Transcript Outline of talk - Respiratory Therapy

‘Golden Hour’
Lung Protective Strategy from Birth
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Proper pressures in the DR
Proper FiO2 in the DR (blended)
Surfactant in the DR
CPAP in the DR
Consistent CPAP in the NICU
Reduced SIMV in the NICU
good judgement
informed jugement
Neo-Puff in the DR
 manual
ventilation of
babies <30 weeks gest.
 Used for all transport
ventilation for all babies
Neo-Puff Infant Resuscitator
easy to use,
manually operated
gas-powered.
Controlled and Precise Peak Inspiratory
Pressure (PIP)
The Neopuff™ Infant Resuscitator will
inflate the baby’s lungs & provide
optimum oxygenation by delivering
consistent PIP with each breath, limiting
the risks associated with under or over
inflation at uncontrolled pressures.
Consistent and Precise Positive End
Expiratory Pressure (PEEP)
The Neopuff™ Infant Resuscitator
maintains Functional Residual Capacity
(FRC) by providing a consistent PEEP
throughout the resuscitation process.
The desired PIP
is set by turning the
inspiratory pressure control.
The desired PEEP
is set by adjusting the
T-piece aperture.
Pressure/Volume
Over Weaning damages too
Ventilator-Associated Lung Injury
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Barotrauma (air leak)
Oxygen toxicity
Ventilator associated pneumonia
Over-distention
De-recruitment
Biochemical Injury
Cytokines,
prostanoids,
Leukotrienes,
reactive oxygen species,
protease
Distal Organs
neutrophil
MOSF
Death
Biophysical Injury
•Shear
•Overdistention
•Cyclic stretch
•Inc. intrathoracic pressure
•Inc alveolar cap permeability
•Dec cardiac output
•Dec organ perfusion
•Tissue injury secondary to
•Inflamatory mediators/cells
•Impaired O2 delivery
•bacteremia
Slutsky and Tremblay
Am J Respir Crit Care Med
1998; 157: 1721-1725
normal
lungs
5 min of
45 cm H2O
20 min of
45 cm H2O
Dreyfuss, Am J Respir Crit Care Med 1998;157:294-323
14/0
45/10
45/0
Webb and Tierney, Am Rev Respir Dis 1974; 110:556-565
esophageal
intubation
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Pulmonary
Interstitial
Emphesema
to Pneumo-
Assessment
•Chest x-ray AP
•
8 rib conventional
•
9-10 rib Hi-Fi
•Rise & fall of chest (slight per NRP)
•Listen to breath sounds
•Vt 5-7 ml/kg (3-5 spont.)
•follow ABGs
To Increase Mean Airway Pressure
1. Increase flow
2. Increase peak pressure
3. Lengthen inspiratory time
4. Increase PEEP
5. Increase Rate
Pressure Wave
Pressure
Time
TYPES OF MECHANICAL
VENTILATION
negative pressure ventilation
o positive pressure ventilation
o high-frequency ventilation
o non-invasive positive pressure ventilation
o
Body Box:
Outline
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Respiratory mechanics and gas exchange
Factors affecting oxygenation and carbon
dioxide elimination during mechanical
ventilation
Blood gas analysis
Ventilatory management: basics and specifics
High frequency ventilation: the basics
Overview
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Mechanical ventilation is an integral part of
neonatal intensive care, and has led to increased
survival of neonates over the last 3 decades
Advances in knowledge of neonatal respiratory
physiology have led to optimization of techniques
and strategies
Conventional mechanical ventilation (CMV) is
most often used, despite the advent of HFV and
SIMV
Overview
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Respiratory failure in neonates has significant
morbidity and mortality (although less than in the
past)
Optimal ventilatory management will reduce the
risk of chronic lung disease
Optimal ventilatory management should be
individualized and be based upon the
pathophysiology and certain basic concepts of
mechanical ventilation
Concepts
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Goal of mechanical ventilation: to improve gas
exchange and to sustain life without inducing lung
injury
Factors that should influence ventilator adjustment
decisions:
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Pulmonary mechanics
Gas exchange
Control of breathing
Lung injury
Pulmonary mechanics
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Compliance
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Property of distensibility of the lungs and chest wall
Change in volume per unit change in pressure
C = D Volume
D Pressure
Neonatal lung
u Normal 0.003-0.006 L/cm H2O
u with RDS 0.0005-0.001 L/cm H2O
Pulmonary mechanics
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Resistance:
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inherent capacity of the air conducting system (airways
and ETT) and tissues to resist airflow
Change in pressure per unit change in flow
R = D Pressure
D Flow
Total cross-sectional area of airways
Resistance
Length of the airways
Flow rate
Density and viscosity of gas
Pulmonary mechanics
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Location of airway resistance:
Resistance
Distal -->
0
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5
10
15
20
Airway Generation
Distal airways contribute less to resistance due to
increased total cross-sectional area
Small ETT and high flow rates can increase
resistance markedly
Pulmonary mechanics
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Laminar flow (Distal airways)
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Driving pressure proportional to flow
R= 8 n l (n = viscosity ; l = length; r = radius)
p r4
Turbulent flow (Proximal airways)
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Driving pressure proportional to square of flow
Reynolds number (Re) = 2 r V d (d = density)
n
Pulmonary mechanics
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A pressure gradient between the upper airway and
alveoli is necessary for gas flow during inspiration
and expiration
The pressure gradient is required to overcome the
elasticity, resistance, and inertance of the respiratory
system
Equation of motion: P =
1 V+RV+IV
C
Elasticity+Resistance+Inertance
Pulmonary mechanics
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Time constant
l The time taken for the airway pressure (and
volume) changes to equilibrate throughout the
lung is proportional to the compliance and
resistance of the respiratory system
l Time constant = Compliance x Resistance
Pulmonary mechanics
% change in pressure in relation to time
Change
in pressure (%)
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100
80 63
60
99
86
40
20
0
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95 98
1
2
3
4
5
Time constants
Almost full equilibration: 3-5 time constants
Pulmonary mechanics
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Healthy term neonate:
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C = 0.004 L/cm H2O; R = 30 cm H2O/L/sec
T = 0.004 x 30 = 0.12 sec
Time constants Time (sec)
% equilibration
1
2
3
0.12
0.24
0.36
63
86
95
5
0.60
99
RDS: Shorter time constant
Pulmonary mechanics
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Application of the concept of time constant
l Short TI : decreased tidal volume delivery
l Inadequate TE: Gas trapping (
FRC,
inadvertent PEEP)
l Heterogeneous lung disease (BPD):
different regions of the lung have different
time constants; tendency for atelectasis and
hyperexpansion to co-exist
Gas exchange
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Total minute ventilation = tidal vol x freq
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VE = VT x f
Alveolar ventilation (VA) = Useful (fresh gas)
portion of minute ventilation that reaches gas
exchange units; excludes dead space (VD)
VA = (VT-VD) x f
l Alveolar ventilation equation:
VA (L/min) = VCO2
(ml/min) x 0.863 (BTPS
PACO2 (mm Hg)
corr.)
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Gas exchange
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Alveolar gas equation:
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If R=1, each molecule of O2 removed from alveoli is
replaced by one molecule of CO2
PAO2 = PIO2 - PACO2
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Average normal value for R = 0.8
PAO2 = FIO2 x (PB-PH2O) - PACO2x FIO2+ 1- FIO2
R
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PaCO2 = effective PACO2
True PACO2 = PETCO2
Gas exchange
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Ventilation-Perfusion matching:
matching of gas flow and blood flow required for
successful gas exchange
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VA = Alveolar ventilation
Q
Pulmonary blood flow (Fick method: O2)
= 0.863 x R x (CaO2 - CVO2)
PACO2
V/Q mismatching usually relevant to effect on
alveolar-arterial PO2 difference: (A-a)DPO2
Gas exchange
O2-CO2 diagram
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0.2
0.5
1.0
V/Q = 0
Ideal
1.5
V/Q =
40
60
80
100
120
140
P O2 (mm Hg)
8
20
V/Q = 0.84
0
PCO2
40
v
160
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Gas exchange
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Causes of hypoxemia
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V/Q mismatch
Right to left shunt (venous admixture)
Hypoventilation (e.g. in apnea)
Diffusion abnormalities
Causes of hypercapnia
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Hypoventilation
Severe V/Q mismatch
Gas exchange
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Factors involved in gas exchange during
mechanical ventilation
l Oxygenation
l Carbon dioxide elimination
l Gas transport mechanisms
l Patient - ventilator interactions
Gas exchange
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Factors affecting oxygenation
l Mean airway pressure (MAP) : affects V/Q
matching. MAP is the average airway pressure
during respiratory cycle
MAP = K (PIP-PEEP) [TI / (TI+TE)] + PEEP
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Oxygen concentration of inspired gas (FIO2)
Gas exchange
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MAP increases with increasing PIP, PEEP,
TI to TE ratio, rate, and flow
PIP
Pressure
Rate
Flow
TI
PIP
PEEP
PEEP
TI
TE
Time
Gas exchange
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Relation of MAP to PaO2 not linear; is like an
inverted “U”:
l Low MAP:
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Atelectasis--> very low PaO2
High MAP:
hyperinflation--> V/Q mismatch; intrapulmonary
shunt, hypoventilation due to distended alveoli
u decreased cardiac output --> decreased oxygen
transport despite adequate PaO2
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Gas exchange
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For the same change in MAP, changes in PIP
and PEEP improve oxygenation more than
changes in I:E ratio
Reversed I:E ratios increase risk of air-trapping
PEEP levels higher than 6 cm H2O may not
improve oxygenation in neonates
Attainment of optimal MAP may allow
weaning of FIO2
Atelectasis may lead to sudden increase in
required FIO2
Gas exchange
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Carbon dioxide elimination
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Proportional to alveolar ventilation (VA) which depends
on tidal volume (VT) and frequency (rate)
VT changes more effective (but more barotrauma) : dead
space constant, so proportion of VT that is alveolar
ventilation increases to a greater degree with increases in
VT
u VT 4 --> 6cc/kg (50%
) with dead space of 2 cc/kg
increases VA from 2 (4-2) to 4 (6-2) cc/kg/breath
(100% )
Gas exchange
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Clinical estimation of optimal TI and TE:
Short TI
Optimal TI
Long TI
Inadeq VT Short insp. plateau Long plateau
Chest
Wall
Motion
Short TE
Air trapping
Chest
Wall
Motion
Time
Optimal TE
Long TE
Short exp. plateau Long exp. plateau
Gas exchange
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Synchrony vs. Asynchrony + “fighting”
l Synchrony augments ventilation, improves
CO2 elimination, decreases hypoxic
episodes
l Asynchrony leads to poor tidal volume
delivery, and impairs gas exchange
l Active exhalation (exhalation during
ventilator breath) increases risk of hypoxic
episodes
Blood gas analysis
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Arterial blood gas analysis the “gold standard”
Interpretation:
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pH: Is it normal, acidotic, or alkalotic?
PCO2: Is it normal, (respiratory acidosis), or
(respiratory alkalosis)?
HCO3: Is it normal, (metabolic acidosis), or
(metabolic alkalosis)?
Simple disorder or mixed? Compensated or not?
PO2: Normal, hypoxia, or hyperoxia?
Blood gas analysis
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Normal values (1 hr age, not ventilated)
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Target values
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Preterm: pH 7.28-7.32, PCO2 35-45, PO2 50-80
Term: pH 7.30-7.35, PCO2 35-45, PO2 80-95
RDS: pH > 7.25, PCO2 45-55, PO2 50-70
BPD: pH > 7.25, PCO2 45-70, PO2 60-80
PPHN: pH 7.50-7.60, PCO2 25-40, PO2 80-120
Remember! O2 content determined mostly by
SpO2 and Hb%.
Blood gas analysis
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Common errors:
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Infrequent ventilator adjustments made only
when ABG (q4/q6) is obtained. In acute phase
of RDS or PPHN, adjustments should be made
with chest rise, SpO2, TcPO2/PCO2 trends
Room air contamination: PCO2, PO2(if <150
torr ). Amount in butterfly set sufficient !
Liquid heparin /saline contamination: pH same,
but lower PCO2 (mimics compensated metabolic
acidosis)
Ventilatory management
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Indications:
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Clinical: Absolute: Apnea (intractable),
gasping, cyanosis not responsive to O2 by hood
Relative: Severe tachypnea / retractions
Laboratory (while on CPAP or FiO2 > 0.7):
pH < 7.25 with PCO2 > 60
(or) PO2 < 45- 50 and / or SpO2 < 85
Other: Surgical procedures, compromised
airway
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PIP:
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Ventilator settings
affects MAP (PO2) and VT (PCO2)
PIP required depends largely on compliance of
respiratory system
Clinical: gentle rise of chest with breath,
similar to spontaneous breath
Minimum effective PIP to be used. No relation
to weight or airway resistance
Neonate with RDS: 15-30 cm H2O. Start low
and increase.
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PEEP:
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Ventilator settings
affects MAP (PO2), affects VT (PCO2) depending on
position on P-V curve
Volume
PEEP PIP
Pressure
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older infants (e.g. BPD) tolerate higher levels of PEEP
(6-8 cm H2O) better
RDS: minimum 2-3, maximum 6 cm H2O.
Ventilator settings
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Rate:
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affects minute ventilation (PCO2)
In general, rate ---> PCO2
Rate changes alone do not alter MAP (with
constant I:E ratio) or change PO2 , unless PVR
changes with changes in pH
However, if rate --> TE < 3TC --> gas
trapping--> decreased VT--> PCO2
Minute ventilation plateaus, then falls with rate
Ventilator settings
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TI and TE:
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Need to be 3-5 TC for complete inspiration and
expiration (Note: TC exp = TC insp)
Usual ranges:
TI sec TE sec
u RDS
0.2-0.45 0.4-0.6
u BPD
0.4-0.8 0.5-1.5
u PPHN
0.3-0.8 0.5-1.0
Chest wall motion / VT may be useful in
determining optimal TI and TE
Ventilator settings
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I : E Ratio
l When corrected for the same MAP, changes in
I:E ratio do not affect gas exchange as much as
changes in PIP or PEEP
l Changes in TI or TE do not change VT or PCO2
unless they are too short (< 3 TC)
l Reversed I:E ratio: No change in mortality or
morbidity noted in studies. Not often used.
May improve V/Q matching and PO2 at risk of
venous return and gas trapping
Ventilator settings
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FiO2
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affects oxygenation directly
with FiO2 <0.6-0.7, risk of oxygen toxicity less
than risk of barotrauma
to improve oxygenation, increase FiO2 to 0.7
before increasing MAP
during weaning, once PIP is low enough,
reduce FiO2 from 0.7 to 0.4. Maintenance of
adequate MAP and V/Q matching may permit a
reduction in FiO2
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Flow:
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Ventilator settings
affects pressure waveform
minimal effect on gas exchange as long as
sufficient flow used
increased flow--> turbulence
higher flow required if TI short, to maintain TV
flow of 8-10 lpm usually sufficient
change of flow may affect delivery of NO or
anesthesia gases
Ventilatory management
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RDS:
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Pathology: decreased compliance, FRC
Once diagnosis established, and if PO2<50 on
40% oxygen: CPAP (or) early intubation and
surfactant. (Prophylactic CPAP for ELBW not
useful)
Ventilation if FiO2 > 0.7 required on CPAP
Surfactant q 6 hrs if intubated and FiO2 > 0.30.4 (Survanta / Infasurf / Curosurf better than
Exosurf). Usually 1-2, rarely 4 doses required.
Ventilatory management
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RDS (continued):
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Use lowest PIP required
moderate PEEP (4-5 cm H2O)
permissive hypercarbia (PaCO2 45-55 mmHg
instead of 35-45 is safe, and need for
ventilation in first 4 days)
limited use of paralysis, aggressive weaning
chest PT not useful, maybe dangerous in
acute phase (increases IVH)
Ventilatory management
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Chronic lung disease / BPD:
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usually heterogeneous lung disease - different
areas of lung with different time constants
increased resistance, frequent exacerbations
higher PEEP often helpful (4-7 cm H2O)
longer TI and TE, with low rates
hypercarbia and compensated respiratory
acidosis often tolerated to avoid increased
lung injury
Ventilatory management
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PPHN:
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ventilator management controversial
FiO2 adjusted to maintain PaO2 80-100 to
minimize hypoxia-mediated pulmonary
vasoconstriction
ventilatory rates and pressures adjusted to
maintain mild alkalosis (pH 7.5-7.6), usually
combined with bicarbonate infusion
avoid low PaCO2 (<20 mm Hg) to prevent
cerebral vasoconstriction
Volume Guarantee
The ventilator automatically adjusts the inspiratory pressure
according to changes of compliance, resistance or
respiratory drive.
Pressure Support Ventilation
Working Principle of Breath
Termination
Erin Browne
Flow Sensor
Measurement Principle
T = 400°C
no gas flow
with gas flow
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Two tiny platinum wires are heated to 400°C
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Gas flow cools the wire down
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From the amount of cooling the amount of gas flowing can be
calculated
Endotracheal Tube Leak
Lung Function Monitoring
Clinical Applications
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Identification of Lung Overdistention
Prediction of successful extubation
Prediction of risk of BPD development
Response to Surfactant or Brochodilators
Teaching tool
Titration of optimal PEEP
Trend in development of disease
Check of compliance during HFV
recognition of recovery from suctioning
O
S
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High frequency ventilation
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Techniques
HFPPV HFJV
VT
>dead sp > or < ds
Exp
passive
passive
Wave- variable triangular
form
Entrai- none
possible
ment
Freq. 60-150 60-600
(/min)
HFFI
> or <ds
passive
triangular
none
300-900
HFOV
<ds
active
sine wave
none
300-3000
High frequency ventilation
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HFPPV
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conventional ventilators with lowcompliance tubing
ventilatory rates of 60-150/min
not very effective: minute ventilation
decreases with high frequencies
ventilator and circuit design are not optimal
for use at frequencies
High frequency ventilation
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HFJV (e.g. Bunnell Life Pulse HFJV)
l adequate gas exchange with lower MAP
l Servo pressure reflects volume ventilated:
u increases with improving compliance or
resistance or by peri-ET leaks
u decreased by worsening compliance,
resistance, obstruction, or pneumothorax
l Larger babies: 300 bpm; smaller ones: 500
bpm
High frequency ventilation
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HFJV (contd.)
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MAP controls PaO2, DP (and frequency) control
PaCO2. (MAP controls lung volume. PaO2 will not
respond to increased MAP if FRC normal)
smaller TV (DP) with higher PEEP better than
larger TV with lower PEEP (--> hypoxia with
hypocarbia)
Optimal PEEP: no drop in SpO2 when CMV off
Parallel conventional ventilation recruits alveoli
(use low rate : 1-3 bpm; 0-1 bpm if air leak)
High frequency ventilation
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HFOV (e.g. Sensormedics 3100A)
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Generally used at more MAP than CMV; optimal
MAP difficult to determine as CXR “rib space
counting” not very accurate
Frequency: 5-10 Hz better for CO2 elimination;
10-15 Hz better for improving oxygenation
maybe useful in airleak syndromes
maybe useful in PPHN; may decrease need for
ECMO esp. if combined with NO
High frequency ventilation
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HFFI (e.g. Infant Star with HFFI module)
l active expiration in Infant Star model
makes operation more like HFOV
l clinical studies have not shown it to be
superior to conventional ventilation
l more convenient: single ventilator for
CMV and HFV makes initiation and
weaning easier
High frequency ventilation
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Uses of HFOV/ HFJV/ HFFI :
l “rescue” for severe RDS
l air leak syndromes (pneumothorax, PIE)
l PPHN
Primary use controversial: risk of hypocarbia
(-->PVL) higher, and reduction of BPD or
airleaks seen in some, but not all, studies.
Summary
The practice of the art of mechanical
ventilation lies in the application of the underlying
science and physiologic concepts to the specific
clinical situation
An individualized flexible approach aimed at
maintaining adequate gas exchange with the
minimum of ventilatory support, both in
magnitude and duration, should optimize the
possible outcome
Combining IMV and HFV
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