Corresponding Bundle Element:

Inspiratory plateau pressures maintained < 30 cm H2O for mechanically ventilated patients.

Related Measures

Inspiratory Plateau Pressure Goal

Background:

Patients with sepsis are at increased risk for developing acute respiratory failure, and most patients with severe sepsis and septic shock will require endotracheal intubation and mechanical ventilation. Nearly 50 percent of patients with severe sepsis will develop acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). Patients with lung injury will have bilateral patchy infiltrates on chest x-ray, low paO2:FIO2 ratios (less than 300 for ALI or less than 200 for ARDS), and pulmonary capillary wedge pressure less than 18 cm H20, although this last measure is often clinically not available. 

High tidal volumes that are coupled with high plateau pressures should be avoided in ALI/ARDS. Clinicians should use as a starting point a reduction in tidal volumes over 1 to 2 hours to a “low” tidal volume (6 mL·kg^-1·lean body weight^-1) as a goal in conjunction with the goal of maintaining end-inspiratory plateau pressures of < 30 cm H2O. 

Mortality Reduction:

The largest trial of a volume- and pressure-limited strategy showed a 9 percent decrease of all-cause mortality in patients ventilated with tidal volumes of 6 mL/kg of estimated lean body weight (as opposed to 12 mL/kg) while aiming for a plateau pressure of < 30 cm H2O. [1]

The formal ARDSnet protocol for mechanical ventilation is available at http://www.ardsnet.org/system/files/Ventilator+Protocol+Card.pdf and is encouraged for use in septic patients.

Permissive Hypercapnia:

Hypercapnia (allowing PaCO2 to increase above normal, so-called permissive hypercapnia) can be tolerated in patients with ALI/ARDS if required to minimize plateau pressures and tidal volumes.

Although an acutely elevated PCO2 may have physiologic consequences that include vasodilatation and increased heart rate, blood pressure, and cardiac output, allowing modest hypercapnia in conjunction with limiting tidal volume and minute ventilation has been demonstrated to be safe in small, nonrandomized series. [2,3] No upper limit for PCO2 has been established. Some authorities recommend maintaining pH at > 7.20–7.25, but this has not been prospectively established. The use of hypercarbia is limited in patients with preexisting metabolic acidosis and is contraindicated in patients with increased intracranial pressure. [4] Sodium bicarbonate infusion may be considered in select patients to facilitate use of permissive hypercarbia. [1] Experimental models suggest that respiratory acidosis may confer protection against various forms of inflammatory injury. [6]

Positive End-Expiratory Pressure (PEEP):

Provide adequate supplemental oxygen to maintain a pulse oximetric saturation of > 90 percent. A minimum amount of PEEP should be set to prevent lung collapse at end expiration. Setting PEEP based on severity of oxygenation deficit and guided by the FIO2 required to maintain adequate oxygenation is one acceptable approach.

For patients supported by mechanical ventilation or who are appropriate candidates for a pressurized face mask, PEEP or continuous positive airway pressure may be used to increase mean and end-expiratory airway pressures, allowing the reduction of the oxygen concentrations below potentially toxic levels (FIO2 < 0.60).

Grading the Evidence: [See Ranking the Evidence]

The Grade 1 recommendations below are based on strong evidence for care based on a number of qualitative considerations. “B” level evidence generally derives from randomized control trials with certain limitations or very well-done observational or cohort studies. “C” level evidence reflects well-done observational or cohort studies with controls. “D” level evidence generally reflects case series data or expert opinion.

• The 2008 Surviving Sepsis Campaign Guidelines recommends that clinicians target a tidal volume of 6 ml/kg (predicted) body weight in patients with ALI/ARDS (Evidence Grade 1B). The Campaign also recommends that plateau pressures be measured in patients with ALI/ARDS and that the initial upper limit goal for plateau pressures in a passively inflated patient be less than or equal to 30 cm H2O. Chest wall compliance should be considered in the assessment of plateau pressure (Grade 1C).

Rationale: Over the past 10 years, several multi-center randomized trials have been performed to evaluate the effects of limiting inspiratory pressure through moderation of tidal volume. [1,6-9] These studies showed differing results that may have been caused by differences between airway pressures in the treatment and control groups. [1,10] The largest trial of a volume- and pressure-limited strategy showed a 9 percent decrease of all-cause mortality in patients with ALI or ARDS ventilated with tidal volumes of 6 mL/kg of predicted body weight (PBW), as opposed to 12 mL/kg, and aiming for a plateau pressure less than or equal to 30 cm H2O. [1] The use of lung protective strategies for patients with ALI is supported by clinical trials and has been widely accepted, but the precise choice of tidal volume for an individual patient with ALI may require adjustment for such factors as the plateau pressure achieved, the level of positive end-expiratory pressure (PEEP) chosen, the compliance of the thoracoabdominal compartment and the vigor of the patient’s breathing effort. Some clinicians believe it may be safe to ventilate with tidal volumes higher than 6 ml/kg PBW as long as the plateau pressure can be maintained less than or equal to 30cm H2O. [11,12] The validity of this ceiling value will depend on breathing effort, as those who are actively inspiring generate higher trans-alveolar pressures for a given plateau pressure than those who are passively inflated. Conversely, patients with very stiff chest walls may require plateau pressures higher than 30 cmH2O to meet vital clinical objectives. One retrospective study suggested that tidal volumes should be lowered even with plateau pressures that are less than or equal to 30 cm H20. [13] An additional observational study suggested that knowledge of the plateau pressures was associated with lower plateau pressures; however, in this trial, plateau pressure was not independently associated with mortality rates across a wide range of plateau pressures that bracketed 30 cm H2O. [14] The largest clinical trial employing a lung protective strategy coupled limited pressure with limited tidal volumes to demonstrate a mortality benefit. [1]

High tidal volumes that are coupled with high plateau pressures should be avoided in ALI/ARDS. Clinicians should use as a starting point the objective of reducing tidal volumes over 1 to 2 hours from its initial value toward the goal of a “low” tidal volume (≈6 mL per kilogram of predicted body weight) achieved in conjunction with an end-inspiratory plateau pressure less than or equal to 30 cm H2O. If plateau pressure remains >30 after reduction of tidal volume to 6 ml/kg/PBW, tidal volume should be reduced further to as low as 4 ml/kg/PBW. 

No single mode of ventilation (pressure control, volume control, airway pressure release ventilation, high frequency ventilation, etc.) has been consistently shown advantageous when compared with any other that respects the same principles of lung protection. 

• The Surviving Sepsis Campaign recommends that hypercapnia (allowing PaCO2 to increase above its pre-morbid baseline, so-called permissive hypercapnia) be allowed in patients with ALI/ARDS if needed to minimize plateau pressures and tidal volumes (Grade 1C).

Rationale: An acutely elevated PaCO2 may have physiologic consequences that include vasodilation as well as an increased heart rate, blood pressure, and cardiac output. Allowing modest hypercapnia in conjunction with limiting tidal volume and minute ventilation has been demonstrated to be safe in small, nonrandomized series. [2,3] Patients treated in larger trials that have the goal of limiting tidal volumes and airway pressures have demonstrated improved outcomes, but permissive hypercapnia was not a primary treatment goal in these studies. [1] The use of hypercapnia is limited in patients with preexisting metabolic acidosis and is contraindicated in patients with increased intracranial pressure. Sodium bicarbonate or tromethamine infusion may be considered in selected patients to facilitate use of permissive hypercarbia. [15,16]

• The Surviving Sepsis Campaign recommends that positive end-expiratory pressure (PEEP) be set so as to avoid extensive lung collapse at end-expiration (Grade 1C).

Rationale: Raising PEEP in ALI/ARDS keeps lung units open to participate in gas exchange. This will increase PaO2 when PEEP is applied through either an endotracheal tube or a face mask. [17-19] In animal experiments, avoidance of end-expiratory alveolar collapse helps minimize ventilator-induced lung injury (VILI) when relatively high plateau pressures are in use. One large multi-center trial of the protocol-driven use of higher PEEP in conjunction with low tidal volumes did not show benefit or harm when compared to lower PEEP levels. [20] Neither the control nor experimental group in that study, however, was clearly exposed to hazardous plateau pressures. A recent multi-center Spanish trial compared a high PEEP, low-moderate tidal volume approach to one that used conventional tidal volumes and the least PEEP achieving adequate oxygenation. A marked survival advantage favored the former approach in high acuity patients with ARDS. [21] Two options are recommended for PEEP titration. One option is to titrate PEEP (and tidal volume) according to bedside measurements of thoracopulmonary compliance with the objective of obtaining the best compliance, reflecting a favorable balance of lung recruitment and overdistention. [22] The second option is to titrate PEEP based on severity of oxygenation deficit and guided by the FIO2 required to maintain adequate oxygenation. [1] Whichever the indicator — compliance or oxygenation — recruiting maneuvers are reasonable to employ in the process of PEEP selection. Blood pressure and oxygenation should be monitored and recruitment discontinued if deterioration in these parameters is observed. A PEEP >5 cm H20 is usually required to avoid lung collapse. [23]

References:

1. The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. New England Journal of Medicine. 2000;342:1301–1308.
2. Hickling KG, Henderson S, Jackson R. Low mortality rate in adult respiratory distress syndrome using low-volume, pressure-limited ventilation with permissive hypercapnia: A prospective study. Critical Care Medicine. 1994;22:1568–1578.
3. Bidani A, Cardenas VJ, Zwischenberger JB. Permissive hypercapnia in acute respiratory failure. Journal of the American Medical Association. 1994;272:957–962.
4. Tasker RC. Combined lung injury, meningitis and cerebral edema: How permissive can hypercapnia be? Intensive Care Medicine. 1998;24:616–619.
5. Laffey JG, et al. Therapeutic hypercapnia reduces pulmonary and systemic injury following in vivo lung reperfusion. American Journal of Respiratory and Critical Care Medicine. 2000;162:2287–2294.
6. Amato MB, Barbas CS, Medeiros DM, et al. Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome. New England Journal of Medicine. 1998;338(6):347-354.
7. Brochard L, Roudot-Thoraval F, Roupie E, et al. Tidal volume reduction for prevention of ventilator-induced lung injury in acute respiratory distress syndrome. American Journal of Respiratory and Critical Care Medicine. 1998;158(6):1831-1838.
8. Brower RG, Fessler HE, Shade DM, et al. Prospective, randomized, controlled clinical trial comparing traditional versus reduced tidal volume ventilation in acute respiratory distress syndrome patients. Critical Care Medicine. 1999;27:1492-1498.
9. Stewart TE, Meade MO, Cook DJ, et al. Evaluation of a ventilation strategy to prevent barotrauma in patients at high risk for acute respiratory distress syndrome. New England Journal of Medicine. 1998;338:355-361.
10. Eichacker PQ, Gerstenberger EP, Banks SM, et al. Meta-analysis of acute lung injury and acute respiratory distress syndrome trials testing low tidal volumes. American Journal of Respiratory and Critical Care Medicine. 2002;166:1510-1514.
11. Tobin MJ. Culmination of an era in research on the acute respiratory distress syndrome. New England Journal of Medicine. 2000;342:1360-1361.
12. Marini JJ, Gattinoni L. Ventilatory management of acute respiratory distress syndrome: A consensus of two. Critical Care Medicine. 2004;32:250-255.
13. Hager DN, Krishnan JA, Hayden DL, et al. Tidal volume reduction in patients with acute lung injury when plateau pressures are not high. American Journal of Respiratory and Critical Care Medicine. 2005;172:1241-1245.
14. Ferguson ND, Frutos-Vivar F, Esteban A, et al. Airway pressures, tidal volumes, and mortality in patients with acute respiratory distress syndrome. Critical Care Medicine. 2005 Jan;33(1):21-30.
15. Kallet RH, Jasmer RM, Luce JM, Lin LH, Marks JD. The treatment of acidosis in acute lung injury with tris-hydroxymethyl aminomethane (THAM). American Journal of Respiratory and Critical Care Medicine. 2000 Apr;161(4 Pt 1):1149-1153.
16. Weber T, Tschernich H, Sitzwohl C, et al. Tromethamine buffer modifies the depressant effect of permissive hypercapnia on myocardial contractility in patients with acute respiratory distress syndrome. American Journal of Respiratory Critical Care Medicine. 2000;162:1361-1365.
17. Marini JJ, Ravenscraft SA. Mean airway pressure: Physiologic determinants and clinical importance—Part I: Physiologic determinants and measurements. Critical Care Medicine. 1992;20:1461-1472.
18. Gattinoni L, Marcolin R, Caspani ML, Fumagalli R, Mascheroni D, Pesenti A.. Constant mean airway pressure with different patterns of positive pressure breathing during the adult respiratory distress syndrome. Bulletin Europeen dePhysiopathologie Respiratoire. 1985;21:275-279.
19. Pesenti A, Marcolin R, Prato P, Borelli M, Riboni A, Gattinoni L.. Mean airway pressure vs. positive end-expiratory pressure during mechanical ventilation. Critical Care Medicine. 1985;13:34-37.
20. The National Heart, Lung, and Blood Institute ARDS Clinical Trials Network. Higher versus lower positive end-expiratory pressures in patients with the acute respiratory distress syndrome. New England Journal of Medicine. 2004;351(4):327-336.
21. Villar J, Kacmarek RM, Pérez-Méndez L, Aguirre-Jaime A, for the ARIES Network. A high PEEP-low tidal volume ventilatory strategy improves outcome in persistent ARDS. A randomized controlled trial. Critical Care Medicine. 2006 May;34(5):1311-1318.
22. Amato MB, Barbas CS, Medeiros DM, et al. Beneficial effects of the “open lung approach” with low distending pressures in acute respiratory distress syndrome. A prospective randomized study on mechanical ventilation. American Journal of Respiratory and Critical Care Medicine. 1995;152:1835-1846.
23. Gattinoni L, Caironi P, Cressoni M, et al. Lung recruitment in patients with acute respiratory distress syndrome. New England Journal of Medicine. 2006;354:1775-1786.

Content adapted extensively from:

• Dellinger, RP, Levy, MM, Carlet, JM, et al. Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2008. Critical Care Medicine. 2008;36(1):296-327.
• Sevransky JE, Levy MM,  Marini JJ. Mechanical ventilation in sepsis-induced acute lung injury/acute respiratory distress syndrome: An evidence-based review. Critical Care Medicine. 2004;32[Suppl.]:S548–S553.