ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Positive end-expiratory pressure (PEEP)

Positive end-expiratory pressure (PEEP)
Authors:
Rommel Sagana, MD
Robert C Hyzy, MD
Section Editor:
Polly E Parsons, MD
Deputy Editor:
Geraldine Finlay, MD
Literature review current through: Jan 2024.
This topic last updated: Oct 14, 2022.

INTRODUCTION — Positive end-expiratory pressure (PEEP) is used therapeutically during mechanical ventilation (extrinsic PEEP). It can also be a complication of incomplete expiration and airtrapping (intrinsic PEEP).

Clinical aspects of extrinsic and intrinsic and PEEP are discussed in this topic review. High levels of PEEP that have been investigated in patients with acute respiratory distress syndrome as well as the application of PEEP in patients with dynamic hyperinflation from asthma and chronic obstructive pulmonary disease are described separately. (See "Invasive mechanical ventilation in acute respiratory failure complicating chronic obstructive pulmonary disease", section on 'Dynamic hyperinflation' and "Invasive mechanical ventilation in adults with acute exacerbations of asthma", section on 'Adding extrinsic PEEP to offset intrinsic PEEP' and "Acute respiratory distress syndrome: Ventilator management strategies for adults", section on 'Further titration/increase in PEEP (high PEEP)'.)

DEFINITION — Positive end-expiratory pressure (PEEP) is the alveolar pressure above atmospheric pressure that exists at the end of expiration. There are two types of PEEP:

●Extrinsic PEEP – PEEP that is provided by a mechanical ventilator is referred to as applied PEEP

●Intrinsic PEEP – PEEP that is secondary to incomplete expiration is referred to as intrinsic PEEP or auto-PEEP

APPLIED (EXTRINSIC) PEEP — Applied PEEP is usually one of the first ventilator settings chosen when mechanical ventilation is initiated. It is set directly on the ventilator. (See "Overview of initiating invasive mechanical ventilation in adults in the intensive care unit", section on 'Indications'.)

Indications — The optimal level of applied PEEP in most mechanically ventilated patients is unknown. Typically, a small amount of PEEP is applied routinely in most patients undergoing mechanical ventilation (3 to 5 cm H2O; also known as "physiologic" PEEP; although technically zero PEEP is physiologic). In select populations (eg, acute respiratory distress syndrome), PEEP is applied to prevent cyclic opening and closing of alveoli (and thereby prevent ventilator-induced lung injury) and to maintain adequate oxygenation (>5 cm H2O; "supraphysiologic" PEEP). The potential benefits of applied PEEP are best studied in acute respiratory distress syndrome (ARDS).

Routine mechanical ventilation — Low levels of applied PEEP are indicated for most patients undergoing mechanical ventilation (eg, 3 to 5 cm H2O). PEEP mitigates end-expiratory alveolar collapse (a consequence of the endotracheal tube bypassing the glottic apparatus) and may reduce the incidence of ventilator-associated pneumonia and lung injury [1,2]. Some authors have suggested routine use of a higher level of PEEP such as 8 cm H2O [3]. However, data are limited in patients who do not have ARDS [2-5], although:

●A randomized trial of 131 nonhypoxemic (partial pressure of arterial oxygen to fraction of inspired oxygen ratio [PaO2/FiO2] >250) patients undergoing mechanical ventilation received either applied PEEP at 5 to 8 cm H2O (85 percent received 5 cm H2O) or no applied PEEP [2]. Applied PEEP was associated with a lower incidence of ventilator-associated pneumonia (9 versus 25 percent) and a lower likelihood of developing hypoxemia (19 versus 54 percent). There were no differences in mortality, length of intensive care unit (ICU) stay, or length of hospital stay. Applied PEEP is associated with decreased leakage of posterior pharyngeal secretions into the lower airway, providing a potential mechanism for this benefit [4].

One review attempted to determine the optimal mechanical ventilation settings for patients with healthy lungs undergoing nonemergency surgery to reduce postoperative pulmonary complications (PPC) [6]. Compared with use of lower PEEP (2 to 4 cm H2O), higher PEEP (12 cm H2O including recruitment maneuvers) during operative ventilation does not decrease PPCs. Hypotension occurred more often in the higher PEEP arm.

●Another randomized trial of 980 mostly surgical patients without ARDS who were not expected to be extubated within 24 hours and most of whom received pressure controlled ventilation compared an initial low PEEP strategy (range 0 to 5 cm H2O) with a high PEEP strategy (PEEP 8 cm H2O) [5]. In the low PEEP arm, patients were placed on PEEP at 5 cm H2O and FiO2 between 0.21 and 0.6; PEEP was down-titrated every 15 minutes by 1 cm H2O to a minimum of 0 cm H2O, to target an oxygen saturation (SpO2) greater than 92 percent or PaO2 greater than 60 mmHg. The higher PEEP strategy started with and maintained PEEP at 8 cm H2O for a similar targeted SpO2 and PaO2. Although the PEEP was lower in patients ventilated with the low PEEP strategy (mean approximately 3 cm H2O versus 8 cm H2O), the range was wide (1.8 to 4.5) and the level gradually increased over five days closer to 5. There was no difference between the strategies in ventilator-free days, oxygenation, need for rescue therapy, or mortality. However, several limitations prevent firm conclusions including heterogeneity among the patients, a paucity of patients consistently on PEEP <2 cm H2O, and lack of gold standard for PEEP settings in this population. Although more patients in the low PEEP group developed ARDS (2.7 percent) than in the high PEEP group (2.7 versus 1 percent), this difference was not significant. Routine use of either strategy in patients without ARDS cannot be justified at this time. A meta-analysis reviewed higher PEEP versus lower PEEP strategies for patients in the ICU without acute respiratory distress syndrome [7]; 2307 patients from 24 trials were included. Although no significant difference was found between high and low PEEP applications in in-hospital mortality, high PEEP decreased the incidence of ARDS and hypoxemia and increased the level of PaO2/FiO2. However, PEEP administration does not prevent the development of ARDS and this finding may simply reflect improved oxygenation [8].

Acute respiratory distress syndrome — Applied PEEP, usually at levels ≥5 cm H2O, are indicated in most patients with acute respiratory distress syndrome (ARDS) and other types of hypoxemic respiratory failure. The major benefit for applied PEEP in this population is improvement in oxygenation. There has been significant research done in an attempt to determine the optimal PEEP in patients with ARDS. A network meta-analysis reported that among patients with moderate to severe ARDS, a high PEEP strategy without recruitment maneuver is associated with a lower mortality than a low PEEP strategy [9], while a Cochrane review failed to find a mortality difference [10]. Most trials titrate PEEP while holding other ventilator settings constant. Data suggest optimal PEEP may depend on the tidal volume. Changing the tidal volume done during a best PEEP trial may lead to different best PEEP settings in the same patient [11]. Studies in a pediatric population appear to validate the use of applied PEEP as pediatric intensivists generally use less PEEP and higher FiO2 than what is recommended by the ARDS Network (ARDSNet). A trial demonstrated that pediatric patients with ARDS managed with lower PEEP relative to FiO2 than recommended by the ARDSNet model had higher mortality [12].

The benefits, harms, and application of applied PEEP in this clinical setting are discussed separately. (See "Acute respiratory distress syndrome: Ventilator management strategies for adults", section on 'Further titration/increase in PEEP (high PEEP)' and "Acute respiratory distress syndrome: Ventilator management strategies for adults".)

Patients with auto-PEEP — Applied PEEP can mitigate the effects of auto-PEEP (also known as intrinsic PEEP) in patients who have an expiratory airflow limitation (eg, acute exacerbations of asthma and chronic obstructive pulmonary disease). The application of extrinsic PEEP in patients with auto-PEEP should always be less than the measured auto-PEEP (50 percent or no greater than 80 percent). The use of applied PEEP in this setting is discussed in greater detail, separately. (See 'Treatment' below and "Invasive mechanical ventilation in acute respiratory failure complicating chronic obstructive pulmonary disease", section on 'Dynamic hyperinflation' and "Invasive mechanical ventilation in adults with acute exacerbations of asthma", section on 'Adding extrinsic PEEP to offset intrinsic PEEP'.)

Cardiogenic pulmonary edema — Applied PEEP has been used in patients with cardiogenic pulmonary edema to improve cardiac function. However, the data indicate that PEEP provides little additional benefit beyond the positive pressure ventilation alone. This was illustrated by a trial of 12 patients receiving mechanical ventilation, during which left ventricular performance was assessed by echocardiography before and after applied PEEP was increased by 10 cm H2O [13]. Left ventricular performance did not change when applied PEEP was increased.

Intraoperative patients — The optimal strategy for mechanically ventilating patients intraoperatively is described separately. (See "Mechanical ventilation during anesthesia in adults".)

Postoperative patients — The application of PEEP has been employed in postoperative patients in an effort to prevent atelectasis and atelectrauma that can occur in injured lung when undergoing ventilation [14-16].

The application of PEEP as an alveolar recruitment maneuver may be beneficial in the postoperative setting. One single center study of 320 patients who had undergone elective cardiac surgery and were mechanically ventilated for hypoxemia compared an intensive recruitment strategy with a moderate strategy [16]. An intensive strategy consisted of two rounds (four hours apart) of three cycles of 60 second lung inflation with PEEP 30 cm H2O, pressure controlled ventilation, driving pressure 15 cm H2O, respiratory rate 15/minute, inspiratory time 1.5 seconds, and fraction of inspired oxygen 0.4 followed by low tidal volume ventilation and a PEEP setting of 13 cm H2O, while a moderate strategy consisted of two rounds (four hours apart) of three cycles of 30 second inflation with continuous positive pressure at 20 cm H2O, and fraction of inspired oxygen 0.6 followed low tidal volume ventilation and a PEEP setting of 8 cm H2O. Intensive recruitment maneuvers resulted in fewer pulmonary complications (severity score 1.8 versus 2.1), and decreased ICU length of stay (3.8 versus 4.8 days) and mortality (2.5 versus 4.9 percent), without increasing the incidence of barotrauma. Flaws in the study design including small sample size, and lack of adjustment for confounding variables and control group, as well as poor generalizability limit interpretation such that further trials demonstrating similar benefit are needed before aggressive recruitment maneuvers can be routinely recommended in the postoperative setting.

Additional details regarding recruitment in patient with ARDS are provided separately.

Other — Applied PEEP has also been used in patients with flail chest (to stabilize the chest wall) or tracheobronchomalacia (to maintain patency of the airways during expiration) with mixed results [1].

Contraindications — There are no absolute contraindications to applied PEEP. However, applied PEEP can have adverse consequences (especially at high levels) and should be used cautiously in patients who have intracranial abnormalities, unilateral or focal lung disease, hypotension, hypovolemia, pulmonary embolism, dynamic hyperinflation without airflow limitation, or a bronchopleural fistula. It may also have undesirable consequences in patients undergoing prone ventilation.

Intracranial disease — Increased intrathoracic pressure due to applied PEEP could theoretically decrease cerebral venous outflow, leading to increased intracranial pressure, decreased mean arterial pressure, or both. The result may be decreased cerebral perfusion pressure and neurologic deterioration.

Whether this actually occurs is uncertain. Observational studies with patients who had acute stroke or acute subarachnoid hemorrhage found that incremental elevation of applied PEEP was associated with diminished cerebral perfusion pressure (due to decreased mean arterial pressure) [17,18]. In contrast, another observational study with patients who had traumatic brain injury found that applied PEEP was associated with increased cerebral perfusion pressure (due to decreased intracranial pressure) [19]. The reason for the conflicting results is uncertain, but may be related to varying effects of the different intracranial abnormalities.

Given the uncertainty that exists, it is prudent to monitor both the mean arterial blood pressure and intracranial pressure (if available) whenever applied PEEP is used in a patient with an intracranial abnormality. Reduction of applied PEEP should be considered if the mean arterial blood pressure decreases or intracranial pressure increases. (See "Evaluation and management of elevated intracranial pressure in adults".)

Focal lung disease — Applied PEEP can worsen hypoxemia in patients with focal lung disease (eg, pneumonia). This probably occurs because the applied PEEP compresses intra-alveolar capillaries in the uninvolved lung, diverting blood flow to the injured lung [20]. This increases intrapulmonary shunting.

Hypotension — Positive pressure ventilation increases intrathoracic pressure, which can decrease venous return, reduce cardiac output, and potentially cause hypotension [21]. This is exacerbated by applied PEEP, especially in hypovolemic patients. In euvolemic patients, applied PEEP up to 20 cm H2O is generally well tolerated from a hemodynamic standpoint, as demonstrated by a trial of eight patients with ARDS [22]. Incremental increases of applied PEEP from 10 to 20 cm H2O caused hypotension in only one patient, while gastric mucosal perfusion (a marker of systemic hypoperfusion) and cardiac index were unchanged in the remaining patients. A technique is being developed that estimates the cardiac output from changes in the pulmonary shunt at different levels of PEEP; the technique is not yet available for routine clinical use [23]. (See "Clinical and physiologic complications of mechanical ventilation: Overview", section on 'Hypotension'.)

Hyperinflation without flow limitation — Applied PEEP should not be used to treat auto-PEEP that exists in the absence of an expiratory flow limitation. Applied PEEP in this setting can worsen alveolar pressure and increase the risk of complications such as pulmonary barotrauma or hypotension.

Prone patients — In patients who are mechanically ventilated in the supine position, 10 cm H2O of applied PEEP is associated with similar redistribution of ventilation and blood flow to the dependent (ie, dorsal) portion of the lung, thereby maintaining a constant amount of ventilation-perfusion (V/Q) mismatch [24]. In contrast, in patients who are mechanically ventilated in the prone ventilation, 10 cm H2O of applied PEEP is associated with a redistribution of blood flow to the dependent (ie, ventral) portion of the lung that is out of proportion to the redistribution of ventilation, thereby exacerbating the V/Q mismatch. A study of prone ventilation in ARDS patients comparing a low PEEP (ARDSNET) strategy to two other PEEP strategies, including a conventional high PEEP protocol (EPVENT-2 trial), found mechanical power decreased when patients on the high PEEP protocol were positioned supine, but nevertheless remained higher than that seen when ventilated by the low PEEP approach [25]. This suggests that higher levels of applied PEEP may be less beneficial, or potentially harmful, in patients undergoing prone ventilation.

Tools for titrating applied PEEP — The titration of PEEP is critical for managing patients with ARDS. Most experts use oxygenation using the strategy outlined in the ARMA trial (table 1). However, several tools are available but with the exception of utilizing oxygenation, most of the tools listed below are not suitable for routine use nor has their use been associated with improved outcomes:

●Oxygen – For the initial setting of PEEP, we use the strategy outlined in ARMA [26] (table 1), a strategy associated with improved outcomes. (See "Acute respiratory distress syndrome: Ventilator management strategies for adults", section on 'Positive end-expiratory pressure (PEEP), fraction of inspired oxygen, oxygenation target'.)

●Esophageal pressure – Esophageal pressure (PES) is an estimate of pleural pressure. It can be measured with an esophageal balloon catheter and then used to calculate the transpulmonary pressure:

Transpulmonary pressure = airway pressure - pleural pressure

The transpulmonary pressure can then be adjusted by titrating applied PEEP, since airway pressure is related to applied PEEP. Titrating applied PEEP to an end-expiratory transpulmonary pressure between 0 and 10 cm H2O may reduce cyclic alveolar collapse, while maintaining an end-inspiratory transpulmonary pressure ≤25 cm H2O may reduce alveolar overdistension [27].

The value of measuring esophageal pressure was evaluated in two trials:

An initial trial (EPvent) randomly assigned 61 patients with ARDS to one of the following mechanical ventilation strategies [27]:

-Adjustment of the FiO2 and applied PEEP to achieve specific transpulmonary pressures, as measured with an esophageal balloon during an end-expiratory occlusion maneuver

-Adjustment of the FiO2 and applied PEEP according to a table of ventilator combinations, an approach similar to that used in the ARMA trial described above (table 1)

Both strategies were designed to maintain a PaO2 between 55 and 120 mmHg (7.32 to 16 kPa), or an oxyhemoglobin saturation between 88 and 98 percent. The group whose applied PEEP was guided by esophageal pressure measurements was managed with significantly higher total PEEP (18 versus 12 cm H2O) and had a significantly higher PaO2/FiO2 ratio (280 versus 191 mmHg [37.2 versus 25.4 kPa]), both assessed at 72 hours. The esophageal pressure group also had an almost statistically significant reduction in 28-day mortality (17 versus 39 percent, adjusted relative risk 0.46, 95% CI 0.19-1.00). There was no difference in the number of ICU-free days or ventilator-free days. However, this study had an unblended single-center design and was stopped early for benefit which may have overestimated the true effect.

•In a multicenter phase 2 confirmatory trial (EPvent-2) of 200 patients with severe ARDS (PaO2/FiO2 ratio ≤200 mmHg), PES-guided titration of PEEP was compared with empirical high PEEP-FiO2 titration (eg, similar to that in the table (table 2)) (see "Acute respiratory distress syndrome: Ventilator management strategies for adults", section on 'Open lung ventilation') [28]. The goal oxygenation was to maintain a PaO2 between 55 and 80 mmHg (7.32 to 10.7 kPa), or an oxyhemoglobin saturation between 88 and 93 percent. PES-guided PEEP titration did not improve the composite outcome of death and the number of mechanical ventilation-free days but did decrease the need for rescue therapy (eg, prone positioning, recruitment maneuvers, extracorporeal membrane oxygenation, inhaled pulmonary vasodilators), perhaps indicating improved oxygenation with PES-guided PEEP strategies. The rate of barotrauma was no different between the groups (5 versus 6 percent).

We believe PES-guided PEEP should not be used routinely in most centers. Improved oxygenation alone is insufficient to warrant a change in routine clinical practice [26,29]. It is difficult for most centers to justify the inconvenience and cost of obtaining the necessary equipment and expertise without more certain evidence of clinical benefit. However, in centers that already have the necessary equipment and expertise, PES-guided PEEP may be helpful in the management of patients with ARDS, especially if there are concerns that airway pressures do not accurately reflect distending pressures in the lung (eg, when there is external compression of the lung due to abdominal compartment syndrome, chest wall deformities, or large pleural effusion).

●Pressure-volume (PV) curves – In many patients with early ARDS, PV curves appear flat at low lung volumes (low compliance), become steeper at higher lung volumes (higher compliance), and then flatten again at even higher lung volumes (figure 1). The lower inflection point is the transition from low to higher compliance, while the upper inflection point is the transition from higher to low compliance. There are two methods of titrating applied PEEP that require a PV curve:

•The first method involves using a level of applied PEEP that is slightly above the lower inflection point (figure 1) [30-32]. The trials of open lung ventilation described above are examples of this method. Specifically, they used an applied PEEP that was 2 cm H2O greater than the lower inflection point that was chosen.

•The second method involves using a level of applied PEEP that matches the pressure at which lung compliance is maximized. This is determined from the PV curve (slope equals compliance) or by stepwise titration of applied PEEP with calculation of compliance at each step [33,34]. Compliance is calculated using the equation Crs = VT/(Ppl - PEEP), where Crs is the compliance, VT is the tidal volume, and Ppl is the plateau airway pressure. Measurement of the plateau airway pressure is described separately. (See "Diagnosis, management, and prevention of pulmonary barotrauma during invasive mechanical ventilation in adults", section on 'Prevention'.)

Regardless of which method is chosen, inflation beyond the upper inflection point can result in alveolar overdistension and pulmonary barotrauma, as well as impaired cardiac filling and oxygen delivery [35].

There are significant limitations to using PV curves to identify the level of applied PEEP necessary for open lung ventilation [33,36-41]. Among the limitations, the lower inflection point cannot be identified in some patients and neuromuscular blockade or apneic-level sedation is generally required to accurately construct a PV curve [33,37]. A novel approach to plotting a PV curve that doesn't require neuromuscular blockade has been used in several clinical trials [42,43]. Following five cycles of controlled ventilation, the inspiratory to expiratory ratio is set to 80 percent, the respiratory rate is set to five breaths per minute, and the tidal volume is set to 500 mL [44]. Inspiratory flow is then administered for 9.6 seconds, during which a PV curve is generated on the ventilator screen. From this curve, the lower inflection point can be determined. This approach appears promising but requires validation.

●Lung ultrasound – The effects of applied PEEP on lung aeration can be directly visualized by lung ultrasound [45]. While this may prove useful in the future, additional experience is necessary before lung ultrasound is used to titrate PEEP in patients with ARDS.

●Oxygen delivery – Applied PEEP can be titrated to a maximum oxygen delivery (DO2). This method involves calculating the DO2 at each level of applied PEEP, then using the applied PEEP that corresponds with the best DO2 for ongoing mechanical ventilation. The calculation of DO2 is discussed elsewhere. (See "Oxygen delivery and consumption".)

AUTO (INTRINSIC) PEEP — Incomplete expiration prior to the initiation of the next breath causes progressive air trapping (ie, dynamic hyperinflation). This accumulation of air increases alveolar pressure at the end of expiration, which is referred to as auto-PEEP.

This section focuses on auto-PEEP that develops during mechanical ventilation. Auto-PEEP that develops during spontaneous breathing is discussed separately. (See "Dynamic hyperinflation in patients with COPD".)

Causes — There are three common situations during which auto-PEEP develops: high minute ventilation, expiratory flow limitation, and expiratory resistance.

High minute ventilation — A high minute ventilation is caused by large tidal volumes, a high respiratory rate, or both. Either alteration can create auto-PEEP.

●Large tidal volumes increase the volume that must be exhaled prior to the next breath. The larger the tidal volume, the less likely that the full tidal volume will be exhaled before the onset of the next breath.

●High respiratory rates decrease the duration of expiration. The faster the respiratory rate, the shorter the expiratory time and the less likely that the full tidal volume will be exhaled before the onset of the next breath.

Expiratory flow limitation — An expiratory flow limitation exists when expiratory flow is slowed by airway narrowing due to collapse, bronchospasm, inflammation, or remodeling (figure 2). It increases the likelihood that the full tidal volume will not be exhaled before the onset of the next breath and auto-PEEP will develop.

Most patients with chronic obstructive pulmonary disease (COPD) have an expiratory flow limitation. As a result, such patients are prone to developing auto-PEEP when mechanical ventilation is initiated [46].

A patient's expiratory flow limitation is not routinely assessed in critical care units because it requires neuromuscular paralysis, specialized techniques, or both to be measured [47,48]. However, it appears that expiratory flow limitation is more prominent when patients are supine rather than semirecumbent [48].

Expiratory resistance — Expiratory resistance is conceptually similar to expiratory flow limitation in that it slows expiration and increases the likelihood that the full tidal volume will not be exhaled before the onset of the next breath. However, expiratory resistance is unrelated to the airways. Examples of expiratory resistance include a narrow diameter or kinked endotracheal tube, inspissated secretions, exhalation or PEEP valves, and patient-ventilator asynchrony. (See "Overview of initiating invasive mechanical ventilation in adults in the intensive care unit", section on 'Follow-up'.)

Potential sequelae — Auto-PEEP increases intrathoracic pressure, which can decrease venous return, reduce cardiac output, and potentially cause hypotension. This is most pronounced in hypovolemic patients. (See "Clinical and physiologic complications of mechanical ventilation: Overview", section on 'Hypotension'.)

Auto-PEEP can also cause alveolar overdistension, increasing the likelihood of pulmonary barotrauma and ventilator-associated lung injury. Alveolar overdistension can also cause hypoxemia if V/Q mismatch increases due to compression of adjacent pulmonary blood vessels. (See "Diagnosis, management, and prevention of pulmonary barotrauma during invasive mechanical ventilation in adults" and "Ventilator-induced lung injury".)

Finally, auto-PEEP increases the work required for a patient to trigger a ventilator breath when pressure-triggering is being used. This is because the patient must generate enough negative pressure to overcome the trigger sensitivity plus the auto-PEEP, rather than the trigger sensitivity alone (figure 3). As an example, a patient whose auto-PEEP is 8 cm H2O and whose ventilator has a trigger sensitivity of -2 cm H2O needs to generate -10 cm H2O of negative pressure to trigger a breath. In contrast, a patient who has no auto-PEEP only needs to generate the -2 cm H2O of negative pressure that is necessary to overcome the trigger sensitivity. Inability to trigger breaths may cause patient-ventilator asynchrony, dyspnea, and insufficient ventilation [49]. (See "Overview of initiating invasive mechanical ventilation in adults in the intensive care unit", section on 'Trigger sensitivity' and "Overview of initiating invasive mechanical ventilation in adults in the intensive care unit", section on 'Follow-up'.)

Assessment — Auto-PEEP can be detected using ventilator-generated flow versus time graphs, or palpation plus auscultation of the chest. With flow versus time graphs, the upstroke that indicates inspiratory flow will begin before the expiration tracing reaches zero flow if auto-PEEP exists. With palpation and auscultation, inspiratory airflow will be heard before the expiratory airflow ceases. Palpation and auscultation can confirm that auto-PEEP is present, but it is unreliable for determining its absence [50].

Another approach exists that can quantitate the auto-PEEP. Specifically, the auto-PEEP is determined by measuring the end-expiratory alveolar pressure and then subtracting the applied PEEP:

Auto-PEEP = end-expiratory alveolar pressure - applied PEEP

The end-expiratory alveolar pressure is measured by applying an end-expiratory breath hold and reading the airway pressure directly from the ventilator during the breath hold. The applied PEEP is set on the ventilator.

Auto-PEEP is difficult to quantitate accurately, as illustrated by the following examples:

●Widespread airway closure in patients with severe asthma can falsely lower the end-expiratory alveolar pressure measurement [51]. As a result, marked dynamic hyperinflation and auto-PEEP may be unrecognized.

●Expiratory muscle activity in non-paralyzed patients can falsely elevate the end-expiratory alveolar pressure measurement (figure 4) [52]. This can lead to the inappropriate and potentially harmful treatment of presumed auto-PEEP. (See 'Treatment' below.)

The second situation described above can be avoided by carefully palpating for the absence of expiratory muscle activity prior to measuring the end-expiratory alveolar pressure [53]. This coincides with the onset of inspiration because the expiratory muscle must relax in order for the inspiratory muscles to decrease intrathoracic pressure [54].

Treatment — Steps should be taken to correct auto-PEEP as soon as it is identified. Initial efforts should focus on determining and treating the underlying cause. When auto-PEEP persists despite management of its underlying cause, applied PEEP may be helpful if the patient has an expiratory flow limitation.

When a high minute ventilation is the presumed cause of auto-PEEP, the minute ventilation should be decreased by lowering the tidal volume or respiratory rate. This frequently requires a strategy of permissive hypercapnia. (See "Permissive hypercapnia during mechanical ventilation in adults".)

When an expiratory flow limitation due to obstructive airways disease is the presumed cause of auto-PEEP, the duration of expiration should be prolonged. This can be accomplished by increasing the inspiratory flow, decreasing the tidal volume, or decreasing the respiratory rate.

Treatment with bronchodilators, steroids, and antibiotics may also be beneficial. In a study of 25 patients with COPD and acute respiratory failure, expiratory flow limitation was present in 96 percent of the patients at the initiation of mechanical ventilation [55]. The prevalence of expiratory flow limitation decreased to 47 percent at the time of extubation and 40 percent at the time of ICU discharge, indicating that expiratory flow limitation may respond to therapy. (See "COPD exacerbations: Management".)

When increased expiratory resistance is the presumed cause of auto-PEEP, the source of increased resistance should be identified and corrected. This may require sedation, pharmacologic paralysis, or replacement of the endotracheal tube or ventilator tubing.

Applied PEEP — Small amounts of applied PEEP can decrease auto-PEEP in patients who have an expiratory flow limitation [56-58]. This can be conceptualized as the applied PEEP holding open the narrowed airways during expiration, improving expiratory airflow, and allowing more complete expiration prior to the onset of the next breath. Additional benefits of using applied PEEP to offset auto-PEEP include decreased oxygen consumption and improved gas exchange. The latter is due to opening the small airways in the dependent lung zones and distributing inspired gas more homogeneously [59-61].

Applied PEEP should always be less than the measured auto-PEEP [62]. Otherwise, alveolar pressure may increase, placing the patient at increased risk for complications such as pulmonary barotrauma or hypotension (figure 5). One study even suggested that applied PEEP does not need to exceed the measured auto-PEEP for this to occur. Rather, it can occur if the applied PEEP is greater than 85 percent of the measured auto-PEEP [63]. Given the potential inaccuracy of auto-PEEP measurements, it is prudent to set applied PEEP to a level that is less than 50 percent of the measured auto-PEEP. Research has shown that mechanical ventilation with PEEP induces longitudinal atrophy by displacing the diaphragm in caudal direction and reducing the length of fibers. As a result, muscle fibers generate less force causing diaphragm weakness [64]. This may exacerbate diaphragm weakness in critically ill patients thus prolonging mechanical ventilation. This advocates for maintaining the lowest required PEEP setting.

Applied PEEP should not be used to counter auto-PEEP in patients who do not have an expiratory flow limitation. Applied PEEP may increase alveolar pressure and increase the risk of both barotrauma and hemodynamic compromise in this setting [65].

SUMMARY AND RECOMMENDATIONS

●Definition – Positive end-expiratory pressure (PEEP) is the alveolar pressure above atmospheric pressure that exists at the end of expiration. PEEP that is applied through a mechanical ventilator is referred to as applied PEEP (also called extrinsic PEEP), whereas PEEP that is secondary to incomplete exhalation is referred to as auto-PEEP (also called intrinsic PEEP). (See 'Definition' above.)

●Applied PEEP – The optimal level of applied PEEP in most populations is unknown. In general:

•A small amount of applied PEEP (3 to 5 cm H2O) is used in most mechanically ventilated patients to mitigate end-expiratory alveolar collapse. (See 'Indications' above.)

•A higher level of applied PEEP (>5 cm H2O) is sometimes used to improve hypoxemia or reduce ventilator-associated lung injury in patients with acute respiratory distress syndrome or other types of hypoxemic respiratory failure, and offset the effects of auto-PEEP in patients with expiratory airflow limitation. (See 'Indications' above.)

•Improvement in P:F ratio with a higher level of applied PEEP is associated with improved mortality in patients with moderate-to-severe ARDS. (See 'Indications' above.)

•There are no absolute contraindications to applied PEEP. However, applied PEEP can have adverse consequences (especially at high levels) and should be used cautiously in patients with intracranial abnormalities, unilateral or focal lung disease, hypotension, hypovolemia, dynamic hyperinflation without airflow limitation, or a bronchopleural fistula. (See 'Contraindications' above.)

●Auto-PEEP

•There are three common situations during which auto-PEEP develops: high minute ventilation, expiratory flow limitation, and expiratory resistance. (See 'Causes' above.)

•Auto-PEEP increases intrathoracic pressure, which can decrease venous return, reduce cardiac output, and potentially cause hypotension. It can also cause alveolar overdistension, increasing the likelihood of pulmonary barotrauma and ventilator-associated lung injury. Finally, auto-PEEP increases the work required for a patient to trigger a ventilator breath if pressure-triggering is being used. (See 'Potential sequelae' above.)

•Auto-PEEP can be detected using ventilator-generated flow versus time graphs or by palpation and auscultation of the chest. It can be detected and quantitated by measuring the end-expiratory alveolar pressure and then subtracting the applied PEEP. (See 'Assessment' above.)

•Steps should be taken to correct auto-PEEP as soon as it is identified. Initial efforts should focus on determining and treating the underlying cause. When auto-PEEP persists despite management of its underlying cause, applied PEEP may be helpful if the patient has an expiratory flow limitation. (See 'Treatment' above.)

•For patients with auto-PEEP and an expiratory flow limitation, we suggest administering applied PEEP at a level that is 50 percent of the measured auto-PEEP (Grade 2C). (See 'Treatment' above.)

  1. Smith, RA. Physiologic PEEP. Respir Care 1988; 33:620.
  2. Manzano F, Fernández-Mondéjar E, Colmenero M, et al. Positive-end expiratory pressure reduces incidence of ventilator-associated pneumonia in nonhypoxemic patients. Crit Care Med 2008; 36:2225.
  3. Neto AS, Barbas CSV, Simonis FD, et al. Epidemiological characteristics, practice of ventilation, and clinical outcome in patients at risk of acute respiratory distress syndrome in intensive care units from 16 countries (PRoVENT): an international, multicentre, prospective study. Lancet Respir Med 2016; 4:882.
  4. Lucangelo U, Zin WA, Antonaglia V, et al. Effect of positive expiratory pressure and type of tracheal cuff on the incidence of aspiration in mechanically ventilated patients in an intensive care unit. Crit Care Med 2008; 36:409.
  5. Writing Committee and Steering Committee for the RELAx Collaborative Group, Algera AG, Pisani L, et al. Effect of a Lower vs Higher Positive End-Expiratory Pressure Strategy on Ventilator-Free Days in ICU Patients Without ARDS: A Randomized Clinical Trial. JAMA 2020; 324:2509.
  6. Simonis FD, Juffermans NP, Schultz MJ. Mechanical ventilation of the healthy lungs: lessons learned from recent trials. Curr Opin Crit Care 2021; 27:55.
  7. Yi H, Li X, Mao Z, et al. Higher PEEP versus lower PEEP strategies for patients in ICU without acute respiratory distress syndrome: A systematic review and meta-analysis. J Crit Care 2022; 67:72.
  8. Pepe PE, Hudson LD, Carrico CJ. Early application of positive end-expiratory pressure in patients at risk for the adult respiratory-distress syndrome. N Engl J Med 1984; 311:281.
  9. Dianti J, Tisminetzky M, Ferreyro BL, et al. Association of Positive End-Expiratory Pressure and Lung Recruitment Selection Strategies with Mortality in Acute Respiratory Distress Syndrome: A Systematic Review and Network Meta-analysis. Am J Respir Crit Care Med 2022; 205:1300.
  10. Santa Cruz R, Villarejo F, Irrazabal C, Ciapponi A. High versus low positive end-expiratory pressure (PEEP) levels for mechanically ventilated adult patients with acute lung injury and acute respiratory distress syndrome. Cochrane Database Syst Rev 2021; 3:CD009098.
  11. McKown AC, Semler MW, Rice TW. Best PEEP trials are dependent on tidal volume. Crit Care 2018; 22:115.
  12. Khemani RG, Parvathaneni K, Yehya N, et al. Positive End-Expiratory Pressure Lower Than the ARDS Network Protocol Is Associated with Higher Pediatric Acute Respiratory Distress Syndrome Mortality. Am J Respir Crit Care Med 2018; 198:77.
  13. Fellahi JL, Valtier B, Beauchet A, et al. Does positive end-expiratory pressure ventilation improve left ventricular function? A comparative study by transesophageal echocardiography in cardiac and noncardiac patients. Chest 1998; 114:556.
  14. Wetterslev J, Hansen EG, Roikjaer O, et al. Optimizing peroperative compliance with PEEP during upper abdominal surgery: effects on perioperative oxygenation and complications in patients without preoperative cardiopulmonary dysfunction. Eur J Anaesthesiol 2001; 18:358.
  15. Good JT Jr, Wolz JF, Anderson JT, et al. The routine use of positive end-expiratory pressure after open heart surgery. Chest 1979; 76:397.
  16. Costa Leme A, Hajjar LA, Volpe MS, et al. Effect of Intensive vs Moderate Alveolar Recruitment Strategies Added to Lung-Protective Ventilation on Postoperative Pulmonary Complications: A Randomized Clinical Trial. JAMA 2017; 317:1422.
  17. Georgiadis D, Schwarz S, Baumgartner RW, et al. Influence of positive end-expiratory pressure on intracranial pressure and cerebral perfusion pressure in patients with acute stroke. Stroke 2001; 32:2088.
  18. Muench E, Bauhuf C, Roth H, et al. Effects of positive end-expiratory pressure on regional cerebral blood flow, intracranial pressure, and brain tissue oxygenation. Crit Care Med 2005; 33:2367.
  19. Huynh T, Messer M, Sing RF, et al. Positive end-expiratory pressure alters intracranial and cerebral perfusion pressure in severe traumatic brain injury. J Trauma 2002; 53:488.
  20. Hasan FM, Beller TA, Sobonya RE, et al. Effect of positive end-expiratory pressure and body position in unilateral lung injury. J Appl Physiol Respir Environ Exerc Physiol 1982; 52:147.
  21. Pinsky MR. Cardiovascular issues in respiratory care. Chest 2005; 128:592S.
  22. Bruhn A, Hernandez G, Bugedo G, Castillo L. Effects of positive end-expiratory pressure on gastric mucosal perfusion in acute respiratory distress syndrome. Crit Care 2004; 8:R306.
  23. Sundaresan A, Chase JG, Hann CE, Shaw GM. Cardiac output estimation using pulmonary mechanics in mechanically ventilated patients. Biomed Eng Online 2010; 9:80.
  24. Petersson J, Ax M, Frey J, et al. Positive end-expiratory pressure redistributes regional blood flow and ventilation differently in supine and prone humans. Anesthesiology 2010; 113:1361.
  25. Boesing C, Graf PT, Schmitt F, et al. Effects of different positive end-expiratory pressure titration strategies during prone positioning in patients with acute respiratory distress syndrome: a prospective interventional study. Crit Care 2022; 26:82.
  26. Acute Respiratory Distress Syndrome Network, Brower RG, Matthay MA, et al. 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.
  27. Talmor D, Sarge T, Malhotra A, et al. Mechanical ventilation guided by esophageal pressure in acute lung injury. N Engl J Med 2008; 359:2095.
  28. Beitler JR, Sarge T, Banner-Goodspeed VM, et al. Effect of Titrating Positive End-Expiratory Pressure (PEEP) With an Esophageal Pressure-Guided Strategy vs an Empirical High PEEP-Fio2 Strategy on Death and Days Free From Mechanical Ventilation Among Patients With Acute Respiratory Distress Syndrome: A Randomized Clinical Trial. JAMA 2019; 321:846.
  29. Bernard GR. PEEP guided by esophageal pressure--any added value? N Engl J Med 2008; 359:2166.
  30. Muscedere JG, Mullen JB, Gan K, Slutsky AS. Tidal ventilation at low airway pressures can augment lung injury. Am J Respir Crit Care Med 1994; 149:1327.
  31. Mancebo J. PEEP, ARDS, and alveolar recruitment. Intensive Care Med 1992; 18:383.
  32. Dreyfuss D, Saumon G. Should the lung be rested or recruited? The Charybdis and Scylla of ventilator management. Am J Respir Crit Care Med 1994; 149:1066.
  33. Ward NS, Lin DY, Nelson DL, et al. Successful determination of lower inflection point and maximal compliance in a population of patients with acute respiratory distress syndrome. Crit Care Med 2002; 30:963.
  34. Suter PM, Fairley B, Isenberg MD. Optimum end-expiratory airway pressure in patients with acute pulmonary failure. N Engl J Med 1975; 292:284.
  35. Dambrosio M, Roupie E, Mollet JJ, et al. Effects of positive end-expiratory pressure and different tidal volumes on alveolar recruitment and hyperinflation. Anesthesiology 1997; 87:495.
  36. Crotti S, Mascheroni D, Caironi P, et al. Recruitment and derecruitment during acute respiratory failure: a clinical study. Am J Respir Crit Care Med 2001; 164:131.
  37. Decailliot F, Demoule A, Maggiore SM, et al. Pressure-volume curves with and without muscle paralysis in acute respiratory distress syndrome. Intensive Care Med 2006; 32:1322.
  38. Gattinoni L, D'Andrea L, Pelosi P, et al. Regional effects and mechanism of positive end-expiratory pressure in early adult respiratory distress syndrome. JAMA 1993; 269:2122.
  39. Maggiore SM, Jonson B, Richard JC, et al. Alveolar derecruitment at decremental positive end-expiratory pressure levels in acute lung injury: comparison with the lower inflection point, oxygenation, and compliance. Am J Respir Crit Care Med 2001; 164:795.
  40. Mergoni M, Martelli A, Volpi A, et al. Impact of positive end-expiratory pressure on chest wall and lung pressure-volume curve in acute respiratory failure. Am J Respir Crit Care Med 1997; 156:846.
  41. O'Keefe GE, Gentilello LM, Erford S, Maier RV. Imprecision in lower "inflection point" estimation from static pressure-volume curves in patients at risk for acute respiratory distress syndrome. J Trauma 1998; 44:1064.
  42. Gattinoni L, Caironi P, Cressoni M, et al. Lung recruitment in patients with the acute respiratory distress syndrome. N Engl J Med 2006; 354:1775.
  43. Grasso S, Stripoli T, De Michele M, et al. ARDSnet ventilatory protocol and alveolar hyperinflation: role of positive end-expiratory pressure. Am J Respir Crit Care Med 2007; 176:761.
  44. Lu Q, Vieira SR, Richecoeur J, et al. A simple automated method for measuring pressure-volume curves during mechanical ventilation. Am J Respir Crit Care Med 1999; 159:275.
  45. Bouhemad B, Brisson H, Le-Guen M, et al. Bedside ultrasound assessment of positive end-expiratory pressure-induced lung recruitment. Am J Respir Crit Care Med 2011; 183:341.
  46. Armaganidis A, Stavrakaki-Kallergi K, Koutsoukou A, et al. Intrinsic positive end-expiratory pressure in mechanically ventilated patients with and without tidal expiratory flow limitation. Crit Care Med 2000; 28:3837.
  47. Gay PC, Rodarte JR, Hubmayr RD. The effects of positive expiratory pressure on isovolume flow and dynamic hyperinflation in patients receiving mechanical ventilation. Am Rev Respir Dis 1989; 139:621.
  48. Valta P, Corbeil C, Lavoie A, et al. Detection of expiratory flow limitation during mechanical ventilation. Am J Respir Crit Care Med 1994; 150:1311.
  49. Gurevitch MJ, Gelmont D. Importance of trigger sensitivity to ventilator response delay in advanced chronic obstructive pulmonary disease with respiratory failure. Crit Care Med 1989; 17:354.
  50. Kress JP, O'Connor MF, Schmidt GA. Clinical examination reliably detects intrinsic positive end-expiratory pressure in critically ill, mechanically ventilated patients. Am J Respir Crit Care Med 1999; 159:290.
  51. Leatherman JW, Ravenscraft SA. Low measured auto-positive end-expiratory pressure during mechanical ventilation of patients with severe asthma: hidden auto-positive end-expiratory pressure. Crit Care Med 1996; 24:541.
  52. Lessard MR, Lofaso F, Brochard L. Expiratory muscle activity increases intrinsic positive end-expiratory pressure independently of dynamic hyperinflation in mechanically ventilated patients. Am J Respir Crit Care Med 1995; 151:562.
  53. Zakynthinos SG, Vassilakopoulos T, Zakynthinos E, Roussos C. Accurate measurement of intrinsic positive end-expiratory pressure: how to detect and correct for expiratory muscle activity. Eur Respir J 1997; 10:522.
  54. Brochard L. Intrinsic (or auto-) positive end-expiratory pressure during spontaneous or assisted ventilation. Intensive Care Med 2002; 28:1552.
  55. Alvisi V, Romanello A, Badet M, et al. Time course of expiratory flow limitation in COPD patients during acute respiratory failure requiring mechanical ventilation. Chest 2003; 123:1625.
  56. Smith TC, Marini JJ. Impact of PEEP on lung mechanics and work of breathing in severe airflow obstruction. J Appl Physiol (1985) 1988; 65:1488.
  57. Kondili E, Alexopoulou C, Prinianakis G, et al. Pattern of lung emptying and expiratory resistance in mechanically ventilated patients with chronic obstructive pulmonary disease. Intensive Care Med 2004; 30:1311.
  58. Caramez MP, Borges JB, Tucci MR, et al. Paradoxical responses to positive end-expiratory pressure in patients with airway obstruction during controlled ventilation. Crit Care Med 2005; 33:1519.
  59. Rossi A, Santos C, Roca J, et al. Effects of PEEP on VA/Q mismatching in ventilated patients with chronic airflow obstruction. Am J Respir Crit Care Med 1994; 149:1077.
  60. Guerin C, LeMasson S, de Varax R, et al. Small airway closure and positive end-expiratory pressure in mechanically ventilated patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1997; 155:1949.
  61. Glérant JC, Leleu O, Rose D, et al. Oxygen consumption and PEEPe in ventilated COPD patients. Respir Physiol Neurobiol 2005; 146:117.
  62. Tuxen DV. Detrimental effects of positive end-expiratory pressure during controlled mechanical ventilation of patients with severe airflow obstruction. Am Rev Respir Dis 1989; 140:5.
  63. Ranieri VM, Giuliani R, Cinnella G, et al. Physiologic effects of positive end-expiratory pressure in patients with chronic obstructive pulmonary disease during acute ventilatory failure and controlled mechanical ventilation. Am Rev Respir Dis 1993; 147:5.
  64. Lindqvist J, van den Berg M, van der Pijl R, et al. Positive End-Expiratory Pressure Ventilation Induces Longitudinal Atrophy in Diaphragm Fibers. Am J Respir Crit Care Med 2018; 198:472.
  65. Marini JJ. Should PEEP be used in airflow obstruction? Am Rev Respir Dis 1989; 140:1.
Topic 1642 Version 26.0

References

1 : Physiologic PEEP

2 : Positive-end expiratory pressure reduces incidence of ventilator-associated pneumonia in nonhypoxemic patients.

3 : Epidemiological characteristics, practice of ventilation, and clinical outcome in patients at risk of acute respiratory distress syndrome in intensive care units from 16 countries (PRoVENT): an international, multicentre, prospective study.

4 : Effect of positive expiratory pressure and type of tracheal cuff on the incidence of aspiration in mechanically ventilated patients in an intensive care unit.

5 : Effect of a Lower vs Higher Positive End-Expiratory Pressure Strategy on Ventilator-Free Days in ICU Patients Without ARDS: A Randomized Clinical Trial.

6 : Mechanical ventilation of the healthy lungs: lessons learned from recent trials.

7 : Higher PEEP versus lower PEEP strategies for patients in ICU without acute respiratory distress syndrome: A systematic review and meta-analysis.

8 : Early application of positive end-expiratory pressure in patients at risk for the adult respiratory-distress syndrome.

9 : Association of Positive End-Expiratory Pressure and Lung Recruitment Selection Strategies with Mortality in Acute Respiratory Distress Syndrome: A Systematic Review and Network Meta-analysis.

10 : High versus low positive end-expiratory pressure (PEEP) levels for mechanically ventilated adult patients with acute lung injury and acute respiratory distress syndrome.

11 : Best PEEP trials are dependent on tidal volume.

12 : Positive End-Expiratory Pressure Lower Than the ARDS Network Protocol Is Associated with Higher Pediatric Acute Respiratory Distress Syndrome Mortality.

13 : Does positive end-expiratory pressure ventilation improve left ventricular function? A comparative study by transesophageal echocardiography in cardiac and noncardiac patients.

14 : Optimizing peroperative compliance with PEEP during upper abdominal surgery: effects on perioperative oxygenation and complications in patients without preoperative cardiopulmonary dysfunction.

15 : The routine use of positive end-expiratory pressure after open heart surgery.

16 : Effect of Intensive vs Moderate Alveolar Recruitment Strategies Added to Lung-Protective Ventilation on Postoperative Pulmonary Complications: A Randomized Clinical Trial.

17 : Influence of positive end-expiratory pressure on intracranial pressure and cerebral perfusion pressure in patients with acute stroke.

18 : Effects of positive end-expiratory pressure on regional cerebral blood flow, intracranial pressure, and brain tissue oxygenation.

19 : Positive end-expiratory pressure alters intracranial and cerebral perfusion pressure in severe traumatic brain injury.

20 : Effect of positive end-expiratory pressure and body position in unilateral lung injury.

21 : Cardiovascular issues in respiratory care.

22 : Effects of positive end-expiratory pressure on gastric mucosal perfusion in acute respiratory distress syndrome.

23 : Cardiac output estimation using pulmonary mechanics in mechanically ventilated patients.

24 : Positive end-expiratory pressure redistributes regional blood flow and ventilation differently in supine and prone humans.

25 : Effects of different positive end-expiratory pressure titration strategies during prone positioning in patients with acute respiratory distress syndrome: a prospective interventional study.

26 : Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome.

27 : Mechanical ventilation guided by esophageal pressure in acute lung injury.

28 : Effect of Titrating Positive End-Expiratory Pressure (PEEP) With an Esophageal Pressure-Guided Strategy vs an Empirical High PEEP-Fio2 Strategy on Death and Days Free From Mechanical Ventilation Among Patients With Acute Respiratory Distress Syndrome: A Randomized Clinical Trial.

29 : PEEP guided by esophageal pressure--any added value?

30 : Tidal ventilation at low airway pressures can augment lung injury.

31 : PEEP, ARDS, and alveolar recruitment.

32 : Should the lung be rested or recruited? The Charybdis and Scylla of ventilator management.

33 : Successful determination of lower inflection point and maximal compliance in a population of patients with acute respiratory distress syndrome.

34 : Optimum end-expiratory airway pressure in patients with acute pulmonary failure.

35 : Effects of positive end-expiratory pressure and different tidal volumes on alveolar recruitment and hyperinflation.

36 : Recruitment and derecruitment during acute respiratory failure: a clinical study.

37 : Pressure-volume curves with and without muscle paralysis in acute respiratory distress syndrome.

38 : Regional effects and mechanism of positive end-expiratory pressure in early adult respiratory distress syndrome.

39 : Alveolar derecruitment at decremental positive end-expiratory pressure levels in acute lung injury: comparison with the lower inflection point, oxygenation, and compliance.

40 : Impact of positive end-expiratory pressure on chest wall and lung pressure-volume curve in acute respiratory failure.

41 : Imprecision in lower "inflection point" estimation from static pressure-volume curves in patients at risk for acute respiratory distress syndrome.

42 : Lung recruitment in patients with the acute respiratory distress syndrome.

43 : ARDSnet ventilatory protocol and alveolar hyperinflation: role of positive end-expiratory pressure.

44 : A simple automated method for measuring pressure-volume curves during mechanical ventilation.

45 : Bedside ultrasound assessment of positive end-expiratory pressure-induced lung recruitment.

46 : Intrinsic positive end-expiratory pressure in mechanically ventilated patients with and without tidal expiratory flow limitation.

47 : The effects of positive expiratory pressure on isovolume flow and dynamic hyperinflation in patients receiving mechanical ventilation.

48 : Detection of expiratory flow limitation during mechanical ventilation.

49 : Importance of trigger sensitivity to ventilator response delay in advanced chronic obstructive pulmonary disease with respiratory failure.

50 : Clinical examination reliably detects intrinsic positive end-expiratory pressure in critically ill, mechanically ventilated patients.

51 : Low measured auto-positive end-expiratory pressure during mechanical ventilation of patients with severe asthma: hidden auto-positive end-expiratory pressure.

52 : Expiratory muscle activity increases intrinsic positive end-expiratory pressure independently of dynamic hyperinflation in mechanically ventilated patients.

53 : Accurate measurement of intrinsic positive end-expiratory pressure: how to detect and correct for expiratory muscle activity.

54 : Intrinsic (or auto-) positive end-expiratory pressure during spontaneous or assisted ventilation.

55 : Time course of expiratory flow limitation in COPD patients during acute respiratory failure requiring mechanical ventilation.

56 : Impact of PEEP on lung mechanics and work of breathing in severe airflow obstruction.

57 : Pattern of lung emptying and expiratory resistance in mechanically ventilated patients with chronic obstructive pulmonary disease.

58 : Paradoxical responses to positive end-expiratory pressure in patients with airway obstruction during controlled ventilation.

59 : Effects of PEEP on VA/Q mismatching in ventilated patients with chronic airflow obstruction.

60 : Small airway closure and positive end-expiratory pressure in mechanically ventilated patients with chronic obstructive pulmonary disease.

61 : Oxygen consumption and PEEPe in ventilated COPD patients.

62 : Detrimental effects of positive end-expiratory pressure during controlled mechanical ventilation of patients with severe airflow obstruction.

63 : Physiologic effects of positive end-expiratory pressure in patients with chronic obstructive pulmonary disease during acute ventilatory failure and controlled mechanical ventilation.

64 : Positive End-Expiratory Pressure Ventilation Induces Longitudinal Atrophy in Diaphragm Fibers.

65 : Should PEEP be used in airflow obstruction?

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟