Approach Cyanosis Final

Approach to a baby with
cyanosis
Objectives
• Cyanosis : types
• Differentials: cardiac vs. non cardiac
• Approach
• Case scenarios
Cyanosis
 Greek word “kuaneos” meaning dark blue
 Bluish discolouration of skin, nail beds, and
mucous membranes.
 Depends on absolute concentration of
reduced haemoglobin (> 3 g/dl in arterial
blood and >5 g/dl in capillary blood)
Pediatric Cardiology for Practitioners- Myung K Park

Types of cyanosis
ACROCYANOSIS CENTRAL CYANOSIS DIFFERENTIAL

CYANOSIS
Physiological Pathological
upto 72 hrs Requires Definitive
Large arterio- immediate congenital heart
venous oxygen evaluation anomalies (right-
difference to-left shunt
through PDA)
Differentials
Cyanotic heart disease Non cardiac causes

 Decreased pulmonary  Respiratory
blood flow disorders
 Increased pulmonary  Persistent fetal
blood flow circulation
 Severe pulmonary  Central nervous
venous congestion system disorders
 Miscellaneous
Approach
Pulse
Confirm oximetry
Clinical Blood gas
central (preductal
evaluation analysis
cyanosis and
postductal)
Approach contd…………….
Cardiac or
Chest Hyperoxia
non Management
radiograph test
cardiac
Approach contd………
Age at presentation of cyanosis
0-7 days 7-28 days >28 days
TGA Truncus TOF like physiology
arteriosus
PS +IVS TAPVC TGA, ASD
HLHS TGA,VSD Truncus Arteriosus
Severe Ebstein TOF PPHN group

Anomaly
TAPVC
(obstructed)
Approach contd………
Pulse oximetry
 Simultaneous measurements from the right

hand and a foot: flow patterns through the
ductus arteriosus.
 Avoid left hand.
 Confirms/ rejects central cyanosis
 R  L ductal shunting if differential cyanosis
Clinical evaluation: some pointers
 Tachypnea with distress  Tachypnea, no/ less distress

 Crepitations +  Crepts -, except with PVH
 Cyanosis mild/uniform  Cyanosis variable/ uniform
 Responsive to oxygen  No/ minimal response to
 Improves with crying oxygen, Worsens with crying
 Age: usually at birth  Usually after 24 hrs
NON CARDIAC CARDIAC

What next? Hyperoxia Test
Right radial
Pulse ox reading artery ABG in
<85% in room air room air
Repeat radial 100% oxygen by

artery ABG hood for 15 min.
Jones, 1976
Interpret? Blood gas analysis
 Low pH  Low pH
 Elevated PaCO2  Normal or low PaCO2
 PaO2 >250 mm Hg after  PaO2 < 100 mm Hg/ Rise
hyperoxia test (passed <10-30 mm Hg (failed
hyperoxia test) hyperoxia test)
 Respiratory acidosis  Metabolic acidosis
predominantly predominantly
NON CARDIAC CARDIAC

If still in dilemma?
Hyperoxia Hyperventilation Test
 Intubation & hyperventilation
Rationale: Pulmonary vasodilation, decreases right to

left shunt at atrial or ductal level
Possible
PPHN
Approach contd………. (X Ray)
Pulmonary vasculature (Normal)
RDPA
X-Ray: Decreased vascularity
• Dark Lung Field

•Thin peripheral
vessels
•Small Hila
Cyanotic heart defects with
decreased vascularity (examples)
Critical Pulmonary Tetralogy of Fallot
stenosis/pulmonary physiology
atresia with intact  TOF (VSD/ PS)
ventricular Septum  DORV/ VSD/ PS
 AVSD/ PS
 TGA/ VSD/ PS
 Single ventricle/ PS
 Tricuspid atresia with
restrictive VSD and/ or
PS
Increased vascularity
• Right des. PA dilated

• Prominent hilar
vessels
• Pulm. vasculature
traced till lateral
3rd of lung field
• End on vessels >4
in one lung field
Cyanotic heart defects with
increased vascularity (examples)
Transposition Admixture physiology
physiology without PS
 Complete TGA  At systemic or right atrial level:
 DORV/ subpulmonic TAPVR, Mitral/ Aortic atresia
VSD (Taussig Bing) with IVS
 At left atrial level: Tricuspid
atresia
 At ventricle/ great artery level:
Single ventricle, Complete
AVSD with straddling AV valve,
DORV/ subaortic or inlet VSD,
Persistent truncus arteriosus
Pulmonary venous hypertension
•Perihilar Haze
•Fluid in fissures
•Kerley’s Lines
Cephalization
Causes
•Obstructed TAPVR
•HLHS/ Mitral atresia with
restrictive ASD
Questions which need to be
answered
 Is there an imminent risk of death?

 What group of cardiac lesion?
 What further investigations?
 When to intervene?
Making an exact diagnosis may not always

be possible.
ECG: INTERPRETATION
 Axis : Leads I and aVF are used
1. P axis:P wave must be upright in leads I and aVF.
0 to +90 degree = normal
+90 to +180 degree = Atrial inversion
0 to _90 degree = Ectopic atrial pacemaker/ AV
junctional rhythm
2. QRS axis: QRS axis is perpendicular to lead with

equiphasic QRS complex (R=S)
3. T axis: T waves must be upright in lead I and aVF

Normal QRS axis
Age Mean ( Range )
<1 wk ard +135
1week -1 month +110 (+30 to +180)
1-3 months +70 ( +10 to+125)
3 month- 3 years +60 ( +10 to 110 )
>3 years +60 ( +20 to 120 )
Adult +50 (-30 to +105)
Abnormal QRS axis
 LAD –QRS axis is less then lower limit of
normal for age.
(a) LVH (b) LBBB
(c) Left anterior hemiblock
 RAD –QRS axis is greater then upper limit of
normal for age.
(a) RVH (b) RBBB
 Superior QRS axis: S>R in aVF
(a) Endocardial cushion defect (ECD)
(b) Tricuspid atresia
(c) RBBB
Further Evaluation
 Echocardiography: To confirm the type of
lesion
 Cardiac catheterisation studies
 Angiography: confirmation, haemodynamics,
oxygenation, intervention
 MRI: diagnostic for anomalies in pulmonary
arteries, aorta, and vena cava
Mangement: Role of PG E1
Indications:
 Cyanotic newborn suspected to have duct
dependent lesion
 Echo proven duct dependent cardiac lesions
Dose: 0.01mcg/kg/min to 0.1 mcg/kg/min;
gradually dec. to 0.025 mcg/kg/min before
stopping (Neofax 2010)
Side effects: Apnea, pulmonary congestion,
fever, hypotension, seizures, and diarrhea
Case 1
A neonate is profoundly cyanosed and
lethargic in his cot at 22 hours of life.
 Clinical examination reveals a soft systolic
murmur heard at the left sternal edge and a
single second heart sound
 Blood gas: unavailable
 ECG :normal neonatal pattern
 Chest X ray: available
Cardiomegaly with typical egg on
side appearance, increased
pulmonary blood flow
Transposition of great arteries

CASE 2
A 3 mo infant presented with bluish
discoloration of lips on crying since past 2
weeks
 No H/o suck-rest –suck cycle/ sweating/ cough
or breathlessness
 Clinical examination reveals HR:110/min,
RR:28/min. Central cyanosis+ worsening on
crying. Apex beat in 4th ICS inside MCL . ESM
Grade 3/6 best heard in Pulmonary area. S1 N S2
single
 ECG and chest X ray is available
Boot shaped heart with right sided RAD with RVH
aortic arch
Tetralogy of Fallot
Case 3
Preterm (34 wks) neonate born by normal
vaginal delivery with mild respiratory
distress and cyanosis
 Put on CPAP
 Spo2 decreased from 95% on room air to
78% on 45% Fio2
 RR=60/min with Intercostal recession with
decreased air entry on the left
 CVS: S1 S2 normal. No murmur
Air fluid levels in chest with defect in
diaphragm
Congenital diaphragmatic hernia

Approach Cyanosis Final

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Approach to a baby with

• Differentials: cardiac vs. non cardiac

Pediatric Cardiology for Practitioners- Myung K Park

ACROCYANOSIS CENTRAL CYANOSIS DIFFERENTIAL

Cyanotic heart disease Non cardiac causes

Severe Ebstein TOF PPHN group

 Simultaneous measurements from the right

 Tachypnea with distress  Tachypnea, no/ less distress

NON CARDIAC CARDIAC

Repeat radial 100% oxygen by

NON CARDIAC CARDIAC

 Intubation & hyperventilation

Rationale: Pulmonary vasodilation, decreases right to

• Dark Lung Field

• Right des. PA dilated

 Is there an imminent risk of death?

Making an exact diagnosis may not always

2. QRS axis: QRS axis is perpendicular to lead with

3. T axis: T waves must be upright in lead I and aVF

Transposition of great arteries

Congenital diaphragmatic hernia

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