Transcript Pediatric Critical Care Review Respiratory Review 22% of CCRN

MANAGEMENT OF ILLNESS
RESPIRATORY
PURPOSE OF THE
RESPIRATORY SYSTEM
• Provide oxygen for
metabolism in the
tissues and to
remove carbon
dioxide (the waste
product of
metabolism)
• Gas Exchange
PHYSIOLOGIC FUNCTION
• During inspiration, the diaphragm
contracts, the chest wall
expands and the volume of the
lungs increases. Gas flows from
the atmosphere into the lungs
and oxygen diffuses into the
blood at the alveolar-capillary
interface.
PHYSIOLOGIC FUNCTION
•During expiration the
diaphragm and the chest
wall relax, thoracic volume
decreases, intrathoracic
pressure increases, and gas
flows out.
PHYSIOLOGY
• Wedge pressures (MAP, systolic, diastolic)- catheter
in pulm. Artery branch measuring left atrial pressure.
Average is 20mmHg for syst., 10mmHg for dias.,
mean pressure overall of 15mmHg.
• Increase in hematocrit of 40% increases blood
viscosity thus leading to increased pulm. Vascular
resistance (cyanotic heart disease)
• Resistance is also seen with a decrease in number
of vessels- (hypoplasia, cystic changes)
ANATOMY
• The upper
respiratory tract
(or upper
airway) consists
primarily of the
nose and
pharynx
ANATOMY
The lower
respiratory tract
• Trachea
• Two mainstem
Bronchi
• Lobar Bronchi
• Bronchioles
• Alveolar ducts
• Alveoli
ANATOMY
• The alveoli are
the final
branchings of the
respiratory tree
and act as the
primary gas
exchange units of
the lung.
EMBRYOLOGY OF RESPIRATORY TRACT
• Lung:
• Conception to 16weeks gestation- lungs are just buds on
the primitive gut and start to divide, larynx develops
between wks. 7-10
• 16-24 wks: at 18wks- some of the cells become type II
(important for surfactant synthesis)
• 24 wks to birth- 26wks alveolar ducts appear, 30wks alveoli
and capillaries appear, cells differentiate into type 1 & 2
cells
• Birth- first breath is initiated d/t chest recoil after thorax has
passed through birth canal (pressure).
• Afterbirth- airway dimensions will continue to increase until
about 8 yrs. –adult chest wall configuration not reached
until age 3.
EMBRYOLOGY OF RESPIRATORY TRACT
• Nose
• Nasal cavities form around 4 wks. Obligatory nose-breathers
until 6mons d/t obstruction encountered by elongated
esophagus touching the soft palate. By 6mos the larynx
grows thus minimizing mouth breathing.
• Pharynx
• About 4wks begins to establish structure
• Larynx
• Vocal cords appear at 8wks
• Trachea
• Begins development at 24 days
AIRWAY RESISTANCE
• Airway resistance (the effort or force required
to move air into the lungs) is greater in
children than in adults because children’s
airways are narrower than those of adults.
• When there’s edema or swelling in the airway
due to an irritant or infectious process, the
airway is further narrowed, increasing the
airway resistance even more.
AIRWAY RESISTANCE
• Increased
airway
resistance
makes the child
work harder to
breathe and is
indicated by:
•Increased
respiratory
rate
•Retractions
•Nasal flaring
ANATOMY
• Lung compliance (i.e., lung distensibility) is affected
by surfactant and by the elasticity of lung tissue.
• Surfactant is a complex substance consisting of
lipids and proteins, formed by alveolar type II cells
(type II pnemocytes). Since surfactant decreases
surface tension at the air fluid interface, insufficient
surfactant results in atelectasis and decreased lung
compliance. Surfactant is necessary for sustained
inflation of the lung. Surfactant production
increases during the later stages of pregnancy
ANATOMY
• The unit of gas
exchange is the alveoli
• Encased in network of
pulmonary capillaries
where gas exchange
takes place by simple
diffusion
• Type I (gas exchange)
and Type II (surfactant)
epithelial cells
RESPIRATORY
DISORDERS
BRONCHOPULMONARY
DYSPLASIA (BPD)
• BPD is a chronic lung disease characterized by:
• Respiratory distress
• Oxygen dependency persisting beyond 36 weeks
corrected gestation age
• Abnormal chest radiographs
• Clinically, O2 dependency at 1 month post natal age
• Mixed disorder:
• Obstructive: increased airway resistance
• Restrictive: decreased compliance
BRONCHOPULMONARY DYSPLASIA
CONTRIBUTING FACTORS
• High impaired oxygen concentration: capillary
proliferation, interstitial fibrosis
• Positive pressure ventilation with airway damage
from high pressure: barotrauma, alveolar over
distention
• Prolonged intubation resulting in reduced
mucociliary function and increased dead space
• Permissive Hypercapnea
BRONCHOPULMONARY DYSPLASIA
CONTRIBUTING FACTORS
• Meconium aspiration
• Disruption of surfactant production
• PPHN: persistent shunting across the PDA,
increased pulmonary vascular resistance,
ventilation-perfusion mismatch
• CHF
• Pulmonary hemorrhage
• Severe neonatal pneumonia
• Abnormal inflammatory response to
injury
MECONIUM ASPIRATION
BPD SYMPTOMS
• Tachypnea, retractions, FTT, hypoxia, hypercapnia, resp.
acidosis, crackling, wheezing on auscultation,
bronchospasm
• Can cause SIADH- Na & fluid retention
• Pulm. HTN- leading to RV failure, tachycardia,
hepatomegaly, periorbital edema, and S2 gallop
rhythm
• HTN d/t increased renin and catecholamine activity
• BPD tantrums- irritability, agitation, duskiness,
hypercarbia, hypoxemia (usually during bowel
movements)
BPD DIAGNOSTICS
• ABG’s- low O2, increased CO2, and compensated
resp. acidosis
• ECG- RV enlargement d/t increase in pulm. Vascular
resistance leading to RV afterload
• CXR- scattered infiltrates, atelectasis, hyperinflation,
cardiomegaly
• PFT’s- low FRC, increased WOB, higher airway
resistance and oxygen consumption,
• Echocardiogram- pulm. HTN, RV enlargement
• Cardiac Cath (rare)- FTT or increased pulm. HTN to
determine extent of disease.
BPD MANAGEMENT
• O2 management- supplemental (92%-95%), CPAP at
the earliest- may mitigate the need for mech.
Ventilation, tracheostomy
• Medication: Bronchodilators (albuterol mainly for acute
episodes, anticholinergic (atrovent, steroids, diuretics
(SIADH) such as Lasix or Bumex
• Nutrition: enteral feeds preferred
• Long-term hospitalization will require monitoring and
follow with speech, PT, OT in order minimize gaps with
cognitive and developmental achievements.
TRACHEOESOPHAGEAL FISTULA
(TEF)
Two Forms:
•Esophageal atresia
•Tracheoesophageal fistula
TRACHEOESOPHAGEAL
FISTULAS (TEF)
• Congenital defect occurring during the
4th week of gestation when the
embryonic foregut divides into the
trachea, larynx, and lungs anteriorly, and
the esophagus posteriorly
• The prenatal history often includes a
history of polyhydramnios (inability of the
infant to swallow amniotic fluid into the
gut)
RELATIVE FREQUENCIES OF OCCURRENCE OF THE
VARIOUS TYPES OF ESOPHAGEAL ATRESIA (EA)
WITH AND WITHOUT TRACHEOESOPHAGEAL
FISTULA (TEF).
FIGURE 4. Relative frequencies of occurrence of the various types of esophageal atresia (EA) with and without tracheoesophageal fistula
(TEF).
TEF: PRE-OPERATIVE MANAGEMENT
• Avoid use of pacifiers which will stimulate
production of oral secretions
• Prone positioning with an elevated HOB 30
degrees to lessen the chance of aspiration of
stomach contents into the lungs via the fistula
• Ensure adequate oxygenation and ventilation:
respiratory distress related to gaseous distention
of the stomach with impingement on the
diaphragm
TEF: PRE-OPERATIVE
MANAGEMENT
• Low pressure positive pressure
ventilation if needed to avoid
gaseous distention of the stomach
when there is no outlet for
decompression
• Ensure optimal fluid and electrolyte
balance: NPO, IVF, TPN
TEF: POST OPERATIVE CARE
• Gastrostomy tube is returned to gravity drainage
until the infant can tolerate feedings
• Optimize nutrition: TPN, enteral feeds after
evaluation of the esophageal anastomosis
• Pain management
• Gastric decompression: do not manipulate NG
tubes placed in surgery
TEF: POST-OPERATIVE MANAGEMENT
• Optimal oxygenation and ventilation:
• Mechanical Ventilation is weaned as soon as
possible
• ETT suctioning needs to be done with a premeasured catheter to only the tip of the ETT to
avoid tracheal suture line stress
• Hemodynamic stability: observe for hypovolemia due
to 3rd spacing
• Assess the extrapleural chest tube for presence of
saliva which may indicate anastomosis leak
ACUTE RESPIRATORY
INFECTIONS
CROUP
RSV PNEUMONIA
EPIGLOTTITIS PERTUSSIS
ACUTE
LARYNGOTRACHEOBRONCHITIS
(LTB)
• Most common of the
croup syndromes
• Generally affects children
younger than
5 years
• Organisms responsible
• RSV, parainfluenza virus,
Mycoplasma
pneumoniae, influenza
A and B
CROUP
• Is usually preceded by an
upper respiratory
infection that proceeds
to laryngitis and then
descends into the
trachea, causing
inflammation of the
mucosal lining and
subsequent narrowing of
the airway.
CROUP
PATHOPHYSIOLOGY
• Cricoid cartilagenarrowest segment
of the upper airway
in infants and small
children
• Swelling & secretions
lead to increased
airway resistance
CROUP
CLINICAL MANIFESTATIONS
• Barking cough &
hoarseness
• Inspiratory stridor and
varying degrees of
respiratory distress
• Nasal flaring
• Tracheal tugging
• Retractions
• Low grade fever
CROUP
DIAGNOSTIC TESTS
• A/P CXR“steeple sign”
• Lateral
radiograph-normal
epiglottis
THERAPEUTIC MANAGEMENT
Airway management
• A steamy bathroom at home
• In the hospital, hoods for infants or mist tents
• Maintain hydration—PO or IV
• High humidity with cool mist
• Nebulizer treatments
• Racemic Epinephrine (mucosal
vasoconstriction)
• Steroids (reduce subglottic edema and
inflammation)
CROUP
PATIENT MANAGEMENT
• Minimize
agitation
• Antipyretics
• Enteral feedings
• Intubation for
severe respiratory
distress
QUESTION
Nurse Amy is assessing
a child with croup in
the emergency
department. The child
has a sore throat and is
drooling. Examining the
child’s throat using a
tongue depressor
might precipitate
which of the following?
A. Sore throat
B. Inspiratory stridor
C. Complete
obstruction
D. Respiratory tract
infection
QUESTION
Which of the following
clinical manifestations
is an indication of the
need for an artificial
airway in a 2 y/o child
with
Laryngotracheobronchitis
A. Elevated
temperature
B. Increased
mucous
production
C. Metabolic
acidosis
D. Persistent
agitation/lethargy
EPIGLOTTITIS
• Severe, lifethreatening, rapidly
progressive infection
of epiglottis
• Usually occurs in
children 2-6 years
• Mortality 8-12% of
hospitalized children
EPIGLOTTITIS
CLINICAL MANIFESTATIONS
Four D’s & S
• Drooling
• Dysphagia
• Dysphonia
• Distress
• Stridor
• Fever with
abrupt onset
• Sore throat
• Muffled voice
• Tripod position
EPIGLOTTITIS
Tripod
position
EPIGLOTTITIS
DIAGNOSTIC TESTS
• Avoid invasive
procedures if
epiglottitis is
suspected!!
• Lateral neck x-raydiagnostic
• Blood cultures
(once airway is
stable)
EPIGLOTTITIS
PATIENT MANAGEMENT
• Prevention- Hib
vaccine
• OR for laryngoscopy
& intubation
• Maintain comfort
• Intubation** (careful
with accidental
extubation)
Respiratory
Infection
Etiology
Epiglottitis
H-flu
Betahemolytic
Streptococ
cus
Pneumoco
cci
Croup
Viral or
Bacterial
Typical
Age
Range
2-6 years
Diagnosed
with lateral
neck film
Management
Clinical
Symptoms
Abrupt
fever
Drooling
Stridor
Tripod
position
Thumb sign
on x-ray
3 months -5 Low fever
years
Barking
Cough
“Steeple
sign” on xray
OR for
laryngoscopy
and intubation
Maintain
Comfort
Sedation
Racemic
epinephrine
Cool
humidified
oxygen
BRONCHIOLITIS
• Acute inflammatory
disease of the lower
respiratory tract
• Results in the
obstruction of small
airways
BRONCHIOLITIS: PATHOPHYSIOLOGY
• Respiratory syncytial virus (RSV) is the leading
cause of bronchiolitis.
• Bronchiolitis occurs when viruses or other
infectious agents invade the mucosal cells
lining the bronchial and bronchioles, causing
the cells to die.
• Cell death results in cell debris that clogs and
obstructs the bronchioles and irritates the
airway.
BRONCHIOLITIS: PREVENTION
• Preventative therapy
may be indicated for
RSV bronchiolitis in
high risk infants
• Synagis (Palivizumab)
is given for 5
consecutive months
during RSV season
which is between…..
November
and
April
QUESTION
A 10 month old w/
bronchiolitis is
intubated in the EC
due to an acute
deterioration in her
respiratory status.
Post intubation ABG
follows:
• pH 7.31
• pCO2 50
• pO2 80
• HCO3 22
• O2 sat 95%
QUESTION
The
blood
gas
reflects:
CONT.
a. Respiratory
acidosis
b. Respiratory
alkalosis
c. Metabolic
acidosis
d. Metabolic
alkalosis
ABG’S
Normal
Values:
•pH: 7.34-7.45
•pC02: 35-45
•HC03: 22-26
•P02: 80-100
PNEUMONIA
• Pneumonia is an acute
inflammation or
infection of the
respiratory bronchioles,
alveolar ducts and sacs,
and alveoli (the
parenchyma) of the
lungs that impairs gas
exchange.
PNEUMONIA ETIOLOGY
• Infection of the
lung usually
caused by
viruses or
bacteria
• Etiologic Agent
varies with age
• RSV
• Influenza
• Paraflu
• Streptococci
• Staphylococci
PNEUMONIA
CLINICAL MANIFESTATIONS
• High fever
• Cough chest
pain
• URI symptoms
• Respiratory
distress
• Cyanosis
• Apnea (infants)
PERTUSSIS
• Known as whooping
cough- contagious acute
respiratory tract infection
• Caused by gram negative
coccobacillus Bordetella
pertussis
• Transmitted through
inhalation of contaminated
respiratory droplets or by
direct contact with
contaminate articles
PNEUMONIA & PERTUSSIS
PATIENT MANAGEMENT
• Hydration
• Analgesics
• Supplemental oxygen
(intubation
depending on
severity)
• NPO
• Steroids
• Antibiotics
STATUS ASTHMATICUS
STATUS ASTHMATICUS
ETIOLOGY
Characterized by:
• Airway
inflammation
• Mucosal edema
• Airway plugging
• Bronchospasm
(mainly smooth
muscle )
MECHANISMS OF OBSTRUCTION IN
ASTHMA
QUESTION
12 y/o male is
admitted to the PICU
following an acute
asthma attack. He
has received multiple
albuterol treatments.
The following
measurements are
obtained:
•BP 130/78
•HR 68
•RR 48
•FiO2 0.6
•O2 Sat 88%
QUESTION (
Physical
findings could
include which
of the
following:
CONT)
a. Wheezing &
coughing
b. Coughing &
grunting
c. Pleural rub &
wheezing
d. Stridor &
bronchospasm
STATUS ASTHMATICUS
CLINICAL MANIFESTATIONS
•  Respiratory
Effort
•  Cardiac
Output
• Metabolic
Acidosis
• Altered LOC
STATUS ASTHMATICUS
DIAGNOSTIC STUDIES
•CXR
•CBC
•ABG
•Basic
Metabolic
Panel
QUESTION
The use of an
inhaled beta 2adrenergic agonist
in the
management of a
child with status
asthmaticus would
include which of
the following
medications?
a. Isoproterenol
(Isuprel)
b. Methylprednisolon
e (Solu-Medrol)
c. Albuterol
(Ventolin)
d. Ipratropium
bromide
(Atrovent)
STATUS ASTHMATICUS
PATIENT MANAGEMENT
• Continuous
Assessment
• Medications
• Mechanical
Ventilation
• Supportive Care
CYSTIC FIBROSIS
CYSTIC FIBROSIS
• Chronic,
autosomal
recessive
inherited disorder
of the exocrine
glands that
affects multiple
organ systems
• Most common
lethal, inherited
disease of
Caucasians of
European origin
but is found in
every ethnic &
racial group
CYSTIC FIBROSIS
• Exocrine glands are glands that secrete their
products (including hormones and other
chemical messengers) into ducts (duct glands)
that lead directly into the external environment
• They are the counterparts to Endocrine glands,
which secrete their products (hormones)
directly into the bloodstream (ductless glands)
or release hormones (paracrines) that affect
only target cells nearby the release site.
CYSTIC FIBROSIS
• Life expectancy for the person with the disease is
around 31-32 years
• The gene responsible for cystic fibrosis is located on
chromosome 7q.
• It encodes a membrane associated protein called
the cystic fibrosis transmembrane regulator (CFTR)
• Exact function of the gene is unknown, but it
appears to help regulate chloride and sodium
transport across epithelial membranes.
CYSTIC FIBROSIS
PATHOPHYSIOLOGY
learn.genetics.utah.edu
www.aurorahealthcare.org
CYSTIC FIBROSIS
TREATMENT
• Treatment for cystic fibrosis is life long.
• Aimed at maximizing organ function and quality
of life & forestalling the complications
• Current treatments delay the decline in organ
function
• Targets for therapy - Lungs, GI tract/Nutrition &
the Reproductive organs (including Assisted
Reproductive Technology (ART)), Transplantation
& Gene therapy
Davies J et al. Cystic Fibrosis. BMJ. 2007 Dec 15;335(7632):1255–59.
CYSTIC FIBROSIS
TREATMENT
- ANTIBIOTICS COVERAGE • Based on culture (deep throat/sputum/BAL)
• Aminoglycoside + Semisynthetic
PCN/Cephalosporin (SYNERGY testing)
• Home/hospital
• Minimum of 10 – 14 days or until:
- symptoms resolved
- PFT’s (FEV1) within 10% of baseline/higher
- suppressed organisms
- to avoid resistant bacteria
• Drug levels – Hearing loss( ↑peak) & kidney
damage (↑trough)
CORNERSTONES OF
PULMONARY MANAGEMENT
• Regular visits to CF
Center
• Good nutrition enzymes replacement
in pancreatic
insufficiency, Vitamins
A,D,E & K ;high-calorie
meals
• Anti inflammatory
drugs
- Steroids (inhaled,
oral), Ibuprofen,
Macrolides
• Active lifestyle
AEROSOLIZED MEDICATIONS THAT
HELP LOOSEN SECRETIONS INCLUDE
• dornase alfa (Pulmozyme®)
- recombinant human DNase
- breaks down DNA (neutrophils) in
sputum
- ↓viscosity17 ;
- ↑5- 7% FEV1
• hypertonic saline16
•  adrenergic/cholinergic agonists
-improves ciliary motility
• N-acetylcysteine (Mucomyst)
- Bad smell
TREATMENT OF AIRWAY INFECTIONS
- MECHANICAL TECHNIQUES  to dislodge sputum and
encourage
expectoration :
- Chest physical
therapy
- ThAIRapy vest
- Intrapulmonary
percussive
ventilator(IPV)
- acapella® (PEP)
 Aerobic exercise