1
ANATOMIC ALETERATION OF THE LINGS
a. During normal intrauterine fetal development
- the fetus periodically demonstrates normal
rapid, shallow respiratory chest movements
- pulmonary fetal fluid moves into and out of the
oropharynx
- glottis remains closed
-
b. During periods of fetal hypoxemia
- fetus may demonstrate very deep
- gasping inspiratory movements that may force
the contents of the nasooropharynx to pass
through the glottis into the airway
- aspirate may contain meconium and amniotic
fluid
MECONIUM
- material that collects in the intestine of the fetus
and forms the first stools of the newborn
- odorless, thick, sticky, blackish green material
- heterogeneous mixture of intestinal tract
secretions, amniotic fluid, pulmonary fetal fluid,
and intrauterine debris
Aspiration of meconium leads to one or more of the
following complications:
1. MAS causes a chemical pneumonitis
- characterized by an acute inflammatory
reaction and edema of the bronchial mucosa
and alveolar epithelium
- leads to excessive bronchial secretions and
alveolar consolidation
- Meconium also promotes the growth of
bacteria
MAJOR
- can also interfere with alveolar pulmonary
CHANGES ASSOCIATED WITH MAS ARE AS
surfactant production
FOLLOWS:
2. Physical presence of the meconium may result
in an upper airway obstruction at birth because
of the high viscosity of the meconium
- clumps of meconium can rapidly migrate past
the glottis and penetrate the smaller airways
- meconium may already be present in the distal
airways at birth
- when thick particulate meconium is aspirated
into the small airways, the meconium can
partially or totally obstruct the airways
- Airways that are partially obstructed are
affected by a “ball-valve” effect
- Excessive hyperinflation may lead to alveolar
rupture and air leak syndromes such as s
pneumomediastinum or pneumothorax.
3. As a consequence of the hypoxemia
associated with MAS, infants with the condition
often develop hypoxia-induced pulmonary
arterial vasoconstriction and vasospasm,
which cause pulmonary hypertension.
- blood shunting from right-to-left
- intrapulmonary shunts are also occasionally
seen
- pulmonary hypoperfusion
- persistent pulmonary hypertension of the
neonate
-
PATHOLOGIC OR STRUCTURAL
 Physical presence of the meconium leading to:
ALWINA S. DAGGONG
BSRT 2D
 2

 Partially obstructed airways, air trapping, and

alveolar hyperinflation
 Pulmonary air leak syndromes
(pneumomediastinum or pneumothorax) RADIOLOGIC FINDINGS (Chest Radiograph)

 Totally obstructed airways and absorption

atelectasis
 Edema of the bronchial mucosa and alveolar
epithelium
 Excessive bronchial secretions
 Alveolar consolidation (or secondary infection)
 Disrupted pulmonary surfactant production

ETIOLOGY AND EPIDEMIOLOGY

- 10,000 to 15,000 infants are diagnosed with

MAS annually
- 30% of them will require mechanical ventilation
- 10% to 15% will develop pneumothorax
- fetal hypoxemia and stress
- rarely is seen in infants born at less than 36
weeks
- Post-term infants are especially at risk for MAS
- Other infants who are at high risk for MAS are
those who are small for gestational age

CLINICAL DATA OBTAINED AT THE PATIENT’S

BEDSIDE GENERAL MANAGEMENT OF MECONIUM
ASPIRATION SYNDROME
The Physical Examination

1. Vital Signs
 Increased Respiratory Rate (Tachypnea)

 Increased Heart Rate (Pulse) and Blood

Pressure Apnea

2. Clinical Manifestations Associated with More

Negative Intrapleural Pressure during
Inspiration

3. Chest Assessment Findings

4. Expiratory Grunting
5. Cyanosis
6. Common General Appearance
7. Barrel chest (when airways are partially
obstructed)

ALWINA S. DAGGONG
BSRT 2D
 3

Congenital heart diseases (CHDs) Etiology and Epidemiology

 CHDs can involve the interior walls of the heart,
valves inside the heart, or arteries and veins
that carry blood to the heart or body
 CHDs are the most common type of birth
defect, affecting 8 of every 1000 newborns.
 nearly 40,000 infants are born with a heart
defect each year in the United States, and
more than 1 million adults are living with CHD
here
CHDs commonly encountered by the respiratory
therapist include:
- patent ductus arteriosus (PDA),
- atrial septal defect (ASD),
- ventricular septal defect (VSD),
- tetralogy of Fallot (TOF), and
- transposition of the great arteries (TGA)
HYPEROXIA TEST
- determine whether the infant’s cyanosis is
caused by lung disease or a CHD (e.g., TOF or
TGA)
- The general procedure required for the
hyperoxia test is as follows:
 First, obtain an arterial blood
gas (ABG)
 If hypoxemia is present, the
infant is then placed on an
FIO2 of 1.0 (e.g., head hood)
for 10 minutes
 followed by a second ABG
PATENT DUCTUS ARTERIOSUS
Anatomic Alterations of the Heart
Patent ductus arteriosus
- congenital heart defect in which the ductus
arteriosus
- normally open during fetal life, fails to close
shortly after birth
- a portion of the oxygenated blood from the
aorta flows through the open ductus back to the
pulmonary artery
- pathophysiologic effect of a PDA is a left-to-
right shun
- PDA results in excessive blood flow through
the pulmonary circulation and hypoperfusion of
the systemic circulation
- prematurity, low birth weight, high altitude and
low atmospheric oxygen tension, hypoxia, and
a variety of chromosomal abnormalities
- more common in premature
- twice as common in girls as in boys
Diagnosis
- based upon its characteristic clinical finding
- confirmed by echocardiography
- echocardiographic imaging
- Doppler color flow mapping
-
CLINICAL MANIFESTATION
- When PDA is complicated by persistent
pulmonary hypertension of the newborn, the
clinical manifestations include:
tachycardia, dyspnea, differential cyanosis,
low PaO2 and SpO2, increased PaCO2, loud
systolic/diastolic murmur at the upper left
sternal border, cardiomegaly, left subclavicular
thrill, prominent left ventricular impulse,
bounding pulse, , and widened pulse pressure.
- Complications of PDA in the newborn include
pulmonary edema, congestive heart failure,
intraventricular hemorrhage, necrotizing
enterocolitis, and bronchopulmonary dysplasia
due to prolonged ventilator and/or oxygen
support
- PDA patients who are 3 to 6 weeks old
commonly present with tachypnea,
diaphoresis, inability or difficulty with feeding,
and weight loss or no weight gain
- In the adult whose PDA has gone
undiagnosed, the signs and symptoms include
congestive heart failure, atrial arrhythmia, and
differential cyanosis

Treatment

ALWINA S. DAGGONG
BSRT 2D

- Medication
- catheter-based procedures
- surgery
- oxygen therapy protocol
- bronchopulmonary hygiene therapy protocol,
- lung expansion therapy protocol
- aerosolized medication therapy protocol
- and ventilator support protocols
ATRIAL SEPTAL DEFECT
Anatomic Alterations of the Heart
Atrial septal defect
- a hole in the septal wall between the right and
left atrium
2 most common types of ASD: ostium secundum ASD
and the primum ASD
1. ostium secundum ASD
- caused by arrested growth of the secundum
septum or excessive absorption of the primum
septum
- resulting in an atrial septal wall defect
- presents as an isolated cardiac defect in the
fossa ovali
2. primum ASD
- caused by arrested growth of the apical portion
of the atrial septum
- associated with an anterior mitral valve clef
DEGREE OF PATHOPHYSIOLOGY ASSOCIATED
WITH AN ASD DEPENDS ON:
(1) the pulmonary and systemic vascular resistances
(2) the compliance of the left and right ventricles, and
(3) the size of the ASD
ETIOLOGY AND EPIDEMIOLOGY
- common and account for approximately 13% of
all patients with CHD
- over 1900 infants in the United States are born
each year with an ASD
- ASDs are not known, abnormal genes in
combination with certain maternal risk factors
are believed to play a role
DIAGNOSIS
- based upon its characteristic clinical
manifestations and confirmed by
echocardiography
- 2-dimensional echocardiographic imaging and
Doppler color flow mapping is both sensitive
and specific for the identification of ASD.
CLINICAL MANIFESTATIONS
4
- can present at any age
- small ASD, the baby may not have any
remarkable signs or symptoms
- clinical manifestations are dependent on the
size of the defect and the degree of shunting
between the atria
- some infants with a moderate to large ASD
- older patient, common signs and symptoms
include
- In all ages, a moderate to large ASD
TREATMENT
- based on the seriousness of the signs and
symptoms and the size of the ASD
- Catheter-based procedures/surgery
- oxygen therapy protocol, bronchopulmonary
hygiene therapy protocol, lung expansion
therapy protocol, aerosolized medication
therapy protocol, and ventilator support
protocols
VENTRICULAR SEPTAL DEFECT
Anatomic Alterations of the Heart
Ventricular septal defect
- an opening in the ventricular septum of the
heart
- may be one or more openings in different
locations of the ventricular septum
common locations include:
 Conoventricular Ventricular Septal Defect
 Inlet Ventricular Septal Defect
 Perimembranous Ventricular Septal Defect
 Muscular Ventricular Septal Defect
At birth, the following physiologic events normally
occur: (1) an immediate fall in pulmonary vascular
resistance, (2) the removal of the low resistance
placenta from circulation
(3) the closure of the ductus arteriosus
A VSD has the following two net effects:
1. the influx of blood into the right ventricle from
the left ventricle increases the right ventricular
pressure and volume
2. the circuitous route of blood through the lungs
and back to the heart causes a volume
overload
ETIOLOGY AND EPIDEMIOLOGY
- most common congenital heart disorder
- 50% of all patients with CHD
- prevalence of VSD is about 42 of 10,000
babies each year
- causes of VSDs are not known
- abnormal genes in combination with certain
maternal risk factors
DIAGNOSIS
ALWINA S. DAGGONG
BSRT 2D

- based upon its characteristic clinical findings
and confirmed by echocardiography
- 2-dimensional echocardiographic imaging and
Doppler color flow mapping
CLINICAL MANIFESTATIONS
- When the VSD is moderate or large, the early
clinical manifestations include tachycardia,
tachypnea, increased work of breathing, poor
weight gain, failure to thrive, and diaphoresis
- Cardiac clinical manifestations include systolic
murmurs at the mid-to-lower left sternal border,
an increased second heart sound (S2),
diastolic murmurs at the apex (indicates a
Qp/Qs of 2 :1 or greater), and diastolic
murmurs at the midto-lower sternal border
- In patients with VSD and aortic regurgitation,
the left ventricle is especially overloaded
- Clinical features include neck pulsations,
bounding pulse, wide pulse pressure, early
diastolic murmur, diaphoresis, and vigorous
precordial movement
- volume and pressure loads on the left and right
ventricles. The chest radiograph may show
increased pulmonary vascular markings, and
enlargement of the left atrium, left ventricle and
pulmonary artery
TREATMENT
- medications to support the heart (e.g., digitalis
and diuretics)
- oxygen therapy protocol, bronchopulmonary
hygiene therapy protocol, lung expansion
therapy protocol, aerosolized medication
therapy protocol, and ventilator support
protocols—are all administered as needed
TETRALOGY OF FALLOT ANATOMIC
ALTERATIONS OF THE HEART
Tetralogy of Fallot (TOF) is a congenital heart defect
with the following four major anatomic alterations:
 Stenosis of the pulmonary artery
 Deviation of the aorta to the right
 Ventricular septal defect
 Right ventricular hypertrophy
The pathophysiologic effects—and clinical
symptoms—of TOF are largely dependent upon the
degree of right ventricular outflow tract obstruction
5
One of the unique physiologic features of TOF is that
the right ventricular outflow tract obstruction often
fluctuates in response to transient increases and
decreases in the resistance caused by obstruction.
ETIOLOGY AND EPIDEMIOLOGY
- prevalence of TOF in the United States is about
4 per 10,000 live births, and it accounts for
about 7% to 10% of the CHDs
- about 1600 infants are born each year with
TOF
- most common congenital heart disorder to
require intervention in the first year of life and
occurs equally in males and female
- causes of TOF are not known, abnormal genes
in combination with certain maternal risk
factors
DIAGNOSIS
- confirmed by echocardiography
- electrocardiogram and chest radiography
- Cardiac catheterization
CLINICAL MANIFESTATIONS
- depends on the degree of right ventricular
outflow tract obstruction
- cyanosis—i.e., “hypercyanotic “or “tet” spells
- Oxygen saturation during hypercyanotic spells
is low
- prominent right ventricular impulse and systolic
thrill
- early systolic click (called an aortic ejection
click) along the left sternal border may be heard
- Symptoms of heart failure may be present
- heart murmur is commonly heard
TREATMENT
- medical care
- surgical palliative care and
- intracardiac repair, and
- long-term postoperative care
- need for medical intervention
- intravenous prostaglandin therapy (alprostadil)
- knee-chest positioning
- Intracardiac repair
- oxygen therapy protocol, bronchopulmonary
hygiene therapy protocol, lung expansion
therapy protocol, aerosolized medication
therapy protocol, and ventilator support
protocols—are all administered as needed
Transposition of the Great Arteries
Anatomic Alterations of the Heart
Transposition of the Great Arteries
ALWINA S. DAGGONG
BSRT 2D
 6

- most common cyanotic congenital heart lesion - oxygen therapy protocol, bronchopulmonary
that presents in neonate hygiene therapy protocol, lung expansion
- a congenital heart defect in which the therapy protocol, aerosolized medication
pulmonary artery and the aorta are switched in therapy protocol, and ventilator support
position, or transposed protocols—are all administered as needed
- the most common form of TGA is the
dextrotransposition of the great arteries
- results in a pulmonary and systemic circulation
that functions in “parallel,” rather than “series.”
- This heart defect produces a right-to-left
shunt—a cyanotic disorder
The most common heart defects are the following:
 Atrial septal defect
 Ventricular septal defect
 Patent ductus arteriosus
 When no other heart defects are present, it is
called Simple Transposition of the Great
Arteries (simple TGA)
 When other defects are present, it is a Complex
Transposition of the Great Arteries (complex
TGA)
ETIOLOGY AND EPIDEMIOLOGY
- prevalence of TGA ranges from 2.3 to 4.7 per
10,000 live births
- approximately 1900 babies are born with TGA
each year
- associated with poor nutrition during
pregnancy, rubella, or other viral illness during
pregnancy, alcoholism, maternal age over 40
years, and Down’s syndrome
DIAGNOSIS
- based on clinical suspicion of an underlying
cyanotic CHD and is confirmed by
echocardiography

CLINICAL MANIFESTATIONS
Infants with TGA
- cyanosis, tachypnea (respiratory rates >60
breaths/min), poor feeding, and clubbing of
fingers and toes
- When there is a VSD, a pan systolic murmur is
usually present within a few days after birth at
the lower left sternal borders
In the patient with left ventricular outflow obstruction
- there may be a systolic ejection murmur3 along
the upper left sternal border

TREATMENT
- directed at stabilizing the patient’s cardiac and
pulmonary function and ensuring adequate
systemic oxygenation
- prostaglandin E1 (alprostadil) therapy
- balloon atrial septostomy (BAS)
- surgical repair

ALWINA S. DAGGONG
BSRT 2D

CROUP
- “barking or brassy sound” associated with a
partial upper airway obstruction
- Inspiratory barking sound heard in a patient
with a partial upper airway obstruction
- croup and laryngotracheobronchitis (LTB)
- Acute epiglottitis
- two types of partial upper airway disorders—
LTB and acute epiglottis
ANATOMIC ALTERATIONS OF THE UPPER
AIRWAY
LARYNGOTRACHEOBRONCHITIS
- can affect the lower laryngeal area, trachea,
and occasionally the bronchi
- synonym for “classic” subglottic obstruction
- inflammatory process that causes edema and
swelling of the mucous membranes
- when edema develops in the upper airway,
fluid spreads and accumulates quickly
throughout the connective tissue
- The edema and swelling in the subglottic
region decrease the ability of the vocal cords to
abduct (move apart) during inspiration.
ACUTE EPIGLOTTITIS
- a life-threatening emergency
- inflammation of the supraglottic region, which
includes the epiglottis, aryepiglottic folds, and
false vocal cords
- does not involve the pharynx, trachea, or other
subglottic structure
- As the edema in the epiglottis increases, the
lateral borders curl and the tip of the epiglottis
protrudes posteriorly and inferiorly
The major pathologic or structural changes associated
with inspiratory stridor are as follows:
 LTB
 EPIGLOTTITIS
ETIOLOGY AND EPIDEMIOLOGY
1. Laryngotracheobronchitis
- parainfluenza viruses cause most cases of LTB
- also may be caused by influenza A and B,
respiratory syncytial virus (RSV), herpes
simplex virus, Mycoplasma pneumoniae,
rhinovirus, and adenoviruse
- seen in children 6 months to 5 years of age
- Boys are affected slightly more often than girls
- The onset of LTB is slow
- most common during the fall and winter
- child’s voice is hoarse, and the inspiratory
stridor is typically loud and high in pitch
7
Acute Epiglottitis
- a bacterial infection that is almost always
caused by Haemophilus influenzae type B
- transmitted via aerosol droplets
- other causes of epiglottitis include aspiration of
hot liquid and trauma from repeated intubation
attempts
- may develop in all age groups
- most often occurs in children 2 to 6 years of age
- Boys are affected more often than girls
- onset of epiglottitis is usually abrupt
- As the supraglottic area becomes swollen,
breathing becomes noisy, the tongue is often
thrust forward during inspiration, and the child
may drool
- typically seen in patients with neck trauma and
- those who have been intubated repeatedly,
and in drug abuse (crack cocaine) case
CLINICAL DATA OBTAINED AT THE PATIENT’S
BEDSIDE The Physical Examination
1. Vital signs
- Increased Respiratory Rate (Tachypnea)
- Increased Heart Rate (Pulse) and Blood
Pressure
2. Chest Assessment Findings
3. Inspiratory Stridor
- slight narrowing of the upper (extrathoracic)
airway that naturally occurs during inspiration
is insignificant
- when the cross-section of the upper airway is
reduced because of the edema, the child will
generate stridor during inspiration
4. Cyanosis
5. Use of Accessory Muscles During Inspiration
6. Substernal and Intercostal Retractions
LATERAL NECK RADIOGRAPH
- Haziness in the subglottic area (LTB)
- Haziness in the supraglottic area (epiglottitis)
- Classic “thumb sign” (epiglottitis)
ANTERIO-POSTERIOR NECK RADIOGRAPH
- “Steeple point” or “pencil point” narrowing of
the upper airway (LTB)
- A lateral neck radiograph is usually done first
to rule out the diagnosis of epiglottitis
- “thumb sign”
- “pencil point” or “steeple point”
ALWINA S. DAGGONG
BSRT 2D
 8

4. Antibiotic Therapy
- Because acute epiglottitis is almost always
caused by H. influenzae type B, appropriate
antibiotic therapy is part of the treatment plan
- Ceftriaxone (Rocephin) and Ampicillin/
sulbactam (Unasyn)

5. Endotracheal Intubation or Tracheostomy

- If the patient is anxious, restless, or
uncooperative, restraints and sedation may be
needed to prevent accidental extubation
- After intubation, the patient should be
transferred to the intensive care unit (ICU) and
placed on continuous positive airway pressure
(CPAP) or pressure support ventilation
- Mechanical ventilation

GENERAL MANAGEMENT OF
LARYNGOTRACHEOBRONCHITIS AND
EPIGLOTTITIS
- Early recognition of epiglottitis may save a
patient’s life; it is a true airway emergency
- Once the diagnosis is suspected or confirmed
by the lateral neck radiograph, examination or
inspection of the pharynx and larynx is only to
be done in the operating room under general
anesthesia with a fully trained team
- The patient with a confirmed diagnosis of
acute epiglottitis should be intubated
immediately
AFTER THE DIAGNOSIS IS ESTABLISHED, THE
GENERAL MANAGEMENT OF LTB AND ACUTE
EPIGLOTTITIS IS AS FOLLOWS:
1. Supplemental Oxygen
- hypoxemia and significant work of breathing is
associated with both LTB and epiglottitis,
supplemental oxygen may be required
- Oxygen therapy should be started when the
patient’s SpO2 is under 92%

2. Racemic Epinephrine
- Aerosolized racemic epinephrine is
administered to children with LTB
- Using the patient’s LTB score, the
administration of racemic epinephrine protocol
is as follows:
- • 3–5: Consider racemic epinephrine
- • >6: Administer racemic epinephrine 0.5 mL in
3 mL normal saline

3. Corticosteroids
- such as dexamethasone, have been shown to
reduce the severity and duration of LTB
- given when the patient presents with moderate
to severe symptoms

ALWINA S. DAGGONG
BSRT 2D