OS 215 Reproductive Ma.

Esterlita Villanueva-Uy

Neonatal Resuscitation and Depressed Infant Exam 2

OUTLINE
I. How does a baby receive oxygen after birth?
A. Before birth (in utero)
B. Transition to neonatal circulation
C. At completion of this normal transition
D. What can go wrong during transition?
E. How can you tell if a newborn had in
utero or perinatal compromise?
F. Risk factors associated with need for
resuscitation
II. APGAR Score
How does a baby receive Oxygen after birth?
A. Before birth (in utero)
 Lungs have no ventilatory purpose, gasless (because it
is fluid-filled), and have decreased blood flow
- only 10% of the blood goes into the
pulmonary circulation (due to high resistance in
the lungs) while the other 90% is shunted through
the ductus arteriosus and goes to the systemic
circulation Fetal PO2 = 24-28mmHg; Adult PO2=50-
60mmHg
 Placenta is the gas-exchange organ- “lungs”
- it has very low resistance compared to high
resistance of the peripheral circulation
 Right to left shunts:
- foramen ovale
- ductus arteriosus
resistance < Systemic
Vascular resistance –
note: There is only functional closing of the foramen ovale
and ductus arteriosus during delivery. The actual closing
of these two shunts takes several days to complete.
Pulmonary hypertension in the newborn happens if there is no
increase in PBF and no decrease in PVR. The lungs remain
constricted and the baby becomes cyanotic.
C. At completion of this normal transition
 Baby breathing and using his lungs
 Crying moves the fluid out of his lungs
 Oxygen and gaseous distension make pulmonary
vessels relax
 Baby turns from blue to pink
D. What can go wrong during transition?
 90% of the time, transition is very smooth. 10% would
need resuscitation. But what could possibly go wrong?
 Baby does not breathe sufficiently to force fluid or
foreign material (meconium) from the alveoli, thus lungs
will not be filled with air.
 Excessive blood loss (ex. Abruption placenta) or poor
cardiac contractility (ex. Due to infection) will result to no
increase in blood pressure hence the shunts remain
open
 Lack of oxygen or gaseous distension will cause
sustained constriction of the pulmonary arterioles hence
not enough blood will be brought to the lungs(Persistent
Pulmonary Hypertension of the Newborn)

E. How can you tell if a newborn had in utero or

perinatal compromise?
In an experiment done in the 60s, they observed
newly born baboons whose heads were wrapped in
plastic after being born. The following changes (in
chronological order) were observed as they
desperately gasped for air and progressive hypoxia
occurred:

Figure 1. Fetal Circulation. Maternal blood carrying food and

oxygen for the fetus goes to the umbilical vein (vessel with
highest oxygenation) and into the ductus venosus. From the
inferior vena cava, blood goes to the right atrium and is shunted
through the foramen ovale into the left atrium. From the left
atrium, blood goes to the left ventricle and eventually to the aorta.
Blood from the superior vena cava goes to the right atrium, into
the right ventricle and into the pulmonary artery. Blood is then
shunted into the ductus arteriosus and then goes to the aorta.

B. Transition to Neonatal Circulation

Table 1.Changes occurring during delivery and their effects.

Changes Effects
Umbilical cord is clamped Eliminate the placenta
Expansion of the lungs
resulting in a ten-fold
First breath is taken increase Pulmonary Blood
Flow (PBF) and a ten-fold
decrease in Pulmonary
vascular resistance (PVR)
Blood flow increases to the
Lung fluid gradually
lungs  pulmonary vein 
leaves the alveoli
left atrium
Blood flow to lung Closes foramen ovale
increases and Left atrial
pressure > Right atrial
pressure
Pulmonary vascular Closes the ductus arteriosus
Rapid breathing
Primary apnea
Irregular gasping
Secondary apnea
Rapidb
HYPOXIA
Figure 2. Physiologic changes associated with primary and
secondary apnea. Initial oxygen deprivation results in a transient
period of rapid breathing. If such deprivation persists, breathing
movements cease (primary apnea). This is accompanied by a
decrease in heart rate and loss of neuromuscular tone. Blood
pressure compensates and increases. If oxygen deprivation and
asphyxia persists, the infant will develop deep gasping
respirations, followed by secondary apnea. This is associated

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 OS 215 Reproductive Ma. Esterlita Villanueva-Uy

Neonatal Resuscitation and Depressed Infant Exam 2

with a further decline in heart rate, falling blood pressure and loss Color Blu or pale Pink body Completely
of neuromuscular tone. pink
 The same response can be said about newborns in Mnemonic:
utero or perinatal compromise. An objective measure A – appearance (color)
that can tell you whether the newborn is in perinatal P – pulse rate (heart rate)
compromise or not can be obtained through APGAR G – grimace (reflex irritability)
Score. A – activity (muscle tone)
 Apnea is the best indicator of neonatal compromise R – respiration
because it is the earliest manifestation. Blood
pressure is the last to go. 1 minute APGAR Score
 In primary apnea, when hypoxic stimulus is removed, - more of a measure of state of infant in utero,
the baby will start breathing. In secondary apnea, or how bad his or her condition in the womb was
removing hypoxic stimulus will not make the newborn - use to identify the need for immediate
breathe. resuscitation
 In the clinics, primary and secondary apnea cannot be
differentiated, so when faced with an apneic newborn, 5 minute APGAR Score and particularly the change in
always assume that the baby might already be in the score between 1 and 5 minutes
secondary apnea so resuscitate aggressively. - useful index of the effectiveness of
resuscitation efforts
F. Risk Factors Assoc. with Need for Resuscitation - a score of less than 3 could lead to the
- be aware of these Risk Factors so you can have all development of cerebral palsy
equipment ready in the OR
 Most infants at birth are in excellent condition, as indicated by
1. Maternal APGAR Scores of 7 to 10, and they require no aid other than
infection aminionitis perhaps simple nasopharyngeal suction. Median score is 9
pneumonia, asthma, ARDS due to acrocyanosis related to temperature instability
Lungs (Adult respiratory distress
 Scoring an infant should be logical. An infant would logically
syndrome)
not have good activity if heart sounds are not present.
arrythmia, structural defects,
heart
failure  An infant with a score of 4 to 6 at 1 minute demonstrates
blood anemia, hemoglobinopathies depressed respirations, flaccidity and pale to blue color.
blood vessel SLE, DM, HPN Heart rate and reflex irritability, however, are good.
uterus hypertonus, rupture
genetic, drugs, PTL (Preterm  Infants with scores of 0 to 3 usually have slow and inaudible
others heart rates and depressed or absent reflex responses.
labor) , MG (multiple gestation),
abnormal FP (fetal presentation)
A Depressed Infant
2. Placenta
age postmaturity  The only way to check if infant is depressed is through
size, abruption, previa the APGAR score.
morphology  Low APGAR score (0-5) in 5 minutes
 May be due to a lot of reasons:
3. Fetal - Maternal sedation or anesthesia
umbilical knot, prolapse, compression, - Substance abuse
cord thrombosis - Trauma
blood anemia - Infection
metabolic IEM (Inborn errors of - Congenital anomalies
metabolism) - CNS disorders
others infection, hydrops, MG - Cardiovascular disorders
- Neuromuscular disorders
APGAR Score
 Does not necessarily mean that infant is asphyxiated

 Objective method of quantifying the newborn’s condition A. Perinatal asphyxia

 Conveys information about the newborn’s overall status
and response to resuscitation  Interference in gas exchange between organ systems of
 Not used to decide how or when to resuscitate – it is mother and fetus resulting in impairment of tissue
measured in the 1st and then 5th minute after delivery of perfusion and oxygenation of vital organs in the fetus
the baby. If sufficient distress is noted before the 1st  Lactic acidosis and hypercapnea
minute, when APGAR scoring hasn’t yet been done,  Multi-organ damage
then infant must be resuscitated.
 Assigned at 1 and 5 minutes of life New ACOG/AAO Definition
 When <7, additional scores every 5 min for up to 20  All four requirements must be met
minutes 1. Evidence of antenatal distress
APGAR SCORE - Meconium stained fluid, electronic fetal
SIGN 0 1 2 heart rate abnormality, fetal tachycardia
Heart Rate Absent <100 >100 2. Low APGAR score (3 or less in the first 5
Respiration Absent Slow, Good, mins.)
irregular crying 3. Evidence of end organ damage
Muscle Limp Some Active - Brain, lungs, gastrointestinal and
Tone flexion Motion kidney damages
Reflex No Grimace Cough, 4. Acid-base abnormality (ph <7.0)
irritability response sneeze, cry
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 OS 215 Reproductive Ma. Esterlita Villanueva-Uy

Neonatal Resuscitation and Depressed Infant Exam 2

3. Pulmonary blood flow decrease in hypoxemia

B. Criteria that Suggest an Intrapartum Timing but and asphyxia
Nonspecific to Asphyxial Insults
=from this point on, these are the slides in the powerpoint
 A sentinel hypoxic event occurring immediately before or which were skipped by Dr. Uy, except those in bold. So
during labor
please read these parts. =)
 A sudden and sustained fetal bradycardia or absent fetal
variability in presence of late decelerations
 Apgar score of 0-3 beyond 5 minutes D. Injury from Asphyxia
 Onset of multi-system involvement within 72 hours of birth
 Early imaging study showing evidence of acute non-focal
cerebral abnormality

C. Changes in Cardiac Output, Percentage

Distribution, Heart Rate, and Pulmonary Blood
Flow During Asphyxia - What happens during
asphyxia?

- absence of blood flow from placenta to baby will

lead to hypoxia
- carbon dioxide is not released
- hypoperfusion will cause baby to undergo
anaerobic metabolism and thus develop acidosis
- fetus becomes a preferential organ organism:
blood flow to brain, heart and adrenal glands
are increased while blood flow to other organs
will be compromised: New development regarding mechanism of brain
injury in the term neonate due to asphyxia: cell death
1. Fetal cardiac output and percentage distribution occurs during oxidative stress, inflammation, and
during asphyxia DURING REPAIR STAGE. Why is there injury during
the repair stage? Cytotoxic effects of oxygen radicals
after blood flow to the tissues is re-established and
Cardiac Output (ml/min/kg) molecular oxygen is re-introduced into the
tissue. REPERFUSION INJURY
700
600 1. Generation of Oxygen Radicals
500
400 • Hypoxanthine degradation by
300 hypoxanthine oxidase and oxygen  oxygen
200 radicals
100 • Blood vessels dilated by and oxygen
0 radicals generated by prostaglandin
Normal Asphyxia • Proteases and lipases eat up plasma
membrane and lead to radical oxygen
species generation

Figure 3. Difference in total fetal cardiac output in

normal and asphyxiated newborns

Distribution of Cardiac Output (%)

60

50

40
Normal
30
Asphyxia
20 Figure 5. Conversion of ATP into hypoxanthine. When
10 ischemia occurs, ATP is converted into hypoxanthine after
0
a series of steps.
Placenta
Brain

Spleen
Heart

Gut
Lungs
Adrenals

U. Body
L. Body

Kidney

Figure 4. Distribution of cardiac output in normal and

asphyxiated newborns. In asphyxia, placenta has
greatest allocation of blood. There is also preferential
perfusion to the brain, the heart, and the adrenals.

2. Heart rate response to hypoxemia and asphyxia

- Heart rate decreases in response to
hypoxemia and asphyxia

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 OS 215 Reproductive
Neonatal Resuscitation and Depressed Infant
Release of Reactive Oxy
Pathophysiolog
Ischemia
Figure 6. The release of reactive oxygen species and
DNA strand
its effects. Ischemia leads to the production of
reactive oxygen species, which in turn causes tissue
breakage
damage and further cell death.
2. Neurotoxicity is secondary to increase in:
• Increase turnover of NA into MHPG (3-
methoxy-4-hydroxyphenylglycol)
• Excitatory amino acids
- Glutamate and aspartate
• Membrane Prostaglandins
Adenosine and gamma aminobutyric
Release of proteases, progress through neonatal encephalopathy
myeloperoxidase,
acid
damage
prostaglandins
Vasodilation
E. Resuscitation:Immediate Treatment of
Asphyxia!
1. Airway
2. Breathing
- room air vs. 100% oxygen
- bad effects of excessive oxygen:
Cell death
decreased cerebral blood flow and
Reperfusion
increased oxygen radicals
- new studies showing that room air
leads to higher 5th minute APGAR
score, shorter time to first breath,
and less neurologic impairment
3. Circulation
Tissue damage
4. Drugs
F. Risks of Permanent Sequelae
Table 2. Classifying the Degree of Encephalopathy to
Establish the “Pretest” Probability of Poor Outcome.
September 16, 2008 Tuesday
Ma. Esterlita Villanueva-Uy
Exam 2
- Sarnat scoring determines/ predicts how severe
ATP depletio
the cerebral palsy is/ will be
- Not rare for sarnat score to increase and progress
G. Neonatal Encephalopathy and Cerebral Palsy
The Report of ACOG’s Task Force on Neonatal
Encephalopathy and Cerebral Palsy
1.
Calcium influ
Neonatal encephalopathy
- Defined clinically on the basis of findings
to include a combination of abnormal
consciousness, tone and reflexes, feeding,
ROS
respiration or seizure and can result from a
myriad of conditions
Phospholipase act
- May or may not result in permanent
brain damage
- Term or near term
2. Cerebral Palsy
- Chronic
Lipid peroxidation
disability of the CNS
Arachidonic rele
characterized by aberrant control of
movement and posture, appearing early in
life and not as a result of a progressive
neurologic damage
- Spastic diplegia
- Pathway from intrapartum hypoxic-
ischemic injury to subsequent CP must
Prot
- Why do we need to predict the
development of cerebral palsy?
 This disease is usually detected around
1-2 years of age. Early detection and
intervention like physical therapy and
maternal counseling lead to less
sequelae
3. Epidemiology
Neonatal encephalopathy
Phag
- Majority (70%) of NE due to events
arising before labor
H. Criteria to Define an Acute Intrapartum Event
Sufficient to Cause Cerebral Palsy
Essential Criteria
 Evidence of a metabolic acidosis in fetal umbilical
arterial cord blood obtained at delivery
 Early onset of severe or moderate neonatal
ROS release
encephalopathy in infants at 34 or more weeks of
gestation
 Cerebral palsy of the spastic quadriplegic or dyskinetic
type
 Exclusion of other identifiable etiologies such as trauma,
coagulation disorders, infectious conditions or genetic
disorders
I. Possible Post Resuscitation Strategies
1. Hypothermia
 Decrease of 2-6% below baseline
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 OS 215 Reproductive Ma. Esterlita Villanueva-Uy

Neonatal Resuscitation and Depressed Infant Exam 2

 Started <6 hours after hypoxic insult

 Decrease brain metabolism Kidneys • Acute tubular • Monitor urine output
 Better neurologic outcome acidosis • Restrict fluids if
oliguria is present
2. Selective Head Cooling (Gunn 1998) • Monitor serum
In selective head cooling, the hypothermic baby electrolyte levels
is said to have a band around his/her head that is Brain • Apnea • Monitor for apnea
maintained at a temperature of 33oC. • Seizures • Monitor glucose and
electrolyte levels
Infants Control (10) Minimal(6) Mild(6) • Avoid hyperthermia
CT scan • Consider
Severe 1 2 0 anticonvulsant
Mild changes 4 1 2 Gastroin- • Ileus • Delay initiation of
Normal 2 1 4 testinal • Necrotizing feeding
EEG enterocolitis • Administer
Abnormal 2 3 0 intravenous fluids
Normal 4 2 6 • Consider parenteral
Dead 2 1 0 nutrition
Severe 1 1 0 Metabolic/ • Hypoglycemia • Monitor blood
handicap Hematolo- • Hypocalcemia/ glucose
Mild to 2 1 0 Gic Hyponatremia • Monitor electrolyte
moderate • Anemia levels
Normal at 6-12 5 2 6 • Thrombocyto- • Monitor hematocrit
mos penia • Monitor platelets
Neonatal Resuscitation Algorithm (next page)
3. Whole Body Cooling (Shankaran Pediatrics
2002) Notes:
• Mnemonic for the first questions to ask:
In a study done, it was noted that there were Nucleotides TACG
improvements in the following parameters: hypotension, • Routine Care
renal failure, length of hospital stay, oxygen use, and o Warmth: Equipment to be used such as
seizures; however, the samples are still too small since it radiant warmers should be pre-warmed
is an ongoing study. before delivery
o Aiway: semi-sniffing head position (to
Hypothermia (9)Normothermia (10) align airway, slightly chin-up)
Hypotension 8 10 o Dry: dry with linen; replace wet linens
PPHN 3 2 with dry ones
Renal failure 3 5 o Assessing Color: note for
Hepatic dysfunction 1 1 acrocyanosis(pink but with pale
DIC 1 1 nailbeds) which may be secondary to
Death 2 3 mechanical problems after birth
Days on oxygen 6.8 8.4
Length of stay 14.9 21.6 • To stimulate: flick the toes or rub the back but
Discharge status don’t take too long to avoid compromising the
baby. If the baby doesn’t breathe immediately,
Gavage feeding 0 2
assume secondary apnea.
Abnormal Neuro exam 1 4
• Things to assess to decide whether to resuscitate
Seizure (on meds) 0 2
o Color
Abnormal MRI 3 3
o Heart/Pulse Rate
Table 3. Neonatal Postresuscitation Complications o Respiration
and Actions • PPV without chest compression
Organ Potential Post Resuscitation o Breathe-2-3-breathe-2-3
System Complication Action o 40 breaths/min
Lungs • Pulmonary • Maintain adequate o 100% O2 ideally
Hypertension oxygenation and • Types of Positive Pressure Ventilation
• Pneumonia ventilation o Bagmask
• Pneumothorax • Consider antibiotics  Ambubag: self-inflating w/ one-
• Transient • Delay oral feeding if way valve therefore cannot be
Tachypnea respiratory distress used for free-flow O2
• Meconium is evident  Anesthesia Bag: needs O2 for
aspiration • Consider surfactant inflation
syndrome therapy o Laryngeal mask: used when the baby
• Surfactant cannot be intubated
deficiency • PPV w/ Chest Compressions
o Heart rate is checked for 6seconds
Cardiovas- • Hypotension • Monitor blood (multiplied by 10) because you have to
cular pressure and heart do everything in 30s.
rate o Cadence: 1-and-2-and-3-and-breathe
• Consider inotrope o 90 compressions,30 breaths per min
(eg. Dopamine) or • 2 Methods of Chest Compression
volume replacement

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 OS 215 Reproductive Ma. Esterlita Villanueva-Uy

Neonatal Resuscitation and Depressed Infant Exam 2

o Two-finger: 1 hand at the back of the 2. Heart rate <100

baby for support; 3. Persistent cyanosis despite O2 support
 Pointer + middle • Indications for chest compressions: HR<60 after
 Middle+ ring 30 sec of PPV
o Two- thumb: more stable • Landmark for chest compressions: imaginary
*depth: 1/3 of AP diameter mammary line
• Epinephrine • Room air resuscitation is sometimes better than
o IV: 0.1ml/kg, 1cc syringe the 100% O2
o ET(endotracheal tube): 1ml/kg, 3-5cc • Best way to asses if endotracheal tube is in:
syringe (1:10,000 dilution) increase in HR
• Causes of bradycardia
o Adult: MI
o Child: Myocardial hypoxia secondary to
pulmonary cause

Neonatal Resuscitation Algorithm

If preterm:
A. Oxygenation
• O2 blender
• O2 sat goal 90-95%
• Ambu w/o reservoir: 40% (mixed w/ room air)
• Ambu w/ reservoir: roughly 100%
B. Thermoregulation
• Preterms are at risk for hypothermia
• Use radiant warmer, dry baby and replace wet
with dry linen
• If <28 weeks, ziplock is used as a warming back

Withdrawing resuscitation:
• If there are no signs of life with continuous and
adequate resuscitation, rescue efforts are
stopped after ten minutes

Jeopardy Notes:
• Most important single step in resuscitation is
pulmonary ventilation
• Three indications for PPV
1. Apnea

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 OS 215 Reproductive Ma. Esterlita Villanueva-Uy

Neonatal Resuscitation and Depressed Infant Exam 2

If meconium stained:

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Iris. Hannie. Ezra. Dianne