Respiratory Support of the Neurocritically Ill: Airway, Mechanical Ventilation, and Management of Respiratory Diseases

Subscribers, click on headers and sub-headers below to view full topic content.


Respiratory complications are a significant source of morbidity and mortality after brain or spinal cord injury. Neurocritically ill patients may develop respiratory problems for a variety of reasons. They may develop aspiration due to inability to protect their airway as a result of primary brain injury; they may hypoventilate in the setting of myasthenic crisis, they may suffer complications of their intensive care unit (ICU) stay or they may present with underlying lung disease that worsens. As the severity of illness and overall complexity of patients managed in the neurological critical care unit (NCCU) increases, those caring for these patients need expertise in the management of respiratory disease. This chapter will review fundamental elements of respiratory physiology, pathophysiology, and support.

Physiology and Pathophysiology of the Respiratory System

Control of breathing

The medulla and pons are responsible for neurologic control of breathing. Respiratory rhythm is controlled by neurons in the ventral medulla (pre-Botzinger complex).1 Input is received by peripheral and central baroreceptors and chemoreceptors that terminate in the dorsomedial and ventral medulla.2,3 In addition, neurons in the parabrachial nucleus in the pons modulate respiratory rate and tidal volume.4 Central chemoreceptors increase respiratory drive in response to hypercapnic academia.5 Lesions to the brainstem result in abnormal breathing patterns: Cheyne-Stokes respirations can be seen in patients with bilateral hemispheric or diencephalic lesions as well as patients with bilateral pontine lesions;6 central neurogenic hyperventilation and apneustic breathing with pontine lesions;7,8 and ataxic breathing with medullary lesions to the pre-Botzinger complex.9

Central and Obstructive Apneas

As described above, pH and carbon dioxide drive respirations via chemoreceptors.5 Patients with a central apnea may have reduced drive of the respiratory pacemaker neurons or may have a decreased respiratory drive due to a diminished chemoreceptor response that is secondary to disease states that lead to chronic hypoventilation and respiratory acidosis (example, chronic obstructive pulmonary disease).10 Primary central apnea is rare and is referred to as “Ondine’s curse” after the water nymph that cursed her lover to cease breathing if he ever fell asleep. Lesions in the ventrolateral medulla to the chemoreceptors, or spinal cord damage to the autonomic neurons, can lead to this disease.11 Medications, specifically opioids, are a common cause of secondary central apnea. Patients who are chronic opioid users are also at risk for ataxic breathing.12

Obstructive sleep apnea (OSA) occurs secondary to a narrowed upper airway. In these patients, decreased airway pressure causes a sudden closure of the airway and cessation of respiration. The patient will awaken secondary to hypercarbia and hypoxia and begin breathing again. Obesity is a risk factor for OSA due to increased soft tissue in the pharynx. Anatomic variants that decrease the size of the airway can also lead to OSA (small maxilla and mandible and size of the tonsils and adenoids). Additionally, patient positioning and secretions influence the risk for OSA.13 It is a concern in the NCCU because the severity of OSA may be worsened in a patient with brain injury, and patients are at risk for developing OSA after brain injury.

Airway Protection and Aspiration

Normal swallowing and cough allow for airway protection and the prevention of aspiration. Swallowing consists of three phases: the oral phase, the pharyngeal phase and the esophageal phase.14 The pharyngeal phase is most involved in airway protection and preventing aspiration.15 The tongue base moves solids or liquids toward the pharynx by moving posteriorly while the larynx moves up and forward under the tongue base, pulling open the upper esophageal sphincter.14 Other airway protective mechanisms occur during this phase to avoid aspiration: the soft palate rises and the nasopharynx closes, pushing material down into the esophagus;14 the true and false vocal folds adduct to close the larynx;14,15 and the epiglottis moves backward to cover the trachea.15

Aspiration can occur before, during or after swallowing. When it occurs, the normal reflex is to cough.15 Aspiration that occurs during swallowing can be seen in patients with an impaired voluntary cough.16 The ability to cough is particularly impaired in neuropathic and neuromuscular disorders such as myasthenic crisis or Guillain-Barré Syndrome (see below). Dysphagia from stroke can be seen with both brainstem and cortical lesions.17 Lesions to the anterior insula demonstrate a delay in pharyngeal swallowing and supraglottic aspiration.18 Right-sided strokes additionally have delay at each stage of pharyngeal swallowing, leading to an increase in aspiration.19

When aspiration does occur, aspiration pneumonitis or pneumonia can develop. Aspiration pneumonitis is caused by sterile, acidic stomach contents entering the airway, resulting in a chemical inflammatory injury to the lungs; aspiration pneumonia is caused by oropharyngeal secretions colonized with bacteria entering the airway, resulting in infection.20 The use of medications for ulcer prophylaxis can cause gastric contents to become colonized with bacteria by increasing the pH of the stomach.21 Enteral feedings are also associated with colonization of the stomach with Enterobacteriaceae.22 Feeding a patient via nasogastric tube versus percutaneous endoscopic gastrostomy (PEG) tube has shown similar rates of aspiration, though over the long-term a PEG tube is more comfortable for a patient.20 Feeding patients via a post-pyloric tube has not shown to decrease the incidence of pneumonia compared to gastric enteral feeds.23

Neuromuscular Respiratory Failure

Neuromuscular respiratory failure may occur in a variety of diseases, including Guillain-Barré Syndrome and its variants, chronic idiopathic demyelinating polyneuropathy, myasthenia gravis, amyotrophic lateral sclerosis (ALS) and other motor neuron diseases, muscular dystrophies and myopathies. Respiratory failure can occur by three means in these patients: 1) weakness of the inspiratory muscles, producing hypoventilation and hypercapnia; 2) weakness of the expiratory muscles, causing impaired cough and clearing of secretions; and 3) weakness of the bulbar muscles, leading to an inability to protect the airway and aspiration.24 Management of respiratory failure often requires endotracheal intubation, mechanical ventilation and clearing secretions.24 Progression of respiratory muscle weakness can be followed by measuring forced vital capacity (FVC) and negative inspiratory force (NIF). A FVC less than 1 L (or less than 20 to 25 mL/kg) or a NIF less than 20 cm H2O implies significant respiratory weakness.25 In patients with bulbar weakness that impairs the accuracy of these tests, the clinician should follow clinically. Asking the patient to count from 1 to 20 can be used as a marker for vital capacity. Neck flexion weakness often correlates with diaphragm weakness, and use of accessory muscles and paradoxical breathing are additional signs of impending respiratory failure. As respiratory failure progresses, patients will also develop worsening hypercapnia due to decreased tidal volumes. Shunting at the lung bases initially preserves oxygen saturation, and hypoxia will not occur until late in the process.26 Non-invasive ventilation (NIV) can be considered in patients without bulbar impairment who have neuromuscular respiratory failure.27,28 Patients who have continued or worsening shortness of breath, increased work of breathing, tachypnea or hypercapnia despite initial management with NIV should be endotracheally intubated.

Table 1 – Neurological causes of respiratory failure
Respiratory Chapter_Table 1_Neurological Causes

Nursing Assessment

Patients admitted to a NCCU must be carefully assessed. Small changes with quick provider notification and intervention may be highly influential to a patient’s long term outcome. Assessment skills must be keen to all body systems, with specific attention to neurological and respiratory status.

Though a thorough neurological exam must be completed with great frequency, specific components that affect the respiratory system include assessment of cranial nerves V, VII, IX, and XII, cough and gag reflexes, motor strength in patients with spinal cord injuries above the level of T10 or neuromuscular disorders, and level of consciousness. See Table 2 for additional assessment details. Abnormal findings in any of these areas may prompt additional assessment or early intervention, including placement of an artificial airway to prevent respiratory arrest.

Table 2 – Nursing Neurological Assessment related to Ventilation and Respiration29,30

Respiratory Chapter_Table 2_Nursing Neuro Assessments related to Ventilation and Respiration

Table 3 – Abnormal Respiratory Patterns33

Respiratory Chapter_Table 3_Abnormal Respiratory Patterns

Airway Management

Indications for Intubation

There are five common reasons for which a patient may need to be intubated:34

  • Hypoxic respiratory failure – low arterial oxygen saturation by pulse oximetry or arterial blood gas
  • Hypercarbic respiratory failure – a failure to ventilate indicated by hypercapnia or by inadequate breaths on physical exam
  • Airway protection – in patients who have a decreased level of consciousness (Glasgow Coma Scale ≤ 8) or bulbar dysfunction
  • Expected neurological or cardiopulmonary deterioration
  • Planned surgical or endovascular interventions

The incidence of endotracheal intubation in the NCCU ranges from 25-39%. Over two-thirds of patients need to be intubated for airway protection.35,36 Over a quarter need to be intubated for anesthesia. The remainder (<10%) are intubated for primary respiratory failure.35

Airway Assessment

Patients requiring intubation should be assessed for a difficult airway and for ability to bag-mask ventilate (BMV).34

First, one can determine if a patient might have a difficult airway using the “LEMON” mnemonic.37

L = Look externally

E = Evaluate the mouth opening and airway position

M = Mallampati score

O = Obstruction

N = Neck mobility

Figure 1 – Mallampati Classifications
Respiratory Chapter_Figure 1_Mallampati Classification

The “OBESE” mnemonic can be used to evaluate for the capacity to BMV.38

O = Obese (BMI > 26 kg/m2)

B = Bearded

E = Elderly (Age > 55 years old)

S = Snoring history

E = Edentulous

Consideration can be given to calling for anesthesia back-up or having assist devices such as fiberoptic devices or a laryngeal mask airway in patients who are at risk for a difficult airway or inability to BMV.34

Table 4 – Potential for a difficult airway in the neurocritical care unit
Respiratory Chapter_Table 4_Potential for a difficult airway

Pre-Intubation Neurological Assessment

A focused and succint neurological exam is important for estabilishing a baseline prior to sedation and intubation.34

Exam elements should include the following:

  • Level of consciousness
  • Pupil reflex
  • Corneal reflex
  • Gaze
  • Face symmetry
  • Gag reflex
  • Cough reflex
  • Motor response in each extremity
  • Presence or absence of seizure activity or other abnormal movements


Rapid sequence intubation is an effective method of emergently intubating patients at risk for aspiration of stomach contents.39 The patient is pre-oxygenated with 100% oxygen. Typically, a nonrebreathing bag reservoir facemask is used. However, since this must be interrupted during intubation, a high-flow nasal cannula can be used to decrease hypoxia and allow for apneic oxygenation.40 An induction agent and neuromuscular blocking agent are then administered. The patient is intubated once loss of consciousness and paralysis has occurred.39 Traditionally, cricoid pressure is applied prior to intubation to decrease the risk of aspiration. However, there is little evidence that this maneuver is helpful in reducing the incidence of aspiration.41

Respiratory Chapter_Pharm

Special considerations are frequently necessary in the neurocritically ill population. Patients with elevated intracranial pressure (ICP) or at risk for elevated ICP should be intubated by the most experienced clinician on the team to avoid unnecessary airway manipulation.34 Both the reflex sympathetic response (RSR) and the direct laryngeal reflex can cause a rise in ICP. The RSR is both increased heart rate and increased blood pressure, leading to increased ICP, and the direct laryngeal reflex can raise ICP independently.42-44 In addition to ICP, the clinician must all be aware of the patient’s cerebral perfusion pressure (CPP). CPP is dependent on both ICP and mean arterial pressure (MAP), the latter often being reduced by induction drugs.


CPP is a surrogate for cerebral blood flow. Thus, hypotension should be avoided so that CPP is maintained. Assuming that ICP is less than 20 mm Hg, the MAP should be maintained at 80 mm Hg to avoid a CPP less than 60 mm Hg throughout the procedure.34

In patients with a cervical spine injury, extreme care must be taken to guarantee spine stabilization. A second clinician has to manually stabilize the head and neck, ensuring inline immobilization.45

Nursing Interventions - Intubation

During intubation, great caution should be used while intubating a patient with increased intracranial pressure.34 As both hypotension related to the use of induction agents as well as hypertension related to the RSR are possible, a pre-intubation plan should be discussed with the interprofessional team prior to RSI.42,43 Additional equipment that should be ready to use includes suction, colorimetric EtCO2 detector or EtCO2 monitor, and video laryngoscope or bronchoscope if the airway has any potential to be difficult.46 An advanced airway surgical tray should be available especially in cases of traumatic injury. In patients with neurological injury, adequate oxygenation throughout intubation must be maintained as cerebral tissues may be hypoxic and at risk for ischemia.47 Close monitoring by the nurse during intubation can cue the provider to halt an attempt, administer oxygen via BVM, and attempt again after oxygen saturation returns to adequate levels.

Patient positioning during intubation is usually supine to allow the proceduralist to visualize the vocal cords. However, this position is contraindicated in patients with increased intracranial pressure.48 Once the airway is secure and normotension has been achieved, the patient’s position should be quickly returned to head of bed 30° to improve venous jugular drainage. In trauma patients, hyperextension of the neck is contraindicated and a jaw thrust maneuver should be used to visualize the vocal cords and prevent any further cervical spinal cord injury.45

Mechanical Ventilation

The general principles of mechanical ventilation are to ventilate, avoiding hypo- or hypercapnia, and to oxygenate with the least amount of oxygen needed. In addition, mechanical ventilation can decrease a patient’s work of breathing. The exact ventilator settings will be patient dependent, though the clinician should avoid lung injury by giving volumes that are 6-8 mL/kg ideal body weight and avoiding high plateau pressures (≥ 30 mm H20).49,50

Table 5 – Frequently used ventilator settings
Respiratory Chapter_Table 5_Frequently used ventilator settings

In patients with brain ischemia from any cause, hyperventilation should be avoided except in cases of emergency treatment of intracranial hypertension, since hypocarbia may lead to cerebral vasoconstriction. Patients with traumatic brain injury who underwent hyperventilation had increased volumes of hypoperfused brain and a total decrease in cerebral blood flow despite improved CPP and ICP measurements.51 Not uncommonly, patients exhibit centrally driven hyperventilation, which can be mediated by both pontine lesions or by cortical brain injury, leading to respiratory alkalosis and hypocapnea.8 There is no clear data that patients should be sedated to blunt this response.

Table 6 – Commonly encountered problems with mechanical ventilation

Respiratory Chapter_Table 6_Commonly encountered problems with mechanical ventilation


The best method to wean a patient in the NCCU from mechanical ventilation is not known. Coma alone is not a reason to delay weaning. Spontaneous awakening trials (SATs) and spontaneous breathing trials (SBTs) have been recommended in the general critical care population because of associations with fewer number of ventilator days, decreased incidence of delirium and improved functional outcomes.52 However, patients in the NCCU have special considerations. Pauses in sedation can lead to increased ICP and possible decreases in CPP.53 Thus, abrupt weaning methods may not be safe in patients with intracranial hypertension or those who need analgesia and sedation to manage ICP. In one prospective observational study, the trial of interrupted sedation had to be aborted in one-third of comatose patients because of ICP crisis.54 A risk-benefit analysis must be considered in these patients prior to weaning.

Nursing Interventions – Spontaneous Awakening Trials

Though our patient populations may be challenging, there may be some benefit to a daily sedation vacation when executed safely. SATs should be completed on patients that have an advanced airway, are mechanically ventilated, and are receiving continuous infusion sedation/analgesia. When the SATs are paired with an SBT, a synergistic effect is seen with patients more likely to pass their breathing trials and get successfully extubated.55 However, adequate screening of the safety of an SAT/SBT is vitally important in the neurocritical care unit. Contraindications to tapering or discontinuing sedation can be seen in table 7. Additional considerations should be given to patients during end of life care, as analgesia and sedation may be used differently for this population prior to extubation.

If patients do not meet any of the exclusion criteria for an SAT, sedation can be discontinued, with signs and symptoms of SAT intolerance also listed in Table 7. During an SAT, patients are at high risk for unplanned extubation and may require direct supervision by a nurse to prevent harm. Endotracheal tubes should be firmly secured and restraints may be applied, though their use remains somewhat controversial.56,57

Intermittent boluses of intravenous analgesia may be used at this time if pain is present, but should not be used for sedation.58 If patients exhibit SAT failure, sedation should be reinitiated at half the previous dose and titrated up until goal parameters are achieved.58 In patients who cannot tolerate an SAT due to agitation, consideration can be given to using dexmedetomidine, which does not depress the respiratory drive.59 Once agitation has been successfully treated, an SAT may be reattempted.

Several non-NCCU studied protocols indicate that a patient passes their SAT or progresses from SAT to SBT when they are able to follow simple commands.58,60 In the NCCU patient, this may be difficult because of their underlying neurological injury. More evidence is needed in this population in order to make any strong recommendations.61

Table 7 – Spontaneous Awakening Trials58

Respiratory Chapter_Table 7_Spontaneous Awakening TrialsBpm, breaths per minute; SpO2, peripheral capillary oxygenation saturation; pbtO2, partial pressure of brain tissue oxygenation

Table 8 – Patient readiness for a spontaneous breathing trial

Respiratory Chapter_Table 8_Patient readiness for a spontaneous breathing trial

ICP, intracranial pressure; RASS, Richmond Agitation-Sedation Scale; SpO2, peripheral capillary oxygen saturation; PaO2, partial pressure of oxygen; FiO2, fraction of inspired oxygen; PaCO2, partial pressure of carbon dioxide; PEEP, positive end-expiratory pressure; RR, respiratory rate; VT, tidal volume; NIF, negative inspiratory force; HR, heart rate; MAP, mean arterial pressure

Table 9 – Indications for stopping a spontaneous breathing trial
Respiratory Chapter_Table 9_Indications for stopping a spontaneious breathing trial
RSBI, rapid shallow breathing index; RR, respiratory rate; VT, tidal volume; PaCO2, partial pressure of carbon dioxide; SpO2, peripheral capillary oxygen saturation; PaO2, partial pressure of oxygen; HR, heart rate; SBP, systolic blood pressure


When to extubate a neurocritically ill patient is not always a simple decision. Many times these patients meet respiratory criteria for extubation, but they are still at risk for not protecting their airways.62 Extubation failure rates in patients with primary brain injury can range from 15-35%63-66 and can be higher (30-40%) in patients with neuromuscular disease.67 Delaying extubation also has risk. Patients can develop ventilator associated pneumonia and have an increased length of stay in the intensive care unit.68 Patients with two of the following have been found to have a likelihood ratio of 3.8 for extubation failure: weak cough, secretions and inability to follow commands. However, the inability to follow commands should not preclude a patient from a trial of extubation. In addition, inability to tolerate an SBT due to agitation does not exclude a patient from a trial of extubation if the patient otherwise meets extubation readiness.69

Many studies have attempted to predefine a GCS that will predict extubation success, with varied results. Patients with GCS scores as low as 3 and 4 have been extubated safely,68 whereas others have shown that a GCS score > 7 and ability to follow commands predicts extubation success.64,70 Other scales, such as the FOUR Score have also not been necessarily predictive of who will tolerate extubation.62 Most recently, a GCS > 10 has been demonstrated to predict extubation success. In addition, patients who were successfully extubated all opened their eyes spontaneously and followed commands, and visual pursuit and swallowing attempts in a multivariate analysis were associated with extubation success.71

Table 10 – Factors indicating possible extubation success
Respiratory Chapter_Table 10_Factors indicating possible extubation success


Patients who cannot be extubated safely must undergo a tracheostomy. The incidence of tracheostomy placement in neurocritically ill patients ranges from 14-35%,36,63 compared to 7-13% in non-neurologically injured patients.63,72 After undergoing a tracheostomy, neurocritical care patients are faster to wean from the ventilator than general ICU patients.72 Given that many of these patients underwent tracheostomy for airway protection and not because of primary lung pathology, it is not surprising that they can be liberated from the ventilator more quickly. The best timing for placement of a tracheostomy is not known. A randomized trial of early (up to day 3 from intubation) vs. late (days 7-14 from intubation) tracheostomy in stroke patients did not demonstrate improved outcomes with early tracheostomy.73 They did, however, show that early tracheostomy is safe and feasible and may decrease the need for sedation in the NCCU. Patients should proceed to tracheostomy after failing extubation or once it is recognized that a trial of extubation is not reasonable, assuming that this is consistent with a patient’s goals of care. Tracheostomy placement can be associated with transient intracranial hypertension. To avoid elevations in ICP and lowering of CPP, the head of bed may be kept at 30 degrees, hypotension during the procedure should be avoided, bronchoscopy should be minimized or thin bronchoscopes used to avoid hypoventilation, and hypoxia and adequate analgesia should be given for the procedure.74

Tracheostomy can be performed via percutaneous dilatation or a traditional surgical technique. The overall complication rate of percutaneous dilatational tracheostomy (PDT) is lower (3%) than surgical tracheostomy (12%), including lower rates of bleeding and infection when PDT is performed with bronchoscopy.75 Additionally, PDT allows for the procedure to be performed at the bedside in the ICU. Granulation tissue forms after tracheostomy, though only 3-12% will have complications from tracheal stenosis. Other rare (<1%) late complications that can occur are tracheo-innominate artery and tracho-esophageal fistulas.76

Nursing Management of Mechanical Ventilation

The threshold for intubating a patient with a neurological injury is low in many clinicians’ minds. Because of this, many nurses in NCCUs care for patients requiring mechanical ventilation. There are several considerations specific to this population.

  1. Suctioning should not be completed on a regular basis but as needed. Frequent suctioning may lead to hypertensive episodes as well as bouts of increased intracranial pressure leading to decreased cerebral perfusion pressure. Lidocaine administered via the endotracheal tube may help alleviate the intracranial hypertension related to suctioning, but more evidence is needed to make this a mainstay of treatment.77
  2. Ventilator settings should be titrated to achieve normocapnea and normal peripheral capillary oxygen saturation (SpO2). However, during times of intracranial hypertension, hyperventilation can be used as a rescue therapy. While this therapy may lower intracranial pressure, it also decreases cerebral blood flow and can lead to ischemia.1 Because of this, hyperventilation should only be maintained for a short period of time. Additionally, FiO2 should be titrated to maintain adequate oxygen levels but avoid oxygen toxicity.78
  3. Many patients with sudden neurological injuries have an increased risk for acute respiratory distress syndrome (ARDS).79,80 While managing ventilator settings for patients that progress to ARDS, increasing PEEP settings will be needed to maintain oxygen saturations and improve alveoli recruitment. This increased PEEP can cause an increase in intrathoracic pressure, leading to decreased ventricular filling and subsequent decreased cardiac output.81 The increased intrathoracic pressure can also decrease jugular drainage from the cranial vasculature, leading to worsening ICP and cerebral edema.

ARDS management may also include certain novel treatments like proning, high frequency jet oscillation, or extracorporeal membrane oxygenation. Severe neurological injury and intracranial hypertension is a common contraindication to these more radical interventions.82,83 The interdisciplinary team should carefully consider the patient’s status and prognosis prior to moving forward with any advanced treatments with family involvement in the plan of care discussion.

Management of Common Respiratory Diseases

Upper Airway Obstruction

Obstructive airway disease can affect the upper or lower airways. When upper airway obstruction occurs, there is decreased ventilation and increased work of breathing, which leads to hypercarbia and then hypoxia. The addition of supplemental oxygen alone will not effectively manage a patient with upper airway obstruction. Ultimately, the cause of the obstruction must be treated or the airway secured.84 A frequent cause of airway obstruction is post-extubation laryngeal edema (PLE); it is the cause of 15% of all reintubations.85 The majority of patients will develop symptoms within 30 minutes of extubation, and almost half within five minutes of extubation.86 Stridor, a high-pitched sound caused by narrowing of the airway, is sometimes present with PLE. The reported incidence of associated stridor varies from 3% to 30%.87 Absence of a cuff leak suggests a higher risk for PLE. However, the presence of a cuff leak does not preclude that a patient will not develop airway obstruction from PLE.88

Corticosteroids can be used for prevention and treatment of PLE. A meta-analysis demonstrated that the use of steroids four hours prior to planned extubation in high-risk patients prevented the development of PLE and need for reintubation.89 In a patient who develops PLE, intravenous methylprednisolone or dexamethasone can be given for 24-48 hours post-extubation to decrease the inflammatory response. Nebulized epinephrine is also used for treatment since it aids in vasoconstriction. The optimal dosing of both medications is unclear.90

Table 11 – Causes of Upper Airway Obstruction

Respiratory Chapter_Table 11_Causes of Upper Airway Obstruction


Atelectasis is a common reason for impaired gas exchange in the NCCU. A positive end-expiratory pressure (PEEP) of 5 cm H2O is frequently used to prevent atelectasis. A PEEP of 5 cm in normal lungs and a PEEP of 10 cm in abnormal lungs correlate with minimal pulmonary vascular resistance.91 In patients undergoing general anesthesia, a PEEP of 10 cm H2O has also been shown to prevent atelectasis. Vital capacity maneuvers (VCM) (e.g. airway pressure of 40 cm H2O for 15 seconds) can open atelectatic lungs. Continuing with supra-physiologic PEEP (10 cm H2O) after a VCM can help prevent reoccurrence of atelectasis.92 VCMs using 30 cm H2O can decrease atelectasis but are not as effective as airway pressures of 40 cm H2O.92,93 Patients with higher body mass indices are at increased odds for developing atelectasis and may require higher airway pressures to open the alveoli.93 Patients should be monitored for barotrauma or hemodynamic instability from decreased cardiac output during a VCM.93

Acute Severe Asthma

Acute severe asthma (previously status asthmaticus) is refractory to beta agonists and must be treated as a medical emergency. The mainstay of treatment is supplemental oxygen for goal oxygen saturation > 90%, short-acting beta-2-agonists (most commonly albuterol) and corticosteroids (methylprednisolone 80 mg/day). Patients may manifest with accessory muscle use, pulsus paradoxus and tachycardia. Wheezing is a less useful predictor of airway obstruction. Heliox, a combination of helium and oxygen, can improve airway resistance by increasing laminar flow of air. Magnesium 2 g intravenous can also be considered in an effort to relax respiratory smooth muscle. Importantly, acute severe asthma is reversible and most patients recover. Underlying infection should be ruled out as a cause for the exacerbation.94

Respiratory Chapter_Acute Severe Asthma

Chronic Obstructive Pulmonary Disease (COPD) Exacerbation

COPD exacerbations are associated with increased morbidity and mortality. Patient who have had more than one exacerbation in the previous year, previous hospitalization for a COPD exacerbation or a forced expiratory volume over one second of less than 50% are at increased risk for future exacerbations.95

Inhaled long-acting bronchodilators combined with inhaled corticosteroids (with or without long-acting anticholinergics) are the mainstay for prevention of COPD exacerbations and improvement of symptoms and lung function. During a COPD exacerbation, short-acting bronchodilators are used to alleviate symptoms. Short-acting anticholinergics can also be added for an exacerbation. In patients with hypoxia, supplemental oxygen should be given to maintain oxygen saturations between 89-92%. Systemic glucocorticoids and antibiotics aid in shortening the exacerbation and decreasing the risk of relapse and improving lung function and oxygen saturation.95 A short duration of steroids (seven days or fewer) is as effective as a longer duration of steroids in improving lung function and symptoms. In addition, there is not an increase in treatment failure or relapse with the shorter duration of steroids.96 Prednisone 40 mg daily for five days is recommended. Antibiotics are given in patients who require intubation or who have worsening shortness of breath and increased sputum production and purulence.

Endotracheal intubation may be required for patients having a COPD exacerbation. However, a trial of non-invasive ventilation (NIV) should be considered first in patients who are safe to protect their airway from a neurological standpoint. Patients managed with NIV may avoid the need to be intubated. In addition, they have decreased mortality, shorter hospital stays and less hospital-acquired pneumonia.97

Respiratory Chapter_COPD

Hospital-Acquired Pneumonia (HAP) and Ventilator-Associated Pneumonia (VAP)

Pneumonia can be clinically difficult to diagnosis. The American Thoracic Society and the Infectious Disease Society of America have defined pneumonia as “a new lung infiltrate plus clinical evidence that the infiltrate is of an infectious origin, which include the new onset of fever, purulent sputum, leukocytosis, and decline in oxygenation.”98 Patients in the NCCU are at risk for HAP and VAP. HAP is pneumonia that occurs >48 hours after hospital admission, and VAP is pneumonia that occurs >48 hours after endotracheal intubation. Cultures should be obtained, preferably non-invasively, in patients suspected of having HAP or VAP. Empiric coverage can be started to cover methicillin-resistant Staphylococcus aureus, Pseudomonas aeruginosa, and Gram-negative bacilli. Antibiotic treatment should continue for seven days and be narrowed once an organism is identified. For patients with ventilator-associated tracheobronchitis, it is not clear that antibiotics improve clinical outcome, though they may decreased ventilator days.99

Pulmonary Edema

Patients in the NCCU can develop pulmonary edema acutely or as an exacerbation of underlying heart failure. Generally, osmotic pressure in the lungs is greater than hydrostatic pressure, preventing fluid from accumulating in the interstitial spaces of the lungs. When hydrostatic pressure exceeds osmotic pressure, the alveoli will fill with fluid and impede oxygenation and decrease lung compliance.100 In cardiac pulmonary edema, insufficient cardiac output leads to vasoconstriction to maintain blood pressure and increased afterload, further impeding blood flow from the left ventricle. Increased volume and higher pressure in the left ventricle results in fluid entering into the pulmonary vasculature.100 Neurogenic pulmonary edema results from an outpouring of catecholamines when intracranial pressure is abruptly increased from brain or spinal cord injury.101 Sudden increases in systemic vascular resistance lead to hydrostatic pulmonary edema.101,102 Patients can also develop Takotsubo’s cardiomyopathy, cardiac injury from sympathetic over-activation leading to cardiogenic pulmonary edema.101 Regardless of the etiology, diuretics are the main treatment for pulmonary edema. Supplemental oxygen and mechanical ventilation are used to treat hypoxic respiratory distress or failure. Non-invasive ventilation (NIV) may have a role in select patients with pulmonary edema who do not have impaired mental status or ability to protect the airway and do not have intracranial hypertension. NIV can recruit alveoli and move interstitial fluid back into the pulmonary capillaries, improving oxygenation. NIV also improves cardiac output by decreasing afterload.100

Respiratory Chapter_Pulmonary Edema

Pleural Effusions

Pleural effusions are commonly seen in critically-ill patients for a variety of reasons: fluid resuscitation, atelectasis, decreased mobility secondary to sedation, VAP and occult pulmonary embolism all contribute.103 Patients that may be at increased risk for developing pleural effusions are those with advanced age, hypoalbuminemia, more severe illness, longer ICU stays and prolonged need for mechanical ventilation.104 Pleural effusions can be diagnosed on chest x-ray, but both CT and ultrasonography are more sensitive. Ultrasound also has the advantage of helping to determine the type of effusion – transudative (anechoic) or exudative (echogenic).103

The clinical implication of pleural effusions in the NCCU depends, in part, on the etiology of the effusions. Large pleural effusions can affect mechanical ventilation, pulmonary function and oxygenation. Diagnostic thoracentesis is not necessary in all patients with pleural effusions unless there is concern for an infectious or malignant etiology or other uncertainty in diagnosis. Usually, transudative effusions do not require drainage and can be treated with diuresis if needed. Drainage options for pleural effusions include thoracentesis, placement of a small-bore (pigtail) catheter and placement of a chest tube (if hemothorax or persistent empyema is present).103 To avoid re-expansion pulmonary edema, no more than one liter should be removed with thoracentesis.105

Table 12 – Light’s Criteria for Diagnosis of Exudative Pleural Effusion106

Respiratory Chapter_Table 12_Light's Criteria for Diagnosis of Exudative Pleural Effusion

Acute Respiratory Distress Syndrome (ARDS)

In 2011, the European Society of Intensive Care Medicine endorsed by the American Thoracic Society and the Society of Critical Care Medicine updated the definition of ARDS using the Berlin definition.107 This new definition eliminates the category of acute lung injury and seeks to stage ARDS as mild, moderate or severe depending on the degree of oxygen impairment present.107

Table 13 – Berlin definition of acute respiratory distress syndrome
Respiratory Chapter_Table 13_Berlin definition of acute respiratory distress syndrome

The mainstay of treatment in ARDS is lung protective ventilation. Patients have limits on tidal volumes (6 mL/kg of ideal body weight) and plateau pressures (≤ 30 cm H20), and are given appropriate PEEP to maintain adequate oxygenation (oxyhemoglobin saturation of 88-95% or partial pressure of arterial oxygen of 55-80 mm Hg).108 Of note, patients receiving lung protective ventilation can develop hypercapnia, which could be detrimental to a neurologically injured patient with cerebral edema. In these patients, a modified ARDS protocol can be used so that permissive hypercapnia is avoided.109 An ICP monitor can also be considered in patients in whom hypercapnia is unavoidable.110 In patients with severe hypoxia, prone ventilation can be considered and may be more effective in obese patients.111,112 High-frequency oscillatory ventilation can also be considered and has been shown to improve oxygenation when implemented early.113 However, it is not clear that it improves mortality.114

Respiratory Chapter_ARDS

Pulmonary Embolism (PE)

PE occurs in less than 1% to 2% of patients in the ICU.115,116 Higher incidences are seen in patients with brain injury or coma (9-17%).116 Patients at increased odds for developing a PE in the ICU include those with hypoxemia (PaO2:FiO2 < 300) or spinal fractures and those who are unable to receive chemical prophylaxis for deep venous thrombosis (DVT).116 Because of a recent neurosurgical procedure or intracranial hemorrhage, when to start chemical DVT prophylaxis safely can be a concern. It is generally thought safe to begin low-dose heparin therapy after a neurosurgical procedure117,118 or within 48 hours of a clinically stable intracerebral hemorrhage without increased risk of bleeding.119 When a PE is suspected, the preferred diagnostic test is a spiral CT. Once a PE is diagnosed, anticoagulation should be initiated. If anticoagulation is contraindicated, placement of an inferior vena cava (IVC) filter is recommended. Patients with IVC filters should still be anticoagulated once their risk of bleeding resolves.120

Respiratory Chapter_PE


A pneumothorax can occur in the setting of thoracic trauma, iatrogenic or spontaneously. Primary spontaneous pneumothorax occurs in patients without underlying lung pathology, and secondary spontaneous pneumothorax occurs in those patients with primary lung disease, most commonly COPD.121 Iatrogenic pneumothorax occurs in 3% of critical care patients; barotrauma is the most common cause (1.3%), followed by central venous catheter insertion (0.9%) and thoracentesis (0.7%).122 An upright inspiratory chest x-ray is the preferred imaging modality for diagnosis.123 Patients with small pneumothoraces who are not mechanically ventilated can be managed conservatively and followed with serial chest x-rays. Patients with large pneumothoraces or symptoms of shortness of breath should be treated with a chest tube to allow the lung to re-expand.121,123 All patients who are mechanically ventilated require a chest tube because the positive pressure ventilation maintains the air leak.124 Once the lung has re-expanded on chest x-ray and there no evidence of an air leak, the chest tube can be removed.121

Tension pneumothorax occurs when air in the pleural space cannot escape during expiration, leading to increasing intrapleural pressure, distended neck veins, hypotension and tracheal deviation. In these cases, needle thoracostomy positioned in the second intercostal space can be life-saving. In cases where the diagnosis is not clear and the patient is sufficiently clinically stable, a chest x-ray should be obtained first.125 In addition, the standard length of an angiocatheter used for needle thoracostomy will be too short in up to 50% of patients secondary to body habitus.126 Definitive treatment for tension pneumothorax is a chest tube.

Nursing Interventions for Common Respiratory Diseases

Many hospital-acquired conditions have evidence-based care bundles focused on prevention, as preventing an injury is beneficial not only to the patient but also to the institution. Two interventions are specifically discussed throughout the literature for prevention of ventilator-acquired pneumonia: head of bed greater than or equal to 30˚ and oral care with chlorhexidine gluconate. 127,128 The most obvious intervention for VAP prevention is to extubate the patient. Daily assessment for need of mechanical ventilation should be discussed with the interprofessional team, and NCCU patients should be extubated quickly if possible. After the patient is extubated, several non-invasive treatments can be used to prevent respiratory complications in the NCCU. Chest physiotherapy with either a vest or vibratory positive expiratory pressure (PEP) device may help mobilize secretions.129 For patients unable to follow commands, the vest is recommended, as the vibratory PEP device requires a tight lip seal around the mouthpiece to vibrate the inferior lung tissues. Incentive spirometry can be used to prevent post-operative atelectasis in patients who have normal inspiratory force.

Another common complication in the NCCU is deep vein thrombosis and pulmonary embolism. Administration of chemical prophylaxis in addition to sequential compression devices should be initiated, even in patients who have had neurological surgery.130 Patient ambulation may also assist with DVT prevention by way of improving venous return. Progressive mobility for appropriate patients has also been shown effective in decreasing the incidence of delirium and improving functional outcomes at discharge.131

Non-Invasive Ventilation (NIV) Management

The use of NIV is recommended during acute exacerbations of COPD or congestive heart failure.97 132 NIV can also be used for some acute neuromuscular diseases, such as myasthenia gravis.27 NIV can prevent invasive mechanical ventilation, which increases the risk of a slew of hospital-acquired conditions and lengthens ICU length of stay. While NIV may be beneficial to some patients, signs and symptoms of respiratory failure with NIV should prompt early notification of the provider teams for quick intervention. If patients can maintain oxygenation and ventilation with NIV, skin protection of the nasal bridge with use of hydrocolloid can prevent pain and pressure injury development.

Fit of the NIV mask is extremely important to maintenance of the pressures required for NIV. Masks should fit snuggly on the face without audible leakage. Two modes are used with NIV: continuous positive airway pressure (CPAP) or bi-level positive airway pressure (BiPAP). CPAP assists with chronic intermittent airway obstructions (such as those seen with obstructive sleep apnea) by keeping a low, continuous amount of positive pressure in the airways. In contrast, BiPAP has two levels of pressure that alternate with inspiration and exhalation, much like a pressure support setting on a ventilator. All pressure levels can be titrated to maximize oxygenation and ventilation. Because of the high pressures and tight fitting mask, NIV should be used with caution in patients with decreased or altered level of consciousness. In addition, enteral nutrition via a nasogastric tube and NIV has been associated with airway complications, leading to a significantly longer need for NIV.133 NIV should be used cautiously in these patients.


Respiratory complications are an important source of morbidity and mortality in the NCCU. Hence, those caring for neurocritically ill patients need to demonstrate expertise in the management of respiratory disease. The conditions described in this chapter need to be anticipated, recognized and managed early, aggressively and confidently. The outcomes of mechanically ventilated, neurocritically ill patients have improved and continue to improve due to new medical and surgical therapies for severe neurologic disease, improved mechanical ventilation and general ICU practices, more sophisticated prevention of secondary neurological injury, and dedicated treatment in specialized NCCUs. It has to be realized that a) many neurocritically ill patients do not have a problem with respiration but with airway control and can often be successfully weaned after tracheostomy, b) even patients not cooperative due to their brain lesion may be to extubate successfully, c) mechanical ventilation is a powerful tool to steer cerebral oxygenation and hemodynamics, d) neurocritically ill patients deserve lung-protective ventilation and use of PEEP the same as other general ICU patients, and e) additional pulmonary disease will further and substantially compromise the course of the neurocritically ill patient and should be avoided, if possible, and treated aggressively.


  1. Smith JC, Ellenberger HH, Ballanyi K, Richter DW, Feldman JL. Pre-Botzinger complex: a brainstem region that may generate respiratory rhythm in mammals. Science 1991;254:726-9
  2. Feldman JL, Ellenberger HH. Central coordination of respiratory and cardiovascular control in mammals. Annu Rev Physiol 1988;50:593-606
  3. Weston MC, Stornetta RL, Guyenet PG. Glutamatergic neuronal projections from the marginal layer of the rostral ventral medulla to the respiratory centers in rats. J Comp Neurol 2004;473:73-85
  4. Chamberlin NL, Saper CB. Topographic organization of respiratory responses to glutamate microstimulation of the parabrachial nucleus in the rat. J Neurosci 1994;14:6500-10
  5. Richerson GB. Serotonergic neurons as carbon dioxide sensors that maintain pH homeostasis. Nat Rev Neurosci 2004;5:449-61
  6. Lee MC, Klassen AC, Heaney LM, Resch JA. Respiratory rate and pattern disturbances in acute brain stem infarction. Stroke 1976;7:382-5
  7. Plum F, Alvord EC, Jr. Apneustic Breathing in Man. Arch Neurol 1964;10:101-12
  8. Plum F, Swanson AG. Central neurogenic hyperventilation in man. AMA Arch Neurol Psychiatry 1959;81:535-49
  9. Gray PA, Janczewski WA, Mellen N, McCrimmon DR, Feldman JL. Normal breathing requires preBotzinger complex neurokinin-1 receptor-expressing neurons. Nat Neurosci 2001;4:927-30
  10. Tatsumi K, Kimura H, Kunitomo F, Kuriyama T, Watanabe S, Honda Y. Sleep arterial oxygen desaturation and chemical control of breathing during wakefulness in COPD. Chest 1986;90:68-73
  11. Schestatsky P, Fernandes LN. Acquired Ondine's curse: case report. Arq Neuropsiquiatr 2004;62:523-7
  12. Walker JM, Farney RJ, Rhondeau SM, et al. Chronic opioid use is a risk factor for the development of central sleep apnea and ataxic breathing. J Clin Sleep Med 2007;3:455-61
  13. White DP. Pathogenesis of obstructive and central sleep apnea. Am J Respir Crit Care Med 2005;172:1363-70
  14. Miller AJ. The neurobiology of swallowing and dysphagia. Dev Disabil Res Rev 2008;14:77-86
  15. Matsuo K, Palmer JB. Anatomy and physiology of feeding and swallowing: normal and abnormal. Phys Med Rehabil Clin N Am 2008;19:691-707, vii
  16. Pitts T, Bolser D, Rosenbek J, Troche M, Sapienza C. Voluntary cough production and swallow dysfunction in Parkinson's disease. Dysphagia 2008;23:297-301
  17. Smith Hammond CA, Goldstein LB, Zajac DJ, Gray L, Davenport PW, Bolser DC. Assessment of aspiration risk in stroke patients with quantification of voluntary cough. Neurology 2001;56:502-6
  18. Daniels SK, Foundas AL. The role of the insular cortex in dysphagia. Dysphagia 1997;12:146-56
  19. Robbins J, Levine RL, Maser A, Rosenbek JC, Kempster GB. Swallowing after unilateral stroke of the cerebral cortex. Arch Phys Med Rehabil 1993;74:1295-300
  20. Marik PE. Aspiration pneumonitis and aspiration pneumonia. N Engl J Med 2001;344:665-71
  21. Garvey BM, McCambley JA, Tuxen DV. Effects of gastric alkalization on bacterial colonization in critically ill patients. Crit Care Med 1989;17:211-6
  22. Bonten MJ, Gaillard CA, van der Geest S, et al. The role of intragastric acidity and stress ulcus prophylaxis on colonization and infection in mechanically ventilated ICU patients. A stratified, randomized, double-blind study of sucralfate versus antacids. Am J Respir Crit Care Med 1995;152:1825-34
  23. Marik PE, Zaloga GP. Gastric versus post-pyloric feeding: a systematic review. Crit Care 2003;7:R46-51
  24. Racca F, Del Sorbo L, Mongini T, Vianello A, Ranieri VM. Respiratory management of acute respiratory failure in neuromuscular diseases. Minerva Anestesiol 2010;76:51-62
  25. Ahmed S, Kirmani JF, Janjua N, et al. An Update on Myasthenic Crisis. Curr Treat Options Neurol 2005;7:129-41
  26. Rabinstein AA. Acute Neuromuscular Respiratory Failure. Continuum (Minneap Minn) 2015;21:1324-45
  27. Rabinstein A, Wijdicks EF. BiPAP in acute respiratory failure due to myasthenic crisis may prevent intubation. Neurology 2002;59:1647-9
  28. Seneviratne J, Mandrekar J, Wijdicks EF, Rabinstein AA. Noninvasive ventilation in myasthenic crisis. Arch Neurol 2008;65:54-8
  29. Hickey JV, Kanusky JT. Overview of neuroanatomy and neurophysiology. In: Hickey J, ed. The clinical practice of neurological and neurosurgical nursing. 7th ed. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins; 2014.
  30. Jarvis C. Physical examination & health assessment. 7th ed. St. Louis: Elsevier, Inc.; 2016.
  31. Hinchey JA, Shephard T, Furie K, et al. Formal dysphagia screening protocols prevent pneumonia. Stroke 2005;36:1972-6
  32. Razi E, Moosavi GA, Omidi K, Khakpour Saebi A, Razi A. Correlation of end-tidal carbon dioxide with arterial carbon dioxide in mechanically ventilated patients. Arch Trauma Res 2012;1:58-62
  33. Stewart-Amidei C, Blissitt P, Brooks L. Assessment. In: Bader M, Littlejohns L, eds. AANN Core Curriculum for Neuroscience Nursing. 5th ed. Glenview, IL: American Association of Neuroscience Nurses; 2010.
  34. Seder DB, Riker RR, Jagoda A, Smith WS, Weingart SD. Emergency neurological life support: airway, ventilation, and sedation. Neurocrit Care 2012;17 Suppl 1:S4-20
  35. Karanjia N, Nordquist D, Stevens R, Nyquist P. A clinical description of extubation failure in patients with primary brain injury. Neurocrit Care 2011;15:4-12
  36. Kurtz P, Fitts V, Sumer Z, et al. How does care differ for neurological patients admitted to a neurocritical care unit versus a general ICU? Neurocrit Care 2011;15:477-80
  37. Reed MJ, Dunn MJ, McKeown DW. Can an airway assessment score predict difficulty at intubation in the emergency department? Emerg Med J 2005;22:99-102
  38. Crosby ET, Cooper RM, Douglas MJ, et al. The unanticipated difficult airway with recommendations for management. Can J Anaesth 1998;45:757-76
  39. Sinclair RCF, Luxton MC. Rapid sequence induction. Continuing Education in Anaesthesia, Critical Care & Pain 2005;5:45-8
  40. Miguel-Montanes R, Hajage D, Messika J, et al. Use of high-flow nasal cannula oxygen therapy to prevent desaturation during tracheal intubation of intensive care patients with mild-to-moderate hypoxemia. Crit Care Med 2015;43:574-83
  41. Butler J, Sen A. Best evidence topic report. Cricoid pressure in emergency rapid sequence induction. Emerg Med J 2005;22:815-6
  42. Shribman AJ, Smith G, Achola KJ. Cardiovascular and catecholamine responses to laryngoscopy with and without tracheal intubation. Br J Anaesth 1987;59:295-9
  43. Walls RM. Rapid-sequence intubation in head trauma. Ann Emerg Med 1993;22:1008-13
  44. Perkins ZB, Wittenberg MD, Nevin D, Lockey DJ, O'Brien B. The relationship between head injury severity and hemodynamic response to tracheal intubation. J Trauma Acute Care Surg 2013;74:1074-80
  45. Hastings RH, Wood PR. Head extension and laryngeal view during laryngoscopy with cervical spine stabilization maneuvers. Anesthesiology 1994;80:825-31
  46. Reynolds SF, Heffner J. Airway management of the critically ill patient: rapid-sequence intubation. Chest 2005;127:1397-412
  47. Davis DP, Dunford JV, Poste JC, et al. The impact of hypoxia and hyperventilation on outcome after paramedic rapid sequence intubation of severely head-injured patients. J Trauma 2004;57:1-8; discussion -10
  48. Feldman Z, Kanter MJ, Robertson CS, et al. Effect of head elevation on intracranial pressure, cerebral perfusion pressure, and cerebral blood flow in head-injured patients. J Neurosurg 1992;76:207-11
  49. Serpa Neto A, Cardoso SO, Manetta JA, et al. Association between use of lung-protective ventilation with lower tidal volumes and clinical outcomes among patients without acute respiratory distress syndrome: a meta-analysis. JAMA 2012;308:1651-9
  50. Vasilyev S, Schaap RN, Mortensen JD. Hospital survival rates of patients with acute respiratory failure in modern respiratory intensive care units. An international, multicenter, prospective survey. Chest 1995;107:1083-8
  51. Coles JP, Minhas PS, Fryer TD, et al. Effect of hyperventilation on cerebral blood flow in traumatic head injury: clinical relevance and monitoring correlates. Crit Care Med 2002;30:1950-9
  52. Morandi A, Brummel NE, Ely EW. Sedation, delirium and mechanical ventilation: the 'ABCDE' approach. Curr Opin Crit Care 2011;17:43-9
  53. Skoglund K, Enblad P, Marklund N. Effects of the neurological wake-up test on intracranial pressure and cerebral perfusion pressure in brain-injured patients. Neurocrit Care 2009;11:135-42
  54. Helbok R, Kurtz P, Schmidt MJ, et al. Effects of the neurological wake-up test on clinical examination, intracranial pressure, brain metabolism and brain tissue oxygenation in severely brain-injured patients. Crit Care 2012;16:R226
  55. Barnes-Daly MA, Phillips G, Ely EW. Improving Hospital Survival and Reducing Brain Dysfunction at Seven California Community Hospitals: Implementing PAD Guidelines Via the ABCDEF Bundle in 6,064 Patients. Crit Care Med 2017;45:171-8
  56. Kiekkas P, Aretha D, Panteli E, Baltopoulos GI, Filos KS. Unplanned extubation in critically ill adults: clinical review. Nurs Crit Care 2013;18:123-34
  57. Tominaga GT, Rudzwick H, Scannell G, Waxman K. Decreasing unplanned extubations in the surgical intensive care unit. Am J Surg 1995;170:586-9; discussion 9-90
  58. Kress JP, Pohlman AS, O'Connor MF, Hall JB. Daily interruption of sedative infusions in critically ill patients undergoing mechanical ventilation. N Engl J Med 2000;342:1471-7
  59. Reade MC, Eastwood GM, Bellomo R, et al. Effect of Dexmedetomidine Added to Standard Care on Ventilator-Free Time in Patients With Agitated Delirium: A Randomized Clinical Trial. JAMA 2016;315:1460-8
  60. Girard TD, Kress JP, Fuchs BD, et al. Efficacy and safety of a paired sedation and ventilator weaning protocol for mechanically ventilated patients in intensive care (Awakening and Breathing Controlled trial): a randomised controlled trial. Lancet 2008;371:126-34
  61. Blackwood B, Burns KE, Cardwell CR, O'Halloran P. Protocolized versus non-protocolized weaning for reducing the duration of mechanical ventilation in critically ill adult patients. Cochrane Database Syst Rev 2014:CD006904
  62. Ko R, Ramos L, Chalela JA. Conventional weaning parameters do not predict extubation failure in neurocritical care patients. Neurocrit Care 2009;10:269-73
  63. Pelosi P, Ferguson ND, Frutos-Vivar F, et al. Management and outcome of mechanically ventilated neurologic patients. Crit Care Med 2011;39:1482-92
  64. Anderson CD, Bartscher JF, Scripko PD, et al. Neurologic examination and extubation outcome in the neurocritical care unit. Neurocrit Care 2011;15:490-7
  65. Wendell LC, Raser J, Kasner S, Park S. Predictors of extubation success in patients with middle cerebral artery acute ischemic stroke. Stroke Res Treat 2011;2011:248789
  66. Vallverdu I, Calaf N, Subirana M, Net A, Benito S, Mancebo J. Clinical characteristics, respiratory functional parameters, and outcome of a two-hour T-piece trial in patients weaning from mechanical ventilation. Am J Respir Crit Care Med 1998;158:1855-62
  67. Wu JY, Kuo PH, Fan PC, Wu HD, Shih FY, Yang PC. The role of non-invasive ventilation and factors predicting extubation outcome in myasthenic crisis. Neurocrit Care 2009;10:35-42
  68. Coplin WM, Pierson DJ, Cooley KD, Newell DW, Rubenfeld GD. Implications of extubation delay in brain-injured patients meeting standard weaning criteria. Am J Respir Crit Care Med 2000;161:1530-6
  69. Wang J, Ma Y, Fang Q. Extubation with or without spontaneous breathing trial. Crit Care Nurse 2013;33:50-5
  70. Namen AM, Ely EW, Tatter SB, et al. Predictors of successful extubation in neurosurgical patients. Am J Respir Crit Care Med 2001;163:658-64
  71. Asehnoune K, Seguin P, Lasocki S, et al. Extubation Success Prediction in a Multicentric Cohort of Patients with Severe Brain Injury. Anesthesiology 2017;127:338-46
  72. van der Lely AJ, Veelo DP, Dongelmans DA, Korevaar JC, Vroom MB, Schultz MJ. Time to wean after tracheotomy differs among subgroups of critically ill patients: retrospective analysis in a mixed medical/surgical intensive care unit. Respir Care 2006;51:1408-15
  73. Bosel J, Schiller P, Hook Y, et al. Stroke-related Early Tracheostomy versus Prolonged Orotracheal Intubation in Neurocritical Care Trial (SETPOINT): a randomized pilot trial. Stroke 2013;44:21-8
  74. Kleffmann J, Pahl R, Deinsberger W, Ferbert A, Roth C. Effect of percutaneous tracheostomy on intracerebral pressure and perfusion pressure in patients with acute cerebral dysfunction (TIP Trial): an observational study. Neurocrit Care 2012;17:85-9
  75. Polderman KH, Spijkstra JJ, de Bree R, et al. Percutaneous dilatational tracheostomy in the ICU: optimal organization, low complication rates, and description of a new complication. Chest 2003;123:1595-602
  76. Epstein SK. Late complications of tracheostomy. Respir Care 2005;50:542-9
  77. Bilotta F, Branca G, Lam A, Cuzzone V, Doronzio A, Rosa G. Endotracheal lidocaine in preventing endotracheal suctioning-induced changes in cerebral hemodynamics in patients with severe head trauma. Neurocrit Care 2008;8:241-6
  78. Hlatky R, Valadka AB, Gopinath SP, Robertson CS. Brain tissue oxygen tension response to induced hyperoxia reduced in hypoperfused brain. J Neurosurg 2008;108:53-8
  79. Hendrickson CM, Howard BM, Kornblith LZ, et al. The acute respiratory distress syndrome following isolated severe traumatic brain injury. J Trauma Acute Care Surg 2016;80:989-97
  80. Hoesch RE, Lin E, Young M, et al. Acute lung injury in critical neurological illness. Crit Care Med 2012;40:587-93
  81. Luecke T, Pelosi P. Clinical review: Positive end-expiratory pressure and cardiac output. Crit Care 2005;9:607-21
  82. Fessler HE, Derdak S, Ferguson ND, et al. A protocol for high-frequency oscillatory ventilation in adults: results from a roundtable discussion. Crit Care Med 2007;35:1649-54
  83. Messerole E, Peine P, Wittkopp S, Marini JJ, Albert RK. The pragmatics of prone positioning. Am J Respir Crit Care Med 2002;165:1359-63
  84. McPherson K, Stephens RC. Managing airway obstruction. Br J Hosp Med (Lond) 2012;73:C156-60
  85. Epstein SK, Ciubotaru RL. Independent effects of etiology of failure and time to reintubation on outcome for patients failing extubation. Am J Respir Crit Care Med 1998;158:489-93
  86. Francois B, Bellissant E, Gissot V, et al. 12-h pretreatment with methylprednisolone versus placebo for prevention of postextubation laryngeal oedema: a randomised double-blind trial. Lancet 2007;369:1083-9
  87. Wittekamp BH, van Mook WN, Tjan DH, Zwaveling JH, Bergmans DC. Clinical review: post-extubation laryngeal edema and extubation failure in critically ill adult patients. Crit Care 2009;13:233
  88. Ochoa ME, Marin Mdel C, Frutos-Vivar F, et al. Cuff-leak test for the diagnosis of upper airway obstruction in adults: a systematic review and meta-analysis. Intensive Care Med 2009;35:1171-9
  89. Jaber S, Jung B, Chanques G, Bonnet F, Marret E. Effects of steroids on reintubation and post-extubation stridor in adults: meta-analysis of randomised controlled trials. Crit Care 2009;13:R49
  90. Pluijms WA, van Mook WN, Wittekamp BH, Bergmans DC. Postextubation laryngeal edema and stridor resulting in respiratory failure in critically ill adult patients: updated review. Crit Care 2015;19:295
  91. Canada E, Benumof JL, Tousdale FR. Pulmonary vascular resistance correlates in intact normal and abnormal canine lungs. Crit Care Med 1982;10:719-23
  92. Neumann P, Rothen HU, Berglund JE, Valtysson J, Magnusson A, Hedenstierna G. Positive end-expiratory pressure prevents atelectasis during general anaesthesia even in the presence of a high inspired oxygen concentration. Acta Anaesthesiol Scand 1999;43:295-301
  93. Rothen HU, Sporre B, Engberg G, Wegenius G, Hedenstierna G. Re-expansion of atelectasis during general anaesthesia: a computed tomography study. Br J Anaesth 1993;71:788-95
  94. Shah R, Saltoun CA. Chapter 14: Acute severe asthma (status asthmaticus). Allergy Asthma Proc 2012;33 Suppl 1:S47-50
  95. Holmquist L, Russo CA, Elixhauser A. Hospital Stays for Lung Cancer, 2006: Statistical Brief #63. Healthcare Cost and Utilization Project (HCUP) Statistical Briefs. Rockville (MD)2006.
  96. Ma Z, Zhang W. Short-term versus longer duration of glucocorticoid therapy for exacerbations of chronic obstructive pulmonary disease. Pulm Pharmacol Ther 2016;40:84-90
  97. Lindenauer PK, Stefan MS, Shieh MS, Pekow PS, Rothberg MB, Hill NS. Outcomes associated with invasive and noninvasive ventilation among patients hospitalized with exacerbations of chronic obstructive pulmonary disease. JAMA Intern Med 2014;174:1982-93
  98. American Thoracic S, Infectious Diseases Society of A. Guidelines for the management of adults with hospital-acquired, ventilator-associated, and healthcare-associated pneumonia. Am J Respir Crit Care Med 2005;171:388-416
  99. Kalil AC, Metersky ML, Klompas M, et al. Management of Adults With Hospital-acquired and Ventilator-associated Pneumonia: 2016 Clinical Practice Guidelines by the Infectious Diseases Society of America and the American Thoracic Society. Clin Infect Dis 2016;63:e61-e111
  100. Skinner J, McKinney A. Acute cardiogenic pulmonary oedema: reflecting on the management of an intensive care unit patient. Nurs Crit Care 2011;16:193-200
  101. Davison DL, Terek M, Chawla LS. Neurogenic pulmonary edema. Crit Care 2012;16:212
  102. Mascia L. Acute lung injury in patients with severe brain injury: a double hit model. Neurocrit Care 2009;11:417-26
  103. Maslove DM, Chen BT, Wang H, Kuschner WG. The diagnosis and management of pleural effusions in the ICU. J Intensive Care Med 2013;28:24-36
  104. Mattison LE, Coppage L, Alderman DF, Herlong JO, Sahn SA. Pleural effusions in the medical ICU: prevalence, causes, and clinical implications. Chest 1997;111:1018-23
  105. Feller-Kopman D, Berkowitz D, Boiselle P, Ernst A. Large-volume thoracentesis and the risk of reexpansion pulmonary edema. Ann Thorac Surg 2007;84:1656-61
  106. Light RW, Macgregor MI, Luchsinger PC, Ball WC, Jr. Pleural effusions: the diagnostic separation of transudates and exudates. Ann Intern Med 1972;77:507-13
  107. Force ADT, Ranieri VM, Rubenfeld GD, et al. Acute respiratory distress syndrome: the Berlin Definition. JAMA 2012;307:2526-33
  108. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network. N Engl J Med 2000;342:1301-8
  109. Haddad SH, Arabi YM. Critical care management of severe traumatic brain injury in adults. Scand J Trauma Resusc Emerg Med 2012;20:12
  110. Mrozek S, Constantin JM, Geeraerts T. Brain-lung crosstalk: Implications for neurocritical care patients. World J Crit Care Med 2015;4:163-78
  111. Guerin C, Reignier J, Richard JC, et al. Prone positioning in severe acute respiratory distress syndrome. N Engl J Med 2013;368:2159-68
  112. De Jong A, Molinari N, Sebbane M, et al. Feasibility and effectiveness of prone position in morbidly obese patients with ARDS: a case-control clinical study. Chest 2013;143:1554-61
  113. Camporota L, Sherry T, Smith J, Lei K, McLuckie A, Beale R. Physiological predictors of survival during high-frequency oscillatory ventilation in adults with acute respiratory distress syndrome. Crit Care 2013;17:R40
  114. Sud S, Sud M, Friedrich JO, et al. High-frequency ventilation versus conventional ventilation for treatment of acute lung injury and acute respiratory distress syndrome. Cochrane Database Syst Rev 2013:CD004085
  115. Patel R, Cook DJ, Meade MO, et al. Burden of illness in venous thromboembolism in critical care: a multicenter observational study. J Crit Care 2005;20:341-7
  116. Bahloul M, Chaari A, Kallel H, et al. Pulmonary embolism in intensive care unit: Predictive factors, clinical manifestations and outcome. Ann Thorac Med 2010;5:97-103
  117. Cerrato D, Ariano C, Fiacchino F. Deep vein thrombosis and low-dose heparin prophylaxis in neurosurgical patients. J Neurosurg 1978;49:378-81
  118. Frim DM, Barker FG, 2nd, Poletti CE, Hamilton AJ. Postoperative low-dose heparin decreases thromboembolic complications in neurosurgical patients. Neurosurgery 1992;30:830-2; discussion 2-3
  119. Boeer A, Voth E, Henze T, Prange HW. Early heparin therapy in patients with spontaneous intracerebral haemorrhage. J Neurol Neurosurg Psychiatry 1991;54:466-7
  120. Kearon C, Akl EA, Comerota AJ, et al. Antithrombotic therapy for VTE disease: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest 2012;141:e419S-94S
  121. Baumann MH, Strange C, Heffner JE, et al. Management of spontaneous pneumothorax: an American College of Chest Physicians Delphi consensus statement. Chest 2001;119:590-602
  122. de Lassence A, Timsit JF, Tafflet M, et al. Pneumothorax in the intensive care unit: incidence, risk factors, and outcome. Anesthesiology 2006;104:5-13
  123. MacDuff A, Arnold A, Harvey J, Group BTSPDG. Management of spontaneous pneumothorax: British Thoracic Society Pleural Disease Guideline 2010. Thorax 2010;65 Suppl 2:ii18-31
  124. Pollack MM, Fields AI, Holbrook PR. Pneumothorax and pneumomediastinum during pediatric mechanical ventilation. Crit Care Med 1979;7:536-9
  125. Cullinane DC, Morris JA, Jr., Bass JG, Rutherford EJ. Needle thoracostomy may not be indicated in the trauma patient. Injury 2001;32:749-52
  126. Stevens RL, Rochester AA, Busko J, et al. Needle thoracostomy for tension pneumothorax: failure predicted by chest computed tomography. Prehosp Emerg Care 2009;13:14-7
  127. Fields LB. Oral care intervention to reduce incidence of ventilator-associated pneumonia in the neurologic intensive care unit. J Neurosci Nurs 2008;40:291-8
  128. Yokoe DS, Anderson DJ, Berenholtz SM, et al. A compendium of strategies to prevent healthcare-associated infections in acute care hospitals: 2014 updates. Infect Control Hosp Epidemiol 2014;35:967-77
  129. Gosselink R, Bott J, Johnson M, et al. Physiotherapy for adult patients with critical illness: recommendations of the European Respiratory Society and European Society of Intensive Care Medicine Task Force on Physiotherapy for Critically Ill Patients. Intensive Care Med 2008;34:1188-99
  130. Nyquist P, Bautista C, Jichici D, et al. Prophylaxis of Venous Thrombosis in Neurocritical Care Patients: An Evidence-Based Guideline: A Statement for Healthcare Professionals from the Neurocritical Care Society. Neurocrit Care 2016;24:47-60
  131. Schweickert WD, Pohlman MC, Pohlman AS, et al. Early physical and occupational therapy in mechanically ventilated, critically ill patients: a randomised controlled trial. Lancet 2009;373:1874-82
  132. Vital FM, Ladeira MT, Atallah AN. Non-invasive positive pressure ventilation (CPAP or bilevel NPPV) for cardiogenic pulmonary oedema. Cochrane Database Syst Rev 2013:CD005351
  133. Kogo M, Nagata K, Morimoto T, et al. Enteral Nutrition During Noninvasive Ventilation: We Should Go Deeper in the Investigation-Reply. Respir Care 2017;62:1119-20

Access to this content is restricted to Neurocritical Care ON CALL subscribers.
Not a subscriber? Click Here to Subscribe.
Already purchased a subscription? Click on the headers to access the full topic content.