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Ventilator Management: What Does It All Mean?
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
Ventilator Management: What Does It All Mean? By Mitchell R. Goldstein, MD, FAAP
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he 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 pressurelimited 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
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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. Goldstein, MD, FAAP, Department of Neonatal Medicine, 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
arly 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 btortureQ despite 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
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end expiratory ventilator pressure may not be as advantageous 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.
Table 1. Pulmonary Function Abbreviations and Calculations Vt Airway flow Airway pressure VtEXP
Pulmonary Function VtINSP
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he 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 commonly 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 expiratory tidal volumes should be distinguished. Inspiratory tidal volume is a gauge of adequacy of spontaneous ventilation but cannot be used to measure the effectiveness 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 spontaneous VtINSP approaches VtEXP of the ventilator, inferences can be made regarding the neonate’s ability to take over more ventilation and perhaps readiness for extubation to NCPAP.13
VE
PTP PES
PIP Kt
Crs Rrs KtINSP
KtEXP
Tidal volume V PAW
Expiratory tidal volume Inspiratory tidal volume Minute ventilation
Transpulmonary pressure Esophageal pressure
Intrapleural pressure Time constants
Compliance of the respiratory system Resistance of the respiratory system Inspiratory time constants Expiratory time constants
Volume of air either exhaled or inhaled Flow of air either exhaled or inhaled This is determined by compliance, resistance, tidal volume, and flow rate Volume of air exhaled Volume of air inhaled Amount of gas expired over 1 min [RespRate (patient) VtEXP (spontaneous)] + [VentRate VtEXP (ventilator)] Pressure exerted on the lungs to initiate inspiration Airway pressure exerted on the esophagus during inspiration. This will be diminished when the endotracheal tube is in place. Pressure within the pleural cavity Time it takes for pressure to equilibrate between proximal airway and alveoli. Kt = Crs Rrs Elasticity or distensibility of the lung Capacity of the airway or lung to resist airflow Time to effective delivery of pressurized gas to level of alveolus Time required for alveolus to empty and recalibrate to effective PEEP
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?
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evaluating the progress of weaning from mechanical ventilation using the assist modes.
Compliance
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n understanding of the differences between compliance 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). Transpulmonary 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 statically. 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
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 surfactant delivery, the loop will move toward the yellow diagram showing improved compliance.
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’s beak 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
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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 measurements, and prevent consideration of extubation due to a falsely elevated work of breathing.
Time Constants
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.
currently be the most important tool available to clinicians in avoiding significant barotraumas.23
Resistance
A
n understanding of resistance is also important to modern ventilation techniques. An elevated resistance 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 encountered during intubation must be taken seriously in the evaluation of the weaning neonate. Excessively small endotracheal tubes can worsen the appearance of respiratory 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 independent of the flow. Turbulent flow is inherently more
T
ime 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
A
s 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 anesthesia. 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 F 0.3 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?
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 mechanical 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
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he 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 intermittent 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 morbidities 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
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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 synchronized 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 timecycled 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 expiration, 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 mechanism. 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
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increase during inspiration but did not provide for a mechanism to terminate the breath. Newer ventilators use sophisticated pneumotachographs to measure flow directly at the patient wye. Relative to older synchronization techniques, flow sensing 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 control 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 practical. 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, prediction of expiratory leaks around the tube was not possible. Attempts to measure tidal volumes at the valve inside the ventilator were uncertain because of compliance 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 neonatology 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 hemorrhage.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 oscillators, 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 Ventilator 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 highfrequency 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?
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 frequency ventilation or PSV offer even more possibility for improved outcomes.46
References 1. Gregory GA, Kitterman JA, Phibbs RH, Tooley WH, Hamilton WK. Treatment of the idiopathic respiratory-distress syndrome with continuous positive airway pressure. N Engl J Med. 1971;284:1333 - 1340. 2. Dunn PM. Respiratory distress syndrome. Continuous positive airway 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 device for CPAP by nasal route. Crit Care Med. 1975;3:76 - 78. 6. Ammari A, Suri M, Milisavljevic V, et al. Variables associated with 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 of underwater bubble continuous positive airway pressure with ventilatorderived continuous positive airway pressure in premature neonates ready for extubation. Biol Neonate. 1998;73:69 - 75. 8. Liptsen E, Aghai ZH, Pyon KH, et al. Work of breathing during nasal continuous positive airway pressure in preterm infants: a comparison of bubble vs variable-flow devices. J Perinatol. 2005;25:453 - 458. 9. Update: ralstonia species associated with Vapotherm oxygen delivery 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 Dis Child. 1989;64:108 - 113. 11. Sinha SK, Donn SM. Neonatal ventilation: present and future directions. Indian Pediatr. 1998;35:595 - 600. 12. Bernstein G, Heldt GP, Mannino FL. Increased and more consistent tidal volumes during synchronized intermittent mandatory ventilation in newborn infants. Am J Respir Crit Care Med. 1994;150:1444 - 1448. 13. Bhutani VK. Clinical applications of pulmonary function and graphics. Semin Neonatol. 2002;7:391 - 399. 14. Silva NG, Gerhardt T, Claure N, Duara S, Bancalari E. Effect of chestwall distortion on the measurement of pulmonary mechanics in preterm infants. Pediatr Pulmonol. 1995;20:34 - 39. 15. Abbasi S, Bhutani VK. Pulmonary mechanics and energetics of normal, non-ventilated low birthweight infants. Pediatr Pulmonol. 1990;8:89 - 95. 16. Balsan MJ, Jones JG, Watchko JF, Guthrie RD. Measurements of pulmonary mechanics prior to the elective extubation of neonates. Pediatr Pulmonol. 1990;9:238 - 243. 17. Cogswell JJ, Hatch DG, Hull D, Milner AD, Taylor BW. Static pulmonary compliance in early childhood. Arch Dis Child. 1973;48:324.
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18. de Mello RR, Dutra MV, Ramos JR, Daltro P, Boechat M, Andra de Lopes JM. Lung mechanics and high-resolution computed tomography of 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 of pulmonary function. Clin Perinatol. 1991;18:581 - 609. 20. Merth IT, de Winter JP, Borsboom GJ, Quanjer PH. Pulmonary function 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 of breathing in healthy infants. J Formos Med Assoc. 1994;93:110 - 116. 22. Yeh TF, Lilien LD, Barathi A, Pildes RS. Lung volume, dynamic lung compliance, and blood gases during the first 3 days of postnatal life in 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 using volume-pressure loops. Pediatr Pulmonol. 1988;5:10 - 14. 24. Carlo WA, Ambalavanan N. Conventional mechanical ventilation: traditional and new strategies. Pediatr Rev. 1999;20:e117 - e126.3 25. Frappell PB, MacFarlane PM. Development of mechanics and pulmonary reflexes. Respir Physiol Neurobiol. 2005;149:143 - 154. 26. Walsh MC, Carlo WA. Sustained inflation during HFOV improves pulmonary mechanics and oxygenation. J Appl Physiol. 1988;65:368 - 372. 27. Rosen WC, Mammel MC, Fisher JB, et al. The effects of bedside pulmonary 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 Hum Dev. 1986;13:127 - 136. 30. Abubakar KM, Keszler M. Patient-ventilator interactions in new modes 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 patienttriggered ventilators. Am Rev Respir Dis. 1993;148:358 - 364. 32. John J, Bjorklund LJ, Svenningsen NW, Jonson B. Airway and body 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 flowtriggering in pressure support ventilation (PSV) for neonates using an animal model. Anaesth Intensive Care. 1995;23:302 - 306. 34. Abd El-Moneim ES, Fuerste HO, Krueger M, et al. Pressure support ventilation combined with volume guarantee versus synchronized intermittent mandatory ventilation: a pilot crossover trial in premature infants in their weaning phase. Pediatr Crit Care Med. 2005;6:286 - 292. 35. Badgwell M, Swan J, Foster AC. Volume-controlled ventilation is made possible in infants by using compliant breathing circuits with large compression volume. Anesth Analg. 1996;82:719 - 723. 36. High-frequency oscillatory ventilation compared with conventional mechanical ventilation in the treatment of respiratory failure in preterm infants. The HIFI Study Group. N Engl J Med. 1989;320:88 - 93. 37. Kinsella JP, Gerstmann DR, Clark RH, et al. High-frequency oscillatory ventilation versus intermittent mandatory ventilation: early hemodynamic effects in the premature baboon with hyaline membrane disease. Pediatr Res. 1991;29:160 - 166. 38. deLemos RA, Coalson JJ, Gerstmann DR, et al. Ventilatory management of infant baboons with hyaline membrane disease: the use of high frequency ventilation. Pediatr Res. 1987;21:594 - 602. 39. deLemos RA, Gerstmann DR, Clark RH, Guajardo A, Null Jr DM. High frequency ventilation—the relationship between ventilator design and clinical strategy in the treatment of hyaline membrane disease and its complications: a brief review. Pediatr Pulmonol. 1987;3:370 - 372. 40. deLemos RA, Coalson JJ, Meredith KS, Gerstmann DR, Null Jr DM. A comparison of ventilation strategies for the use of high-frequency oscillatory ventilation in the treatment of hyaline membrane disease. Acta Anaesthesiol Scand Suppl. 1989;90:102 - 107.
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41. deLemos RA, Coalson JJ, deLemos JA, King RJ, Clark RH, Gerstmann DR. Rescue ventilation with high frequency oscillation in premature baboons with hyaline membrane disease. Pediatr Pulmonol. 1992;12:29 - 36. 42. Bancalari A, Gerhardt T, Bancalari E, et al. Gas trapping with high-frequency ventilation: jet versus oscillatory ventilation. J Pediatr. 1987;110:617 - 622. 43. Marlow N. High frequency ventilation and respiratory distress syndrome: do we have an answer? Arch Dis Child Fetal Neonatal Ed. 1998;78:F1 - F2.
44. Bhuta T, Henderson-Smart DJ. Elective high frequency jet ventilation versus conventional ventilation for respiratory distress syndrome in preterm infants. Cochrane Database Syst Rev. 2000; CD000328. 45. Jirapaet KS, Kiatchuskul P, Kolatat T, Srisuparb P. Comparison of high-frequency flow interruption ventilation and hyperventilation in persistent pulmonary hypertension of the newborn. Respir Care. 2001;46:586 - 594. 46. Mammel MC. New modes of neonatal ventilation: let there be light. J Perinatol. 2005;25:624 - 625.
Ventilator Management: What Does It All Mean? By Mitchell R. Goldstein, MD, FAAP
T
he 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 pressurelimited 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
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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. Goldstein, MD, FAAP, Department of Neonatal Medicine, 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
arly 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 btortureQ despite 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
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end expiratory ventilator pressure may not be as advantageous 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.
Table 1. Pulmonary Function Abbreviations and Calculations Vt Airway flow Airway pressure VtEXP
Pulmonary Function VtINSP
T
he 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 commonly 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 expiratory tidal volumes should be distinguished. Inspiratory tidal volume is a gauge of adequacy of spontaneous ventilation but cannot be used to measure the effectiveness 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 spontaneous VtINSP approaches VtEXP of the ventilator, inferences can be made regarding the neonate’s ability to take over more ventilation and perhaps readiness for extubation to NCPAP.13
VE
PTP PES
PIP Kt
Crs Rrs KtINSP
KtEXP
Tidal volume V PAW
Expiratory tidal volume Inspiratory tidal volume Minute ventilation
Transpulmonary pressure Esophageal pressure
Intrapleural pressure Time constants
Compliance of the respiratory system Resistance of the respiratory system Inspiratory time constants Expiratory time constants
Volume of air either exhaled or inhaled Flow of air either exhaled or inhaled This is determined by compliance, resistance, tidal volume, and flow rate Volume of air exhaled Volume of air inhaled Amount of gas expired over 1 min [RespRate (patient) VtEXP (spontaneous)] + [VentRate VtEXP (ventilator)] Pressure exerted on the lungs to initiate inspiration Airway pressure exerted on the esophagus during inspiration. This will be diminished when the endotracheal tube is in place. Pressure within the pleural cavity Time it takes for pressure to equilibrate between proximal airway and alveoli. Kt = Crs Rrs Elasticity or distensibility of the lung Capacity of the airway or lung to resist airflow Time to effective delivery of pressurized gas to level of alveolus Time required for alveolus to empty and recalibrate to effective PEEP
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?
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evaluating the progress of weaning from mechanical ventilation using the assist modes.
Compliance
A
n understanding of the differences between compliance 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). Transpulmonary 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 statically. 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
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 surfactant delivery, the loop will move toward the yellow diagram showing improved compliance.
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’s beak 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
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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 measurements, and prevent consideration of extubation due to a falsely elevated work of breathing.
Time Constants
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.
currently be the most important tool available to clinicians in avoiding significant barotraumas.23
Resistance
A
n understanding of resistance is also important to modern ventilation techniques. An elevated resistance 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 encountered during intubation must be taken seriously in the evaluation of the weaning neonate. Excessively small endotracheal tubes can worsen the appearance of respiratory 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 independent of the flow. Turbulent flow is inherently more
T
ime 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
A
s 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 anesthesia. 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 F 0.3 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?
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 mechanical 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
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he 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 intermittent 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 morbidities 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
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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 synchronized 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 timecycled 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 expiration, 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 mechanism. 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
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increase during inspiration but did not provide for a mechanism to terminate the breath. Newer ventilators use sophisticated pneumotachographs to measure flow directly at the patient wye. Relative to older synchronization techniques, flow sensing 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 control 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 practical. 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, prediction of expiratory leaks around the tube was not possible. Attempts to measure tidal volumes at the valve inside the ventilator were uncertain because of compliance 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 neonatology 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 hemorrhage.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 oscillators, 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 Ventilator 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 highfrequency 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?
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 frequency ventilation or PSV offer even more possibility for improved outcomes.46
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18. de Mello RR, Dutra MV, Ramos JR, Daltro P, Boechat M, Andra de Lopes JM. Lung mechanics and high-resolution computed tomography of 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 of pulmonary function. Clin Perinatol. 1991;18:581 - 609. 20. Merth IT, de Winter JP, Borsboom GJ, Quanjer PH. Pulmonary function 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 of breathing in healthy infants. J Formos Med Assoc. 1994;93:110 - 116. 22. Yeh TF, Lilien LD, Barathi A, Pildes RS. Lung volume, dynamic lung compliance, and blood gases during the first 3 days of postnatal life in 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 using volume-pressure loops. Pediatr Pulmonol. 1988;5:10 - 14. 24. Carlo WA, Ambalavanan N. Conventional mechanical ventilation: traditional and new strategies. Pediatr Rev. 1999;20:e117 - e126.3 25. Frappell PB, MacFarlane PM. Development of mechanics and pulmonary reflexes. Respir Physiol Neurobiol. 2005;149:143 - 154. 26. Walsh MC, Carlo WA. Sustained inflation during HFOV improves pulmonary mechanics and oxygenation. J Appl Physiol. 1988;65:368 - 372. 27. Rosen WC, Mammel MC, Fisher JB, et al. The effects of bedside pulmonary 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 Hum Dev. 1986;13:127 - 136. 30. Abubakar KM, Keszler M. Patient-ventilator interactions in new modes 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 patienttriggered ventilators. Am Rev Respir Dis. 1993;148:358 - 364. 32. John J, Bjorklund LJ, Svenningsen NW, Jonson B. Airway and body 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 flowtriggering in pressure support ventilation (PSV) for neonates using an animal model. Anaesth Intensive Care. 1995;23:302 - 306. 34. Abd El-Moneim ES, Fuerste HO, Krueger M, et al. Pressure support ventilation combined with volume guarantee versus synchronized intermittent mandatory ventilation: a pilot crossover trial in premature infants in their weaning phase. Pediatr Crit Care Med. 2005;6:286 - 292. 35. Badgwell M, Swan J, Foster AC. Volume-controlled ventilation is made possible in infants by using compliant breathing circuits with large compression volume. Anesth Analg. 1996;82:719 - 723. 36. High-frequency oscillatory ventilation compared with conventional mechanical ventilation in the treatment of respiratory failure in preterm infants. The HIFI Study Group. N Engl J Med. 1989;320:88 - 93. 37. Kinsella JP, Gerstmann DR, Clark RH, et al. High-frequency oscillatory ventilation versus intermittent mandatory ventilation: early hemodynamic effects in the premature baboon with hyaline membrane disease. Pediatr Res. 1991;29:160 - 166. 38. deLemos RA, Coalson JJ, Gerstmann DR, et al. Ventilatory management of infant baboons with hyaline membrane disease: the use of high frequency ventilation. Pediatr Res. 1987;21:594 - 602. 39. deLemos RA, Gerstmann DR, Clark RH, Guajardo A, Null Jr DM. High frequency ventilation—the relationship between ventilator design and clinical strategy in the treatment of hyaline membrane disease and its complications: a brief review. Pediatr Pulmonol. 1987;3:370 - 372. 40. deLemos RA, Coalson JJ, Meredith KS, Gerstmann DR, Null Jr DM. A comparison of ventilation strategies for the use of high-frequency oscillatory ventilation in the treatment of hyaline membrane disease. Acta Anaesthesiol Scand Suppl. 1989;90:102 - 107.
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41. deLemos RA, Coalson JJ, deLemos JA, King RJ, Clark RH, Gerstmann DR. Rescue ventilation with high frequency oscillation in premature baboons with hyaline membrane disease. Pediatr Pulmonol. 1992;12:29 - 36. 42. Bancalari A, Gerhardt T, Bancalari E, et al. Gas trapping with high-frequency ventilation: jet versus oscillatory ventilation. J Pediatr. 1987;110:617 - 622. 43. Marlow N. High frequency ventilation and respiratory distress syndrome: do we have an answer? Arch Dis Child Fetal Neonatal Ed. 1998;78:F1 - F2.
44. Bhuta T, Henderson-Smart DJ. Elective high frequency jet ventilation versus conventional ventilation for respiratory distress syndrome in preterm infants. Cochrane Database Syst Rev. 2000; CD000328. 45. Jirapaet KS, Kiatchuskul P, Kolatat T, Srisuparb P. Comparison of high-frequency flow interruption ventilation and hyperventilation in persistent pulmonary hypertension of the newborn. Respir Care. 2001;46:586 - 594. 46. Mammel MC. New modes of neonatal ventilation: let there be light. J Perinatol. 2005;25:624 - 625.