G) mid and late diastolic murmurs
Duration
• the leaflets of the mitral valve fail to close properly
• allowing blood to leak back from left ventricle to left atrium
Mitral valve prolapse
o Diastolic blowing murmur
o Begin immediately after S2
o Early diastolic backflow from the great artery into the heart through an incompetent semilunar valve (AR, PR)
Early Diastolic Murmurs
Mid-diastolic Murmurs
o Diastolic rumbling murmur
o Excessive flow through a normal-sized atrioventricular valve is heard as a mid-diastolic rumble “relative stenosis”
o Valve is held partially closed by AR jet, a mid-diastolic murmur results, called the “Austin-Flint murmur”
o Atrial contraction pushing blood through the narrowed valve into the ventricle
o MS, TS -> low-frequency murmurs , rare
Late Diastolic Murmurs
CONTINUOUS MURMURS
o Begin in systole and continue into, and often, through diastole
o Because of the constant pressure gradient between the aorta and pulmonary arteries and increases during systole
o Always are vascular in origino Aortopulmonary (PDA, surgical AP shunts)
Loudest in systole and soft during diastole [“machinery” characteristic]
o Arteriovenous connections (AV fistula,
coronary-cameral fistula)
Louder in diastole
o Turbulent flow through veins (venous hum)
INNOCENT MURMURS
Noisy blood flow coursing through a structurally
normal heart
> 50% of children, 3-4 y Factor Increased cardiac output : excited,
anemic, febrile Low in intensity, low in frequency SEM, continuous murmur (venous hum) Dynamic auscultation Venous hum; upright > supine Still murmur; supine > upright
o Continuous murmur
o Low frequency noise
o Incessant when patient is
upright
o This murmur will decease with maneuvers that occlude the neck veins
Venous Hum
o Intensity changes with rotation of head