Tidal Volume-Targeted Ventilation

As described in Chapter 15 , two fundamentally different approaches to positive pressure ventilation are possible. In pressure-controlled (PC) ventilation, the primary control variable governing gas delivery to the lungs is inflation pressure, and the tidal volume delivered to the lungs is the dependent variable that changes as the baby breathes and lung compliance and resistance change. In volume-controlled (VC) ventilation, tidal volume delivery is directly controlled and pressure becomes the dependent variable, changing as necessary to compensate for the baby breathing and to overcome resistive and elastic forces of the lungs ( Fig. 20-1 ).

FIG 20-1

Key differences between volume-controlled (VC) and pressure-controlled (PC) ventilation. Volume delivered into the ventilator circuit is the primary control variable in VC. Circuit pressure rises passively and reaches its peak just before exhalation. The device generates whatever pressure is needed to deliver the set volume. Inflation pressure is the primary control variable in PC ventilation. Delivered volume is proportional to inflation pressure and compliance of the respiratory system; therefore the tidal volume will vary with changes in respiratory mechanics.

PC, time-cycled, continuous-flow ventilation has been the standard of care in neonatal ventilation for more than 30 years because early attempts at VC ventilation in small preterm neonates were unsuccessful with the devices available at the time. The perceived advantages of PC ventilation are the ability to directly control the inflation pressure and time and to ventilate despite large leaks around the uncuffed endotracheal tubes used with neonates. A preoccupation with high inflation pressure as the chief culprit in ventilator-induced lung injury and air leak has led to a deeply ingrained “barophobia” that has persisted despite mounting evidence that pressure by itself, without generating excessively large tidal volume, is not the main cause of lung injury.

Rationale for Tidal Volume-Targeted Ventilation

Preclinical studies clearly demonstrate that tidal volume, rather than inflation pressure, is the critical determinant of ventilator-induced lung injury. Dreyfuss and colleagues demonstrated as early as 1988 that severe acute lung injury occurred in animals ventilated with large tidal volume, regardless of whether that volume was generated by a high or low inflation pressure ( Fig. 20-2 ). On the other hand, animals whose chest wall and diaphragmatic excursion were limited by external binding experienced much less lung damage despite being exposed to the same high inflation pressure. This work and other similar experiments clearly show that excessive tidal volume, not pressure per se, is chiefly responsible for lung injury. Pressure, without correspondingly high volume, is not by itself injurious to the lungs, although it could be injurious to immature airways.

FIG 20-2

Rodents with normal lungs were ventilated with high inflation pressure (45 cm H 2 O) and no restriction on chest wall movement ( red ), high inflation pressure but with chest wall movement restricted by a tight elastic bandage around chest and abdomen ( blue ), or high negative extrathoracic pressure ( yellow ). Pulmonary edema was assessed by measuring the extravascular lung water content (Qwl/BW). Changes in permeability were assessed by determining the bloodless dry lung weight (DLW/BW) and the distribution space of 125 I-labeled albumin (Albumin space). Large tidal volume was associated with high degree of acute lung injury, whether it was generated by high positive inflation pressure or negative pressure. In contrast, despite exposure to the same high inflation pressure, when the tidal volume was limited by restricted thoracic excursion, there was significantly less acute lung injury.

(Adapted from Dreyfuss D, Soler P, Basset G, Saumon G. High inflation pressure pulmonary edema. Respective effects of high airway pressure, high tidal volume, and positive end-expiratory pressure. Am Rev Respir Dis . 1988;137(5):1159-1164.)

An equally compelling reason for tidal volume-targeted ventilation (VTV) is the extensive body of evidence documenting that both hypercarbia and hypocarbia are associated with neonatal brain injury. Despite increasing awareness of its adverse consequences, inadvertent hyperventilation remains a common problem with pressure-limited ventilation, especially early in the clinical course when the baby starts breathing, lung compliance changes rapidly in response to clearing of lung fluid, surfactant is administered, and lung volume is optimized. Luyt et al. demonstrated that 30% of ventilated infants had at least one blood gas with PaCO 2 < 25 torr during the first day of life.

While there are important differences in how volume targeting is achieved with various ventilators, the primary benefit of VTV probably rests in the ability to regulate and maintain an appropriate tidal volume (V T ), regardless of how that goal is achieved. When V T is the primary control variable, inflation pressure will fall as lung compliance and patient inspiratory effort improve, resulting in real-time weaning of pressure, in contrast to intermittent manual lowering of pressure in response to blood gases. Real-time lowering of pressure avoids excessive V T and achieves a shorter duration of mechanical ventilation. The inflation pressure will also rise if for some reason the set V T is not delivered. Two meta-analyses that included a combination of several different modalities of VC and targeted ventilation documented a number of advantages of VC/VTV, compared to pressure-limited ventilation, including significant decrease in the combined outcome of death or bronchopulmonary dysplasia (BPD), lower rate of pneumothorax, less hypocarbia, decreased risk of severe intraventricular hemorrhage/periventricular leukomalacia, and significantly shorter duration of mechanical ventilation ( Table 20-1 ). These results are very encouraging, but some limitations should be recognized. Included studies were quite small, used a variety of modalities, and many of the key outcomes reported in the meta-analysis were not prospectively collected or defined. In some of the studies, other variables beyond volume versus pressure targeting also differed. The studies focused on short-term physiologic outcomes, rather than BPD as a primary outcome. Except for one follow-up study based on parental questionnaire, no long-term pulmonary or developmental outcomes have been reported as of this writing.

TABLE 20-1

Documented Benefits of Volume-Targeted Ventilation

Outcome No. of Studies No. of Subjects RR (95% CI) or Mean Diff (95% CI)
Mortality 11 759 0.73 (0.51-1.05)
BPD at 36 weeks 9 596 0.61 (0.46-0.82)
Any IVH 11 759 0.65 (0.42-0.99)
Cystic PVL 7 531 0.33 (0.15-0.72)
Grade 3-4 IVH 11 707 0.55 (0.39-0.79)
Pneumothorax 8 595 0.46 (0.25-0.86)
Any hypocarbia 2 58 0.56 (0.33-0.96)
Failure of assigned mode 4 405 0.64 (0.43-0.94)
Duration of supplemental oxygen (days) 2 133 −1.68 (−2.5 to −0.88)

RR , Risk ratio; BPD , bronchopulmonary dysplasia; IVH , intraventricular hemorrhage; PVL , periventricular leukomalacia.

(Data from Peng W, Zhu H, Shi H, Liu E. Volume-targeted ventilation is more suitable than pressure-limited ventilation for preterm infants: a systematic review and meta-analysis. Arch Dis Child Fetal Neonatal Ed . 2014;99(2):F158-165.)

Indicates a statistically significant benefit of volume-targeted ventilation.

Volume-Controlled versus Volume-Targeted Ventilation

VC, also known as volume-cycled, ventilators deliver a constant, preset V T into the ventilator circuit with each inflation. In theory, these ventilators allow the operator to select V T and respiratory rate and therefore directly control minute ventilation. Pressure rises passively, in inverse proportion to lung compliance, as the V T is delivered, reaching its peak just before the ventilator cycles off, allowing little time for intrapulmonary gas distribution. The ventilator delivers the set V T into the circuit, generating whatever pressure is necessary to overcome lung compliance and airway resistance, up to a set safety pop-off, typically set at a pressure >40 cm H 2 O. A maximum inflation time is also set as an additional safety measure. The ventilator cycles into expiration when the preset V T has been delivered or when the maximum inflation time has elapsed. The latter ensures that with very poor lung compliance, the ventilator does not generate a very prolonged inflation in an attempt to deliver a set V T that cannot be reached at the pressure pop-off value.

The major limitation of any VC ventilator is that what is controlled is the volume injected into the ventilator circuit and NOT the V T that enters the patient’s lungs . This limitation is based on the fact that the V T is measured at the ventilator end of the circuit and does not account for compression of gas in the circuit and humidifier or distention of the compliant circuit. In large patients with cuffed endotracheal tubes (ETTs), this loss is negligible and easily compensated for. But such is not the case in small preterm infants, whose lungs are only a fraction of the total volume of the circuit ( Fig. 20-3 ). Most modern ventilators have provisions to compensate for circuit compliance/gas compression, but this ability breaks down with the ubiquitous and highly variable leak around uncuffed ETTs used in newborn infants. These limitations can be overcome to a degree by using a separate flow sensor at the airway opening to monitor exhaled V T . This will allow the user to manually adjust the set V T (also known as V del ) to achieve the desired exhaled V T . Unfortunately, the ETT leak is usually variable, and thus frequent monitoring and adjustment may be necessary. An alternate approach to VC is to rely on clinical assessment of adequacy of chest rise and breath sounds to set the V del , which typically needs to be set at 10 to 12 mL/kg, to achieve effective V T of 4 to 5 mL/kg, and to make subsequent adjustments based on blood gas measurement. Despite these limitations, VC has been shown to be feasible even in small preterm infants when a flow sensor at the airway opening is used.

FIG 20-3

Functional limitation of volume-controlled ventilation in newborn infants. Volume-controlled ventilation regulates the volume of gas delivered into the proximal end of the ventilator circuit (V Tdelivered ). The volume of gas entering the lungs (V TLung ) is affected by three factors: (1) tubing compliance (C T ), (2) compressible volume of the circuit and humidifier, and (3) magnitude of the leak around an uncuffed endotracheal tube (ETT). In newborn infants the volume of the lungs is only a fraction of the circuit/humidifier volume and often poorly compliant. Thus the loss of volume to compression of gas in the circuit and to stretching of the compliant circuit is very substantial. Variable leak around ETTs makes compensation very challenging.

Neonatal Tidal Volume-Targeted Ventilation

In contrast to traditional VC ventilation, V T -targeted ventilation modalities are modifications of pressure-controlled ventilation designed to deliver a target V T by microprocessor-directed adjustments of inflation pressure or inflation time. Some devices regulate V T delivery based on flow measurement during inflation and others during exhalation. Each approach has advantages and disadvantages: leak is greater during inflation and thus exhaled V T more closely approximates true V T . Use of exhaled V T results in regulation of the peak pressure based on the previous ventilator cycle, whereas using inflation volume makes same-cycle control possible, but it is then not possible to compensate for ETT leak in real time. If the inflation volume were 10 mL and the ETT leak 50%, then the baby would be getting a V T of only 5 mL. When a large ETT leak is present, exhaled V T may underestimate true volume and inspiratory measurement will overestimate the true V T that enters the lungs. On balance, the use of exhaled V T appears to offer the best balance of safety and effectiveness. Newer modalities of VTV have increasingly come to closely resemble volume guarantee ventilation, which focuses on expired V T , as described below.

Volume Guarantee

Volume guarantee (VG) is an option available on the Dräger Babylog 8000+, the VN 500 (Dräger Medical, Lübeck, Germany), and the Leoni Plus (Heinen + Löwenstein GmbH, Bad Ems, Germany—not available in the United States). More recently, a version of VG has been implemented on the Avea ventilator (CareFusion, San Diego, CA) and the GE Engström Carestation (GE Healthcare, Chicago, IL). VG may be combined with any of the basic ventilator modes (continuous mandatory ventilation, assist/control [AC], synchronized intermittent mandatory ventilation [SIMV], pressure support ventilation). It is a volume-targeted, time- or flow-cycled, pressure-controlled form of ventilation. The operator chooses a target V T and a pressure limit up to which the ventilator operating pressure (working pressure) may be adjusted. The microprocessor compares the exhaled V T of the previous inflation and adjusts the working pressure up or down to target the set V T ( Fig. 20-4 ). The algorithm limits the pressure increment from one inflation to the next to a percentage of the amount needed to reach the target V T to avoid excessive oscillations, up to a maximum increase of 3 cm H 2 O. Consequently, with rapid, large changes in compliance or patient inspiratory effort, several cycles are needed to reach target V T . If the ventilator is unable to reach the target V T with the set inflation pressure limit, a “low V T ” alarm will sound, alerting the operator that an assessment is needed. The VG modality, as implemented on the Dräger Babylog 8000+ and VN 500 ventilators, which are designed specifically for newborn infants, employs separate controls for triggered and untriggered inflations. This is an important feature when ventilating spontaneously breathing preterm infants whose respiratory effort is highly variable, because as with all forms of synchronized ventilation, the V T is determined by a combination of the positive pressure from the ventilator and the negative intrapleural pressure resulting from the spontaneous effort of the infant ( Fig. 20-5 ). Consequently VG leads to a more stable V T than would be seen in similar modalities that use a single control algorithm ( Fig. 20-6 ). The impact of VG with the dual control algorithm compared to simple PC ventilation is seen in Figure 20-7 . A secondary safety feature designed to prevent delivery of excessively large inflations terminates an inflation on the same cycle if the V T target is exceeded by >30% based on inspiratory volume measurement (corrected for leakage). In an awake, actively breathing infant the variable patient contribution to transpulmonary pressure is always perturbing the equilibrium, causing the V T to fluctuate around the target V T . Thus the term volume guarantee is arguably a misnomer. However, there is good evidence that a completely constant V T leads to atelectasis over time; thus a physiologic variability of V T is actually desirable.

FIG 20-4

Principles of operation of volume guarantee. The device compares the measured tidal volume to the target volume and automatically regulates the PIP (peak inflation pressure, working pressure) within preset limits (as low as end-expiratory pressure to as high as the pressure limit) to achieve the tidal volume that is set by the user. Regulation of PIP is in response to exhaled tidal volume to decrease error due to ETT leak. The PIP increase from one cycle to the next is limited to avoid overshoot and undesirable oscillations. If tidal volume exceeds 130% of target, inflation will be terminated at that point (a secondary safety volume-limit function).

FIG 20-5

In an awake, breathing infant the tidal volume that enters the lungs is generated by the transpulmonary pressure, the sum of the negative intrathoracic pressure generated by the infant’s spontaneous respiratory effort and the positive inflation pressure generated by the ventilator. Because the respiratory effort of a preterm infant is variable and inconsistent, the infant’s contribution to the transpulmonary pressure is variable, thus resulting in a variable tidal volume.

FIG 20-6

A, Because the respiratory effort of a preterm infant is variable and inconsistent, the infant’s contribution to the transpulmonary pressure is variable, thus resulting in a variable tidal volume. In this graph, the infant’s own inspiratory effort is drawn in blue, superimposed on the ventilator pressure. This contribution is not measured or displayed by the ventilator. When an actively breathing infant who was contributing substantially to the transpulmonary pressure fails to take a breath before the next ventilator cycle, there will be a large drop in delivered tidal volume. The ventilator adjusts the working pressure based on the tidal volume of the previous cycle, but the infant again resumes its breathing, resulting in large fluctuations in tidal volume. Because of the limited increment in working pressure from breath to breath, it takes several cycles to reach the target tidal volume when the infant remains apneic. B, The VG function as implemented on the Dräger devices has a separate control algorithm to regulate triggered and untriggered inflations. The microprocessor will use the working pressure for the previous cycle of the same type (triggered or untriggered) as a starting point for the adjustment. Consequently, the transpulmonary pressure remains more stable, resulting in more stable tidal volume delivery.

FIG 20-7

The impact of volume guarantee (VG) with dual control algorithm versus PC ventilation. Flow is displayed at the top, pressure in the middle, and tidal volume (V T ) at the bottom. Relatively stable V T is seen in the first part of the recording while peak inflation pressure (PIP) is highly variable. After VG is turned off, PIP becomes fixed (after it is manually lowered in two steps), while V T begins to fluctuate from inflation to inflation, because now we see the impact of a fixed PIP on top of a highly variable and sometimes absent spontaneous effort of the baby.

The VG modality, as implemented on a Dräger ventilator, has been studied more thoroughly than other modes of VTV. VG reduces the incidence of hypocarbia and the number of excessively large V T s. Specific clinical guidelines for VG have been published and are also provided below and in Table 20-2 . VG has been shown to be more effective when used with AC than with SIMV, probably because all inflations are subject to volume targeting.

TABLE 20-2

Clinical Guidelines for Volume-Targeted Ventilation

Recommendation Rationale
Initiation of VTV

  • Implement VTV as soon as feasible

  • Choose basic mode of synchronized ventilation: PC-AC or PC-PSV is preferred

  • If using SIMV + PSV, be aware that only the SIMV inflations are volume guaranteed

  • Select backup rate about 10 breaths below spontaneous breathing rate: 30/min for term, 40/min for preterm infants

  • Select PEEP appropriate to the infant’s diagnosis, current condition, and FiO 2

  • Ensure that flow sensor is calibrated and functioning properly

  • Select target V T :

    • 4.5 mL/kg for typical preterm infant with RDS

    • 5-6 mL/kg if <700 g

    • 5-6 mL/kg if MAS, air-trapping

    • 6 mL/kg if >2 weeks

  • Set PIP limit 3-5 cm H 2 O above expected PIP need

  • If V T target not met, ensure ETT is in good position, then increase PIP limit if needed

  • Confirm adequacy of support by observing chest rise, auscultating breath sounds, and monitoring SpO 2 and obtaining blood gas

  • If converting from PC to VTV, match the V T generated by PC mode if PaCO 2 was satisfactory and increase PIP limit by 3-5 cm H 2 O

  • Compliance and respiratory effort change rapidly soon after birth

  • These ventilator modes result in more stable V T and lower work of breathing

  • The PSV pressure is a set value, not subject to VG

  • Backup rate is a safety net for apnea. If too low, there will be more fluctuation in SpO 2 and minute ventilation; if too high, there will be more untriggered inflations

  • Because VG uses lowest possible PIP, adequate PEEP is essential to maintain FRC

  • Accurate V T measurement is essential for VTV

  • V T is now the primary control variable

    • Typical V T for average preterm infant

    • Impact of instrumental DS

    • Increased alveolar DS

    • Increased anatomic and alveolar DS

  • To allow adjustment of working pressure both up and down

  • ETT obstructed on carina would cause high PIP, ETT in right bronchus would cause high PIP, volutrauma

  • Recommended V T targets are population averages; individual patients may need higher or lower V T

  • Changing primary control variable does not affect relationship of compliance, PIP, and V T . Allow PIP to float both up and down as needed. Average PIP will be less than or equal to that on PC

Subsequent Adjustment

  • Once range of working PIP is known, set PIP limit 25%-30% above upper end of the range

  • Record and present on rounds range of working PIP as well as PIP limit

  • If indicated, adjust V T in steps of ∼0.5 mL/kg

  • Base V T adjustments on pH, not PaCO 2 ; do not lower V T target if pH is not alkalotic

  • Lower PIP limit as needed to keep it 25%-30% above upper end of the range of PIP

  • Assess patient’s respiratory rate, comfort, oxygen requirement, and working pressure, not just blood gas. Increase V T if necessary to achieve adequate support

  • Always verify appropriateness of support by clinical assessment, especially if large increase in support appears to be needed

  • Use birth weight initially to determine V T target and remember to adjust for weight gain if the baby remains ventilated

  • Important safety feature to alert provider to changes in support

  • PIP limit does not accurately reflect actual level of support

  • This step leads to meaningful change

  • pH, not PaCO 2 is the primary control of respiratory drive. Infants compensate for a base deficit by hyperventilating

  • As compliance and respiratory effort improve, working PIP comes down

  • Tachypnea and retractions indicate increased WOB. If V T is set below patient’s physiologic need, the ventilator lowers the PIP and the infant has to work harder to maintain its MV

  • Machines are fallible. Do not blindly trust any mechanical device

  • Short-term changes in weight after birth reflect fluid shifts, but once baby begins to grow, the V T needs to keep up with current weight


  • When pH is low enough to ensure respiratory drive, weaning is automatic; do not lower target V T to wean, unless patient is alkalotic

  • Withhold or reduce sedation/analgesia

  • Do not reduce V T below 3.5-4 mL/kg

  • Consider raising PEEP to maintain adequate distending pressure as PIP comes down

  • Avoid using SIMV and do not wean backup rate on PC-AC or PC-PSV

  • Observe the graphic display to detect excessive periodic breathing or apnea

  • Physiologic V T need does not decrease, the PIP needed to achieve it does—self-weaning

  • Avoid suppressing the respiratory drive

  • Setting the V T below what the infant needs imposes excessive WOB

  • Automatic lowering of PIP may lead to atelectasis if PEEP is relatively low

  • As PIP comes down, the WOB is gradually shifted from ventilator to infant. The infant controls the ventilator rate

  • Inconsistent respiratory effort may set up the infant for extubation failure


  • Consider extubation if inflation pressure is ≤12-15 cm H 2 O with satisfactory blood gas.

  • Readiness for extubation can be assessed using the SBT

  • Caffeine should always be used prior to extubation of preterm infants ≤32 weeks

  • Distending pressure with CPAP, NIPPV, or HHHFNC should always be used for at least 24 hr post extubation

  • These pressures are low enough to ensure that the infant is able to take over

  • The SBT has been shown to accurately predict extubation readiness

  • Caffeine reduces extubation failure in preterm infants

  • The use of distending airway pressure after extubation reduces the risk of extubation failure

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Jan 30, 2019 | Posted by in PEDIATRICS | Comments Off on Tidal Volume-Targeted Ventilation
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