Objectives:

Upon completion of this chapter, you will be able to:

1. List specific anatomical and physiology features of the neonate.

2. Identify common neonatal pathophysiologies.
3. Implement specific neonatal treatments.

Scenario
Your advanced life support (ALS) crew is working in a tiered rural district and receives a 911 for a routine obstetrical call. Your system
dispatches a basic life support (BLS) unit to obstetrical calls unless there are complications. The BLS unit responds. While monitoring the
radio, you hear an update that the patient is having contractions three minutes apart and has had no prenatal care. The lack of prenatal
care is considered a complication, so you respond to the call. During your response, the BLS crew arrives and advises you that delivery is
imminent. As you arrive on the scene, you see that your BLS crew is attending to an approximately 25-year-old female. They are
preparing for delivery. The BLS crew relays the history of the patient. This is her first pregnancy and she has had no prenatal care. She
states that she bought a pregnancy test at the pharmacy approximately six months ago, and it tested positive. She guesses that her last
period was four weeks prior to her test.
Upon preparing for delivery, you notice thick green meconium staining in the amniotic fluid. You advise your BLS partners to be prepared
to aggressively defend the airway. As the head delivers, you confirm the presence of meconium. You suction the nose and oropharynx,
and continue with delivery. Your partner does the math and estimates the neonate to be approximately 28 weeks of gestation.
The baby delivers and fails to spontaneously breathe. The baby boy has a pulse of 80. You suction the airway again and begin bag valve
mask ventilations. Since there are two EMS units on scene, you elect to send the asymptomatic mother with the BLS crew and to
transport the neonate with your ALS crew. The mother is very reluctant to be separated from her newborn. After explanation of the
situation, however, she agrees. You wrap the newborn in a blanket, carry him to your ambulance, and begin transport. Because you are in
a rural environment, your core hospitals are thirty minutes away. You continue to suction and to ventilate the neonate, with no change in
his status.
One of the hospitals is University Hospital, which has a staffed Neonatal Intensive Care Unit (NICU). This hospital is equal distance from
the other hospitals, so you elect to transport to University Hospital.
The babys condition remains unchanged: there are no spontaneous respirations, but the baby has a brachial pulse of 80 beats per
minute. You intubate the baby with an uncuffed endotracheal tube, using a Miller blade. During intubation, you notice evidence of
meconium staining on the vocal cords. While checking tube placement, you hear rales in the lung fields. You continue to suction the
patient and notice small collections of meconium in the suction canister.
You establish an intraosseous line in the neonates tibia. You attach a monitor and see a low voltage normal sinus rhythm. Online medical
control advises no IV medications but to continue the airway and breathing management.
You arrive at University Hospital. The emergency room staff escorts you to the NICU. The NICU doctor takes your report, agrees with the
estimated age of the baby, and assumes control of patient care. Shortly thereafter, your BLS unit arrives at the emergency room with the
mother, who is still in stable condition.
You continue to follow up on the condition of the neonate. Your thoughts are confirmed that the newborn did have meconium aspiration
syndrome. The baby is in an incubator and on a ventilator. He is receiving IV antibiotics and is being fed through a gastric tube. You find
that the neonate improves slowly, spending eight weeks in the NICU. You learn some time later that the baby was able to fight the
infection and was able to be discharged to home after a total of ten weeks in the hospital.
Overview
In this chapter, we will discuss the emergencies that may be encountered with the neonatal patient. In order to fully understand this, we
will discuss the anatomy and physiology of the neonate, including the amazing changes that take place in the neonates vital organs
during birth. We will study some of the sciences implemented in the NICU, including treatment strategies that may be encountered by the
critical care transport paramedic. With that in mind, this is an important subject for all EMS personnel. 911 EMS personnel will benefit
equally from this chapter, as we may be summoned at any moment to a residence or facility for a neonatal emergency patient.
Birth of humans and animals is a natural process that has occurred throughout history, mostly without intervention. Neonates experiencing
the emergencies that we will discuss will benefit the most from early recognition, treatment, and transport to a facility that provides an
NICU. These facilities have specially trained staff and special equipment to handle neonatal emergencies.

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In the United States, estimates state that approximately six percent of newborns will require emergency life support. Birth weight and
gestational age have a great impact on this need. Sixty-six percent of neonates who have a birth weight of less than 1500 grams will
require support. Seventy to eighty percent of neonates born at or prior to 24 weeks of gestation will not survive.1 With these statistics in
mind, it is important to get a good assessment of the mothers history during obstetrical calls. Is this the mothers first pregnancy? Has she
had a high-risk pregnancy currently or with past children? Has she had prenatal care?
Gestational age, also known as the gestational period, is the time from conception to the birth of the infant. During this time, the baby
develops in the mothers womb. A common method of determining gestational age is taking the day of the beginning of the mothers last
menstrual cycle and adding a fertility window of 10 to 20 days. The gestational age is the time between the tenth day and the current date.
It is important to note that this is an estimate based on averages. Only five percent of newborns are born on their calculated date.2
Gestational Age = Current Date (Beginning of Last Period + 10 Days)
A neonate is defined as a newborn from the moment of birth to 28 days (4 weeks) of age, regardless of gestational age.3 A neonate is
considered premature or preterm if born with a gestational age of less than 37 weeks. A full-term or term neonate is a baby born between
37 and 42 weeks of gestation. A neonate is considered post-term when born after 42 weeks of gestation.
Neonatal Anatomy and Physiology
To consider an infant, especially a neonate, a little adult would be quite wrong in terms of anatomy and physiology. The anatomical and
physiological transitions that the neonate incurs while moving from life intrauterine, or in utero (in the womb), to life outside the womb are
incredible. The majority of the changes focus on the fact that, intrauterine, the babys essential functions are handled by the mother. Once
born, the neonate must function as an independent body.
Airway
Besides just being smaller, the neonatal airway will be much more difficult to manage due to a large tongue designed to suckle. The
Mallampati score is used by anesthesiologists, doctors, and sometimes EMS personnel to rate the probable difficulty of endotracheal
intubation. The Mallampati classification indicates the amount of posterior pharynx visible with the patient sitting up, opening the mouth to
the maximum position, and sticking the tongue out. The theory is that the more visible the posterior pharynx, the less difficult the
intubation.
Class I: soft palate, fauces, uvula, pillars Class II: soft palate,
fauces, portion of uvula Class III: soft palate, base of uvula Class
IV: hard palate only
The Mallampati score.4

A neonate would have a Class 4 Mallampati score due to the large tongue. The trachea is also more superior and anterior, located near
the level of the first or second vertebrae, compared to the adult trachea, positioned at the fourth or fifth cervical vertebrae.
The neonatal airway is yet more complicated. The trachea of the neonate is much more pliable than the adults. In a full-term infant, only
the first cartilaginous ring of the trachea is complete. In firefighter terms, the neonatal trachea is more like a soft suction hose than a hard
suction hose. This pliability makes the airway more susceptible to partial or complete kinking. This can easily occur as a result of
hyperflexion or hyperextension of the patients neck. The very narrow trachea is more at risk for obstruction from respiratory difficulties,
such as meconium aspiration. Meconium aspiration will be further discussed later in this chapter. The neonatal right and left mainstem
bronchi bifurcate at more even angles when compared to the sharp angle of the adult left mainstem bronchus. This is important to
remember during intubation, as it is possible to insert the endotracheal tube too far, intubating either the right or left mainstem bronchus.
A normal neonatal chest x-ray.
Note the flat curves of the rib cage.6

Anatomy and Physiology of the Chest

The muscle tone of the neonate will be significantly weak. This is equally true of the chest cavity. Also, the ribs of the neonate, like most of
its other bones, are not completely calcified and, as a result, are quite pliable and flexible. The same is true of the sternum. This is
necessary to aid in the passage of the baby through the birth canal. When looking at a neonate in the supine position, it can be noted that
the chest cavity appears to be more flat than that of an adult. These flat, pliable ribs are very difficult to expand, or lift, to increase
respiratory volume.5 These facts become treatment factors when providing emergency care of the neonate. Neonates are primarily
abdominal breathers in that they rely heavily on movement of the diaphragm into the abdominal cavity to increase inspiratory volume. This
is necessary to overcome the weak, pliable chest cavity. As the neonate experiences respiratory compromise, it, like adults, will begin to

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require extra work of the accessory chest muscles. As respiratory compromise increases, fatigue of these weak accessory muscles will
occur.
By looking at the two sample x-rays in Figure 2 and Figure 3, it can be noted that the neonatal heart consumes proportionally more of the
chest cavity than that of an adult. This gives the neonatal lungs less room to expand. This fact leads to a diminished pulmonary reserve
capacity. Combine this with the low ability to expand the chest cavity and it becomes obvious why neonates are primarily abdominal
breathers.
The combined results of thermogenesis (heat generation) and the extra work of the newly functioning organs, such as the liver and lungs,
causes a higher metabolic rate in the neonate when compared to an adult. This causes greater oxygen consumption and demand, placing
even more burden on the already challenged neonatal respiratory system.
A normal adult chest x-ray.
Note the round turns in the ribs as compared
to the neonate in Figure 2.7

Pulmonary and Cardiovascular Anatomy and Physiology

Perhaps the most dramatic changes in the pulmonary and cardiovascular anatomy and physiology occur during and shortly after birth. In
utero, the infant receives all oxygenation from the mother through the placenta. At approximately six and a half to seven weeks of
gestational age, the heart is formed and beating, circulating the oxygenated blood from the mother through the developing fetus. A normal
heart rate at this point is between 90 and 110 beats per minute.8 It is not until the twenty-fourth week of gestational age, however, that the
lungs are developed enough to function, if necessary. The lungs are not fully mature until approximately 36 weeks of gestation.9 Even
though the lungs may be developed in utero, they will not function until after delivery. These facts require the heart to bypass developing
lungs, which are not yet capable of providing oxygenation. It is very important to understand this process in utero, because the EMS
provider may encounter the neonate anywhere along the gestational period.
Three main bypasses exist in the neonatal circulatory system. They are the ductus venosus, the foramen ovale, and the ductus
arteriosus.
The placenta serves as the point of exchange for oxygen, carbon dioxide, nutrients, and wastes. The in utero premature neonatal liver is
not capable of performing all of its functions. Thus, throughout fetal development, the liver cannot handle the normal load of blood
circulation. The ductus venosus is a port that remains open to allow the majority of blood from the placenta to bypass the fetal liver and
enter the inferior vena cava for circulation.
Fetal circulation, showing the open foramen ovale,
ductus arteriosus, and ductus venosus.10

In utero, the lungs are fluid-filled and do not have the ability to inspire and expire air. Instead, they are very fragile developing organs. The
foramen ovale is an opening in the interatrial septum that allows blood, oxygenated from the placenta, to flow from the right atrium to the
left atrium for distribution throughout the fetus. This relieves pressure on the right ventricle that, currently, does not need to circulate blood
to the lungs. While transport to the lungs is not necessary, the heart does develop the pulmonary artery for function in the extrauterine
world. While in utero, the ductus arteriosus is a tubular connection between the pulmonary artery and the aorta. Together, the foramen
ovale and the ductus arteriosus allow blood to bypass the developing lungs.
Changes to the special bypasses and the rest of the cardiovascular system occur during birth and the few minutes to days after delivery.
The majority of changes occur as a part of the compression and clamping of the umbilical cord. This stoppage of placental circulation
causes pressure changes within the cardiovascular system. The low pressure placental blood flow stops. An increase in systemic
vascular resistance occurs. The lack of blood flow from the placenta and increased systemic pressure cause the ductus venosus to close.
This initiates perfusion of the kidneys, which begins the renal functions of filtering blood.
In the extrauterine environment, the lungs expand. The first breath of the neonate causes negative thoracic pressure, resulting in a
reduction in pulmonary vascular resistance. Pulmonary blood flow increases, and the lungs begin to fill with blood. This filling reduces
building pressure in the pulmonary artery. The left heart begins to receive oxygenated blood from the pulmonary vein. This initiates a
strengthening of the left heart ionotropic (strength of muscle contractions) functions. With the left atrium functioning at a higher pressure
than the right atrium, the foramen ovale closes. This closes the wall of the septum, and normal extrauterine cardiac flow begins.
The normal extrauterine heart.10
The continuation of oxygenated blood flowing into the left side of the heart causes the left ventricle to increase blood flow and pressure

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into the aorta. This increase in pressure causes a reverse in the flow of blood through the ductus arteriosus. This blood is now highly
oxygenated. This oxygenated blood stimulates vascular constriction of the smooth muscle of the ductus arteriosus and eventual closing of
the duct. In full-term infants, this occurs within hours or days of birth.
Because of the variable time frames, EMS personnel will encounter the neonate in various stages of the closing of the ductus venosus,
foramen ovale, and ductus arteriosus. In a healthy, full-term neonate, this may not be noticeable. In the distressed neonate, however, this
may cause systemic hypotension, and/or pulmonary hypertension.
Pulmonary Pathophysiology
The majority of emergency medical care in the distressed neonate will focus around pulmonary and cardiac problems. We shall now focus
on specific pulmonary problems.
Persistent Pulmonary Hypertension of the Newborn (PPHN)
Persistent pulmonary hypertension is a condition in which the ductus arteriosus and foramen ovale remain open after birth. This syndrome
complicates itself in that the open ductus arteriosus and foramen ovale cause pulmonary hypertension, and the pulmonary hypertension
causes the ductus arteriosus and foramen ovale to remain open. PPHN has many causes. Most of them focus on difficult deliveries that
disrupt the natural transformation of the valves, meconium aspiration syndrome, diaphragmatic hernia, or other congenital disorders.
Meconium Aspiration Syndrome
Meconium is the waste product found in the intestinal tract of infants. In a normal, healthy delivery, this meconium is expelled in the
newborns first bowel movement after birth. In distressed deliveries, the fetus may move its bowels prematurely, causing dispersion of the
meconium into the amniotic fluid. If the neonate inhales or opens its mouth while still in utero, or inhales while still covered in the fluid
post-delivery, the neonate may then aspirate this meconium into the airway and lungs. Damage to the extremely narrow airway and newly
functioning lungs can be devastating. The National Institute of Health estimates that premature meconium expulsion occurs in ten to
fifteen percent of all deliveries. Only two to ten percent of these patients will aspirate the meconium into the lower airways.11 Aspiration
can cause airway obstruction and may cause the surfactant of the aveoli to fail to activate, resulting in poor respiration. Aspiration may
also lead to pneumonia and long-term complications. Maternal diabetes (congenital or gestational) and maternal hypertension is known to
contribute to distressed deliveries and will put the fetus at special risk for meconium aspiration.
Emergency medical treatment of the meconium aspiration syndrome patient should focus on prevention. A mother being transported on a
fetal heart monitor may present with a slowing heart rate. Look carefully for signs of meconium staining in the amniotic fluid prior to birth.
This may appear as darkish green staining or streaking in the amniotic fluid, or may present clearly as the presence of stool. Prepare to
suction and protect the airway appropriately, as soon as the head presents during delivery. Listen to lung sounds for rales or crackles. In
the delivery room or NICU, the neonate may undergo laryngoscopy to view the vocal cords for possible staining. This is not appropriate in
the emergency medical field unless laryngoscopy is being performed for intubation or suctioning. A chest x-ray would also be performed.
A blood sample may indicate alkalosis.
Aggressive prevention and treatment, including proper suctioning, can lead to a positive outcome. Severe patients may require intubation
and mechanical ventilation and will receive antibiotics in the NICU for the treatment or prevention of infection. Brain damage may occur to
the neonate as a result of severe aspiration and lack of oxygenation.
Transient Tachypnea of the Newborn
Before discussing Neonatal Respiratory Distress Syndrome (NRDS), we will discuss a subset of NRDS, known as Transient Tachypnea of
the Newborn. Transient Tachypnea of the Newborn (TTN) is also known as wet lung or Type II Respiratory Distress Syndrome.12 The
name describes the condition, with transient meaning temporary and tachypnea meaning a fast rate of breathing. This syndrome occurs
as a result of the failure of the neonatal lungs to drain their in utero fluid in response to spontaneous respirations. As mentioned in the
pulmonary anatomy and physiology section, the in utero lungs are fluid-filled. The first breath after birth causes a negative pressure in the
lungs, beginning the draining of this fluid and the filling of the lungs with oxygen. With the sustained presence of fluid, less alveolar
surface is available for oxygen exchange. Since the neonate has such a pliable chest, and such a low tidal volume, the neonates only
available natural response is to increase rate of respirations. While this may happen as a result of premature birth, this is most common in
full-term neonates. Neonates born via Cesarean section are at a particular risk, because they do not experience the natural compression
of a vaginal delivery.
The TTN patient will present with typical signs of respiratory distress. Respirations may be above 60 times per minute. Rales or rhonchi
will be present upon auscultation. The patient may grunt. The ultimate diagnosis is made by the chest x-ray, which would show
hyperinflated streaking lungs.
Treatment in the emergency medical environment involves respiratory support with oxygen. Oropharyngeal and deep tracheal suctioning
may be necessary. In the critical care transport environment, you may have to care for a patient who is on IV antibiotics to prevent or treat
pneumonia. The patient may have a gastric feeding tube in place. The neonate may also be receiving Continuous Positive Airway
Pressure (CPAP). This is a treatment for several respiratory conditions of all ages, including sleep apnea. CPAP is used in TTN, because
it pushes a continuous flow of pressure into the lungs. This increase in pressure helps to keep the air passages open and allows the

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healthy alveolar surfaces to function more efficiently. CPAP may be in the form of a mask on the neonates face or may be attached to an
endotracheal tube and ventilator. EMS personnel who encounter a TTN patient on CPAP should receive a briefing on the equipment and
circuitry prior to transporting the patient. If you are planning on transferring the patient to your own ventilator, you must make sure that
your ventilator is CPAP-capable and compatible with the mask and any circuitry that you may transfer. Note the settings and have
everything prepared prior to removing the patient from the existing circuit.
Hyaline Membrane Disease (Neonatal Respiratory Distress Syndrome)
Hyaline Membrane Disease (HMD) is also known as Neonatal Respiratory Distress Syndrome (NRDS). It is a syndrome that is most
common in premature neonates and rarely seen in full term-infants. This disease occurs in over half of neonates born before 28 weeks of
gestation.13 The severity of the disease depends on the gestational age of the neonate. It is worsened by contributing factors, such as
infection or a patent ductus arteriosus. HMD involves the alveolar surfactant. We have discussed that the lungs are barely functional at 24
weeks. This is in part due to the fact that surfactant production begins around the twenty-fourth week. The surfactant consists of
phospholipids and proteins and reduces surface tension in the lungs, particularly at the alveolar level. This reduced surface tension aids in
the gas exchange. In the absence of surfactant, the alveoli collapse, causing atelectasis, the decrease in surface area of the lungs.
Neonates affected by HMD will display shortness of breath, tachypnea, sternal retractions, grunting, nasal flaring, and accessory muscle
use. As discussed in the chest anatomy section, neonates have poor muscle tone and a flat chest. These anatomical weaknesses, when
combined with an extended respiratory disorder such as HMD, will cause the neonate to fatigue quickly, leading to respiratory arrest. EMS
treatment of this neonate will focus on early recognition of respiratory distress using visible signs, the APGAR score, and pulse oximetry.
High-flow oxygen should be provided. Be prepared to intubate and provide ventilations. Mechanical ventilations, when necessary, will also
help to provide pressure on the aveoli, reducing atelectasis.
A reticulogranular chest x-ray of a Hyaline
Membrane Disease neonate.14

Hospital assessment of the HMD patient will include a chest x-ray. Radiologists will look for a reticulogranular (cloudy) appearance. A
blood gas analysis will be performed not only to check oxygen levels but also to check for high levels of carbon dioxide and acidosis.
Acid/base therapy will be performed as necessary. An echocardiogram will be performed to check for a patent ductus arteriosus and other
heart conditions. Long-term treatment of this neonate will most likely involve surfactant replacement therapy, which is most successful
when initiated within six hours of birth. Therefore, EMS personnel must recognize symptoms early and transport a suspected neonate to a
facility capable of providing neonatal intensive care. Check your local transport protocols for details.
Congenital Diaphragmatic Hernia
A Congenital Diaphragmatic Hernia (CDH) is a condition in which the organs of the abdomen have protruded through the diaphragm into
the thoracic cavity. This occurs as the diaphragm is developing during the first trimester, between the seventh and eighth week of
gestation. The stomach, esophagus, and intestines are also still developing at this time. The diaphragm naturally has a hole to allow the
great vessels and the esophagus through to the abdomen. During development, this hole remains loose, and developing organs push
through it. This condition is most common on the left side of the body and is called a Bochdalek hernia.15 This accounts for eighty-five to
ninety percent of all congenital diaphragmatic hernias. In a left-sided hernia, the stomach and small intestine typically are the organs
herniated into the chest cavity. In a right-sided, or Morgagni hernia, the liver and small intestine are usually protruded into the chest cavity.
A Morgagni hernia is very rare but is known to specifically involve the tendon surrounding the esophagus and great vessels. Both forms of
CDH will cause a physical mediastinal shift of the chest cavity. The already compact chest volume is further diminished, making
respirations even more difficult.
The physical decrease in chest volume is not the only problem. Because this condition occurs at such a young gestational age, the
diaphragm, lungs, stomach, intestines, and liver are all still in various stages of development. The physical restrictions on the lungs cause
pulmonary hypoplasia, which is defined as a decrease in the number of alveoli, cells, and airways, resulting in a decreased size and
functionality of the lungs. Also, the decreased alveoli are able to only partially fill with air. A decrease in surfactant causes the alveoli to
deflate quickly.
In a CDH, the stomach and intestines also suffer from a lack of space during development. They are also at risk for a decreased blood
supply during development, caused by the compression of the vessels and organs through the diaphragm.
Assessment of the CDH patient begins with a history of the mother. Mothers who have received prenatal care will most likely know of the
condition prior to birth. Ultrasounds at various stages are able to determine the presence of this condition in utero. Parents who have had
a previous child with a diaphragmatic hernia have a two percent chance of recurrence with future children.
Left-sided Congenital
Diaphragmatic Hernia.16

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Mothers without prenatal care will be unaware of the situation. Neonates with a diaphragmatic hernia will present with abnormal chest
formation, with one side being larger than the other. Due to the absence of organs in the abdomen, the abdomen will appear to be caved
in (concave). The patient will have trouble breathing, tachypnea, tachycardia, and cyanosis. Abnormal breathing may be obvious. Breath
sounds will be uneven. Patients with a rare right-sided hernia may show no signs or symptoms.
Emergency medical treatment of this neonatal patient will focus on respiratory support. A CDH patients severity can vary greatly.
Endotracheal intubation and mechanical ventilation may be necessary, as this patient may be unable to support its own respirations
against the additional pressure of the abdominal contents. Medical control may order rapid sequence intubation or other forms of sedation
and/or pain management, as this neonate will be in severe distress.
In-hospital care may involve the placement of a nasogastric (NG) tube. The objective is to keep the stomach decompressed to allow for
maximum possible lung expansion. Definitive care can require a stay in the NICU to allow for further development of the premature
neonate, making the newborn a better candidate for surgery. During this period, the patient may be quite vulnerable. The most severe
patients may require ECMO, a heart/lung bypass machine. The ultimate solution will be surgery, which will physically move the organs
into the right location and seal the hole in the diaphragm to a normal position.
While this surgery will fix the main problem, the neonate may experience ongoing problems into childhood and even adulthood.
Emergency medical providers may encounter these patients in the field. Many CDH patients will have chronic lung disease, and will
require medication and home oxygen therapy for weeks to years after birth. CDH patients may also have gastric esophageal reflux
disease (GERD). This allows stomach fluids and acids to move up into the esophagus, causing heartburn and long-term damage to the
esophagus. Esophageal reflux can cause feeding problems in the already distressed neonate.
Due to the extensive lung problems, CDH patients may experience Failure to Thrive Syndrome. This condition is defined by the inability of
the neonate to gain or sustain weight and metabolism. The distressed neonate may have a higher Basal Metabolic Rate (BMR) than
normal neonates as they work to repair and grow their bodies. GERD, as described previously, may further complicate the feeding
process.
Cardiovascular Pathophysiology
Congenital heart defects are imperfections in the development of the heart during gestation or chronic failures of the heart to complete the
anatomy and physiology changes discussed earlier in this chapter. According to kidshealth.org, 8 in 1000 neonates are born with some
form of heart defect.17 The defects range in severity, depending upon the amount, pressure, and direction of blood displaced from the
normal flow. Severe defects can lead to an inadequate cardiac output, resulting in poor systemic perfusion to the rest of the body.
Left to Right Shunt Defects
Atrial Septal Defect (ASD) and Ventricular Septal Defect (VSD) are considered left to right shunt defects. This means that the septum is
not completely developed in one or more areas. The end result is that blood is moved from the left atrium or left septum to the right
chambers of the heart, respectively. These defects do not affect the oxygenation of the blood leaving the aorta but can possibly affect the
volume. This is because the pressures on the left side of the heart are greater than those on the right. Blood flows from left to right
through the defect. Thus, there is no mixing of oxygenated blood in the left side. Instead, oxygenated blood remixes with unoxygenated
blood in the right side of the heart. It is then recirculated through the pulmonary system and back into the left side of the heart. These
defects are referred to as acyanotic, meaning that inadequate blood oxygenation is NOT present.
Ventricular Septal Defect
Ventricular Septal Defect (VSD) is considered a shunt defect. In VSD, one or more holes between the atrial and ventricular septum exist.
The severity depends upon how big the hole(s) is. VSD with a small opening may be asymptomatic and therefore may be difficult to
diagnose. A large VSD may be acute or chronic, meaning that it may be diagnosed immediately, or it may take a few years of growth to
appear. Patients with VSD may develop an enlarged right ventricle as a result of the increased pressure leaking from the left ventricle to
the right. A neonate with severe VSD will present to EMS personnel with pulmonary vascular congestion, rales, or crackles. The patient
will have tachypnea, increased respiratory effort. The patients symptoms will be very much like congestive heart failure. A patient
diagnosed with VSD may be receiving diuretic treatments and fluid restrictions. The definitive care for a neonate with VSD is surgery to
repair the hole(s).
Atrial Septal Defect and Patent Foramen Ovale
Atrial Septal Defect (ASD) is an opening between the right and left atria. This is most commonly caused by an incomplete closing of the
foramen ovale. The foramen ovale is the opening between the right and left atrium that allows partial bypass of the lungs while in utero.
Failure of the foramen ovale to close is called Patent Foramen Ovale (PFO). In this condition, the word patent means remaining open,
such as in a patent IV. The clinical manifestations of PFO are similar to that of VSD in that they will present as congestive heart failure.
Over time, enlargements will occur in both the right atrium and the right ventricle. The definitive treatment for a neonate with PFO or other
forms of ASD is surgery to repair the hole.
Patent Ductus Arteriosus
A Patent Ductus Arteriosus (PDA) is a failure of the ductus arteriosus to close shortly after birth, when pulmonary circulation is

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established. Recall that the ductus arteriosus is the main bypass between the pulmonary artery and aorta that shunts blood from the
immature, developing lungs. The ductus arteriosus takes hours to a couple of days to close, so it is impossible to diagnose this problem in
the newborn. PDA is more common in premature or low birth weight infants than in full-term newborns. It is estimated that sixty percent of
patients younger than 28 weeks of gestation will maintain a patent ductus arteriosus. Approximately thirty percent of low birth weight
neonates (less than 2500 grams) will have a PDA.18
The main clinical manifestations of PDA are centered on the pulmonary and cardiovascular systems. PDA will cause congestive heart
failure signs and symptoms. The patient with a serious PDA will display tachypnea, tachycardia, bounding peripheral pulses, and a wide
pulse pressure. Patients will have a heart murmur during systole.
Emergency medical treatment of the PDA patient will focus on respiratory support. In the transport environment, the patient may be
receiving diuretic therapy. The patient may also be receiving two very opposite treatments. If the plan for surgical intervention is surgical
ligation, then the patient may be receiving prostaglandins to actually maintain the PDA in the open position. Prostaglandin promotes
vasodilation and relaxation of the ductus arteriosus. If the patient is not a candidate for surgical ligation, then the patient may be on a
prostaglandin inhibitor called indomethacin, in an attempt to naturally close the ductus arteriosus.
The next group of heart defects is known as obstructive heart defects. They are commonly a result of structural deformity. Severity
depends on the size of the blockage and the cardiovascular regions involved.
Aortic Stenosis (AS) and Pulmonary Stenosis (PS) are two different conditions with very similar manifestations. The difference is simply in
the location. Stenosis refers to narrowing. Thus, AS is a narrowing in the aortic valve, which is located between the left ventricle and the
aortic arch. This narrowing causes the left ventricle to have to work harder, increasing pressure to overcome the restrictions of the narrow
valve. This will lead to left ventricular hypertrophy, enlargement of the left ventricle. This additional pressure will also effect the aorta,
causing stretching.
PS exists in the pulmonary valve, between the right ventricle and the pulmonary artery. This condition will cause hypertrophy of the right
ventricle and increased pressure on the pulmonary artery.
The neonatal AS or PS patient will have dyspnea, with an increase in rate and effort. Although heart sounds are rarely assessed in the
pre-hospital environment, the emergency medical provider may hear a heart murmur on auscultation. Treatment of the AS or PS patient
focuses on supportive therapy. Definitive treatment of AS and PS is a balloon valvuloplasty or angioplasty.19
Coarctation of the Aorta (COA) is a narrowing of the aorta toward the distal end of the aortic arch. This location is clinically significant
because it occurs after the bradiocephalic, left common, and left arteries branch off. This congenital defect accounts for eight to ten
percent of congenital heart defects. The neonate with COA will have an enlarged ventricle, similar to that described in the AS section
previously. The neonate may show congestive heart failure signs. This problem is further complicated by an imbalance in systemic blood
pressure. Because of the location of the coarctation, the upper portion of the body will receive hypertensive blood flow, while the abdomen
and lower extremities will be hypotensive. This places the neonate at a high risk of stroke due to the increased pressure in the cerebral
cortex. While the COA neonate is experiencing a hypertensive crisis in the upper portion of the body, the abdomen and, thus, the
abdominal organs are suffering from a hypotensive crisis. Poor blood flow through the liver and kidneys will cause metabolic acidosis and
renal sepsis.
Transport of the COA neonate may require prostaglandin therapy support, as well as diuretic therapy to treat congestive heart failure
symptoms. Because of the wide scope of systemic effects, the transport team should be prepared to handle multiple IV infusions and
follow strict ongoing assessment orders from the transferring physician that may be unique for each COA patient.
The last two congenital defects to be discussed in this chapter are considered cyanotic heart defects. The congenital heart defects
discussed to this point were acyanotic in that they did not affect oxygenation of blood through the pulmonary system. Complete
Transposition of the Great Vessels and Tetralogy of Fallot are cyanotic in that the pathophysiologies result in poor pulmonary perfusion
and inadequate blood oxygenation.20
Complete Transposition of the Great Vessels
Complete Transposition of the Great Vessels (TGV) is a congenital condition represented by abnormal pathways of the great vessels. In a
normal heart, the pulmonary artery leaves the right ventricle to carry unoxygenated blood to the lungs. The aorta leaves the left ventricle
to carry oxygenated blood to the rest of the body. In TGV, the pulmonary artery exits the left ventricle to the body, while the aorta exits the
right ventricle to the body. This condition alone causes two parallel blood circuits, and circulating blood is never moved through the lungs
for oxygenation. How does the neonate survive? Two factors keep these victims alive. The first is that, in utero, the fetus is receiving
oxygenated blood from the mothers placenta. No blood is circulated through the lungs due to the ductus arteriosus and foramen ovale.
Upon birth, all neonates have a patent ductus arteriosus for a few hours to a few days. This may allow for enough oxygenated blood to
mix with the unoxygenated blood to prevent severe cyanosis and hypoperfusion. The second factor is that approximately twenty-five
percent of TGV patients are also born with VSD.21 These two factors often provide enough mixing of blood for a neonate to survive to
surgery.

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Transposition of the Great Arteries

Emergency medical care of the TGV patient involves good history taken from the mother. This neonate may have only hours to survive,
so an advanced knowledge of the problem is key to survival. In mothers with no prenatal care, early recognition of signs in the neonate is
essential. The neonatal TGV patient will have dyspnea, tachycardia, and cyanosis that are not improving and are quite likely deteriorating
after birth. Definitive care will involve surgery to place the great vessels in their proper alignment, completing the circuit. A TGV neonate in
the transport environment may be on IV prostaglandin to keep the ductus arteriosus open, allowing for the maximum mixing of
oxygenated and unoxygenated blood.
Tetralogy of Fallot
Tetralogy of Fallot (TOF) is a rather complicated cyanotic heart defect. Tetralogy has the prefix tetra, which means four. TOF involves four
defects:

1. Pulmonary Stenosis
2. Ventricular Septal Defect
3. An overriding aorta: A condition in which the aortic valve is enlarged. This enlargement pushes the septum aside and, thus,
receives blood from both the right and left ventricles.
4. Right ventricular hypertrophy: The enlargement of the right ventricle as a result of working at the higher pressures communicated
by the left ventricle.

The pulmonary stenosis and the flow of blood from the right ventricle to the aorta shunt blood flow to the lungs, resulting in inadequate
oxygenation. As ominous as this condition sounds, symptoms can vary from mild to severe. As such, the neonate will present with a range
of signs, including mild to severe dyspnea and cyanosis. Oxygenation will have little effect on moderate to severe patients. Emergency
medical treatment is supportive in nature based on the severity of symptoms. A TOF neonate in the transport environment may be on IV
prostaglandin to keep the ductus arteriosus open, allowing for the maximum mixing of oxygenated and unoxygenated blood.
The Pulmonary and Cardiovascular Neonate
As you may have very well noted by now, the vast majority of this chapter has focused on anatomy, physiology, and pathology of the
neonatal pulmonary and cardiovascular systems. This is because the vast majority of neonatal health issues focus on these two systems.
Almost every condition discussed in the subsequent sections involves respiratory support. Most of the conditions mentioned tachypnea
and/or tachycardia. One last point should be made about the neonatal heart and lungs. As explained previously, neonates have a
decreased muscle tone. This is true of the diaphragm, the accessory muscles, and the cardiac muscle. Also studied has been the relative
lack of space in the thoracic cavity. Because of these factors, the neonate has few options when experiencing shortness of breath or
cardiac issues. Since the neonate experiencing respiratory distress cannot expand its lung volume to compensate, the only mechanism
available to improve respirations is to increase the rate. This is the same with the heart. The weak tone of the cardiac muscle prevents an
increase in ionotrophy (strength of contractions). The only alternative is increased chronotrophy (rate) to increase cardiac output.
Increasing tachypnea and tachycardia should be signs of trouble in the ill neonate. Likewise, slowing respirations and bradycardia should
be a sign of a tiring, decompensating patient.
Thermoregulation Issues of the Neonate
At birth, the neonates surface area to volume ratio is four times that of an adult. That larger surface area also contains very little adipose
tissue, which acts as the insulation of the skin. Thermogenesis (heat generation) is only one and a half times that of an adult. The neonate
has very little muscle tone, which inhibits the ability to shiver to compensate for heat loss. Heat is lost in the neonate through evaporation,
convection, radiation, and conduction. Evaporation is the largest cause of heat loss in the newborn, wet neonate. Convection is the next
largest heat loss mechanism. This poses a more difficult situation in the EMS setting than in a controlled delivery room. The neonate in
our care may be born in a less than desirable location, such as a large, open public place, a residence, or even our ambulance. We must
then transfer that neonate from the place of birth to the hospital, which may involve one or more trips outside. It is relatively easy to set
and to maintain the temperature in a delivery room, while we must constantly be aware of our environment in the EMS world.
Blood Sugar and Metabolism of the Neonate
The glucose requirements of a neonate may vary greatly depending on the gestational age and the maturity of vital organs. Newborns will
have very low glycogen stores in the liver. A premature liver may be unable to store or release glucose. A premature pancreas may be
unable to properly regulate insulin production or release. A distressed neonate may use more glucose than normal, adding hypoglycemia
to their current problem. Blood glucose levels in a full-term neonate should be between 70 and 80 ml/dl.
The metabolism of a healthy neonate is quite higher than that of an adult. Adult metabolisms vary greatly, depending upon gender, height,
weight, age, and health conditions. The Basal Metabolic Rate (BMR) is the number of calories needed simply for survival. In other words,
the BMR is the amount of calories needed daily for a body at rest. BMRs for adults vary between 5 to 10 calories per kilogram of body
weight per day.22Protocols in Neonatal Nursing recommends a BMR of 50 calories per kilogram per day for a healthy neonate.23

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Assessment of the Neonate

Now that we have a vast knowledge of the anatomy, physiology, and pathology of the neonate, we can apply this knowledge in the field
setting. Assessment of the unborn or extrauterine neonate should begin with the mother. When the basics of assessment and treatment of
the mother and neonate are complete, a focused maternal history should be obtained.24 Ask the mother how far along she is or when the
baby is due. This will allow you to approximate the gestational age, allowing you to prepare for the potential complications of prematurity.
Ask the mother if she is expecting a single newborn or multiples. Multiple gestations are at risk for prematurity and may require additional
resources. Ask the mother if her water has broken. This will give you some timeframe for delivery. If it has broken, asking what color the
fluid was, or looking for stains in clothes and linens, will help to determine the presence of meconium. Obtain the mothers medications,
including over-the-counter and possibly illegal drugs. Recent narcotic use may lead to a depressed respiratory system in the neonate.
Determine whether the mother has chronic or gestational diabetes, as the neonate may have hypoglycemia. If care is initiated prior to
delivery, ask the mother about the position of the baby and the possibility of placenta previa. Most mothers with prenatal care would know
if their baby was breech or if placenta previa was present.
Care of the Newborn Neonate
If you are present at the birth of the neonate, it is important to take the proper steps to assure the neonates transition to extrauterine life.
Begin by assuring a clear, patent airway. Suction the neonates mouth and then nose during and immediately after birth. Note for the
presence of meconium. Provide tactile stimulation for the neonate to breathe. Dry the neonate to guard from heat loss and further
stimulate breathing. Answer the following five questions:

1.
2.
3.
4.
5.

Is the airway clear of meconium?

Is the neonate breathing or crying?
How is the neonates muscle tone?
How is the neonates color?
Is the neonate of term gestation or premature?

A tool exists to help the care provider to answer these questions. The APGAR score was developed in 1952 by an obstetrical
anesthesiologist named Virginia Apgar.25 The APGAR scoring system is a universally accepted method of rating five signs that indicate
the overall condition of the neonate. Each sign gets a rating of 0, 1, or 2, and is then added to equal a total. The APGAR scores are
calculated as follows:
APGAR Score Chart

Appearance
Pulse
Grimace
Activity
Respirations

1
Body Pink, Extremities Blue
<100
Grimaces, Cries
Flexion of Extremities
Slow or Irregular

Blue or Pale
Absent
No Response
Limp
Absent

2
Completely Pink
100 or Greater
Cries Vigorously
Active Motion
Good, Adequate

The APGAR score is calculated at one and five minutes extrauterine. It is not necessary to have a score of 10 at one minute for the
neonate to be healthy, but a normal neonate should achieve a 10 by five minutes. This tool is useful in reporting the status of the newborn
neonate to the receiving facility. It is important for the EMS provider to realize, however, that this score is assessed after one minute.
Intervention with the pulseless and/or apneic neonate should begin as soon as possible when the newborn does not respond to tactile
stimulation.
Key Terms28

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Acyanotic: Lacking cyanosis, or absence of inadequate oxygen

Metabolic Rate: The amount of calories per kilogram required p
Ductus arteriosus: A tubular connection between the pulmonary
Ductus venosus: The intrauterine port between the umbilical co
Extrauterine: Development and life of the neonate post-delivery
right atrium and left atrium that allows blood to bypass the lung
gestation. Intrauterine, in utero: Development and life of the ba
muscle contractions. Meconium: The waste product found in th
to 28 days of age.
Premature (Preterm): A neonate born with a gestational age of
gestation. Pulmonary hypoplasia: A decrease in the number of
generation of heat through the bodys normal metabolism.

The normal respiratory rate of a term newborn is 30 to 60 breaths per minute. The term newborns heart rate is normally 100 to 180 beats
per minute.
Emergency Resuscitation of the Distressed Newborn
The American Heart Association provides guidelines for the evaluation and resuscitation of the newborn neonate.26 The guidelines begin
with a 30-second evaluation of the newborn. During this period, the provider is to dry and warm the neonate, answering the five questions
above and providing tactile stimulation. If all questions answer yes AND the patient is breathing AND the patient has a heart rate equal to
or greater than 100, then supportive care is indicated, including supplemental oxygen as needed.
If, after the initial evaluation, the neonate is apneic, and/or has a pulse of less than 100, the guidelines recommend beginning positive
pressure ventilations. Ventilations should be provided at 20 times per minute (one ventilation every three seconds). The guidelines also
call for the consideration of tracheal intubation if the patient does not improve. Provide ventilations for another 30-second period,
evaluating the neonate for color improvement and pulse rate.
If, at the end of the period, the patient is breathing, has a pulse greater than 100, and has good color, ventilations can be terminated and
supportive care continued. If the patient has a pulse between 60 and 100, continue the ventilations. If the patient has a pulse rate of less
than 60, continue ventilations and begin chest compressions. At this point, epinephrine therapy may be indicated. The guidelines call for
.01 to .03 mg per kilogram of 1:10,000 epinephrine. Remember, however, that the AHA guidelines are just that: guidelines. Check your
local pre-hospital care protocols for your appropriate resuscitation orders.
Neonatal Intubation
At several places in this chapter, the need for endotracheal intubation of the neonate has been discussed. In the airway anatomy and
physiology section, discussion included the extreme pliability of the incomplete tracheal rings. The neonatal epiglottis is more oblong
(elongated) in shape than that of an adult. With this in mind, consider the concepts of laryngoscopy. While there are several commercial
types of laryngoscope blades, the Mac (curved) and the Miller (straight) are the most common. The concept of the Macintosh blade is to
slide it into the valleculla, the open slot just superior to the epiglottis. Lifting upward and outward should, in theory, indirectly lift the
epiglottis away from the trachea. The more oblong, pliable epiglottis will be more difficult to displace this way than that of an adult. The
Miller blade is designed to directly lift and sweep the epiglottis out of the way. For the anatomical reasons listed, the Miller blade is more
appropriate to displace the epiglottis and achieve a straight plane in the neonatal airway. Cricoid pressure with the tip of one finger should
be implemented to further achieve this straight plane. Remember that the neonatal trachea is more superior and anterior than that of an
adult. Also, when auscultating the lungs to confirm tube placement, recall that it is equally possible to intubate the left or right mainstem
bronchi.
Advanced Concepts in Neonatal Care:
Deep Tracheal Suctioning
Discussed previously was the need for tracheal suctioning in neonates, such as those who have suffered from meconium aspiration.
Before performing deep tracheal suctioning, check your local transport protocol or online medical control. Protocols for deep tracheal
suctioning may vary greatly. If EMS deep tracheal suctioning of the neonate is indicated, several basic guidelines apply. Apply suctioning
only on the way out. In other words, do not suction while inserting the catheter into the airway. Do NOT use mechanical suctioning
unless the vacuum pressure can be adjusted to the amount of pressure indicated by your protocol. Commercial devices exist to assist
with neonatal endotracheal suctioning. For example, the Cathmark Neonatal Suction Catheter Kit, manufactured by Smiths Medical,

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allows for careful suctioning of the neonate.27

Neonatal Transport Incubators
At several points in this chapter, discussion focused on the importance of thermoregulation of the neonate. Also mentioned was the
difficulty of maintaining an appropriate environment for transporting infants in an ambulance. For this reason, the neonatal incubator must
extend from the NICU to the ambulance. Special transport incubators exist for this purpose. These incubators allow the environment of
the NICU to be duplicated in the transport environment.
Summary
In this chapter, we listed specific anatomical and physiology features of the neonate. We also identified common neonatal
pathophysiologies, and we implemented specific neonatal treatments.
Author: Gary S. Ehling, BA, EMT-P, KY EMS Instructor Copyright (c) CE Solutions, All Rights Reserved.

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