Gentle Ventilation in the NICU

Vol. 14 •Issue 7 • Page 32
Neonatal Care

Gentle Ventilation in the NICU

Support Neonates With Settings That Approximate Physiologic Breathing

Before mechanical ventilation was used to support infants in the 1960s, neonates born more than a month before their due date had little chance of survival, mostly dying from respiratory insufficiency.

In 1963, President John F. Kennedy’s son, Patrick, born six weeks prematurely and weighing 2,100 g, died from respiratory failure a few days after birth. Patrick’s death fueled a flurry of research on understanding and treating neonatal respiratory distress syndrome.

A deficit of surfactant, leading to alveolar collapse and making it difficult for premature infants to breathe, was identified as the culprit in premature respiratory distress syndrome.1 Surfactant is a naturally occurring detergent that lowers alveolar surface tension. This detergent was isolated from cow lungs, purified and, through randomized clinical trials, shown to improve survival when delivered down the breathing tubes of premature infants.2

At the same time the importance of surfactant in neonatal respiratory disease was being discovered, new ventilators were being designed for neonates. The combination of technologic advances and surfactant replacement therapy has resulted in a significant increase in neonatal intensive care units’ survival rates since Patrick Kennedy’s birth and death. Currently, the survival rate for infants born at 26 weeks gestation cared for in our regional perinatal center is more than 90 percent, and for infants born at 24 weeks gestation, 60 percent.


The early ventilator models used in NICUs were scaled down from those designed for 70 kg adults and used on 3 kg neonates. While lifesaving to some neonates, mechanical ventilation was risky business.

The ventilators provided nonsynchronized intermittent mandatory ventilation, raising the potential for patient distress or pneumothoraces when the machine tried to deliver a breath when the infant was exhaling.

It also was difficult to determine which settings would provide adequate gas exchange without leading to barotrauma (pressure-induced lung damage) and volutrauma (stretch-induced tissue disruption) in these tiny patients, some of whom weighed only 500 g with lung volumes of 3 cc. Settings that resulted in normal blood gases in extremely premature infants would quickly lead to lung damage, inflammation (biotrauma), and often, a delayed death from chronic lung disease known as bronchopulmonary dysplasia.

It became clear that using high ventilator settings was an independent risk for lung damage, irrespective of the initial disease severity or underlying reason for initiating mechanical ventilation. While using higher ventilator settings can result in more normal blood gases in the short run, in the long run the resultant tissue disruption and inflammation leads to chronic lung disease.3

In an effort to protect the lungs from ventilator-induced lung injury, the practice of supporting neonates with respiratory insufficiency using assisted ventilation that approximates physiologic breathing rather than targeting normal blood gases, known as gentle ventilation, developed.

In this approach, ventilator settings that avoid excessive chest movement and alveolar overdistension are selected. Relative hypoxia and hypercapnea are tolerated. Lung distension on chest X-ray of 9 to 91/2 ribs expansion on the patient’s right chest are targeted (8 to 81/2 ribs in the case of air leak syndrome). It can be used with conventional and high-frequency ventilation.

Practicing gentle ventilation protects the lung, decreases the length of mechanical ventilation, and decreases the risk for subglottic stenosis, a narrowing of the trachea observed in neonates receiving prolonged mechanical ventilation.4,5


One of the earliest advances in mechanical ventilators used for neonates was synchrony — the ability of the machine to detect the infant’s effort to take a breath. Synchrony can be established in a number of ways. Newer machines can detect chest movements from breathing efforts, a change in airflow initiated by the patient, or a change in gas temperature in the respiratory circuit caused by a patient’s respiratory effort.

Early ventilators used pressure ventilation to minimize pneumothoraces due to rapidly changing compliance in many neonatal respiratory diseases. Newer ventilators have an improved ability to detect and respond to changes in pressure needed to deliver a set tidal volume. Clinicians can use volume ventilation to deliver a physiological breath, while using a pressure safety to limit the peak inspiratory pressure (PIP) used to deliver the set tidal volume.

This approach optimizes ventilation while guarding against excessive peak pressures delivered during times of rapidly changing compliance. It also avoids a full tidal volume breath being delivered unilaterally if an endotracheal tube inadvertently moves into a mainstem bronchus, which isn’t uncommon when extremely low birth weight infants with very short tracheae move or are repositioned.

The advanced sensors in current ventilators that allow synchronized ventilator breaths and combined volume/pressure ventilation result in the ability to deliver a mechanical breath to even the smallest infant with minimal barotrauma or volutrauma, if physiologic ventilator settings are used.

High-frequency oscillatory or jet ventilation also can be used to provide gentle ventilation. If conventional ventilation using physiologic settings fails to provide adequate oxygenation or ventilation, high frequency may be more effective at gas exchange while maintaining relatively low settings.


In premature infants, mask or nasal continuous positive airway pressure may be used to avoid atelectasis and minimize the need for endotracheal intubation with mechanical ventilation. If mechanical ventilation is necessary, large tidal volumes and high peak pressures are avoided because these can lead to tissue disruption and a heightened ventilator-induced inflammatory response.

There are no definitive ventilator settings or target blood gases determined to be optimal in randomized controlled trials in gentle ventilation of neonates. The ventilator settings are chosen to most closely approximate physiologic breathing. Tidal volumes and peak pressures are chosen to mimic spontaneous breathing, with excessive chest movement being avoided.

A tidal volume of 6 cc/kg and PIP of 20 to 25 cm H2O in full-term infants are targeted. Comparable tidal volumes of 6 to 8 cc/kg are used in premature infants, with peak pressures for the smallest premature infants often only reaching 9 cm H2O.

Optimum positive end expiratory pressure (PEEP) is used to avoid atelectasis and minimize hyperoxic lung damage. Because hyperoxia also can lead to lung injury, if there’s a persistent need for oxygen greater than 60 percent, increased PEEP may be beneficial in decreasing oxygen exposure.


As with target ventilator settings, data on optimal target blood gases is limited. A target PaCO2 of 50 to 75 mm Hg appears to be well-tolerated in premature infants, but long-term outcome data isn’t yet available.6 A PaO2 of 50 mm Hg or oxygen saturation of 88 percent to 92 percent is frequently targeted, although current studies investigating the safety of lower target saturations are ongoing.7

Hyperventilation, previously used in full-term infants with persistent pulmonary hypertension (PPHN) to increase pH, improves PaO2 in the short term, but can lead to increased lung damage and hearing loss, doesn’t improve long-term outcome, and should be avoided.8 Normal blood gases are routinely targeted in infants with PPHN (PaCO2 35 to 45 mm Hg, PaO2 60 to 100 mm Hg).

A modified set of target blood gases for infants with congenital diaphragmatic hernia and pulmonary hypoplasia appears to be beneficial. Infants are maintained on 100-percent oxygen for the initial six hours. PIP 20 to 24 cm H2O and PEEP 4 to 5 cm H2O are maintained. PaCO2 of 40 to 65 mm Hg and oxygen saturations > 97 percent with PaO2 80 to 100 mm Hg are targeted. A PaCO2 > 65 mm Hg is tolerated if arterial pH is > 7.20, and postductal oxygen saturations in the 60s are tolerated if preductal saturations are ³ 85 and the infant otherwise is doing well and isn’t acidotic.

Applying this approach can lead to a survival rate among infants with congenital diaphragmatic hernia of greater than 90 percent.9,10 Long-term studies of neurodevelopmental outcome haven’t yet been performed.


Gentle ventilation strategies initially focused on minimizing barotrauma and volutrauma in extremely premature infants with underdeveloped lungs and infants with pulmonary hypoplasia, such as babies with congenital diaphragmatic hernia receiving prolonged mechanical ventilation in the NICU. More recently, gentle ventilation techniques have moved to the delivery room, with mask CPAP being administered to premature infants right at birth to avoid atelectasis and the eventual need for intubation.11

Even resuscitation can be performed using an apparatus designed for neonates to provide CPAP that allows delivery of breaths of preset PIP and PEEP. This minimizes inadvertently high PIPs being delivered in the heat of a resuscitation.

The concepts used in neonatal patients also have been extended to other patients requiring mechanical ventilation, including adults with acute respiratory distress syndrome, for whom gentle ventilation with tidal volumes of 6 to 8 cc/kg has been found to decrease mortality.12,13 Weaning guidelines also have been established for adults.14

While there’s a growing body of literature to support the safety and efficacy of gentle ventilation in a wide range of ages with a broad spectrum of pathophysiologies, the conditions of optimum ventilation strategies and target blood gases, especially in the neonatal population, are areas of ongoing research.15

Patricia R. Chess, MD, is associate professor of pediatrics and biomedical engineering, and ECMO medical director at Golisano Children’s Hospital at Strong, University of Rochester School of Medicine and Dentistry, N.Y.

For a list of references, please call Sharlene George at (610) 278-1400, ext. 1324, or visit

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