1 Sidney Kimmel Medical College of Thomas Jefferson University, Philadelphia, PA, USA
2 Mount Sinai Morningside‐West, New York, NY, USA
3 Harvard Medical School, Boston, MA, USA
Background
Definition and goals of invasive mechanical ventilation
Mechanical ventilation is the process by which a patient’s respiratory requirements are partially or completely supported by a mechanical ventilator.
The primary purpose of mechanical ventilation is to optimize oxygenation and CO2 removal.
The ventilator takes over the work of breathing fully or partially. The ventilator plays an essential role in relieving the systemic effects of respiratory distress, including an increase in oxygen demand by the respiratory muscles and the myocardium. This elevated work of breathing can result in myocardial ischemia and the production of lactate.
In non‐invasive ventilation, positive pressure is delivered through a non‐invasive interface to the patient’s mouth or nose.
In invasive ventilation, the ventilator is connected to a conduit that bypasses the anatomic upper airways and delivers air directly into the trachea. This can be done through a nasotracheal, endotracheal, or tracheostomy tube.
This chapter will explain invasive mechanical ventilation.
Prevalence and impact
A large retrospective study of over 6 million hospitalizations found that 2.8% of the patients received mechanical ventilation and the in‐hospital mortality was 34.5%.
Maintenance of airway patency, such as with expanding neck lesions or airway edema.
Commonly used terms
Predicted body weight (PBW): calculated weight used for weight‐based ventilator settings. It is based on gender and height, accounting for the fact that lung size and capacity will remain the same despite variations in a patient’s weight over time.
Men: PBW = 50 kg + 2.3 kg × (height (inches) – 60).
Women: PBW = 45.5 kg + 2.3 kg × (height (inches) – 60).
Tidal volume (VT): volume of air delivered to the patient per breath. It is expressed in milliliters (mL). Recommended VT for mechanically ventilated patients: lung protective ventilation ≤8 mL/kg PBW; ARDS settings ≤6 mL/kg PBW.
Respiratory frequency (f): number of breaths delivered per minute. Often ranges between 12 and 20/min. Patients with metabolic acidosis usually need a higher rate, whereas those with obstructive disease should be ventilated with lower rates.
Fraction of inspired oxygen (FiO2): concentration of O2 in the inspired gas. It ranges from 0.21 (room air) to 1.0 (100% O2). FiO2 is titrated to maintain a SpO2 of ≥90%, or a PaO2 of ≥60 mmHg. An FiO2 higher than 60% can result in oxygen toxicity.
Positive end‐expiratory pressure (PEEP): set amount of positive pressure in cmH2O that is maintained at the end of expiration. This can be extrinsic or intrinsic. A baseline extrinsic PEEP of 5 cmH2O is frequently used to prevent atelectasis.
Minute ventilation (VE): volume of air exchanged in 1 minute. VE is the product of tidal volume and respiratory frequency VE = (VT × f), expressed in liters per minute (L/min). Range: 5–10 L/min; this can be higher in patients with high minute ventilation requirements, such as sepsis.
Peak inspiratory pressure (Ppeak): highest pressure (expressed cmH2O) recorded during inspiration. It reflects the PEEP, compliance of the lungs/pleura/chest wall system, and the flow resistance of the airways.
Table 21.1Features of hypoxemic and hypercapnic respiratory failure.
Decreased minute ventilation Increased dead space ventilation Increased CO2 production Venous admixture
Sedative overdose CNS injury Neuromuscular disease Severe asthma COPD
Plateau pressure (Pplat): pressure resulting from the elastic recoil of the lung and chest wall at the end of inspiration when the system has reached a no gas flow state. It is assessed by applying a short pause during inspiration. Plateau pressure is also affected by the pleura/chest wall system.
Mean airway pressure (Paw): time‐weighted average pressure during a respiratory cycle.
Compliance (CL): ease with which the lungs can distend. It is the quotient of the change in volume and the change in pleural pressure (CL = ∆V/∆P) and is expressed in L/cmH2O.
Static compliance (CS): compliance measured in conditions of no gas flow; CS = VT/(Pplat – PEEP).
Dynamic compliance (CD): compliance measured during gas flow and therefore affected by resistance; CD = VT/(Ppeak – PEEP).
Airway resistance (Rinsp): resistance to airflow during inspiration. It is determined as the ratio of the pressure gradient needed to overcome airways resistance (Ppeak – Pplat) and the inspiratory flow rate (Vinsp); R = (Ppeak – Pplat)/Vinsp.
Inspiratory time (TI): time in seconds required to deliver VT at a specified flow rate (TI = VT/flow). A longer Ti increases the Paw. A shorter Ti delivers VT faster.
Inspiratory rise time: time in seconds required to reach the set peak inspiratory pressure. It can be adjusted to match patient effort. For patients with high VT demand the rise time can be shortened.
Inspiratory flow rate (Vinsp): rate at which gas is delivered to the patient’s lungs during the inspiratory phase (expressed as L/min). This is normally set at 40–100 L/m. A higher Vinsp delivers VT faster and shortens inspiratory time.
Trigger sensitivity: level of spontaneous effort needed to trigger a machine breath. This can be set based on flow or pressure thresholds. Typical settings are –2 cmH2O or 50% change of bias flow.
Autocycling: ventilator breath is initiated in absence of patient respiratory effort or set rate. This can be due to a leak in the system, such as a faulty exhalation valve or damaged ventilator tubing.
I:E ratio: inspiratory to expiratory time ratio. Depends mainly on respiratory rate; inspiratory time has less impact. Inspiration time is normally shorter than expiratory time, at least 1:3. In airflow obstruction, it takes longer for the expiration phase, and so a longer I:E ratio is desired.
Setting the ventilator
The clinician must set the parameters listed here, based on the indication for mechanical ventilation, the patient’s underlying clinical condition, and defined therapeutic endpoints.
Mode: the mode of mechanical ventilation refers to the shape of the inspiratory pressure or flow characteristics and will determine if a patient can augment the VT or respiratory rate using his or her own efforts. Modes are usually volume pre‐set or pressure pre‐set. For most patients, an assist control mode is used. A mode such as volume control or pressure‐regulated volume control (PRVC) is most commonly used to assure desired tidal volume. Weaning from mechanical ventilation is often performed using pressure support mode. (See explanation of modes later.)
Tidal volume: The tidal volume VT is determined by the predicted body weight and generally set at 6–8 mL/kg PBW.
Respiratory rate: the respiratory rate is set based on the clinical indication for mechanical ventilation. For patients with sepsis, metabolic acidosis, or conditions with high minute ventilation requirements, it is set at a higher rate of 20/min. Patients with ARDS ventilated with low tidal volumes may need an even higher rate. In obstructive disease, a low rate of 10–12/min is set to allow sufficient time for exhalation.
FiO2: The FiO2 is initially set at 100% and titrated down to maintain oxygen saturation of 90% at the lowest possible FiO2.
PEEP: this is often initiated at 5 cmH2O. PEEP is set at higher levels in disease such as ARDS, when implementing ‘open lung strategy’ to provide adequate oxygenation and prevent atelectasis.
Ventilator phases
There are three phases in a ventilatory cycle: what starts the breath, what is the goal that must be reached, and how the breath ends so that expiration can occur.
Trigger
This is the phase in which the breath is initiated. There are three basic types of triggers:
Time: a breath is delivered at a set frequency per minute.
Pressure: a breath is delivered when the ventilator senses patient effort in the form of negative pressure.
Flow: a breath is delivered when the ventilator senses patient effort in the form of a decrease in flow. Flow triggering reduces the effort required from the patient and is the most commonly used trigger variable.
Limit
This is the phase in which a positive pressure breath is delivered that is governed by a set limit. The limit is the variable that needs to be reached and maintained before inspiration ends. While the limit cannot be exceeded, it does not terminate the inspiratory cycle. There are three commonly used limit variables:
Pressure: a set pressure is targeted during inspiration. Flow and volume are variable and dependent on the lung compliance and airway resistance.
Flow: a set flow is targeted. Airway pressure is variable and dependent on the lung compliance and airway resistance.
Volume: a set tidal volume is targeted.
Cycle
This is the phase in which inspiration ends and the breath cycles from inspiration to expiration.
Volume cycled: breath cycles from inspiration to expiration after a pre‐set tidal volume is met (i.e. volume control ventilation).
Time cycled: breath cycles from inspiration to expiration after a prespecified inspiratory time (i.e. pressure control ventilation).
Flow cycled: breath cycles from inspiration to expiration after inspiratory flow decreases to a prespecified level (i.e. pressure support ventilation).
Pressure cycled: during volume control ventilation, breath cycles from inspiration to expiration if airway pressure exceeds the set limit regardless of the volume delivered.
Modes of mechanical ventilation
The modes of mechanical ventilation are best separated into full ventilatory support modes and partial ventilatory support modes. In full ventilator support modes, there are mandatory breaths that are set to ensure the minimum minute ventilation. Partial support modes such as pressure support are patient triggered, provide varying ventilatory support, and are often used for weaning from mechanical ventilation.
Assist control refers to patient‐triggered breaths which are assisted during full ventilator support. The ventilator delivers mandatory breaths and the patient has the option of triggering additional breaths that are assisted by the ventilator and have exactly the same control parameters as the mandatory breaths.
The common ventilator modes are listed in Table 21.2.
Volume control (VC)
Commonly used mode.
The tidal volume is set and guaranteed. This results in a consistent minute ventilation regardless of the lung resistance, compliance, or of the patient’s ability to contribute to the breathing effort.
While this may be beneficial in patients with hypercapnic respiratory failure requiring controlled and efficient ventilation, it may be detrimental to patients with increased resistance or decreased compliance as it can lead to higher airway pressures.
The breath is flow targeted and volume cycled. Since flow is the limit variable, it remains constant throughout inspiration. Since volume is the cycle variable, inspiration ends after delivery of the set tidal volume.
The clinician usually sets the f, VT, inspiratory flow rate, flow waveform, FiO2, and PEEP.
Advantages: guaranteed minute ventilation.
Disadvantages: patient dyssynchrony and difficulty controlling the plateau pressure.
Pressure control (PC)
A constant pressure is delivered throughout inspiration. The delivered volume will therefore vary depending on the patient’s lung compliance and airway resistance.
The breath is pressure targeted and time cycled. Since pressure is the limit variable it remains constant throughout inspiration. Since time is the cycle variable, inspiration ends after predetermined time.
The clinician sets the f, inspiratory pressure, TI, FiO2, and PEEP.
Initial settings:
f: 12–14 breaths/min.
Inspiratory pressure: 20–24 cmH2O, not to exceed 30 cmH2O, and titrated to achieve tidal volumes of 6–8 mL/kg PBW.
TI: 0.9–1.0 seconds.
FiO2: 100%.
PEEP: 5 cmH2O.
Advantages: patient comfort, decelerating flow pattern, plateau pressure can be regulated, and can be used with cuffless endotracheal tube.
Disadvantages: tidal volume is not guaranteed.
Pressure‐regulated volume control (PRVC)
Commonly used mode.
Dual control pressure ventilation mode. It is a variant of pressure controlled ventilation but resolves the disadvantage of variable tidal volumes (due to changes in lung characteristics over the respiratory failure course) by adjusting the delivered pressure on a breath by breath basis to reach a set tidal volume. The ventilator uses the Pplat to provide the desired tidal volume using the lowest possible pressure.
There are two unique features:
It does not allow the pressure to rise above a level set at 5 cmH2O below the pressure alarm limit. If that pressure is reached, the breath automatically cycles off to expiration.
Decelerating flow pattern.
Advantages: decreases the risk of barotrauma, decreased work of breathing, improved gas distribution, and decreased airway resistance.
Disadvantages: may worsen auto‐PEEP since the flow is decelerating and in effect prolonging inspiratory time. It may not provide adequate flow for patients who are flow starving, thus increasing work of breathing. May result in very variable tidal volumes if the patient intermittently makes a significant inspiratory effort. If there are inherent leaks in the system (such as loss of volume due to chest tubes), the device may not be able to obtain the Pplat and this will cause the mode to autocycle, leading to dyssynchrony.
Pressure support (PS)
Mode in which all breaths are triggered by the patient. It can only be used for patients who are breathing spontaneously.
Pressure limited and flow cycled. Since the breath is pressure limited, a constant pressure is maintained throughout inspiration. Since it is flow cycled, the ventilator continues to deliver the breath until the inspiratory flow has decreased to a specific level (e.g. 25% of the peak inspiratory flow), and expiration then follows. The delivered tidal volume depends on the patient’s lung compliance and airway resistance.
The clinician sets the inspiratory pressure, sensitivity, PEEP, and FiO2.
Tidal volumes are variable and dependent on lung compliance and resistance and respiratory muscle strength.
This mode is often used for weaning from mechanical ventilation.
Advantages: facilitates weaning, less sedation is needed, and improved patient comfort.
Disadvantages: needs close monitoring and tidal volumes are variable.
Volume support (VS)
Mode similar in concept to PRVC. Each breath is pressure supported to attain a volume target.
The breath is patient triggered, pressure limited, and flow cycled. The pressure support for each breath is calculated by the compliance measured during the previous breath.
As the patient is recovering and making sufficient respiratory efforts, the amount of pressure support provided will decrease.
Advantages: guaranteed minimum tidal volume and patient comfort.
The ventilator delivers a set number of mandatory breaths while still allowing the patient to take spontaneous breaths. The mandatory breaths can be any of the previously mentioned control modes (i.e. VC, PC, PRVC). The spontaneous breaths can be pressure supported.
Advantages: by progressively decreasing the frequency of the mandatory breaths, it was theorized that this mode would allow reconditioning of patients’ respiratory muscles and accelerate weaning.
Disadvantages: large trials have shown this mode to prolong weaning compared with weaning using pressure support mode or T‐piece.
Airway pressure release ventilation (APRV)
Generally a rescue mode for severe hypoxemic respiratory failure.
Variant of bilevel ventilation in which a relatively high airway pressure P high is maintained for a prolonged period with brief time of pressure at a lower level P low . The inflation of the lung is allowed by the time spent at P high . Then the brief exhalation is followed by inflation again.
Initial settings:
Phigh: 30 cmH2O.
Plow (PEEP): 0 cmH2O.
Thigh: 4 seconds.
Tlow: 0.5 seconds.
FiO2: 100%.
Pressure support: 5 cmH2O (if patient is triggering breaths).
Advantages: inflation pressures are maintained thus promoting lung recruitment, which has theoretical advantages in conditions such as ARDS. It is also a lung protective mode as the set pressures cannot be exceeded. Patient is able to breath spontaneously thus decreasing the need for heavy sedation.
Disadvantages: ventilation occurs only in the limited time of low pressure PL which can result in hypercapnia. Tidal volumes can be higher than the target low tidal volume ventilation. There is also a risk of barotrauma due to auto‐PEEP.
Troubleshooting the ventilator
The ventilator is a life‐sustaining device. A malfunction or impairment of gas exchange due to the ventilator or the patient’s own disease can lead to a rapid and fatal patient decompensation. It is therefore essential to understand the ways by which the ventilator or the circuit can fail and how to identify problems.
High pressure alarm
Indicates an elevated airway pressure. Airway pressures may be elevated due to the underlying respiratory disorder, but also for reasons such as the patient coughing or biting the endotracheal tube, as well as partial or complete occlusion of the endotracheal tube.
An assessment of the peak pressure and the plateau pressure can help identify the etiology if not evident on examination, with the pressure gradient between peak inspiratory and plateau pressures being proportional to the airways flow resistance.
Increased Ppeak with normal Pplat: consider obstructive processes (high pressure gradient):
Indicates a leak somewhere in the patient–ventilator circuit.
The clinician should always suspect and investigate the following:
Air leak due to deflated or damaged cuff.
Tube displacement or extubation.
Patient disconnection from the ventilator.
Systematic approach to respiratory deterioration in an unstable, mechanically ventilated patient
Listen to the lungs bilaterally for wheezing, or asymmetric reduced breath sounds, which could indicate a pneumothorax or atelectasis.
Pass a suction catheter through the endotracheal tube. If it passes easily, this rules out biting, kinking, or obstruction of the tube secondary to secretions.
Disconnect the patient from the ventilator and manually ventilate. If it is difficult to manually ventilate the patient, this indicates increased airway resistance or decreased compliance. If the patient is very easy to manually ventilate, consider a leak or displaced endotracheal tube.
Disease‐oriented settings
ARDS
ARDS is a complex response to local and systemic inflammation as a result of either direct or indirect injury to the lung. It most commonly arises due to underlying sepsis, aspiration of gastric contents, pneumonia, multiple transfusions, or trauma. This condition is characterized by non‐cardiogenic pulmonary edema, hypoxemia, diffuse alveolar damage, heterogeneous disease distribution, and decreased lung compliance.
Beside supportive care and treating the underlying cause, mechanical ventilation treatment strategies focus on maximizing ventilator settings to improve hypoxemia and to decrease ventilator‐associated lung injury. The landmark ARDSNet study demonstrated that ventilating patients with lower VT leads to improved mortality.
While patients on mechanical ventilation are usually started on a VT of 8 mL/kg PBW, patients with ARDS are started with VT at 6 mL/kg PBW.
The respiratory rate needs to be adjusted to compensate for the smaller VT while maintaining adequate VE.
Further adjustment in f will be made based on pH assessment from an arterial blood gas, with the goal of maintaining serum pH ≥7.15.
Perform an inspiratory pause to measure the plateau pressure (Pplat). If Pplat >30 mmHg, decrease VT by 1 mL/kg PBW to a minimum VT of 4 mL/kg PBW. Remember to increase the respiratory rate.
The PEEP should be increased proportionally to the FiO2 requirement:
FiO2
0.3
0.4
0.5
0.6
0.7
0.8
0.9
1
PEEP
5
5–8
8–10
10
10–14
14
14–18
18–25
The Surviving Sepsis guidelines on the management of ARDS in a setting of sepsis include use of low tidal ventilation, titrating plateau pressure to 30 cmH2O, and use of PEEP.
Obstructive airways disease: status asthmaticus, acute COPD exacerbation
Obstructive airways diseases such as status asthmaticus and acute COPD exacerbation result in the inability to ventilate adequately. The airflow obstruction prevents full exhalation due to flow and time limitation; air trapping occurs and intrathoracic pressure may rise with resulting dynamic hyperinflation. When severe, this leads to decreased venous return and hypotension. Additionally, the alveolar hypoventilation leads to increased PaCO2 and respiratory acidosis.
Auto‐PEEP refers to PEEP, not set by the clinician, due to incomplete expiration with alveolar air trapping. In obstructive lung diseases, this auto‐PEEP is due to expiratory flow limitation from bronchospasm and edema. A rapid respiratory rate can worsen auto‐PEEP due to the expiratory time limitation.
Ventilator settings in patients with acute exacerbation from severe asthma or COPD are geared to optimizing ventilation while preventing auto‐PEEP. This is achieved by setting a lower respiratory rate, which allows a favorable I:E ratio and sufficient time for full exhalation.
Start with a VT of 8 mL/kg PBW.
A respiratory rate of 10–12 breaths per minute is a reasonable starting point.
Monitor for auto‐PEEP by monitoring the flow and volume curves to see that expiration is achieved prior to initiation of a new breath. Measure auto‐PEEP at end expiration.
Strategies that improve the I:E ratio and allow longer time for expiration include the following:
Decrease the respiratory rate.
Decrease the VT.
Increase the inspiratory flow rate.
Decrease the inspiratory time.
Serial arterial blood gases should be performed to monitor for CO2 retention and respiratory acidosis. Elevated PaCO2 and serum pH as low as 7.15 can be tolerated. This approach is termed permissive hypercapnia.
Cardiovascular effects of mechanical ventilation (heart–lung interactions)
Mechanical ventilation can affect cardiac performance by affecting preload, afterload, and cardiac contractility. The net effect can result in serious hemodynamic consequences, that if not identified and prevented, may complicate the underlying disease management and can worsen clinical outcomes.
Effect on venous return and cardiac output
Positive pressure ventilation causes a decrease in venous return, resulting in a decrease in preload and possibly a decrease in cardiac output. This effect is accentuated by PEEP and may lead to worsening hypotension, especially in patients presenting with hypovolemia and shock.
Effect on PVR
PVR
PVR is elevated at lung volumes above FRC due to compression of alveolar vessels and at lung volumes below FRC due to tortuous extra‐alveolar vessels. PVR is optimal at FRC.
PVR increases in severe hypoxemia. Hypoxic pulmonary vasoconstriction develops when regional PaO2 decreases to less than 60 mmHg.
High tidal volumes and severe hypoxemia increase PVR. Elevated PVR increases RV afterload, so RV cardiac output may be reduced.
Effect on left heart function
Positive pressure ventilation may decrease LV afterload which leads to increase in cardiac output.
Increase in intrathoracic pressure lowers the transmural pressure of the thoracic aorta. The transmural pressure is the difference between the pressure in the vessel and the pleural pressure. The higher intrathoracic pressure decreases the transmural pressure, thus reducing LV afterload and increasing stroke volume.
In patients with severe heart failure, removal of positive pressure during weaning from mechanical ventilation can lead to decompensation. Transitioning to non‐invasive ventilation may be beneficial.
Auto‐PEEP
Auto‐PEEP refers to PEEP, not set by the provider, due to incomplete expiration with alveolar air trapping.
Auto‐PEEP can occur due to increased minute ventilation, expiratory flow limitation (COPD, asthma), or expiratory resistance (secretions, patient–ventilator asynchrony).
Effects of auto‐PEEP are due to the increase in intrathoracic pressure. Clinical findings include tachycardia and hypotension.
Complications and prevention
Barotrauma
Barotrauma is a well recognized complication of mechanical ventilation. It occurs when elevated airway pressures result in damage to the lungs that manifests as extra‐alveolar air. This is usually caused by a combination of high tidal volumes and diseased lungs.
Manifestations of barotrauma are pneumothorax, pneumomediastinum, or pneumopericardium. While some forms of barotrauma require only observation, others require urgent and invasive interventions such as the placement of a chest tube. Patients on positive pressure mechanical ventilation who develop pneumothorax generally require a chest tube.
Conditions at risk for barotrauma include: ARDS, COPD, and pulmonary fibrosis.
Ventilator‐associated events and pneumonia
A ventilator‐associated event (VAE) is defined by the CDC as worsening oxygenation following more than 2 days of increasing FiO2 or PEEP requirement.
A VAP occurs after more than 2 days of mechanical ventilation, and requires a change in temperature, WBC, antibiotic administration, and laboratory growth of bacteria. VAP has been demonstrated to increase the mortality of critically ill patients by up to 30%, as well as prolonging the ICU and hospital stay.
For more detailed information on VAE and VAP, please refer to Chapter 46.
Ventilator ‘bundles’ have been developed to prevent VAE and usually include the following measures: elevation of the head of the bed to at least 30°, oral care, endotracheal tube with subglottic suctioning (unsettled), daily assessment for readiness to extubate, and the prevention of stress ulcer bleeding and venous thromboembolism.
Gastric stress ulcer bleeding
Patients with critical illness undergoing mechanical ventilation are at increased risk for the development of stress ulcers. These can in turn result in life‐threatening gastrointestinal bleeding and the need for transfusion of blood products.
Stress ulcer prophylaxis is initiated for patients with expected mechanical ventilation for more than 48 hours using H2 receptor antagonists or proton pump inhibitors.
Deep venous thrombosis
Mechanically ventilated patients are at risk of developing venous thromboembolic events due to venous stasis and a prothrombotic state from the critical illness.
Pharmacologic prophylaxis is generally initiated using unfractionated or low molecular weight heparin. Intermittent pneumatic compression is also used in most patients.
Reading list
Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000; 342:1301–8.
Dellinger RP, et al; Surviving Sepsis Campaign Guidelines Committee including the Pediatric Subgroup. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med 2013; 41:580–637.
Leatherman J. Mechanical ventilation for severe asthma. Chest 2015; 147:1671–80.
Modrykamien A, Chatburn RL, Ashton RW. Airway pressure release ventilation: an alternative mode of mechanical ventilation in acute respiratory distress syndrome. Cleve Clin J Med 2011; 78:101–10.
Papadakos PJ, Lachmann B. Mechanical Ventilation: Clinical Applications and Pathophysiology, 1st edition. Philadelphia: Elsevier Saunders, 2007.
Rittayamai N, Katsios CM, Beloncle F, Friedrich JO, Mancebo J, Brochard L. Pressure‐controlled vs volume‐controlled ventilation in acute respiratory failure. Chest 2015; 148:340–55.
Serpa Neto A, 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.
Slutsky AS, Ranieri VM. Ventilator‐induced lung injury. N Engl J Med 2013; 369:2126–36.
Tobin MJ. Principles and Practice of Mechanical Ventilation, 3rd edition. New York: McGraw‐Hill, 2013.
Wunsch H, Linde‐Zwirble WT, Angus DC, Hartman ME, Milbrandt EB, Kahn JM. The epidemiology of mechanical ventilation use in the United States. Crit Care Med 2010; 38:1947–53.
Only gold members can continue reading. Log In or Register to continue
