Mechanical Ventilation of the Neonate: Principles and Strategies

Transcription

1 12 Current Respiratory Medicine Reviews, 2012, 8, Mechanical Ventilation of the Neonate: Principles and Strategies Steven M. Donn * Department of Pediatrics, Division of Neonatal-Perinatal Medicine, C.S. Mott Children s Hospital, University of Michigan Health System, Ann Arbor, MI , USA Abstract: The advent of microprocessor-based technology has revolutionalized the treatment of respiratory failure in the newborn. Clinicians are now able to customize ventilatory strategies to the specific pathophysiology of the patient. Sophisticated monitoring provides breath-to-breath feedback on patient-ventilator interactions. This paper will focus upon the basic principles of mechanical ventilation, and will review various strategies that may be employed to manage the wide range of respiratory disorders encountered by preterm and term newborn infants, including respiratory distress syndrome, meconium aspiration syndrome, persistent pulmonary hypertension of the newborn, and bronchopulmonary dysplasia. Keywords: Newborn, prematurity, respiratory failure, mechanical ventilation. INTRODUCTION Newborns with respiratory failure have been treated with mechanical ventilation since the early 1960s. The first attempts at assisted ventilation were performed with adult ventilators, modified to fit small babies, which achieved token success but were very problematic in meeting the unique needs of these relatively small patients [1]. The development of continuous flow techniques, whereby the baby had a fresh gas source from which to breathe between mechanical breaths, was a major advance and became the mainstay of treatment for more than a quarter of a century. Virtually all infants, irrespective of their underlying lung disease, were ventilated with time-cycled pressure-limited (TCPL) ventilators using the intermittent mandatory ventilation (IMV) mode. As more and more preterm babies survived, the challenges and limitations of the first generation neonatal mechanical ventilators became more apparent, as did the recognition that not all babies nor their pulmonary problems were alike. Technological enhancements brought high-frequency ventilation (HFV) to the neonatal intensive care unit (NICU) in the 1980s as an alternative to conventional mechanical ventilation (CMV). The use of pulse oximetry to assess oxygenation non-invasively became widespread practice. The 1990s saw the incorporation of the microprocessor into the ventilator, along with the development of lightweight, low deadspace transducers rendering the ability to more accurately measure airway flow and pressure, create volume measurements, and provide instantaneous feedback with both data and real-time pulmonary graphics [2]. This also led to the development of patient-triggered ventilation (PTV) [3] and, to a large extent, led to the evolution of patient- and disease-specific strategies. *Address correspondence to this author at the F5790 C.S. Mott Children s Hospital, 1500 E. Medical Center Drive, Ann Arbor, MI , USA; Tel: ; Fax: ; smdonnmd@med.umich.edu This era has also been marked by significant pharmacological advances in treating newborns with respiratory failure, including antenatal corticosteroids to induce fetal lung maturation, exogenous surfactant to treat respiratory distress syndrome (RDS), cyclo-oxygenase inhibitors to close a patent ductus arteriosus (PDA), and inhaled nitric oxide (ino) to reduce pulmonary vascular resistance in persistent pulmonary hypertension of the newborn (PPHN). BASIC PRINCIPLES OF MECHANICAL VENTILATION Indications Mechanical ventilation is used to provide all or part of the work of breathing when a newborn is unable to achieve adequate pulmonary gas exchange, exhibiting either hypoxemia, hypercapnia, or both. Mechanical ventilation may also be necessary in situations where lung function is normal, but respiratory drive is inadequate. This can occur if the baby is pharmacologically depressed (for example, after maternal narcotics or magnesium sulfate therapy), has neuromuscular disease, or exhibits central nervous system depression for any reason, such as intracranial hemorrhage, hypoxic-ischemic encephalopathy, or central apnea. Extrapulmonary conditions, such as airway or cranio-facial anomalies, may also require mechanical respiratory support. Oxygenation The major determinants of oxygenation are the fraction of inspired oxygen (FiO 2 ) and the mean airway pressure [4]. Increases in the fraction of inspired oxygen may be used to overcome alveolar hypoxia, reduce pulmonary vasoconstriction, and improve ventilation-perfusion mismatch. Care must be taken with its use in very preterm babies, as it has been associated with the subsequent development of retinopathy of prematurity [5]. Mean airway pressure refers to the average pressure applied to the lung during the respiratory cycle. It may be graphically depicted as the area under the curve for a single ventilator cycle. It is used to recruit lung volume and to 1-8 /12 $ Bentham Science Publishers

2 Mechanical Ventilation of the Neonate Current Respiratory Medicine Reviews, 2012, Vol. 8, No increase the surface area of the lung exposed to gas exchange. Optimally, the lung should be ventilated at functional residual capacity. Ventilating above this point may expose the lung to excessive pressure (barotrauma) and volume (volutrauma), and ventilating below this point may subject the lung to atelectotrauma, where lung units are injured by the repetitive opening an closing of this still delicate (and developing) tissue [6]. Several factors contribute to mean airway pressure. Positive end-expiratory pressure (PEEP) has the greatest effect, as every 1 cm H 2 O increase in PEEP results in a 1 cm H 2 O increase in mean airway pressure. Peak inspiratory pressure (PIP) also contributes to mean pressure, and the longer the inspiratory time (T i ), the greater the effect. Ventilator rate may have a small effect on mean airway pressure, as there is more area under the curve for a given time at a faster rate, if all other conditions are kept constant. Rise time, a feature on some ventilators that offer variable inspiratory flow, may also be used to qualitatively adjust inspiratory flow to avoid pressure overshoot or air hunger, conditions which may cause rheotrauma. Ventilation Ventilation refers to the removal of carbon dioxide. During conventional ventilation, the amount of carbon dioxide removed is proportional to the tidal volume (V T ), which in turn is determined by the difference between PIP and PEEP (often referred to as amplitude), and frequency (rate) [7]. Thus, to increase ventilation, amplitude or tidal volume can be increased by raising the PIP, lowering the PEEP, or doing both, or by increasing the rate. During HFV, carbon dioxide removal is proportional to the rate and the square of the V T [8]. This is why even small changes in amplitude can have a profound effect on arterial carbon dioxide tension, much more so than altering the rate. Monitoring of the Ventilated Newborn Although mechanical ventilation is a life-saving tool, it is not without hazards and potential complications and demands constant clinical vigilance. Newborns receiving mechanical ventilation should be monitored closely for the development of situations which could lead to lung or systemic injury. Fortunately, present day ventilators are equipped with numerous alarms which alert clinicians when various parameters can not be met or are exceeded. Virtually all NICUs now monitor oxygenation continuously with pulse oximetry [9]. This device displays the percent saturation of hemoglobin and is relatively accurate. However, clinicians must realize that the linearity between arterial oxygen tension and saturation disappears as saturation approaches 98%. Use of dual site pulse oximetry has been used to detect right-to-left shunting in babies with PPHN and can be used as an adjunct to manage systemic blood pressure in this condition. Transcutaneous monitoring of both oxygen and carbon dioxide is possible [10]. Electrodes are affixed to the skin, heated, and used to approximate the arterial tensions of these gases. Earlier versions required substantial heating to 43 or 44 degrees Centigrade and produced burns if left in situ too long. A newer version appears to have overcome this problem. End-tidal carbon dioxide (capnometry) is another technique that is available, but it has not been utilized very much, probably because its use increases ventilator deadspace and there is little clinical information regarding its utility in the newborn [11]. One of the most important advances in monitoring was the advent of real-time pulmonary graphics [2]. Breath-tobreath displays of waveforms (pressure, flow, and volume), and displays of pulmonary mechanics (flow-volume, pressure-volume, and other loops) provide the clinician with a wealth of information regarding the status of the baby and the interaction between the baby and the ventilator. Several conditions may be seen graphically before they are clinically apparent, such as gas trapping and hyperinflation. Digital displays of V T, and minute ventilation may decrease the frequency of blood gas analyses, and trends in parameters such as compliance and resistance provide objective assessments of treatments such as surfactant or bronchodilators. Conventional Mechanical Ventilation Conventional mechanical ventilation refers to a form of assisted ventilation in which the delivered gas volumes approach physiologic tidal volumes, and the patterns of breathing attempt to mimic physiologic breathing. It may also be referred to as tidal ventilation. There are several different ways in which this is accomplished in clinical practice. Conventional ventilators are commonly designated by their modalities, such as pressure-targeted or volumetargeted, which are really a reflection of how gas flow is delivered to the patient. Continuous Flow Ventilation Continuous flow ventilation is utilized in traditional TCPL ventilation. Bias gas flow through the ventilator circuit is set by the clinician. When the exhalation valve closes, this flow is diverted to the patient and the lungs are inflated. The rate of inspiratory flow and the tidal volume delivered to the patient, are determined by lung mechanics. Cycling is accomplished by setting a fixed inspiratory time, although many newer ventilators allow the clinician to use flow cycling (described below). Peak pressure is also set by the clinician. Setting the proper circuit flow is important. If too low, the peak pressure may not be reached; if set too high, hyperinflation, turbulence (and inefficient gas exchange), and inadvertent PEEP may result. Variable Flow Ventilation Variable flow ventilation produces a rapidly accelerating inspiratory flow waveform, which subsequently decelerates fairly quickly. It results in rapid pressurization of the ventilator circuit and delivery of peak pressure and peak volume delivery early in inspiration. It may thus be considered to be a front end loaded breath [12]. This gas flow pattern is utilized in both pressure control ventilation (PCV) and pressure support ventilation (PSV) [13]. Both of these modalities are pressure limited and delivered tidal

3 14 Current Respiratory Medicine Reviews, 2012, Vol. 8, No. 1 Steven M. Donn volume will be proportional to lung compliance. PCV was originally time cycled, but several ventilators now offer flow cycling. PSV is flow cycled and time limited. Theoretical advantages of variable flow include treatment of homogeneous lung disease characterized by the need for a high opening pressure (such as RDS), as well as situations characterized by high resistance, where a higher flow rate may be beneficial in overcoming this. Constant Flow Ventilation Constant flow ventilation is utilized in volume targeted ventilation [12]. Gas flow accelerates to a pre-selected limit and is then held constant until a targeted volume of gas is delivered, and then decelerates. This type of flow delivery results in achieving peak pressure and peak volume delivery late in the inspiratory phase, and thus it is a back end loaded breath. It produces a square flow waveform. This should be advantageous when lung disease is heterogeneous to avoid over-ventilation of compliant areas and underventilation of atelectatic areas. It should also offer advantages in disease states characterized by rapidly changing compliance, as the pressure will be automatically adjusted to provide the desired tidal volume. Recent advances in some ventilators allow clinicians to select a decelerating waveform, but the advantages of such are yet to be determined. Modes of Ventilation Modes of ventilation refer to the way that breaths are delivered to the patient. In intermittent mandatory ventilation (IMV), the clinician sets a rate at which the ventilator is to cycle, and mechanical breaths are delivered to the baby at regular intervals, irrespective of the baby s own spontaneous breathing, which is supported only by PEEP. This often results in asynchronous breathing, where the baby may be exhaling against positive pressure. Asynchrony has been shown to result in inefficient gas exchange, widely variable tidal volume delivery, air leaks, increased work of breathing [13], and irregularity of arterial blood pressure and cerebral blood flow velocity [14]. The latter has a strong association with intraventricular hemorrhage in preterm babies [14]. Synchronized intermittent ventilation (SIMV) is a form of patient triggered ventilation (PTV). It is similar to IMV except that when it is time to cycle a mechanical breath, the ventilator will look for the initiation of a spontaneous breath and then synchronize the mechanical breath to the spontaneous breath. If the baby fails to breath or fails to trigger the breath, the mechanical breath will still be delivered. Again, spontaneous breaths between mechanical breaths are supported only by PEEP. Assist/control ventilation (A/C) can be used to achieve full synchrony between mechanical and spontaneous breaths [15]. Each time that the baby starts to breathe and exceeds the assist sensitivity or trigger level, a mechanical breath will be provided. Thus, the baby controls the ventilatory rate. Assist sensitivity is usually based on an inspiratory flow change, and enables even the tiniest babies to avail themselves of this method. If the patient fails to trigger the ventilator, breaths are provided at intervals defined by the control rate (e.g., if the control rate is 30/min, the ventilator will cycle 2 sec after the prior breath if no patient effort is detected). Clinicians must be aware that as long as the baby is breathing above the control rate, further reduction in the control rate will have no impact on gas exchange. Thus, the primary weaning strategy should be the reduction in peak pressure during pressure targeted ventilation (TCPL or PCV). Pressure support ventilation was introduced into neonatal intensive care in the early 1990s. It is a spontaneous mode of ventilation, in which an inspiratory pressure assist can be applied to fully or partially support spontaneous breaths. PSV is flow cycled and pressure and time limited. It is generally used in combination with SIMV, but it may be a stand alone mode if the baby has reliable respiratory drive [13]. It is most often utilized during the weaning phase of mechanical ventilation, where it mimics A/C; the SIMV breaths are used as control breaths, and the PSV breaths are the assist breaths. PSV will decrease the patient work of breathing and facilitates weaning by unloading the respiratory musculature during spontaneous breathing [16]. Cycling Mechanisms Cycling refers to the way in which inspiration is transitioned to expiration, and the way in which expiration is transitioned to inspiration. Mechanisms of cycling include time, flow, and volume. However, because cuffed endotracheal tubes are not used in the newborn, there is always some degree of leak around the endotracheal tube precluding volume as a reliable cycling mechanism in neonatal intensive care. Time cycling is the oldest and widest practice method. Inspiration ends after a preset time elapses. Time cycling may be the primary mechanism, but it is also used as a backup mechanism to flow cycling. Time cycling gives the clinician the ability to determine how long a breath will last. Consideration needs to be given to the respiratory time constant, the product of resistance and compliance, which determines how much time is necessary for the equilibration of pressure (and volume) in the lung. Expiratory time needs to be 4-5 times the length of the time constant to avoid gas trapping. Flow cycling can be used to terminate inspiration based on the natural decay of the inspiratory flow waveform. Here, the clinician can choose a point on the decelerating limb where the breath should be terminated. This is usually 5-15% of the peak inspiratory flow rate. The ventilator recognizes this point, which is just before the baby is terminating his own breath, and inspiration ends, cycling directly into expiration. In other words, the baby does not achieve a zero flow state just prior to expiration. There are two major advantages to using flow cycling. First, it achieves complete synchrony between the ventilator and the baby. The baby initiates the breath and terminates the breath, thus establishing both the ventilator rate and the inspiratory time. Secondly, it is a safeguard against gas trapping during PTV. If time cycling is utilized during PTV and the baby becomes tachypneic, the faster the baby breathes, the shorter the expiratory time becomes because the inspiratory time is fixed. At rapid rates, the baby could inverse the

4 Mechanical Ventilation of the Neonate Current Respiratory Medicine Reviews, 2012, Vol. 8, No inspiratory:expiratory ratio with resultant gas trapping and inadvertent PEEP. With flow cycling, because inspiration always ends at a percentage of peak inspiratory flow, the ratio will be maintained, and the inspiratory time will get shorter. When flow cycling is working successfully, the actual inspiratory time will be shorter than the set inspiratory time, which becomes a limit variable. High-Frequency Ventilation High-frequency ventilation (HFV) differs from CMV in two major ways. First, the delivered gas volumes are less than the anatomical deadspace, generally 1-3 ml/kg. Thus, it is non-tidal ventilation. Second, these devices operate at very rapid rates. There are two preeminent forms of HFV, high-frequency jet ventilation (HFJV) and high-frequency oscillatory ventilation (HFOV), as well as some hybrids. From a practical standpoint, most of the principles of mechanical ventilation for CMV also apply to HFV. Oxygenation is proportional to mean airway pressure. Ventilation differs slightly, however, in being the product of frequency (rate) and the square of the delivered gas volume. Even small changes in the determinant of the delivered volume (PIP and PEEP) can have profound effects on carbon dioxide elimination and must thus be monitored aggressively [17]. High-Frequency Jet Ventilation HFJV is accomplished by the delivery of high velocity pulsations directly into the airway or proximal endotracheal tube. Rates vary from breaths per minute. HFJV is used in tandem with a conventional ventilator, which provides PEEP and can be used to deliver occasional mechanical breaths, or sighs. HFJV relies on passive exhalation (the elastic recoil of the lungs) to drive expired gas from the airway. It has proven to be very effective in treating air leaks, such as pulmonary interstitial emphysema [18] and recurrent pneumothorax, and in the management of major airway disruptions, such as tracheo-esophageal fistula and broncho-pleural fistula [19]. High-Frequency Oscillatory Ventilation HFOV is provided by a stand alone device. It functions at a faster rate than HFJV, generally in the 8-15 Hz range. It utilizes active exhalation, where expired gas is actively removed from the airway during exhalation. A unique feature of HFOV is the uncoupling of oxygenation, controlled by adjustments in the mean airway pressure, and ventilation, controlled by adjustments in the amplitude. Unlike CMV (or HFJV), these adjustments can be made independent of one another without adversely affecting the other. HFOV has been used as a primary strategy for all types of respiratory disorders in the newborn, but it is more frequently utilized as a rescue tool for intractable respiratory failure unresponsive to CMV [17]. DISEASES AND STRATEGIES The newborn infant may be affected by numerous respiratory disorders with very different pathophysiologic features. In the early era of mechanical ventilation, when all that was available was TCPL ventilation and IMV, clinicians tended to treat virtually all of the disorders similarly. Better understanding of cardiopulmonary pathophysiology and enhanced ventilatory diagnostic and therapeutic techniques has greatly (and fortuitously) altered the approach to one which is both disease- and patient-specific. Respiratory Distress Syndrome RDS is the most common respiratory illness among infants born prematurely. It results from both anatomical and biochemical abnormalities of the underdeveloped lung. Affected infants display underdeveloped alveoli, small and poorly supported airways, and protein and fluid leak into the air spaces. They lack pulmonary surfactant, leading to impaired gas exchange and progressive atelectasis, resulting in increased work of breathing. The chest wall is usually more compliant than the lungs, adding to difficulty in breathing. The biochemical abnormality is surfactant deficiency. Exogenous surfactant is provided to help establish an air-liquid interface, maintaining the alveolar surface free of liquid to facilitate gas exchange, and to reduce the collapsing forces that can lead to progressive atelectasis [20]. RDS is a low lung volume disease. Goals of mechanical ventilation should be aimed at establishing normal functional residual capacity and ventilating the lung at a point where compliance is best. PEEP is used to maintain a degree of alveolar distension at end-expiration, to take advantage of the Laplace relationship, lower surface tension, and decrease the work of breathing. PIP is used to provide driving pressure to expand the lungs, and to establish the amplitude and hence, V T delivery. Different approaches have been espoused. CMV strategies have utilized both pressure-targeted and volume-targeted ventilation [21, 22]. As additional evidence has accumulated, it appears that volume-targeted ventilation may reduce the duration of mechanical ventilation and the incidence of air leaks, with a strong trend to reducing BPD [23]. A recent study also showed improved pulmonary outcomes at one year corrected age [24]. PTV, although offering many short term benefits, has not been shown to decrease BPD [25], nor has permissive hypercapnia [26, 27]. In a similar vein, HFOV has been utilized as a primary strategy. The evidence, on balance, is that although some short term physiologic advantages have been demonstrated, long term outcomes are no better than with CMV. Two very similar studies, one using HFOV vs SIMV [28], and one using HFOV vs TCPL ventilation [29], with about 25% of the CMV infants receiving PTV, had disparate results. One study using HFJV as a primary strategy showed a slight reduction in the need for supplemental oxygen at discharge [30]. An important question that still needs to be addressed is what are the clinically relevant outcome measures of neonatal ventilation studies [31]? It appears that BPD may now be more a function of extreme prematurity than a complication of mechanical ventilation [32]. Meconium Aspiration Syndrome Meconium aspiration syndrome (MAS) continues to be a significant problem despite the myriad of advances in

5 16 Current Respiratory Medicine Reviews, 2012, Vol. 8, No. 1 Steven M. Donn perinatal care. It is characterized by the aspiration of meconium-stained amniotic fluid, respiratory distress, and a typical radiographic appearance of fluffy infiltrates and hyperexpansion. The disorder results from both direct and indirect effects of meconium on the lung. Meconium may obstruct small airways, increasing the risk of gas trapping and air leak. It may incite inflammation, leading to impaired gas exchange. It can inactivate surfactant. It may contribute to increased pulmonary vascular resistance and secondary PPHN (see below) [33]. In contrast to RDS, MAS is a high lung volume disease. The goals of mechanical ventilation are to accomplish adequate pulmonary gas exchange without increasing the risks of hyperinflation, gas trapping, air leak, and PPHN. Multiple approaches to managing severe respiratory failure from MAS have been attempted. CMV strategies should address the pathophysiology. PEEP can be used to stent open the smaller airways. Use of short inspiratory times and slower rates may avoid gas trapping. Theoretically, constant flow ventilation should be of benefit when disease is patchy, but a definitive study has not yet been accomplished. Clinicians have utilized HFV to treat MAS. Combining exogenous surfactant and HFJV improves oxygenation [34]. HFOV has also been used, especially in conjunction with inhaled nitric oxide (ino), used to dilate the pulmonary vasculature and decrease right-to-left shunting [35]. Infants who continue to exhibit intractable respiratory failure may be candidates to undergo extracorporeal membrane oxygenation therapy (ECMO), which has a 94% survival rate in babies with an estimated mortality of >80%. Unfortunately, ECMO is an expensive and highly technological treatment, and it is not universally available. Persistent Pulmonary Hypertension of the Newborn PPHN is characterized by a group of disorders in which the normal fall in pulmonary vascular resistance that is supposed to happen at birth does not occur. Elevated pulmonary vascular resistance leads to diminished pulmonary blood flow and the shunting of de-oxygenated blood across the fetal channels- the foramen ovale and/or the ductus arteriosus. The pathophysiology may be thought of as a vicious circle, where hypoxemia leads to acidosis, acidosis exacerbates pulmonary vascular constriction, which reduces pulmonary blood flow. This decreases oxygen uptake and carbon dioxide removal, further contributing to tissue hypoxia and more acidosis. In addition, acidosis and decreased pulmonary blood flow may damage the pulmonary epithelium and inhibit production of surfactant from Type II cells. PPHN may be an idiopathic primary disorder, or it may be secondary to a host of disorders, including RDS, MAS, sepsis/pneumonia, congenital diaphragmatic hernia, pulmonary hypoplasia, and even transient tachypnea of the newborn. Ventilatory management of PPHN depends on a large extent to what the underlying pathophysiology is. This is nicely illustrated by the history of the disorder. It was first described by Gersony et al. in 1969 in newborns with severe hypoxemia and clear lung fields [36]. In the late 1970s, when Peckham and Fox showed that hyperventilation could radically improve oxygenation below some critical value of p a CO 2 [37], it became the standard treatment, even in babies with MAS or other parenchymal lung disease. There is little doubt that many infants suffered significant complications from hypocapnia, hyperoxia, and extreme alkalosis. CMV strategies need to be carefully planned to avoid complications, especially those that might contribute to elevated pulmonary vascular resistance, including hyperinflation and high intrathoracic pressure, and the avoidance of extremes of oxygen and carbon dioxide tensions. Similar cautions need to be applied to HFV, as well. The advent of ino has changed the approach to PPHN. This selective pulmonary vasodilator relaxes the pulmonary vascular endothelium, resulting in decreased pulmonary vascular resistance, breaking the vicious circle of PPHN. For ino to work, however, the lung must be adequately inflated. It appears that the combined use of HFOV and ino works better than either therapy alone [38]. ECMO may be considered in term or late preterm infants with intractable failure. Its success rate depends on the underlying disease. Bronchopulmonary Dysplasia Bronchopulmonary dysplasia (BPD), also referred to as chronic lung disease (CLD), is the most common respiratory sequel of prematurity. Initially, BPD was thought to represent the traumatic effects of pressure and oxygen therapy. However, recent evidence suggests a multifactorial etiology, with the common denominator being a reduction in the number of alveoli [32]. Various definitions have been used in the medical literature, including the need for supplemental oxygen at 36 weeks postmenstrual age. Using this, the incidence among very low birth weight (<1500 g) infants is 30-40%. Infants with BPD are likely to be <1500 g at birth and many received only modest ventilatory and oxygen support. Their chest radiographs show a diffuse, hazy pattern with fine, lacy infiltrates. Histopathologically, they show decreased alveolarization, minimal small airways disease, and less inflammation and fibrosis than was seen in an earlier era. The foremost goal of mechanical ventilation is to avoid further lung injury. Re-adjusting one s expectations of gas exchange is necessary to achieve this. Rapid rate (>60 breaths/min) CMV did not show any benefits over slower rate ventilation [39]. Using modest levels of PEEP (6 cm H 2 O) was associated in improved oxygenation without a concomitant increase in carbon dioxide tensions [40], perhaps by helping to stent the airways. Short term success has been demonstrated anecdotally for PTV [41], PSV [42], and HFOV [41], and the use of ino [43, 44], but no long term outcome measures have been adequately evaluated. Careful attention must be paid to adjunctive treatments, including the nutritional approach and evaluation of cardiac function. SUMMARY Neonatal intensive care, especially mechanical ventilation, has changed dramatically in the past 30 years. No longer are all infants treated the same, no matter what the cause of their respiratory failure. Mechanical ventilation is now a multi-faceted treatment, offering numerous options to attack complex pathophysiology.

6 Mechanical Ventilation of the Neonate Current Respiratory Medicine Reviews, 2012, Vol. 8, No Unfortunately, the evidence base for the newer therapies has yet to be fully elicited. Until such time as a definitive answer is reached, clinicians should adopt a physiologybased strategy. Consider the underlying problem and decide the best way to overcome this while minimizing the risks of aggravating the condition or injuring the patient further. Careful use of monitoring techniques and frequent reassessment of the baby will help to guide this approach. REFERENCES [1] Delivoria-Papadopoulos M, Levison H, Swyer PR. Intermittent positive pressure respiration as a treatment in severe respiratory distress syndrome. Arch Dis Child. 1965; 40: [2] Donn, SM (ed.). Neonatal and Pediatric Pulmonary Graphics: Principles and Clinical Applications. Armonk, NY, Futura Publishing Co., [3] Donn SM, Nicks JJ, Becker MA: Flow-synchronized ventilation of preterm infants with respiratory distress syndrome. 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N Engl J Med. 2006; 355: Received: November 15, 2010 Revised: December 9, 2010 Accepted: January 2, 2011