Pediatric and Neonatal Respiratory Care Embryologic Development

Pediatric and Neonatal
Respiratory Care
Embryologic Development
Germ Layers of the Embryo
Endoderm Mesoderm Ectoderm
Respiratory Dermisand Epiderm is, Hair,

Tract Muscles andN ails
D igestiveTract, B one, Lensof Eyeand
Bladderand connectiveand SkinGlands
Thyroid lym phtissue
Liverand R eproductive& Central and
Pancreas C ardiovascular Peripheral
S ystem NervousS ystem
Development of the
Pulmonary System
Embryonic Period
Pseudoglandular Period
Canalicular Period
Saccular and Alveolar Period
Embryonic Period
 From Conception to 4-
6 weeks gestation
 Development of
proximal airways
 0-24 days one central
tube
 24 days - primitive
lung bud appears
Embryonic Period (continued)
 26-28 days form right
and left lung buds
 Primitive airways
progress in dividing
 Lobar bronchi - day 31
 diaphragm starts and
is completely
developed by 8th
week
Pseudoglandular Period
 7-16 week gestation
 development of
conducting airways
 7th week - epiglottis
formation starts
 7th week - choana
disintegrates and
palates development
begins
Pseudoglandular Period (cont.)
 8th week - vocal cord
development begins
 Lung resembles gland
 Dichotomy results
 11th week - cartilage
in airways appears
 12th week - major
lobes identifiable
Pseudoglandular Period (cont.)
 13th week - goblet
cells form
 13th-24th week
bronchial glands
develop
 10 week - ciliated cells
start to appear
Canalicular Period
 17-24 weeks gestation
 Development of
acinus
 Tremendous amount
of vasularization
 Outpouchings appear
on wall of bronchioles
Canalicular Period (continued)
 Two types of cells
start to differentiate
 Capillaries present but
too far away from
alveolar cavity
Saccular (Alveolar) Period
 24th week - birth
 Development of gas
exchange units
 25th-26th week
alveolar-capillary
membrane able to
sustain extrauterine
life
Saccular Period (continued)
 28-29th week
terminal sacs line with
mature Type II cells -
surfactant appears
 34-36th week
mature alveolar
structure evident
 approximately 55
million alveoli (10 m2)
C. Development of the fetal lung:
1. Week 4 of gestation: Lung starts to form as an out-
pouching of the esophagus.
2. Week 7 of gestation: Diaphragm starts to form.
3. Week 10 of gestation: Cartilagenous rings of the
trachea and lymphatic of the respiratory system start
to form.
4. Week 22-24 of gestation: Significant development of
all cartilagenous support of the conducting airways is
developed.
5. Week 26-28 of gestation: Alveolar ducts and sacs have
developed and alveolar type II cells begin to appear.
The number of alveoli necessary to support extra-
uterine life is now present.
6. At normal birth: The number of alveoli is about 24
million. Alveoli continue to develop after birth until there are
about 300 million alveoli at adulthood.
Fetal Lung Fluid
 Composition
 Different than amniotic fluid
 Decreased levels of bicarbonate and protein
 Increased levels of Sodium and Chloride
Fetal Lung Fluid cont.
 Function: Maintain patency

Term = 20-30 ml/kg in lungs
Production decreases days prior to clinical
detection of labor
Determination of Lung Maturity
 Shake (Foam) Test

 LS ratio (Lecithin to sphingomyelin ratio)
 Lungs mature when 2:1 (35 weeks)
 PG detection (Phosphatidylglycerol)
 Lipid
 Absent until about 35 weeks gestation
Lung Maturity Cont.
 FLM or FP Assay – Fluorescence

Polarization
 Surfactant to Albumin
 Quick and Reliable
 Lung Profile
 L:S and PG detection
SURFACTANT
Type II pneumocytes produces surfactant in the alveoli.
First appearance is between 26th-28th weeks of gestation.
Mature surfactant is made up of lipids and glycoproteins.
The main phospholipids that make up of mature surfactant are

Phosphatidylcholine (PC) and
phosphatidylglycerol (PG).
Surfactant Function
Decreases Surface Tension
Maintains Compliance and FRC
Tests for Adequate Surfactant Production
Shake Test
LS Ratio
Amniocentesis
Surface Tension and Surfactant Development:
1. Appearance of surfactant is between 26-28 weeks of gestation. At
this time, lecithin and sphingomyelin appear in the pulmonary
and amniotic fluid.
2. As gestation proceeds, the volume of lecithin in the pulmonary
fluid increases, whereas sphingomyelin levels remain constant.
3. At 35 weeks of gestation, lecithin levels increase significantly.
4. L/S ratio can be determined intrauterinely by analysis of amniotic
fluid or Amniocentesis. L/S ratio interpretation.
a. L/S ratio of 2:1-pulmonary maturity, can support extrauterine
life.
b. L/S ratio of <2:1-incidence of dev’t of respiratory distress
syndrome increases.
c. L/S ratio of <1:1-incompatible of extrauterine existence.
5. Surface tension is the cohesive forces of a fluid that tends to hold
the walls of the alveoli together in a partially collapsed newborn’s
lungs.
6. Laplace Law states that the radius of the alveoli decreases, the
surface tension increases.
7. Surfactant is a substance found on the alveolar wall that lowers
surface tension easing the newborn’s respiratory efforts.
8. Surfactant is secreted by alveolar cells or produced by Type II
pneumocytes that appear in 28 weeks of gestation.
Development of the
Cardiovascular System
Development of Cardiovascular System
 3rd week - two tubes

surrounded by
myocardial tissue
 Tubes fuse form
single chamber
(continued)
 4th week - heart
begins to beat
 Heart begins to twist
and fold
 Eventually will form
four chambers
(continued)
 Sinus venosus - horns
at bottom of
embryonic heart - will
become vena cava’s
and portion of right
atrium
 Truncus arteriosus -
will form pulmonary
artery and aorta
(continued)
 Bends in middle - S
shape
 Rapid growth
 Development of
chambers
 Blood flow begins -
one way flow
(continued)
 5th week - heart takes
on shape of adult
heart
 Developing veins and
arteries couple the
heart to circulatory
system
 Separate blood paths
created
(continued)
 Four chambers
formed with openings
between the atria and
the ventricles
 Truncus arteriosus
allows blood to exit
right ventricle
Fetal Circulation
Fetal Circulation
 Pressure in the fetal vasculature

 Systemic – Low resistance
 Placental – Low resistance
 Pulmonary – High resistance
Characteristics of Fetal Circulation
 Normal shunts in the fetus

 Foramen ovale – bypasses lung
 Ductus arteriosus – bypasses lung
 Ductus venosus – bypasses liver
Placental Development
 Placenta organ of
respiration for fetus
 Umbilical arteries carry
unoxygenated blood from
fetus
 Intervillous space acts as
alveolar-capillary
membrane
 Umbilical vein carries
oxygenated blood to fetus
Umbilical Cord
 Life line
 Wharton’s Jelly
 2 arteries and 1 vein
Amniotic Fluid
 1 liter at term
 Constantly recirculated and replenished
through lung fluid and urination
 Amount of fluid depends on recirculation
Function of Amniotic Fluid
 Thermoregulation
 Facilitation of movement
 Shock Absorber
Fetal Circulation
 Flow chart of the most
oxygenated fetal blood
 Bypasses liver -
ductus venosus
 Bypasses lungs -
foramen ovale
Fetal Circulation (continued)
 Flowchart of
least
oxygenated fetal
blood
 Small amount
feed lungs (high
resistance)
 Most bypasses
lungs - ductus
arteriosus
FETAL LUNG CIRCULATION
 Cardiac development occurs between the 4th and 7th week
gestation.
 The foramen ovale is a one-way flap in the atrial septal wall
Blood bypasses the lungs because of the high right sided

pressures.
 The ductus arteriosus is a connection between the PA and t
Aorta - shunts blood away from the lungs.

 Fetal PVR is high, within 24hr after birth, PVR should fall t
1/2 SVR
 The ductus should close within 10-24 hrs after birth.
 Fetal lung does not participates in gas exchange.
 About 10% of blood goes to lungs for tissue development

• Placenta->umbilical vein->ductus venosus
(bypassing the liver)
• Blood entering the right atrium from the

inferior vena cava->foramen ovale-> left
atrium
• the well oxygenated blood from the placenta

enters mainly the left side of the heart, rather
than the right side, and is pumped by the left
ventricle -> head and forelimbs
• only 10% of the blood flows through the

lungs; immediately after birth, virtually all the
blood flows through the lungs.
 Specific Anatomical Structure
- lungs are nonfunctional
- liver is only partially functional
 not necessary for the fetal heart to pump much blood
through either the lungs or liver
 The fetal heart must pump large quantities of
blood through the placenta.
• superior vena cava->tricuspid valve -
>right ventricle
• this blood is mainly deoxygenated blood

from the head region of the fetus, & it is
pumped by the right ventricle-> pulmonary
artery -> ductus arteriosus -> descending
aorta -> two umbilical arteries -> placenta,
where the deoxygenated blood becomes
oxygenated.
• closure of foramen ovale
•The low right atrial pressure & the high left

atrial pressure that occur secondarily to the
changes in pulmonary and systemic
resistances at birth cause blood now to
attempt to flow backward through the
foramen ovale
• the small valve that lies over the foramne

ovale on the left side of the atrial septum
closes over this opening thereby preventing
further flow through the foramen ovale.
• closure of the ductus arteriosus
• the increased systemic resistance

elevates the aortic pressure while the
decreased pulmonary resistance reduces
the pulmonary arterial pressure.
• blood begins to flow backward from the

aorta into the pulmonary artery through
the ductus arteriosus rather than in the
other direction as in fetal life.
•Functional closure- after only a10-24

hours the musle wall of the ductus
arteriosus constricts
- within 1-8 days the constriction is usually
sufficient to stop all blood flow
• Anatomic closure-during the next 1-4
months the ductus arteriosus
anatomically occluded
- growth of fibrous tissue into its lumen
CARDIOPULMONARY EVENTS AT BIRTH
Primary Changes in Pulmonary and Systemic
Vascular Resistances at Birth
1. loss of the tremendous blood flow through the
placenta
2. the pulmonary vascular resistance greatly
decreases as a result of expansion of the lungs.
• vessels are no longer compressed and the
resistance to blood flow decreases

• hypoxia of the lungs causes considerable tonic
vasoconstriction of the lung blood vessels

• vasodilation takes place when aeration of the lungs
eliminates the hypoxia.

All these changes together reduce the resistance to
blood flow through the lungs 5x, which reduces the
pulmonary arterial pressure, right ventricular
pressure, and right atrial pressure.
 Closure of the Foramen Ovale
 The low right atrial pressure and the high left atrial
pressure that occur secondarily to the changes in
pulmonary and systemic resistances at birth cause blood
now to attempt to flow backward through the foramen
ovale
 The small valve that lies over the foramen ovale on the
left side of the atrial septum closes over this opening,
thereby preventing further flow through the foramen
ovale
 Closure of the Ductus Arteriosus
 The increased systemic resistance elevates the aortic
pressure while the decreased pulmonary resistance
reduces the pulmonary arterial pressure.
 Blood begins to flow backward from the aorta into the
pulmonary artery through the ductus arteriosus, rather
than in the other direction as in fetal life.
 Functional closure - after only a few hours, the muscle
wall of the ductus arteriosus constricts.
 Anatomic closure - during the next 1 to 4 months, the
 Closure of the Ductus Venosus

 In fetal life, the portal blood from the fetus's
abdomen joins the blood from the umbilical
vein, and these together pass by way of the
ductus venosus directly into the vena cava
immediately below the heart but above the
liver, thus bypassing the liver.
 Within 1 to 3 hours the muscle wall of the
ductus venosus contracts strongly and closes
this avenue of flow.
 The portal venous pressure rises from near 0
to 6 to 10 mm Hg, which is enough to force
portal venous blood flow through the liver
sinuses.
 In one of several thousand infants, the ductus fails to

close, resulting in a patent ductus arteriosus,
 The failure of closure has been postulated to result
from excessive ductus dilation caused by vasodilating
prostaglandins in the ductus wall.
 Aministration of the drug indomethacin, which
blocks synthesis of prostaglandins, often leads to
closure.
FETAL VS INFANT CIRCULATION
• FETAL • INFANT
• Low pressure system • High pressure system

• Right to left shunting • Left to right blood flow
• Lungs non-functional • Lungs functional
• Increased pulmonary resistance • Decreased pulmonary
resistance
• Decreased systemic resistance
• Increased systemic resistance
CHANGES IN CARDIOVASCULAR
STRUCTURES AFTER BIRTH
• FETAL STRUCTURE • ADULT STRUCTURE
 Foramen ovale  Fossa ovalis
 Umbilical vein (internal)  Ligamentum teres
 Ductus venosus
 Ligamentum venosum
 Umbilical arteries and
abdominal ligaments  Medial umbilical ligaments,
superior vesicular artery

(supplies bladder)
 Ductus arteriosus  Ligamentum arteriosum

ASSESSMENT OF THE NEWBORN
MATERNAL FACTORS
 Previous pregnancy complication
 Diabetes mellitus
 Pregnancy Induced hypertension
 Maternal age<17 y/o
 Maternal age above 35 y/o
 Placenta previa
 Placenta abruptio
 Alcohol consumption
 Smoking
 Drug use
FETAL ASSESSMENT
1. Ultrasonography
 Position of the fetus and placenta
 Measure fetal growth
 Identify possible anomalies
 Qualitatively assess amniotic fluid
2. Amniocentesis
Amniotic fluid may be inspected for meconium, bloo
and fetal cells.
 Lecithin/Sphingomyelin ratio (L:S ratio)
Normal is 2:1
Relates to lung maturity
If less than 2:1, then administer pulmonary surfac
 Phosphatidylglycerol (PG)
Appears at approx. 35 – 36 wks of gestation

B. FETAL ASSESSMENT
3. Fetal Heart Rate Monitoring
Normal: 120-160 beats/min
4. Fetal blood gas analysis
Normal: ph: 7.35 – 7.25
C. EVALUATION OF THE NEWBORN
 The initial new born care following delivery includes warming,
positioning the head, drying, and suctioning.

1. Apgar score
 Describes the condition of the NB immediately after birth.
 Done after 1 and 5 minutes after delivery
 The higher the score the better condition of the infant
a. 7-10 points – provide routine care

b. 4- 6 points – support infant wit oxygen, warmth, and general
stimulation
c. 0-3 points – CPR
2. Silverman-Anderson Scoring System

 Determine the severity of Respiratory distress
 Lower score indicates less distress
a. 0-3 – No respiratory distress to mild respiratory
distress
b. 4-6 – Moderate respiratory distress
c. 7-10 – Severe respiratory distress

3. Assessment of Gestational Age

a. Ballard Score
 Good method to determne gestational a
and physical maturity

 Score of 40 correlates with 40 weeks
gestation
 Includes 6 physical and 6 neurologic sig
38-42 wks – term

before 38 wks – pre term
after 42 wks - posterm
4. Newborn’s Classification by Weight and Gestation
a. Birth Weight:
Low Birth Weight - <2,500 g

Very Low Birth Weight - <1,500 g
Extremely low Birth Weight - <1000 g
b. Size for Age:
SGA – below the 5th percentile for the gestational
AGA – appropriate for gestational age. 10th – 90th
percentile
LGA – above the 90th percentile
5. Vital Signs
a. Respiratory Rate – 40 – 60 per minute
b. Heart Rate – 120 – 160 beats/min
c. Temperature – 36 – 37 deg C.
d. Blood pressure – 60/40 mmHg

6. Arterial Blood Gas
pH – 7.35 – 7.45 ( not <7.25 at birth)
PaCo2 – 35 to 45 mmHg
PaO2 – 50-80 mmHg
HCO3 – 20 – 26 mEq/L
BE - -5 to +5
Neurological Exam
• Reflex exams
– Rooting reflex
• Gently stroke corner of mouth
• Infant should turn head towards side stroked
– Suck reflex
• Place pacifier or clean finger into mouth
• Infant should begin to suck
Neurological Exam
• Reflex exams
– Grasp reflex
 Place index finger into infant’s palm
 Grasp finger & place your thumb over fingers
 Gently pull infant to sitting position
 Assess degree of head control
 Healthy infant can keep head upright
Neurological Exam
• Reflex exams
– Moro reflex
• Slowly lower infant
• Just before he
touches bed, quickly
remove your finger
allowing him to fall to
bed
• Arms should extend
up & out, hips &
knees should flex
Adult versus Pediatric Airways
ANATOMICAL FEATURE PRESENTATION IN CHILDREN CLINICAL SIGNIFICANCE
TONGUE Larger in relation to the oral Tongue is a natural airway
cavity obstructer
Tonsils, adenoids, and Larger in size; large amount of These are potential areas for
pharyngeal lymphoid lymphoid tissue in pharynx swelling, which can cause upper
tissue airway obstruction; they may also
bleed significantly during trauma
or intubation, obstructing views
and risking aspiration
Epiglottis Larger, less flexible, and omega Can make visualization difficult
shaped; lies more horizontally during intubation
Epiglottis and laryngeal Angle between is more acute Can make direct visualization
opening difficult during intubation and
blind nasal intubation
Glottis Higher and more anterior Can make direct visualization more
difficult during intubation
Cricoid ring Narrowest portion of the airway Uncuffed tubes create seal at the
cricoid ring
Cricothyroid membrane Smaller; virtually nonexistent in Needle cricothyrotomy and surgical

children younger than 3 years cricothyrotomy are difficult in
infants and small children
Extrathoracic trachea More malleable Increased risk of collapse during

respiratory distress
Trachea Smaller diameter Endotracheal tube misplacement

and
accidental extubation are more
frequent
Airway Ribs and sternum are mostly
cartilage (infants); ribs lay more Airway obstruction is more common
horizontal as a result of swelling
Thoracic cage Ribs and sternum are mostly The thoracic cage offers little
cartilage (infants); ribs lay more stability; the chest wall will collapse
horizontal with negative pressures; retractions
are more pronounced in infants
Diaphragm Main action for breathing in Infants known as “belly breathers”;

infants increases WOB when increasing
tidal
volume
Mainstem bronchus Right mainstem angle lower Right mainstem intubation and right
foreign
body obstruction are more frequent
Conducting airways Smaller in diameter More pronounced distress during

reactive airways disease
Chest wall Higher compliance

RESPIRATORY CARE
A. OXYGEN THERAPY
1. O2 Hood
 Loosely enclosed environment placed over the infa
head
 Minimum flow of 7lpm to prevent CO2 buildup
 Can deliver up to 100% Oxygen
 Monitor O2 by placing analyzer probe near the
patient’s mouth
 Usually equipped with a temperature probe – mus
monitor temperature to
prevent excess cooling from aerosol.
1. Too hot – infant may become apneic
2. Too cool – could cause increase in O2 consump
 Can be very loud inside the hood

RESPIRATORY CARE
A. OXYGEN THERAPY
2. Incubator
 Good for neonates only
 Small, whole body environment
 Precise control over environment including FiO2,
humidity, temperature
 With red flag warning sign
 Hazards
 a. Skin burns
 b. Hearing damage
 c. Electrical shock
RESPIRATORY CARE
A. OXYGEN THERAPY
3. Radiant Warmer
 Totally open to room air
 Must be combined with an oxygen hood or other oxyg
delivery device
 Helpful in decreasing insensible water loss as it provid
neutral thermal environment

 Allows easy access to infant
*** Safe levels of Oxygen Therapy***

FiO2 - <50%
SPO2 – 88% - 94%
PaO2 – 60 – 80 mmHg
RESPIRATORY CARE
B. AIRWAY MANAGEMENT
1. Intubation
 The infant’s age and weight can be used to estimate proper ET tube
size and depth of insertion.
 Most neonatal tubes are uncuffed to eliminate cuff-related problems.
 Miller (straight) blade is usually used during intubation
2. Suctioning
 Oral and pharyngeal suctioning of infants can be done with bulb
syringe.
 DeLee trap or a mechanical vacuum source with catheter is used in
nasopharyngeal and nasotracheal suctioning.
 Recommended suction pressures for neonates range from -40 - -60
mmHg.
 Do not pre oxygenate infants below 1 month old with 100% FiO2
 Raise FiO2 by 10% or 15% for at least 1 minute before suctioning.
 Limit duration to 5 seconds or less.
RESPIRATORY CARE
B. AIRWAY MANAGEMENT
3. Neonatal Resuscitation
 Immediately after delivery, the infant is assessed for
presence of meconium, breathing or crying, muscle tone,

color and term of gestation.
 If with presence of meconium, the mouth and nose is
suctioned.
 If the infant has absent or depressed respirations or a HR
<100 beats/min, positive pressure ventilation (PPV) with

100% O2 is provided with BVM.
 After application of PPV for 30 seconds, heart rate is
reassessed. If the heart rate is <60 beats/min, start chest

compressions and maintain PPV.
If HR remains <60 beats/min, appropriate medications are
given.
If with spontaneous breaths and HR >100 beats/min, PPV
RESPIRATORY CARE
C. NITRIC OXIDE THERAPY
 Inhaled Nitric Oxide (INO) is a selective pulmonary vasodilator
used to treat newborns who require mechanical ventilation for

hypoxic respiratory failure.
 It is indicated in term or near term neonate of more than 34
weeks gestation who have persistent pulmonary hypertension

(PPHN)
 The normal starting dose is 20 parts per million (ppm).
 The INO is discontinued once a final dose of 1 ppm is reached.
D. EXTRACORPOREAL MEMBRANE OXYGENATION

 Modified form of cardiopulmonary bypass used to provide
relatively long term pulmonary or cardiopulmonary life

support.
 Two types: 1. Venoarterial (VA) – both heart and lung function
is supported
blood taken from RA; CO2 removed, O2
added; heated returned right common carotid artery
CONGENITAL HEART DEFECTS
OF THE NEWBORN
GENETICS
• Gene abnormalities in only 10% of CHD
• Trisomies 21, 13, 15, 18, XO
• Mutations of genes which encode for
transcription factorsTBX5ASD,VSD
 NKX2.5ASD
• Region of chromosome 22 important in heart
development, 22q11.2
deletionconotruncus, branchial arch, face
ENVIRONMENT
• RUBELLA
• TERATOGENS
CHD
• LR SHUNTS: all “D’s” in their names
– NO cyanosis
– Pulmonary hypertension
– SIGNIFICANT pulmonary hypertension is
IRREVERSIBLE
• RL SHUNTS: all “T’s” in their names
– CYANOSIS (i,.e., “blue” babies)
– VENOUS EMBOLI become SYSTEMIC
• OBSTRUCTIONS
LR
NON CYANOTIC
• ASD
• VSD IRREVERSIBLE
PULMONARY
• ASVD HYPERTENSION
IS THE MOST
• PDA FEARED
CONSEQUENCE
VENTRICULAR SEPTAL DEFECT
 Sometimes called a hole in the heart, this
defect — the most common congenital heart
defect — occurs when the muscular wall
(septum) separating the bottom chambers of
the heart (right and left ventricles) doesn't fully
form. The hole allows oxygen-rich blood to
leak from the left ventricle into the right
ventricle, instead of moving into the aorta and
on to the body. In the right ventricle, the
oxygen-rich blood mixes with blood that
doesn't have enough oxygen in it.
(management)
 This defect can lead to heart failure, high blood
pressure in the lungs (pulmonary
hypertension), infection of the heart
(endocarditis), irregular heartbeats
(arrhythmias) and delayed growth. Small holes
may heal on their own or cause no symptoms.
Larger holes may require surgery to stitch the
hole closed or to cover the hole with a patch.
ATRIAL SEPTAL DEFECT
 Atrial septal defect is a hole that occurs when
the muscular wall (septum) separating the top
two chambers of the heart (right and left atria)
doesn't close properly. This allows oxygen-rich
blood from the left atrium to flow into the right
atrium, where it mixes with blood that doesn't
have adequate oxygen in it. Blood from the left
atrium should normally flow into the left
ventricle and on to the aorta and the rest of the
body.
(management)
 Minor cases may cause no symptoms and may

not require treatment. Larger defects may
require surgery or cardiac catheterization to
repair the hole.
PATENT DUCTUS ARTERIOSUS
 Before birth, a blood vessel called the ductus
arteriosus connects the pulmonary artery — the
artery carrying blood to your lungs — and the
aorta, the large artery that carries blood away
from the heart. Before a baby is born, the ductus
arteriosus allows blood to bypass the lungs
because the baby receives oxygen through the
placenta and umbilical cord. The ductus
arteriosus normally closes within soon after birth.
If the ductus arteriosus remains open (patent),
some blood that should flow through the body
goes to the lungs.
(management)
 This defect can cause heart failure or an
infection of the heart (endocarditis). In infants,
it can be closed with medications. In older
children and adults, surgery is performed to
close the vessel.
PULMONARY VALVE STENOSIS
 In this condition, blood flow from one of the
heart's bottom chambers, the right ventricle, to the
pulmonary artery is slowed by narrowing at the
pulmonary valve. When there's narrowing
(stenosis), the right ventricle must pump harder to
get blood into the artery that carries blood to the
lungs (pulmonary artery). Pulmonary valve
stenosis may occur along with other defects, such
as thickening of the muscle of the right ventricle
below the valve.
(management)
 In many cases, pulmonary valve stenosis is mild
and doesn't require treatment. But because it can
cause heart failure, arrhythmias or enlargement of
the right heart chambers, it may be necessary to
correct the defect. In many cases, a balloon
(pulmonary valvuloplasty) opens the narrowed
valve. In some cases, especially in people with
other heart defects, surgery may be necessary to
replace the diseased valve with an artificial valve.
AORTIC STENOSIS
AORTIC STENOSIS
 Aortic stenosis is a defect that narrows or

blocks the aortic valve opening, making it
difficult for the heart to pump blood into the
aorta — the main artery leading away from the
heart — on to the rest of your body.
AORTIC STENOSIS
(management)
 The defect can cause the heart to get bigger,
left-sided heart failure, abnormal heart rhythms
(arrhythmias), infections of the heart
(endocarditis) and fainting. Treatment includes
surgery to repair or replace the valve or, in
young children, widening of the valve through
a surgical procedure called balloon
valvuloplasty, in which a balloon-like device
widens the valve so that blood can flow
through.
COARCTATION OF THE AORTA
 This is a narrowing (coarctation) in a portion of

the heart's main artery (aorta). Coarctation
forces the heart to pump harder to get blood
through the aorta and on to the rest of the
body.
(management)
 Coarctation of the aorta can cause several life-
threatening complications, including severe high
blood pressure, a bulge in the aorta that can burst
(aortic aneurysm), infection of the heart
(endocarditis), brain hemorrhage, stroke, heart
failure and premature coronary artery disease.
Repair is typically recommended before age 10,
either by surgically removing the affected portion
or widening it through a surgical procedure called
balloon angioplasty and placement of a mesh
tube that can hold the aorta open (stent).
TRANSPOSITION OF GREAT
ARTERIES
ARTERIES
 With this defect, the positions of the aorta — the
main artery leading away from the heart — and
the pulmonary artery, which leads to the lungs,
are reversed (transposed). The aorta and
pulmonary artery are, together, sometimes
referred to as the great arteries. In transposition
of the great arteries, the aorta arises from the
right ventricle instead of the left ventricle and the
pulmonary artery arises from the left ventricle
instead of the right. This prevents nourishing
oxygenated blood from reaching the body.
ARTERIES
(management)
 This condition would quickly be fatal to a
newborn except it's generally accompanied by
another defect — commonly a septal defect or
patent ductus arteriosus — that allows oxygen-
rich blood to get to the body. Surgery to repair
the condition is usually necessary shortly after
birth.
TETRALOGY OF FALLOT
TETRALOGY OF FALLOT
 This defect is a combination of four (tetralogy)

heart defects. The four defects typically are
ventricular septal defect (VSD), pulmonary
valve stenosis, a misplaced aorta and a
thickened right ventricular wall (right ventricular
hypertrophy). They usually result in an
insufficient amount of oxygenated blood
reaching the body.
TETRALOGY OF FALLOT
(management)
 Complications of tetralogy of Fallot (fuh-LOE)
include cyanosis — sometimes called "blue
baby syndrome," since the lips, fingers and
toes may have a bluish tinge from lack of
oxygen — as well as poor eating, physical
inability to exercise, irregular heartbeats
(arrhythmias), delayed growth and
development, and stroke. Surgery to repair the
defects is required early in life.
DEFECT OF THE TRICUSPID VALVE
 This is a defect of the tricuspid valve, which
controls blood flow between the heart's right
atrium, which is an upper chamber of the heart,
and the right ventricle, a bottom chamber of the
heart. The valve is positioned lower than normal
into the right ventricle instead of remaining
between the atrium and the ventricle. The
incorrectly formed ventricle is too small and the
atrium too large, and neither functions properly.
The valve often allows blood to leak from the
ventricle into the atrium. This defect often occurs
along with other heart defects.
(management)
 Some people have symptoms early in life,

including heart failure and life-threatening
irregular heartbeats (arrhythmias). Other
people may have no signs or symptoms until
adulthood. Treatment is with medications or
with surgery.
ATRIOVENTRICULAR SEPTAL
DEFECT
DEFECT
 This is a combination of defects, including a large
hole in the center of the heart and a single
common valve instead of the separate tricuspid
and mitral valves. Also called atrioventricular
septal defect, this defect is classified by whether
it's only partial (involving only the upper chambers
of the heart), or complete (in which blood can
travel freely among all four chambers of the
heart). Both forms of the defect allow extra blood
to circulate to the lungs, causing the heart to
enlarge.
DEFECT
(management)
 The condition occurs most often in children
with Down syndrome. Infants may also have
trouble breathing and not grow well. Surgery is
often done in infancy to close the hole and
reconstruct the valves.
HYPOPLASTIC LEFT HEART
SYNDROME
SYNDROME
 In this condition found in babies, the left side of
the heart is underdeveloped (hypoplastic),
including the aorta, aortic valve, left ventricle and
mitral valve. As a result, the baby's body doesn't
receive enough oxygen. In the first few days after
a baby is born, the ductus arteriosus remains
open (patent), allowing normal blood flow. But
when the ductus arteriosus naturally closes, signs
and symptoms begin, including a bluish cast to
the skin from lack of oxygen (cyanosis), difficulty
breathing and being unable to feed.
SYNDROME
(management)
 Hypoplastic left heart syndrome is sometimes
found during ultrasound exams before a baby
is born. Treatment options for this life-
threatening condition are a heart transplant or
a multistage surgical procedure done during
the first few years of life.
TRUNCUS ARTERIOSUS
TRUNCUS ARTERIOSUS
 This is a defect in which the normally separate
pulmonary artery and aorta merge into one single large
vessel (truncus) arising from the two bottom chambers
of the heart (right and left ventricles). Many people who
have this defect also have a large ventricular septal
defect, which turns the right and left ventricles into a
single chamber. This allows red oxygenated blood and
blue unoxygenated blood to mix. Too much blood may
flow to the lungs, flooding them and making it difficult to
breathe. It can also result in life-threatening pulmonary
hypertension — high blood pressure in the lungs.
TRUNCUS ARTERIOSUS
(management)
 Surgery is needed to close the septal defect

with a patch and to separate the pulmonary
arteries from the trunk.
NEONATAL AND PEDIATRIC RESPIRATORY
DISORDERS
A. NEONATAL RESPIRATORY DISORDERS
1. RESPIRATORY DISTRESS SYNDROME

 Developmental disorder rather than a disease
 Incidence increases with decreasing gestational age
 Affects premature infants with inadequate amounts of
surfactant
 Corticosteroids and thyroid hormone increases the rate
of synthesis
MANIFESTATIONS
 Tachypnea
 Retractions
 Nasal flaring
 Expiratory grunt
 Fine inspiratory crackles

DISORDERS
RADIOGRAPHY
 Diffuse reticulogranular pattern
 Air-bronchogram sign
 Contracted lung volume
MANAGEMENT
 Prevent hypoxia
 Optimize fluid management
 Reduce metabolic demands
 Prevent worsening atelectasis and pulmonary
edema
 Minimize lung injury due to barotrauma or oxygen
DISORDERS
SURFACTANT ADMINISTRATION
 4ml/kg
 How to administer?
Head and body inclined down; head turned to the left
Head and body inclined down; head turned to the right
Head and body inclined up; head turned to the left
Head and body inclined up; head turned to the right
OXYGEN
 Maintain PaO2 50 – 80 mmHg
 Avoid high O2
DISORDERS
CPAP
 Start at 4 to 6 cmH2O
MECHANICAL VENTILATION
 PCO2 >50 mmHg
 PaO2 <50 mmHg
 Severe Apnea
 O2 <90% with FiO2 >50%
 Initial Settings:
PIP: < 30 cmH2O

PEEP: 4 to 6 cmH2O
RR: 20 – 30 bpm
I.T: 0.4 – 0.5
FiO2: 50 - 100
DISORDERS
2. TRANSIENT TACHYPNEA OF THE NEWBORN
 RDS type II
 Most common diagnosis of respiratory distress in
the newborn
 Remember often “term infants” may be a little early
 Ineffective clearance of amniotic fluid from lungs
with delivery
 Most often seen at birth or shortly after
MANIFESTATION:
 Tachypnea 60-150 bpm
 Nasal flaring
 Grunting
 Retracting
 Fine Rales
 Cyanotic
DISORDERS
RADIOGRAPHY:
 Prominent Perihilar streaking
 Hyperinflation
 Fluid in fissure
MANAGEMENT:
 Treat signs and symptoms
 Support infant
 May need O2
 Probably too tachypneic to PO feed so start IV fluids
 Be patient!!
DISORDERS
3. MECONIUM APIRATION SYNDROME
 Most often found in post date infants > 40 weeks, but may
occur in infants >34 weeks

 Infant passes meconium due to varying degrees of asphyxia
in utero
 Obstruction of large and small airways with aspirated
meconium
 Aspiration may occur:
in utero
intrapartum
postpartum period
MANIFESTATION:
 Tachypnea
 Nasal flaring
 Grunting
 Retracting
 Apnea/ irregular respiratory pattern
 Decreased breath sounds/ wet/ rhonchi
DISORDERS
RADIOGRAPHY:
 Increased AP diameter
 Hyperinflation
 Atelectasis
 Pneumothorax
DISORDERS
4. BRONCHOPULMONARY DYSPLASIA (BPD)
 Chronic lung disease that follows MV and O2 therapy
for acute respiratory distress after birth in

premature newborns
MANIFESTATION:
 Increased airway resistance
 Tachypnea
 Retractions
 Cyanosis
 Occasional grunting
 Wheezes
 Hypercarbia
DISORDERS
RADIOGRAPHY:
 Diffuse haziness due to accumulation of exudative fluid
 Multicystic or spongelike, with alternating areas of emphysema
 Stage 1: Characteristic features of RDS or complications of RDS

 Stage2: Fine or course interstitial opacities, diffuse distribution. In
severe cases, changes are widespread and coarse.
 Stage 3: characterized by a classic bubbly appearance and irregular
dense areas, opaque areas
 Stage 4: hyperexpansion of the lung, expanding bubbles.
Pulmonary hyperinflation is seen in the most severe cases
MANAGEMENT:
 Mechanaical ventilator
 Oxygen therapy
 Diuretics
DISORDERS
5. ACYANOTIC CONGENITAL HEART DISEASES
Classification:
1. Those producing Volume overload
 Communication between systemic and pulmonary sides
of the circulation
 AV valve regurgitation: increase vol. load
 Cardiomyopathy: decreased cardiac muscle function:
atrial and ventricular filling pressure

2. Those that cause increase in pressure load
 Ventricular outflow obstruction
 Narrowing of one of the great vessels (CoA)

DISORDERS
LESION SYMPTOMS PE CXR TREATMENT
A. ATRIAL Usually asx; Systolic ejection Enlargement of Surgery or

SEPTAL DEFECT Large lesion; murmur at left RV/RA; may transcatheter
feeding mid upper have Increase closure
intolerance; easy sternal border pulmonary
fatigability vascularity
B. Small: asx; Systolic murmur Normal to Small:

VENTRICULAR Large: dyspnea minimal reassurance
SEPTAL DEFECT poor growth cardiomegaly; Large: medical
cardiac ailure may have management and
increased surgery
pulm. Bld. flow
DISORDERS
3. PATENT Small: asx Bounding Large: Surgical closure

DUCTUS Large: heart peripheral cardiomegaly;
ARTERIOSUS failure; growth pulses; prominent
retardation continouos pulmonary
murmur artery with
(machinery) increase pulm.
vascularity
4. BP in legs are Cardiomegaly Surgery

COARCTATION lower; pulses in with
OF AORTA legs are weaker pulmonary
congestion
DISORDERS
6. CYANOTIC CONGENITAL HEART DISEASES
Classification:
1. Those with decreased blood flow
 Degree of cyanosis depends on degree of obstruction to
pulmonary blood flow

 Mild obstruction: cyanosis maybe absent at rest
 Severe: blood flow may be dependent on PDA
2. Those with increased pulmonary blood flow

 No obstruction to pulmonary blood flow
 Cyanosis due to abnormal connections or total mixing of
systemic and pulmonary circulation

DISORDERS
1. TETRALOGY Cyanosis noted Dusky blue skin; COEUR EN Medical and

OF FALLOT 1st yr of life; gray sclerae; SABOT (boot or surgical ( blalock
dyspnea on clubbing wooden shoe); taussig shunt
exertion relieved hypertrophy of then corrective
by squatting RV; decreased surgery
pulm. Bld. flow
a. Pulmonary stenosis (RV obstruction)

b. VSD
c. Dextroposition of the aorta with septal override
d. RV hypertrophy
DISORDERS
2. Cyanosis snd Murmurs may Mild Medical

TRANSPOSITIO tachypnea noted be absent or cardiomegaly emergency with
N OF GREAT within 1st hr of with soft systolic with normal to surgery
ARTERIES life ejection increased
murmur; failed pulm. Bld. flow
hyperoxia test
DISORDERS
B. PEDIATRIC RESPIRATORY DISEASES
1. SUDDEN INFANT DEATH SYNDROME (SIDS)

 Leading cause of death among infants younger than 1 year.
 The diagnosis is based on the presumptive a previously
healthy baby dies during sleep.
 Usually hits during winter and at night
 Also known as cot death or crib death
RISK FACTORS:
1. Prone sleeping position
2. Low birth weight
3. 5 minute APGAR score <7
4. Multiple births
5. Maternal Smoking
DISORDERS
Prevention:
 Receive early and regular prenatal care
 Do not smoke
 Back to sleep
 Select bedding carefully

DISORDERS
2. CYSTIC FIBROSIS
 An inherited autosomal recessive trait that affects all exocrine glands
 Affects the chromosome 7
 Characterized by three clinically observable d/o:
1. pulmonary disease
2. pancreatic insufficiency
3. sweat chloride concentrations
MANIFESTATION:
Skin that tastes salty
Increased mucus production with frequent coughing spells
Frequent pulmonary infections leading to pneumonia and bronchitis
Dehydration
Infertility in men
Diarrhea or bulky, foul-smelling, and greasy stools
Poor weight gain and stunted growth in children
Stomach pain secondary to obstruction of the liver, gallbladder, and/
or pancreas
Digital clubbing, hypoxemia, cyanosis, and dyspnea
Atelectasis
Pneumothorax
DISORDERS
DIAGNOSIS:
1. Sweat chloride test
 Gold standard
 >60 mEq indicates positive CF
RADIOGRAPHY:
 Appear normal on onset
 Hyperinflation and air trapping upon progression
 Bilateral lobe infiltrates
 Pneumothorax
MANAGEMENT:
 Pancreatic enzyme supplementation
 Bronchial hygiene
 Diet:
Low fat, High protein , High Calorie

DISORDERS
3. EPIGLOTTITIS AND CROUP
A. EPIGLOTTITIS
 Severe obstruction secondary to supraglottic swelling.
 Affects the aryepiglottic folds and arytenoid cartilage
B. CROUP
 Viral disorder of the upper airway that normally results
in subglottic swelling and obstruction

 Also known as laryngotracheobronchitis
 Three types
1. Laryngotracheitis
2. Spasmodic croup
3. Laryngotracheobronchitis
DISORDERS
PRESENTATION EPIGLOTTITIS CROUP
AGE 2 – 6 years 6 mos – 6 yrs
Rate of onset Rapid (often only hours) Slow (2-3 dyas)
Infectious origin Haemophilus influenza type B Parainfluenza virus
Clinical presentation High fever, anxious, leaning May be febrile or afebrile, hoarse,
forward, drooling, low-pitched barky cough, tight uppe airway
stridor, muffled voice, no cough stridor
CXR Swollen, edematous epiglottis Narrowing of the subglottic airway

(thumb sign), and supraglottic (hourglass) seen on AP neck film
structures seen on lateral neck
film
Seasonal Incidence Any season Usually winter

DISORDERS
TREATMENT:
 Immediate establishment of airway
 Oxygen Therapy
 Cool mist Therapy
Croup – racemic Epi and dexamethasone(0.3mg/kg)

 Epiglottitis – do not attempt to intubate
- emergency tracheostomy
END
ADULT/PEDIA MECHANICAL
VENTILATION
What is Mechanical Ventilation?
 Is a useful modality for patients who are unable to

sustain the level of ventilation necessary to maintain
the gas exchange functions
 Is a SUPPORTIVE therapy, it’s not a curative

Goals:
 Provide adequate oxygenation
 Support muscle ventilation
 Remove carbon dioxide
 Reduce work of breathing
 Recruitment and preservation of lung
volume
 Airway resistance: The degree of airflow
obstruction in the airways.
Clinical condition that increase airway resistance
Type Clinical conditions
COPD -Emphysema
-chronic bronchitis
-asthma
-bronchiectasis
Mechanical obstruction -postintubation obstruction
-foreign body aspiration
-endotracheal tube
-condensation in ventilator circuit

Cont.
Airway resistance is calculated by:
PRESSURE CHANGE ( peak inspiratory pres.- plateau pres.)

FLOW
Raw= P
V
 Lung Compliance: The degree of lung expansion
per unit pressure change.
Low compliance: Means that the volume change is mall per

unit pressure change. Most commonly clinical conditions
( e.g., acute respiratory distress syndrome or ARDS ) low
lung compliance is associated with refractory hypoxemia.
High compliance: means that the volume change is large

per unit pressure change.. Emphysema is an example of
high compliance where the gas exchange process is
impaired.
C= _V_
P
Corrected tidal volume: respiratory rate total x 3

1000
Types:
o Static Compliance:
Corrected Tidal Volume
Plateau pressure-PEEP
o Dynamic Compliance:
Corrected Tidal Volume
Peak inspiratory pressure-PEEP
Deadspace Ventilation
 Is a wasted ventilation or a condition in which

ventilation is in excess of perfusion.
3 types of deadspace ventilation

1. Anatomic
2. Alveolar
3. Physiologic
Anatomic Deadspace:
The volume occupying the conducting
airways that does not take part in gas exchange. For a tidal
volume of 500 mL, about 150 mL of this volume is wasted
.
Decrease in tidal volume causes a relatively
higher anatomic deaspace to tidal volume percent. TV 500
decreased 300 mL.
ex. 150/500 = 0.3 or 30%

150/300 = 0.5 or 50%
Alveolar Deadspace:
The normal lung volume that has become
unable to take part in gas exchange because of reduction
or lack of pulmonary perfusion. May cause by some clinical
condition.
Physiologic Deadspace:
Sum of anatomic deadspace and alveolar
deadspace. Under normal conditions, it is about the same
as anatomic deadspace.
Mechanical Dead Space
 The volume of gas that is re-breathed during

ventilation
 Anything added to the ventilator circuit between the
Y-connector and the patient
 Corrugated tubing
 HME’s
 Inline suction catheters

Indications
 Apnea
 Acute ventilatory failure
 Impending ventilatory failure
Hazards and Complications
 Barotrauma / Volutrauma
 Ventilator Associated Pneumonia
 Oxygen toxicity
 Diaphragm atrophy
 Intrinsic-PEEP/ auto-PEEP
Origin of mechanical ventilation
 Negative pressure ventilation:

Pressure lower than atmospheric pressure is
applied to the extrathoracic space during inspiration.
ex: iron lung & chest cuirass
 Positive pressure ventilation:
Pressure higher than atmospheric pressure is
applied to the intraalveolar space during inspiration.
The negative and positive pressure mechanical
ventilator
2 Main Modes
 Volume control ventilation:

Is a preset of a volume pattern, and it operates as
a volume controller.
Is a independent variable and pressure is a
dependent variable. The airway pressure during this
mode of ventilation are affected by the changing
compliance and resistance.
What do you set?
You set:
 Volume Controlled Tidal Volume

Peak Flow
Rate
FiO2
PEEP
 Pressure-Controlled Ventilation
A preset of peak inspiratory pressure is used

to provide ventilation. Pressure is the dependent
variable and volume is a dependent variable and the
ventilator operates as a pressure controller.
The pressure remain constant throughout
inspiration.
What do you set?
You set:
Pressure Limit
 Pressure Controlled Time spent in inspiration

(I Time)
Rate
FiO2
PEEP
Volume vs. Pressure
MODES of Ventilation
 Assist Control Ventilation (A/C)
 Controlled Mandatory Ventilation (CMV)
 Synchronized Intermittent Mandatory
Ventilation (SIMV)
 Pressure Control Ventilation
 Spontaneous Mode
Pressure support ventilation (PSV)
Positive end-expiratory pressure (PEEP)
 Assist Control mode A/C: (full support) mainly use in
adult
-Preset rate and tidal volume (sometimes PIP), full mechanical
breath is delivered either triggered by patient’s respiratory efforts,
or–if not sufficient the preset mechanical rate is maintained
automatically.
USES: for patients who have a very weak respiratory effort, allows
synchrony with the patient but maximal support. Not a weaning
mode, as at any rate they are getting complete mechanical
support.
 Controlled mandatory ventilation (CMV): full
control
-The ventilators deliver the preset tidal volume at a time-

triggered frequency and all breathing are coming from the vent.
USES: Should only be used when the patient is properly medicated
with a combination of sedatives, respiratory depressants and
neuromuscular blockers. Sometimes indicated if the patient
“fights” the ventilator in the initial stages of mechanical ventilator
support.
 Synchronized intermittent mandatory ventilation
(SIMV): partial support
-Is the mode in which the ventilator delivers either assisted

breaths to the patient at the beginning of a spontaneous breaths
or time-triggered mandatory breaths.
USES: It provide partial ventilatory support, i.e., a desire to have
the patient actively involved in providing part of the minute
volume.
 Pressure control ventilation:
-The pressure-controlled breaths are time-triggered by a preset
frequency. Once inspirations begins, a pressure plateau is created
and maintained for a preset inspiratory time. Airway pressure and
inspiratory time are controlled.
USES: Usually indicated for patients with severe ARDS who require
extremely high peak inspiratory pressures during mechanical
ventilation in volume-controlled mode.
 Spontaneous
-Spontaneous mode is not an actual mode since the frequency

and tidal volume during spontaneous breathing are determined by
the patient.
USES: To provide inspiratory flow to the patient in a timely manner;
flow adequate to fulfil a patient’s inspiratory demand (i.e,. Tidal
volume or inspiratory flow); and adjunctive modes such as PEEP to
complete a patient’s spontaneous breathing effort.
 Pressure-Control Ventilation:
-The patient initiates every breath and the ventilator delivers
support with the preset pressure value. Is used to lower the work
of spontaneous breathing and usually applied in the SIMV mode
when the takes spontaneous breaths.
 Positive End Expiratory Pressure:

-Is not commonly regarded as a “stand alone” mode, rather it is
applied in conjunction with other ventilator modes. It is often used
to improve the patient’s oxygenation status, especially in
hypoxemia.
Advanced Mode of Ventilation
 Pressure-regulated volume control (PRVC)

 Inverse ratio ventilation (IRV)
 Airway pressure release ventilation (APRV)
 High-frequency oscillatory ventilation (HFOV)
 Pressure regulated volume control:
-A control mode, which delivers a set tidal volume with each
breath at the lowest possible peak pressure. Deliver the breath with
a decelerating flow pattern that is thought to be less injurious to the
lung.
 Inversed ratio ventilation:

-Pressure control mode
-can increase MAP without increasing PIP: Improve oxygenation
but limit Barotrauma. Significant risk of air trapping
 Airway pressure release ventilation (APRV)

-Has two CPAP or pressure levels—high pressure/Pinsp and low
pressure/PEEP, and the patient is allowed to breathe
spontaneously without restriction.
 High-frequency oscillatory ventilation (HFOV)
-HFOV does not have a tidal volume setting and it delivers
extremely small volumes at high frequency. Its main application is
to minimize development of lung injury while providing mechanical
ventilation.
Who needs a Mechanical Ventilator
 Can’t oxygenate (low paO2/SPO2)

 Can’t ventilate (high PCO2)
 Can’t participate or low airway (low GCS)
 If you’re not sure whether or not the patient needs a
mechanical ventilator, then the patient needs a
ventilator support.
Set the Tidal Volume and Rate: the goals that
does not no harm
 Normal Lungs:
 Vt of 10-12 ml/kg IBW
 Rate 8-12
 Restrictive Lungs:
 Vt of 4-8ml/kg IBW
 Rate 15-25 (watch I:E ratio for enough exhalation time)
 Airways Obstruction and Resistance:
 Vt of 8-10 ml/kg IBW
 Rate 8-12
Applications
Determine the weight
Pressure < 10 kgs Volume > 10 kg
Initial set-ups Initial set-ups

 pressure - Vt: 8-12/
pedia 5-10 ml/kgs
 PIP: pedia 10-15 cm H2O - rate: 12-20
adult < 35 cm H2O - flow: pedia 30-40 lpm
 Rate: Pedia 20-40 adult: 40-60 lpm
Adult 12-20
 Flow rate: pedia 8-12 lpm
adult 40-60 lpm
 PEEP: 3-5 cm H2O
Flow Patterns
selection depends of lung condition
 Constant Flow – Square waveform
 Provides the shorted Ti
 Ascending Ramp
 Not generally used
 Sine Flow
 Tapered flow may more evenly distribute gas to
lungs
 Descending Ramp
 Attempts to meet pt flow demand, flow is
greatest at the beginning of inspiration
Formulas:
Tidal Volume: calculated base on gender and height( frame
size)
Women IBW (lbs) = 105 + 5 (H in inches - 60)
Men IBW (lbs) = 106 + 6 (H in inches - 60)
Ex: patient height 5 ft 3 and his weights 150 kg
105 + 5 x (63 - 60)
105 + (5 x 3)
105 + 15 = 120 lb (ideal body weight)
120 lb + 2.2 lb/kg = 55 kg
Vt= 12 mL/kg x 55 kg = 660 mL

Interrelation of Vt, flow, I Time, Exp Time, TCT, and
RR
 minute ventilation (Ve) = Vt x f
 Total cycle time (TCT) = Ti +Te
 RR (frequency) = Ve / Vt or 60sec / TCT
 Ti = (60 / f) – TE or TC – Ti
 Te = ( 60 / f) – Ti or TC – Te
 I:E Ratio = Ti : Te
 flowrate = Vt / (Ti / 60)
Adjusting the ventilator settings
 PCO2 too High

 PCO2 too Low
 PaO2 too High
 PaO2 too Low
 PIP too high
PCo2 too high
 Patient’s minute ventilation is too low

 Increase rate and tidal volume or both
 If using PC ventilation increase PIP
 If PIP too high, increase the rate
 sometimes, you have to live with the high pCo2, so
use bicarbonate to increase the pH to >7.20 mmHg
PCo2 too low
 Minute ventilation is too high

 Lower the rate or tidal volume
 Don’t need to lower the TV if the PIP is <20
 If patient is spontaneously breathing, consider
lowering the pressure support if spontaneous TV
>7ml/kg.
PaO2 is too High
 Decrease the FiO2.

 When FiO2 is less than 40%, decrease the PEEP to
3-5 cm H2O.
 Wean the PEEP no faster than about 1 every 8-12
hours. Sudden decease in PEEP may lead to
precipitous decrease in oxygenation and FRC.
 While patient is on ventilator, don’t wean FiO2 to
<25% to give the patient a margin of safety in case
the ventilator quits.
PaO2 too low
 Increase either the FiO2 or the mean airway
pressure (MAP).
 Try to avoid FiO2 >70%.
 Increasing the PEEP is the most efficient way of
increasing the MAP in the PICU.
 Can also increase the I-time to increase the MAP
(PC).
 Can increase the PIP in Pressure Control to increase
the MAP,
 May need to increase the PEEP to over 10, but try to
stay <15 if possible.
PIP too high
 Decrease the PIP (PC) or the TV (VC).

 Increase the I-time (VC).
 Change to another mode of ventilation. Generally,
pressure control achieves the same TV at a lower PIP
than volume control.
 If the high PIP is due to high airway resistance,
generally the lung is protected from barotrauma
unless air-trapping occurs.
Vent. Settings to improve oxygenation
Ventilator settings are adjusted to:

1. normalize blood gases (oxygenation, ventilation)
2. improved patient-ventilator synchrony/decrease
respiratory distress
3. wean a patient from ventilator support
 PCO2 varies to minute volume
 blood oxygen levels can affected by two – the
FiO2 AND PEEP levels. In general the higher the
FiO2 and PEEP level, the higher PaO2/SaO2
 PaO2 excessive high >100 mm Hg: lower the
parameter ( FiO2/PEEP)
 PaO2 and FiO2 is low (<60 mmHg or <90%):
either FiO2 or PEEP should be increased
 V/Q imbalance (indicated by an PO2 > 60 mm Hg
on a FIO2 < 0.6): Increased FiO2
 Shunting (indicated by an PO2 < 60 mm Hg on a
FIO2 > 0.6): Increased FiO2 won’t help, must be
added PEEP or increase.
ALARMS
 High pressure alarm
+10 - 15 to PIP
problems: cough, kinking or biting, water obstruction, secretions,
brochospasm
 Low pressure alarm
-10 – 15 to PIP or above baseline airway pressure
problems: May indicates leak, deflate cuff or disconnect
 High minute ventilation
+20% of Ve
problems: Tachypnea, oversensitive
 Low minute ventilation
-20% of Ve
problems: leaks, decrease in rate
Weaning from Mechanical
Ventilator
Weaning: is a process of withdrawing mechanical
ventilator support and the WOB from the
ventilator to the patient.
Weaning procedure:
-a weaning approached to wean a patient off
mechanical ventilation by using a set of clinical
measurements as guided.
 Spontaneous
 Synchronized intermittent mandatory ventilation
(SIMV)
 Pressure support ventilation (PSV)
Spontaneous breathing -may use T-tube, CPAP, or automatic tube
compensation;
-Let patient breathe spontaneously for up to 30 min

If patients tolerates 4 step consider
extubation when blood gas and vital -May use low level pressure support (up to 8 cm H2O
for adults and 10 cm H2O for paediatrics
signs are satisfactory
-assess patient
-reduce SIMV (ventilator) frequency by 1 to 3 breaths

per min.
SIMV -monitor SpO2, obtain ABG as needed
If patients tolerated 3 step -reduce SIMV frequency further until a frequency of 2

consider extubation when blood gas to 4/min is reached.
and vital signs are satisfactory
-PSV may be used on conjunction with spontaneous

PSV breathing or SIMV mode
If patients tolerated 3 step -start PSV at a level of 5 to 15 cm H2O -40 cm H2O

consider extubation when blood gas -Decrease pressure support level 3 to 6 cm H2O
and vital signs are satisfactory intervals until of close to 5 cm H2O is reached.
Weaning Failure
 as either the failure of spontaneous breathing trial

or the need for reintubation within 48 hours
following extubation. Patients who fail the SBT often
exhibits the following clinical signs: tachypnea,
tachycardia, hypertansion, hypotension, hypomia,
acidosis, or arrhythmias.
Weaning success
 an absence of ventilatory support 48 hours following the

extubation. While the spontaneous breaths are unassisted
by mechanical ventilation, or continuous positive airway
pressure may be used to support and maintain adequate
spontaneous ventilation and oxygenation.

Pediatric and Neonatal Respiratory Care Embryologic Development

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Pediatric and Neonatal Respiratory Care Embryologic Development

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Pediatric and Neonatal

Endoderm Mesoderm Ectoderm

Respiratory Dermisand Epiderm is, Hair,

 Function: Maintain patency

 Shake (Foam) Test

 FLM or FP Assay – Fluorescence

The main phospholipids that make up of mature surfactant are

 3rd week - two tubes

 Pressure in the fetal vasculature

 Normal shunts in the fetus

Blood bypasses the lungs because of the high right sided

Aorta - shunts blood away from the lungs.

 Fetal lung does not participates in gas exchange.

 About 10% of blood goes to lungs for tissue development

• Blood entering the right atrium from the

• the well oxygenated blood from the placenta

• only 10% of the blood flows through the

• this blood is mainly deoxygenated blood

•The low right atrial pressure & the high left

• the small valve that lies over the foramne

• the increased systemic resistance

• blood begins to flow backward from the

•Functional closure- after only a10-24

resistance to blood flow decreases

vasoconstriction of the lung blood vessels

eliminates the hypoxia.

 Closure of the Ductus Venosus

 In one of several thousand infants, the ductus fails to

• Low pressure system • High pressure system

superior vesicular artery

 Ductus arteriosus  Ligamentum arteriosum

 Pregnancy Induced hypertension

 Maternal age<17 y/o

 Maternal age above 35 y/o

 Position of the fetus and placenta

 Measure fetal growth

 Identify possible anomalies

 Qualitatively assess amniotic fluid

Appears at approx. 35 – 36 wks of gestation

positioning the head, drying, and suctioning.

 Done after 1 and 5 minutes after delivery

 The higher the score the better condition of the infant

a. 7-10 points – provide routine care

2. Silverman-Anderson Scoring System

 Lower score indicates less distress

a. 0-3 – No respiratory distress to mild respiratory

c. 7-10 – Severe respiratory distress

3. Assessment of Gestational Age

 Good method to determne gestational a

and physical maturity

38-42 wks – term

Low Birth Weight - <2,500 g

b. Heart Rate – 120 – 160 beats/min

d. Blood pressure – 60/40 mmHg

Cricothyroid membrane Smaller; virtually nonexistent in Needle cricothyrotomy and surgical

Extrathoracic trachea More malleable Increased risk of collapse during

Trachea Smaller diameter Endotracheal tube misplacement

Diaphragm Main action for breathing in Infants known as “belly breathers”;

Conducting airways Smaller in diameter More pronounced distress during

Chest wall Higher compliance

 Can deliver up to 100% Oxygen

 Monitor O2 by placing analyzer probe near the

* Safe levels of Oxygen Therapy*