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

Physical Examination in CVS

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

Pulse Oximetry Screening

Ewer AK and Martin GR. Pediatrics 2016;138(5).

Test – Positive

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

Clubbing fingers

Long-standing arterial desaturation (usually longer than 6 months)

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

Central Venous Pressure(CVP)

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

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

Right thoracotomy; RMBTS, ASD repair, MV surgery

Left thoracotomy; LMBTS, PDA, COA repair

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

Heart Sounds

First heart sound (S1)

TV and MV closure

Second heart sound(S2)

AV and PV closure

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

S1 TV and MV closure S2 AV and PV closure

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

Lubb-dupp-da Da-lubb-dupp

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

Systolic Murmurs

• the leaflets of the mitral valve fail to close properly

• allowing blood to leak back from left ventricle to left atrium

Mitral valve prolapse

Diastolic Murmurs

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)

Differential diagnosis of

Systolic murmur at

LUPSB

Differential diagnosis of Systolic murmur at LLPSB

*increases the cardiac output (e.g., fever, anemia, anxiety, exercise)

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

Common Innocent Heart Murmurs in Infants and Children

Diagram of innocent heart murmurs in children

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

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