Prone Position in ARDS

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Acute respiratory distress syndrome is a rapidly progressive and often fatal condition with a mortality of >50%. ARDS is encountered by nurses in all hospitals settings- from small rural hospitals to large urban centers. Patients may quickly become too unstable for transport, therefore it is imperative that nurses are familiar with ARDS therapies, including prone positioning. In this module we will discuss ARDS and the use of prone positioning in depth.

Prone Position in ARDS – What is ARDS?

Acute respiratory distress syndrome (ARDS) was first identified in 1967 during the Vietnam War as a distinctively new subset of hypoxemic respiratory failure (1) and first defined in 1994 by the Berlin definition as the acute onset of hypoxemia with bilateral frontal infiltrates on chest radiograph and no evidence of left atrial hypertension (2).

In 1994, the American and European Consensus Conference (AECC) established the specific criteria to describe acute lung injury (ALI) and ARDS. These criteria included acute onset, bilateral lung infiltrates of chest x-ray, no evidence of elevated left atrial pressure and severe hypoxemia, assessed by the arterial oxygen tension to inspired oxygen fraction (PaO2/FiO2) ratio. (1). According to the above guidelines, ALI existed at a PaO2/FiO2 of =/< 300mmHg, and ARDS was diagnosed when PaO2/FiO2 =/< 200mmHg. (1).

In 2011, the European Society of Intensive Care Medicine proposed the Berlin ARDS definition to replace the AECC definition due to the limitation of diagnostic reliability. The Berlin definition used more specific criteria, which will be discussed at length in this presentation (1).

After years of extensive research- we know now that it is a complicated clinical condition caused by an inflammatory immune response resulting in endothelium permeability, non-cardiogenic pulmonary edema, and atelectasis.

Sources of lung injury that could lead to ARDS: sepsis, pneumonia, aspiration, trauma, blood transfusion, drug overdose, acute pancreatitis, shock, aspiration, cardiac reperfusion after surgical procedures such as liver transplantation or cardiac artery bypass, toxic inhalation such as smoke, DIC, and pulmonary contusion (2).

The Incidence of ARDS in the United States is approximately 60 cases/ 100,000 population per year (3). 10-23% of mechanically ventilated patients meet ARDS criteria (3).  Mortality associated with ARDS is 40-58%, and some studies have shown an approximate decrease in mortality by 50% when prone positioning is used (3).

Pathophysiology Breakdown: The Exudative Phase

The pathophysiology of ARDS can be broken down into 3 phases: exudative, proliferative, and fibrotic (3). 

The cause of the initial lung injury ultimately leading to ARDS can be either indirect or direct. In direct cases, the injurious agent reaches the lung through the airways or by trauma to the chest. In indirect, the injurious agent arrives at the lungs through the bloodstream. 

A direct or indirect agent injures alveolar capillary endothelial cells and type I pneumocytes (alveolar epithelial cells). This leads to a loss of the normally tight alveolar barrier to fluid and macromolecules, causing protein-rich edema fluid to accumulate in the interstitial and alveolar spaces (3).

Clinical Disorders Associated with the Development of ALI/ARDS

Credit: Atabai K, Matthay MA. Thorax 2000 / Frutos-Vivar F. et al. Curr Opin Crit Care. 2004

Pro-inflammatory cytokines and lipid mediators are increased in this acute phase, leading to the recruitment of leukocytes (especially neutrophils) into the pulmonary interstitium and alveoli (3). In addition, condensed plasma proteins aggregate in the air spaces with cellular debris and dysfunctional pulmonary surfactant- this forms hyaline membrane whorls (3).

Alveolar edema predominantly involves dependent portions of the lung with diminished aeration. As edema progresses, there is often a collapse of large sections of dependent lung, which in turn, contributes to decreased lung compliance. Consequently, intrapulmonary shunting and hypoxemia develop and the work of breathing increases, leading to dyspnea.

All of this is then exacerbated by microvascular occlusion that results in reductions in pulmonary arterial blood flow to ventilated portions of the lung (increased dead space! Helloooo V/Q mismatch!) and in pulmonary hypertension (3).

This means that in addition to severe hypoxemia, hypercapnia secondary to an increase in pulmonary dead space can be prominent in early ARDS. The exudative phase is typically the first 7 days of illness after exposure to an ARDS risk factor. Symptoms usually present within 12-36 hours of initial insult but can be delayed by 5-7 days (3).

So what will a patient look like in this phase? Typically dyspneic, with a sensation of rapid shallow breathing and an inability to get enough air. Tachypnea and increased work of breathing may progress rapidly from mild hypoxemia with a low oxygen requirement to severe hypoxemia with progressively increasing oxygen requirement with associated respiratory fatigue leading to respiratory failure- and ultimately a need for mechanical ventilation. An early hallmark clinical sign of ARDS is profound hypoxemia that is resistant to oxygen therapy. Not all patients with ARDS require endotracheal intubation but it should not be delayed if it is clinically indicated.

Laboratory values are generally nonspecific and are primarily indicative of underlying clinical disorders.

The chest x-ray will show infiltrates involving up to 75% of the lung fields but is often indistinguishable from cardiogenic pulmonary edema (CPE) (3). It’s possible to have both CPE and ARDS exist concurrently, and it is safer to assume that there is a component of ARDS and initiate therapies to reduce lung injury rather than ignore early radiographic findings. Both CPE and ARDS may share bilateral airspace opacifications, but ARDS is not typically associated with cardiomegaly or cephalization of the pulmonary vasculature (4). When trying to differentiate between CPE and ARDS on a basic chest radiograph, some findings that are helpful to keep in mind: while cardiogenic pulmonary edema typically begins centrally and ARDS will typically present with a uniform opacification (4). Pleural effusions are more often present in CPE and will respond to diuretic therapy, whereas pleural effusions in ARDS will persist despite diuresis (4). Kerley B lines are a common finding in CPE, whereas they are not typically found in a patient with ARDS (4). Radiographic and physical exam evidence of cardiogenic pulmonary edema (pleural effusions, cardiomegaly, peripheral edema, clinical heart failure) should be considered in patients with bilateral opacities and respiratory failure (3).

So basically in this phase, the patient looks like that patient whom you’re staring at wondering what’s wrong with them. They are obviously ill, but you just can’t figure out why. Lots of nonspecific findings and they look like there is impending doom.

Pathophysiology Breakdown: The Proliferative Phase

This phase typically occurs between days 7-21 of ARDS progression (3). Patients improve and are frequently extubated from mechanical ventilation during the proliferative phase.

 In terms of histology, this is where you will see the first signs of improvement. There is the initiation of lung repair, an organization of alveolar exudates, and a shift from neutrophil dense infiltrates to lymphocyte infiltrates (3).

 Despite this, some patients continue to experience dyspnea, tachypnea, and hypoxemia. Some patients will also begin to develop progressive lung injury and begin to show signs of pulmonary fibrosis.

Pathophysiology Breakdown: The Fibrotic Stage

The majority of patients recover from ARDS within 3-4 weeks; however, some patients develop a fibrotic stage of ARDS that often includes extended mechanical ventilation needs or noninvasive supplemental oxygen requirements (3). Low tidal volume and high peep mechanical ventilation along with steroids therapy (when appropriate) may prevent or reduce fibrosis. 

Histologically, the alveolar edema and inflammatory exudates that typically resolve, instead convert to extensive alveolar-duct and interstitial fibrosis (3). This disruption leads to emphysema-like pulmonary changes (3). 

The physiologic consequences include an increased risk of pneumothorax, reductions in lung compliance, and increased pulmonary dead space (3). 

Patients in this late phase experience a substantial burden of excess morbidity.

How Steroids Can Alter the Progression of ARDS

As explained previously, the majority of the pathological insult in ARDS occurs within the first 7 days during the exudative phase. The evolution of pulmonary and systemic inflammation during the first week will dictate the physiological progression from exudative to fibrosis. 

Patients who fail to improve in their mechanical ventilation requirements (PEEP and PaO2/FiO2 requirements), static lung compliance, and degree of infiltration on chest x-ray by day 7 of mechanical ventilation exhibit persistently high levels of circulating inflammatory markers, and a higher mortality rate. 

Since the direction of systemic inflammatory response is established early in the disease, there have been studies evaluating the effects of early administration of methylprednisolone and the effects on disease trajectory. 

Meduri (5) conducted a study that initiated prolonged low dose methylprednisolone (1mg/kg/d) within 72 hours of diagnosed ARDS in order to study the effects of ICU length of stay and length of mechanical ventilation by inducing a down-regulation of systemic inflammation. This particular study had fairly impressive results. By study day 7, 54% of patients in the treatment group were breathing without assistance versus 25% of patients in the placebo group (5). There was also a statistically significant decrease in ICU morality within the treatment group (20.6% vs 42.9%, p= 0.03) (5). 

Improvement by day 7 also correlated to survival by day 7 and overall hospital survival (5). While the use of steroids is not the primary method of treating ARDS, there is evidence showing that early and prolonged administration of glucocorticoids can lead to more ventilator-free days and decreased overall mortality by preventing the progression to fibrosis. I encourage you to investigate your particular hospital’s policy regarding ARDS and read additional studies pertaining to the use of steroids in ARDS treatment as the above is only a snapshot of one particular study and not a meta-analysis. It is generally accepted that steroids may help prevent fibrosis if given early, but as we well know there are many side effects which may outweigh the benefits in some patients.

Case Study: Patient Introduction

You are an ACP working in a busy Medical ICU. You are coming in to start your shift, and receive sign out on your patients. There was one admission overnight. A 23-year-old male, Shawn, who was brought into the emergency department from a concert venue with severe alcohol intoxication. He just graduated from college and was celebrating (too vivaciously) with his family and friends at the Jason Aldean concert.

Per his mom, he went for a run in the morning and came back to get ready for the tailgate. They started drinking around noon, and Shawn ventured off with some friends later in the afternoon. It wasn’t until several hours later that his family started to worry, and later got a call from the local emergency department that Shawn was in their care. He was found by EMS to be highly intoxicated and he was unable to comply with basic procedures, so he was taken to the hospital for further evaluation.

In the ER, he was given fluids; basic labs were drawn- including a blood alcohol level and toxicology screen. Labs were all within normal limits. His blood alcohol level was 250 mg/dL. Unfortunately, during his otherwise routine stay- Shawn vomited and aspirated.

Due to his severe intoxication and mental status impairment, Shawn wasn’t able to protect his airway and required intubation. It was at this point that he was admitted to the medical ICU for further care. Since he’s healthy, my initial plan is to extubate him early in the day once his sedation wears off and he passes a spontaneous breathing trial (SBT).

Case Study: Physical Exam

Vital Signs: Temperature: 37C tympanic, HR 97, BP 128/90, respiratory rate 25, SpO2 93% on volume control (VC) mechanical ventilation with settings of 60% fraction of inspired oxygen (FIO2), RR 18, PEEP 5, tidal volume (TV) 350.

HENT: Pupils are equal, round and reactive to light bilaterally. Moist mucous membranes. Native teeth intact.

Cardiovascular: Heart rate and rhythm regular. No murmurs, rubs or gallops. No peripheral edema. Nail beds pink, capillary refill <2 seconds.

Pulmonary: Intubated on VC, appears comfortable but tachypneic above set ventilator rate. No evidence of auto-PEEP. Diffuse crackles and rhonchi in all lung fields.

Gastrointestinal: Normoactive bowel sounds. Abdomen is symmetric, soft and nontender to palpation.

GU: Foley catheter in place draining yellow urine.

Skin: Intact. No rashes, lesions. Normal skin turgor.

Neurological: Unable to participate in physical examination due to intubation and sedation. No focal deficits noted. Appropriate response to painful stimuli.

You ask the nurse to hold his sedation and ask the respiratory therapist to transition him to 40% CPAP once he is awake and able to tolerate an SBT. The nurse calls you to the bedside 20 minutes later because he is failing his SBT and she wants to know if we should re-sedate him and give him more time. The patient is diaphoretic, tachypneic with a respiratory rate of 40/min, SpO2 of 85%, and tachycardic with a HR 127. What are your next steps? What is possibly driving this clinical change in an otherwise healthy young adult?

Initially, you decide to lightly re-sedate him, switch him back to full ventilation and 100% FiO2 to allow for his Spo2 to recover and order some diagnostic tests. First, you order basic lab work (CBC, CMP, lactate, coagulation studies, and an ABG). You also order a portable chest x-ray.

Diagnosing ARDS – The Berlin Criteria

A diagnosis of ARDS is made when a patient meets the Berlin criteria.  The Berlin criteria require that all four of the following are met (2):

1. 1. Timing: Symptoms have begun within 1 week of known clinical insult, or the patient has new or worsening respiratory symptoms over the past week
   2. Chest Imaging: Bilateral infiltrates consistent with diffuse pulmonary edema must be present on either a chest x-ray or chest CT scan that is not explained by pleural effusions, lobar collapse, lung collapse or pulmonary nodules
   3. Origin of edema: Respiratory failure must not be fully explained by cardiac failure or fluid overload. In the previous AECC definition, a cardiogenic cause of pulmonary edema had to be excluded by pulmonary artery catheterization showing a pulmonary artery occlusion pressure (PAOP) of <18. Since adopting the Berlin criteria, this has been phased out in favor of using an objective study to rule out hydrostatic pulmonary edema- such as an echocardiogram.
   4. Oxygenation: A moderate to severe impairment of oxygenation must be present- as defined by PaO2/FiO2. There is a direct correlation between the severity of hypoxemia and the severity of ARDS diagnosis:Mild ARDS—The PaO2/FiO2 ratio is > 200, but ≤ 300, on a ventilator with a positive end-expiratory pressure (PEEP) or continuous positive airway pressure ≥ 5 cm H2O. This used to be referred to as acute lung injury- this phrase is now replaced with mild ARDS.

Moderate ARDS—The PaO2/ FiO2 ratio is > 100, but ≤ 200 mmHg, on a ventilator with a PEEP ≥ 5 cm H2O.

Severe ARDS—The PaO2/ FiO2 ratio is ≤ 100 on a ventilator with a PEEP ≥ 5 cm H2O

Case Study: Early Results

You receive the lab results, which show that most everything is normal aside from a minor leukocytosis of 14,000.

His ABG is as follows: pH 7.45/CO2 26/ HCO3 22/ PaO2 105 on 100% FiO2.

Using the previous information regarding PaO2/FiO2, what stage of ARDS is the patient experiencing?

Using these numbers, the patient would have a PaO2/FiO2 of 105 (105/1(for 100%) compatible with moderate ARDS. In this particular patient, we can assume that the inciting incident was the episode of aspiration on stomach contents prior to intubation in the emergency department. Below is his chest x-ray immediately post-intubation compared to the chest x ray obtained after failing SBT.

What are our next steps in management?

Since ARDS is an inflammatory process set off due to an underlying disease process, our focus is to treat the underlying disease (in this case, aspiration pneumonia/pneumonitis) and support the respiratory system through the ARDS process.

What Do We Do With the Ventilator in ARDS?: Que the ARDSNet Protocol

The ARDS Network is an NIH based research network formed to carry out multi-center clinical trials focused on the treatment of ARDS. The goal of the Network was to efficiently test promising agents, devices, or management strategies to improve the care of patients with ARDS (8).

ARDSNet provides evidence-based guidance for the management of ARDS. The cornerstone of therapies are low tidal volume and high PEEP mechanical ventilation, and the conservative use of intravenous fluids (when there is no organ dysfunction caused by tissue hypoperfusion) in conjunction with the use of diuretics to hasten mechanical ventilation liberation (8).

The basics of the ARDSnet ventilator guidelines that practitioners should be aware of include ventilator setup and adjustment, oxygenation goal, plateau pressure goal, and ventilator weaning. As you move forward and read the guidelines associated with ventilation management in the ARDS patient, you will notice that there is an emphasis on low tidal volume ventilation. As a side effect of this guideline, patients are more likely to become hypercarbic, and subsequently, acidotic. The purpose of ventilator management is to allow the damaged and inflamed lungs to heal. In order for this to be successful, practitioners utilize a “permissive hypercapnia” philosophy. This means that evidence shows it is better to have patients who are hypercapnic and acidotic (to an extent) than to have a normal blood gas with ventilator settings that damage the lungs. The idea is that in ARDS we must allow the lungs to heal, even if the blood gas is not perfect. The focus of ARDS mechanical ventilation should be focused on optimizing the patient’s ventilation while protecting the lungs, and not driven by perfecting the ABG results.

Part I: Ventilator Set-up and Management

• The goal of mechanical ventilation in ARDS is to minimize inflammation by reducing baro/volutrauma to the lungs. In ARDS, the lungs are stiff and each ventilator breath causes alveolar shear, which, in turn, worsens the inflammation and perpetuates the cycle of increased inflammation and decreased gas exchange across the injured alveoli. By reducing tidal volume and increasing PEEP we can decrease alveolar shear.

• To lessen the opportunity of ventilator-associated lung injury, we use low tidal volume ventilation with high PEEP coupled with a high respiratory rate. As a surrogate of lung stiffness, we use Plateau pressure. If the plateau pressure is consistently above 30, this is an indicator that we are stretching the injured, stiff lungs too much and causing further injury.

• Below is the step-wise approach used by ARDSNet (8) to achieve adequate ventilation and oxygenation in the ARDS patient without adding insult to injury. You will notice that some of the calculations rely on the patients predicted body weight, which can be quickly and easily calculated using free online based calculators (such as MedCalc).

 Step-Wise Approach used by ARDSNet

1. Calculate predicted body weight (PBW)
   -Males = 50 + 2.3 [height (inches) – 60] and
   -Females = 45.5 + 2.3 [height (inches) -60]
2. Select any ventilator mode
3. Set ventilator settings to achieve initial VT = 8 ml/kg PBW
4. Reduce VT by 1 ml/kg at intervals ≤ 2 hours until VT = 6ml/kg PBW.
5. Set initial rate to approximate baseline minute ventilation (not > 35bpm).
6. Adjust VT and RR to achieve pH and plateau pressure goals below.

pH goal: 7.30- 7.45

Acidosis Management: (pH < 7.30)

If pH 7.15-7.30: Increase RR until pH > 7.30 or PaCO2 < 25

(Maximum set RR = 35).

If pH < 7.15: Increase RR to 35.

If pH remains < 7.15, VT may be increased in 1 ml/kg steps until pH >7.15 (Pplat target of 30 may be exceeded). May give NaHCO3

Alkalosis Management: (pH > 7.45) Decrease vent rate if possible. Consider sedation to facilitate.

Consider the effect of acidosis rather than the absolute number. Some patients may have hypotension, arrhythmias etc. at a Ph of 7.2 while others may tolerate a Ph of 7.1 without issues. In general the approach is one of “permissive acidosis”, meaning acidosis is permitted as much as possible in order to ensure lung-protective ventilation is maximized.

I:E Ratio Goal: Recommend that duration of inspiration be <duration of expiration.

Plateau Pressure Goal: ≤ 30 cm H2O

• The plateau pressure is the amount of pressure applied to the terminal airways and alveoli. It’s measured by using a 0.5 – 1-second inspiratory pause at end-inspiration, with a goal of <30 cm H2O. As you are titrating ventilator settings, the increasing PEEP coupled with decreased lung compliance can cause increased plateau pressure- leading to a higher risk of alveoli overdistension and lung injury. The use of tidal volumes >6-8 mL/kg can add to the risk of overdistension and ventilator-associated volumtrauma.
• Check Pplat (0.5 second inspiratory pause), at least q 4h and after each change in PEEP or VT.
• If Pplat > 30 cm H2O: decrease VT by 1ml/kg steps (minimum = 4ml/kg). As you begin to decrease the tidal volume especially if using volumes of 4mL/kg, make sure to check frequent ABGs to avoid losing the ground you gained correct acidemia.
• If Pplat < 25 cm H2O and VT< 6 ml/kg, increase VT by 1 ml/kg until Pplat > 25 cm H2O or VT = 6 ml/kg.
• If Pplat < 30 and breath stacking or dys-synchrony occurs: may increase VT in 1ml/kg increments to 7 or 8 ml/kg if Pplat remains < 30 cm H2O.

Please note that plateau pressures may be artificially elevated it patients are ventilator asynchronous or breathing against the ventilator.

Oxygenation Goal: PaO2 55-80 mmHg or SpO2 88-95%

• Use a minimum PEEP of 5 cm H2O. Consider the use of incremental FiO2/PEEP combinations to a max FiO2 of 100% and max PEEP of 24 to achieve goal.
• The physiologic reason behind using high levels of PEEP is to avoid the repetitive opening and closing of the atelectatic alveoli that can induce or worsen ventilator-induced lung injury. The idea is to keep the alveoli open at end-inspiration and to preserve the inspiratory lung recruitment (9).
• Below is information showing the incremental increase in PEEP with the associated down-titration of FiO2 (8).

Part II: Weaning

A. Conduct a Spontaneous Breathing Trial Daily When:

1. FiO2 ≤ 0.40 and PEEP ≤ 8 OR FiO2 < 0.50 and PEEP < 5.
2. PEEP and FiO2 ≤ values of previous day.
3. Patient has acceptable spontaneous breathing efforts. (May decrease vent rate by 50% for 5 minutes to detect effort.)
4. Systolic BP ≥ 90 mmHg without vasopressor support.
5. No neuromuscular blocking agents or blockade.

B. Spontaneous Breathing Trial (SBT):

If all above criteria are met and subject has been in the study for at least 12 hours, initiate a trial of UP TO 120 minutes of spontaneous breathing with FiO2 < 0.5 and PEEP < 5:

–Place on T-piece, trach collar, or CPAP ≤ 5 cm H2O with PS < 5

–Assess for tolerance as below for up to two hours:

1. SpO2 ≥ 90: and/or PaO2 ≥ 60 mmHg
2. Spontaneous VT ≥ 4 ml/kg PBW
3. RR ≤ 35/min
4. pH ≥ 7.3
5. No respiratory distress (distress= 2 or more)

– HR > 120% of baseline

– Marked accessory muscle use

– Abdominal paradox

– Diaphoresis

– Marked dyspnea

1. If tolerated for at least 30 minutes, consider extubation.
2. If not tolerated resume pre-weaning settings.
   

   Additional information and printable algorithm cards regarding the ARDSNet protocol can be found on their website www.ardsnet.org.

Case Study: Ventilator Management

Using the previous information, and knowing that your patient is a 23-year-old 6’2” male, what will you set the initial tidal volume to?

Initially, 8mL/kg PBW would be tidal volume of 658 mL. Since 6mL/kg PBW is also acceptable, we will start there.

What tidal volume would that be?

493 mL! Still some pretty big breaths! You select AC as your ventilator mode, set the FiO2 to 100% TV to 490, respiratory rate of 20 to start, and turn the PEEP up to 18. You let him rest for 30 minutes, and get your first ABG, which is as follows: pH 7.13/ CO2 65/ HCO3 25/ PaO2 76.

What changes will you make?

Per ARDSNet, you will increase the ventilator rate to correct the acidemia, and the PEEP to help with persistent hypoxemia. Recheck an ABG and follow this pattern until the pH is >7.3 or the CO2 is <25. For the next several hours, you follow this protocol, but the patient is remaining acidotic and his PaO2/FiO2 remains low. You’ve tried several times to titrate the PEEP up in order to bring the FiO2 below 100%, but his SpO2 precipitously drops to the low 80% range each time you try. His PEEP has been titrated up to 24, and his FiO2 remains at 100%.

After several ABGs with worsening acidosis, you decide to initiate chemical paralysis to ensure that you have complete control of his ventilation and respiratory effort. At times, adequate sedation is not enough to overpower the body’s innate respiratory drive and chemical paralysis is needed to physically take complete control of the patients respiratory effort and work towards correcting the profound acidosis.

You also initiate a steroid regimen since it is early in the disease process and can help decrease the likelihood of ARDS progressing to the fibrotic stage. Your patient is 190 lbs, and the recommended dose of methylprednisolone in ARDS is 1mg/kg/day. This comes out to 86mg/day, which will be scheduled to start this evening.

What next?

Prone Position in ARDS: What Is It and Why Are We Doing It?

Prone positioning is a therapeutic modality that has been used to aid in oxygenation in patients diagnosed with ARDS. It involves turning the patient completely over onto his or her stomach in the face-down position (10).

Prone positioning has been used with success for many years in patients who have developed ARDS, and there have been numerous RCTs confirming that oxygenation is significantly improved in patients who are in the prone position rather than in a supine position.

Prone positioning first came into practice in the 1970s after the introduction of CT scanning. It was observed on CT scans that lung consolidation and edema was primarily in the dependent lung regions with the aerated portion of the lung is in the non-dependent areas (11).

According to the PROSEVA study (12), patients should be considered for prone positioning if they have ARDS secondary to sepsis and if their PaO2/FiO2 <150. When this guideline was followed within the first 26 hours of intubation and used for >16 hours/day, patients showed improved mortality, improved oxygenation, and improved lung compliance.

Although there is an improvement in patient arterial oxygen saturation in the prone position, it is likely due to the homogenous redistribution of alveolar stress in the prone position versus the supine position rather the original hypothesis of better aerating nondependent areas of lung.

The mechanisms by which prone positioning may benefit patients with acute respiratory distress syndrome (ARDS) undergoing mechanical ventilation include improving ventilation–perfusion matching (2), increasing end-expiratory lung volume (3), and preventing ventilator-induced lung injury by more uniform distribution of tidal volume through lung recruitment and alterations in chest wall mechanics (12).

When To Initiate Prone Position in ARDS

• There is no hard and fast rule as to when to initiate prone therapy. There are patient specific factors that must be considered as well as hospital resources. It is a resource-intensive process and requires vigorous monitoring.
• The literature is suggesting that earlier proning may be better for both short and long-term outcomes. Currently is it often used as a last resort, whereas it may have more benefit when used early.
• One of the strongest recommendations comes from the surviving sepsis campaign, which says the following about ARDS in sepsis: “We recommend using prone over supine position in adult patients with sepsis-induced ARDS and a PaO2 /F IO2 ratio < 150 (strong recommendation, moderate quality of evidence).” (16)
• As you can imagine this would require a great many more patient receive prone therapy than currently do so. It remains an area of great debate but there is some strong evidence suggesting that earlier proning may be superior, hence this recommendation.
• In the PROSEVA trial patients were included if they were on more than 60% Fi02 and 6>cm of water of PEEP with a Pa02/Fi02 ratio of <150. It is very important to note that all patients underwent a “stabilization” periods of 12-24 hours (12). In other words they had to demonstrate persistent hypoxia for this length of time before prone positioning was initiated. This is important because many patients are hypoxemic prior to ventilator changes and an adequate rest period post-intubation.
• As you can see a Pa02/Fi02 ratio of <150 has been a popular milestone. Clinical practices vary and an individualized choice has to be made for reach patient. It is also important to remember that low-tidal volume, high PEEP therapy is likely synergistic with proning therapy.

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