John T. Gallagher, MPH, RRT‐NPS
Critical Care Coordinator, Pediatric Respiratory Care
University Hospitals, Rainbow Babies & Children’s Hospital
Cleveland, Ohio John.Gallagher@uhhospitals.org
yyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyy
yyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyy
yyyyyyyyyyyyyyyyyyyyyyyyyyyyyyyooooooooooooooo
oooooooooooooooooooooooooooooooooooooooooo
oooooooooooooooooooooooooooooooooooooooooo
oooooooooooooooooooooooooooooooooooooooooo
oooooooooooooooooooooooooooooooooooooooooo
oooooooooooooooooooooooooooooooooooooooooo
ooooooouuuuuuuuuuuuuuuuuuuuuuuuuuuuuuuuuu
uuuuuuuuuuuuuuuuuuuuuuuuuuuuuuuuuuuuuuuu
uuuuuuuuuuuuuuuuuuuuuuuuuuuuuuuuuuuuuuuu
uuuuuuuuuuuuuuuuuuuuuuuuuuuuuuuuuuuuuuuu
uuuuuuuuuuuuuuuuuuuuuuuuuuuuuuuu
ƒThe Lung
ƒThe Baby
ƒThe Machines
ƒThe Evidence
ƒThe Practice
General Precautions
y RDS occurs in roughly 50% of infants born < 30 weeks gestation
y Failure to give antenatal steroids for expected preterm infants significantly increases risk of RDS
y Highest incidence of BPD results from care provided in first 24 hours
y Greatest chance for IVH exists when unstable MAP and a PaCO2 > 66 occur simultaneously
y Grade III/IV IVH and/or PVL increases the chances of developing cerebral palsy, developmental delays, and seizure disorders
Neonatal Considerations
y
y
y
y
y
y
Stages of Lung Development
Respiratory Distress Syndrome
The Role of Surfactant
Susceptibility to Injury
Risk of Infection
Bronchopulmonary Dysplasia
http://www.epigee.org/fetal3.html
Stages of Lung Development
y
y
y
y
y
Embryonal Stage
Pseudoglandular Stage
Canalicular Stage
Saccular Stage
Alveolar Stage
4 – 8 weeks
8 – 16 weeks
17 – 26 weeks
26 – 36 weeks
36 weeks ‐ term
Embryonal Stage
y Weeks 3 ‐ 8 y Primitive development
y First 2 months of gestation
y Lung bud emerges from pharynx at 26 days
y Elongates and forms 2 buds & trachea
y Separation from esophagus
y Airway branching occurs, 10 R, 9 L
y Mesenchyme is undifferentiated
y Diaphragm complete by week 7
4 Weeks
5 Weeks
6 & 8 Weeks
(Walsh, Czervinske, & DiBlasi, 2010)
Pseudoglandular Stage
y Weeks 8 – 16
y Extensive subdivision of conducting airways
y Permanent patterning
y Subsequent growth is in size only
y Most peripheral are terminal bronchioles
y Cilia appear on trachea & mainstem at 10 wks
y Cilia appear on peripheral airways by 13 wks
y T‐Lymphocytes found by 14 wks
y Maybe the beginnings of cartilage?
Canalicular Stage
y Weeks 17 – 26
y Appearance of vascular channels, capillaries
y Capillaries develop at 20 weeks
y
y
Increasing number by 22 weeks
Epithelial cells differentiate into type I & II cells
y
Occurs at 20 – 22 weeks
VIABILITY BEGINS
y Survival becomes possible at 22 – 24 weeks
y Acinus formation
y Gas exchange possible
y
Saccular Stage
y Weeks 26 – 36
y Formerly thought of as the last stage
y Terminal structures are saccules
y
y
Smooth‐walled, cylindrical Secondary crests protrude into saccules
y
Capillary net drawn in
Further separation results
y Subsaccules with surrounding capillaries
y “Alveoli” once bordered on three sides
y
Alveolar Stage
y Week 36 – Term
y Debate over inception of alveoli
y Maturation & proliferation a post‐natal event
y Alveoli at birth: 20 – 150 million
y Mean number: 50 ‐ 100 million at term birth
y Adults have 300 million
y Lungs are not done growing at birth!
Fetal Lung Fluid
y
y
y
y
y
y
y
Fetal lungs secrete 250 – 300 ml liquid /day
Flows from terminal airways up to oropharynx
Swallowed or expelled into amniotic fluid
Essential for normal lung development
Pulmonary circulation is major source
Production / Drainage balance is essential
Clearance continues in first hours after birth
Post‐natal Lung Growth
y
y
y
y
y
y
Up to 80% of total alveoli may develop after birth
Lung volume will increase 23‐fold
Alveolar number will increase 6‐fold
Majority of formation occurs within 1.5 years
Lungs then grow proportionally with body
Alveoli continue to grow in size until thoracic growth is completed Pulmonary Hypoplasia
y
y
y
y
y
y
y
y
y
Too few cells, too few alveoli, too few airways
Present in 10 – 25% of neonatal autopsies
Diaphragmatic hernia – 1 in 4000 births
Compression of lung is major factor
Earlier compression is greatest severity
Osteogenesis imperfecta
Thoracic Dystrophies, tumors, etc
Oligohydraminos
Glucocorticoids? Alveolar Cell Development
y During development, epithelial cells differentiate into highly specialized type I and type II pneumocytes
y Type I pneumocyte – squamous cells
y Gas permeable membrane y Type II pneumocyte – cuboidal appearing
y Surfactant production, storage, secretion, reuse
y Surfactant
y Lowers surface tension within alveolus
y Inadequate development will likely lead to Respiratory Distress Syndrome (RDS)
Respiratory Distress Syndrome
y First described in 1903
y Affects premature infants with inadequate lung development
y Dx in 60% of infants born < 28 weeks
y Occurs in 10 % of preterm births (< 37 weeks)
y Mortality rate 5‐10%, 5th leading cause of death < 1 yo
y Higher Risk
y Diabetic mothers
y Multiple births
y C‐Sect before onset of labor
Respiratory Distress Syndrome
y Associated with a deficiency of pulmonary surfactant and abnormal lung surface tension properties
y Results from immature cell and vascular development of the lungs
y Develops into:
y Reduced alveolar recruitment
y Decreased FRC
y Decreased Compliance
y Increased Resistance
y V/Q Mismatch
The Role of Surfactant
y A complex aggregate of phospholipids and surfactant – specific proteins produced endogenously
y Major components are preserved across species
y Saturated phosphatidycholine species
y Surfactant protein B
y Surfactant protein C
y Secreted in sufficient amounts to prevent RDS after 35 weeks gestation
y Given exogenously to treat the effects of RDS by reducing surface tension and activating Type II cells
Factors that Modify Surfactant Function
y Inactivation ‐ commonly caused by lung injury
y Activation ‐ by interaction of lung with surfactant
y Antenatal Steroids
y Increase activation
y Decrease inhibition
y Improve dose‐response curve for surfactant
y Increase in Gestational Age
y Increase in lung gas volume
y Lung less easily injured
y Endogenous surfactant less sensitive to inactivation
y More activation of treatment surfactant
Susceptibility to Injury
y Lung Development
y Free Radicals
y Reactive Oxygen Species (ROS)
y Induce tissue damage via oxidative stress
y Antioxidants
y Mechanical Ventilator Induced Lung Injury (VILI)
y Immaturity
y Inflammation
y Trauma
Lung Injury
y Ventilator induced lung injury (VILI) is characterized by:
y Barotrauma – Excessive pressure in airways
y Volutrauma ‐ Excessive tidal volume delivery y Atelectrauma – Shear injury related to repetitive cycling of distal airways at suboptimal lung volumes
y Biotrauma – consequent release of biochemical substances that instigate pulmonary inflammation Risk of Infection
y Chorioamnionitis
y Clinical associations
y Preterm Premature Rupture of Membranes (PPROM)
y
y
Gestational Age
y
y
Decreased incidence of RDS
Chorio = decreased death < 26 wks
VLBW infants: Ventilated vs. Not Ventilated
y
Chorio = increased BPD if ventilated > 7 days
Bronchopulmonary Dysplasia
y First described in 1967 by Northway & Assoc.
y Lung injury from prolonged exposure to high FiO2 and high ventilating pressures.
y Can result from the treatment of RDS
y Pathophysiology linked to four factors
y Oxygen toxicity
y Barotrauma
y Presence of PDA
y Fluid overloading
Delivery Room y 2010 NRP Guidelines emphasize need for effective ventilation
y Use of t‐piece resuscitators gain wide attention
y Research suggest variability by clinician Delivery Room y T‐Piece Resuscitator
Xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx
xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx
xxxxxxxxxxxxxxxxxxxxxxxxxxxxxx
xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx
xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx
xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx
xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx
xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx
xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx
xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx
xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx
Fisher & Paykal
NeoForce
GE Healthcare
Transporting Infants
Neopuff™
Powerless, Pneumatically driven, Manually controlled pressure control ventilation
MVP 10™
Powerless, Pneumatically driven, Manually controlled pressure control ventilation
CrossVent II™
Powered, Pneumatically driven, Electronically controlled pressure & volume control ventilation
Transporting Infants
By Air
By Land By ICU
http://www.umc.edu/
http://iuhealth.org/health‐professionals/lifeline/services/pediatric‐neonatal/
http://kalittamedflight.com/equipment/equipment‐details/
Intensive Care Ventilation
y Non‐Invasive Ventilation
y Limited Frequency of 1 – 50/min
y Conventional Ventilation
y Frequency of 1‐150/min
y High Frequency Ventilation
y Frequency of 150‐900/min
AL VENTILATOR
IC
N
A
H
EC
M
S:
T
EN
T
N
CO
DANGEROUS!
Non‐Invasive Ventilation
y Why NIV?
y Even short‐term invasive mechanical ventilation in RDS has been associated with
y
y
y
Inflammation and injury
Reduced efficacy of endogenous surfactant
Arrest of alveolar growth and development
y Early in the evolution of the science
y Nasal interface dilemma
Drager BabyFlow
RAM Cannula
Non‐Invasive Ventilation
y Nasal Intermittent Mandatory Ventilation (NIMV)
y Nasal Neurally Adjusted Ventilatory Assist (NNAVA)
y Sigh Continuous Positive Airway Pressure (SiPAP)
y Nasal High Frequency Ventilation (NHFV)
Diblasi, Respiratory Care, 2011
Non‐Invasive Ventilation
y No difference in choice of NIMV vs SiPAP
y Both a valid option to CMV
y Theoretical benefits of both styles
y Vt enhancement
y Improved FRC
y Improved Paw
y Reduced apneas
Ricotti, et al, J Matern Fetal Neonatal Med, 2013
Conventional Ventilation
y
y
y
y
y
y
y
y
VIP Bird Gold Ventilator
AVEA Ventilator
Bear Cub 750
Newport Wave
Newport e360
Drager Babylog VN500
SERVO‐i Ventilator
GE Carestation
Drager Babylog VN500
Conventional Ventilation
Conventional Ventilation
y Volume Control
y Constant volume
y Constant flow rate
y Lower Paw
y Better MV control
y Not favorable with cuffless ETT
y Original NICU vent
y Fallen out of favor
Conventional Ventilation
y Pressure Control
y Preset pressure limit
y Variable flow rate / Decelerates
y Higher Paw
y Less MV control
y More favorable with cuffless ETT
y 2nd generation NICU vent
y Commonly used
Conventional Ventilation
y Dual Control
y “Volume‐targeted, Pressure‐limited”
y Variable flow rate
y Microprocessor servo‐
controls the pressure level in response to airway resistance and lung compliance
y Comfort of pressure control, maintenance of volume
Key Points to CMV
y Developing a neonatal unit ventilation protocol for the preterm baby is best approach
y Delivery Room
y Non‐invasive support
y Intubation Criteria
y Surfactant Administration
y Vent modes & setting
y Escalating criteria
y Weaning / Extubating
y Post‐extubation care
Sant’Anna & Kezler, 2012 Pediatrics
High Frequency Ventilation
y High Frequency Oscillatory Ventilation
y SensorMedics 3100A Ventilator
y
Operating as an independent ventilator, the 3100A delivers tidal
volumes less than dead space with an active exhalation feature while maintaining a constant mean airway pressure
y High Frequency Jet Ventilation
y Bunnell Life Pulse Ventilator
y
Used in conjunction with a conventional ventilator, the Life Pulse delivers jet pulses to the airways through a separate side lumen to the endotracheal tube
3100A
Why do dogs pant?
The developers of the oscillator wanted to know!
•3100A approved in 1991 for Neonatal Application for the treatment of all forms of respiratory failure. •3100B approved in 1995 for Pediatric Application, for patients >35kg with no upper weight limit. For treating selected patients failing conventional ventilation.
Working with the oscillator is like a day at the beach.
It’s all about the air currents and waveforms!
Flow Properties
y Bulk Axial Flow
y Asymmetrical Velocity Profiles /
Taylor Dispersion
y Augmented Diffusion
y Pendelluft
Theory of Ventilation
HFOV delivers very small tidal volumes at very high rates via a sinusoidal waveform, all while maintaining a continuous, optimal lung volume In CMV, controls for oxygenation and ventilation are overlapped
20
15
Ventilation
Pressure (cmH2O)
10
Oxygenation
5
0
Time (sec)
1 Conventional
20
HFOV
15
Pressure (cmH2O)
10
5
0
Time (sec)
1 20
In HFOV, controls for oxygenation and ventilation are relatively separate
Ventilation
HFOV
15
Pressure (cmH2O)
10
Oxygenation
5
0
Time (sec)
1 HFOV Operation
•
•
•
•
•
•
Electrically powered, electronically controlled piston‐diaphragm oscillator Paw of 3 ‐ 45 cmH2O
Pressure Amplitude from 8 ‐ 110 cmH2O
Frequency of 3 ‐ 15 Hz
Inspiratory Time 30% ‐ 50%
Flow rates from 0 ‐ 40 LPM
•
Oxygenation is primarily controlled by the Mean Airway Pressure (Paw) and the FiO2
•
Ventilation is primarily determined by the stroke volume of the piston. SV is determined by Amplitude and Frequency.
Oxygenation
• The Paw is used to inflate the lung and optimize the alveolar surface area for gas exchange.
• Paw = Lung Volume
Mean Airway Pressure (Paw)
Paw is created by a continuous bias flow of gas past the resistance (inflation) of the balloon on the mean airway pressure control valve.
“Super‐CPAP” system to maintain lung volume
•
PVR is increased with:
• Atelectasis • Loss of support for extra‐alveolar vessels • Over expansion
• Compression of alveolar capillary bed
•
The lung must be recruited, but guard against over expanding.
V/Q Matching
Image courtesy of
Alveolar ventilation during CMV is defined as
F x Vt
Alveolar Ventilation during HFV is defined as
F x Vt 2
* Therefore, changes in volume delivery (as a
function of Delta-P, Freq., or % Insp. Time)
have the most significant affect on CO2
elimination
Amplitude (∆P)
Primary control of CO2 is by the stroke volume produced by the Power Setting.
Gerstmann D.
proximal
90% pressure attenuation occurs when using a 2.5 ETT
trachea
alveoli
P
T
1 Hz = 60 cycles
•
The stroke volume will increase if
– The amplitude increases (higher delta P) – The frequency decreases (longer cycle time)
Stroke
volume
% i‐Time
• The % Inspiratory Time
controls the time for
piston displacement,
controlling CO2
elimination.
• Increasing %
Inspiratory Time will
also affect lung
recruitment by
increasing delivered
Paw.
•
•
•
•
•
•
I/E Ratio adjustable with Inspiratory time control
Inspiratory time = Forward movement piston
Expiratory time = Backward movement piston
Backward movement piston = active exhalation Recommended Insp. time = 33% (prevents air‐trapping)
33%
+
‐‐
67%
Inspiratory time adjustable: 30% - 50%
Piston Position
Which mode should I use?
y Preventing CLD?
y No evidence
y HFO or HFJ?
y No difference
y CV vs. HFO?
y No difference in LOV or Mortality
y Better oxygenation with HFO at 72 hours
Duyndam, et al, Critical Care 2011 Which mode should I use?
y HFOV vs. SIMV
y VLBW infants were extubated sooner on HFOV
y Improved respiratory outcome with HFOV
y No increase in associated morbidities with HFOV
Courtney, et al, NEJM 2002 Courtney, et al, NEJM 2002 Inhaled Nitric Oxide
y FDA approved to treat infants (>34 wks) with hypoxic respiratory failure with associated pulmonary hypertension
y Ballard, et al 2006 found iNO improved pulmonary outcomes for preterm infants (BPD)
y NIH Consensus statement 2011 suggest that iNO use in preterm had equivocal results
Home Care Ventilation
y Tracheostomy rates for ELBW and VLBW are higher than previously reported
y Survival rights are high and are increasing for the smaller patients
y Developmental delay is common among all infants requiring prolonged mechanical ventilation
Overman, et al, Pediatrics 2013
Home Care Ventilation
y Family preparation
y Trach
y Ventilator
y Resuscitation
y Selection of ventilator
y Portability
y Sophistication
y DME support
y Professional home care
http://www3.gehealthcare.com/
Way to Go!
http://slodive.com/inspiration/thumbs‐up‐symbol/
John.Gallagher@uhhospitals.org
John T. Gallagher MPH, RRT‐NPS
Critical Care Coordinator, Pediatric Respiratory Care
University Hospitals, Rainbow Babies & Children’s Hospital
References
Bancalari, E. (2008). The Newborn Lung. Philadelphia: Saunders.
Donn, S., & Sinha, S. (2012). Manual of Neonatal Respiratory Care. New York: Springer.
Walsh, B., Czervinske, M., & DiBlasi, R. (2010). Perinatal and Pediatric Respiratory Care. St. Louis: Saunders.
Whitaker, K. (2001). Comprehensive Perinatal & Pediatric Respiratory Care.
Clifton Park: Delmar.