Protecting the Intubated Patient

1 Comment

Intub RMWhile much focus is put on intubation in the ED, post-intubation ventilator management is arguably just as critical to the patient’s ultimate outcome 

While much focus is put on intubation in the ED, post-intubation ventilator management is arguably just as critical to the patient’s ultimate outcome 


Intub W

Hundreds of thousands of patients are mechanically ventilated in the emergency department (ED) annually [1]. Only recently has mechanical ventilation in the ED received much attention, both in terms of clinical practice and associated outcomes. Intubating a patient can be an emotionally charged and possibly technically challenging process, and it is not unusual to feel that the emergency physician’s job is done once this task is complete. Post-intubation ventilator management, however, is arguably just as important, if not more so. The initiation of mechanical ventilation can be a life-saving intervention, but the way in which a ventilator is managed after endotracheal intubation can directly impact outcomes.  

Ventilator-associated lung injury (VALI) is a broad term that refers to how a ventilator can propagate injury in already damaged lungs, or initiate injury in relatively normal lungs [2]. To distension, specifically regional overdistension, as well as repetitive opening and closing of alveolar units. High volume lung injury is typically thought of in terms of “barotrauma” (i.e. extra-alveolar air) and “volutrauma” (i.e. excessive lung stretch). Low volume lung injury occurs when collapsed alveoli at end- expiration re-open during inspiration. This repetitive opening and closing can lead to surfactant dysfunction and epithelial injury, and is coined “atelectrauma”. The net effect of the above factors can lead to the translocation of various mediators from the lung and into the systemic circulation. This is thought to be responsible for the multi-organ dysfunction associated with VALI, and is referred to as “biotrauma”.  


Why should Emergency Physicians care? Studies have shown that VALI can occur in the first few hours of mechanical ventilation [3,4].  Given the increasing ED boarding times for critically ill patients, the duration of mechanical ventilation in the ED is often more than sufficient to begin the process of lung injury. So it is possible that the institution of lung-protective ventilation strategies in the ED can mitigate VALI and the negative clinical outcomes associated with it. Maybe just as important, mechanical ventilator settings in the ED are influential on subsequent ventilator settings in the intensive care unit (ICU) [5].  As a result, improper ventilator settings in the ED have the potential to cause ongoing injury long after the patient has left the department.

So what can we do in the ED to help protect our patients from potential VALI?  A lung-protective ventilation strategy attempts to limit overdistension, as well as low volume derecruitment, while also addressing other potential contributors to lung injury, such as excessive oxygen administration. Pertinent ventilator parameters typically manipulated are: 1) tidal volume, 2) positive end-expiratory pressure (PEEP), and 3) the fraction of inspired oxygen (FiO2).

  1. Normal mammalian tidal volume, indexed to size, is less than 7 mL/kg [6]. Animal models and human data have established that tidal volume is a major risk for VALI. 
  2. PEEP serves to stabilize alveoli, preventing end-expiratory collapse, decreasing the likelihood of atelectrauma. 
  3. Excessive oxygen administration, in the form of high FiO2, can promote alveolar collapse, and increasing evidence suggests that excessive oxygen exposure has negative clinical outcomes [7,8,9].

Beyond the three parameters mentioned above, another important assessment for VALI potential is inspiratory plateau pressure. As mentioned above, overdistention is a key driver of VALI; lung inflation and distention are governed by transalveolar pressure, which is alveolar pressure minus pleural pressure. Plateau pressure is a surrogate for transalveolar pressure, and limiting this pressure serves to limit excessive stretch. Patient groups that can benefit from a lung-protective approach include those with acute respiratory distress syndrome (ARDS) and those at risk for the syndrome (the majority of patients intubated in the ED).

ARDS is a complex pattern of inflammatory lung injury that leads to impaired gas exchange. It is defined by the presence of bilateral alveolar infiltrates and arterial hypoxemia, and can be further classified as mild, moderate, or severe depending on the degree of impaired oxygenation [10]. It is associated with a mortality rate of around 40%, as well as long-term survivor morbidity [11]. Typically thought of as a syndrome associated with the intensive care unit (ICU), data from academic EDs suggest that a significant minority (~8.5%) of mechanically ventilated patients have ARDS while in the ED5. The ARMA trial [12]  demonstrated a 9% mortality reduction when a tidal volume of 6mL/kg predicted body weight (PBW) was used as compared to 12 mL/kg PBW. Said differently, a relatively normal tidal volume will decrease mortality in ARDS versus a doubling of that tidal volume. Plateau pressure was also limited to 25-30 cm H2O in the “low” tidal volume group versus 45-50cm H2O in the conventional group.


PEEP 288Patients at risk for ARDS, but without the syndrome, will comprise most of the patients ventilated in the ED. While lung-protective ventilation has convincing survival benefit in ARDS, more recent observational studies and a small, randomized trial from the ICU suggest a benefit of lung-protective ventilation in all patients [13,14]. Specifically, higher tidal volume use in critically ill patients at risk for ARDS has been linked with the subsequent development of ARDS after ICU admission. In further support of the effect of relatively brief periods of ventilation on outcome, data from the operating room support the use of lung-protective ventilation to reduce post-operative pulmonary and non-pulmonary complications [4].

The data on mechanical ventilation practices in the ED suggest that VALI is a potential problem in these patients. In a single center cohort study of mechanically ventilated ED patients with severe sepsis and septic shock, lung-protective ventilation was used in only 27% of patients, PEEP was uniformly set at 5 cm H2O, and FiO2 was kept close to 100%. In just over two-thirds of patients, no ventilator parameters were adjusted during the ED stay [3].  In keeping with the concept that what occurs in the ED influences subsequent care, the first ventilator setting in the ICU was the same as the last ventilator setting in the ED 86% of the time, and 25% of patients were exposed to the same tidal volume used in the ED for 24 hours.  Among 22 patients who met criteria for ARDS while in the ED, only 4 (18%) received low tidal volume ventilation during the ED stay, and the median time exposed to an FiO2 of 100% was nearly 5 hours in this subset. In a follow-up study that involved four academic EDs, mechanical ventilation practices were summarized as using higher than recommended tidal volumes, high FiO2, low PEEP, and infrequent monitoring of plateau pressure [5]. We believe the weight of evidence regarding VALI and ED ventilator practices demonstrates a great opportunity to improve delivery of care and clinical outcomes.

The take away points from this article are: 1) How the ventilator is managed, even for relatively brief periods, can influence outcome; 2) ARDS is a syndrome that is not confined to the ICU, and ventilated ED patients will have ARDS. Tidal volume should be set at 6mL/kg PBW, plateau pressure should be limited to <30 cm H2O, and PEEP and FiO2 should be titrated with the aid of a PEEP-FiO2 table; 3) Ventilator settings can influence the development of ARDS in at-risk patients. Given the risk/benefit of lung-protective ventilator settings in this cohort, this approach should be used as well. We recommend targeting a tidal volume of 6-8mL/kg PBW with a plateau pressure of 25-30 cmH2O; setting a PEEP of at least to 5 cm H2O, with higher levels in patients at increased risk for atelectrauma (e.g. obesity). We also recommend against initiating FiO2 at 100%, but rather starting at 30-40% and titrating higher only if needed (and in conjunction with PEEP). Finally, it should be stressed that a catchall protocol approach to mechanical ventilation is impossible for every patient. The great majority of all ventilated patients will tolerate a lung-protective approach easily, however it is up to the clinician to ensure adequate tolerance in any particular patient.

ARDS is a devastating complication of mechanical ventilation and is associated with substantial mortality and morbidity.  It is difficult to treat after onset and therefore prevention of this complication is paramount. Lung-protective ventilation reduces mortality in patients with ARDS, and is beneficial in those at risk for its development.  Several knowledge gaps exist with respect to the long-term clinical outcomes associated with lung protective ventilation in the ED. A lung-protective ventilation strategy in the ED has the potential to reduce iatrogenic VALI and can be instituted in the majority of ventilated ED patients.

Brian Fuller, MD and Brian Cohn, MD are assistant professors of EM at Washington University in St. Louis.

1. Easter BD, Fischer C, Fisher J. The use of mechanical ventilation in the ED. Am J Emerg Med. 2012 Sep;30(7):1183-8.
2. Slutsky AS, Ranieri VM. Ventilator-induced lung injury. N Engl J Med. 2014 Mar 6;370(10):980.
3. Fuller BM, Mohr NM, Drewry AM, Carpenter CR. Lower tidal volume at initiation of mechanical ventilation may reduce progression to acute respiratory distress syndrome: a systematic review. Crit Care. 2013 Jan 18;17(1):R11.
4. Futier E, Constantin JM, Paugam-Burtz C, et al; IMPROVE Study Group. A trial of intraoperative low-tidal-volume ventilation in abdominal surgery. N Engl J Med. 2013 Aug 1;369(5):428-37.
5. Fuller BM, Mohr NM, Miller CN, et al. Mechanical ventilation and acute respiratory distress syndrome in the emergency department: a multi-center, observational, prospective, cross-sectional study. Chest. 2015 Mar 5.
6. Tenney SM, Remmers JE. Comparative quantitative morphology of the mammalian lung: diffusing area. Nature. 1963 Jan 5;197:54-6.
7. Kilgannon JH, Jones AE, Shapiro NI, et al; Emergency Medicine Shock Research Network (EMShockNet) Investigators. Association between arterial hyperoxia following resuscitation from cardiac arrest and in-hospital mortality. JAMA. 2010 Jun 2;303(21):2165-71.
8. Kilgannon JH, Jones AE, Parrillo JE, et al; Emergency Medicine Shock Research Network (EMShockNet) Investigators. Relationship between supranormal oxygen tension and outcome after resuscitation from cardiac arrest. Circulation. 2011 Jun 14;123(23):2717-22.
9. Rachmale S, Li G, Wilson G, Malinchoc M, Gajic O. Practice of excessive F(IO(2)) and effect on pulmonary outcomes in mechanically ventilated patients with acute lung injury. Respir Care. 2012 Nov;57(11):1887-93.
10. ARDS Definition Task Force, Ranieri VM, Rubenfeld GD, Thompson BT, et al. Acute respiratory distress syndrome: the Berlin Definition. JAMA. 2012 Jun 20;307(23):2526-33.
11. Rubenfeld GD, Herridge MS. Epidemiology and outcomes of acute lung injury. Chest. 2007 Feb;131(2):554-62.
12. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network. N Engl J Med. 2000 May 4;342(18):1301-8.
13. Determann RM, Royakkers A, Wolthuis EK, et al. Ventilation with lower tidal volumes as compared with conventional tidal volumes for patients without acute lung injury: a preventive randomized controlled trial. Crit Care. 2010;14(1):R1.
14. Fuller BM, Mohr NM, Dettmer M, et al. Mechanical ventilation and acute lung injury in emergency department patients with severe sepsis and septic shock: an observational study. Acad Emerg Med. 2013 Jul;20(7):659-69. 


1 Comment

Leave A Reply