Taking Ownership of the Ventilator – How to Manage and Troubleshoot

Evan Miller, DO (EM Resident Physician, Allegheny General Hospital) and Maxim Dzeba, MD (EM Attending Physician, Allegheny General Hospital) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) & Justin Bright, MD (@JBright2021)

Case Scenarios

You are the overnight senior resident in the ED managing a 27 year-old asthmatic male who has been in respiratory distress for the past few hours. You make the decision to intubate given the patient’s declining mental status and increasing fatigue. The respiratory therapist asks if you want to set the patient’s respiratory rate at his current 24 breaths per minute.

You received sign-out from the day resident about an intubated patient in room 5. The patient is an 81 year-old female who presented seven hours prior and was intubated after being diagnosed with severe sepsis due to pneumonia. The patient’s blood pressure has been steadily decreasing and repeat chest xray showed diffuse bilateral opacities which was worse than prior imaging. The patient is 80 kg and 5’3” tall. She was started on VCV rate 14, tidal volume 600, PEEP 10, FiO2 80%. Are these the correct settings?

Your overnight junior calls for your help with his decompensating intubated patient. The patient is a 54 year-old male with a history of COPD who was intubated ten minutes ago. The ventilator is alarming due to high pressures. The patient’s current vitals are HR 140, BP 80/50, SpO2 82%. The ventilator settings are VCV rate 12, tidal volume 450, PEEP 15, FiO2 100%. You quickly disconnect the circuit but the patient is not improving. What do you do next?

As you are managing these critical patients, a nurse tells you that the 16 year-old female in room 1 who was intubated for airway protection for a suspected drug-induced encephalopathy has a low pressure alarm. You enter the room and see an obese young female who is bucking the vent and thrashing around. You perform an inspiratory pause and find the plateau pressure to be low with a continuously low peak pressure.

Introduction

The care of critically ill, mechanically ventilated (MV) patients is essential to the practice of emergency medicine. While emergency physicians are experts at securing even the most difficult airways, much less time is spent on learning the intricacies of mechanical ventilation. Increasing emergency department (ED) boarding time has been associated with negative outcomes.1 Fuller et al (2015) found emergency physicians had suboptimal adherence to best practice guidelines for mechanically ventilated patients in the ED. This was correlated with increased intensive care unit (ICU) length of stay (LOS) and higher rates of morbidity and mortality. In that study the median ED LOS was 3.4 hours with a range of 1.1 to 18.3 hours. Due to this increased ED LOS, it is imperative ED physicians are comfortable with initial ventilator settings, best practices, and perhaps the most difficult yet most important task of ventilator troubleshooting.2

Basics of Mechanical Ventilation

Indications and Pathophysiology

The emergency physician will intubate for one of four main reasons: a) inability to ventilate; b) inability to oxygenate; c) anticipated clinical course; and d) airway protection.3

There are two main goals of respiration: supplying oxygen demand and eliminating carbon dioxide (CO2). Ventilation is defined as the elimination of CO2 from the body. Adequate ventilation is matching minute ventilation with metabolic demand, while hypoventilation is the inability to keep up with metabolic demand resulting in hypercapnia and eventually acidosis.

Minute ventilation (VE) is the measurement of air inhaled or exhaled per minute and is found by multiplying the respiratory rate (RR) by the tidal volume (VT) [VE = RR x VT]. When dealing with a patient who was intubated for inability to ventilate, these two parameters (RR, VT) can be modified to correct the hypoventilation. Common causes of low RR include any CNS depressant/injury, while causes of low VT include poor respiratory muscle contraction due to neuromuscular disorders or poor chest wall mechanics.4

Oxygenation is any process that leads to the delivery of O2 to the tissues. There are many causes of hypoxemia including low inspired FiO2 (altitude, medical error), V/Q mismatch, hypoventilation, diffusion defect, and low mixed venous oxygen.5  Shunt and dead space ventilation are the two major mechanisms that cause significant abnormalities in gas exchange.

Shunt is perfusion without ventilation. This occurs when the blood passes from the right heart to the left heart without passing any areas of ventilation. An intra-cardiac right to left shunt is an easy representation of this. Intrapulmonary causes include consolidation, pulmonary edema, and atelectasis. In these situations, increasing the FiO2 to 100% will not improve the oxygenation as the blood is not being exposed to areas of ventilation. The treatment for shunt induced hypoxemic respiratory failure is positive end expiratory pressure (PEEP).6,7 PEEP recruits collapsed alveoli and works to decrease the shunted areas. One method to determine the proper amount of PEEP is to use the Acute Respiratory Distress Syndrome Network (ARDSNet) PEEP/FiO2 table (http://www.ardsnet.org/files/ventilator_protocol_2008-07.pdf). Ideally, the goal is to use the lowest amount of PEEP to maintain an oxygen saturation of 88 – 95%.8

Dead space is any area of ventilation without perfusion. The traditional example of dead space is seen with a massive pulmonary embolism, but this can also be seen in cases of low cardiac output. Iatrogenic causes of dead space include alveoli over distension secondary to breath-stacking in an intubated COPD patient. Increased dead space can lead to both hypoxemia and hypercapnia.4

Modes and variables

There are several different modes and variables to understand when setting up MV.

Breath types: There are three main types of breaths that a ventilator can supply. The most basic is a mandatory breath which is initiated, controlled, and ended by the machine itself. The second type is an assisted breath which is initiated by the patient but controlled and ended by the machine (based on variables set by the provider).  The third type is a spontaneous breath which is initiated, controlled, and ended by the patient.

Trigger: An assisted breath is triggered by a set negative airway pressure or flow. When an intubated patient attempts to take a breath, the negative pressure or change in flow is sensed by the vent and a breath is delivered. This setting is generally standard and not often manipulated by ED physicians.

Cycle: The cycle is the main distinction between ventilator modes. The “cycling” is when the ventilator switches from inspiration to expiration. Volume-cycled: the machine delivers a set volume at which point it stops the flow and allows for expiration. Pressure-cycled: the machine delivers a breath until it reaches a set pressure at which point it stops the flow and allows for expiration. The volume will vary with each breath depending on lung compliance.

Respiratory rate: This variable sets a minimum number of breaths that must be given per minute. For example, in an assist mode, if you set the rate at 12 the ventilator will break the minute up into 12 five second blocks. If the patient initiates a breath during these five seconds, the ventilator will count that breath. If the patient does not initiate a breath by that time, the ventilator will deliver a mandatory breath ensuring a minimum number of breaths per minute.9

Inspiratory to expiratory (I:E) ratio: This variable is a factor of the inspiratory time which is the VT divided by the flow rate (VT / FR). The standard flow rate is 60 L/min. The I:E can be increased by: 1) decreasing the tidal volume; 2) increasing the inspiratory flow; or 3) decreasing the respiratory rate. A normal I:E would be 1:2 or 1:3 vs. a patient with COPD where an appropriate I:E would be 1:4 or above.

Positive end-expiratory pressure: PEEP is used to increase functional residual capacity (FRC) by preventing alveolar collapse at the end of expiration and recruiting fluid filled or atelectatic alveoli. The starting PEEP is usually set at 5 cm H2O as this is believed to be equivalent to physiologic levels. In patients with ARDS, the PEEP is adjusted based on the PEEP / FiO2 tables.8

Fraction of inspired oxygen: FiO2 is usually started at 100% and is titrated down to a SpO2 of > 88% (or PaO2 > 55 mm Hg) with a goal FiO2 of < 60% as soon as possible.10 In patients who are intubated for airway protection and have no issues with ventilation or oxygenation, it is reasonable to start the FiO2 at lower levels. Increased FiO2 allows for a higher PAO2 at a low alveolar ventilation L/min.

Tidal Volume: VT is set in volume-cycled modes and is the minimum volume delivered per breath. It is important to note that the tidal volume should be calculate using the ideal body weight (aka predicted body weight) rather than the actual weight.

Predicted body weight (in kg)
Males: 50 + 2.3 (height [inches] – 60)
Females: 45.5 + 2.3 (height [inches] – 60)

Modes:

Assist-control ventilation (ACV) provides the highest level of ventilatory support3. In this mode, every breath is supported by the ventilator, including any breaths above the set rate. ACV can be either volume-cycled (volume-targeted) or pressure-cycled (pressure-targeted).

In volume-cycled ACV the physician will establish a set VT to be delivered with each breath ensuring a minimum volume per breath. The trigger can either be an elapsed time (minimum set rate) or a spontaneous breath. Major disadvantages of this include auto-PEEP with associated lung injury (discussed later) and decreased cardiac output.

In pressure-cycled ACV the physician will establish a set rate, flow, and pressure. Each breath will cycle after the set pressure is reached thereby decreasing peak inspiratory pressure (discussed later). However the tidal volume is variable which each breath and is dependent upon the lung compliance.

Pressure-support ventilation (PSV) is used primary for weaning purposes or during stable ventilatory support periods. Each breath is patient-triggered and pressure-cycled. This mode provides extra pressure support to help the patient overcome the inherent resistance of the ventilator circuit.

Other available modes include synchronized intermittent mandatory ventilation, bilevel, and control mode ventilation.

Ventilatory settings

General settings for initiation of MV using the “lung-protective” strategy are as follows:8,10

  • Assist control mode – volume-cycled
  • Tidal volume 6 mL/kg IBW
    • Alternatively starting at 8 mL/kg IBW and reducing by 1 mL/kg every 2 hours until tidal volume is 6 mL/kg4
  • RR 14-16 breaths/min (can titrate to a max of 35 to keep pH above 7.15)
  • FiO2 100% with rapid titration based on SpO2
  • PEEP 5 to 7 cm H2O
  • Keep plateau pressures below 30 cm H2O

For patients with contraindications for permissive hypercapnia (discussed below):

  • Tidal volume 8 mL/kg IBW
  • RR 12-20 breaths per minute

Special Scenarios

Acute Respiratory Distress Syndrome (ARDS)

Acute respiratory distress syndrome is a severe cause of hypoxemic respiratory failure. ARDS is caused by both direct and indirect lung injury which causes an exudative alveolar filling. This leads to a severe VQ mismatch. While ARDS is not commonly encountered in the ED due to its delayed time of onset, most patients that are intubated in the ED have significant risk factors for its development. These risk factors include severe sepsis, chest trauma, and pneumonia.

Historically, tidal volumes were set as 10-12 mL/kg even though the normal tidal volumes of spontaneous breathing is 5-7 mL/kg IBW. It was later discovered that these elevated volumes lead to alveolar over distension causing alveolar rupture and release of inflammatory cytokines. These effects in turn can lead to: 1) Barotrauma, which includes pneumothorax, pneumomediastinum, and pneumopericardium, occurs when the structural integrity of the alveolus is disrupted due to elevated transalveolar pressures; 2) Volutrauma is due to the overdistention of the alveolus resulting in lung parenchyma damage; and 3) Biotrauma which is a multi-organ injury due to the inflammatory cytokines.11

The high mortality of ARDS led to a randomized control trial performed by ARDSNet in 2000 which found a significant reduction in morbidity and mortality when volumes were set at 6 mL/kg IBW and plateau pressures were kept below 30 cm H2O.8 The low tidal volume strategy is designed to prevent worsening lung injury that could be caused by alveolar over-distension. These lower tidal volume are combined with higher respiratory rates to provide adequate minute ventilation.8

table1
Table (1): Berlin Definition of Acute respiratory Distress Syndrome.12

Permissive hypercapnia

The lung-protective settings usually result in a retention of CO2 and therefore a degree of acidosis, this is referred to as permissive hypercapnia. Previously, MV was used to normalize arterial blood gas numbers, specifically the pH and arterial carbon dioxide tension (PaCO2). The current thought process is to minimize the risks of MV while still maintaining an adequate gas exchange. Permissive hypercapnia is acceptable as long as the pH remains above 7.15-7.20. If the pH falls below 7.15, you can increased the RR to a maximum of 30-35 breaths/min.10 Due to this acidosis, permissive hypercapnia is contraindicated in patients with acute brain injury, fulminant hepatic failure, severe pulmonary hypertension, or severe metabolic acidosis.9,13

Asthma and COPD

The major concern for mechanically ventilated patients with obstructive airway disease is dynamic hyperinflation (also known as auto-PEEP, intrinsic PEEP, breath stacking, or air trapping). This condition occurs when gas becomes trapped in the lungs during mechanical ventilation. The air trapping is caused by inadequate time for exhalation allowing for delivery of the next breath before the patient has time to completely exhale. This leads to increased alveolar pressures, decreased venous return, and decreased cardiac output ultimately leading to hemodynamic instability. Auto-PEEP can be detected on the ventilator waveform because the flow will not return to zero before the next breath (figure 1).

table2
Figure (1). Dynamic hyperinflation: Top image shows how the trapped gas will result in increased lung volume resulting in decreased ventilation/oxygenation and increased intrathoracic pressure. Bottom image shows how the waveform does not reach zero/baseline before delivery of the next breath.11

Strategies to avoid auto-PEEP would be any factor that increases the I:E ratio which include decreasing the respiratory rate and/or tidal volume, or increasing the inspiratory flow rate (the standard flow rate is 60 L/min, this can be increased up to 80-100 L/min).6 These factors allow more time for the patient to complete exhalation minimizing the risk of hyperinflation. In severe cases, deep sedation and paralysis may be necessary to improve ventilator synchrony and avoid auto-PEEP.11

Other special topics

Elevated intracranial pressure: Ii any case of elevated ICP, hypoxia and hypercapnia need to be avoided. Permissive hypercapnia is contraindicated due to association with cerebral vasodilatation which could lead to increased cerebral blood flow and therefore increased intracranial pressure.11

Severe metabolic acidosis: Patients with severe metabolic acidosis (e.g. diabetic ketoacidosis or salicylate toxicity) usually increase their minute ventilation to help compensate for the acidosis. This is usually accomplished by increasing their respiratory rate. When these patients are placed on MV, it is important to consider setting the RR close to the pre-intubation rate as well as closely monitoring the pH.6

Shock: High amounts of PEEP can result in increased intrathoracic pressures which decrease cardiac preload and exacerbate hypotension. Addressing volume status, preferably prior to intubation, and keeping PEEP at 5 cm H2O is advised.7

Troubleshooting the ventilator

General effects of intubation include:

  • Post-intubation hypotension
  • Decreased venous return due to increased intrathoracic pressure
  • Acidemia
  • Acute lung injury / acute respiratory distress syndrome
  • Increased intracranial pressure
  • Ventilator-induced pneumonia
    • Strategies to reduce this include:
      • Elevate the head of the bed 30-45 degrees
      • Maintaining endotracheal tube cuff pressure at 20 cm H2O
      • Placing a naso- or oro-gastric tube to avoid overdistention
    • Oxygen toxicity – the exact cause and mechanism is still controversial however supraphysiologic levels of oxygen has been associated with increased mortality and worse neurologic outcomes in post arrest patients

Step-wise approach

There is a broad differential in any mechanically ventilated distressed patient including anxiety and pain as well as tension pneumothorax and auto-PEEP. The first step is identifying the level of distress as well as the overall hemodynamic stability.

In a hemodynamically stable patient, a focused systematic approach can be safely utilized.7,15

1) Obtaining a history from the bedside staff – this includes reason for and difficulty of intubation, ETT depth, current ventilator settings, and any recent changes including ventilator settings, new medications, or invasive procedure attempts (e.g. chest tube, central line).

2) Performing a physical exam – this includes examining the ETT for migration, air leak, or kinking. This also includes assessing need for continued intubation. For example, if a previously healthy patient was intubated for airway protection for a suspected drug overdose and is now awake and following commands, weaning to extubate could be an option. Evaluation for equal breath sounds and chest rise should be performed as well. Assess for hypoxia via pulse oximetry and/or arterial blood gas.

3) Checking the ventilator – evaluate the patient’s synchrony with the machine as well as the waveform searching of possible auto-PEEP.

4) Monitoring lung mechanics – please see measuring pressures section below.

5) Examining a chest x-ray or bedside ultrasound – examine the chest x-ray for worsening clinical condition, pneumothorax, and ETT tube position. Bedside ultrasound can be utilized for evaluation of pneumothorax.

6) Evaluating adequacy of analgosedation – after all other causes have been evaluated, the patient’s need for analgesia, sedation, and possibly paralysis should be assessed (e). The modified Society for Critical Care Medicine’s algorithm for sedation and analgesia on UpToDate can be utilized.

Measuring pressures – monitoring lung mechanics

Peak airway pressure (PAP): The peak pressure (Ppeak) is the amount of pressure that is required to deliver the set tidal volume from the ventilator circuit to the alveoli. The PAP is measured at the end of inspiration and is a function of both the airway resistance and the compliance of the lung. Therefore, if the tidal volume remains constant, a change in the PAP would be due to either a change in the airway resistance or in the compliance.  In VCV, the increase in PAP would not affect the delivery of the set volume. However, in PCV, the increase in the peak pressure would result in less volume be delivered (since the set pressure is constant).

Ppeak ≈ (Resistance + Compliance)

Plateau pressure (Pplat): The plateau pressure is measured by using the “inspiratory hold” technique. After the ventilator completes delivery of the breath, the machine will pause resulting in no airflow between the ventilator and patient; this allows for the equalization of pressures. Since the plateau pressure is measure when there is no airflow, it is therefore only a measurement of compliance.

Pplateau ≈ Compliance

Based on the above information, the difference between the Ppeak and Pplat would be proportional to the airway resistance.

Ppeak — PPlateau≈ Airway resistance

The normal measured airway resistance should be less than 10 cm H2O (with an adequate sized ETT).11

Using Pressures to troubleshoot

We can now apply the above information in a case of a crashing ventilator-dependent patient.

  1. If the peak pressure is elevated while the plateau pressure remains unchanged, that means there is an issue with the airway resistance. [ΔPPeak – PPlat would be increased]
  2. If both pressures are increased, then this would mean there is an issue with the compliance of the lungs and chest wall. [ΔPPeak – PPlat would be unchanged or decreased]
  3. If the peak pressure would be decreased, then there is either an air leak or the patient is hyperventilating enough to pull the air instead of having it pushed under pressure.
  4. No change in peak or plateau and patient still having respiratory distress, pulmonary embolism should be considered.11
Using pressures to troubleshoot
Increased Resistance

High peak pressure

Increased Compliance

High peak and plateau

Low Peak
·    ETT obstruction by kinking or patient biting tube

·    Airway obstruction (secretions, mucus, blood)

·    Bronchospasm

Extra-thoracic

·    Abdominal compartment syndrome

·    Ascites

·    Large body habitus

·    Positioning

Intra-thoracic

·    Pneumothorax

·    Pneumonia

·    ARDS

·    Atelectasis

·    Auto-peep

·    Pulmonary edema

·    R mainstem intubation

 

·  Cuff Leak

·  ETT dislodgement

·  Ventilator malfunction

·  Vent circuit is disconnected

 

Abdominal compartment syndrome is due to elevated abdominal compartment pressures. These elevated pressure result in compression of the diaphragm and lead to elevated peak and plateau pressures. Symptoms include hypotension, difficulty ventilating, decreased urine output, and cardiac arrest. Treatment includes decompression, sedation and/or paralysis, and urgent surgical consultation.6

In a hemodynamically unstable patient, the EM physician must know how to quickly react in order to prevent worsening patient condition and death. A common mnemonic used to respond to a deteriorating patient is DOPE. This stands 1) Dislodgement, 2) Obstruction, 3) Pneumothorax, and 4) Equipment failure.7,11

The first step should be disconnecting the patient from the ventilator and proceeding to manually bag with a bag valve mask and 100% FiO2. This step alone will help identify if the distress is due to the equipment failure or auto-PEEP. If there was a large exhalation immediately after disconnecting the circuit with immediate improvement in stability, auto-PEEP was likely to be the cause. If the patient improves with BVM then the ventilator needs to be investigated for equipment failure or patient-ventilator asynchrony due to inadequate sedation. Asynchrony can be improved by addressing adequacy of sedation as well as tailoring vent settings to match the patient’s efforts with required support.11 Double-cycling is an example of asynchrony in which there are back to back ventilator delivered breaths. This occurs when the patient wants a higher flow rate than what is set. This can be alleviated by increasing the flow rate.13

If the patient does not improve, next assess the difficulty of ventilation. If it is “too easy” to ventilate, a dislodgement or air leak could have occurred. If it is “too difficult” to ventilate, a suction catheter should be passed through the tube to asses for ETT obstruction or kinking.

If the above measures fail and the patient continues to decline, pneumothorax must be considered. This can be evaluated with auscultation, chest x-ray, or bedside ultrasound. If necessary, a needle chest decompression followed by a decompressive chest tube should be performed.

Case answers

Case #1: No. This patient is at risk for auto-PEEP. If this patient’s vent was set for a rate of 24 this would allow for 2.5 seconds per breath. Even if the inspiratory flow would be increased to 100 L/min, that would only allow for a maximum of 2.4 seconds for exhalation. This would result in an I:E of 1:2.4 which is significantly less than the recommended 1:4 to 1:5.

Case #2: The tidal volume in the scenario was set to 600 mL. Given this patient’s current condition she would be at risk for ARDS and the lung protective strategy should be utilized. The patient’s height is 5’3” and an appropriate tidal volume would be 400 mL (http://www.mdcalc.com/ideal-body-weight/).

Case #3: This is an example of a hemodynamically unstable patient. In the case, the patient was removed from the ventilator and BVM was utilized. In going through the stepwise approach you find that the ETT is in good place and is not obstructed. You place the ultrasound on the left chest and quickly identify an acute tension pneumothorax. You perform a needle decompression with immediate patient improvement. Afterwards you place a tube thoracostomy and decrease the PEEP to 5.

Case #4: On your physical exam you notice the patient has “tongued” the tube out of place and therefore has self-extubated. You reassess the patient’s mental status and confirm that the patient is currently alert and oriented, following commands, and is able to protect her airway. The patient is eventually discharged from the department in the custody of her concerned parents.

Must Know Information

Vent Basics

  • Understand the importance of the initial ventilator settings
  • Utilize the lung protective settings when applicable
    • Use 6-8 mL/kg using predicted/ideal body weight
  • Understand how permissive hypercapnia can be utilized to prevent ARDS

Crashing Patients

  • Have a standardized approach to a crashing patient
  • Understand the DOPE mnemonic
    • Dislodgement, obstruction, pneumothorax, equipment failure
  • Consider adequate sedation/analgesia
  • Understand how peak and plateau pressures can be utilized to help diagnose an acutely crashing patient

References / Further Reading

  1. Chalfin DB, et al. Impact of delayed transfer of critically ill patients from the emergency department to the intensive care unit. Crit Care Med 2007;35:1477-1483
  2. 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;148:365-374
  3. Adams J. Emergency Medicine: Clinical Essentials. Philadelphia, PA: Elsevier/Saunders; 2013.
  4. Marino, P. L., & Sutin, K. M. (2007). The ICU book. Philadelphia: Lippincott Williams & Wilkins.
  5. Mosier JM, Hypes C, Joshi R, Whitmore S, Parthasarathy S, Cairns CB. Ventilator Strategies and Rescue Therapies for Management of Acute Respiratory Failure in the Emergency Department. Annals of Emergency Medicine2015;66(5):529–541.
  6. Wood SL, Kloot TVder. Ventilator Management in The Intubated Emergency Department Patient. EM Critical Care2013;3(4). Available at: http://www.ebmedicine.net/topics.php?paction=showtopic&topic_id=378. Accessed January 15, 2016.
  7. Owens W. Ventilator Management And Troubleshooting In The Emergency Department. EM Critical Care2014;4(5). Available at: http://www.ebmedicine.net/topics.php?paction=showtopic&topic_id=416. Accessed January 15, 2016.
  8. 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 N Engl J Med2000;342(18):1301–1308.
  9. Rosen, P., Marx, J. A., Hockberger, R. S., Walls, R. M., & Adams, J. (2006). Rosen’s emergency medicine: Concepts and clinical practice. Philadelphia, PA: Mosby Elsevier.
  10. Wood S, Winters ME. Care of the Intubated Emergency Department Patient. The Journal of Emergency Medicine2011;40(4):419–427.
  11. Archambault PM, St-Onge M. Invasive and Noninvasive Ventilation in the Emergency Department. Emergency Medicine Clinics of North America30:421–449.
  12. Acute Respiratory Distress Syndrome. Jama 2012;307(23).
  13. Santanilla JI, Daniel B, Yoew M-E. Mechanical Ventilation. Emergency Medicine Clinics of North America2008;26:849–862.
  14. Kilgannon JH, Jones AE, Shapiro NL, et al. Association between arterial hyperoxia following resuscitation from cardiac arrest and in-hospital mortality. JAMA. 2010;303(21):2165-2171.
  15. Winters ME, DeBlieux PMC, Santanilla JI. Emergency Department Resuscitation of the Critically Ill. Dallas, TX: American College of Emergency Physicians; 2011.
  16. Please see the NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary http://www.ardsnet.org/files/ventilator_protocol_2008-07.pdf

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