he Respiratory System in Babies

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What is respiration?
Respiration is the act of breathing in and out. When you breathe in, you take in oxygen. When you breathe
out, you give off carbon dioxide.

What makes up the respiratory system?

The respiratory system is made up of the organs involved in the interchanges of gases:

 Nose

 Mouth

 Throat (pharynx)

 Voice box (larynx)

 Windpipe (trachea)

 Airways (bronchi)

 Lungs

The upper respiratory tract includes the:

 Nose

 Air-filled space above and behind the nose (nasal cavity)

 Sinuses

The lower respiratory tract includes the:

 Voice box

 Windpipe

 Lungs

 Airways (bronchi and bronchioles)

 Air sacs (alveoli)

What do the lungs do?

 The lungs take in oxygen. The body's cells need oxygen to live and carry out their normal functions. They
also get rid of carbon dioxide. This is a waste product of the cells.

The lungs are 2 cone-shaped organs. They are made up of spongy, pinkish-gray tissue. They take up most
of the space in the chest, or the thorax (the part of the body between the base of the neck and diaphragm).
They are inside a membrane called the pleura.

The lungs are separated by an area (called the mediastinum) that has the following:

 Heart and its large vessels

 Windpipe

 Food pipe (esophagus)

 Thymus gland

 Lymph nodes

The right lung has 3 lobes. The left lung has 2 lobes. When you breathe, the air:

 Enters the body through the nose or mouth

 Travels down the throat through the voice box and windpipe

 Goes into the lungs through tubes (mainstem bronchi):

o One of these tubes goes to the right lung and one goes to the left lung

o In the lungs, these tubes divide into smaller bronchi

o Then into even smaller tubes called bronchioles

o Bronchioles end in tiny air sacs called alveoli

Breathing in babies
An important part of a baby's lung development is the production of surfactant. This is a substance made
by the cells in the small airways. By about 35 weeks of pregnancy, most babies have developed
enough surfactant. It is normally released into the lung tissues. There it helps to keep the air sacs (lung
alveoli) open. Premature babies may not have enough surfactant in their lungs. They may have trouble
breathing.

Respiratory Distress Syndrome (RDS) in

Premature Babies
What is respiratory distress syndrome in premature babies?
What is respiratory distress syndrome in premature babies?

Respiratory distress syndrome (RDS) is a common problem in premature babies. It causes babies to need
extra oxygen and help with breathing. The course of illness with RDS depends on:

 The size and gestational age of your baby

 How serious the illness is

 Whether your baby has an infection

 Whether your baby has a heart defect called patent ductus arteriosus

 Whether your baby needs a machine to help him or her breathe (ventilator)

RDS typically gets worse over the first 2 to 3 days. It then gets better with treatment.

What causes RDS in premature babies?

RDS occurs when there is not enough surfactant in the lungs. Surfactant is a liquid made by the lungs that
keeps the airways (alveoli) open. This liquid makes it possible for babies to breathe in air after delivery.
An unborn baby starts to make surfactant at about 26 weeks of pregnancy. If a baby is premature (born
before 37 weeks of pregnancy), he or she may not have made enough surfactant yet.

When there is not enough surfactant, the tiny alveoli collapse with each breath. As the alveoli collapse,
damaged cells collect in the airways. They further affect breathing. The baby has to work harder and
harder to breathe trying to reinflate the collapsed airways.

As the baby's lung function gets worse, the baby takes in less oxygen. More carbon dioxide builds up in the
blood. This can lead to increased acid in the blood (acidosis). This condition can affect other body organs.
Without treatment, the baby becomes exhausted trying to breathe and over time gives up. A ventilator must
do the work of breathing instead.

Which premature babies are at risk for RDS?

RDS occurs most often in babies born before the 28th week of pregnancy. Some premature babies get RDS
severe enough to need a breathing machine (ventilator). The more premature the baby, the higher the risk
and the more severe the RDS.

Most babies with RDS are premature. But other things can raise the risk of getting the disease. These
include:

 The baby is a boy or is white

 The baby has a sibling born with RDS

 C-section (Cesarean) delivery, especially without labor. Going through labor helps babies' lungs become
ready to breathe air.

 The baby doesn’t get enough oxygen just before, during, or after birth (perinatal asphyxia)

 The baby has trouble maintaining body temperature (cold stress)

 Infection

 The baby is a twin or other multiple (multiple birth babies are often premature)

 The mother has diabetes (a baby with too much insulin in his or her body can delay making surfactant)

 The baby has a condition called patent ductus arteriosus (PDA)

What are the symptoms of RDS in premature babies?

These are the most common symptoms of RDS:
 Breathing problems at birth that get worse

 Blue skin color (cyanosis)

 Flaring nostrils

 Rapid breathing

 Grunting sounds with breathing

 Ribs and breastbone pulling in when the baby breathes (chest retractions)

The symptoms of RDS usually get worse by the third day. When a baby gets better, he or she needs less
oxygen and mechanical help to breathe.

The symptoms of RDS may look like other health conditions.

How is RDS in premature babies diagnosed?

RDS is usually diagnosed by a combination of these:

 Baby’s appearance, color, and breathing efforts. These can point to a baby's need for help with
breathing.

 Chest X-rays of the lungs. X-rays make images of bones and organs.

 Blood gas tests. These measure the amount of oxygen, carbon dioxide and acid in the blood. They may
show low oxygen and higher amounts of carbon dioxide.

 Echocardiography. This test is a type of ultrasound that looks at the structure of the heart and how it is
working. The test is sometimes used to rule out heart problems that might cause symptoms similar to RDS.
It will also show whether a PDA may be making the problem worse.

How is RDS in premature babies treated?

Treatment will depend on your child’s symptoms, age, and general health. It will also depend on how
severe the condition is.

Treatment for RDS may include:

 Placing a breathing tube into your baby's windpipe (trachea)

 Having a ventilator breathe for the baby

 Extra oxygen (supplemental oxygen)

 Continuous positive airway pressure (CPAP). This is a breathing machine that pushes a continuous flow of
air or oxygen to the airways. It helps keep tiny air passages in the lungs open.

 Artificial surfactant. This helps the most if it is started in the first 6 hours of birth. Surfactant replacement
may help make RDS less serious. It is given as preventive treatment for some babies at very high risk for
RDS. For others who become sick after birth, it is used as a rescue method. Surfactant is a liquid given
through the breathing tube.

 Medicines to help calm the baby and ease pain during treatment

What are possible complications of RDS in premature babies?

 Babies sometimes have complications from RDS treatment. As with any disease, more severe cases often
have greater risks for complications. Some complications of RDS include:

 Lungs leak air into the chest, the sac around the heart, or elsewhere in the chest

 Chronic lung disease (bronchopulmonary dysplasia)

How can RDS in premature babies be prevented?

Preventing a premature birth is the main way to prevent RDS. When a premature birth can’t be prevented,
you may be given corticosteroids before delivery. These medicines may greatly lower the risk and severity
of RDS in the baby. These steroids are often given between 24 and 34 weeks of pregnancy to women at
risk of early delivery. They may sometimes be given up to 37 weeks. But if the delivery is very quick or
unexpected, there may not be time to give the steroids. Or they may not have a chance to start working.

Key points about RDS in premature babies

Respiratory distress syndrome (RDS) is a common problem in premature babies. It can cause babies to
need extra oxygen and help with breathing.

RDS occurs most often in babies born before the 28th week of pregnancy and can be a problem for babies
born before 37 weeks of pregnancy.

RDS typically gets worse over the first 2 to 3 days. It then gets better with treatment.

Treatment may include extra oxygen, surfactant replacement, and medicines.

Preventing a premature birth is the main way to prevent RDS.

Next steps
Tips to help you get the most from a visit to your child’s healthcare provider:

 Know the reason for the visit and what you want to happen.

 Before your visit, write down questions you want answered.

 At the visit, write down the name of a new diagnosis, and any new medicines, treatments, or tests. Also
write down any new instructions your provider gives you for your child.

 Know why a new medicine or treatment is prescribed and how it will help your child. Also know what the
side effects are.

 Ask if your child’s condition can be treated in other ways.

 Know why a test or procedure is recommended and what the results could mean.

 Know what to expect if your child does not take the medicine or have the test or procedure.

 If your child has a follow-up appointment, write down the date, time, and purpose for that visit.

 Know how you can contact your child’s provider after office hours. This is important if your child
becomes ill and you have questions or need advice.

Bayi Muda adalah bayi dengan rentang usia mulai dari baru lahir hingga sebelum genap
berusia 2 (dua) bulan.
 RI D. Buku bagan manajemen terpadu balita sakit (MTBS). Direktorat Bina Kesehatan Anak. Jakarta.
2008.

Apnea of Prematurity
What is apnea of prematurity?
Apnea is a term that means breathing has stopped for more than 20 seconds. It can happen in full-term
babies, but it's more common in premature babies. The more premature the baby, the greater the chances
that apnea will occur.

What causes apnea of prematurity?

In premature babies, the part of the brain and spinal cord that controls breathing is not yet mature enough
to allow nonstop breathing. Apnea of prematurity can cause babies to have large bursts of breath followed
by periods of shallow breathing or stopped breathing. The condition may have other causes. Some of these
include:

 Bleeding in or damage to the brain

 Lung problems

 Infections

 Digestive problems such as reflux. Reflux is when the stomach contents move back up into the esophagus.

 Too low or too high levels of chemicals in the body, such as glucose or calcium

 Heart or blood vessel problems

 Triggering reflexes that lead to apnea. This might be from feeding tubes, suctioning, or a baby's neck
position.

 Changes in body temperature

What are the symptoms of apnea of prematurity?

Apnea of prematurity is when a baby’s breathing has stopped for 20 seconds or more. Other signs and
symptoms that may happen with apnea include:

 Bluish color to the skin (cyanosis)

 Decrease in heart rate

 Low oxygen levels

The symptoms of apnea of prematurity may look like other health conditions. Make sure your child sees
his or her healthcare provider for a diagnosis.

How is apnea of prematurity diagnosed?

It's important to find out if the apnea is caused by prematurity or if it is caused by another problem. Your
baby’s healthcare provider will examine your baby. He or she will check many of your baby's body
systems to find out what might be causing the apnea. Your baby’s breathing rate, heart rate, temperature,
and blood pressure will be continuously checked. Tests used to diagnose the problem may include:

 Blood oxygen levels. Babies have their oxygen levels continuously checked.
 Blood tests. These check blood counts, blood sugar levels, and electrolyte levels. They also check for
signs of infection.

 Lab tests. The fluid around the brain and spinal cord, urine, and stool may be checked for infection and
other problems.

 X-ray, ultrasound, or other imaging studies. The healthcare provider may order X-rays or other pictures
of the upper airways and lungs, brain, heart, or digestive system.

 Sleep studies. Vital signs and oxygen levels are checked.

How is apnea of prematurity treated?

Many premature babies will “outgrow” the condition by the time they reach the date that would have
been the 36th week of pregnancy. If treatment is needed, it may include:

 General care. This includes control of body temperature, proper body position, and extra oxygen.

 Nasal continuous positive airway pressure (CPAP). A steady flow of air is delivered through the nose
into the airways and lungs. Nasal intermittent positive pressure ventilation may be added to CPAP.

 Medicines. Methylxanthine is used to stimulate breathing.

Your baby may also need blood transfusions, depending on the cause of apnea.

What are possible complications of apnea of prematurity?

Premature babies may have many problems. They often have to stay in the hospital for long periods of
time. Apnea of prematurity is one of the problems of babies born too early. A slow heart rate and
decreased oxygen levels in the blood may happen with apnea of prematurity. These babies are at risk for
respiratory failure and death. They may also have long-term lung problems.

How is apnea of prematurity managed?

Most premature babies outgrow apnea as they mature. But sometimes your baby may be sent home with an
apnea monitor. It should be used whenever you or your infant is sleeping and when you are busy. The
apnea monitor alarms are very loud so don't place the monitor next to your baby’s head. Check every alarm
signal, even if you think it is a false alarm.

Key points about apnea of prematurity

 Apnea is a term that means breathing has stopped for more than 20 seconds. It can happen in full-term
babies, but it's more common in premature babies.

 Apnea of prematurity may not have a cause other than your baby's having an immature central nervous
system.

 Many premature babies will "outgrow" apnea of prematurity by the time they reach the date that would
have been the 36th week of pregnancy.

 Sometimes a baby is sent home with an apnea monitor.

Next steps
Tips to help you get the most from a visit to your healthcare provider:

 Know the reason for your visit and what you want to happen.

 Before your visit, write down questions you want answered.

 Bring someone with you to help you ask questions and remember what your provider tells you.

 At the visit, write down the name of a new diagnosis, and any new medicines, treatments, or tests. Also
write down any new instructions your provider gives you.

 Know why a new medicine or treatment is prescribed, and how it will help you. Also know what the side
effects are.

 Ask if your condition can be treated in other ways.

 Know why a test or procedure is recommended and what the results could mean.

 Know what to expect if you do not take the medicine or have the test or procedure.

 If you have a follow-up appointment, write down the date, time, and purpose for that visit.

 Know how you can contact your provider if you have questions.

Anatomy & physiology

Respiratory System

At birth the alveoli are thick walled and only number 10% of the adult total.
Lung growth occurs by alveolar multiplication until 6 - 8 years. The airways
remain relatively narrow until then, which results in a high incidence of
airway disease. Ventilation is almost entirely diaphragmatic.

During the first 2 years of life the geometry of the rib cage changes, with
the gradual development of the "bucket handle" configuration seen in the
adult. Ribs tend to be more horizontal in infants and this limits the potential
for thoracic expansion. The "ventilatory pump" (rib cage, diaphragm,
abdominal and accessory muscles) tends to be less efficient in young
children due to instability of the chest wall as well as the tendency of the
diaphragm to easily tire. This is a result of its relative paucity of type-1
muscle fibres. The combination of a high airway resistance and low
compliance results in a short time constant and therefore a rapid
respiratory rate. The respiratory pattern is sinusoidal with no expiratory
pause seen.

Oxygen consumption in young children is high: approximately 7 ml/kg/min

at birth (c.f. 3-4 ml/kg/min in adults). The metabolic cost of respiration is
higher than in adults and may reach 15% of total oxygen consumption.
Similarly the metabolic rate in infants is almost twice that of adults and
consequently alveolar minute volume is greater and the FRC relatively low.
As a result both inhalational induction and awakening at termination of
anaesthesia is more rapid. Similarly, hypoxia also occurs much more
rapidly.

The outward recoil of the chest wall in infants and young children is low, but
the inward lung recoil is similar to that of a young adult. As the FRC is the
lung volume at which the outward recoil of the chest wall exactly balances
that of the inward recoil of the lungs, this leads to a reduced in FRC.
However it is maintained by other mechanisms (e.g. laryngeal braking
during expiration and active diaphragmatic and intercostal expiratory tone)
in the awake state, although not necessarily during anaesthesia,
contributing to rapid desaturation. The closing volume is greater than the
FRC until 6-8 years due to the poor elastic properties of infant lungs, so
airways closure occurs during normal tidal ventilation. This leads to an
increase in alveolar-arterial oxygen tension difference and a normal PaO2
of 9-9.5 kPa.

The physiological dead space is approx. 30% of the tidal volume, as in

adults, but the absolute volume is small, so that any increase caused by
apparatus deadspace has a proportionally greater effect on small children.
During anaesthesia, deadspace must be kept to a minimum, and the
resistance of breathing apparatus should be kept low.

These changes in lung mechanics compared to those of adults increase

the susceptibility of infants to respiratory infection and also to the adverse
ventilatory effects of anaesthesia. Secretions resulting from cholinergic
activity or an URTI may cause respiratory difficulty. This includes breath
holding and coughing on induction of inhalational anaesthesia, as well as
an increased incidence of bronchospasm and even more significantly,
laryngospasm.

Distribution of ventilation and perfusion is different in children. In

spontaneously breathing adults, ventilation and perfusion are distributed
preferentially to dependent lung areas, with the diversion of ventilation to
the non-dependent areas during IPPV. However in spontaneously
breathing children, the situation is similar to that seen in the ventilated
adult, with uppermost areas being better ventilated and lowermost better
perfused. This leads to an increased V/Q mismatch as compared to adults.

Lung Mechanics of the Neonate Compared with the Adult

Variable Neonate Adult

Compliance (ml/cmH2O) 5 100

Resistance (cmH2O/l/s) 30 2

Time constant (s) 0.5 1.3

Respiratory rate (breaths/min) 32 15

Respiratory Variables in the Neonate

Tidal volume 7 ml/kg

Deadspace Tidal vol. X 0.3 ml.

Respiratory rate Neonate: 32 breaths/min

Age 1-13: (24 � age) 2 breaths/min

Minute ventilation 220 ml/kg/min

Alveolar ventilation 140 ml/kg/min

FRC 30 ml/kg
The narrowest part of the pre-pubertal upper airway is at the cricoid ring
C3/4, and thus if oedema develops there is no possibility of expansion.
1mm of oedema can lead to a 60% reduction in internal diameter. The
larynx is high and anteriorly placed. It is opposite C3 in premature
neonates, C3-4 in full term neonates and reaches C4 in adulthood. The
trachea is short, only 4 cm at birth, and the angle of the carina is wider.

Neonates are obligatory nose breathers, which may be a problem if the

nose blocked e.g. by a NG tube.

Cardiovascular System

Infants have a high cardiac output (commensurate with their high metabolic
rate) of approx. 200 ml/kg/min (2-3 times that of adults.) 60% (by weight) of
a baby's heart is non-contractile (30% in adults) with a thick muscular right
ventricle. Thus ventricular compliance is poor. This increase in cardiac
output is produced by an increase in heart rate, as they are unable to
increase their stroke volume. Babies can tolerate a HR up to 200/min
without evidence of heart failure.

Tachyarrythmias are uncommon in the absence of cardiac disease.

Cardiac arrest is usually secondary to extreme bradycardia/asystole; VF is
rare in normally connected hearts due to the low muscle mass found in
infant hearts. However bradycardia occurs readily in presence of hypoxia
and vagal stimulation (as children do have a relatively high vagal tone).
Rapid treatment with O2 or atropine (20 g/kg iv.) is required.

BP is low at birth (approx. 80/50) secondary to a low SVR, due to the large
proportion of vessel-rich tissues in children. BP increases within the 1st
month to approx. 90/60 and reaches adult levels at approx. 16 years. As a
guide for neonates, especially those born pre-term; a mean BP in mmHg of
at least the gestational age in weeks should be achieved.
Variation of HR with Age

Age Mean value Normal range

Neonate 140 100-180

1 year 120 80-150

2 years 110 80-130

6 years 100 70-120

12 years 80 60-100

Neonates have a reactive pulmonary vasculature, and reversion to a

transitional circulation may occur during the first few weeks of life,
precipitated by an increase in PVR (e.g. secondary to acidosis, hypoxia or
hypercapnia) and a decrease in SVR (e.g. most anaesthetics).

Monitoring of CVS

- ECG: RAD and RV dominance at birth, resembles adult ECG by about 1

year.

- NIBP, unless regular ABG are necessary. The complication rate of

arterial cannulation is much higher in children. Slow continuous flushing
should be used (and volume of fluid infused carefully measured) as
intermittent flushing has been shown to cause retrograde flow from the
radial artery to the carotid artery, risking cerebral emboli.

- CVP: Useful in the treatment of fluid imbalance or haemorrhage. Femoral

venous cannulation is often technically easier than the internal jugular vein,
especially in small children, is a safer route and carries a lower
complication rate
Blood Volume. This can show a variation of up to +/- 20% at birth
depending on the stage at which the umbilical cord is clamped. Blood
losses >10% circulating volume should be replaced with blood, to maintain
the Hct>30.

Average blood volume

At birth 90 ml/kg

Infant & young child 80 ml/kg

> 6-8 years 75 ml/kg

An alternative method of estimating blood volume at birth which takes into

account degree of transfusion from the placenta is (50ml+Hct)/kg.

Haemoglobin

75-80% Hb is HbF at birth. The decrease in blood volume and HbF occur
before HbA haemopoiesis is fully established at 6 months. Hb decreases
from approximately 160g/l at birth to about 90-100 g/l at 6-10 weeks,

HbF has lower 2,3-DPG content and therefore a higher affinity for O2. The
Oxygen Dissociation Curve (ODC) is thus shifted to the left. Metabolic
acidosis, which persists from foetal life into infancy and a high CO2
resulting from a high metabolic rate help to improve oxygen delivery to the
tissues by shifting the curve to the right. Respiratory alkalosis caused by
hyperventilation reduces oxygen availability and should be avoided.
Haemorrhage must be monitored carefully and blood for transfusion should
be warmed and filtered. If small volumes are required, or blood loss is
rapid, replacement can be syringed in via 3-way tap. Otherwise a burette
should be used.

Metabolism and Homeostasis

Renal Function and Fluid Balance

Total Body Water as Percentage of Body Weight:

Premature 85%

Neonate 80%

Infant 75%

Adult 65%

The proportion of total body water present as ECF exceeds ICF at birth.
This ratio gradually reverses with age. There is a considerable reduction in
total body water during the first few days of life, with concomitant changes
in drug distribution. Fluid turnover is much greater in infants (15% of total
body water/day) due to their relative inability to concentrate urine. Thus
interruption of fluid intake in infants can rapidly lead to dehydration. This is
especially true of premature infants, who have increased insensible losses
due to a high surface area to volume ratio. However, overloading a neonate
can result in the re-opening of a patent ductus ateriosus.

GFR and tubular reabsorption rate are reduced until 6-8 months; thus a
decreased ability to handle excessive water loads exists. Both GFR and
RBF are low in first 2 years of life. This immature renal function causes a
relative inability to handle excessive sodium loads, and may lead to the
accumulation and toxicity of drugs that are renally excreted.

Fluid Therapy

Temperature Regulation and Maintenance

Children have a high surface area to volume ratio (2.5 times greater in
neonates than in adults); and their natural insulation is poor at birth. Thus
they are susceptible to heat loss to the surrounding environment. This is
reflected by the fact that the thermoneutral environment is 34 C for
premature babies, 32 C for neonates and 28 C for adults. Note that even
incubators are unable to provide a thermoneutral environment for a naked
pre-term infant.

Infants less than 3 months old depend upon non-shivering thermogenesis.

This is achieved by increasing the metabolism of brown fat; this causes an
increase in oxygen consumption, which may stress the immature
respiratory system and may even cause respiratory failure. The control of
brown fat metabolism is compromised by general anaesthesia, so it is
important to maintain body temperature by other means during surgery: viz.
wrapping limbs in orthopaedic wool/padding or using a space blanket,
placing the baby on a pre-heated blanket, humidifying and warming
inspired gases. Care must also be taken not to over-heat neonates as they
have poorly developed sweating mechanisms.

A decrease in core temperature may lead to respiratory depression,

reduced cardiac output, prolongation of the action of drugs (esp. muscle
relaxants) and increased risks of hypoventilation, regurgitation and
aspiration in the post-operative period.

NB: Malignant hyperpyrexia is extremely rare in children < 3 years.

CNS

At birth myelination is incomplete. This results in an altered control of

ventilation, with periodic breathing and apnoeas seen up to about 60 weeks
post-conceptual age. This immaturity causes an increased sensitivity to the
respiratory depressant effects of narcotics and volatile agents.