RESPIRATORY Flashcards
Fanaroff 11th; chapters 62,63,64,65,66,67,68,69,70,38,37
most effective treatment for RDS in neonatology
antenatal corticosteroids and postnatal surfactant
lung structural development “stages”
embryonic, pseudoglandular, canalicular, saccular and alveolar;
embryonic period
lobar airway 37 days
segmental airway 42 days
subsegmental bronchi 48 days
mesenchyme
pseudoglandular stage
5-18 weeks; airway branching is complete;
cuboidal cells filled with glycogen; major components of lungs are completed
in what stage airway, arteries and veins have developed?
18 weeks, pseudoglandular stage
canalicular stage
16-25 weeks; transformation of the previable lung to the potentially viable lung that can exchange gas
3 major events:
-appearance of acinus(berry-like clustering oof cells at the distal ends of respiratory brioncholes)
-epithelial differentiation (development of the air-blood barrier)
-start of the surfactant synthesis (recognizable type II cells)
what is the first critical step for the development of the future gas exchange surface?
saccular branching (acinus: 6 branching generations of respiratory brioncholes, alveolar ducts, and alveoli)
saccular stage
24 weeks to term; terminal sac is developing respiratory bronchiole (alveolar duct) to about 32 weeks(initiation of alveolarization)
type I pneumocytes: modulate gas exchange
type II pneumocytes: synthesis and secretion of surfactant
when is the most rapid rate of accumulation of the alveoli?
32 weeks till first months after delivery
factors that delay/interfere with alveolarization?
mechanical ventilation antenatal and postnatal glucocorticoids pro-inflammatory mediators chorioamninitis hyperoxia or hypoxia poor nutrition
factors that stimulate alveolarization?
vit A(retinoids) and thyroxin
stages of branching
airway branching, saccular branching, alveolarization
number of distal structures
24 weeks: 65000
adult: 500 million
fetal lung fluid
high chloride; bicarb and protein low;
what can completely stop fetal lung fluid production?
epinephrine IV
delay clearance of fetal lung fluid can cause what?
transient respiratory difficulties
what causes secondary pulmonary hypoplasia?
restricted lung growth (mass, effusion, external compression)
renal agenesis (potter syndrome) and prolonged oligohydramnios
congenital diaphragmatic hernia
absence of fetal breathing
pulmonary sequestrations
portion of the lungs that are in isolation from neighboring lung tissue and with no communication th the bronchial tree
alveolar macrophages
immune cells; functions: immune surveillance, phagocytosis, antigen presentation, interaction with adaptive immune cells, surfactant homeostasis; fetus normally do NOT have macrophages; they populate in lungs with an onset of breathing; *chorioamnionitis can mature and stimulate macrophages prior the delivery
surfactant composition
70-80% phospholipids (60% are saturated) , 8% protein, 10% neutral lipids
what is measured for fetal lung maturity?
AF Phosphatidylglyceroid
4 proteins in surfactant
SP-A (innate host defense protein); not used for RDS
SP-B (surface absorption of lipids and low surface tension on surface area compression); lack of SP-B lethal respiratory failure
SP-C only in type II cells; similar to SP-B
SP-D similar to SP-A; used in surfactant for ventilator mediated inflammation
surfactant synthesis and secretion
type II cells;
synthesis: ?
secretion: stimulated by adenosine triphosphate mechanical stretch (distention or hyperinflation)
what is primary cause of RDS?
surfactant deficiency
surfactant pool sizes
long delay between synthesis and secretion balanced by slow catabolism and clearance: this is favorable for surfactant treatment strategies
alveolar life cycle of surfactant
lamellar bodies “unravel” tubular myelin …?
physiologic effects of surfactant in the preterm lung
alveolar stability (prevent from collapsing, and keep interstitial fluid from entering the alveolus, normalize size) pressure-volume curves (increases maximal volume at max pressure, increase in lung volume increase gas exchange, stabilization of the lung on deflation
Lung maturation
surfactant appearance, induced lung maturation, glucocorticoids, intrauterine infections
defined by lack of RDS generally, present after 35 weeks of normal gestation
surfactant appearance test
L/S ration lecithin to sphingomyelin
fetal stress, fetal growth restriction or preeclampsia induce lung maturation
FALSE
fetal exposure to inflammation may have short time benefits of decreasing RDS
TRUE
corticosteroids and lung maturation
induce lung maturation by increasing the surface area for gas exchange; decrease pulmonary edema; induce surfactant synthesis; improve response to postnatal surfactant;
other use of maternal corticosteroids
PDA, IVH, NEC, increase kidney function and postnatal BP
clinical observations
respiratory rate, retractions, nasal flaring, grunting, cyanosis
work of breathing components
elastic and resistive
elastic component
work required to stretch the lungs and chest wall during a tidal inspiration
resistive component
work required to overcome friction caused by lung tissue movement and gas flow through the airways
respiratory rate
TV 6-7ml/kg; 40-60 bpm
retractions
substernal, subcostal, intercostal; caused by negative intrapleural pressure generated by the contraction of the diaphragm and other respiratory muscles and the mechanical properties of the lung and chest wall
suggest low lung compliance, obstruction or atelectatis
what increases retractions?
RDS (lung stiffness); airway obstruction, misplacement of ETT, pneumothorax, atelectasis
grunting definition
neonates attempt to close (adduct) their vocal cords during the initial phase of expiration, holding gas in the lungs and producing an elevated transpulmonary pressure in the absence of airflow. The elevated pressure and corresponding increased lung volume result in the enhancement of the ventilation-perfusion ratio (V̇/Q̇). During the last part of the expiratory phase, gas is expelled from the lungs against partially closed vocal cords, causing an audible grunt
compensatory mechanism to maintain FRC and maximize pO2 (partial pressure of oxygen)
central cyanosis
check tounge and oral mucosa; desaturated hemoglobin
assessing pulmonary function
pulse oximetry and blood gas
pressure of alveolar oxygen
PaO2
optimal gas exchange
appropriate matching of the alveolar gas with the mixed venous blood
mixed venous blood composition and volume include what?
arterial blood gas content, cardiac output, oxygen consumption, and carbon dioxide production
what does the quantity of oxygen bound to hemoglobin depends on?
PaO2 and oxygen dissociation curve
arterial oxygen content
CaO2; sum of hemoglobin bound and dissolved oxygen
indexes used to estimate the degree of oxygen derangement
- arterial-alveolar oxygen tension ratio
- alveolar-arterial oxygen tension gradient mmHg
- oxygen ration mmHg
oxygenation index
OI
pulse oximetry
measures the amount of hemoglobin molecules that is bound with oxygen
ideal oxygen saturation
currently UNKNOWN; AAP guideline recommendation 90-95%
hyperoxia test
differentiate between primary lung disease and congenital heart disease with right-to-left shunting
hyperoxia-hyperventilation test
distinguish between structural congenital heart disease and PPHN (both have right to left shunting)
preductal
right hand
postductal
left hand/ or any foot
respiratory physiologic measurements
airflow (pneumotachometer), lung volume, pressure
functional residual capacity FRC
the volume of gas in the lungs that is in direct communication with the airways at the end of expiration; oxygen storage compartment; volume of gas left in the lung after a normal expiration
thoracic gas volume
total volume of gas in the thorax at the end of expiration
tidal volume
volume of gas in and out of the lungs in a single breath
pressure
transpulmonary vs transrespiratory
respiratory mechanics
compliance, resistance, time constant, forced expiratory maneuvers, forced oscillation technique, work of breathing
lung compliance
measure of elasticity; reciprocal: elestance
resistance
measure of the friction encountered by gas flowing through the nasopharynx, trachea, and bronchi and by tissue moving against tissue. reciprocal: conductance
equation of motion
relationship between pressure, flow, volume, and the elastic, resistive, and inertial components of the respiratory system
time constant
duration (expressed in seconds) necessary for a step (e.g., pressure or volume) change to partially equilibrate throughout the lungs; resistance * compliance
work of breathing
a measure of the energy expended in inflating the lungs and moving the chest wall
goal of respiratory support
optimize oxygenation and CO2 elimination with the lowest possible ventilator settings to minimize lung injury
RDS pathologic diagnosis
surfactant deficiency; risk factors: GA and low BW; predominant factors: elective deliveries, maternal DM and perinatal hypoxia-ischemia; white boys ;)
RDS pathophysiology
diffuse atelectasis; impaired or delay surfactant synthesis and secretion
is RDS genetic?
too rare to determine
RDS radiographic findings
diffuse reticulogranular pattern, giving the classic ground-glass appearance in both lung fields with superimposed air bronchograms
RDS clinical presentation
grunting, retractions, nasal flaring, cyanosis, increased oxygen requirement
RDS RX
positive pressure ventilation, surfactant therapy, inhaled NO, assessment of blood gas(pulse oximetry, noninvasive carbone dioxide monitoring-capnography; arterial sampling), acid-base therapy, CV management, ABX
positive pressure ventilation
invasive: via an endotracheal tube utilize a time-cycled, pressure-limited mode, or volume-controlled mode with synchronized ventilated breaths; jet, oscillator, and conventional
noninvasive: CPAP, Noninvasive positive-pressure ventilation (NIPPV) increases tidal and minute volumes, improves lung recruitment, decreases work of breathing, may reduce apnea of prematurity, and may reduce the need for mechanical ventilation
benefits of CPAP
maintenance of a constant airway opening pressure, establishment, and maintenance of functional residual capacity, reduction of pharyngeal or laryngeal obstruction, improvement of oxygenation, and release of surfactant stores
reduces barotrauma, volutrauma, airway damage, and risk of secondary infections, and enhances mucociliary transport.
surfactant therapy
4 types approved for use in the US; bovine, porcine and synthetic mix of SP-B and SP-C protein; no proven adverse effects; INSURE technique (INtubate, SURfactant, Extubate)
inhaled Nitric Oxide therapy (iNO)
for preterm infants at risk for developing BPD or in RDS that is complicated by pulmonary hypertension
pulse oximetry
Continuous noninvasive measurement of arterial hemoglobin oxygen saturation
UAC placement
high T6-T8 (above aortic bifurcation); low L3-L4
complication of UAC
blanching or cyanosis of part or all of a distal extremity or the buttock area, resulting either from vasospasm or a thrombotic or embolic incident
use heparin to avoid thrombi
flushing can cause retrograde blood flow and transient elevated BP
increase in bloodstream infection (ideal not more than 3 days)
Allen test for radial artery line to establish the presence of adequate collateral circulation to the fingers
acid-base therapy
use of sodium bicarbonate has adverse effects and not recommended
CV management of the RDS
decreased perfusion can be caused by lactic acidemia or metabolic acidosis (monitor BP via A-line), use of pressors and monitor cortisol levels
PDA complications
what can happen after surfactant administration to the CV system
unrecognized overdistension of the lungs by excessive mechanical ventilation support can decrease systemic venous return to the heart and result in a decrease in cardiac output. Xray will show: squeezed-heart silhouette and flattened diaphragm are found,
vital signs, peripheral pulses, capillary refill, and urine output as surrogate markers of adequate cardiac output.
ABX in RDS
pneumonia indistinguishable from RDS on x-ray
Penicillin combined with an aminoglycoside is recommended for 48h until blood culture results are back
what is the major contributor to long injury?
mechanical ventilation
noninvasive respiratory support modalities
single level pressure support: CPAP, HFNC
bilevel: BiPAP, SiPAP
nasal NIPPV
CPAP in RDS
prevent collapse of alveoli at end-expiration, maintaining some degree of alveolar inflation; helps maintain functional residual capacity and to facilitate gas exchange; useful in treating apnea of prematurity
CDP continous distending pressure
can be provided by CPAP and PEEP
clinical indications of CPAP
delivery room resuscitation RDS post-extubation support apnea mild upper airway obstruction
types of CPAP
flow driven
bubble CPAP
ventilator-derived CPAP
HFNC
1-8 L/min; issues with sizing and leaks(no baseline pressure); use: after birth, post-extubation, apnea
noninvasive nasal ventilation
PEEP, PIP, RR, inspiratory time can be manipulated
CPAP complications
nasal trauma lung overinflation increase or air leaks can increase intrathoracic pressure and decrease venous return and cardiac output to high cause carbone dioxide retention gastric distention (OG)
indication for assisted ventilation
absolute:
failure to initiate or sustain spontaneous breathing
persistent bradycardia
major airway or pulmonary malformations (diaphragmatic hernia, severe hydrops
sudden respiratory or cardiac collapse with As and Bs (not responding to mask ventilation or pulmonary hemorhage)
Relative: “50-50 rule”
likelihood of subsequent respiratory failure
surfactant administration
impaired gas exchange
worsening As
need to maintain airway patency
need to control carbon dioxide elimination
medication-induced respiratory depression (magnesium, anesthetics, analgesics)
sepsis, MAS, PPHN
General Principles of Assisted Ventilation
oxygenation
ventilation
time constant
PEEP/ positive end expiration pressure
baseline pressure, the lowest level to which airway pressure falls; PEEP increases mean airway pressure (mean Paw)
PIP/ peak inspiratory pressure
driving pressure, increases mean Paw; establishes the upper limit of the amplitude
determinants of oxygenation in Assisted Ventilation
fraction of inspired oxygen mean airway pressure PEEP PIP inspiratory time frequency gas flow rate
determinants of ventilation in Assisted Ventilation
tidal volume amplitude PIP-PEEP frequency minute volume: conventional (freq*TV) high-freq (freq*TV square) expiratory time (I:E ratio)
ventilation
carbon dioxide removal; tidal volume (TV) and frequency
tidal volume TV
amplitude of mechanical breath: the difference between PIP and PEEP
amplitude too high, newborn will do what?
infant’s hypercapnic drive will be abolished, and the baby will “ride” the ventilator rate
amplitude too low, newborn will do what?
baby will compensate by increasing the spontaneous breathing rate
time constant
the time required to allow pressure and volume equilibration in the lungs; product of compliance and resistance
conventional mechanical ventilator vs high frequency
CMV delivers physiological tidal volumes HFV delivers TV that is less than physiologic dead space
CMV types
ventilatory modalities (control the type of ventilation) ventilatory modes (determine the breath type)
control variables (ventilatory modalities)
time, pressure, volume, only one can be controlled
phase variables (ventilatory modes)
trigger, limit, cycle, PEEP
modes of ventilation
intermittent mandatory ventilation IMV: set rate, supported by PEEP
synchronized intermittent mandatory ventilation SIMV, supported by PEEP
assist/control A/C set minimal breath rate
pressure support ventilation PSV
starting TV reference
4-6ml/kg preterm; 5-8ml/kg term
starting PEEP reference
4-6 cm h2o
when infant is ready to wean?
improved gas exchange and pulmonary mechanics, more spontaneous breathing
what is most common reason for failure to wean
failure to wean
what is the best way to wean
change one parameter at the time (does NOT apply to HFOV), reduce the most harmful one first
what is the best predictive value of positive extubation
attention to spontaneous breathing
High Frequency Ventilation HFV
delivered gas volumes are less than the anatomic dead space and are provided to a patient at a very rapid rate; carbon monoxide is a product of frequency, set amplitude lower than CMV, shorter inspiratory time (less barotrauma); higher PEEP than CMV; does NOT mimic spontaneous breaths; airway resistance (not long compliance) is the major determinant of gas distribution
JET
OSCILLATOR
JET in what conditions?
active inspiration, passive exhalation; 360-450bpm
“air leaks”, pulmonary interstitial emphysema, E/T artesia or fistulas
HFOV in what conditions?
active inspiration, active exhalation; 8-15Hz (480-900bmp); best to deliver iNO;
monitoring ventilated infants
- clinical evaluation
- assessment of gas exchange
- chest imagining
- pulmonary functions and mechanics testing
- extrapulmonary monitoring (ECHO)
oxygenation depends on what?
ventilation-perfusion matching
movement of CO2 depends on what?
alveolar ventilation
base deficit
product of metabolic acidosis; 3-5mEq/L health infant; 5-10 should be ok
complications od assisted ventilation
airway:
UPPER: trauma, abnormal dentition, esophageal perforation, nasal septal injury, acquired palatal groove
TRACHEA: mucosal metaplasma, subglottic cysts, tracheal enlargement, vocal cord paralysis, subglottis stenosis, necrotizing tracheobronchitis
LUNGS: VAP, air leaks, ventilator-induced lung injury, BPD
air leaks examples
pneumomediastinum (nitrogen washout?)
pneumothorax
pulmonary interstitial emphysema (PIE)
pneumopericardium (air from pleural space or mediastinum enters pericardial sac)
pneumoperitoneum (rupture or perforation of abdominal viscus
pneumothorax ventilator causes?
high inspiratory pressure and unevenly distributed ventilation
certain diseases: MAS, CF, pulmonary hypoplasia
clinical S&S:
ASYMPTOMATIC: none, just xray
Deterioration in labs or bedside monitoring findings
Acute clinical deterioration
tension pneumotorax clinical evaluation
agitation and worsening respiratory distress
diminished or absent breath sound sounds on affected side
contralateral shift of heart sounds at the PMI
mixed acidosis and hypoxemia on CBG
transillumination: increased light on involved side
tension pneumothorax RX
thoracentesis (needle aspiration)
thoracostomy (chest tube)
PIE pulmonary interstitial emphysema
most compliant portion of the terminal airway ruptures, gas leaks into interstitial space
xray: fine linear or radial radiolucencies
pneumopericardium/cardiac tamponade
air completely encircling the heart
pulmonary injury sequence in VILI
barotrauma (too much pressure)
volutrauma ( too much gas, overdistention)
atelectrauma (repetitive opening and closing of lung units)
biotrauma (infection, inflammation, stress)
rheotrauma (inappropriate flow)
Bronchopulmonary Dysplasia BPD
chronic respiratory insufficiency
supplemental oxygen requirements
abnormal xray at 36 weeks GA
caused by: excessive TV
right to left shunting
high pulmonary resistance (early RDS, MAS)
left to right shunting
high systemic vascular resistance
nonpulmonary etiologies of respiratory distress
thermal instability, circulatory problems, cardiac diseases, neuromuscular diseases, sepsis, anemia, polycythemia, methemoglobinemia
agenesis
total absence of pulmonary parenchyma, supporting vasculature and bronchi; antenatal US: mediastinal shift without diaphragmatic hernia
pulmonary hypoplasia
result of deficient or incomplete development of the lung parenchyma leading to decreased number of distal airways, alveoli, and associated pulmonary vessels
primary
secondary: oligohydramnios (renal malformation, prolonged AF leak, placental abnormalities, IUGR
space-occupying lesion (hernia)
cystic lung disease
cardiac malformations (cardiomegaly)
absence ob abnormal diaphragmatic activity
congenital diaphragmatic hernia
(CDH) results from a developmental defect during the formation of the diaphragm that permits abdominal contents to herniate into the thoracic cavity
CDH types
posterolateral (Bochdalek) most common anterior (Morgagni) central 1 in 2000-3000 live births more common on L side
CDH clinical presentation
severy respiratory distress, cyanosis, scaphoid abdomen, absence of breath sounds
xray: bowel loops in chest cavity, OG tube in thorax
CDH management
ECMO criteria
gentle ventilation and permissive hypercapnia HFOV, low PIP
preductal sat above 85%, postductal dont matter
CO2 less or equal to 65, pH at least 7.25
dont use iNO
delay surgical therapy until stable and improvement of PPHN
CDH long term complications
pulmonary
GERD
hypoxemia: developmental delay
scoliosis
Alveolar Capillary Dysplasia
fatal; hypoxemia and PPHN not responding to treatment in first 48 hours
congenital pulmonary lymphangiectasia
CPL, dilation of lymphatic vessels in multiple areas of the lungs
intractable respiratory failure, cyanosis, and hypoxia associated with bilateral chylothoraces in the first few hours of life
nonimmune hydrops
xray: hyperinflation of the lung with bilateral interstitial infiltrates and bilateral pleural effusions
DX: lung biopsy: increased fibrous tissue with dilation of cystic lymphatic spaces and collapsed alveoli
poor prognosis if symptomatic early
chylothorax
accumulation of lymphatic fluid (chyle) in the pleural cavity
xray: pleural effusion, compression of the lung on the affected side, and displacement of the heart to the opposite side
DX: analysis of pleural fluid
RX: supportive, spontaneous resolution within 4-6 weeks
Congenital Cystic Pulmonary Malformations
congenital pulmonary airway malformations
bronchopulmonary sequestration
bronchogenic cyst
congenital lobar emphysema
congenital pulmonary airway malformations
(CPAM) constitutes multiple different hamartomatous lesions arising from the abnormal branching of the immature bronchial tree
4 types
bronchopulmonary sequestration
(BPSs) are microscopic cystic masses of nonfunctioning lung tissue thought to arise from the primitive foregut. Usually not connected to the main airway, and their blood supply arises from the systemic circulation intralobar sequestration (ILS) extralobar sequestration (ELS)
bronchogenic cyst
single cyst lined by respiratory epithelium and covered with elements of the tracheobronchial tree, including cartilage and smooth muscle
treatment: complete surgical excision
congenital lobar emphysema
postnatal overdistension of one or more segments or lobes of the lung
Pulmonary Arteriovenous Malformation
malformations are direct communications between the smaller pulmonary arteries and veins, allowing blood to bypass the capillary system
meconium
comprised of desquamated fetal intestinal cells, bile acids, minerals, and enzymes, including alpha1 antitrypsin and phospholipase A2, as well as swallowed amniotic fluid, lanugo, skin cells, and vernix caseosa
MAS mechanisms
complete or partial obstruction of airways, inflammation, complement activation and cytokine production, inhibition of surfactant synthesis and function, apoptosis of epithelial cells, and increased pulmonary vascular resistance
typical MAS infant
postmaturity, with evidence of weight loss; cracked, peeling skin; and long nails, together with heavy staining of nails, skin, and umbilical cord with a yellowish pigment
barrel chest
rales
xray: coarse, irregular pulmonary densities with areas of diminished aeration or consolidation
MAS suctioning
amnioinfusion: not recommended
intrapartum: not recommended
routine intubation and suctioning: not recommended
MAS NICU
supportive respiratory and CV care ABX HFOV surfactant lavage complicated by PPHN, iNO should be considered
neonatal pneumonia
early: 3-7 days, aspiration of infected amniotic fluid, ruptures membranes, birth canal bacteria; Group B Streptococcus (GBS), herpes simplex and other TORCH, candidal infections
late: VAP, hospital-acquired; viral can take longer to develop because of the virus incubation period
xray: nonspecific, but persist for weeks
neonatal pneumonia RX
broad spectrum ABX till culture comes back
early: amp and gent
late: vanco and gent or nafcillin and gent
Transient Tachypnea of the Newborn
TTN from pulmonary edema secondary to inadequate or delayed clearance of fetal alveolar fluid
48-72 hours
risk factors: premature or elective cesarean delivery without labor, large birth weight, maternal diabetes, maternal asthma, twin pregnancy, and male gender
transient nature of this disease
no specific RX
wheezing syndrome early in life
pulmonary hemorrhage
defined as a gush of blood through an endotracheal tube in intubated neonates associated with a worsening clinical picture, requiring increased ventilatory support and blood product transfusion
before 72 hours of life, median 40 hours
risk factors:extreme prematurity, surfactant administration, patent ductus arteriosus (PDA) with left-to-right shunting, multiple birth, and male gender
pulmonary hemorrhage patho
pathophysiology of pulmonary hemorrhage is believed to be secondary to a sudden decrease in pulmonary vascular resistance, causing increased left-to-right shunting and pulmonary vascular engorgement, pulmonary edema, and ultimately, rupture of pulmonary capillaries
pulmonary hemorrhage treatment
increase in PEEP (stops bleeding) avoid suctioning epinephrine: not sure blood products exogenous surfactant administration prophylactic indomethacin
Pulmonary Air Leak Syndromes
pneumothorax pneumomediastinum pulmonary interstitial emphysema pneumopericardium pneumoperitoneum subcutaneous emphysema
rib cage abnormalities
asphyxiating thoracic dystrophy (Jeune syndrome) thanatophoric dysplasia achondrogenesis homozygous achondroplasia osteogenesis imperfecta (severe form) Ellis-van Creveld syndrome (chondroectodermal dysplasia) hypophosphatasia spondylothoracic dysplasia rib-gap syndrome
Phrenic Nerve Injury
Phrenic nerve injury with paralysis of the diaphragm is an unusual cause of respiratory distress
C3 to C5
breathing activity fetus
11 weeks
neonatal respiratory activity
irregular with spontaneous changes alternating between eupnea, apnea, periodic breathing, and tachypnea
laryngeal chemoreflex
reflex-induced apnea
response to instilling saline in the oropharynx
Hering-Breuer reflex
Stimulation of pulmonary stretch receptors through increasing lung volume causes shortening of inspiratory time, prolongation of expiratory time, or both
prevents long overdistention on CPAP
breathing neurotransmitters
adenosine, GABA, prostaglandins, endorphins, and serotonin(SIDS)
apnea
the cessation of breathing for greater than 15-20 seconds. Shorter events (<15 seconds) may also be identified as apnea if accompanied by oxygen desaturation and bradycardia
apnea types
central, obstructive, mixed
ABD definition
defined as >10 seconds if accompanied by bradycardia (HR <100 beats/minute) and desaturation (SpO2 <80%)
apnea clinical association
sepsis
intracranial hemorrhage, hypoxic-ischemic encephalopathy, and brain malformations
NEC
RSV
anemia
hypoglycemia, hypocalcemia and electrolyte imbalances, temperature instability, and metabolic acidosis
opiates, benzodiazepines, magnesium sulfate, and prostaglandin
ALTE vs BRUE
apparent life-threatening event(old definition) vs Brief Resolved Unexplained Events(new terminology)
apnea treatment
HFNC
Methylxanthines: aminophylline
theophylline and caffeine
Xanthine
nasal and nasopharyngeal lesions
Pyriform Aperture Stenosis Nasolacrimal Duct Cysts Choanal Atresia Congenital Nasal Masses Nasopharyngeal Teratoma Mucosal Obstruction Continuous Positive Airway Pressure Trauma
Oral and Oropharyngeal Lesions
micrognathia, glossoptosis, and posterior tongue displacement and subsequent airway obstruction
Pierre Robin sequence, Treacher Collins syndrome, Goldenhar syndrome, Crouzon disease, Down syndrome
Lymphatic Malformations
Oral Cavity Cysts
Laryngeal Lesions
Laryngomalacia (stridor) Bifid or Absent Epiglottis Laryngeal Cysts Vocal Cord Paralysis Laryngeal Web Congenital Subglottic Stenosis Subglottic Hemangioma Laryngeal Cleft Congenital high airway obstruction syndrome (CHAOS) Intubation Trauma
Bronchopulmonary dysplasia
the most important respiratory complication of preterm birth, and it is associated with long-term respiratory morbidities
NIH BPD definition
severity-based definition of BPD into three categories based on the duration and level of oxygen therapy required:
mild
moderate
severe
BPD pathogenesis
injury to developing lung secondary to prolonged mechanical ventilation with high airway pressures and inspired oxygen concentration
BPD pathogenic factors
prematurity
pre- and postnatal infections
mechanical trauma from positive pressure ventilation
oxygen toxicity
pulmonary edema secondary to increased pulmonary blood flow from patent ductus arteriosus (PDA) acts on the immature alveolar and vascular structure of the immature lung
BPD pulmonary functions
low compliance, low to normal functional residual capacity (FRC), and high airway resistance
fibrosis, edema, overdistention, and collapse of lung parenchyma
increased work of breathing that contributes to the hypoventilation and hypercapnia
minute ventilation increased
CO2 retention
hypoxemia and require supplemental oxygen to maintain acceptable oxygenation levels
does surfactant reduce BPD
no
what can reduce BPD?
steroids NO
less invasive ventilation MAYBE/individualized
volume-targeted ventilation
targets in oxygen saturation (low YES, but cause NEC)
postnatal systemic corticosteroids YES, has side effects
inhaled steroide YES, but side effects
caffeine YES
vit. A YES
iNO ?
postnatal systemic corticosteroids
decrease bronchospasm
management of established BPD
respiratory support bronchodilator therapy corticosteroids therapy management of pulmonary hypertension fluid management nutrition infection prevention
ECMO
Extracorporeal membrane oxygenation
ECMO definition
cardiopulmonary bypass support for term and late preterm infants with severe, life threatening, hypoxic respiratory failure. Affected infants present within the first 2 weeks of life, and the majority of these also have persistent pulmonary hypertension of the neonate
allowing the lung to rest and recover until pulmonary arterial pressures decline and blood flow to the lung is restored
iNO inhaled Nitric Oxide
a noninvasive inhalational therapy that can elicit selective pulmonary vasodilation
PPHN persistent pulmonary hypertension of the neonate
pulmonary vascular resistance approaches or exceeds systemic vascular resistance, offering significant impedance to pulmonary blood flow
PPHN desaturated blood
Desaturated blood returning to the right heart is shunted to the systemic circulation (following the path of least resistance) across one or both persistent fetal channels, the patent ductus arteriosus (PDA) and the foramen ovale, resulting in marked cyanosis
what diagnosis will benefit from surfactant?
MAS, RDS, or pneumonia
what diagnosis will NOT benefit from surfactant?
CDH and HRF, nor in infants with isolated PPHN
ECMO types
venoarterial (VA) bypass
venovenous (VV) bypass
oxygenation on ECMO
varying blood flow through the ECMO circuit. The higher the volume of cardiac output diverted through the membrane lung, the better the oxygen delivery from the ECMO circuit
blood flow in ECMO
80-100ml/kg; weaning at 10-20ml/kg
no pressors and vasodilators needed
mild sedation
ECMO anticoagulation
Systemic anticoagulation therapy with unfractionated heparin: Activated clotting times (ACTs), antifactor Xa assays or Thromboelastography (TEG)
Bivalrudin if heparin can NOT be used because of HIT
ECMO ventilator support
“lung rest” on CMV rate 10; PEEP(use higher), PIP
maintain FRC and to allow for continued pulmonary toilet
advantage of VV ECMO
avoidance of carotid artery cannulation, bot NO cardiac support provided to the infant
ECMO criteria
Gestational age of 34 weeks or older
Normal cranial ultrasound or stable grade I or II intraventricular hemorrhage
Absence of complex congenital heart disease
Less than 10-14 days of mechanical ventilation
Reversible lung disease, including congenital diaphragmatic hernia
Failure of maximum medical therapy
No lethal congenital anomalies or evidence of irreversible brain damage
ECMO oxygenation criteria
Oxygenation Index (OI): OI = (MAP × FiO2 × 100)/PaO2 The usual criterion is OI of 35-60 for 0.5-6 hours.
Alveolar-Arterial Oxygen (Aado2) Gradient (at Sea Level)
AaDO2 = FiO2 (P − 47) − PaO2 − PaCO2 (FiO2 + (1 − FiO2)/R)
Usual criterion is AaDO2 > 605-620 mm Hg for 4-12 hours.
Partial Pressure of Arterial Oxygen
Usual criterion is PaO2 < 60 mm Hg for 2-12 hours.
Acidosis and Shock
Usual criterion is pH < 7.25 for longer than 2 hours or with hypotension
what exam needs to be done before ECMO
ECHO to R/O serious congenital heart disease
potent vasodilators
tolazoline, nitroprusside, prostoglandin E and prostoglandin D
Nitric Oxide NO
inhaled NO decrease pulmonary vascular resistance and improve pulmonary blood flow without compromising systemic blood pressure or worsening V/Q mismatch
NO life
short-life (seconds) dose 5-20ppm
testing for NO toxicity
methemoglobin
treatment alternative to iNO
Revatio (Sildenafil PDE5)-long-term not recommended
Milrinone
tidal volume
amount fo gas moved during one normal inspiration and expiration
Functional Residual Capacity FRC
volume of gas left in the lung after a normal expiration
residual volume
minimum lung volume possible-air left in lung after max expiration
vital capacity
maximum amount of air that can be moved
total lung capacity
total amount of volume present in lung
minute volume
combination of tidal volume and respiratory rate
anatomic dead space
part of airway where NO gas exchange occurs
physiological deas space
alveoli that is ventilated but under or not perfused
V/Q ratio
balance between ventilation (airflow at the alveoli) and perfusion (blood flow entering the lungs)
V/Q mismatch
lungs are ventilated but not perfused
or lungs are perfused but not ventilated
leads to hypoxemia and hypercarbia
lung development is completed by what age?
16-18 years of age
asphyxia symptoms
progressive hypoxia, hypercarbia, acidosis
side effects of Prostoglandin E
apnea or respiratory depression
side effect of methylxanthine
gastroesophageal reflux
anatomic dead space
conducting airway
wasted ventilation
the amount of ventilation that does NOT participate in gas exchange
oxyhemoglobin dissociation curve
a relation between dissolved oxygen and the affinity for oxygen by the hemoglobin molecule
oxyhemoglobin curve shifts to the right
caused by decrease in pH
oxyhemoglobin dissociation curve shifts to the left
caused by increase in pH
chronic hypoxia caused what electrolyte imbalance
decreased chloride
respiratory distress may lead to what?
hypoglycemia
false reading on pulse oximetry is due to what?
phototherapy
PEEP may cause an increase in what?
PVR pulmonary vascular resistance
increased PEEP cause what?
barotrauma
what factor increases PVR
sepsis
side effect of surfactant
pulmonary hemorrhage
normal ABG values
pH (between 7.35 - 7.45);
CO2 (between 35 - 45 mmHg);
HCO3 (22-26 mEq/L)
“sigh: setting in HFV
decrease microatelectasis and recruit alveoli
how antenatal steroids work?
accelerate the rate of glycogen depletion
results in thinning the intra-alveolar septa and increases the size of the alveoli.
burned out xray
over exposed xray
intrauterine pass of meconium theory include what?
maternal HTN
