UTHSCSA Pediatric Resident Curriculum for the PICU
RESPIRATORY FAILURE
& ARDS
RESPIRATORY FAILURE
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Inability of the pulmonary system to meet the metabolic
demands of the body through adequate gas exchange.
Two types of respiratory failure:
 Hypoxemic
 Hypercarbic
Each can be further divided into acute and chronic.
Both types of respiratory failure can be present in the same
patient.
CENTRAL ETIOLOGIES
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Trauma: head injury, asphyxiation, hemorrhage
Infection: meningitis, encephalitis
Tumors
Drugs: narcotics, sedatives
Neonatal apnea
Severe hypoxemia or hypercarbia
Increased ICP from any of the above causes
OBSTRUCTIVE ETIOLOGIES
Upper Airway
Lower Airway
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Anatomic: choanal atresia,
tracheomalacia, tonsillar
hypertrophy, laryngeal web,
vascular rings, vocal cord
paralysis, macroglossia
Aspiration: mucus, foreign
body, vomitus
Infection: epiglottitis,
abscesses, laryngotracheitis
Tumors: hemangioma, cystic
hygroma, papilloma,
Laryngpospasm
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Anatomic: bronchomalacia,
lobar emphysema
Aspiration: FB, mucus,
meconium, vomitus
Infection: pneumonia,
pertussis, bronchiolitis, CF
Tumors: teratoma,
bronchogenic cyst
Bronchospasm
RESTRICTIVE ETIOLOGIES
Lung Parenchyma
Chest Wall
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Anatomic: agenesis, cyst,
pulmonary sequestration
Atelectasis
Hyaline membrane disease
ARDS
Infection: pneumonia,
bronchiectasis, pleural
effusion, Pneumocystis
carinii
Air leak: pneumothorax
Misc: hemorrhage, edema,
pneumonitis, fibrosis
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Muscular: diaphragmatic
hernia, myasthenia gravis,
muscular dystrophy,
botulism
Skeletal: hemivertebrae,
absent ribs, fused ribs,
scoliosis
Misc: distended abdomen,
flail chest, obesity
HYPOXEMIA
V/Q mismatch

Most common reason. Blood perfuses non-ventilated
lung. Seen in atelectasis, pneumonia, bronchiectasis
Global hypoventilation: apnea
Right-to-left shunt

Intracardiac lesions, e.g., tetralogy of Fallot
Incomplete diffusion

Oxygen must diffuse across increased distance secondary
to interstitial edema, fibrosis, or hyaline membrane.
Low inspired FiO2: high altitude
HYPERCARBIA
Pump Failure
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Reduced central drive: apnea, metabolic alkalosis, drugs,
brainstem injury, hypoxia
Muscle fatigue: muscular dystrophy
Increased pulmonary workload: decreased compliance,
increased obstruction
Increased CO2 production: fever, seizure, malignant
hyperthermia
Increased dead space: V/Q mismatch (ventilation of
non-perfused lung)
PHYSICAL EXAM
 Tachypnea
 Dyspnea
 Retractions
 Nasal flaring
 Grunting
 Diaphoresis
 Tachycardia
 Hypertension
 Altered mental status

Confusion
 Agitation
 Restlessness
 Somnolence
 Cyanosis (need 5mg/dl
of unoxygenated blood)
CXR FINDINGS
 CXR may be normal if problem is with upper airway
 Can see hyperinflation, atelectasis, infiltrate,
cardiomegaly
 Additional studies may be needed, e.g., chest CT,
barium swallow, echocardiogram
BLOOD GAS
 For any age patient, breathing room air, respiratory
failure is defined as arterial pCO2 > 50mm Hg or
arterial pO2 < 60mm Hg.
 If the patient is hyperventilating, a normal pCO2 is
disturbing.
 The above definition assumes the absence of an
anatomic shunt.
 Chronic hypercarbic respiratory failure will often
have a normal pH because of compensatory
metabolic alkalosis.
MANAGEMENT
REMEMBER PALS
Airway
Breathing
Circulation
AIRWAY
 Repositioning
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Position of comfort
Jaw thrust/chin lift
 Oral airway
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Unconscious patients only
 Nasal trumpet
 Nasal or mask CPAP
 Bag-mask ventilation
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Use during preparation for intubation
 Tracheal intubation
BREATHING
 Decrease respiratory workload
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ß-agonists
Decadron or steroids
Antibiotics
CPAP
 Supplemental O2
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Nasal cannula
Closed face mask
Non-rebreather
 Counteract drug effects
 Bag-mask ventilation
 Mechanical ventilation
CIRCULATION
Suppress anaerobic metabolism and acidosis
Correct anemia to improve oxygen delivery
Ensure adequate cardiac output
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Inotropes: oxygen, vasopressors
Fluid boluses
ARDS
 A patient must meet all of the following:

Acute onset of respiratory symptoms
 CXR with bilateral infiltrates
 No evidence of left heart failure
 PaO2/FiO2 < 200mm Hg (regardless of PEEP)

American-European Consensus Conference on ARDS (Am J Resp
Crit Care Med 149:818, 1994)
 The following are implied:

Previously normal lungs
 Decreased lung compliance
 Increased shunting
 Hypoxemic respiratory failure
ETIOLOGY
 ARDS represents about 3% of PICU admissions.
 Numerous precipitating events:
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Trauma
Pneumonia
Burns
Sepsis
Drowning
Shock
PATHOPHYSIOLOGY
 Acute Injury
 Latent Period
 Early Exudative Phase
 Cellular Proliferative Phase
 Fibrotic Proliferative Phase
Royall and Levin
J Peds 112:169-180;
335-347, 1988
PATHOLOGY OF ARDS
Green arrows point to hyaline membrane
Blue arrows point to type II pneumocytes and alveolar macrophages
MANAGEMENT
 Meticulous supportive care is the mainstay of therapy
 Prevent secondary lung injury
 Ensure adequate cardiac output
 Limit secondary infections
 Drugs
 Good nutrition
VENTILATOR STRATEGIES
The hallmark of ARDS is heterogeneous lung.
 Limit Barotrauma
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Keep PIP <35 cm H2O
Use pressure-control
ventilation
Use TV of 6-10cc/kg
Keep rate <30 bpm
Permissive hypercapnia
Use bicarb or THAM to
keep pH >7.20
 Limit O2 Toxicity

Give enough PEEP to
lower FiO2 to <60%
while maintaining O2
>90%.
 PEEP <15 cm H2O
shouldn’t decrease
cardiac output.
 Increase mean airway
pressure with inverse
ratio (I>E) ventilation.
CARDIAC OUTPUT
 Keep cardiac output >4.5 L/min/m2.
 Keep O2 delivery >600 ml O2/min/m2.
 Keep Hct >30%, higher if signs of heart failure.
 Use inotropes to augment cardiac output.
 Ensure adequate preload.
LIMIT SECONDARY INFECTIONS
 Wash your hands.
 Use the gut as soon as possible for nutrition and
meds.
 Discontinue indwelling catheters as soon as
possible.
 Have high index of suspicion.
 Treat infections early, but tailor antibiotics to culture
results.
DRUGS
 Diuretics: a dry lung is a good lung.
 Inotropes
 Steroids: 2mg/kg/day begun after a week into the
course may be of benefit, otherwise don’t use.
 Pulmonary vasodilators (nitric oxide, prostaglandins,
nitroprusside): of little benefit. NO may be of benefit
in some patients.
 Surfactant replacement: probably no benefit
 NSAIDs: no clinical benefit
NUTRITION
 Ensure adequate calories as soon as possible:
 50-60kcal/kg/day in infants
 35-45kcal/kg/day in older children.
 After day 4, increase calories by 25-50% above
baseline.
 Begin enteral feeds as soon as is safe.
 “Pulmonary” formulas probably of little benefit.
MORTALITY/MORBIDITY
 Published mortality is 50% in children.
 Pulmonary failure accounts for only 15% of the
deaths.
 Lung function usually returns to normal within 18
months after leaving the hospital.