• Positive end expiratory pressure (PEEP) is the supra-atmospheric pressure present in the alveoli at the end of expiration.
• During mechanical ventilation, PEEP is generated by valves incorporated into the ventilator or externally applied to the expiratory side of the respiratory circuit.
• PEEP has effects on the pulmonary and cardiovascular systems.
  • Pulmonary: Increases functional residual capacity (FRC) by preventing collapse and contributes to the re-opening of distal airways and alveoli; optimizes ventilation and hence V/Q matching.
  • Cardiac: Decreases venous return to the heart, and diminishes cardiac output. This effect is more pronounced in patients with normal lung compliance and/or hypovolemia.
  • "Best PEEP" is the level of end expiratory pressure required to produce maximal oxygen transport, while maintaining an adequate cardiac output necessary to deliver the arterial oxygen to the peripheral tissues. It represents the point of equilibrium between the effects on the respiratory and cardio-circulatory system.

• "Physiologic PEEP" is present in all spontaneously breathing subjects and is produced by narrowing of the glottis during exhalation. Physiologic PEEP is estimated to be around 3–5 cm H₂O.
• "Extrinsic PEEP" is applied to the airways of patients on ventilator support with the goal of improving oxygenation and respiratory mechanics. Clinicians may select different levels of PEEP depending on a patient's clinical condition, and the respiratory and hemodynamic response to the initial setting.
• PEEP's effects on respiratory function:
  • Stabilizes lung parenchyma by maintaining the patency of distal airways and alveoli especially in the dependent areas of the lung that tend to collapse in patients under general anesthesia. Patent alveoli can be ventilated and participate in oxygenation of pulmonary blood (V/Q matching). This is manifested as an increase in SpO₂, PaO₂, and decrease in intrapulmonary shunt fraction.
  • Increases FRC by contributing to the re-opening of collapsed alveoli
  • Prevents cyclic opening and closing of alveoli during the respiratory cycle. This repeated opening and closing has been associated with alveolar damage and the systemic release of inflammatory mediators. Theoretically, they can contribute to the development of multi-organ failure.
  • Extrinsic PEEP may decrease work of breathing in patients with airway flow limitation on partial respiratory support.
  • Overdistension is associated with decreased lung compliance and increased dead space ventilation.
• PEEP's effects on cardiovascular function:
  • Increases mean airway pressure that gets partially transmitted to the heart and increases the transmural pressure. As a result, this can compromise venous return to the right atrium, and reduce cardiac output. On the contrary, in patients with reduced left ventricle function, PEEP decreases the relative afterload of the LV. LV dysfunction can result in decreased pulmonary volume and compliance. As a result, greater (more negative) inspiratory pressures, and hence transmural pressures, are required to maintain tidal volumes. The addition of PEEP can partially offset this.
  • Alveolar overdistension results in compression of alveolar capillaries and increased pulmonary vascular resistance; this results in increased right ventricular afterload and can impair right ventricular output.
• PEEP's effects on neurologic function:
  • Levels >10 cm H₂O may increase intracranial pressure (ICP) by impeding venous drainage from the brain. Thus, in patients with increased ICP, judicious PEEP titration is recommended, taking into consideration both changes in oxygen delivery to the brain and intracranial compliance.
  • PEEP use with the intent of maintaining positive pressure in the intracranial venous sinuses is a frequently reported practice. However, there is no conclusive evidence to suggest that PEEP alone is sufficient to prevent venous air embolism (VAE) in neurosurgical procedures. In addition, in patients with a patent foramen ovale, it can increase the mean intrathoracic pressures and theoretically favor the entry of an embolus into the left heart.
• PEEP's effects on renal function:
  • If PEEP compromises cardiac output, it can decrease renal perfusion and activate the renin–angiotensin–aldosterone system (RAAS). The RAAS causes an increase in solute and water reabsorption at the glomerular level, and reduced urinary output.

PEEP exerts most of its direct effects at the level of the alveoli and distal bronchi. Atelectasis, however, occurs mostly in the dependent portions of the lungs during general anesthesia or with the use of neuromuscular blockade.

• Atelectasis is considered a pre-inflammatory state, and can serve as a nidus for infection and contribute to pulmonary complications.
• "Intrinsic PEEP": Although the therapeutic effects of physiologic and extrinsic PEEP are often discussed, "intrinsic" PEEP (or auto-PEEP) should also be considered. Intrinsic PEEP is caused by alveolar air trapping secondary to incomplete breath exhalation. This incomplete expiration results in supra-atmospheric alveolar pressure and increased lung volume. There are 3 possible mechanisms leading to the development of intrinsic PEEP:
  • Dynamic hyperinflation, caused by large tidal volumes and high respiratory rate, which does not allow full lung exhalation before the next breath starts.
  • Airway flow limitation, caused by ‘premature’ small airway collapse that is typical of patients with increased closing volumes (e.g., COPD).
  • Increased expiratory resistance, as seen with a kinked endotracheal tube, small diameter endotracheal tube, or airway obstruction by bronchial secretions.
• Extrinsic and intrinsic PEEP can both contribute to barotrauma.

• Obesity: A greater degree of atelectasis occurs during general anesthesia in obese patients. Application of PEEP/CPAP by a face mask should begin prior to induction with the patient in reverse Trendelenburg position. During the case, PEEP at a level of 10 cm H₂O combined with frequent recruitment maneuvers (40–60 cm H₂O for 6–8 seconds) has been shown to be effective. Continue PEEP until extubation and consider CPAP in the PACU.
• Laparoscopic surgery decreases FRC and respiratory compliance by moving the diaphragm cephalad, and causing atelectasis. PEEP alone (at a level of 10 cm H₂O) does not improve oxygenation; however, in combination with frequent recruitment maneuvers and beach chair positioning, PEEP has been shown to improve oxygenation, end expiratory lung volume, and respiratory compliance (3) [B].

Pediatric Considerations

FRC decreases under general anesthesia and paralysis. In infants, who typically have very compliant chest walls, PEEP helps in maintaining the FRC, because it compensates for the prevailing tendency toward alveolar collapse that results from the interaction between the uneven and opposing forces generated by lung elastic recoil (favoring collapse) and by the smaller forces generated by the chest wall (promoting lung expansion). PEEP at levels of 3–6 cm H2O has been shown to increase FRC in ventilated children without respiratory disease. Its effects on increasing FRC is more pronounced in children receiving 100% FiO2 (prevention of reabsorption atelectasis is the likely mechanism). Optimal intraoperative PEEP settings have not been clearly established for children, but likely vary depending on age, comorbidities, and body size.

One lung ventilation: Application of low to moderate levels of PEEP to the dependent lung can improve arterial oxygenation depending upon individual amounts of atelectasis, presence of intrinsic PEEP, and TV settings (4) [A]. PEEP usually improves oxygenation in patients who respond to recruitment maneuvers. Conversely, by increasing mean pressure in the dependent lung, it can shunt blood to the non-dependent and non-ventilated lung, worsening V/Q mismatch.

Prone positioning: Benefits are probably less pronounced, and optimal levels are likely lower than in the same subjects in the supine position. This is due to the different effects on the distribution of ventilation and perfusion as compared to supine subjects, leading to greater V/Q mismatch in prone patients (2) [B].

COPD: These patients are prone to develop intrinsic PEEP and require personalized ventilator management; the I:E ratio should be adjusted to provide a longer expiratory time. A low respiratory rate is also recommended. The application of low levels of extrinsic PEEP (less than intrinsic PEEP) in supported ventilator modes can help alleviate intrinsic PEEP by maintaining the peripheral bronchi open. In particular, during one lung ventilation, these patients tend to develop intrinsic PEEP. The application of extrinsic PEEP may worsen air trapping.

Asthma: Flow limitation and airway inflammation can result in intrinsic PEEP. Thus, as in COPD patients, low respiratory rates and adequate expiratory time should be established. PEEP in controlled, mechanical ventilation may lead to hyperinflation. Conversely, spontaneously breathing patients will have a reduced work of breathing with modest amounts of PEEP.

Acute respiratory distress syndrome (ARDS): PEEP increases oxygenation and improves respiratory mechanics by minimizing the amount of cyclic opening and closing of alveoli (associated with the systemic release of inflammatory markers and multiple organ dysfunction). Current evidence recommends the use of higher levels of PEEP for PaO2:FiO2 levels 200 mm Hg and lower levels of PEEP for PaO2:FiO2 between 201–300 mm Hg. It is recommended that PEEP be increased with FiO2 in a stepwise fashion to maintain end expiratory transpulmonary pressure (Ttp) between 0–10 cm H2O. Ttp can be calculated by subtracting the esophageal pressure (a surrogate of pleural pressure) from airway pressure. Esophageal balloon catheters can be used to measure esophageal pressure (6) [B]. In patients with ARDS, an initial higher level of PEEP (>12 cm H2O) may confer a survival benefit with respect to lower levels (7) [A].

The typical initial setting of PEEP is 5 cm H2O; titration is usually up or down by 2–3 cm H2O while monitoring for changes in: Hemodynamics: Heart rate, BP, and urine output Arterial line (if present): Changes in pulse pressure or stroke volume variation, possibly reversed by volume loading. Oxygenation: Increases in SpO2 saturation and PaO2 on arterial blood gases. ETCO2: Increased values may suggest decreased intrapulmonary shunt or increased cardiac output (improved CO2 delivery for exhalation). Respiration mechanics: A reduced gradient between plateau pressure and end expiratory pressure suggests a PEEP-induced increase in lung recruitment shown by an increase in respiratory compliance. However, high PEEP can cause barotrauma such as pneumothorax or subcutaneous emphysema. Peak and airway pressures must be constantly monitored. FiO2 titration: High FiO2 can result in absorption atelectasis; if possible, titrate FiO2 downward. Intrinsic PEEP is suspected when the expiratory flow waveform fails to return to 0 at the end of expiration. "Best PEEP": Requires concurrent measurements of the cardiac output and PaO2. Outcome studies of PEEP during anesthesia: There is no sufficiently powered study to indicate any improvement in mortality or in pulmonary complications following the use of PEEP. There is, however, data indicating higher PaO2/FiO2 ratios on postoperative day 1 and less atelectasis by CT scan in patients who received PEEP during anesthesia (5) [A]. Contraindications: PEEP should be avoided or used cautiously in patients with the following conditions: Hypotension/hypovolemia Increased ICP Focal pneumonias: PEEP may cause overdistension of alveoli in the healthy lung, causing compression of their capillaries and leading to diversion of blood flow to the affected lung segments, causing hypoxemia. Bronchopleural fistulas: PEEP may lead to overpressurization of the pleural cavity causing a tension pneumothorax. PEEP can also delay healing of a bronchopleural fistula (1) [A].

Lung compliance = Vt/(Ppl - PEEP); Vt = Tidal volume, Ppl = Plateau pressure

• Functional Residual Capacity
• Acute Respiratory Distress Syndrome
• Laparoscopy

Justin C. Shields , MD

andrea Vanucci , MD, DEAA