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Positive end-expiratory pressure (PEEP)

Positive end-expiratory pressure (PEEP)
Authors:
Rommel Sagana, MD
Robert C Hyzy, MD
Section Editor:
Ellen L Burnham, MD
Deputy Editors:
Geraldine Finlay, MD
Paul Dieffenbach, MD
Literature review current through: Apr 2025. | This topic last updated: Feb 07, 2025.

INTRODUCTION — 

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

Clinical aspects of extrinsic and intrinsic PEEP are discussed in this topic. Additional information regarding PEEP application in patients with acute respiratory distress syndrome and 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'.)

●(See "Invasive mechanical ventilation in adults with acute exacerbations of asthma".)

●(See "Acute respiratory distress syndrome: Ventilator management strategies for adults", section on 'Further titration/increase in PEEP (high PEEP)'.)

DEFINITION — 

PEEP is the alveolar pressure above atmospheric pressure that exists at the end of expiration. There are two types of PEEP:

●Extrinsic PEEP – PEEP provided externally by a mechanical ventilator is referred to as extrinsic or applied PEEP.

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

EXTRINSIC (APPLIED) PEEP — 

Extrinsic PEEP is a ventilator setting. (See "Overview of initiating invasive mechanical ventilation in adults in the intensive care unit", section on 'Indications'.)

Indications

Routine application — In most patients undergoing mechanical ventilation, a small amount of PEEP is routinely applied. In patients with healthy lungs, this is usually 3 to 5 cm H2O.

PEEP is applied to mitigate end-expiratory alveolar collapse during passive exhalation. It may also reduce the incidence of ventilator-associated pneumonia (VAP) and lung injury [1,2]. Routine application of small amounts of PEEP is often called "physiologic PEEP" because it preserves a physiologic end-expiratory volume (functional residual capacity) compared with zero PEEP, which leads to lower volumes and alveolar collapse.

Acute respiratory distress syndrome — In acute respiratory distress syndrome (ARDS), PEEP is applied (≥5 cm H2O) to prevent cyclic opening and closing of alveoli, and thereby reduce ventilator-induced lung injury and maintain adequate oxygenation. The initial titration of PEEP and use of high PEEP as a rescue strategy for refractory hypoxemia in ARDS are discussed in a separate topic. (See "Acute respiratory distress syndrome: Ventilator management strategies for adults", section on 'Positive end-expiratory pressure (PEEP), fraction of inspired oxygen, oxygenation target' and "Acute respiratory distress syndrome: Ventilator management strategies for adults", section on 'Further titration/increase in PEEP (high PEEP)'.)

Patients with intrinsic PEEP — In patients with expiratory airflow limitation due to airway disease (eg, acute exacerbations of asthma and chronic obstructive pulmonary disease), extrinsic PEEP can mitigate the increased work of breathing caused by intrinsic PEEP. Extrinsic PEEP in patients with intrinsic PEEP should be less than the measured intrinsic PEEP (50 percent to ≤80 percent). The use of extrinsic PEEP in this setting is discussed below and separately. (See 'Increasing applied PEEP in patients with airway disease' 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".)

Cardiogenic pulmonary edema — Successful use of extrinsic PEEP in patients with cardiogenic pulmonary edema is discussed separately. (See "Noninvasive ventilation in adults with acute respiratory failure: Benefits and contraindications", section on 'Acute cardiogenic pulmonary edema'.)

Intraoperative patients — Intraoperative PEEP is typically individualized according to patient and surgical factors. PEEP prevents atelectasis and assists in maintaining adequate oxygenation. Initial settings are typically 5 to 8 cm H2O. The optimal intraoperative strategy is described separately. (See "Mechanical ventilation during anesthesia in adults".)

Postoperative patients — Extrinsic PEEP is used postoperatively to prevent atelectasis and atelectrauma [3-8]. Limited data suggest benefit from PEEP, but trials have not directly compared PEEP with a no PEEP strategy. The optimal level remains unknown. Further trials demonstrating benefit are needed before aggressive recruitment can be routinely recommended in the postoperative setting.

●One single-center study of 320 patients who had undergone elective cardiac surgery and were mechanically ventilated compared an intensive recruitment strategy (30 cm H2O PEEP recruitment followed by 13 cm H2O) with a moderate strategy (20 cm H2O PEEP recruitment followed by 8 cm H2O) [5]. Intensive recruitment maneuvers resulted in fewer pulmonary complications (severity score 1.8 versus 2.1), and decreased intensive care unit length of stay (3.8 versus 4.8 days) and mortality (2.5 versus 4.9 percent), without increasing the incidence of barotrauma. However, the sample size was small and there was a lack of adjustment for confounding variables and poor generalizability to other types of surgery.

●Another randomized noninferiority trial of 980 mostly surgical patients compared an initial low PEEP strategy (range 0 to 5 cm H2O) with a high PEEP strategy (PEEP 8 cm H2O) to target an oxygen saturation >92 percent or partial arterial oxygen tension (PaO2) >60 mmHg [6]. Similar rates of ventilator-free days, oxygenation, need for rescue therapy, and mortality were reported. However, several issues including heterogeneity among the patients, a paucity of patients consistently on PEEP <2 cm H2O, and lack of a gold standard for PEEP settings in this population limit interpretation.

Other non-ARDS or nonsurgical patients — Most clinicians initiate PEEP in non-ARDS and nonsurgical patients at 3 to 5 cm H20, although limited data suggest that routine use of a higher level of PEEP (eg, 5 to 8 cm H2O) may prevent VAP or reduce the likelihood of developing hypoxemia [9]. As an example, a meta-analysis of 24 trials compared higher PEEP with lower PEEP strategies in 2307 mechanically ventilated patients without ARDS [7]. High PEEP decreased the incidence of hypoxemia and increased the PaO2/fraction of inspired oxygen (FiO2) ratio, without an impact on mortality.

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].

Relative contraindications — There are no absolute contraindications to extrinsic PEEP. However, extrinsic 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 due to hypovolemia or pulmonary embolism, dynamic hyperinflation without airflow limitation, pronation, or a bronchopleural fistula.

Intracranial disease — The absolute effect of PEEP on cerebral perfusion pressure (CPP) is uncertain. In theory, increased intrathoracic pressure due to extrinsic PEEP may decrease cerebral venous outflow, leading to increased intracranial pressure (ICP), decreased mean arterial pressure (MAP), or both. The result may be decreased CPP and neurologic deterioration.

However, data are conflicting as to whether this actually occurs during PEEP application. Given the uncertainty, it is reasonable to monitor both the MAP and ICP (if feasible) when PEEP is applied. PEEP should be reduced if the MAP decreases or ICP increases. (See "Evaluation and management of elevated intracranial pressure in adults".)

Data describing the impact of PEEP on ICP are limited. Observational studies in patients who had acute stroke or acute subarachnoid hemorrhage found that increases in extrinsic PEEP were associated with diminished CPP due to decreased MAP [10,11]. In contrast, another observational study in patients with traumatic brain injury found that extrinsic PEEP increased CPP due to decreased ICP [12]. While uncertain, the conflicting outcomes may be due to differences in the underlying intracranial abnormalities.

Unilateral or focal lung disease — Extrinsic PEEP can worsen hypoxemia in patients with focal lung disease (eg, lobar pneumonia). This probably occurs because an excess of extrinsic PEEP compresses intra-alveolar capillaries in the uninvolved lung, thereby diverting blood flow to the injured lung, worsening ventilation/perfusion (V/Q) mismatch (figure 1), and precipitating shunt [13]. The concepts of V/Q mismatch and shunt are discussed separately. (See "Measures of oxygenation and mechanisms of hypoxemia", section on 'Ventilation-perfusion mismatch'.)

We suspect this adverse effect when oxygenation decreases following an increase in extrinsic PEEP. When suspected, we decrease PEEP. If hypoxemia persists, we position the patient in a decubitus position with the uninvolved lung down to improve V/Q matching.

Hypotension due to hypovolemia or right ventricular dysfunction — Positive pressure ventilation increases intrathoracic pressure, which can decrease venous return, reduce cardiac output, and cause hypotension [14]. This process is exacerbated by extrinsic PEEP, especially when patients have hypovolemia, hemodynamically significant pulmonary embolism, or right ventricular (RV) failure (eg, RV infarction, pulmonary hypertension).

When present, this phenomenon will result in a fall in central venous oxyhemoglobin saturation when PEEP is increased; this finding can assist in diagnosis.

In hypovolemic patients, we administer fluids to improve RV preload and offset this effect. Helpful strategies for those with RV failure include minimizing PEEP to maintain oxygenation and reducing RV afterload with inhaled pulmonary vasodilators. In patients with RV failure, small fluid boluses (eg, 250 to 500 mL) may be appropriate.

In euvolemic patients, extrinsic PEEP up to 20 cm H2O is generally well tolerated [15]. In a study of eight euvolemic patients with ARDS, increasing PEEP from 10 to 20 cm H2O caused hypotension in only one patient while cardiac output and systemic hypoperfusion were unchanged in the remaining seven patients. Whether this applies to non-ARDS patients is unclear. (See "Clinical and physiologic complications of mechanical ventilation: Overview", section on 'Hypotension'.)

Countering intrinsic PEEP in those without airflow limitation — Applying excess PEEP to counter intrinsic PEEP in the absence of airflow limitation can worsen hyperinflation and alveolar pressure, increasing the risk of complications, such as pulmonary barotrauma or hypotension. This is discussed in more detail below. (See 'Increasing applied PEEP in patients with airway disease' below.)

Bronchopleural fistula — Extrinsic PEEP may prevent healing in patients with a bronchopleural fistula (BP). In addition, large BP fistulas also rapidly dissipate PEEP, making it problematic to use this modality in this setting. (See "Bronchopleural fistula in adults", section on 'General supportive care' and "Diagnosis, management, and prevention of pulmonary barotrauma during invasive mechanical ventilation in adults", section on 'Ventilator management'.)

Tools for titrating extrinsic PEEP (in ARDS) — PEEP titration is critical for managing patients with ARDS. Most experts use a strategy that improves outcomes [16] and titrates oxygen according to the patient's oxygenation (table 1). (See "Acute respiratory distress syndrome: Ventilator management strategies for adults", section on 'Positive end-expiratory pressure (PEEP), fraction of inspired oxygen, oxygenation target'.)

Several additional tools are available. However, most are not routinely used since they do not improve outcomes compared with PEEP titration (table 1):

●Esophageal pressure (PES) – PES is an estimate of pleural pressure, which can be used to titrate PEEP. While this strategy improves oxygenation, it does not improve patient-important outcomes, is inconvenient and costly, and requires expertise for interpretation [16,17]. However, in centers that have the equipment and expertise, PES-guided PEEP may be used when 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, significant obesity, chest wall deformities, or large pleural effusion).

PES 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 is then adjusted by titrating extrinsic PEEP. Titrating 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 [18].

PES-guided PEEP titration has been studied in two major trials:

•EPvent – An initial trial (EPvent) randomly assigned 61 patients with ARDS to FiO2 and PEEP adjustment using either PES or a standard titration approach (table 1)[18]. 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. PES-guided PEEP titration was associated with improved oxygenation. There was also a nonsignificant improvement in mortality, although the study was likely underpowered.

•EPvent-2 – In a 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') [19]. The goal 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 or 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). The rate of barotrauma was similar between the groups (5 versus 6 percent).

●Pressure-volume (PV) curves – PV curves can be measured manually at the bedside. However, their use has fallen out of favor since they require an esophageal balloon, are cumbersome, and have limited data to support their routine use. PV curves may also be obtained from ventilator waveform tracings, but have not been shown to impact outcome in clinical trials.

In many patients with ARDS, PV curves have two inflection points (figure 2). 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. However, the lower inflection point cannot be identified in some patients and neuromuscular blockade or apneic-level sedation is generally required to construct an accurate curve [20,21].

●Lung compliance – Compliance is defined as the change in lung volume per unit change in pressure and is the slope of the PV curve (figure 2). Similar to titration using the PV curve, selecting a PEEP that maximizes compliance should avoid both atelectasis and overdistension. Typically, static rather than dynamic compliance measurements (using an inspiratory pause) are used. Allowing time for lung recruitment between measurements may improve their accuracy. Titration with this method may improve the PaO2/FiO2 ratio compared with titration to oxygenation, but has not been shown to definitively impact outcomes in ARDS [22].

●Lung ultrasound – Lung ultrasound can directly visualize the effects of extrinsic PEEP on lung aeration [23]. Additional experience and outcome data are necessary before routine use.

●Oxygen delivery (DO2) – Extrinsic PEEP can be titrated to target maximum DO2. This method involves calculating the DO2 at each level of applied PEEP, then using the PEEP that corresponds with the best DO2 for ongoing mechanical ventilation. However, this method has fallen out of favor since the calculation of DO2 requires a pulmonary artery catheter, which is no longer routinely placed in ventilated patients. Calculation of DO2 is discussed separately. (See "Oxygen delivery and consumption".)

●Electrical impedance tomography (EIT) – EIT is a noninvasive imaging technique that provides real-time regional lung information to guide PEEP titration [24,25]. One meta-analysis demonstrated that EIT-guided PEEP titration resulted in improved lung compliance and lowered driving pressure compared with other methods [24]. The impact on clinically meaningful outcomes is unknown. Further studies are required before EIT can be routinely used to guide PEEP titration.

INTRINSIC (AUTO) PEEP

Definition and physiology — Intrinsic PEEP (auto-PEEP) exists when incomplete expiration occurs prior to the initiation of the next breath. The accumulation of air increases alveolar pressure at the end of expiration. Because air accumulates in the lung with each breath, progressive hyperinflation ensues, which is termed dynamic hyperinflation (DHI) or "breath stacking" (figure 3). In the absence of acute barotrauma, a new equilibrium is achieved with substantially higher lung volumes and airway pressures. In pressure modes, breath stacking will lead to reduced tidal volumes (VT) as end-expiratory volumes and airway pressures increase.

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

Potential sequelae — The complications of intrinsic PEEP include the following:

●Cardiovascular compromise – Intrinsic PEEP increases intrathoracic pressure, which can decrease venous return, reduce cardiac output, and cause hypotension. If severe, progressive cardiovascular collapse culminating in cardiac arrest with pulseless electrical activity may occur [26]. Intravascular volume depletion and sedatives can accelerate the deterioration. (See "Clinical and physiologic complications of mechanical ventilation: Overview", section on 'Hypotension'.)

●Barotrauma and lung injury – Intrinsic PEEP can cause alveolar overdistension, risking pulmonary barotrauma and ventilator-induced lung injury. Alveolar overdistension can also cause hypoxemia if ventilation/perfusion 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".)

●Increased work of breathing (WOB) – Intrinsic PEEP increases the work required for a patient to trigger a ventilator breath. The patient must generate enough negative pressure to overcome the trigger sensitivity (a ventilator setting) plus intrinsic PEEP rather than the trigger sensitivity alone (figure 4 and figure 5).

As an example, a patient whose intrinsic PEEP is 8 cm H2O and the pressure trigger sensitivity is -2 cm H2O needs to generate a pressure of -10 cm H2O to trigger a breath. In contrast, a patient without intrinsic PEEP only needs to generate a pressure of -2 cm H2O to trigger a ventilator breath. This concept applies to flow-triggers as the intrinsic PEEP still needs to be overcome before inspiratory flow can be achieved; however, the increased inspiratory base flow does appear to reduce intrinsic PEEP and decrease WOB to some extent compared with pressure-triggered modes (figure 6) [27]. Inability to trigger breaths may cause patient-ventilator asynchrony, dyspnea, and insufficient ventilation [28]. (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'.)

Evaluating suspected intrinsic PEEP — Intrinsic PEEP should be suspected in patients who develop a rapid breathing rate in association with elevated peak pressures, particularly in patients with underlying obstructive lung diseases, such as asthma and chronic obstructive pulmonary disease (COPD). Hypotension indicates life-threatening intrinsic PEEP and is a worrisome sign.

Detecting intrinsic PEEP — Suspected intrinsic PEEP can be confirmed in several ways:

●Nonquantitative (ventilator graphics) – This is the most common approach used because it is practical and reliable. This method uses ventilator graphics with or without palpation plus auscultation of the chest.

When intrinsic PEEP is present, the flow versus time graph demonstrates initiation of inspiratory flow before the expiration tracing reaches zero flow (figure 7). In addition, auto-PEEP may be seen on ventilator graphics as a progressive rise in peak airway pressures during volume-targeted ventilation (figure 3) [27,29-31]

With palpation and auscultation, inspiratory airflow is heard before the expiratory airflow ceases. Palpation and auscultation can confirm intrinsic PEEP but are unreliable for determining its absence [32].

●Quantitative (airway pressure [Paw]) – Intrinsic PEEP can be estimated by measuring Paw during an expiratory pause. Most ventilators provide a value using the following formula (waveform 1):

Intrinsic PEEP = end-expiratory Paw - applied PEEP

Ideally, intrinsic PEEP should be <10 cm H2O.

However, this method is frequently inaccurate.

•Intrinsic PEEP is only accurate when the patient is paralyzed or exhibiting negligible abdominal and chest wall muscle engagement during exhalation. We do not encourage paralysis for this indication only, but intrinsic PEEP can be measured while the patient is paralyzed for another indication. (See "Neuromuscular blocking agents in critically ill patients: Use, agent selection, administration, and adverse effects", section on 'Clinical use'.)

Expiratory muscle activity in nonparalyzed patients can falsely elevate Paw. This can lead to the inappropriate and potentially harmful treatment of presumed auto-PEEP [33]. To avoid this inaccuracy, we palpate for the absence of expiratory muscle activity prior to measuring the Paw [34,35].

•Also leading to inaccuracy is widespread airway closure in patients with severe bronchospasm, which can falsely lower the Paw [36]. As a result, DHI and intrinsic PEEP may be unrecognized. Patients with severe asthma, high airway pressures, and an elevated respiratory rate should be assumed to have significant hyperinflation. Sedation or neuromuscular blockade may be needed to facilitate a more regulated breathing pattern and more accurate measurements; however, intrinsic PEEP may remain falsely low until bronchospasm is at least partially treated.

Determine the etiology — The three most common situations during which intrinsic PEEP develops are high minute ventilation (Ve), expiratory flow limitation, and increased expiratory resistance. More than one abnormality may be present simultaneously. These etiologies can be determined by examining the patient and the ventilator settings and graphics.

High minute ventilation — High Ve is caused by large VT, a high respiratory rate, or both. Evidence of high Ve can be determined by examining the patient and ventilator settings (eg, set VT, actual inspired and expired volume, set and actual respiratory rate). In some cases, the high Ve is due to underlying disorders (eg, acute respiratory distress syndrome, COPD exacerbation), pain, anxiety or delirium, intracranial pathology, or incorrect ventilator settings (eg, following adjustment after transport).

The mechanism that underlies intrinsic PEEP due to high Ve is the following:

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

●High respiratory rates decrease the duration of expiration. The higher respiratory rate shortens the expiratory time (Te) and reduces the likelihood that full VT exhalation occurs before the onset of the next breath.

Expiratory flow limitation due to airway disease — Expiratory flow limitation (figure 3) exists when expiratory flow is limited by airway narrowing due to airway collapse, bronchospasm, inflammation, or airway remodeling (figure 8). This increases the likelihood that the full VT will not be exhaled before the onset of the next breath. Expiratory flow limitation is not routinely assessed because it requires neuromuscular paralysis, specialized techniques, or both [37,38]. Thus, we rely on clinical examination, clinical judgment, and ventilator graphics to make this assessment. This assessment is described in a separate topic. (See "Assessment of respiratory distress in the mechanically ventilated patient", section on 'Cardiorespiratory stability' and "Assessment of respiratory distress in the mechanically ventilated patient", section on 'An increase in the Ppeak with a widening of the delta Ppeak – Pplat' and "Assessment of respiratory distress in the mechanically ventilated patient", section on 'Maintenance of airway pressure, reduction in tidal volume, and delayed return of expiratory flow'.)

Most patients with COPD and asthma exacerbations have an expiratory flow limitation. Thus, these patients are prone to developing intrinsic PEEP during mechanical ventilation [39]. Ventilator management of such patients is discussed separately. (See "Invasive mechanical ventilation in acute respiratory failure complicating chronic obstructive pulmonary disease" and "Invasive mechanical ventilation in adults with acute exacerbations of asthma".)

Other causes of increased expiratory resistance — Examples of other conditions that increase expiratory resistance include a narrow-diameter or kinked endotracheal tube (ETT), inspissated secretions, ventilatory circuit abnormalities (eg, faulty exhalation or PEEP valves), and patient-ventilator asynchrony [40]. This assessment is discussed separately. (See "Assessment of respiratory distress in the mechanically ventilated patient", section on 'Cardiorespiratory stability' and "Assessment of respiratory distress in the mechanically ventilated patient", section on 'An increase in the Ppeak with a widening of the delta Ppeak – Pplat' and "Assessment of respiratory distress in the mechanically ventilated patient", section on 'Maintenance of airway pressure, reduction in tidal volume, and delayed return of expiratory flow'.)

Treatment — Once identified, we correct intrinsic PEEP (algorithm 1). The initial approach differs depending on whether the presentation is life-threatening (hemodynamically unstable) or stable.

Life-threatening intrinsic PEEP — We suspect life-threatening intrinsic PEEP in an intubated patient with respiratory distress and rising peak pressures in association with acute hypotension.

●When suspected, we immediately disconnect the ETT from the ventilator. This life-saving maneuver is the most effective means of testing for and abolishing hemodynamically significant intrinsic PEEP. Gas escaping from the ETT over several seconds after disconnection may be heard and hypotension typically improves promptly, although may not resolve.

●Most well-sedated patients demonstrate lower airway pressures after reconnection to the ventilator; however, ventilator settings or other treatments must be adjusted within minutes to prevent recurrence. Thus, we proceed with detailed evaluation and targeted management as outlined below. (See 'Non-life-threatening intrinsic PEEP' below.)

Initial evaluation and management of the unstable ventilated patient with respiratory distress are discussed in detail separately. (See "Assessment of respiratory distress in the mechanically ventilated patient", section on 'Cardiorespiratory instability'.)

Non-life-threatening intrinsic PEEP — We treat intrinsic PEEP by simultaneously correcting likely underlying causes and making ventilator adjustments.

Addressing reversible etiologies — Initial efforts should focus on identifying and treating underlying reversible conditions contributing to intrinsic PEEP.

●High Ve associated with patient respiratory efforts – For patients with high Ve, we treat the presumed cause (eg, pain, anxiety or delirium, too awake). (See "Sedative-analgesia in ventilated adults: Management strategies, agent selection, monitoring, and withdrawal".)

If the reason for the high ventilation is unclear or not reversible (eg, inoperable intracranial or other pathology), we sometimes sedate the patient to meet ventilator-set parameters. (See "Sedative-analgesia in ventilated adults: Management strategies, agent selection, monitoring, and withdrawal".)

●Bronchospasm – We typically treat patients with airflow limitation due to bronchospasm with inhaled or nebulized bronchodilators and glucocorticoids. (See "Acute exacerbations of asthma in adults: Emergency department and inpatient management" and "COPD exacerbations: Management".)

●Extrinsic or occlusive airway obstruction – For patients with other forms of obstruction not necessarily associated with airway disease (eg, mucus impaction, secretions, kinked ETT, faulty ventilatory circuit components), we address each etiology (eg, aggressive suctioning [including bronchoscope-directed suctioning, if required], ETT replacement, ventilatory circuit change). (See "Assessment of respiratory distress in the mechanically ventilated patient".)

●Hypovolemia – When hypovolemia is suspected as an exacerbating factor, we administer intravenous fluids. (See "Treatment of severe hypovolemia or hypovolemic shock in adults".)

Initial ventilator adjustments — The main determinants of intrinsic PEEP are Ve and Te. The initial ventilator strategy to reduce intrinsic PEEP is to decrease total Ve followed by prolonging Te [30,41]. We generally make these adjustments at the bedside and monitor the effects in real time.

When adjusting the ventilator settings, we aim for a decreased but adequate Ve to target a pH ≥7.2, an inspiratory plateau pressure <30 cm H2O, and an intrinsic PEEP <10 cm H2O.

Reducing respiratory rate and tidal volume — In patients with auto-PEEP, we reduce Ve. This is achieved through a reduction in respiratory rate (often done first) and/or VT (ie, the determinants of Ve).

Reducing respiratory rate also prolongs Te, and therefore has a robust effect on intrinsic PEEP. Calculating a target Ve using a newly reduced rate and volume helps make this strategy effective (eg, 8 to 10 L/minute).

The strategies of decreasing the respiratory rate and VT can lead to respiratory acidosis. However, permissive hypercapnia is acceptable, provided the arterial pH does not fall much below 7.2 or lead to hemodynamic instability. The effects of respiratory acidosis are generally better tolerated than the consequences of barotrauma from auto-PEEP. The indications, contraindications, and technique of permissive hypercapnia and management of barotrauma are discussed separately. (See "Permissive hypercapnia during mechanical ventilation in adults" and "Diagnosis, management, and prevention of pulmonary barotrauma during invasive mechanical ventilation in adults".)

Reduce inspiratory time — In most patients with intrinsic PEEP, we also prolong Te by raising the inspiratory flow rate to shorten inspiratory time (Ti) (figure 9). Ensuring that the patient's intrinsic Ti closely matches the duration of the tidal breath delivered by the ventilator may decrease ineffective triggering and WOB [42,43].

Reducing Ti is typically less effective than adjusting respiratory rate or VT for several reasons, which should be monitored at the bedside. As examples:

●In patients with bronchial hyperresponsiveness, increased inspiratory flow may trigger bronchoconstriction.

●In patients with airway diseases, inspiratory flow may be limited by high airway resistance, leading to elevated peak airway pressures.

●At lower levels of Ve (eg, <10 L/minute), some evidence suggests that increasing the inspiratory flow rate has less of an ameliorative effect on DHI than at higher levels [44].

●Increasing inspiratory flow may lead to an increase in the spontaneous respiratory rate and thus not achieve a decrease in DHI [45].

Persistent intrinsic PEEP — For patients in whom initial treatments and ventilator adjustments fail to correct intrinsic PEEP, additional measures are needed. These include increasing trigger sensitivity and, in patients with airflow limitation due to airway disease, the application of extrinsic PEEP [44-46]. We generally make these adjustments at the bedside and monitor the effects in real time.

Optimizing inspiratory trigger sensitivity — For nonparalyzed patients with persistent intrinsic PEEP, increasing the sensitivity of the inspiratory trigger may reduce ineffective triggering and lower WOB [42,47-49]. While optimizing triggering decreases WOB to a small degree for any patient on the ventilator, the excess work to trigger inspiration is typically unimportant in those without intrinsic PEEP.

In patients with COPD, WOB can typically be reduced by switching to a flow trigger (if not already performed) and adjusting the trigger sensitivity to the lowest level needed to initiate a breath without false-triggering and overventilation (also known as "auto-cycling") (figure 6) [27,50-52]. We typically trial settings of 0.7 to 1 L/minute. (See "Invasive mechanical ventilation in acute respiratory failure complicating chronic obstructive pulmonary disease", section on 'Trigger sensitivity'.)

Increasing applied PEEP in patients with airway disease — For nonparalyzed patients with persistent intrinsic PEEP and airway disease leading to expiratory airflow limitation (eg, asthma, COPD, bronchiectasis, cystic fibrosis), we suggest applying extrinsic PEEP to reduce WOB (figure 10 and figure 11 and figure 5). Extrinsic PEEP reduces the work required to trigger a breath in the setting of intrinsic PEEP and may also improve gas exchange. In patients without diffuse airway disease, the extrinsic PEEP may increase alveolar pressure and risk of barotrauma or hemodynamic compromise. Effective levels of extrinsic PEEP should lead to minimal increases in airway pressures (in volume modes) or reductions in VT (in pressure modes). (See 'Expiratory flow limitation due to airway disease' above.)

●Typical settings – Extrinsic PEEP should not exceed 80 percent of the measured intrinsic PEEP to avoid worsening DHI (figure 11) [53,54]. However, given the potential inaccuracy of intrinsic PEEP measurements, we typically apply PEEP to <50 percent of the measured intrinsic PEEP [55]. Significant increases in airway pressures (or fall in VT in pressure modes) after applying PEEP suggest exacerbation of hyperinflation rather than improvement and should prompt decreasing the amount of PEEP applied (See 'Detecting intrinsic PEEP' above.)

●Mechanism – In mechanically ventilated patients with COPD, extrinsic PEEP has been shown to decrease WOB and improve patient-ventilator synchrony (figure 10 and figure 11), although it may not decrease DHI [31,55-58]. As an example, a patient whose intrinsic PEEP is 8 cm H2O and whose ventilator has a trigger sensitivity of -2 cm H2O needs to generate a pressure of -10 cm H2O to trigger a breath. Extrinsic PEEP reduces this gradient and therefore the work required to trigger the next breath. Extrinsic PEEP may also improve gas exchange by opening the small airways in the dependent lung zones and distributing inspired gas more homogeneously [59-61].

●Avoidance in those without airway disease – Extrinsic PEEP should not be used to counter intrinsic PEEP in patients who do not have an expiratory flow limitation due to an airway disease. The risk of increasing alveolar pressure and subsequent risk of both barotrauma and hemodynamic compromise are significantly higher in this setting than in those with airway diseases [62].

When extrinsic causes of increased expiratory resistance result in intrinsic PEEP, the source of increased resistance should be identified and corrected. This may require sedation, pharmacologic paralysis, or replacement of the ETT or ventilator tubing. (See 'Other causes of increased expiratory resistance' above.)

SUMMARY AND RECOMMENDATIONS

●Definition – Positive end-expiratory pressure (PEEP) is the alveolar pressure above atmospheric pressure that exists at the end of expiration. (See 'Definition' above.)

●Extrinsic PEEP – PEEP that is applied through a mechanical ventilator is referred to as extrinsic or applied PEEP. The optimal level of extrinsic PEEP in most populations is unknown. In general, the following applies (see 'Indications' above):

•In most mechanically ventilated patients, a small amount of extrinsic PEEP (3 to 5 cm H2O) is used to mitigate end-expiratory alveolar collapse. (See 'Routine application' above.)

•In patients with hypoxemic respiratory failure, a higher level of extrinsic PEEP (>5 cm H2O) is sometimes used to improve hypoxemia or reduce ventilator-induced lung injury and, when expiratory airflow limitation is present, offset the effects of intrinsic PEEP. (See 'Acute respiratory distress syndrome' above and 'Cardiogenic pulmonary edema' above.)

•There are no absolute contraindications to extrinsic PEEP. However, extrinsic PEEP should be used cautiously in patients with intracranial abnormalities, unilateral or focal lung disease, hypotension due to hypovolemia or right ventricular dysfunction, dynamic hyperinflation (DHI) without airflow limitation, or a bronchopleural fistula. (See 'Relative contraindications' above.)

•In acute respiratory distress syndrome, several tools are available to titrate PEEP. However, most clinicians titrate to hypoxemia using the strategy outlined in the table (table 1) since this strategy has been associated with improved outcomes. (See 'Tools for titrating extrinsic PEEP (in ARDS)' above.)

●Intrinsic PEEP physiology and evaluation – Intrinsic PEEP (also known as auto-PEEP) exists when incomplete expiration occurs prior to the initiation of the next breath. The accumulation of air increases alveolar pressure at the end of expiration. Because air accumulates in the lung with each breath, progressive hyperinflation ensues, which is termed DHI or "breath stacking" (figure 3).

•Intrinsic PEEP can cause cardiovascular collapse, barotrauma, lung injury, and increase the work of breathing (WOB). (See 'Potential sequelae' above.)

•Intrinsic PEEP should be suspected in patients who develop a rapid breathing rate in association with elevated peak pressures with or without hypotension, particularly in patients with underlying obstructive lung diseases, such as asthma and chronic obstructive pulmonary disease.

•Intrinsic PEEP can be detected using ventilator-generated flow versus time graphs (figure 7 and figure 3). It can be quantitated by measuring the end-expiratory airway pressure during an expiratory pause and then subtracting the extrinsic PEEP. However, it requires paralysis for accurate determination. (See 'Evaluating suspected intrinsic PEEP' above.)

●Intrinsic PEEP treatment – Steps should be taken to correct intrinsic PEEP as soon as it is identified (algorithm 1). (See 'Treatment' above.)

•Those with hypotension should undergo immediate disconnection of the endotracheal tube from the ventilator. This potentially life-saving maneuver is diagnostic and therapeutic. Treatment of reversible causes and adjustment of ventilator settings must be performed immediately after reconnection to prevent recurrence. (See 'Life-threatening intrinsic PEEP' above.)

•Reversible causes of high minute ventilation (Ve) and expiratory resistance should be promptly diagnosed and treated. (See 'Addressing reversible etiologies' above and 'Determine the etiology' above.)

•Ventilator management of significant intrinsic PEEP includes reducing respiratory rate, reducing tidal volumes (VT), and, if needed, further prolonging expiratory time by increasing inspiratory flow. We typically adjust settings to achieve a decreased but adequate Ve (pH ≥7.2), an inspiratory plateau pressure <30 cm H2O, and (if accurately measurable) an intrinsic PEEP <10 cm H2O. (See 'Initial ventilator adjustments' above.)

●Improving WOB for persistent intrinsic PEEP – For nonparalyzed patients with persistent intrinsic PEEP despite the above measures, additional ventilator adjustments may decrease WOB. (See 'Persistent intrinsic PEEP' above.)

•Patients with increased WOB due to intrinsic PEEP require optimization of their trigger sensitivity to decrease inspiratory work. A flow trigger of 0.7 to 1 L/minute is often effective.

•For nonparalyzed patients with persistent intrinsic PEEP due to airway disease, we suggest increasing extrinsic PEEP by 50 percent of the measured intrinsic PEEP (Grade 2C). Significantly increased airway pressures or falling VT with this intervention indicate worsening hyperinflation and require decreasing extrinsic PEEP. (See 'Increasing applied PEEP in patients with airway disease' above.)

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Topic 1642 Version 29.0

References

1 : Physiologic PEEP

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

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

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

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

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

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 : 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.

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

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

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

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

14 : Cardiovascular issues in respiratory care.

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

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

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

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

19 : 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.

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

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

22 : Individualized PEEP setting in subjects with ARDS: a randomized controlled pilot study.

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

24 : Electrical impedance tomography-guided positive end-expiratory pressure titration in ARDS: a systematic review and meta-analysis.

25 : Personalized positive end-expiratory pressure in spontaneously breathing patients with acute respiratory distress syndrome by simultaneous electrical impedance tomography and transpulmonary pressure monitoring: a randomized crossover trial.

26 : Circulatory arrest induced by intermittent positive pressure ventilation in a patient with severe asthma.

27 : Inspiratory effort and measurement of dynamic intrinsic PEEP in COPD patients: effects of ventilator triggering systems.

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

29 : Novel aspects of pulmonary mechanics in intensive care.

30 : Determinants of dynamic hyperinflation in a bench model.

31 : Continuous positive airway pressure reduces work of breathing and dyspnea during weaning from mechanical ventilation in severe chronic obstructive pulmonary disease.

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

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

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

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

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

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

38 : Detection of expiratory flow limitation during mechanical ventilation.

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

40 : Expiratory asynchrony.

41 : The effects of ventilatory pattern on hyperinflation, airway pressures, and circulation in mechanical ventilation of patients with severe air-flow obstruction.

42 : Optimization of respiratory muscle relaxation during mechanical ventilation.

43 : Cycling of inspiratory and expiratory muscle groups with the ventilator in airflow limitation.

44 : Effect of prolongation of expiratory time on dynamic hyperinflation in mechanically ventilated patients with severe asthma.

45 : Intubation and mechanical ventilation of the asthmatic patient in respiratory failure.

46 : Intubation and mechanical ventilation of the asthmatic patient in respiratory failure.

47 : Regulation of inspiratory neuromuscular output during synchronized intermittent mechanical ventilation.

48 : Patient-ventilator interaction.

49 : The inspiratory workload of patient-initiated mechanical ventilation.

50 : Flow-triggering reduces inspiratory effort during weaning from mechanical ventilation.

51 : Inspiratory muscle work of breathing during flow-by, demand-flow, and continuous-flow systems in patients with chronic obstructive pulmonary disease.

52 : 2019 Year in Review: Patient-Ventilator Synchrony.

53 : Mechanical ventilation of the patient with severe chronic obstructive pulmonary disease.

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

55 : Physiologic effects of positive end-expiratory pressure in patients with chronic obstructive pulmonary disease during acute ventilatory failure and controlled 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 : Should PEEP be used in airflow obstruction?