Anda di halaman 1dari 34



Revision course_Primaries 2013

Cardiorespiratory changes at birth

Tongo O. O (FWACP Paed)
Lungs and Circulation

In the fetus
 In utero, the fetus is dependent on the
placenta as the organ of gas
 Air sacs (alveoli) are filled with fetal
lung fluid
Oxygenation before birth
Oxygenation before birth
Lungs and Circulation

In the fetus
 Arterioles are
 Pulmonary blood
flow is diminished
 Blood flow is
diverted across
ductus arteriosus
Lungs and Circulation

• Lung fluid appears during 2nd trimester

• Close to term,
• rate of lung fluid production reduces, reabsorption
• Just before onset of labour,
• β adrenergic activity converts chloride secreting alveolar
cell to sodium absorbing cells

• By the time of delivery, lung fluid is 30ml/kg in the

term foetus
Lungs and Circulation
Fetal lung fluid clearance

 Up to 75% cleared by term

 Improved with labour before delivery

 Improved with vaginal delivery

 Facilitated with effective initial breaths

 Impaired by
 Apnea at birth with no lung expansion

 Shallow ineffective respirations

Lungs and Circulation
After delivery
 Lungs expand with air
 Fetal lung fluid leaves alveoli
Lungs and Circulation

After delivery
 Pulmonary
arterioles dilate
 (endothelin,
prostacyclin &
nitric oxide)
 Pulmonary blood
flow increases
Lungs and Circulation
 After delivery
 Blood oxygen
levels rise
 Ductus
 Blood flows
through the
lungs to pick up
Oxygenation After birth
Major changes within seconds after birth:

 Fluid in the alveoli is absorbed

 Umbilical arteries and vein constrict

 Systemic vascular resistance increases

 Blood vessels in lung tissue relax

What Can Go Wrong During Transition

 Insufficient ventilation, airway blockage, or

 Excessive blood loss or poor cardiac
contractility from acidosis after prolonged
 Sustained constriction of pulmonary
What Can Go Wrong During Transition

Pulmonary blood flow

 Decreases with hypoxemia and acidosis

due to vasoconstriction
 Increases with ventilation, oxygenation,
and correction of acidosis
Lungs and Circulation
Cardiac function and compensatory mechanisms
in asphyxia
 Initial response
 Constriction of vascular beds in lungs, intestines,
kidneys, muscle, and skin to redistribute blood flow
to heart and brain

 Late effects
 Myocardial function may be impaired, cardiac
output decreases, and multiorgan damage may
Primary & Secondary Apnea

10 Apnoea
 Rapid attempts to breathe

 Respirations cease
 Heart rate decreases
 Blood pressure is usually
Heart rate
 Responds to stimulation

20 Apnoea
 Respirations cease

 Heart rate decreases


 Blood pressure decreases

 No response to stimulation
If a baby does not begin breathing immediately
after being stimulated, he is likely in secondary
apnoea and will require positive-pressure
ventilation. Continued stimulation will not help
Signs of a Compromised Newborn

 Good tone with

 Persistent Cyanosis cyanosis

 Bradycardia

 Low blood pressure

 Depressed
respiratory effort
 Poor muscle tone  Poor tone with
 Tachypnoea
Approximately 10% of newborns require some
assistance to begin breathing at birth;
Only 1% need extensive resuscitative measures
(intubation, chest compressions, and/or
medications) to survive.
At every delivery,
there should be at least
one person whose
primary responsibility is
the baby and who is
capable of initiating
Preparation for Resuscitation Personnel
and Equipment
 Trained person to initiate resuscitation at every
 Recruit additional personnel, if needed for more
complex delivery (multiple, instrumental/operative deliveries)
 Prepare necessary equipment
 Turn on radiant warmer
 Check resuscitation equipment

 Team concept
The ABCs of Resuscitation:

Airway (position and clear if necessary)

Breathing (stimulate to breathe)

Circulation (assess heart rate and color)

Resuscitation Flow Diagram
Resuscitation Flow Diagram
After the initial steps, further actions are
based on evaluation of:
 Respirations

 Heart Rate

 Color

Ventilation is the most important step

in neonatal resuscitation!
Preterms are at higher risk of requiring assistance

 Possible surfactant deficiency

 Increased heat loss, poor temperature
 Possible infection
 Susceptible to intracranial hemorrhage
Clinical chemistry of the newborn
Glucose homeostasis
• Physiologic drop in blood sugar levels in 1st 2 hours after
birth which normalizes thereafter except in high risk
• Exclusively breastfed babies able to maintain glucose
levels on the amount of breastmilk available in the 1st
• Able to use other fuels like ketones for brain metabolism
• Ability to produce ketones is suppressed by addition of
formula feeds
• It is NOT necessary to monitor RPG in term well
breastfeeding infants
Clinical chemistry of the newborn
Hypoglycaemia (RPG < 2.2mmol/l, 10th centile)
• Profound/prolonged hypoglycaemia results in
neuroglycopenia which may be symptomatic or
• May result in permanent brain damage
• RPG monitoring mandatory in high risk groups
Risk factors;
• Small for gestational Age babies
• Large for gestational Age babies
• Infants of diabetic mothers
Clinical chemistry of the newborn
• Prematurity
• Sepsis
• Inborn errors of metabolism

Hyperglycaemia (RPG > 8mmol/l)

 Elevated blood sugar is equally dangerous to the newborn
 Preterm infants have limited ability to handle glucose load
 Sepsis and asphyxia are predisposing factors
 Babies <32weeks and <1500g are most vulnerable
Clinical chemistry of the newborn

 Glucose infusion of >10mg/kg/min

 Drugs-Theophyllines (Aminophylline)
 Respiratory Distress
 Stress-painful procedures
 Transient Neonatal Diabetes Mellitus
 Permanent neonatal DM
 Total Parenteral Nutrition
 Insulin resistance
Clinical chemistry of the newborn

Fluid and electrolytes

• Newborns redistribute body fluids in the 1st few
days after birth
• There is a net fluid loss in the first week of life in
AGA babies
• Newborns particularly preterms experience huge
transepidermal fluid losses
• Excessive fluid and sodium administration
adversely affect the outcome in babies with RDS
& other respiratory problems, PDA
Clinical chemistry of the newborn
 Newborns especially preterms have limited ability to
concentrate urine in the face of water deprivation
(SG 1.006 – 1.012)
 Urine output in the 1st 24hours of life < 1ml/kg/hr
 Thereafter post natal diuresis 2 – 4mls/kg/hr (wt loss
< 10% bt wt in wk 1)
 Diuresis delayed in RDS (onset heralds
 Sodium administration should only be commenced
after post natal diuresis @2 – 4 meq/kg/d
Clinical chemistry of the newborn
Hyponatraemia (Serum Na <125meq/l)
 Serious problem in newborns with adverse CNS
 Results from inadequate intake, haemodilution or
excessive loss
 Inadequate intake (infusion of hypotonic fluids)
 Haemodilution (SIADH, AKI, oxytocin to mother via
hypotonic fluids)
 Excessive loss (3rd space losses like GI obstruction,
reckless diuretic therapy, vomiting & diarrhoea, CAH)

 Monitor electrolytes and urea, urinary output, weight,

urine specific gravity, plasma osmolarlity
Clinical Chemistry of the newborn
Suggested further reading

• Calcium homeostasis
• Hypocalcaemia
• Acid base balance and blood gas results