Introduction

Mechanical ventilation is ubiquitously deployed in the Neurological Critical Care Unit (NCCU). Special concerns about the effects of neurologic injury on ventilation complicate the care of ventilated patients in the NCCU and those with brain injury who are cared for in surgical and medical intensive care units (ICUs). Among all patients who are intubated in any ICU, 20% will be intubated secondary to neurologic injury [1]. Clinicians who care for neurologically impaired patients are often confronted with complex clinical challenges against a backdrop of limitations imposed by the need to preserve brain function. These problems require practitioners to incorporate novel strategies for the management of the ventilators that seem to operate outside the norms established for medical and surgical ICUs, and they often require solutions that are not well addressed by existing literature. It is necessary to understand the important clinical issues associated with different types of neurologic injury and to view them in the context of expanding evidence. Clinicians can focus on these issues as the starting point of a series of strategies directed toward enhancement of brain outcomes.

Intubation

Comatose or obtunded patients often present with airway occlusion caused by their altered mental status. One of the first concerns in patients with impaired consciousness is the tendency of the tongue to occlude the airway, which occurs most frequently when patients have suddenly lost consciousness from anesthesia or acute neurologic injury [2]. Other concerns in unconscious patients include loss of bulbar reflexes, inhibited cough reflexes, extinction of the gag reflex, and impaired swallowing mechanisms, all of which can be related to specific damage to cranial nerves (e.g., the glossopharyngeal, vagus, and hypoglossal nerves) that affects respiration and the bulbar protective response [3]. In general, any patient who the practitioner feels is at risk for aspiration is a candidate for intubation. Standard guidelines for intubation have been established based on the Glasgow Coma Scale (GCS) [4]. While these guidelines are helpful and provide a guidepost to care, three factors should be considered when evaluating a patient’s need for intubation: (1) Are the gag and cough reflexes intact? (2) Will the patient be neurologically impaired for a long period of time? (3) Is the patient in a monitored setting where he can be easily intubated if necessary? It is our observation that patients who meet these criteria can be safely observed and intubated at a later time if they deteriorate. In our unit, the time limit for observation in the unintubated state is usually 24–72 h. If a patient’s mental status does not improve during that period, we often intubate. This practice is not data driven but is based on a clinical observation that patients who do not recover within that time period usually need to be intubated for reasons other than airway protection, such as aspiration pneumonia.

Central Control of Ventilation

Neural control of respiration depends on both conscious and automatic components that are controlled from the cortex and nuclei in the pons and medulla, respectively. Automatic respiration is a homeostatic mechanism by which ventilation may be continuously adjusted to regulate acid–base status and ensure adequate oxygenation to meet the metabolic requirements of the body. It is controlled by areas of the dorsolateral tegmentum, the pons, and medulla in the region of the nucleus tractus solitarius and retroambigualis. Pathways that affect respiration include descending pathways in the ventrolateral columns of the spinal cord [5]. Altered patterns of respiration observed following neurologic injury result from damage to the automatic respiration mechanism and include Cheynes–Stokes breathing, apneustic breathing, cluster breathing, and ataxic breathing.

The most commonly observed alteration in respiratory pattern in patients with brain injury is tachypnea, which often results in hypocapnia and may produce dramatic immediate effects on ICP. Frequently seen as a result of diffuse cortical and subcortical injury in awake and comatose patients, tachypnea is related to a change in the detection and response to CO2 and may be mediated through physiologic changes to the dorsal regulatory group of the medulla, where CO2-driven, centrally mediated respiratory drive originates. This occurs as a result of reflexive responses to brain injury or it can be the direct effect of brain injury on the regulatory group. Moreover, alterations in breathing patterns can be seen in patients who appear to be neurologically intact [5–8]. A common syndromic respiratory pattern seen in brain injury that reflects this trend toward tachypnea is Cheynes–Stokes respiration. The Cheynes–Stokes pattern of disordered breathing has been related to the disruption between the bilateral cortical hemispheres and dysfunction of the medial forebrain structures [5–8]. It is typified by an alternation between hyperventilation and hypoventilation in a consistent, cyclical manner and is usually related to an increased dependency on the arterial carbon dioxide partial pressure (PaCO2), which acts as a trigger for respiratory drive.

Other variations in breathing patterns are classically described in a number of texts [3, 5–8]. Apneustic breathing, which is characterized by long respiratory pauses after which air is retained and then released, occurs with lesions of the lower half of the tegmentum of the pons [3, 5–8]. Cluster breathing is a group of quick breaths that occur in an irregular sequence in clusters and are regularly separated by long pauses; this pattern is often associated with low pontine or high medullary lesions [7, 8]. Ataxic breathing is a form of respiration that is reflected by complete loss of rhythmicity of breathing. The breaths are irregularly timed with variable tidal volumes, usually of smaller sizes. This pattern is associated with long pauses and can be confused with cluster breathing, except that the associated rhythm is irregular and is highly variable [7, 8]. It is important to note that as patterns of disrupted breathing associated with damage to specific areas of the midbrain, pons, and medulla are observed, they are representative of damage to the brain that is irreversible and portend an ominous prognosis for the patient [3, 5–8].

Gas Exchange

The use of the ventilator affects ICP and the parenchyma of brain-injured patients in many ways. One of the most important issues affected by the ventilator is brain oxygenation. The ventilator is a major component of the strategies designed to address brain oxygenation; however, no large studies have systematically examined the role of different ventilator strategies on brain oxygenation. Although strategies that emphasize maximal oxygen support with maximal fractional inspired oxygen (FiO2) have been proposed [9], no study has demonstrated benefit from the prophylactic use of high FiO2 in the setting of brain injury, and there is a hypothetical consideration of lung injury from exposure to high FiO2 in the setting of severe lung injury [9]. As long as blood oxygen saturation is adequate, the use of higher levels of FiO2 appears unnecessary [10]. The use of permissive hypercapnia as a component of a lung-protective mechanical-ventilation strategy has also been considered. Some have expressed concern over the effects of elevated PaCO2 and its effects on elevated ICP [11]. At this time, the risk of elevated ICP as a consequence of mild permissive hypercapnia has not been substantiated, and an effect on outcomes in severe brain injury has not been demonstrated [11].

Oxygenation

At the minimum, careful neurologic monitoring during such proposed interventions would seem prudent. In the past, a prospective study of brain oxygenation has been limited by our inability to measure parenchymal oxygenation directly [12]. In recent years, instrumentation (e.g., jugular venous oxygen sensors and intraparenchymal oxygen sensors) has been developed that can yield direct measurements of brain oxygenation through determination of vascular oxygenation and direct determination of parenchymal oxygen levels [13]. New clinical strategies that emphasize the optimization of these parameters have been developed; however, they have not been tested by well-designed prospective studies [4].

Hypo/hypercapnia

Induced hypocapnia through hyperventilation allows for a dramatic reduction in ICP. This strategy is often employed in ventilated patients by increasing their minute ventilation through increases in the respiratory rate or tidal volume [14, 15]. The goal of hyperventilation is to reduce PaCO2 from a normal range of 40–60 mmHg to a reduced range of 25–35 mmHg [4]. As hypocapnia induces alkalosis-induced vasoconstriction, cerebral blood flow (CBF) is decreased, which causes a drop in brain ICP. This reaction is initiated by arterial constriction in response to changes in pH and is mediated by mechanisms located in the perivascular space of the small arterioles of the brain [3, 5, 14–16]. Change caused by hypocapnia can temporarily shift the autoregulatory curve to the right, resulting in lower ICP and lower CBF at higher mean arterial pressure (MAP) (Fig. 1). As bicarbonate ions shift intracerebrally, this autoregulatory system adapts to higher PaCO2 set points. Hypocapnia then loses its effect on vasoconstriction and shifts the curve back to the left, resulting in higher CBF at lower PaCO2 and similar MAPs. The effect of hypocapnia on ICP will be lost within 6–12 h after initiation. In healthy volunteers, a reduction of CBF to 40% lasts for 30 min after reduction of PaCO2 to 25 mmHg [14–16]. Similar observations have been made in patients with brain injury [17].

Fig. 1
figure 1

Cerebral blood flow versus mean arterial pressure (MAP) with normocapnia (solid line) and hyperventilation (hypocapnia, dashed line)

Full size image

In ventilated patients, alterations in respiratory rate to increase minute ventilation are common strategies to reduce ICP acutely. In a randomized prospective trial, hyperventilation was associated with increased morbidity and early mortality if continued chronically [12, 18]. To date only one randomized prospective study has been conducted that addresses the effects of chronic hyperventilation on clinical outcomes in patients with traumatic brain injury (TBI). It compared outcomes in patients who where hyperventilated for 5 days with a PaCO2 of 25 mmHg to patients with a PaCO2 of 35 mmHg for 5 days. Functional outcomes at 3 and 6 months were recorded. Patients with a GCS of 4–5 had a significantly better functional outcome if they were not hyperventilated [18]. Although this study had significant limitations, including size and biases associated with post hoc analysis, it has become the basis for the class I recommendation against prophylactic hyperventilation in patients with severe TBI [4].

Some practitioners still advocate the use of hyperventilation in the setting of careful monitoring of jugular venous oxygen saturation. They believe that this strategy can be employed safely as long as global brain oxygen levels are monitored by jugular venous oxygen monitors [9]. The present brain trauma guidelines recommend against any strategy that employs preemptive hyperventilation. However, the use of hyperventilation to induce hypocapnia and reduce ICP is effective for short periods in acute neurologic emergency cases that involve elevated ICP.

The Effects of Different Ventilatory Modes, Settings, and Strategies on ICP

As ICUs have become ubiquitous, the monitoring of ICP with intracranial monitors has become commonplace. In studying ventilated patients with brain injury and ICP monitors, researchers have made observations about the relationship of elevated ICP to ventilator modes. An important observation is the relationship of positive end-expiratory pressure (PEEP) to ICP [19–28]. Clinicians have observed that as PEEP increases in patients with lung injury, ICP often increases [28]. Although this observation has not been made in all patients with head injury, it has been observed that ICP can increase to dangerously high levels in response to elevated PEEP [19–28].

PEEP

PEEP mediates changes in ICP through a variety of mechanisms. The close proximity of the thoracic cavity to the cranial vault suggests that increased thoracic pressure caused by increasing PEEP is directly transmitted through the neck to the cranium [29, 30]. In some experimental animal models of brain injury, increasing PEEP by as little as 10 cm H2O shifts the pressure curve beyond the deflection point and causes significant elevations in ICP [20]. In dogs, cats, and rabbits, the effect of increasing PEEP on ICP appears related to direct increases in intrathoracic pressure in response to increased PEEP [31–34]. PEEP has a direct effect on other physiologic parameters in the chest as well. Increasing PEEP increases intrathoracic pressure, peak inspiratory pressure (PIP), and mean airway pressure and decreases venous return, MAP, and cardiac output [31–34]. Each of these can have an independent effect on ICP. Mean airway pressure can cause increased intrathoracic pressure, which in turn, can cause increased ICP. The same holds true for PIP. Elevation in these values can cause an increase in jugular venous pressure and a reduction of venous return, which causes increased blood and CSF volume in the brain’s venous and ventricular systems and results in increased ICP. Decreasing MAP and cardiac output are usually associated with declining ICP levels, as each represents a decline in the space occupied by blood volume within the intracranial space. However, reduction of these can also lead to decreased CBF and decreased brain oxygenation, which can cause elevated ICP [33, 35, 36]. Decreasing venous flow increases cerebral venous congestion. Changes in venous flow caused by changes in PIP, intrathoracic pressure, and PEEP can have a critical effect on ICP in situations in which the ventricular compliance is decreased and ventricular elastance is elevated by space-occupying lesions or TBI. In this setting, small changes in intracranial volume result in steep increases in ICP (Fig. 2) [31–34].

Fig. 2
figure 2

Volume–pressure (Elastance) curve, illustrating the exponential increase of ICP following an increase in the volume of the intracranial compartment. Adapted from Stocchetti et al. [9]

Full size image

Other factors also contribute to increases in ICP in concert with ventilator-mediated changes. These factors include changes in CBF, elevated capillary dilatation secondary to elevated PaCO2, and decreased cardiac output [9–28, 35, 36]. Elevated MAP can also play a role in increasing ICP in this setting. As the MAP rises, the kinetic energy from the artery is more readily transmitted into the parenchymal system [23, 34, 36].

Many human clinical studies have documented the relationship of elevated PEEP to increasing ICP in the setting of brain injury [23–29, 37]. Although PEEP appears to have some effect on ICP, exceptional clinical studies have reported that mean ICP increases up to 14.5 ± 7.7 mmHg in response to as little as 10 cm H2O of PEEP [21, 22, 24, 25]. The variability of the effects of PEEP on ICP in different clinical situations in different individuals suggests that other physiologic factors are in play. The effects of PEEP on ICP appear to be significantly influenced by reductions in the ventricular compliance of brain-injured patients, in whom the ability of the ventricle to buffer against changes in ICP in response to vascular pressure and venous outflow declines. In patients with severe lung injury, the effects of PEEP on increases in intrathoracic pressure are often amplified. Patients who experience changes in lung compliance as well as a decline in ventricular compliance become PEEP sensitive, with greater elevations in ICP in response to increases in PEEP [25, 26]. In patients who experience both decreased ventricular compliance and decreased lung compliance, the effects of elevated PEEP on ICP appear to be greater [27, 37], suggesting that the variability of the effects of PEEP between brain-injured patients may be explained by the susceptibility of the brain to the effect of changes in venous outflow coupled with an increase in the responsiveness of the lungs to changes in PEEP. In short, patients with normal pulmonary compliance generally demonstrate no elevation in ICP with increases in PEEP [37]. Patients with normal ventricular compliance and decreased pulmonary compliance normally do not experience great increases in ICP. If patients have both, they are at greater risk for elevated ICP in response to changes in PEEP.

Recently, clinicians have attempted to optimize ICP and cerebral perfusion pressure in the ICU. PEEP is often required to support patients with TBI and thus improve their oxygenation. Even though increased PEEP leads to elevated ICP and some changes in hemodynamic parameters, in general, no decrease in mortality is associated with its use. PEEP should always be considered an option for patients who require it secondary to severe lung injury, even in the setting of severe brain injury [28, 37].

Head Positioning and PEEP

Head positioning can reduce the impact of increased PEEP on elevated ICP. Abbushi et al. noted that the relationship between ICP and PEEP could be reduced by elevating the head of the bed 30°–45° [29]. In the supine position, PEEP-dependent venous hypertension is clearly transmitted into the intracranial compartment. In the sitting position, PEEP has no influence on most patients. In patients with signs of cerebral edema, the combination of head flexion and rotation caused a dangerous increase in ICP, even in the sitting position [30].

Inspiration (I) and Expiration (E) Ratio (I:E Ratio)

The effect of cycle time of inspiration (I) and expiration (E) on changes in PEEP and ICP has been tested in animals and humans. Experiments in rabbits suggest no effect of inverted I:E ratios on PEEP, ICP, or any other parameter that affects ICP [38]. In human trials, a number of regimens have been employed to explore changing I:E ratios from 1:2 to 1:1 with varying adjusted levels of PEEP, including 5 and 10 cm H2O. In patients with various brain injuries such as stroke, TBI, and intracranial hemorrhage, no direct effect of these inverted ratios was demonstrated on elevations of ICP in the setting of ventilator management [38–41].

Weaning

Weaning and spontaneous breathing trials affect ICP. The transition from controlled ventilation to spontaneous ventilation can be accomplished safely if the patient’s ICP is within the range of normal. In any situation in which patients have markedly high ICP, a spontaneous breathing trial may be associated with significant and meaningful rises in ICP. In a retrospective trial, ICP, cerebral perfusion pressure, MAP, and PaCO2 were examined in patients with severe TBI. Measurements were made before and after changing the mode of ventilator support. Patients who were switched to a spontaneous breathing trial fell into two main groups. In the largest group, ICP remained stable; in the second group, ICP increased from 25 to 33 mmHg. The significant difference between the groups was that second group had an ICP greater than 25 mmHg prior to beginning the spontaneous breathing trial [42]. This study demonstrated that spontaneous breathing trials can increase ICP and that the most important factor predicting this increase is the patient’s ICP prior to beginning the trial [42].

High-Frequency Ventilation

High-frequency ventilation (HFV) is an innovation that may have a dramatic impact on the care of patients with severe lung injury of all types. HFV incorporates high-frequency respiratory rates >150 breaths/min with low tidal volumes, usually 1–5 ml/kg. This unique ventilator technology results in a system of ventilation that separates oxygenation and ventilation. It allows for efficient ventilation and oxygenation with minimal induction of ventilatory-induced lung injury. It also causes a reduced intrathoracic pressure and minimal effect on cerebral venous outflow, which allows for a significant reduction of ICP when compared to conventional modes of ventilation. This technology has a number of variants: high-frequency oscillatory ventilation (HFOV), high-frequency percussive ventilation (HFPV), high-frequency jet ventilation (HFJV), high-frequency flow interruption (HFFI), and high-frequency positive-pressure ventilation (HFPPV). The effects of these ventilator modes are to reduce the mean peak airway pressure and the PIP, thereby reducing the intrathoracic pressure [43]. TBI patients in whom this technology is most likely to be incorporated will have both severe lung injury and TBI. They will have reduced pulmonary compliance and reduced intraventricular compliance and are likely to be sensitive to the effects of PEEP and elevated intrathoracic pressure on ICP.

Animal studies and small human studies have examined the effects of HFV on PEEP and ICP. Studies in canine models of HFJV identified an improved ventricular pressure volume curve and a decrease in elasticity [44]. Studies in other animal models demonstrated minimal effect on ICP, but a significant decline in intrathoracic parameters, such as PIP, mean airway pressure, and intrathoracic pressure [45–47]. In cats, HFV eliminated ventilator-linked fluctuations in both blood pressure and ICP and significantly reduced the peak ICP seen during each cycle. This reduction in ICP was more pronounced as ventricular compliance fell. In the exposed brain of cats, HFV reduced brain movement that represented a decrease in cerebral volume [48].

In humans, a number of small trials with different types of HFV have documented reductions in a variety of pulmonary parameters that affect ICP. The most recent study in patients with acute respiratory distress syndrome and elevated ICP was a small retrospective study from trauma patients observed over 1 year who failed standard mechanical ventilation and were placed on HFPV. Measurements were compared before institution of HFPV and then at 4 and 16 h after HFPV. ICP decreased by 30.9 ± 3.4 vs. 17.4 ± 1.7 (P = 0.01) during HFPV when compared at 16 h to conventional ventilation. PaCO2 and PIP also declined at 16 h [49–51]. Likewise, when 11 patients with multiorgan dysfunction, TBI, and elevated ICP who required PEEP were transitioned to HFJV, a statistically significant fall in ICP of 7.2 mmHg and a concomitant fall in PaO2 from 131 to 101 Torr with a slight decrease in oxygen delivery were seen. They had no change in cardiac output or intrapulmonary shunt fraction [51].

Bronchoscopy

Fiberoptic bronchoscopy can precipitate a rise in ICP. The effect of fiberoptic bronchoscopy on ICP has been examined in a prospective study that was also designed to determine the effects of an optimal anesthetic regimen to reduce ICP elevations in this setting [52]. In this singular trial, patients were paralyzed, their cough reflexes were suppressed with lidocaine, and they were anesthetized with adequate analgesia and sedation. Patients with increased cranial elastance also received a nebulizer of 4% lidocaine. All were preoxygenated. The mean ICP at baseline was 12.6 mmHg; after bronchoscopy, the ICP increased to 38.0 mmHg. Lidocaine did not appear to blunt the cough reflex nor prevent rises in ICP. Despite the anesthetic regimen, ICP increased significantly. Fiberoptic bronchoscopy does cause a significant increase in ICP in head-injured patients, and anesthesia does not safely blunt this effect [52]. While this effect is temporary and reversible, fiberoptic bronchoscopy should be performed cautiously in patients with elevated ICP.

Liberation from Mechanical Ventilation and Extubation in Neurologic Disorders

Little data exist to guide the appropriate decision-making pathways for liberating patients with primarily neurologic injury from the ventilator. New data have changed the strategy of extubation in general medical and surgical ICUs from slow weaning trials to new tactics that employ daily spontaneous breathing trials and rapid liberation [53]. The Society of Critical Care Medicine has suggested that the best evidence supports the weaning pathway that utilizes a standard breathing trial with aggressive liberation of the patient from the ventilator—upon passage of the trial. The literature does not support weaning protocols that incorporate either slow weans through rate reduction in the setting of synchronized intermittent mandatory ventilation or the use of continuous positive airway pressure (CPAP) without periods of rest.

Literature is limited concerning the effects of early ventilation on care in the NCCU. Coplin et al. [54] evaluated a group of neurosurgical patients and patients with neurologic impairment in the NCCU at the University of Washington and detected no differences in outcome when patients were extubated, even if they had GCS scores as low as 3, as long as they retained their cough and had infrequent suctioning requirements. Thirty-nine of 49 patients (80%) with GCS scores ≤8 and 10 of 11 patients (91%) with GCS scores ≤4 were successfully extubated. Patients not liberated had a higher incidence of ventilator-associated pneumonia and longer hospital stays. Affected populations included a group of patients who were expected to make a recovery. Namen et al. attempted to utilize a standard trial of daily breathing instituted by a respiratory therapist; they reported that this strategy was often overridden by the neurosurgical specialist. Among those who where eligible to be extubated but were not, a much higher rate of tracheostomy was reported [55].

In patients with primarily neurologic disorders, strategies that incorporate CPAP with a slow reduction in support and a plan for systematic reductions in respiratory rates are often employed. Although no evidence exists to support the use of these strategies, they are employed by practitioners who have experience with weaning strategies in specialized patient groups with neurologic injury. Weaning trials incorporating CPAP are often used in patients who are intubated for prolonged periods and are recovering from acute peripheral nervous disorders (e.g., myasthenia gravis and Guillain–Barré), where a slow increase in strength, with a gradual increase in functional residual capacity (FRC) and negative inspiratory force (NIF) occur over days to weeks. Additionally, many practitioners will use strategies that incorporate slow decreases in respiratory rate or slow decreases in CPAP or pressure support to obtain FRC and NIF goals indicative of a potential for liberation from mechanical ventilation. These strategies are also used in patients with severely altered mental status and intact mechanical pulmonary systems.

Extubation of patients with severe peripheral nerve disease can be attempted when sufficient respiratory muscle is recovered. Peripheral nerve injury that results in respiratory failure constitutes type II respiratory failure for which good clinical evidence that supports standardized weaning protocols does not exist. Many guidelines based on expert opinion have been proposed and suggest that extubation should only be attempted when sufficient pulmonary recovery has occurred, as indicated by (a) signs of improvement in overall muscle strength, (b) vital capacity (VC) >10 ml/kg, (c) mean inspiratory pressure <−20 cm H2O, (d) FiO2 requirement <40% and PEEP ≥5 cm H2O, and (e) no fever, infection, or other medical complications [3]. In our own unit, a VC of 15–20 ml/kg of ideal body weight is employed, with a suggested NIF in the 20–50 cm H2O range. In addition, an aggressive trial of prolonged spontaneous breathing for 12–24 h is often employed to test for the possibility of fatigability in patients with myasthenia gravis and Guillain–Barré. In rare instances, patients never regain enough strength to be safely extubated and tracheotomies are used as permanent solution or as a bridging tool to extubation.

High cervical spinal cord injury can inhibit many of the reflexes that protect the lung. Often, patients will be awake and aware of their inability to ventilate. In this setting, atelectasis and alveolar hypoventilation develop. Respiratory failure usually involves a scenario of slow decline in which the patient progressively de-recruits alveoli as a result of prolonged alveolar hypoventilation. The PaCO2 slowly rises, with a concomitant decrease in oxygenation, which causes a slow progressive decline, often ending in intubation and ventilator dependency. Patients often exhibit a form of breathing known as paradoxic breathing or diaphragmatic breathing in which the intercostal muscles are de-innervated while the diaphragm is flaccid. In this situation, the chest is flaccid or weak, while the belly expands paradoxically in response to the need to use the diaphragm as the primary muscle of respiration. This condition markedly inhibits the efficiency of ventilation. The level of the spinal injury may give insight into the severity respiratory dysfunction. Injury from C1 to C3 causes apnea. Injury from C3 to C5 is often associated with a mixed presentation in which the patient is able to initiate ventilation but cannot do so with enough efficiency to ventilate independently, or lacks the stamina to remain ventilator independent. Injury below C5 is usually associated with some form of recovery to ventilator independence. Special concerns for these patients revolve around three key clinical obstacles: (1) avoiding atelectasis through maneuvers that promote alveolar recruitment and adequate inflation, (2) aggressive pulmonary toilet to avoid aspiration pneumonia, and (3) education of the patient to use voluntary muscles of respiration and proper positioning to maximize pulmonary function and achieve the other goals outlined above. These patients often experience a reduction of lung parenchymal volume while maintaining stable intrapleural volume. This situation can facilitate the development of small airspaces in the intrapleural space that can enlarge into pneumothoraces and can be aggravated by aggressive recruitment maneuvers. Strategies for liberation of ventilation include prolonged trials of spontaneous ventilation, NIF > 20 cm H2O, as well as VC > 15–20 ml/kg of the patient’s ideal body weight. Pitfalls to be avoided involve the rapid extubation of patients with cervical spine injury within the first 72 h. Often these patients will perform well only to fail as the edema at the site of their injury expands and causes a more devastating injury, leading to respiratory failure. Similarly, patients with partial paralysis from their cervical injuries will breathe well after extubation only to fail as different muscle groups begin to fatigue. There is no easy answer to this dilemma, and these patients require close observation. The clinician must be willing to reintubate if trouble ensues. Often, these patients require a tracheostomy, which frequently becomes a permanent solution. If the injury results in quadriparesis and permanent respiratory paralysis, then a tracheostomy should be pursued as early as medically possible, based on the patient’s medical condition.

Conclusion

A series of special circumstances surround the mechanical ventilation of patients with neurologic injury, including alteration of mental status, bulbar dysfunction, neurogenic pulmonary injury, and the pulmonary mechanical consequences of neurologic injury. When considering a mechanical ventilation strategy, the critical care physician must consider the related issues of optimizing cerebral oxygen delivery and minimizing the impact of positive-pressure ventilation on ICP. Finally, the critical care physician must determine the appropriate time and strategy to liberate the patient from the ventilator.