Mechanical ventilation of adults in the emergency department

INTRODUCTION — Patients present to the emergency department (ED) with a wide range of conditions that may require tracheal intubation or positive-pressure ventilation, including pneumonia, asthma, chronic obstructive pulmonary disease (COPD), cardiogenic pulmonary edema, acute respiratory distress syndrome (ARDS), stroke, trauma, drug overdose, sepsis, shock, and neuromuscular disorders such as myasthenia gravis or Guillain-Barré syndrome.

Once a definitive airway has been secured, ventilatory management ensues. Ventilatory strategies vary according to the clinical scenario, and to provide optimal care, emergency clinicians must understand the fundamental concepts of mechanical ventilation.

This topic review will discuss management of mechanical ventilation in the ED, including ventilator settings, modes of mechanical ventilation, complications of mechanical ventilation, management of ventilated patients in distress, general and disease-specific ventilation strategies, and weaning from ventilatory support [1-5]. Although useful guidelines are provided, clinicians will need to individualize mechanical ventilation strategies based on the clinical scenario. Tracheal intubation and other aspects of airway management are discussed elsewhere. (See "Rapid sequence intubation in adults for emergency medicine and critical care" and "Rapid sequence intubation (RSI) in children for emergency medicine: Approach".)

OBJECTIVES AND OVERVIEW OF MECHANICAL VENTILATION — Clinicians place patients on mechanical ventilation to accomplish any of the following goals, including:

●To secure the airway

●To improve pulmonary gas exchange (ie, reverse hypoxemia or acute respiratory acidosis)

●To relieve respiratory distress (ie, decrease oxygen consumption or address respiratory muscle fatigue)

●To assist with airway and lung healing

●To permit appropriate sedation and neuromuscular blockade

The ventilator simulates four stages of breathing:

1. The ventilator or the patient triggers the initiation of inspiration.

2. The ventilator provides a breath, determined by preset variables (ie, pressure, volume, and flow rate).

3. The ventilator halts inspiration when a preset parameter, such as tidal volume, inspiratory time, or airway pressure, is reached.

4. The ventilator switches to expiration, and the breath is completed. Expiration occurs when the expiratory valve opens and generally involves a passive mechanism generated by the recoil of the chest wall, lungs, and diaphragm.

VENTILATOR SETTINGS — To manage patients requiring mechanical ventilation, emergency clinicians must be familiar with the ventilator apparatus in use at their hospital and understand the various settings that can be modified. In this section, we describe basic ventilator settings of importance to the emergency clinician. More detailed discussions of mechanical ventilation settings are found separately. (See "Overview of initiating invasive mechanical ventilation in adults in the intensive care unit" and "Modes of mechanical ventilation".)

Ventilator settings are adjusted to provide adequate minute ventilation (MV) to meet metabolic demand while minimizing the risk of iatrogenic complications. MV equals tidal volume (TV) multiplied by respiratory rate (RR) (MV = TV x RR). Normal MV ranges from 5 to 10 L/min. The basal ventilatory rate is selected by the clinician. TV is generally based on predicted body weight (PBW) (calculator 1) and varies according to the ventilation mode chosen. The TV based on PBW for males and females is provided in the tables and calculator (table 1 and table 2) (calculator 2). (See 'Modes of ventilation' below.)

●Breath types – Mechanical ventilators can deliver different kinds of breaths. A mandatory breath is started, controlled, and ended by the ventilator, which does all the work. An assisted breath is initiated by the patient but controlled and ended by the ventilator. A spontaneous breath is initiated, controlled, and ended by the patient; the volume of the breath delivered by the ventilator is determined by the patient’s effort, pulmonary compliance, and physiologic reserve. (See "Overview of initiating invasive mechanical ventilation in adults in the intensive care unit", section on 'Indications'.)

●Triggers – An assisted breath can be triggered by either pressure or flow. The pressure trigger requires a demand valve, which senses a negative airway pressure deflection when the patient initiates a breath. A trigger sensitivity threshold of -1 to -3 cmH₂O is common. When the threshold is reached, the ventilator delivers a breath. (See "Overview of initiating invasive mechanical ventilation in adults in the intensive care unit", section on 'Trigger sensitivity'.)

The flow trigger uses a circuit of gas that flows continuously past the patient. A preset change in flow rate, created when the patient initiates a breath, triggers the ventilator to deliver a breath. A basal flow rate of 10 L/minute is common, and a trigger sensitivity threshold of 2 L/minute is frequently used.

Regardless of the trigger mechanism, the threshold must be appropriate. If it is too low, the ventilator will "auto-cycle" (ie, deliver a continual series of breaths), resulting in respiratory alkalosis; if it is too high, the patient will be "locked out" from ventilator-supported breaths while expending considerable energy. In both conditions, the mechanically ventilated patient will appear to be in respiratory distress, and the work of breathing will increase.

●Respiratory rate – The clinician determines the minimum number of breaths per minute (ie, respiratory rate) given to the patient by the ventilator. The rate can be adjusted according to the disease process. (See 'Disease-specific ventilatory management' below and "Overview of initiating invasive mechanical ventilation in adults in the intensive care unit", section on 'Ventilator rate'.)

●Inspiratory-to-expiratory (I:E) ratio – Inspiratory time (I time) is equal to TV divided by flow rate (I time = TV/FR). Decreasing the TV or increasing the flow rate decreases the inspiratory time and decreases the I:E ratio. The normal I:E ratio is 1:2 or 1:3.

Clinicians often reduce the I:E ratio to 1:4 or 1:5 in the presence of obstructive airway disease, which requires greater time for expiration. An inverse I:E ratio may be necessary in states of low lung compliance, such as acute respiratory distress syndrome (ARDS). Inverse-ratio ventilation may improve oxygenation in ARDS without elevating peak alveolar and inspiratory plateau pressures that can lead to further lung injury. (See "Modes of mechanical ventilation", section on 'Inverse ratio ventilation'.)

●Flow – Flow rates and waves represent additional inspiration variables. Flow rates of 60 L/minute are standard. Higher flow rates (up to 100 L/minute) may be required in certain conditions, such as obstructive airway disease (OAD) [6]. In OAD, higher flow rates deliver the desired TV more rapidly, allowing for increased expiratory time. (See "Modes of mechanical ventilation", section on 'Volume-limited ventilation'.)

●Cycling – Ventilator "cycling" refers to the mechanism by which a breath changes from inspiration to expiration. Common methods for cycling a ventilator are volume, flow, and time. Volume-cycled breaths transition from inspiration to expiration after a preset volume of gas is delivered. This is the most common form. Flow-cycled inspiratory breaths transition after a preset airway pressure is reached and flow decreases to a particular rate. Time-cycled inspiratory breaths transition after a predetermined inspiratory time.

Inspiratory hold can also be included in the cycling mechanism. This function keeps air in the lungs at end-inspiration for longer intervals to maximize gas exchange.

●Positive end-expiratory pressure (PEEP) – Applied or extrinsic positive end-expiratory pressure (PEEPe) can be provided by the ventilator to prevent premature airway closure and alveolar collapse at end expiration. PEEPe allows for improved oxygenation by increasing functional residual capacity (FRC), which is the volume at which pressure from elastic recoil equals PEEPe. By improving oxygenation, PEEPe can help clinicians reduce the fraction of inspired oxygen (FiO₂) being provided to the patient. PEEPe is often initially set with a minimum of 5 cmH₂O, a level thought to be equivalent to physiologic PEEPe. (See "Positive end-expiratory pressure (PEEP)".)

●Fraction of inspired oxygen (FiO₂) – FiO₂ is typically set at 1.0 (ie, 100 percent) when mechanical ventilation is initiated. As soon as possible, clinicians should reduce the FiO₂ to nontoxic levels (generally 0.6 or less), provided that an oxygen saturation (SpO₂) of 90 percent or greater can be maintained (PaO₂ above 60 mmHg). (See "Adverse effects of supplemental oxygen".)

MODES OF VENTILATION — The emergency clinician should be familiar with the following modes of mechanical ventilation:

●Assist-control ventilation (ACV)

●Synchronized intermittent mandatory ventilation (SIMV)

●Pressure support ventilation (PSV)

●Positive-pressure noninvasive ventilation (NIV)

ACV is used most frequently in the emergency department (ED) [7]. A brief description of the modes of ventilation of greatest relevance to emergency practice is provided here. There is no evidence that either mode of ventilation is superior to the other in terms of patient outcomes. More detailed discussions of the modes and advanced alternative modes of mechanical ventilation are found separately. (See "Modes of mechanical ventilation" and "High-frequency ventilation in adults".)

●Assist-control ventilation (ACV) – With ACV, every breath is fully supported by the ventilator, regardless of whether the breath is initiated by the patient or the machine. The clinician determines a base ventilatory rate, but the patient is able to breathe faster than this preset rate. ACV provides the patient with increased ventilatory support and reduces the work of breathing. Potential dangers include diminished cardiac output and inappropriate hyperventilation. (See "Clinical and physiologic complications of mechanical ventilation: Overview".)

ACV may be volume- or pressure-cycled. In volume-cycled (ie, volume-targeted) ACV, the clinician determines the tidal volume (TV), inspiratory flow rate, flow waveform, sensitivity to the patient's respiratory effort (ie, trigger), and basal ventilatory rate. When the patient breathes faster than the preset basal ventilatory rate, auto-positive end-expiratory pressure (PEEP) causing excessive peak inspiratory pressure (PIP) and subsequent lung injury may result unless limited by a pressure alarm and "pop-off" valve.

In pressure-cycled (ie, pressure-targeted) ACV, the clinician determines the ventilator's sensitivity to the patient's respiratory effort (ie, trigger) and the basal ventilatory rate. Unlike volume-controlled ACV, however, the clinician determines pressure levels and inspiratory time. TV is not set by the ventilator and is dependent upon airway pressures and the compliance of the lung and chest wall. While this mode allows the clinician to minimize PIP (and associated pressure-induced lung injury), specific TV is not guaranteed and will vary based upon the patient’s airway resistance and lung compliance.

●Synchronized intermittent mandatory ventilation (SIMV) – In SIMV mode, the patient is allowed intermittent spontaneous breaths between the mandated, preset number of ventilator-supported breaths. Spontaneous breaths above the preset ventilatory rate are not supported by the ventilator. Either the patient or the ventilator can trigger the ventilator-supported breaths.

SIMV creates less interference with normal cardiovascular function by decreasing auto-PEEP, lowering mean airway pressures, and preserving respiratory muscle function. However, it does increase the patient’s work of breathing compared with ACV. SIMV also creates the risk of dyssynchrony between patient effort and ventilator-supported breaths. (See "Clinical and physiologic complications of mechanical ventilation: Overview".)

With volume-cycled (ie, volume-targeted) SIMV, the tidal volume, inspiratory flow rate, flow waveform, sensitivity, and basal ventilatory rate are determined by the ventilator. With pressure-cycled (ie, pressure-targeted) SIMV, airway pressures, inspiratory time, sensitivity, and basal ventilatory rate are determined by the ventilator.

SIMV is almost always combined with PSV in order to reduce the amount of work during intermittent spontaneous breaths. Generally, the set respiratory rate should allow 80 percent of breaths to be provided by the ventilator in order to minimize the work of breathing.

●Pressure support ventilation (PSV) – With PSV, each breath must be patient-triggered, so the patient must possess intact respiratory drive. PSV is pressure-cycled and designed to reduce the patient’s work of breathing by partially supporting spontaneous breaths. A minimal amount of pressure support is necessary to compensate for the inherent resistance of the endotracheal tube (ETT) and ventilator circuit; the smaller the ETT diameter, the higher the pressure support required. Most modern ventilators automatically compensate for this increased resistance, even when the PSV is set at zero. PSV is used primarily during stable ventilatory support periods and for weaning patients from ventilatory support. It is contraindicated in paralyzed and heavily sedated patients who cannot initiate a spontaneous breath.

●Positive-pressure noninvasive ventilation (NIV) – NIV includes continuous positive airway pressure (CPAP) and bilevel-positive airway pressure (BPAP), which is CPAP plus PSV. Positive-pressure NIV is delivered through a nasal or facial mask or a helmet, rather than an endotracheal or tracheotomy tube. CPAP is the noninvasive equivalent of continuous PEEP; BPAP is the noninvasive equivalent of ventilator-supported breathing. Contraindications to NIV include the need for a definitive airway, high aspiration risk, and inability to tolerate mask ventilation (table 3). In select patients with acute respiratory distress, NIV has reduced the need for conventional mechanical ventilation. (See "Noninvasive ventilation in adults with acute respiratory failure: Benefits and contraindications".)

COMPLICATIONS — Mechanical ventilation is associated with a number of pathophysiologic derangements that can lead to injury. Among these are:

●Diminished cardiac output and hypotension

●Pulmonary barotrauma (eg, pneumothorax)

●Ventilator-associated lung injury (VALI)

●Auto-positive end-expiratory pressure (auto-PEEP; ie, intrinsic PEEP)

●Elevated intracranial pressure

These complications are discussed in detail elsewhere but are briefly described below. (See "Clinical and physiologic complications of mechanical ventilation: Overview".)

Hypotension and VALI, including barotrauma, are among the more important problems that occur after the institution of mechanical ventilation. Hypotension most often results from a combination of sedation, decreased venous return from elevated intrathoracic pressure, and diminished intravascular volume. These complications are often observed immediately after endotracheal intubation; hence, close monitoring during the post-intubation period is imperative. Barotrauma results from elevated pulmonary pressures. Clinicians can reduce the risk of barotrauma by minimizing plateau airway pressures. Reduced airway pressures, as well as reduced tidal volumes (TVs), also help minimize the risk of VALI. Clinicians need to be aware that some abnormalities, such as an elevated PaCO₂, need not be corrected immediately to achieve physiologic norms or the patient’s baseline, and that attempts to do so may increase the risk of VALI.

Pneumonia is a well-described complication of mechanical ventilation. Clinicians can reduce the risk of ventilator-associated pneumonia (VAP) by elevating the head of the patient’s bed by at least 30 degrees, either by inclining the head of the bed upwards, inclining the entire bed upwards (ie, reverse Trendelenburg), or by placing the patient in a semirecumbent position (ie, not lying flat). Other strategies for reducing the risk of VAP are discussed elsewhere. (See "Risk factors and prevention of hospital-acquired and ventilator-associated pneumonia in adults".)

APPROACH TO VENTILATORY MANAGEMENT

General principles — There is no single optimal mode of mechanical ventilation [8-10]. Diseases and patient condition vary over time, so clinicians should regularly reassess the settings and mode of ventilation. Nevertheless, certain guiding principles should be applied in most instances:

●Minimize plateau pressures and tidal volumes (TVs), allowing hypercapnia, if necessary (except in brain-injured patients), to reduce the risk of lung injury.

●Optimize extrinsic positive end-expiratory pressure (PEEPe) to prevent alveolar collapse and improve oxygenation.

●Reduce inspired oxygen to nontoxic levels (≤60 percent) as quickly as possible.

●Minimize the risk of ventilator-associated pneumonia (VAP) by maintaining the head in an elevated position whenever possible. (See "Risk factors and prevention of hospital-acquired and ventilator-associated pneumonia in adults", section on 'Prevention'.)

Selecting a ventilatory strategy — Emergency clinicians can select among three fundamental strategies for mechanical ventilation: positive-pressure noninvasive ventilation (NIV) and two strategies of invasive positive-pressure ventilation (IPPV), which are low TV ventilation (LTVV; also known as lung-protective invasive positive-pressure ventilation or L-IPPV) and general IPPV.

Below, we describe the basic principles, indications, contraindications, and settings for each. Modifications to these basic approaches may be needed in specific disease states, and these are described in the section on disease-specific management as well as in separate UpToDate topic reviews. (See 'Disease-specific ventilatory management' below.)

●Positive-pressure noninvasive ventilation (NIV) – We use positive-pressure NIV in patients who need respiratory support and do not have contraindications (table 3). NIV has proven most effective in patients with acute exacerbations of chronic obstructive pulmonary disease (COPD) and acute cardiogenic pulmonary edema (CPE). It may also be helpful in the management of immunocompromised patients and select patients with early acute respiratory distress syndrome (ARDS). (See "Noninvasive ventilation in adults with acute respiratory failure: Benefits and contraindications".)

NIV does not secure the airway and should not be used in a patient with high aspiration risk or who cannot tolerate mask ventilation. The clinician must be prepared to intubate the trachea if necessary and acceptable to the patient or health care proxy. The patient should be monitored closely and formally reassessed within 30 minutes of application to ensure improvement or stabilization of respiratory compromise [11].

●Invasive positive-pressure ventilation (IPPV) – In an emergency department (ED) patient starting IPPV, we typically use an LTVV strategy with an initial TV of 6 mL/kg predicted body weight (PBW). In a patient not at high risk for development of ARDS, a reasonable option is a general IPPV strategy with an initial TV of 8 mL/kg PBW. We use an ED lung injury prediction score (EDLIPS) (table 4) of less than five to identify patients not at high risk for ARDS [12]. However, we prefer to set an initial TV of 6 mL/kg in this population given the possible benefits described below and minimal harm with appropriate minute ventilation (MV). The EDLIPS is derived from the lung injury prediction score (LIPS), which is discussed separately [13]. (See "Acute respiratory distress syndrome: Epidemiology, pathophysiology, pathology, and etiology in adults", section on 'Lung injury prediction score'.)

LTVV prevents ventilator-associated lung injury (VALI), including barotrauma, and benefits patients with ARDS, pneumonia, thoracic trauma (eg, pulmonary contusion), and sepsis [14-16]. This is accomplished by using low TVs and minimizing airway and alveolar pressures, even if hypercapnia and mild acidosis result (ie, permissive hypercapnia). The mechanism of benefit and evidence for LTVV are discussed separately. (See "Ventilator-induced lung injury", section on 'Mechanisms' and "Acute respiratory distress syndrome: Ventilator management strategies for adults", section on 'Efficacy and harm'.)

The routine use of LTVV in the ED has been controversial, but early application of LTVV may provide a benefit for multiple reasons [17,18]. The incidence of ED patients at risk of ARDS is approximately 7 percent [19]. Many ED patients who require invasive mechanical ventilation are already at increased risk for developing ARDS, and the use of low TVs helps to prevent a second pulmonary insult from VALI. The mortality benefit of low TVs is greater when initiated early in the patient’s course [20]. Mechanically ventilated ED patients often do not have ventilator adjustments while awaiting transfer to an intensive care unit (ICU) [16,21,22]. Many ED patients who are receiving non-LTVV do not have their ventilator settings changed to LTVV upon ICU arrival [23,24].

A meta-analysis of 11 non-randomized studies (12,912 patients) found that patients started on a LTVV strategy in the ED had decreased occurrence of ARDS, duration of mechanical ventilation and hospitalization, and mortality, although the latter finding was not statistically significant [25]. The ED-based LTVV strategy in the included studies was typically a TV ≤8 mL/kg PBW, which was a mean reduction of 1.5 mL/kg compared with preintervention ventilator settings. In patients ventilated with the LTVV strategy, ARDS occurred less often (5 studies, 7043 patients, 4.5 versus 8.3 percent, odds ratio [OR] 0.57, 95% CI 0.44-0.75) and patients spent less time on a ventilator (6 studies, 7122 patients, mean difference 1.4 days, 95% CI 0.4-2.4 days), had a shorter hospital length of stay (7 studies, 10,163 patients, mean difference 1.2 days, 95% CI 2.3-0.1 days), and had a shorter ICU length of stay (7 studies, 10,163 patients, mean difference 1.0 day, 95% CI 1.7-0.3 days). In 10 studies with 11,086 patients, mortality was non-significantly lower with the LTVV strategy compared with the non-LTVV strategy (23.1 versus 24.5 percent, OR 0.87, 95% CI 0.69-1.09).

Below, we discuss some basic principles and the initial ventilator settings for each strategy.

Implementing the chosen ventilatory strategy

Positive-pressure NIV — The mechanics of noninvasive ventilation (NIV) are described above. (See 'Modes of ventilation' above.)

The following settings are appropriate when initiating bilevel-positive airway pressure (BPAP), the preferred form of positive-pressure NIV (see "Noninvasive ventilation in adults with acute respiratory failure: Practical aspects of initiation", section on 'Initial settings'):

●Inspiratory positive airway pressure (IPAP) 8 to 12 cm H₂O

●Expiratory positive airway pressure (EPAP) 0 to 5 cm H₂O

A gradient of at least 5 cm H₂O between IPAP and EPAP should be maintained. NIV is generally started at an IPAP/EPAP of 10/5 cm H₂O. Both values can be increased gradually over approximately 10 minutes to provide greater ventilatory support. IPAP can be increased up to 20 cm H₂O and EPAP up to 10 to 12 cm H₂O. Continuous pulse oximetry and end-tidal CO₂ monitoring can help determine NIV’s effectiveness in improving oxygenation and ventilation. Clinicians should reassess the patient within 30 minutes to determine if treatment is successful.

LTVV — ED patients requiring tracheal intubation who have or are at risk for developing acute lung injury (ALI) or ARDS are managed using low tidal volume ventilation (LTVV). (See 'Selecting a ventilatory strategy' above.)

Reasonable initial settings are presented in the table (table 5) and include the following (see "Overview of initiating invasive mechanical ventilation in adults in the intensive care unit", section on 'Settings'):

●Assist control mode

●Initial TV of 6 mL/kg PBW (can be as low as 4 mL/kg if ALI/ARDS) (table 1 and table 2) (calculator 2)

●Respiratory rate 16 breaths/minute (range 14 to 22 breaths/minute) to meet the patient’s MV requirements (can titrate up to 35 in order to keep pH above 7.25, as long as there is adequate expiration time to prevent intrinsic PEEP [PEEPi])

●Inspiratory flow rate 60 L/minute (range 40 to 90 L/minute)

●FiO₂ 100 percent (titrate to 60 percent or below as quickly as possible)

●PEEPe of 5 cm H₂O (range 5 to 10 cm H₂O)

●Keep plateau pressures at 30 cm H₂O or less

If an excess degree of hypercapnia develops, the respiratory rate should be maximized to increase the MV. The hypercapnia often caused by LTVV may be minimized by increasing the ventilatory rate to a point just below that at which PEEPi (ie, breath stacking) develops [26]. Ventilators can measure PEEPi, which should be monitored. TV may be increased up to 8 mL/kg PBW if hypercapnia persists. Oxygenation is maintained at appropriate levels by using PEEPe and adjusting the FiO₂ to minimize injurious levels of oxygenation. Ventilator adjustments in a LTVV strategy are presented in the table (table 6) and discussed further separately. (See "Acute respiratory distress syndrome: Ventilator management strategies for adults", section on 'Initial follow-up'.)

LTVV should be used in patients with cerebral injury, stroke, or elevated intracranial pressure since those processes increase the risk of developing ARDS. The respiratory rate and MV should be maximized to avoid hypercapnia and acidosis, which can compromise cerebral perfusion [27]. We recommend not using sodium bicarbonate to control acidemia, which has no proven benefit and may be harmful. Implementation of LTVV may require high levels of sedation with appropriate monitoring. (See "Management of acute moderate and severe traumatic brain injury", section on 'Ventilation'.)

General IPPV — Patients who are not at high risk for the development of ARDS can be managed with general invasive positive-pressure ventilation (IPPV). (See 'Selecting a ventilatory strategy' above.)

Settings consist of the following (see "Overview of initiating invasive mechanical ventilation in adults in the intensive care unit", section on 'Settings'):

●Assist control mode

●Initial TV 8 mL/kg PBW (may be increased to no greater than 10 mL/kg) (table 1 and table 2) (calculator 2)

●Respiratory rate 14 breaths/minute (range 12 to 16 breaths/minute)

●Inspiratory flow rate 40 L/minute (range 40 to 60 L/minute)

●FiO₂ 100 percent (titrate to 60 percent or below as quickly as possible based on pulse oximetry)

●PEEPe of 5 cm H₂O (range 5 to 10 cm H₂O)

The clinician must assess the patient’s response to these settings frequently and adjust them as necessary, guided by oxygenation, partial pressure of carbon dioxode (PaCO₂), plateau pressure, and hemodynamic parameters.

The patient’s baseline lung compliance, airway resistance, and PEEPi should be measured and recorded immediately following the initiation of invasive mechanical ventilation while the patient is paralyzed or heavily sedated.

Clinicians should frequently reassess patient comfort and patient-ventilator synchrony [28]. Adequate patient sedation and analgesia should be provided. (See 'Sedation and analgesia for the ventilated patient' below.)

DISEASE-SPECIFIC VENTILATORY MANAGEMENT

Pulmonary diseases

Asthma and COPD — Patients with asthma and chronic obstructive pulmonary disease (COPD) can present to the emergency department (ED) with impending respiratory failure. The major reason for instituting mechanical ventilation in these patients is the clinical manifestation of respiratory distress related to deteriorating gas exchange. In-depth discussion of management of these patients is detailed separately. (See "Invasive mechanical ventilation in adults with acute exacerbations of asthma" and "COPD exacerbations: Management", section on 'Ventilatory support'.)

For patients with severe asthma or COPD requiring mechanical ventilation, we recommend the following approach:

●Use larger-sized endotracheal tube (ETT; eg, ≥8 mm) (patient weight or attributes suggesting difficult intubation may preclude the use of large tubes)

●Keep minute ventilation (MV) below 115 mL/kg

●Keep tidal volume (TV) below 8 mL/kg

●Maintain respiratory rate at 10 to 14 breaths per minute

●Maintain a high inspiratory flow rate of 80 to 100 L/minute

●Use a lower respiratory rate and higher inspiratory flow rate to allow increased expiratory time with decreased inspiratory-to-expiratory (I:E) ratio (1:3 or 1:4 up to 1:5)

●Maintain plateau pressures below 30 cm H₂O if possible

●Allow hypercapnia for patients with high peak pressures

●Continue comprehensive treatment of the reactive airway disease

As reflected in the settings above, we recommend a strategy of permissive hypercapnia for intubated asthmatics with high peak airway pressures. In addition, we recommend minimizing intrinsic positive end-expiratory pressure (PEEPi). Paralysis may be necessary to prevent patient-ventilator dyssynchrony, minimize PEEPi, and avoid dynamic hyperinflation, although it is preferable to use adequate sedation and analgesia and to avoid the use of neuromuscular blocking agents if possible.

Mechanical ventilation in patients with asthma and COPD can result in high airway pressures, barotrauma, and added morbidity and mortality, all secondary to increased lung volumes and narrowed airways. When intubating these patients, clinicians should use larger-sized ETTs (eg, ≥8 mm) if possible, in order to minimize added airway resistance.

Positive-pressure noninvasive ventilation (NIV) benefits many patients with COPD exacerbations and may be helpful for many asthmatics. In a patient with an asthma exacerbation failing medical therapy, a short trial of NIV (eg, one to two hours, typically bilevel-positive airway pressure [BPAP]) is appropriate, but the threshold to place on mechanical ventilation should be low. Contraindications to NIV include the need for a definitive airway, high aspiration risk, and inability to tolerate mask ventilation (table 3). The evidence for use of NIV in COPD and asthma exacerbations is discussed separately. (See "Noninvasive ventilation in adults with acute respiratory failure: Benefits and contraindications", section on 'Acute exacerbation of chronic obstructive pulmonary disease (AECOPD) with hypercapnic respiratory acidosis' and "Noninvasive ventilation in adults with acute respiratory failure: Benefits and contraindications", section on 'Asthma exacerbation'.)

Hypoxemic respiratory failure — Acute hypoxemic respiratory failure (AHRF) is defined as severe arterial hypoxemia refractory to supplemental oxygen. Ventilation-perfusion (V/Q) mismatch and shunting are the two primary mechanisms for such hypoxemia. Conditions such as pulmonary edema, pulmonary embolus, severe pneumonia, and acute respiratory distress syndrome (ARDS) are often responsible. Positive-pressure NIV can be a useful strategy in selected patients, particularly those with acute COPD exacerbations, acute cardiogenic pulmonary edema, or malignancy. (See 'Selecting a ventilatory strategy' above and "Noninvasive ventilation in adults with acute respiratory failure: Benefits and contraindications" and "Approach to the adult with dyspnea in the emergency department".)

In severe cases, tracheal intubation with mechanical ventilation may be required. In general, we suggest a low tidal volume ventilatory (LTVV) strategy for these patients. (See 'LTVV' above.)

Ventilator settings must be adjusted according to the underlying disease. (See 'Acute cardiogenic pulmonary edema' below and 'ARDS' below.)

Acute cardiogenic pulmonary edema — ED management of the patient with acute cardiogenic pulmonary edema (CPE) may require tracheal intubation and mechanical ventilation to relieve respiratory distress, improve pulmonary gas exchange, and reduce both preload and afterload. Clinicians should implement invasive mechanical ventilation if respiratory failure appears likely or if symptoms fail to respond to standard therapy, including oxygen, vasodilators, diuretics, and positive-pressure NIV. (See "Treatment of acute decompensated heart failure: General considerations" and "Clinical and physiologic complications of mechanical ventilation: Overview".)

Clinicians can initiate mechanical ventilation in these patients using the general invasive positive-pressure ventilation (IPPV) strategy, but if significant edema creates elevated airway pressures, they should change to an LTVV strategy. (See 'General IPPV' above and 'LTVV' above.)

Extrinsic positive end-expiratory pressure (PEEPe) can be increased as tolerated to improve oxygenation and further reduce preload. Excessive PEEPe can result in hypotension in patients dependent on preload to maintain cardiac output (eg, patients with right ventricular dysfunction).

Many patients with acute CPE benefit from NIV treatment. NIV improves cardiac performance and decreases pulmonary edema. However, some patients are not amenable to treatment with NIV (table 3). (See "Noninvasive ventilation in adults with acute respiratory failure: Benefits and contraindications".)

ARDS — Acute respiratory distress syndrome (ARDS) is defined as a syndrome of acute and persistent lung inflammation with increased vascular permeability. ARDS is characterized by four features:

●Timing – Develops within one week of a known clinical insult or new or worsening respiratory symptoms.

●Radiographic appearance – Bilateral opacities not fully explained by effusions, lobar/lung collapse, or nodules.

●Pulmonary edema – Respiratory failure not fully explained by cardiac failure or fluid overload; need objective assessment (eg, echocardiography) to exclude hydrostatic edema if no risk factor is present.

●Compromised oxygenation

•Mild: 200 mmHg <PaO₂/FiO₂ ≤300 mmHg with PEEP or continuous positive airway pressure (CPAP) ≥5 cmH₂O

•Moderate: 100 mmHg <PaO₂/FiO₂ ≤200 mmHg with PEEP ≥5 cmH₂O

•Severe: PaO₂/FiO₂ ≤100 mmHg with PEEP ≥5 cmH₂O

An LTVV strategy is the best approach when performing mechanical ventilation in patients with ARDS. Airway pressures must be reassessed frequently. In patients with severe ARDS, early administration of a neuromuscular blocking agent may be beneficial, and alternative strategies to improve oxygenation may be needed (eg, airway pressure release ventilation [APRV], extracorporeal membrane oxygenation [ECMO]). ARDS is discussed in detail separately. (See 'LTVV' above and "Acute respiratory distress syndrome: Clinical features, diagnosis, and complications in adults" and "Acute respiratory distress syndrome: Fluid management, pharmacotherapy, and supportive care in adults" and "Acute respiratory distress syndrome: Ventilator management strategies for adults" and "Modes of mechanical ventilation", section on 'Airway pressure release ventilation' and "Extracorporeal life support in adults in the intensive care unit: Overview".)

Prone ventilation (ie, ventilation that is delivered with the patient lying in the prone position) may be used in patients with severe ARDS (ie, PaO₂:FiO₂ ratio <150 mmHg with an FiO₂ ≥0.6 and PEEP ≥5 cm H₂O) despite optimized ventilator settings, provided there is no contraindication (table 7) [29]. (See "Prone ventilation for adult patients with acute respiratory distress syndrome", section on 'Indications'.)

In patients with ARDS, prone ventilation has been used for many years to improve oxygenation and outcomes when more traditional modes of ventilation have failed and has shown evidence of a mortality benefit [29-31]. The prone position takes advantage of gravity to conform the shape of the lungs to the chest cavity, thus creating a more favorable and equitable distribution of air. Benefits include reducing ventilator-associated lung injury (VALI), improving V/Q matching, increasing end-expiratory lung volume, improving secretion clearance, and an overall improvement in lung ventilation [30-34]. (See "Prone ventilation for adult patients with acute respiratory distress syndrome", section on 'Physiologic effects on oxygenation'.)

The traditional prone ventilation approach involves the patient spending up to 16 hours in the prone position and the remainder of the day supine, although different proning strategies exist. Challenges of implementing prone ventilation, which may be especially relevant to the ED setting, include requiring intensive resources such as a team of trained staff, specialized expensive rotating mechanical beds, and an increased risk of dislodging tubes, lines, and equipment during patient movements. (See "Prone ventilation for adult patients with acute respiratory distress syndrome", section on 'Prone procedure'.)

Neuromuscular diseases — Patients with neuromuscular disease requiring tracheal intubation can be managed using a general IPPV strategy, provided that no comorbid pulmonary conditions exist. (See 'General IPPV' above and "Respiratory muscle weakness due to neuromuscular disease: Clinical manifestations and evaluation" and "Respiratory muscle weakness due to neuromuscular disease: Management".)

Guillain-Barré syndrome — The respiratory status of patients with Guillain-Barré syndrome (GBS) can deteriorate quickly and unpredictably. Many patients require mechanical ventilation. Respiratory features associated with progression to respiratory failure in patients with severe GBS include:

●Vital capacity less than 20 mL/kg

●Maximal inspiratory pressure less than 30 cmH₂O

●Maximal expiratory pressure less than 40 cmH₂O, or a reduction of more than 30 percent in vital capacity

Clinical features associated with respiratory failure include:

●Time from onset to admission less than seven days

●Inability to cough

●Inability to stand

●Inability to lift the elbows

●Inability to lift the head

Bulbar dysfunction, autonomic dysfunction, and bilateral facial palsy are also associated with the need for mechanical ventilation. (See "Guillain-Barré syndrome in adults: Treatment and prognosis", section on 'Ventilatory status' and "Guillain-Barré syndrome in adults: Pathogenesis, clinical features, and diagnosis".)

Myasthenia gravis — Patients with myasthenic crisis often develop oropharyngeal and respiratory muscle weakness and become unable to protect their airway. Two measures have been found to predict respiratory failure in these patients: decline in functional vital capacity to less than 15 mL/kg of body weight and an inspiratory force of -25 cmH₂O or less. Clinicians should note that muscle weakness may prevent these patients from manifesting accessory muscle use. (See "Myasthenic crisis", section on 'Assessment of respiratory function'.)

Trauma — Clinicians should exercise caution when initiating mechanical ventilation in the trauma patient and should consider the implications of potential hypovolemia, poor lung compliance, abdominal distention, and increased intracranial pressure (ICP).

In the severely injured patient with a traumatic brain injury, in which cerebral autoregulation may be disrupted, hypotension, hypoxemia, and hypercarbia must be avoided. Respectively, these goals are achieved with aggressive volume resuscitation and blood transfusion, oxygen supplementation and appropriate levels of PEEP to maintain the SpO₂ above 93 percent, and appropriate MV to achieve normocarbia while minimizing high airway pressures. A general IPPV strategy is a reasonable approach when initiating mechanical ventilation in these patients; an LTVV strategy may compromise cerebral perfusion and should be avoided. Continuous end-tidal CO₂ monitoring should be used if available. Frequent reevaluation is mandatory to ensure adequate mean arterial pressure (and adequate cerebral perfusion pressure), oxygenation, and normocarbia. (See "Initial management of trauma in adults" and "Management of acute moderate and severe traumatic brain injury" and 'General IPPV' above and 'Elevated intracranial pressure' below.)

In patients with hemorrhagic shock, PEEPe can exacerbate hypotension. Most patients can tolerate a PEEPe of 5 cmH₂O, but higher levels increase intrathoracic pressure and can reduce cardiac preload, and therefore should be avoided. Likewise, elevated plateau pressures can reduce cardiac output and should be avoided in these patients. (See "Approach to shock in the adult trauma patient".)

Patients with significant thoracic trauma (eg, pulmonary contusion) may be difficult to oxygenate and can have poor pulmonary compliance, increasing the risk of barotrauma. For these patients, a higher PEEPe may be required to maintain adequate oxygenation. In addition, an LTVV strategy that minimizes airway pressures and incorporates permissive hypercapnia may be required to minimize reductions in cardiac output, provided there is no concomitant traumatic brain injury [35]. (See 'LTVV' above.)

Elevated intracranial pressure — The goal of management in patients with traumatic brain injury (TBI), stroke, or other causes of elevated intracranial pressure (ICP) is to optimize cerebral perfusion pressure and oxygen delivery. Lung TV ventilation strategies (ie, LTVV) should be avoided in patients with elevated ICP because hypercapnia and acidosis can compromise cerebral perfusion. However, if such patients are at high risk for ARDS, LTVV may be used if hypercapnia and acidosis can be avoided. A PaCO₂ between 35 and 40 mmHg is recommended. (See "Evaluation and management of elevated intracranial pressure in adults".)

Prophylactic hyperventilation therapy (PaCO₂ ≤35 mmHg), once widely recommended after TBI, may cause harm and is contraindicated [36-38]. Hyperventilation can compromise cerebral perfusion immediately following injury when cerebral blood flow may already be reduced. Hyperventilation may be used for a brief period if there is acute neurologic deterioration (eg, herniation) that is unresponsive to a full barrage of standard therapies, including sedation, osmotic diuresis (eg, mannitol), paralysis, and cerebrospinal fluid drainage. Hyperventilation therapy should not extend beyond a brief period (eg, one to two hours) needed to assess the effectiveness of other therapies or to permit transfer to the operating room.

Other conditions

Pregnancy — Pregnant patients normally exhibit a respiratory alkalosis, with a baseline arterial pH of 7.40 to 7.47 and an arterial PaCO₂ of approximately 32 mmHg. Consequently, this PaCO₂ should be considered the target during mechanical ventilation in pregnant patients. Animal studies suggest that higher ventilation rates producing an arterial partial pressure of carbon dioxide significantly below this level may reduce uterine blood flow and thus should be avoided.

The strategy of permissive hypercapnia, which may be necessary when ventilation is difficult, does not appear to affect the fetus adversely (at least to a carbon dioxide level of 60 mmHg). In third-trimester pregnant patients without hypovolemia, higher levels of PEEPe may be needed to prevent atelectasis caused by the gravid uterus. (See "Critical illness during pregnancy and the peripartum period", section on 'Mechanical ventilation' and "Maternal adaptations to pregnancy: Dyspnea and other physiologic respiratory changes", section on 'Physiologic pulmonary changes in pregnancy'.)

Abdominal compartment syndrome — Emergency clinicians need to be cognizant of the physiologic features of abdominal compartment syndrome (ACS), as early diagnosis can improve outcome. In ACS, rising intraabdominal pressure is transmitted to the thorax via an elevated diaphragm, resulting in extrinsic compression of the pulmonary parenchyma, increased intrapulmonary shunt fraction, and increased alveolar dead space, causing hypoxemia and hypercarbia. (See "Abdominal compartment syndrome in adults".)

In mechanically ventilated patients with ACS, peak inspiratory, mean airway, and plateau pressures are increased, while chest wall compliance and spontaneous TV are markedly reduced, creating a risk for barotrauma. In this scenario, a ventilatory strategy utilizing permissive hypercapnia may be useful to reduce airway pressures. Neuromuscular blocking agents may be needed when standard treatments are ineffective. Obtain an immediate surgical consultation when ACS is suspected.

APPROACH TO VENTILATED PATIENT IN DISTRESS — Approach the distressed mechanically ventilated patient in a systematic fashion (algorithm 1) instead of presuming the “bucking” patient is just “fighting” the ventilator and reflexively treating with neuromuscular blocking agents and sedative medications. Otherwise, potentially life-threatening problems, such as a tension pneumothorax, can be missed. Critical aspects of this approach are described below and discussed in greater detail separately. (See "Assessment of respiratory distress in the mechanically ventilated patient".)

●Immediate management – Immediately disconnect the patient from the ventilator and provide bag ventilation at a controlled rate and tidal volume (TV) with 100 percent oxygen when a patient develops severe respiratory distress or hemodynamic instability while receiving mechanical ventilation. This maneuver removes a large number of potential problems and enables the clinician to concentrate on the patient rather than the ventilator.

●Causes of decompensation – A useful mnemonic for the causes of unexpected, acute decompensation of mechanically ventilated patients is DOPE [39]:

•Dislodgement of the endotracheal tube (ETT)

•Obstruction of the ETT

•Pneumothorax

•Equipment failure

Causes and clinical features of respiratory distress in mechanically ventilated patients are summarized in the table (table 8).

●Distress unresolved after disconnecting from ventilator – If the distress has not resolved once the patient is disconnected from the ventilator, search for immediate threats to life, such as a dislodged or obstructed ETT, a tension pneumothorax, disruption of the oxygen supply, or dysrhythmia. Perform a focused history and physical examination, including vital signs. Team members (eg, nurse, respiratory therapist) may provide important history. Assess trends in ventilator parameters, such as a rising plateau pressure. If the cause of distress is not immediately apparent and easily rectified, obtain an immediate portable chest x-ray and electrocardiogram (ECG). Clinicians should perform point-of-care bedside ultrasound for pneumothorax if trained and the equipment is available. (See "Assessment of respiratory distress in the mechanically ventilated patient", section on 'Patients who do not improve'.)

●Further management after life-threatening causes ruled out – Evaluate the patient’s respiratory mechanics and the adequacy of sedation and ventilatory support and treat the underlying cause of patient-ventilator dyssynchrony. Often, respiratory distress can be managed by observing the patient’s breathing pattern and by adjusting controlled variables (eg, TV, respiratory rate, inspiratory flow rate, trigger sensitivity) to match patient demand. As an example, when a patient is “auto-triggering” (ie, triggering frequent breaths) or “locked-out” (ie, failing to trigger breaths), the trigger sensitivity threshold should be made higher or lower, respectively. (See "Assessment of respiratory distress in the mechanically ventilated patient", section on 'Cardiorespiratory stability'.)

Assessment of airway pressures can provide insight into the cause of respiratory difficulty in patients whose problems resolve once they are disconnected from the ventilator or whose problems are less severe and who remain hemodynamically stable. By measuring peak and plateau airway pressures, the clinician can localize problems to the airway or alveoli and determine a differential diagnosis, as shown in the following algorithm (algorithm 2).

•The combination of elevated peak and plateau pressures reflects low compliance from underlying disease, such as pneumothorax, severe pulmonary edema, pulmonary effusion, hyperinflation, or elevated intraabdominal pressure from ascites or compartment syndrome. (See "Assessment of respiratory distress in the mechanically ventilated patient", section on 'An increase in both the Ppeak and Pplat with a delta Ppeak – Pplat that is unchanged or reduced'.)

•The combination of elevated peak pressures with normal plateau pressures suggests an obstruction to air flow within the ventilator circuit (eg, clogged ETT) or the proximal airways (eg, copious secretions, bronchospasm, dynamic hyperinflation [auto-positive end-expiratory pressure (PEEP) or intrinsic PEEPi (PEEPi)]). (See "Assessment of respiratory distress in the mechanically ventilated patient", section on 'An increase in the Ppeak with a widening of the delta Ppeak – Pplat'.)

Dynamic hyperinflation (ie, auto-PEEP) may be confirmed by review of the flow-time waveforms (figure 1). Such patients are difficult to ventilate with a bag. Temporarily disconnecting the ventilator circuit from the ETT, allowing a prolonged expiration, and adjusting settings to prevent further auto-PEEP should resolve this problem. (See "Assessment of respiratory distress in the mechanically ventilated patient", section on 'Dynamic hyperinflation (auto-PEEP)'.)

SEDATION AND ANALGESIA FOR THE VENTILATED PATIENT — In addition to assessing organic causes of distress, clinicians must ensure that the intubated patient receives adequate sedation and analgesia. Preliminary research suggests that a small but concerning number of patients managed with mechanical ventilation in the emergency department (ED) do not receive adequate sedation and analgesia while paralyzed [40]. The risk may be greater when a longer-acting paralyzing medication (eg, rocuronium) is used for rapid-sequence intubation.

A few important principles for providing sedation and analgesia are mentioned below. The subject is discussed in detail separately. (See "Sedative-analgesia in ventilated adults: Management strategies, agent selection, monitoring, and withdrawal" and "Pain control in the critically ill adult patient".)

The Society of Critical Care Medicine’s algorithm for sedation and analgesia of mechanically ventilated patients provides a reasonable approach. We have modified the original version for use in the ED (algorithm 3).

In the ED, it is often better to use short-acting medications when managing acutely unstable patients whose diagnoses may be unclear. Propofol is an excellent short-acting sedative and allows the clinician to perform frequent neurological examinations in patients with brain injury. However, propofol can cause hypotension, and blood pressure support with a vasopressor (eg, phenylephrine) may be needed. The use of propofol and other sedative (and analgesic) agents for longer-term sedation of the critically ill is discussed separately. (See "Sedative-analgesia in ventilated adults: Medication properties, dose regimens, and adverse effects".)

Since tracheal intubation is a very noxious stimulus, we administer analgesics for patient comfort and to reduce the amount of sedative required. Fentanyl, a short-acting analgesic, is often used. Morphine and hydromorphone are also effective. Mechanically ventilated patients expected to have a prolonged ED stay are treated with infusions of sedatives and analgesics titrated to achieve targeted goals based upon pain and sedation/agitation scales, such as the Richmond Agitation-Sedation Scale (RASS) (table 9). (See "Sedative-analgesia in ventilated adults: Management strategies, agent selection, monitoring, and withdrawal", section on 'Initiating sedative-analgesics'.)

WEANING AND DISCONTINUATION OF MECHANICAL VENTILATION — As the need for critical care services and emergency department (ED) lengths of stay increase, emergency clinicians will increasingly be called upon to provide long-term critical care management, including weaning and discontinuation of mechanical ventilation [41,42].

Weaning is the process whereby mechanical ventilatory support is gradually withdrawn and the patient resumes spontaneous breathing. Weaning can be separated into two parts: weaning to partial ventilator support and weaning to discontinuation of support and removal of the endotracheal tube (ETT). Aspects of weaning of particular import to the emergency clinician are described below. Weaning from mechanical ventilation is discussed in detail elsewhere. (See "Weaning from mechanical ventilation: Readiness testing" and "Initial weaning strategy in mechanically ventilated adults" and "Management of the difficult-to-wean adult patient in the intensive care unit".)

Before beginning a weaning trial, clinicians should determine whether the patient is ready using the following criteria as a general guide [43,44]:

●Evidence for some reversal of the underlying cause of respiratory failure

●Adequate oxygenation (PaO₂ >60 mmHg on FiO₂ <0.4; extrinsic positive end-expiratory pressure [PEEPe] <10 cmH₂O; PaO₂/FiO₂ >150 to 300)

●Stable cardiovascular status (heart rate <140; stable blood pressure; no or minimal use of vasopressors)

●No significant respiratory acidosis (pH ≥7.25)

●Adequate hemoglobin (generally >7 g/dL in patients without ischemic cardiac disease or hemoglobin >10 g/dL in patients with ischemic cardiac disease)

●Adequate mentation (arousable; can follow commands reliably; no continuous sedative infusions)

●Stable metabolic status (acceptable electrolyte levels)

Clinicians should adapt these criteria to clinical circumstances; some patients will not satisfy all criteria yet be successfully weaned off mechanical ventilation. Over the years, a wide variety of physiologic indices have been proposed to assist in the discontinuation of ventilatory support. Such indices have varying strengths and weaknesses and different applications. Variables such as respiratory rate, PaO₂/FiO₂ (P/F) ratio, and the rapid shallow breathing index (RSBI) are used.

RSBI is a commonly used assessment tool to determine readiness to wean and discontinue mechanical ventilation in the intensive care unit (ICU). The RSBI measurement consists of a one-minute trial of unassisted breathing with a PEEPe of 0 cmH₂O and pressure support of 0 cmH₂O. At the end of one minute, the average respiratory rate (RR) is divided by the average tidal volume (TV) to obtain the RSBI (ie, RSBI = RR/VT). A number less than or equal to 105 has been found to be most predictive of successful extubation. (See "Weaning from mechanical ventilation: Readiness testing".)

After an initial assessment of weaning, including calculation of an RSBI, we perform a spontaneous awakening trial (SAT) and spontaneous breathing trial (SBT) to determine if the patient is ready for liberation from mechanical ventilation. There are three ways to perform an SBT: putting the patient on minimal pressure support and PEEPe, assessing respiratory parameters (so-called “performing mechanics”); using continuous positive airway pressure (CPAP) alone; or using a T-piece trial, which requires the patient to breathe through the endotracheal tube for a preset period of time with oxygen but without ventilatory support. Institutional approaches vary, but any of the methods described are acceptable. (See "Initial weaning strategy in mechanically ventilated adults".)

The criteria used to assess patient tolerance during an SBT are the respiratory pattern, adequacy of gas exchange, hemodynamic stability, and patient comfort. Generally, if the patient tolerates an SBT lasting 30 minutes, the mechanical ventilator should be discontinued and the ETT removed. A longer SBT (up to 120 minutes) may be necessary if the patient’s condition is more uncertain.

Otherwise healthy patients intubated for a transient problem (eg, acute drug intoxication) can often be extubated rapidly following a brief period of observation. Once the problem has resolved and the patient is awake, breathing spontaneously, and manifesting no signs of respiratory or hemodynamic instability, the ETT can be removed.

SUMMARY AND RECOMMENDATIONS

●Objectives – Mechanical ventilation is performed in the emergency department (ED) to accomplish any of a number of goals, including the following (see 'Objectives and overview of mechanical ventilation' above):

•To secure the airway

•To improve pulmonary gas exchange (ie, reverse hypoxemia or acute respiratory acidosis)

•To relieve respiratory distress (ie, decrease oxygen consumption or respiratory muscle fatigue)

•To permit appropriate sedation and neuromuscular blockade

●Ventilator settings – Ventilator settings are adjusted to provide adequate minute ventilation (MV) while minimizing the risk of iatrogenic complications. MV normally ranges from 5 to 10 L/minute but in a critically ill patient with a higher ventilatory demand, a higher MV may be required. Tidal volume (TV) is generally based on predicted body weight (PBW) (calculator 1) and varies according to the ventilation strategy chosen. The TV based on PBW for males and females is provided in the tables and calculator (table 1 and table 2) (calculator 2). (See 'Ventilator settings' above and 'Modes of ventilation' above.)

●Complications – Complications of mechanical ventilation include diminished cardiac output, hypotension, pulmonary barotrauma (eg, pneumothorax), ventilator-associated lung injury (VALI), ventilator-associated pneumonia (VAP), auto-positive end-expiratory pressure (auto-PEEP; ie, intrinsic PEEP), and elevated intracranial pressure (ICP). (See 'Complications' above.)

●General principles of ventilatory management – There is no single optimal mode of mechanical ventilation; diseases and patient condition vary over time, and ventilator settings must be adjusted accordingly. Nevertheless, certain guiding principles should be applied in most instances, including (see 'General principles' above):

•Minimize plateau pressures and TVs, allowing hypercapnia if necessary (except in brain-injured patients), to reduce the risk of lung injury.

•Optimize extrinsic PEEP (PEEPe) to prevent alveolar collapse and improve oxygenation.

•Reduce inspired oxygen to nontoxic levels (≤60 percent) as quickly as possible.

●Positive-pressure noninvasive ventilation (NIV) – We use NIV in patients who need respiratory support and do not have contraindications (table 3). This is most effective in patients with acute exacerbations of chronic obstructive pulmonary disease (COPD) and acute cardiogenic pulmonary edema. (See 'Positive-pressure NIV' above.)

●Invasive positive-pressure ventilation (IPPV) – In an ED patient who is starting IPPV, we suggest a low tidal volume ventilation (LTVV) strategy with an initial TV of 6 mL/kg PBW (Grade 2C). In a patient not at high risk for development of ARDS (ED lung injury prediction score [EDLIPS] <5) (table 4), a reasonable option is a general IPPV strategy with an initial TV of 8 mL/kg PBW. An LTVV strategy is the standard for ARDS management and prevents ventilator-associated lung injury. It benefits patients at high risk for ARDS, such as those with pneumonia, thoracic trauma (eg, pulmonary contusion), and sepsis. (See 'Selecting a ventilatory strategy' above.)

If an excess degree of hypercapnia develops, the respiratory rate should be maximized to increase the minute ventilation. TV may be increased up to 8 mL/kg PBW if hypercapnia persists. LTVV should be used in patients with cerebral injury, stroke, or elevated ICP, but the respiratory rate and minute ventilation should be maximized to avoid hypercapnia and acidosis, which can compromise cerebral perfusion. (See 'LTVV' above.)

●Disease-specific ventilatory management – Modifications to mechanical ventilation must be made based on the disease process. Approaches to ventilator management for important conditions that confront the emergency clinician are provided in the text. (See 'Disease-specific ventilatory management' above.)

●Managing distress in a ventilated patient – Approach the distressed mechanically ventilated patient in a systematic fashion, as outlined in the attached algorithm (algorithm 1) and table (table 8). Treating the "bucking," distressed patient, presumed to be "fighting" the ventilator, with neuromuscular blocking agents and sedative medications should only occur after a detailed bedside assessment to exclude potentially life-threatening problems, such as a tension pneumothorax. (See 'Approach to ventilated patient in distress' above.)

●Sedation and analgesia – Clinicians must ensure that the intubated patient receives adequate sedation and analgesia (once organic causes of distress are addressed, if present). The Society of Critical Care Medicine's algorithm for sedation and analgesia of mechanically ventilated patients provides a reasonable approach. We have modified the original version for use in the ED (algorithm 3). (See 'Sedation and analgesia for the ventilated patient' above.)