ventilator management: what does it all mean?
TRANSCRIPT
Abstract
Neonatal ventilation has progressed
from a primitive adaptation of adult
ventilatory techniques to its own
science. An understanding of the
fundamental concepts involved is
essential in applying these newer
ventilator modalities to successful care
of the critically ill newborn. A
discussion of pulmonary function and
its application to the newer ventilator
strategies is presented with a historical
approach to the development of the
newer ventilator modalities.
n 2006 Elsevier Inc.
All rights reserved.
Keywords: Ventilation, Neonate,
Pulmonary function
From the Department of Neonatal Medicine,
Pomona Valley Hospital Medical Center, Pomona,
CA; Citrus Valley Medical Center, West Covina, CA;
and Western University Health Sciences, Pomona,
CA.
Address correspondences to Mitchell R. Gold-
stein, MD, FAAP, Department of Neonatal Med-
icine, 1135 South Sunset Ave., Suite # 406, West
Covina, CA 91790.
n 2006 Elsevier Inc. All rights reserved.
1527-3369/06/0602-0137$10.00/0
doi:10.1053/j.nainr.2006.03.003
VentilatorManagement:What Does ItAll Mean?
By Mitchell R. Goldstein, MD, FAAP
The functional differences in the neonatal lung are distinct to the
gestational age of the patient. Term newborn physiology includes a
functional alveolar bed with surfactant function that is not dissimilar to
the adult. The lungs of a 23-week gestation neonate are at a terminal bronchiolar
stage of fetal development in which alveolarization has not yet begun.
Physiologically and structurally, however, the neonate has different needs.
Ventilation must be specifically tailored to the needs of the individual patient.
Conventional mechanical ventilation clearly provides adequate support and
good outcomes for a number of patients but can be the source of barotrauma and
precipitate lung injury in others. Although traditional time-cycled pressure-
limited ventilation has been modified to included strategies to prevent excess
volume generation using newer modes such as Volume Guarantee (VG-Drager),
Pressure Support Ventilation (PSV-Viasys), and Pressure Regulated Volume
Control (PRVC-Maquet), there are still instances where these mechanisms are
insufficient to provide what is needed to prevent lung damage. One must
consider when the baby requires intubation, when conventional mechanical
ventilation should be discontinued, when oscillation becomes necessary, and
when a baby should be extubated.
Noninvasive Ventilation
Early investigations by Gregory and others led to the development of
continuous positive airway pressure (CPAP) for the treatment of respiratory
distress syndrome (RDS).1,2 Continuous positive airway pressure had a major
advantage over previous attempts to ventilate the neonate in that it provided the
necessary pressure to stabilize the airway while limiting the resistance incurred
with the placement of an endotracheal tube. The most challenging part of
delivering CPAP continues to be positioning and maintenance of the CPAP
device. Critics of the use of nasal CPAP (NCPAP) consider it a form of btortureQdespite consistent evidence that it can prevent the occurrence of chronic lung
disease in the most at risk premature populations.3-5 At pressures of 3 to 6 cm
H2O, NCPAP has prevented intubation, excessive periods of ventilation, and
other consequences of chronic ventilation. Nasal CPAP is not a panacea. Rises
in the oxygen requirement and increases in CO2 can indicate developing
atelectasis or excessive work of breathing. These infants may also require
intubation and surfactant where RDS is present. In certain neonatal intensive
care unit environments, NCPAP is much more successful than others.5,6 Recent
studies have demonstrated that the use of CPAP provided through continuous
Newborn and Infant Nursing Reviews, Vol 6, No 2 (June), 2006: pp 79-86 79
Table 1. Pulmonary Function Abbreviations and
Calculations
Vt Tidal volume Volume of air either
exhaled or inhaled
Airway
flow
V Flow of air either exhaled
or inhaled
Airway
pressure
PAW This is determined by
compliance, resistance,
80 Mitchell R. Goldstein
end expiratory ventilator pressure may not be as advan-
tageous as that provided by the bubble devices used in
early studies.7,8 Other devices using humidified high-flow
nasal cannula theoretically simulating CPAP (ie, using a
liter per minute flow without measuring pressure) have not
yet been proven to provide consistent benefit.9 Questions
have been raised about the safety of this mode in the
neonate as well.
tidal volume, and flow rate
VtEXP Expiratory tidal
volume
Volume of air exhaled
VtINSP Inspiratory tidal
volume
Volume of air inhaled
VE Minute ventilation Amount of gas expired over
1 min [RespRate (patient)
� VtEXP (spontaneous)] +
[VentRate �VtEXP (ventilator)]
PTP Transpulmonary
pressure
Pressure exerted on the
lungs to initiate inspiration
PES Esophageal
pressure
Airway pressure exerted on
the esophagus during
inspiration. This will be
diminished when the
endotracheal tube is in
place.
PIP Intrapleural
pressure
Pressure within the pleural
cavity
Kt Time constants Time it takes for pressure to
equilibrate between
proximal airway and
alveoli. Kt = Crs � Rrs
Crs Compliance of the
respiratory system
Elasticity or distensibility
of the lung
Rrs Resistance of the
respiratory system
Capacity of the airway or
lung to resist airflow
KtINSP Inspiratory time
constants
Time to effective delivery
of pressurized gas to level
of alveolus
KtEXP Expiratory time
constants
Time required for alveolus
to empty and recalibrate to
effective PEEP
Pulmonary Function
The newer modes of ventilation are dependent not
only on understanding the basics of bdialingQ in the
numbers but actually being able to read the pulmonary
function scalars and graphics. The ventilator settings
must fit the disease process. An understanding of
pulmonary function is important in any approach to
ventilation.10,11 There are several abbreviations common-
ly used when discussing pulmonary function. Pulmonary
function abbreviations used in this article are defined
in Table 1.
Tidal volume (Vt) monitoring has become a de facto
standard for neonatal ventilation. Inspiratory and expira-
tory tidal volumes should be distinguished. Inspiratory
tidal volume is a gauge of adequacy of spontaneous
ventilation but cannot be used to measure the effective-
ness of mechanical ventilation breaths. Issues of leak and
loss of volume in a compliant ventilator circuit must be
considered carefully. Tidal volume is electronically
integrated from airflow. Airway flow (V) is dependent
on many factors. The physical density of the gas, laminar
nature of the gas flow, and turbulence in the system can
affect the manner in which flow is administered to the
newborn. Airway flow is dependent on the airway
pressure (PAW) delivered over time in producing volume.
Assuming no leak and a noncompliant ventilator circuit,
expiratory tidal volumes are larger than inspiratory tidal
volumes secondary to decompression of the gas, warming
in the tracheobroncheal tree, and humidification (loss of
water). Using different ventilator modalities, VtEXP values
of 2 to 10 mL/kg may be acceptable. Lower values are
common in assisted modes of ventilation and higher tidal
volumes are necessary when only a certain proportion of
breathing is assisted. Particularly, in the premature infant,
5 to 7 mL/kg is considered normal tidal volume.12
Careful monitoring of the Vt along with radiographic
changes can optimize management and minimize over
distention during mechanical ventilation. As the sponta-
neous VtINSP approaches VtEXP of the ventilator, infer-
ences can be made regarding the neonate’s ability to take
over more ventilation and perhaps readiness for extuba-
tion to NCPAP.13
Minute ventilation (VE) is the amount of gas expired
over a minute. This is calculated using VtEXP. Minute
ventilation is defined by:
[RespRate (patient) � VtEXP (spontaneous) + VentRate]� VtEXP (ventilator).
Normal minute ventilation is 250 to 350 mL/kg per
minute. Assist modes of ventilation emphasize the
establishment of normal VE over higher tidal volumes. A
comparison of the contribution of VE from spontaneous
breaths and VE of the mechanical breaths can be useful in
Ventilator Management: What Does It All mean? 81
evaluating the progress of weaning from mechanical
ventilation using the assist modes.
Fig 1. The normal compliance loop in yellow is compared with
decreased compliance loop in blue. This pattern is commonly
seen in RDS. As compliance changes, that is, with surfactan
delivery, the loop will move toward the yellow diagram showing
improved compliance.
Compliance
An understanding of the differences between compli-
ance of the chest wall and the lung is vital to
understanding the principles of mechanical ventilation.
Although no amount of monitoring can substitute for
observation at the bedside, it is critical that there is an
understanding of what exactly is being monitored. There
is a difference between chest wall and total lung
compliance. The overly elastic (compliant) chest wall
can lead the clinician into thinking that the underlying
lung disease is worse than it actually is.14 This, in turn,
can lead to unnecessary ventilation, especially in the
at-risk premature with incomplete ossification of the
chest wall.
Compliance is measured as the lung or tidal volume
over the change in transpulmonary pressure (PTP). Trans-
pulmonary pressure is defined by the difference between
PAW and esophageal pressure (PES) or more accurately
intrapleural pressure (PIP). In the ventilated neonate, this
PES will approach 0 cm. Normal values of compliance
range from 1.3 to 3 mL/cm in neonates.15-22 Lower values
of static compliance have been invariably associated with
extubation failure, whereas high values (z1.3 mL/cm)
were associated with extubation success in 94% of
neonates studied.16 Documentation of an improving
compliance is essential in establishing the appropriate
timing for successful extubation.
Compliance is measured either dynamically or statical-
ly. Static compliance measures the change in pressure as
volume is fixed periodically during decompression.
Dynamic compliance is the slope of the point of end
inspiration and end expiration on the pressure volume
curve. Although it is not truly possible to accurately
describe static changes in pressure with a given volume,
because of its ability to be used continuously in line, there
is less disruption to ventilation. Most conventional
ventilators and conventional pulmonary function monitors
incorporate compliance measures as an enhanced function
set in their newer devices.
Although compliance measures can give a fair
estimation of the adequacy of pulmonary function and
can give a reasonable approximation of the improvement
noted in ventilation after an intervention such as the
administration of surfactant (Fig 1), there are situations
where compliance measurement will not suffice to
complete an understanding of the pathophysiology.
Characteristic of these exceptions to the rule are instances
where the volume displacement of the lung with a given
t
pressure improves beyond its elastic properties and
situations where a worsening compliance fixes the
volume of the lung bregardlessQ of the administered
pressure. Graphically, these situations produce a beaking
of the pressure volume curve with a characteristic bbird’sbeak Q evident in the upper right hand corner of the graph
(Fig 2). Recognition of this pattern is crucial to
avoid unnecessary barotrauma but often cannot be
discerned by measuring tidal volume or compliance
alone.23 In even the most compelling of situations, tidal
volume and compliance can appear normal despite
inordinate pressure administration.
The inspiratory limb and expiratory limb of the
compliance curve differ secondary to changes that have
occurred in the lung resulting in decreased recoil in
expiration. This relationship is referred to as Hooke’s law
and allows ventilation to occur by maintaining volume in
the passively pressurized lung during this phase. If the
lung is allowed to passively deflate, 70% to 80% of the
pressure will be lost within approximately 1 minute. In the
premature infant, with decreased surfactant and concurrent
atelectasis, this process worsens the respiratory symptoms
already seen with RDS.14
Terminal compliance measurement can be used in these
instances to demonstrate where beaking of the pressure
volume curve interferes with the intended ventilation. As
the ratio decreases below 1 and approaches 0, the
excessive pressure is not producing significant volumetric
displacement. Essentially, for the additional pressure cost,
there is no increase in ventilation. A number of the newer
ventilators have incorporated this measure as a guide to
whether the patient is overdistended. This concept may
Fig 2. The upper curve in yellow showed the normal relationship
of volume to pressure. The lower curve in blue shows the
bbeakingQ that is evident with too much pressure. A neonate with
the lower curve without the establishment of adequate ventilation
might be a candidate for high-frequency oscillation.
82 Mitchell R. Goldstein
currently be the most important tool available to clinicians
in avoiding significant barotraumas.23
Resistance
An understanding of resistance is also important to
modern ventilation techniques. An elevated resis-
tance is a major contributor to work of breathing in
neonates. Flow itself may be laminar or turbulent. Laminar
flow is simpler to analyze than turbulent flow. Turbulent
flow occurs with high flow rates, decreases in the diameter
of the airway or endotracheal tube, angulation of the
endotracheal tube in the airway, and/or the normal
branching that occurs in the developing lung.
Total (airway + tissue) respiratory resistance values for
normal neonates range from 20 to 40 cm H2O/L per
second; 50 to 150 cm H2O/L per second is commonly seen
in intubated neonates.24 The increased resistance encoun-
tered during intubation must be taken seriously in the
evaluation of the weaning neonate. Excessively small
endotracheal tubes can worsen the appearance of respira-
tory distress. A less than optimal tube position can produce
dramatic increases in resistance. Higher than necessary
flow rates introduced through the ventilator produce
turbulent flow patterns, higher resistance, and concomitant
increased work of breathing.
Laminar flow is governed by Poiseuille law. Halving
the radius of a tube will increase the resistance by 16
times. With laminar flow, the drop of pressure is related to
the flow rate, and so the bresistanceQ of a tube is inde-
pendent of the flow. Turbulent flow is inherently more
variable because resistance varies with flow. At any given
flow, the pressure change is proportional to the fifth power
of the radius (the Fanning Equation). The implications for
ventilation are clear. The largest possible endotracheal tube
that can be placed bsafely Q should be used. Excessive tube
leak compromises even the best flow compensation
systems, can lead to falsely elevated resistance measure-
ments, and prevent consideration of extubation due to a
falsely elevated work of breathing.
Time Constants
Time constants (Kt) are an important but often
neglected concept and are derived by multiplying
the compliance of the respiratory system (Crs) by the
resistance of the respiratory system (Rrs). This is
expressed as Kt = Crs � Rrs. KtINSP is the time to
effective delivery of the pressurized gas to the level of the
alveolus. KtEXP is the time required for the alveolus to
empty and recalibrate to the effective PEEP. Using a
statistical model and an assumption of uniform lung
compliance, 3*Kt will give a time equivalent at which
point 95% of the alveoli will have equilibrated. Normal
values of Kt are 0.12 to 0.15 seconds. Given a resistance
of 0.1 mL/cm H2O, inspiratory time should generally not
be set longer than 0.36 to 0.45 seconds to minimize the
potential for gas trapping and optimize transmission of
ventilation breaths.25 If the inspiratory time is too short (ie,
less than the time constant), modes of ventilation that
feature breath termination can produce atelectasis and
ventilator failure.
Recoil
As a final step in the approach of modern ventilation
techniques, it is important to understand the different
lung volumes and capacities involved in conventional
ventilation and the normal breathing process. FRC is the
volume of gas in the lung after a normal expiration. The
FRC is determined by the balance between the inward
elastic recoil of the lungs and the outward recoil of the
thoracic cage. FRC decreases with paralysis and anesthe-
sia. FRC for normal infants was measured in one study on
days 1, 2, and 3 and were 2.0 F 0.3, 2.1 F 0.3, and 2.2 F0.3 mL/cm, respectively. For infants with meconium
aspiration, these values were 1.8 F 0.4, 2.3 F 1.1, and
2.2 F 0.6 mL/cm, respectively.22 An FRC that is
inadequate suggests that part of the work of ventilation
is being devoted to open atelectatic areas of lung that do
not have enough pressure during end expiration to prevent
collapse. This relationship can be visualized on a pressure
Ventilator Management: What Does It All mean? 83
volume curve. An inspiratory baseline that is flat almost to
the point of end inspiration is suggestive of inadequate
PEEP and FRC that has not been optimized. An FRC that
exceeds normal can also be visualized as an overly flat
compliance curve despite the clinical appearance of
ventilation improvement.26
As discussed earlier, PAW is the mean pressure
measurement in the airway. Whereas spontaneous breaths
incur a negative flow on scalar tracings, ventilator breaths
are associated with a pressure cost of ventilation and thus
a positive scalar tracing. Pressure measurements can be
used to generate compliance and resistance measures,
which can be important in determining the ventilation
modality with the least pressure cost of ventilation.27
Mean airway pressure is the average of PAW throughout
the entire respiratory cycle. This correlates with mechan-
ical breath tidal volume and PEEP level. The upper limit
of Mean PAW is generally 10 to 15 in the conventionally
ventilated neonate.
State of the Science
The concept of modern ventilation for the neonate
distinguishes itself from previous technologies, not
merely in terms of the different modes of ventilation that
are available for the clinician to choose from, but in the
availability of conceptual pulmonary function monitoring
and in vivo testing that was previously only estimated
radiographically and by blood gas analysis. Early attempts
at intermittent positive pressure ventilation (IPPV) were
confounded by an inability to maintain an adequate FRC
and the resultant barotrauma from requisite reexpansion of
atelectatic areas of the lung with each ventilation. Volume
mode ventilation was used in the early stages of the
development of neonatal ventilation. Overly compliant
tubing, excessive circuit leaking, and equipment designed
primarily for the adult market relegated this modality to
the back shelf for generations of neonates. A significant
improvement in technology was the innovation of inter-
mittent mandatory ventilation (IMV). The concept of
continuous PEEP with flow by ventilation not only
minimized the work of breathing but also prevented
significant atelectasis from occurring with the 0 cm PEEP
modus operandi of IPPV.28,29
Even with this improvement, significant lung morbid-
ities continued to occur. Chronic lung disease was
common in the pre-surfactant era. Morbidities such as
pulmonary interstitial emphysema, pneumothorax, and
bronchopulmonary dysplasia were expected consequences
of extended ventilation. Prophylactic chest tube placement
was a real consideration. The concept of breath-to-breath
monitoring was not the expected norm. Pulmonary
function testing was a curiosity that occurred in only the
most sophisticated centers on an intermittent basis. Even
then, the pneumotachographs were adaptations of adult
models. The dead space of these devices could exceed the
lung volume. At issue was the concept that IMV
represented the evolved state of the art. Patient synchro-
nized ventilation was a concept that might be successful in
the adult world with cuffed endotracheal tubes and
minimal expected tube leak. Issues involved in measuring
low flow rates and the difficulty in preventing auto cycling
were paramount with respect to the obstacles faced in
developing these devices.
The initial synchronized ventilators for neonates were
based on impendence and pressure-driven mechanisms
such as the Greysby capsule (a small pressure capsule the
size of a dime that was taped to the chest wall). The
devices were continuous flow, pressure-limited time-
cycled ventilators. The major difference between these
devices and traditional IMV was that a synchrony signal
passing from the pressure capsule could trigger the
generation of a breath from the ventilator. A fixed
inspiratory time was given and the delivered pressure
was determined by the ventilator. The effectiveness of the
synchronization was determined by the placement of the
capsule. Inadvertent motion, seizures, or hiccoughs could
jeopardize the synchrony of ventilation. In the worse case
situation, the ventilation could be delivered 1808 out of
phase, with inhalation synchronized during the expiration
process. The ventilator breath could not be terminated. A
tachypneic baby could attempt to breathe during expira-
tion, resulting in increased work of breathing. Pulmonary
function monitoring was not built into the ventilator.
Adjunct devices were introduced to measure tidal volumes
and generate flow and pressure scalars. Even with the best
possible pulmonary function monitoring, a discerning eye
was necessary to distinguish when appropriate position of
the capsule had been achieved. Flow delivery was
mediated by solenoid valves. The flow signature of these
ventilators were largely square shaped providing that flow
had been set adequately to generate the set pressure limit.
Higher flows were imprudent but did not produce as much
turbulence as might be expected because of this mecha-
nism. An assist control mode was also available but was
inhibited by an inability to adequately terminate breaths.
Stacking of breaths was common in assist control mode
and produced the potential for inadvertent PEEP and
subsequent barotrauma. Studies of this device indicated
improved patient tolerance and suggested that less sedation
was required for patients on this modality of ventilation
but failed to produce a discernable improvement in
outcome measures. Flow synchronization characteristic
of the newer ventilation modalities was limited to a
demand mode, which would allow a predetermined flow
84 Mitchell R. Goldstein
increase during inspiration but did not provide for a
mechanism to terminate the breath.
Newer ventilators use sophisticated pneumotacho-
graphs to measure flow directly at the patient wye.
Relative to older synchronization techniques, flow sens-
ing allowed for better and faster breath tracking and gave
rise to the possibility of enhanced patient control of
ventilation.30,31 Ventilators produced by Viasys, Maquet
(formerly Servo), Drager, and Puritan-Bennett have all
incorporated some of the newer modalities of flow
control. One of the more popularly used is PSV. Unlike
simple time-cycled pressure-limited SIMV, PSV has no
fixed inspiratory time. The PEEP is set along with a level
of pressure support (PS). It is important to remember that
the level of PS is not equivalent to the PIP commonly
seen in the previous generation of ventilators. The peak
pressure is equivalent to the PEEP + PS. The patient
determines the respiratory rate in certain modes and can
terminate breaths with expiratory effort or as a function of
percent of positive pressure in others. Volume guarantee
(VG) is another commonly used mode. Within set
pressure parameters, breath volume is adjusted based on
the changing compliance of the lung. PIP is adjusted
downward bautomatically.Q More sophistication and con-
trol is possible with adjustments to the flow, which can
help establish a decelerating flow pattern, prevent
excessive acceleration in the inspiratory flow pattern,
and prevent inadvertent auto cycling.32,33
Volume or volume-limited ventilation is now practi-
cal. Before the introduction of proximal flow sensing,
volume-targeted ventilation was impractical. Neonatal
endotracheal tubes are uncuffed often resulting in airway
leaks. In previous volume ventilation modalities, predic-
tion of expiratory leaks around the tube was not
possible. Attempts to measure tidal volumes at the valve
inside the ventilator were uncertain because of compli-
ance changes in the ventilator tubing itself. Again
beginning with a set PEEP, the desired tidal volume is
selected (usually 4-6 mL/kg per breath for premature
infants and as much as 8-10 mL/kg per breath for term).
Enhanced computer-automated predictive models of
ventilation have effective leak compensation. Avoidance
of barotrauma may be possible as btoxicQ pressure levels
are not generated.34,35
High-frequency ventilation was introduced to neona-
tology in the late 1970s. The initial high-frequency trials
were less than encouraging. Data suggested that these
devices did not significantly improve ventilatory outcomes
and might increase the risk of intraventricular hemor-
rhage.36 Progress in acceptance of the devices over the
course of the ensuing years occurred with the recognition
that intervention strategies and normalization of lung
expansion were more efficacious than rescue strategies
that relied on the adequacy of an initial conventional
ventilation strategy to avoid the pitfall of barotraumas and
atelectasis inherent in the earlier research.37 Today, this
ventilatory strategy is in wide use. High-frequency
ventilators can be divided into three classes: true oscil-
lators, jet ventilators, and flow interrupters.
In the United States, the Sensormedics 3100A is the
only true oscillator in clinical use. It has FDA indications
for first intent ventilation as well as rescue strategies.
Research conducted by deLemos et al established the
superiority of these devices over conventional IMV
ventilation in the avoidance of barotrauma-based lung
injury.38-41 In the neonatal age group, ventilation is
established by the selection of a mean airway pressure
adequate to produce a satisfactory FRC (chest radiograph
expanded to 9-10 ribs), frequency selection generally
between 8 and 15 Hz (breaths per second), and amplitude
(pressure distance of the breath from the baseline pressure
in inspiration and expiration). Amplitude selection is
generally clinically based on finding a value that will
produce an badequateQ chest wiggle. Although the
inspiratory time can be adjusted, it is usually fixed at
0.33 or 33% of the entire cycle. The active expiratory
mode, which accounts for 66% of the ventilator cycle, is
important in the rapid elimination of CO2.42
The Bunnell Life Pulse High-Frequency bJet Q Ventila-tor provides small high-frequency breaths using passive
instead of active ventilation. Breaths per minute can be set
from 240 to 660. Amplitude is replaced by PIP selection.
Unlike the oscillator, the Jet relies on passive exhalation
for ventilation. In certain circumstances, the Jet may allow
the selection of a lower mean airway pressure and
avoidance of bchokeQ points, which can occur with higher
amplitudes with high-frequency oscillation. The Jet is used
in coordination with conventional ventilators to facilitate
the transition from conventional ventilation. Both high-
frequency and conventional mode ventilation can be active
simultaneously. The Jet has been used extensively for
rescue in the prevention and amelioration of air leak. As a
first intent ventilator, the Jet may offer certain advantages
as well.43,44
Of historical interest is the InfantStar high-frequency
flow interrupter. Although support for this ventilator has
all but been discontinued, the InfantStar is still in
widespread use in many neonatal units. Its main advantage
over other modalities was its flexibility. The ventilator
could be used for nasal CPAP, SIMV ventilation, as well as
high frequency. The oscillatory effect is produced by
solenoid valves interrupting airflow at the preselected rate,
generally between 8 and 14 Hz. Amplitude is adjusted in
the same way as HFOV. The InfantStar does not rely on
an active expiratory phase (similar to the Jet). Compared
with the other devices available, the InfantStar was less
Ventilator Management: What Does It All mean? 85
powerful, had fewer features, and had more from
amplitude drift; however, its ease of use established it as
the only high-frequency device in many neonatal intensive
care units until recently.45
Conventional ventilation of the neonate has progressed
in sophistication over the years. From the early makeshift
adaptation of adult ventilators and ventilator strategies,
neonatal ventilation has gradually progressed to a science
of its own. Early volume mode ventilation strategies gave
way to IPPV, which was subsequently supplanted by IMV
mode ventilation. Newer modalities including high fre-
quency ventilation or PSV offer even more possibility for
improved outcomes.46
References
1. Gregory GA, Kitterman JA, Phibbs RH, Tooley WH, HamiltonWK. Treatment of the idiopathic respiratory-distress syndrome withcontinuous positive airway pressure. N Engl J Med. 1971;284:1333 -1340.
2. Dunn PM. Respiratory distress syndrome. Continuous positiveairway pressure (CPAP) using the Gregory box. Proc R Soc Med.1974;67:245 -247.
3. Narendran V, Donovan EF, Hoath SB, Akinbi HT, Steichen JJ,Jobe AH. Early bubble CPAP and outcomes in ELBW preterm infants.J Perinatol. 2003;23:195-199.
4. Sahni R, Wung JT. Continuous positive airway pressure (CPAP).Indian J Pediatr. 1998;65:265 -271.
5. Wung JT, Driscoll Jr JM, Epstein RA, Hyman AI. A new devicefor CPAP by nasal route. Crit Care Med. 1975;3:76-78.
6. Ammari A, Suri M, Milisavljevic V, et al. Variables associatedwith the early failure of nasal CPAP in very low birth weight infants.J Pediatr. 2005;147:341-347.
7. Lee KS, Dunn MS, Fenwick M, Shennan AT. A comparison ofunderwater bubble continuous positive airway pressure with ventilator-derived continuous positive airway pressure in premature neonates readyfor extubation. Biol Neonate. 1998;73:69 -75.
8. Liptsen E, Aghai ZH, Pyon KH, et al. Work of breathing duringnasal continuous positive airway pressure in preterm infants: a comparisonof bubble vs variable-flow devices. J Perinatol. 2005;25:453 -458.
9. Update: ralstonia species associated with Vapotherm oxygendelivery devices—United States, 2005. MMWR Morb Mortal Wkly Rep.2005;54:1104-1105.
10. Andreasson B, Lindroth M, Mortensson W, Svenningsen NW,Jonson B. Lung function eight years after neonatal ventilation. Arch DisChild. 1989;64:108-113.
11. Sinha SK, Donn SM. Neonatal ventilation: present and futuredirections. Indian Pediatr. 1998;35:595 -600.
12. Bernstein G, Heldt GP, Mannino FL. Increased and moreconsistent tidal volumes during synchronized intermittent mandatoryventilation in newborn infants. Am J Respir Crit Care Med.1994;150:1444-1448.
13. Bhutani VK. Clinical applications of pulmonary function andgraphics. Semin Neonatol. 2002;7:391 -399.
14. Silva NG, Gerhardt T, Claure N, Duara S, Bancalari E. Effect ofchestwall distortion on the measurement of pulmonary mechanics inpreterm infants. Pediatr Pulmonol. 1995;20:34-39.
15. Abbasi S, Bhutani VK. Pulmonary mechanics and energetics ofnormal, non-ventilated low birthweight infants. Pediatr Pulmonol.1990;8:89-95.
16. Balsan MJ, Jones JG, Watchko JF, Guthrie RD. Measurements ofpulmonary mechanics prior to the elective extubation of neonates. PediatrPulmonol. 1990;9:238-243.
17. Cogswell JJ, Hatch DG, Hull D, Milner AD, Taylor BW. Staticpulmonary compliance in early childhood. Arch Dis Child. 1973;48:324.
18. de Mello RR, Dutra MV, Ramos JR, Daltro P, Boechat M, Andrade Lopes JM. Lung mechanics and high-resolution computed tomographyof the chest in very low birth weight premature infants. Sao Paulo Med J.2003;121:167-172.
19. Gerhardt TO, Bancalari E. Measurement and monitoring ofpulmonary function. Clin Perinatol. 1991;18:581-609.
20. Merth IT, de Winter JP, Borsboom GJ, Quanjer PH. Pulmonaryfunction during the first year of life in healthy infants born prematurely.Eur Respir J. 1995;8:1141-1147.
21. Yau KI, Fang LJ. Pulmonary mechanics and the energetics ofbreathing in healthy infants. J Formos Med Assoc. 1994;93:110 -116.
22. Yeh TF, Lilien LD, Barathi A, Pildes RS. Lung volume, dynamiclung compliance, and blood gases during the first 3 days of postnatal lifein infants with meconium aspiration syndrome. Crit Care Med.1982;10:588-592.
23. Fisher JB, Mammel MC, Coleman JM, Bing DR, Boros SJ.Identifying lung overdistention during mechanical ventilation by usingvolume-pressure loops. Pediatr Pulmonol. 1988;5:10-14.
24. Carlo WA, Ambalavanan N. Conventional mechanical ventila-tion: traditional and new strategies. Pediatr Rev. 1999;20:e117 -e126.3
25. Frappell PB, MacFarlane PM. Development of mechanics andpulmonary reflexes. Respir Physiol Neurobiol. 2005;149:143-154.
26. Walsh MC, Carlo WA. Sustained inflation during HFOVimproves pulmonary mechanics and oxygenation. J Appl Physiol.1988;65:368-372.
27. Rosen WC, Mammel MC, Fisher JB, et al. The effects of bedsidepulmonary mechanics testing during infant mechanical ventilation:a retrospective analysis. Pediatr Pulmonol. 1993;16:147 -152.
28. Cox JM. Techniques in neonatal ventilation. Int Anesthesiol Clin.1974;12:111 -140.
29. Greenough A, Roberton NR. Neonatal ventilation. Early HumDev. 1986;13:127-136.
30. Abubakar KM, Keszler M. Patient-ventilator interactions in newmodes of patient-triggered ventilation. Pediatr Pulmonol. 2001;32:71 -75.
31. Bernstein G, Cleary JP, Heldt GP, Rosas JF, Schellenberg LD,Mannino FL. Response time and reliability of three neonatal patient-triggered ventilators. Am Rev Respir Dis. 1993;148:358 -364.
32. John J, Bjorklund LJ, Svenningsen NW, Jonson B. Airway andbody surface sensors for triggering in neonatal ventilation. Acta Paediatr.1994;83:903-909.
33. Uchiyama A, Imanaka H, Taenaka N, Nakano S, Fujino Y,Yoshiya I. A comparative evaluation of pressure-triggering and flow-triggering in pressure support ventilation (PSV) for neonates using ananimal model. Anaesth Intensive Care. 1995;23:302-306.
34. Abd El-Moneim ES, Fuerste HO, Krueger M, et al. Pressuresupport ventilation combined with volume guarantee versus synchronizedintermittent mandatory ventilation: a pilot crossover trial in prematureinfants in their weaning phase. Pediatr Crit Care Med. 2005;6:286 -292.
35. Badgwell M, Swan J, Foster AC. Volume-controlled ventilation ismade possible in infants by using compliant breathing circuits with largecompression volume. Anesth Analg. 1996;82:719 -723.
36. High-frequency oscillatory ventilation compared with conven-tional mechanical ventilation in the treatment of respiratory failure inpreterm infants. The HIFI Study Group. N Engl J Med. 1989;320:88 -93.
37. Kinsella JP, Gerstmann DR, Clark RH, et al. High-frequencyoscillatory ventilation versus intermittent mandatory ventilation: earlyhemodynamic effects in the premature baboon with hyaline membranedisease. Pediatr Res. 1991;29:160-166.
38. deLemos RA, Coalson JJ, Gerstmann DR, et al. Ventilatorymanagement of infant baboons with hyaline membrane disease: the use ofhigh frequency ventilation. Pediatr Res. 1987;21:594 -602.
39. deLemos RA, Gerstmann DR, Clark RH, Guajardo A, Null JrDM. High frequency ventilation—the relationship between ventilatordesign and clinical strategy in the treatment of hyaline membranedisease and its complications: a brief review. Pediatr Pulmonol.1987;3:370-372.
40. deLemos RA, Coalson JJ, Meredith KS, Gerstmann DR, Null JrDM. A comparison of ventilation strategies for the use of high-frequencyoscillatory ventilation in the treatment of hyaline membrane disease. ActaAnaesthesiol Scand Suppl. 1989;90:102-107.
86 Mitchell R. Goldstein
41. deLemos RA, Coalson JJ, deLemos JA, King RJ, Clark RH,Gerstmann DR. Rescue ventilation with high frequency oscillation inpremature baboons with hyaline membrane disease. Pediatr Pulmonol.1992;12:29 -36.
42. Bancalari A, Gerhardt T, Bancalari E, et al. Gas trapping withhigh-frequency ventilation: jet versus oscillatory ventilation. J Pediatr.1987;110:617-622.
43. Marlow N. High frequency ventilation and respiratory distresssyndrome: do we have an answer? Arch Dis Child Fetal Neonatal Ed.1998;78:F1-F2.
44. Bhuta T, Henderson-Smart DJ. Elective high frequency jetventilation versus conventional ventilation for respiratory distresssyndrome in preterm infants. Cochrane Database Syst Rev. 2000;CD000328.
45. Jirapaet KS, Kiatchuskul P, Kolatat T, Srisuparb P. Comparison ofhigh-frequency flow interruption ventilation and hyperventilation inpersistent pulmonary hypertension of the newborn. Respir Care.2001;46:586 -594.
46. Mammel MC. New modes of neonatal ventilation: let there belight. J Perinatol. 2005;25:624-625.