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StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-.

StatPearls [Internet].

Show detailsTreasure Island (FL): StatPearls Publishing; 2025 Jan-.Search term Positive End-Expiratory Pressure

Alexandra Levine; Jorge I. Mora.

Author Information and Affiliations

Authors

Alexandra Levine1; Jorge I. Mora2.

Affiliations

1 Orlando Health - Orlando Regional Medical Center2 University of Pennsylvania

Last Update: September 14, 2025.

Continuing Education Activity

Positive end-expiratory pressure (PEEP) is a fundamental component of mechanical ventilation used to maintain alveolar patency at the end of expiration, thereby improving oxygenation and reducing the risk of atelectrauma. PEEP is essential in managing acute respiratory distress syndrome, cardiogenic pulmonary edema, and perioperative or postoperative atelectasis. By maintaining positive pressure in the lungs, PEEP enhances functional residual capacity, decreases intrapulmonary shunting, and contributes to improved ventilation-perfusion matching. However, inappropriate application of PEEP may lead to complications such as barotrauma, volutrauma, or compromised hemodynamics due to increased intrathoracic pressure. Optimal PEEP levels vary depending on the patient’s clinical condition and require careful titration. Advanced imaging, arterial blood gases, lung mechanics, and hemodynamic monitoring guide individualized therapy. PEEP is widely used in invasive and noninvasive ventilation strategies in emergency, critical care, and perioperative settings, making its correct implementation vital to improving patient outcomes.

This educational activity enhances clinician competence in understanding the physiologic principles of PEEP and its role in mechanical ventilation management. Participants gain knowledge of current evidence-based approaches to PEEP titration, including strategies for assessing pulmonary mechanics and minimizing ventilator-induced lung injury. Emphasis is placed on identifying appropriate indications and contraindications for PEEP, managing its complications, and applying it effectively across various clinical settings, from acute respiratory failure to chronic ventilatory support. The activity reinforces the value of collaborative decision-making among interprofessional team members such as respiratory therapists, nurses, intensivists, and emergency clinicians to ensure coordinated care, continuous monitoring, and prompt intervention. Effective teamwork improves ventilator management, patient safety, and overall clinical outcomes.

Objectives:

• Identify the physiological principles and clinical indications for using positive end-expiratory pressure in patients who are ventilated.
• Evaluate the potential benefits and complications associated with varying levels of positive end-expiratory pressure in the treatment of acute respiratory failure and the acute respiratory distress syndrome.
• Apply principles of individualized positive end-expiratory pressure treatment for patients with heterogeneous lung pathology, including those with invasive and non-invasive ventilation, such as acute respiratory distress syndrome, chronic obstructive pulmonary disease, or other respiratory conditions. 
• Apply effective communication strategies among the interprofessional healthcare team, including clinicians, respiratory therapists, and nurses, to optimize positive end-expiratory pressure management and improve patient outcomes.

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Introduction

Positive end-expiratory pressure (PEEP) is the positive pressure that remains in the airways at the end of the respiratory cycle (eg, the end of exhalation) and is greater than the atmospheric pressure in patients on mechanical ventilation [1]. PEEP can be classified as extrinsic (applied PEEP), delivered by the ventilator to prevent alveolar collapse, or intrinsic (auto-PEEP), which occurs when incomplete exhalation leads to air trapping. Auto-PEEP may develop in obstructive lung disease, during high respiratory rates, or with excessive tidal volumes, and can complicate mechanical ventilation by increasing work of breathing and impairing hemodynamics. In noninvasive ventilation, an analogous setting is expiratory positive airway pressure (EPAP) in bilevel positive airway pressure modes. Continuous positive airway pressure (CPAP) is not synonymous with PEEP but delivers a constant positive pressure throughout the respiratory cycle; during exhalation, this functions similarly to applied PEEP by maintaining end-expiratory lung volume [[2], [3]]. Recent literature emphasizes that PEEP selection should be individualized based on lung mechanics, oxygenation targets, and patient-specific factors, rather than applied as a fixed value [[2],[3] [4]. In acute respiratory distress syndrome (ARDS), guidelines conditionally recommend higher PEEP strategies in moderate-to-severe disease, supported by physiologic monitoring methods such as driving pressure, compliance curves, and electrical impedance tomography to balance alveolar recruitment against the risk of overdistension [[2],[4],[5],[6]].

Function

Extrinsic PEEP is a ventilator setting that can increase oxygenation. According to Henry’s law, the solubility of a gas in a liquid is directly proportional to the pressure of that gas above the solution’s surface. Thus, increasing PEEP will increase the pressure within the mechanical or noninvasive ventilation system. This external pressure increases oxygen solubility, allowing it to cross the alveolocapillary membrane more easily, increasing the blood’s oxygen content.

PEEP is applied to prevent end-expiratory collapse during passive exhalation. Applying positive pressure inside the airways can open airways that may otherwise collapse, decreasing atelectasis, improving alveolar ventilation, and, in turn, decreasing ventilation/perfusion mismatch [7]. The application of extrinsic PEEP will have a direct impact on oxygenation and an indirect impact on ventilation. The alveolar surface increases by dilating airways, creating more areas for gas exchange and improving ventilation. Nevertheless, extrinsic PEEP should never be used for the sole purpose of increasing ventilation. If carbon dioxide (CO2) is decreased by improving ventilation, pressure support with either bilevel positive airway pressure or invasive ventilation is more appropriate. Selecting and titrating a specific level, especially for patients with ARDS remains challenging despite extensive research on the subject, with current guidelines suggesting higher PEEP strategies in moderate–severe ARDS but emphasizing individualization [[8],[2]]. Furthermore, there is no clear evidence-based guidance regarding initial PEEP settings or how to titrate them early in the course of the illness [[8], [2]]. Many clinicians try a “one-size-fits-all” approach; however, individualized PEEP titration using methods such as driving pressure, compliance, or electrical impedance tomography may offer greater benefit, particularly when tailored to lung injury severity and oxygenation needs [[3], [4]].

Extrinsic PEEP also significantly decreases breathing work [[2], [9]]. In intubated individuals with low lung compliance, breathing can represent up to 30% of total energy expenditure. This increased energy expenditure leads to higher CO2 and lactate production, which can cause acid-base abnormalities. By decreasing the work of breathing, CO2 and lactate production decrease, reducing the need for high minute ventilation (to correct the hypercapnia and acidosis) and thereby decreasing respiratory drive and further decreasing the work of breathing in a positive-feedback loop. Recent physiologic studies confirm that PEEP can also reduce inspiratory effort and mitigate patient self-inflicted lung injury during assisted ventilation [[6]]. Routine application of small amounts of extrinsic 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 lung volumes and alveolar collapse.

Issues of Concern

The use of extrinsic PEEP can also cause several physiologic and clinical complications. Normal respiratory physiology functions as a negative-pressure system. When the diaphragm contracts during inspiration, intrathoracic negative pressure is generated, creating a gradient that draws air into the lungs. This same negative intrathoracic pressure decreases the right atrial (RA) pressure and generates negative pressure on the inferior vena cava, increasing venous return.

The application of extrinsic PEEP changes this physiology. The positive pressure generated by the ventilator or bilevel positive airway pressure is transmitted to the upper airways and ultimately to the alveoli, increasing intrapulmonary and intrathoracic pressure. As a result, RA pressure increases and venous return decreases, reducing preload. The result is a double effect on reduced cardiac output. Lower residual volume means less blood reaches the left ventricle, decreasing cardiac output. The reduced preload positions the heart to work at a less efficient point on the Frank-Starling curve, further reducing cardiac output. The decreased cardiac output decreases mean arterial pressure unless there is a compensatory response of increased systemic vascular resistance. If distributive shock is present (septic, neurogenic, or anaphylactic), systemic vascular resistance is low, worsening the decrease in mean arterial pressure. Extrinsic PEEP would reduce preload and lower the mean arterial pressure further. 

Decreased RA pressure and venous return may benefit patients with cardiogenic pulmonary edema and volume overload. The left ventricle may be overdistended and operating at a less optimal point on the Frank-Starling curve. Decreasing vascular resistance will decrease preload and allow the left ventricle to function more efficiently, thereby increasing cardiac output and improving pulmonary edema. Notably, higher PEEP does not directly improve left ventricular function.[10] Conversely, decreased vascular resistance to the right ventricle reduces pulmonary pressure, reducing pulmonary edema. 

In patients with stroke or subarachnoid hemorrhage, maintaining cerebral perfusion pressure through the effect of extrinsic PEEP on cardiac output and mean arterial pressure is significant. Although PEEP does not directly affect cerebral perfusion pressure, cerebral autoregulation will compensate for changes in mean arterial pressure. If cerebrovascular autoregulation is compromised, a decrease in mean arterial pressure can lead to adverse outcomes.[11]

Extrinsic PEEP can also induce harmful barotrauma, especially in stiff lungs, by increasing plateau pressures. Extrinsic PEEP can also interfere with hemodynamic measurements of right heart catheters. PEEP can affect the geometry and function of the diaphragm by remodeling the muscle fibers due to increased end-expiratory lung volumes.[12] This remodeling reduces muscle length and increases atrophy resulting from the loss of sarcomeres. This longitudinal atrophy is considered an adaptive response of muscles to restore their optimal length for force generation. During ventilator weaning, the rapid release of PEEP upon extubation quickly decreases end-expiratory lung volumes, stretching the adapted, longitudinally atrophied diaphragm fibers to excessive lengths, impairing contraction.[12]  

Patients with chronic obstructive pulmonary disease (COPD) on mechanical ventilation have both intrinsic and extrinsic PEEP, complicating ventilator management. Dynamic hyperinflation and the development of intrinsic PEEP are commonly observed in patients with COPD and acute respiratory failure.[12] Hyperinflation is a progressive (dynamic) because air accumulates in the lungs with each breath due to incomplete exhalation before the next breath. Airflow obstruction secondary to bronchoconstriction, combined with increased minute ventilation (increased respiratory rate and tidal volume) delivered by the ventilator, creates elevated levels of intrinsic PEEP. Patient-ventilator dyssynchrony, increased work of breathing, barotrauma, cardiovascular collapse, and potentially even death can result from high levels of intrinsic PEEP. 

Clinical Significance

Extrinsic PEEP requires an understanding of the type of ventilation (eg, nasal intermittent positive pressure versus invasive mechanical ventilation) and the ventilatory mode (assist-control, synchronized intermittent mandatory ventilation, airway pressure release ventilation). The following principles apply to the use of PEEP in all modes of ventilation:

• Begin with the lowest effective PEEP and increase as tolerated based on the patient’s comfort, oxygenation, and hemodynamic status [[2],[3]]. Current guidelines for ARDS emphasize that initial PEEP should be individualized rather than fixed, using physiologic targets such as driving pressure, compliance, or imaging-based recruitment assessment [[2],[4],[5]].
• Monitor plateau pressures consistently to prevent barotrauma; maintain plateau pressure below 30 cm H2O [[2]].
• Monitor mean arterial pressure while increasing or decreasing PEEP to avoid hemodynamic compromise, as high intrathoracic pressures can reduce venous return and cardiac output [[2],[6]].
• Consider effects on vascular resistance in patients with cardiogenic pulmonary edema. PEEP may reduce left ventricular afterload and improve oxygenation, but excessive levels can impair right ventricular function [[3]]. Premature extubation in this setting can worsen pulmonary edema and lead to reintubation.
• In ARDS, the ARDS Network (ARDSnet) PEEP/FiO2 tables remain a reference, but recent ATS recommendations support higher PEEP strategies in moderate-to-severe ARDS when tolerated, avoiding routine recruitment maneuvers unless indicated. Oxygenation goals include PaO2 55–80 mm Hg or SpO2 88–95%, achieved by titrating PEEP and FiO2 [[2]].

Other Issues

Auto-PEEP or Intrinsic PEEP

Intrinsic, or auto-PEEP, is a complication of mechanically ventilated individuals.[13] Under normal conditions, passive exhalation allows for the complete emptying of air until lung pressure equals atmospheric pressure. When mechanically ventilated, the lungs may not completely deflate, leaving air trapped inside at the end of exhalation. The trapped air generates positive pressure, known as intrinsic or auto-PEEP. With each successive respiratory cycle, air trapping increases. Consequently, the intrathoracic pressure increases, compressing the right atrium and decreasing vascular resistance, causing hypotension, high plateau pressure, and barotrauma. The increased air trapping will also reduce the volume of air inhaled, which increases the work of breathing, oxygen consumption, and carbon dioxide production. This imbalance leads to an increased need for ventilation, a higher respiratory rate, and greater auto-PEEP, perpetuating a vicious cycle.

Factors Leading to Auto-PEEP 

• Airway inflammation and mucus plugs generate dynamic airflow obstruction. Increased expiratory effort increases the pressure around the inflamed or obstructed airways, leading to closure around the plugs and alveolar air trapping.
• High lung compliance, as in COPD, predisposes to dynamic airway collapse during forced exhalation.
• High tidal volume ventilation can result in air trapping if some air is retained when the next breath is delivered.
• High respiratory rates result in shortened expiratory time, increasing air trapping.
• Slow inspiratory flow creates a higher inspiratory-to-expiratory time ratio, resulting in shorter exhalation times and air trapping.

Types of Auto-PEEP

Dynamic hyperinflation with intrinsic expiratory flow obstruction

This is the most common cause of auto-PEEP in patients with COPD because alveolar collapse during expiration leads to air trapping. Low-level extrinsic PEEP can help decrease auto-PEEP by keeping the airways open, encouraging complete exhalation. Airway inflammation and mucus plugs also cause dynamic hyperinflation, although extrinsic PEEP is not as beneficial.

Dynamic hyperinflation without airflow obstruction

This occurs when exhalation time is shortened due to a high respiratory rate, low inspiratory flow, or high tidal volume. Extrinsic PEEP would be detrimental in this case, as it would generate backpressure, preventing airflow from the lungs.

Clinical Clues Suggesting Auto-PEEP

• Incomplete return to baseline on the volume-time curve during mechanical ventilation [14]
• Elevated plateau pressure measurements
• Use of accessory muscles during exhalation (indicates active exhalation by the patient) 
• Decreased blood pressure
• Prolonged expiratory phase
• Sign of respiratory distress

Although there are many reasons for respiratory distress in an intubated individual, the presence of a volume curve that does return to 0 before the next breath is delivered is very highly suggestive of auto-PEEP.

Treating Auto-PEEP

Prompt recognition and intervention are critical to avoid complications such as shock and barotrauma. In the most extreme cases of respiratory distress and associated shock, temporarily disconnecting the patient from the ventilator to allow complete exhalation could be life-saving. In less severe cases, several measures can prevent or treat auto-PEEP:

• Decrease the respiratory rate to allow longer expiratory time and lower the inspiratory-to-expiratory ratio to between 1:3 and 1:5.
• Increasing the inspiratory flow rate to 60 to 100 L/min ensures rapid air delivery during inspiration, allowing longer exhalation.
• Use a square waveform for ventilation flow. While this type of delivery is uncomfortable for the patient, it speeds the inspiration process.
• Reduce tidal volume to decrease the time required for complete exhalation. 
• Reduce respiratory demand by decreasing carbon dioxide and lactate production (control fever and pain, ensure adequate sedation, control anxiety, and treat sepsis).
• Minimize flow obstruction by treating bronchoconstriction with bronchodilators and suctioning mucus plugs. Treat airway inflammation with steroids when indicated.[15]

In cases of dynamic flow obstruction, especially in COPD and alveolar collapse, low-level extrinsic PEEP will maintain airway patency and decrease expiratory resistance.[16]  Extrinsic PEEP will reduce the breathing work for patients with COPD by allowing expiration and decreasing auto-PEEP. However, although asthma is also an obstructive condition, extrinsic PEEP is ineffective due to inflammation-driven obstruction rather than airway collapse.

When extrinsic PEEP is applied to conditions without dynamic airflow obstruction, back pressure prevents air from escaping from the lungs. Notably, extrinsic PEEP initially adds to the auto-PEEP, increasing intrathoracic pressure. Extrinsic PEEP should be maintained below 75% to 85% of the auto-PEEP. The effects are measured by checking the static pressures while increasing extrinsic PEEP in small increments. If the static pressures do not increase, extrinsic PEEP may be beneficial.

Enhancing Healthcare Team Outcomes

All healthcare professionals caring for patients receiving mechanical ventilation should be aware of PEEP's indications and potential adverse effects. One clinician, specifically the respiratory therapist or attending clinician, should adjust the ventilator settings. Nurses who care for patients receiving mechanical ventilation should be aware that high PEEP can lead to barotrauma and a decrease in cardiac output. Protocols should be in place to counter these complications. Patients on mechanical ventilation should be monitored daily to assess the need for changes in ventilator settings. 

Review Questions

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References

1.Acosta P, Santisbon E, Varon J. "The use of positive end-expiratory pressure in mechanical ventilation". Crit Care Clin. 2007 Apr;23(2):251-61, x. [PubMed: 17368169]2.Qadir N, Sahetya S, Munshi L, Summers C, Abrams D, Beitler J, Bellani G, Brower RG, Burry L, Chen JT, Hodgson C, Hough CL, Lamontagne F, Law A, Papazian L, Pham T, Rubin E, Siuba M, Telias I, Patolia S, Chaudhuri D, Walkey A, Rochwerg B, Fan E. An Update on Management of Adult Patients with Acute Respiratory Distress Syndrome: An Official American Thoracic Society Clinical Practice Guideline. Am J Respir Crit Care Med. 2024 Jan 01;209(1):24-36. [PMC free article: PMC10870893] [PubMed: 38032683]3.Edginton S, Kruger N, Stelfox HT, Brochard L, Zuege DJ, Gaudet J, Solverson K, Robertson HL, Fiest KM, Niven DJ, Doig CJ, Bagshaw SM, Parhar KKS. Methods for determining optimal positive end-expiratory pressure in patients undergoing invasive mechanical ventilation: a scoping review. Can J Anaesth. 2024 Nov;71(11):1535-1555. [PMC free article: PMC11602853] [PubMed: 39565498]4.Spatenkova V, Mlcek M, Mejstrik A, Cisar L, Kuriscak E. Standard versus individualised positive end-expiratory pressure (PEEP) compared by electrical impedance tomography in neurocritical care: a pilot prospective single centre study. Intensive Care Med Exp. 2024 Aug 05;12(1):67. [PMC free article: PMC11300775] [PubMed: 39103646]5.Kim YJ, Kim BR, Kim HW, Jung JY, Cho HY, Seo JH, Kim WH, Kim HS, Hwangbo S, Yoon HK. Effect of driving pressure-guided positive end-expiratory pressure on postoperative pulmonary complications in patients undergoing laparoscopic or robotic surgery: a randomised controlled trial. Br J Anaesth. 2023 Nov;131(5):955-965. [PubMed: 37679285]6.Widing H, Pellegrini M, Chiodaroli E, Persson P, Hallén K, Perchiazzi G. Positive end-expiratory pressure limits inspiratory effort through modulation of the effort-to-drive ratio: an experimental crossover study. Intensive Care Med Exp. 2024 Feb 05;12(1):10. [PMC free article: PMC10838888] [PubMed: 38311676]7.Rossi A, Santos C, Roca J, Torres A, Félez MA, Rodriguez-Roisin R. Effects of PEEP on VA/Q mismatching in ventilated patients with chronic airflow obstruction. Am J Respir Crit Care Med. 1994 May;149(5):1077-84. [PubMed: 8173744]8.Millington SJ, Cardinal P, Brochard L. Setting and Titrating Positive End-Expiratory Pressure. Chest. 2022 Jun;161(6):1566-1575. [PubMed: 35131298]9.Siuba MT, Bulgarelli L, Duggal A, Cavalcanti AB, Zampieri FG, Rey DA, Lucena WDR, Maia IS, Paisani DM, Laranjeira LN, Neto AS, Deliberato RO. Differential Effect of Positive End-Expiratory Pressure Strategies in Patients With ARDS: A Bayesian Analysis of Clinical Subphenotypes. Chest. 2024 Oct;166(4):754-764. [PMC free article: PMC11489450] [PubMed: 38768777]10.Fellahi JL, Valtier B, Beauchet A, Bourdarias JP, Jardin F. Does positive end-expiratory pressure ventilation improve left ventricular function? A comparative study by transesophageal echocardiography in cardiac and noncardiac patients. Chest. 1998 Aug;114(2):556-62. [PubMed: 9726745]11.Muench E, Bauhuf C, Roth H, Horn P, Phillips M, Marquetant N, Quintel M, Vajkoczy P. Effects of positive end-expiratory pressure on regional cerebral blood flow, intracranial pressure, and brain tissue oxygenation. Crit Care Med. 2005 Oct;33(10):2367-72. [PubMed: 16215394]12.Petrof BJ, Legaré M, Goldberg P, Milic-Emili J, Gottfried SB. Continuous positive airway pressure reduces work of breathing and dyspnea during weaning from mechanical ventilation in severe chronic obstructive pulmonary disease. Am Rev Respir Dis. 1990 Feb;141(2):281-9. [PubMed: 2405757]13.Mughal MM, Culver DA, Minai OA, Arroliga AC. Auto-positive end-expiratory pressure: mechanisms and treatment. Cleve Clin J Med. 2005 Sep;72(9):801-9. [PubMed: 16193827]14.Blanch L, Bernabé F, Lucangelo U. Measurement of air trapping, intrinsic positive end-expiratory pressure, and dynamic hyperinflation in mechanically ventilated patients. Respir Care. 2005 Jan;50(1):110-23; discussion 123-4. [PubMed: 15636649]15.Laghi F, Goyal A. Auto-PEEP in respiratory failure. Minerva Anestesiol. 2012 Feb;78(2):201-21. [PubMed: 21971439]16.Kondili E, Alexopoulou C, Prinianakis G, Xirouchaki N, Georgopoulos D. Pattern of lung emptying and expiratory resistance in mechanically ventilated patients with chronic obstructive pulmonary disease. Intensive Care Med. 2004 Jul;30(7):1311-8. [PubMed: 15054570]

Disclosure: Alexandra Levine declares no relevant financial relationships with ineligible companies.

Disclosure: Jorge Mora declares no relevant financial relationships with ineligible companies.

Copyright © 2025, StatPearls Publishing LLC.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

Bookshelf ID: NBK441904PMID: 28722933 Share

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• Cite this PageLevine A, Mora JI. Positive End-Expiratory Pressure. [Updated 2025 Sep 14]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-.

In this Page

• Continuing Education Activity
• Introduction
• Function
• Issues of Concern
• Clinical Significance
• Other Issues
• Enhancing Healthcare Team Outcomes
• Review Questions
• References

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