OS 215 Reproductive Ma.

Esterlita Villanueva-Uy

Neonatal Resuscitation and Depressed Infant Exam 2

OUTLINE
I. How does a baby receive oxygen after birth? resistance < Systemic
A. Before birth (in utero) Vascular resistance –
B. Transition to neonatal circulation note: There is only functional closing of the foramen ovale
C. At completion of this normal transition
D. What can go wrong during transition?
and ductus arteriosus during delivery. The actual closing of
E. How can you tell if a newborn had in utero or these two shunts takes several days to complete.
perinatal compromise?
F. Risk factors associated with need for resuscitation
II. APGAR Score Pulmonary hypertension in the newborn happens if there is no
III. A Depressed Infant increase in PBF and no decrease in PVR. The lungs remain
constricted and the baby becomes cyanotic.

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
resistance of the peripheral circulation
Right to left shunts:
- foramen ovale
- ductus arteriosus
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
to high 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:
Breathing

Rapid breathing Primary apnea Irregular gasping Secondary apnea

Figure 1. Fetal Circulation. Maternal blood carrying food and
oxygen for the fetus goes to the umbilical vein (vessel with Heart rate
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 Blood pressure
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. Rapid breathing
Changes Effects
Umbilical cord is clamped Eliminate the placenta Primary apnea
Expansion of the lungs
resulting in a ten-fold Irregular gasping
First breath is taken increase Pulmonary Blood
Flow (PBF) and a ten-fold Secondary apnea
decrease in Pulmonary
vascular resistance (PVR) HYPOXIA
Blood flow increases to the Figure 2. Physiologic changes associated with primary and
Lung fluid gradually
lungs  pulmonary vein  secondary apnea. Initial oxygen deprivation results in a transient
leaves the alveoli
left atrium period of rapid breathing. If such deprivation persists, breathing
Blood flow to lung Closes foramen ovale movements cease (primary apnea). This is accompanied by a
increases and Left atrial decrease in heart rate and loss of neuromuscular tone. Blood
pressure compensates and increases. If oxygen deprivation and
pressure > Right atrial asphyxia persists, the infant will develop deep gasping
pressure respirations, followed by secondary apnea. This is associated
Pulmonary vascular Closes the ductus arteriosus

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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 pink
of neuromuscular tone. Mnemonic:
The same response can be said about newborns in utero A – appearance (color)
or perinatal compromise. An objective measure that can P – pulse rate (heart rate)
tell you whether the newborn is in perinatal compromise or G – grimace (reflex irritability)
not can be obtained through APGAR 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, the - more of a measure of state of infant in utero, or
baby will start breathing. In secondary apnea, removing how bad his or her condition in the womb was
hypoxic stimulus will not make the newborn breathe. - use to identify the need for immediate
In the clinics, primary and secondary apnea cannot be resuscitation
differentiated, so when faced with an apneic newborn,
always assume that the baby might already be in 5 minute APGAR Score and particularly the change in
secondary apnea so resuscitate aggressively. the score between 1 and 5 minutes
- useful index of the effectiveness of resuscitation
F. Risk Factors Assoc. with Need for Resuscitation efforts
- be aware of these Risk Factors so you can have all - a score of less than 3 could lead to the
equipment ready in the OR development of cerebral palsy
1. Maternal Most infants at birth are in excellent condition, as indicated by
infection aminionitis APGAR Scores of 7 to 10, and they require no aid other than
pneumonia, asthma, ARDS perhaps simple nasopharyngeal suction. Median score is 9 due
Lungs (Adult respiratory distress to acrocyanosis related to temperature instability
syndrome)
Scoring an infant should be logical. An infant would logically not
arrythmia, structural defects,
heart have good activity if heart sounds are not present.
failure
blood anemia, hemoglobinopathies An infant with a score of 4 to 6 at 1 minute demonstrates
blood vessel SLE, DM, HPN depressed respirations, flaccidity and pale to blue color. Heart
uterus hypertonus, rupture rate and reflex irritability, however, are good.
genetic, drugs, PTL (Preterm
others Infants with scores of 0 to 3 usually have slow and inaudible
labor) , MG (multiple gestation),
abnormal FP (fetal presentation) heart rates and depressed or absent reflex responses.

2. Placenta A Depressed Infant

age postmaturity
size, abruption, previa The only way to check if infant is depressed is through
morphology the APGAR score.
Low APGAR score (0-5) in 5 minutes
3. Fetal May be due to a lot of reasons:
umbilical knot, prolapse, compression, - Maternal sedation or anesthesia
cord thrombosis - Substance abuse
blood anemia - Trauma
metabolic IEM (Inborn errors of - Infection
metabolism) - Congenital anomalies
others infection, hydrops, MG - CNS disorders
- Cardiovascular disorders
- Neuromuscular disorders
APGAR Score
Does not necessarily mean that infant is asphyxiated
Objective method of quantifying the newborn’s condition
Conveys information about the newborn’s overall status A. Perinatal asphyxia
and response to resuscitation
Not used to decide how or when to resuscitate – it is Interference in gas exchange between organ systems of
measured in the 1st and then 5th minute after delivery of mother and fetus resulting in impairment of tissue
the baby. If sufficient distress is noted before the 1st perfusion and oxygenation of vital organs in the fetus
minute, when APGAR scoring hasn’t yet been done, then Lactic acidosis and hypercapnea
infant must be resuscitated. Multi-organ damage
Assigned at 1 and 5 minutes of life
When <7, additional scores every 5 min for up to 20 New ACOG/AAO Definition
minutes All four requirements must be met
APGAR SCORE 1. Evidence of antenatal distress
SIGN 0 1 2 - Meconium stained fluid, electronic fetal
Heart Rate Absent <100 >100 heart rate abnormality, fetal tachycardia
Respiration Absent Slow, Good, 2. Low APGAR score (3 or less in the first 5
irregular crying mins.)
Muscle Limp Some Active 3. Evidence of end organ damage
Tone flexion Motion - Brain, lungs, gastrointestinal and
Reflex No Grimace Cough, kidney damages
irritability response sneeze, cry 4. Acid-base abnormality (ph <7.0)
Color Blu or pale Pink body Completely

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Iris. Hannie. Ezra. Dianne
 OS 215 Reproductive Ma. Esterlita Villanueva-Uy

Neonatal Resuscitation and Depressed Infant Exam 2

B. Criteria that Suggest an Intrapartum Timing but 3. Pulmonary blood flow decrease in hypoxemia
Nonspecific to Asphyxial Insults and asphyxia
A sentinel hypoxic event occurring immediately before or during =from this point on, these are the slides in the powerpoint
labor
which were skipped by Dr. Uy, except those in bold. So
A sudden and sustained fetal bradycardia or absent fetal
variability in presence of late decelerations please read these parts. =)
Apgar score of 0-3 beyond 5 minutes
Onset of multi-system involvement within 72 hours of birth D. Injury from Asphyxia
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
1. Fetal cardiac output and percentage distribution injury in the term neonate due to asphyxia: cell death
during asphyxia occurs during oxidative stress, inflammation, and
DURING REPAIR STAGE. Why is there injury during
the repair stage? Cytotoxic effects of oxygen radicals
Cardiac Output (ml/min/kg) after blood flow to the tissues is re-established and
molecular oxygen is re-introduced into the tissue.
 REPERFUSION INJURY
700
600 1. Generation of Oxygen Radicals
500
400
• Hypoxanthine degradation by hypoxanthine
300
oxidase and oxygen  oxygen radicals
• Blood vessels dilated by and oxygen radicals
200
generated by prostaglandin
100
• Proteases and lipases eat up plasma
0
membrane and lead to radical oxygen
Normal Asphyxia species generation

Figure 3. Difference in total fetal cardiac output in

ATP
normal and asphyxiated newborns
AMP

Distribution of Cardiac Output (%) Adenosine

Inosine
60
50 Hypoxanthine

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

0
Brain
Placenta

Spleen
Lungs
U. Body
Heart

Gut
Adrenals

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 Ma. Esterlita Villanueva-Uy

Neonatal Resuscitation and Depressed Infant Exam 2

Release of Reactive Oxygen Species

Pathophysiology
Ischemia ATP depletion

Calcium influx

Phospholipase activation

Arachidonic release

Prostaglandins Proteases, lipases

Vasodilation Increase
microvascular
permeability Sarnat scoring determines/ predicts how severe
-
Reperfusion the cerebral palsy is/ will be
- Not rare for sarnat score to increase and
ROS release progress
G. Neonatal Encephalopathy and Cerebral Palsy
ROS
The Report of ACOG’s Task Force on Neonatal
DNA strand Neutrophil
Encephalopathy and Cerebral Palsy
Lipid peroxidation
breakage accumulation
1. Neonatal encephalopathy
Membrane Release of proteases, - Defined clinically on the basis of findings to
myeloperoxidase,
damage
prostaglandins
PMN plugging include a combination of abnormal
of capillaries consciousness, tone and reflexes, feeding,
Phagocytosis respiration or seizure and can result from a
Cell death myriad of conditions
- May or may not result in permanent brain
Ischemia
Tissue damage damage
- Term or near term
Figure 6. The release of reactive oxygen species and
its effects. Ischemia leads to the production of 2. Cerebral Palsy
reactive oxygen species, which in turn causes tissue - Chronic disability of the CNS characterized
damage and further cell death. by aberrant control of movement and
posture, appearing early in life and not as a
2. Neurotoxicity is secondary to increase in: result of a progressive neurologic damage
• Increase turnover of NA into MHPG (3- - Spastic diplegia
methoxy-4-hydroxyphenylglycol) - Pathway from intrapartum hypoxic-ischemic
• Excitatory amino acids injury to subsequent CP must progress
- Glutamate and aspartate through neonatal encephalopathy
• Adenosine and gamma aminobutyric acid - 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
E. Resuscitation:Immediate Treatment of Asphyxia!
maternal counseling lead to less
1. Airway sequelae
2. Breathing 3. Epidemiology
- room air vs. 100% oxygen Neonatal encephalopathy
- bad effects of excessive oxygen: - Majority (70%) of NE due to events arising
decreased cerebral blood flow and
before labor
increased oxygen radicals
- new studies showing that room air H. Criteria to Define an Acute Intrapartum Event
leads to higher 5th minute APGAR Sufficient to Cause Cerebral Palsy
score, shorter time to first breath,
and less neurologic impairment Essential Criteria
3. Circulation Evidence of a metabolic acidosis in fetal umbilical arterial
4. Drugs cord blood obtained at delivery
Early onset of severe or moderate neonatal
F. Risks of Permanent Sequelae encephalopathy in infants at 34 or more weeks of
gestation
Table 2. Classifying the Degree of Encephalopathy to Cerebral palsy of the spastic quadriplegic or dyskinetic
Establish the “Pretest” Probability of Poor Outcome. 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 (eg. Dopamine) or

Decrease brain metabolism volume
Better neurologic outcome replacement

2. Selective Head Cooling (Gunn 1998) Kidneys • Acute • Monitor urine

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

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 OS 215 Reproductive
Neonatal Resuscitation and Depressed Infant
 Anesthesia Bag: needs O2 for
inflation
o Laryngeal mask: used when the baby
cannot be intubated
• PPV w/ Chest Compressions
o Heart rate is checked for 6seconds
(multiplied by 10) because you have to
do everything in 30s.
o Cadence: 1-and-2-and-3-and-breathe
o 90 compressions,30 breaths per min
• 2 Methods of Chest Compression
o Two-finger: 1 hand at the back of the
baby for support;
 Pointer + middle
 Middle+ ring
o Two- thumb: more stable
*depth: 1/3 of AP diameter
• Epinephrine
o IV: 0.1ml/kg, 1cc syringe
o ET(endotracheal tube): 1ml/kg, 3-5cc
syringe (1:10,000 dilution)
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
September 16, 2008 Tuesday
Ma. Esterlita Villanueva-Uy
Exam 2
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
2. Heart rate <100
3. Persistent cyanosis despite O2 support
• Indications for chest compressions: HR<60 after
30 sec of PPV
• Landmark for chest compressions: imaginary
mammary line
• Room air resuscitation is sometimes better than
the 100% O2
• Best way to asses if endotracheal tube is in:
increase in HR
• Causes of bradycardia
o Adult: MI
o Child: Myocardial hypoxia secondary to
pulmonary cause
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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