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Difficult Airway Society Guidelines
How to dominate the Ventilator
Mechanical Ventilation

Difficult Airway Society Guidelines

Difficult Airway Society Guidelines for the management of tracheal extubation

Anaesthesia:Volume 67, Issue 3, pages 318–340, March 2012

Introduction:

Tracheal extubation is a high-risk phase of anaesthesia. The majority of problems that occur during extubation and emergence are of a minor nature, but a small and significant number may result in injury or death.

Problems at extubation: why is extubation hazardous?

1. Problems related to airway reflexes:

The return of airway reflexes depends on many factors, and may be delayed for some hours after removal of the tracheal tube. In practice, exaggerated, reduced (obtunded) and dysfunctional reflexes may all cause problems.

2. Exaggerated laryngeal reflexes:

Breath holding, coughing and bucking (a forceful and protracted cough that mimics a Valsalva manoeuvre) are physiological responses to airway stimulation and are associated with increases in arterial blood pressure, venous pressure and heart rate.

Laryngospasm is a protective exaggeration of the normal glottic closure reflex. Laryngospasm is often triggered by the presence of blood, secretions or surgical debris, particularly in a light plane of anaesthesia. Nasal, buccal, pharyngeal or laryngeal irritation, upper abdominal stimulation or manipulation and smell have all been implicated in the aetiology of laryngospasm.

Laryngospasm causes signs of upper airway obstruction (including stridor) that can precede complete airway obstruction and requires an immediate response. If not relieved promptly, laryngospasm may result in post-obstructive pulmonary oedema (also known as negative pressure pulmonary oedema) and hypoxic cardiac arrest.

3. Reduced airway reflexes:

Upper airway reflexes maintain tone and upper airway patency; laryngeal reflexes protect the lower airway. Reduced laryngotracheal reflexes increase the risk of aspiration and airway soiling. Partial or complete airway obstruction with forceful inspiratory effort generates a significant negative intrathoracic pressure, which opens the oesophagus increasing the risk of regurgitation.

Protective laryngeal reflexes are impaired after tracheal extubation, and may be compromised following airway management with a supraglottic airway device.

This is a particular problem in obese patients and in those with obstructive sleep apnoea (OSA).

4. Dysfunctional laryngeal reflexes:

Paradoxical vocal cord motion describes a rare condition in which vocal cord adduction occurs on inspiration, and can cause stridor following extubation. It is more common in young females and in those with emotional stress. The condition is often misdiagnosed and treated as laryngospasm or bronchospasm. The diagnosis can only be made by direct observation of the vocal cords, and responds to treatment with anxiolytic, sedative or opioid agents.

5. Depletion of oxygen stores at extubation:

Various factors that contribute to rapid depletion of oxygen stores and a reduction in arterial oxygen saturation are summarized:

Pathophysiological	Reduced functional residual capacity
	Hypoventilation)
	Diffusion hypoxia
	Atelectasis
	Ventilation/perfusion mismatch
	Problems related to airway reflexes
	Shivering
	Cardiovascular instability
	Neurological dysfunction
	Metabolic derangement
	Electrolyte disturbances
	Airway injury
Pharmacological	Neuromuscular blocking drugs
	Opioids
	Residual anaesthetic agents
Human & other factors	Inadequate equipment
	Inadequate skilled assistance
	Patient position
	Access to airway e.g. dressings/gastric tubes/rigid fixators
	Interruption of oxygen supply during patient transfer
	Communication difficulties (e.g. language, mental capacity)
	Removal of oxygen by agitated or uncooperative patient

6. Airway injury:

Injury to the airway may be the result of direct trauma following surgical or anaesthetic intervention, or it may be indirect due to subsequent bleeding, swelling or oedema.

Managing extubation:

Extubation is an elective process, and it is important to plan and execute it well.

The guidelines describe the following four steps:

Step 1:	Plan extubation.
Step 2:	Prepare for extubation.
Step 3:	Perform extubation.
Step 4:	Post-extubation care: recovery and follow-up.

The DAS extubation guidelines:

I. DAS extubation guidelines: basic algorithm.

2. DAS extubation guidelines: ‘low-risk’ algorithm:

Sequence for ‘low-risk’ extubation in an awake patient.

1 Deliver 100% oxygen through the breathing system

2 Remove oropharyngeal secretions using a suction device, ideally under direct vision

3 Insert a bite block to prevent occlusion of the tube

4 Position the patient appropriately

5 Antagonise residual neuromuscular blockade

6 Establish regular breathing and an adequate spontaneous minute ventilation

7 Allow emergence to an awake state of eye-opening and obeying commands

8 Minimise head and neck movements

9 Apply positive pressure, deflate the cuff and remove the tube while the lung is near vital capacity

10 Provide 100% oxygen with an anaesthetic breathing system and confirm airway patency and adequacy of breathing

11 Continue delivering oxygen by mask until recovery is complete

Sequence for ‘low-risk’, deep extubation. Deep extubation is a technique that should be reserved for spontaneously breathing patients with uncomplicated airways and only performed by clinicians familiar with the technique.

1 Ensure that there is no further surgical stimulation

2 Balance adequate analgesia against inhibition of respiratory drive

3 Deliver 100% oxygen through the breathing system

4 Ensure adequate depth of anaesthesia with volatile agent or TIVA as appropriate

5 Position the patient appropriately

6 Remove oropharyngeal secretions using a suction device, ideally under direct vision

7 Deflate the tracheal tube cuff. Airway responses such as cough, gag or a change in breathing pattern indicate an inadequate depth and the need to deepen anaesthesia

8 Apply positive pressure via the breathing circuit and remove the tracheal tube

9 Reconfirm airway patency and adequacy of breathing

10 Maintain airway patency with simple airway manoeuvres or oro-/nasopharyngeal airway until the patient is fully awake

11 Continue delivering oxygen by mask until recovery is complete

12 Anaesthetic supervision is needed until the patient is awake and maintaining their own airway

3. DAS extubation guidelines: ‘at-risk’ algorithm:

Sequence for LMA exchange in ‘at-risk’ extubation.

1 Administer 100% oxygen

2 Avoid airway stimulation: either deep anaesthesia or neuromuscular blockade is essential

3 Perform laryngoscopy and suction under direct vision

4 Insert deflated LMA behind the tracheal tube

5 Ensure LMA placement with the tip in its correct position

6 Inflate cuff of LMA

7 Deflate tracheal tube cuff and remove tube whilst maintaining positive pressure

8 Continue oxygen delivery via LMA

9 Insert a bite block

10 Sit the patient upright

11 Allow undisturbed emergence from anaesthesia

Sequence for use of a remifentanil infusion for ‘at-risk’ extubation.

1 Consider postoperative analgesia. If appropriate, administer intravenous morphine before the end of the operation

2 Before the end of the procedure, set the remifentanil infusion at the desired rate

3 Antagonise neuromuscular blockade at an appropriate phase of surgery and emergence

4 Discontinue anaesthetic agent (inhalational agent or propofol)

5 If using inhalational agent, use high-flow oxygen-enriched gas mixture to aid full elimination and monitor its end tidal concentration

6 Continue ventilation

7 Laryngoscopy and suction should be performed under direct vision if appropriate

8 Sit the patient upright

9 Do not rush, do not stimulate, wait until the patient opens their eyes to command

10 Discontinue positive pressure ventilation

11 If spontaneous respiration is adequate, remove the tracheal tube and stop the infusion

12 If spontaneous respiration is inadequate, encourage the patient to take deep breaths and reduce the infusion rate

13 When respiration is adequate, remove the tracheal tube and discontinue the remifentanil infusion, taking care to flush residual drug from the cannula

14 After extubation, there is a risk of respiratory depression and it is essential that the patient is closely monitored until fully recovered

15 Remember that remifentanil has no long-term analgesic effects

16 Remember that remifentanil can be antagonised by naloxone

Sequence for use of an airway exchange catheter for ‘at-risk’ extubation.

1 Decide how far to insert the AEC. It is essential that the distal tip remains above the carina. If there is any un certainty about the position of the tracheal tube tip, its position relative to the carina should be checked with a fibreoptic bronchoscope before AEC insertion. An AEC should never be inserted beyond 25 cm in an adult patient

2 When the patient is ready for extubation, insert the lubricated AEC through the tracheal tube to the predetermined depth. Never advance an AEC against resistance

3 Employ pharyngeal suction before removal of the tracheal tube

4 Remove the tracheal tube over the AEC, while maintaining the AEC position (do not advance the AEC)

5 Secure AEC to the cheek or forehead with tape

6 Record the depth at the teeth/lips/nose in the patient’s notes

7 Check that there is a leak around AEC using an anaesthetic circuit

8 Clearly label the AEC to prevent confusion with a nasogastric tube

9 The patient should be nursed in a high dependency or critical care unit

10 Supplemental oxygen can be given via a facemask, nasal cannula or CPAP mask

11 The patient should remain nil by mouth until the AEC is removed

12 If the presence of the AEC causes coughing, check that the tip is above the carina and inject lidocaine via the AEC

13 Most patients remain able to cough and vocalise

14 Remove the AEC when the airway is no longer at risk. They can be tolerated for up to 72 hours

Sequence for use of an airway exchange catheter for reintubation.

1 Position the patient appropriately

2 Apply 100% oxygen with CPAP via a facemask

3 Select a small tracheal tube with a soft, blunt bevelled tip (for example, the tube developed for use with an intubating LMA (Intavent Direct Ltd, Maidenhed UK).

4 Administer anaesthetic or topical agents as indicated

5 Use direct or indirect laryngoscopy to retract the tongue and railroad the tracheal tube (with the bevel facing anteriorly) over the AEC

6 After reintubation, confirm the position of the tracheal tube with capnography

Conclusion:

The DAS extubation guidelines promote the concept of an extubation strategy, involving a stepwise approach to planning, preparation and risk stratification, aimed at clear identification and management of patients ‘at risk’ during extubation.

SOURCE: Guidelines: Difficult Airway Society Guidelines for the management of tracheal extubation. Anaesthesia: Volume 67, Issue 3, pages 318–340, March 2012

Further Reading:

1. The Physiology of Extubation Failure: Podcast.

2. The Pathomechanics of Extubation Failure. PulmCCM Journal.

How to dominate the Ventilator

Scott Weingart MD RDMS FACEP

Two Strategies of Ventilation

Injury:	This strategy is for patients with lung injury and those prone to lung injury. Essentially this means every intubated patient except those with…
Obstruction:	Use this strategy when patients are in the midst of an Asthma/COPD exacerbation.

Injury Strategy

Based on ARDSnet (ARMA Study-N Engl J Med 2000;342,1301-1308)

Mode

Assist Control (AC)-Volume

Tidal Volume (Vt)=Protection

	6-8 cc/kg, based on PBW (see last page). If ALI/ARDS, the goal is to get down to 6 cc/kg.
	Injured lungs are baby lungs.
	This setting should not be altered to fix ventilation.
	It only gets changed for lung protection (i.e. to prevent barotrauma/volutrauma).

Flow Rate (IFR)=Comfort

	60-80 lpm
	This setting controls how quickly the air goes in.

Rate (RR)=Ventilation

	Initially 18, adjust based on CO2 and ventilatory needs.
	Va (Alveolar Ventilation) for a normal CO2 when not intubated is 60 cc/kg/min.
	We need to double that to 120 cc/kg/min when intubated b/c of increased deadspace.
	Need double that volume (240 cc/kg/min) to send CO2 from 40 to 30.
	Try to keep mildly hypercarbic.

FiO2/PEEP=Oxygenation

Many ventilator evils would be fixed if these were on one knob

	Start at 100% and PEEP of 0 or 5.
	Wait 5 minutes and then draw an ABG.
	Then set the FiO2 to 30% and start titrating based on the chart. Go up every 5-10 minutes; quicker if low saturation.

OXYGENATION GOAL: PaO2 55-80 mmHg or SpO2 88-95%

Use a minimum PEEP of 5 cm H2O. Consider use of incremental FiO2/PEEP combinations such as shown below (not required) to achieve goal.

Many doctors, even in specialties that should know better, are irrationally afraid of PEEP.

Check Plateau Pressure

	Check it after initial settings and at regular intervals thereafter.
	Use the inspiratory hold button, hold for 0.5 sec—look at pressure gauge.
	The peak pressure is essentially meaningless.
	Plateau pressure must be maintained <30 cm H20. Keep lowering the Vt until Plat <30. You may need to go as low as 4 cc/kg.

Note: The plateau pressure is the pressure applied (in positive pressure ventilation) to the small airways and alveoli. The peak pressure is the pressure measured by the ventilator in the major airways, and it strongly reflects airways resistance.

The figure above is a waveform of a patient on volume control ventilation with a 0.8 second inspiratory hold. (Courtesy: Critical Care Medicine Tutorials)

Disadvantages of this strategy

	It is not the most comfortable strategy of ventilation for awake, spontaneously breathing patients.
	Use sedation/pain medications.
	Give enough flow; if you see the patient sucking the straw, increase the IFR setting

Obstructive Strategy

Goal is to give as much expiratory time as possible

Mode-Assist Control

Vt-8 cc/kg by PBW (Predicted Body Weight)

IFR-80-100 lpm

PEEP-0

FiO2-use whatever you need, most folks are fine at 40%

RR-Start at 10 bpm. Look for I:E of 1:4 or 1:5 Adjust the rate to achieve this.

Permissive Hypercapnia

	Patients will need tons of sedation/opioids.
	Keep pH above 7.1; rarely, you may need a bicarb drip to accomplish this.
	Give enough flow; if you see the patient sucking the straw, increase the IFR setting

AutoPEEP and Airtrapping

They decrease venous return, impede expiration, & impede spontaneous ventilation.

Other Concerns:

Large Tubes:

At least 8.0 size ETT whenever possible, for both male and female patients. Pulmonary toilet and ICU care is miserable with small tubes. Biofilm forms within the first two days reducing tube size dramatically.

Ventilator Alarms:

Treat them like a code announcement. The closest person should run to the patient’s bedside and assess the situation.

Mechanical Ventilation Protocol Summary

NIH NHLBI ARDS Clinical Network

INCLUSION CRITERIA:

Acute onset of

	PaO2/FiO2 ≤ 300 (corrected for altitude)
	Bilateral (patchy, diffuse, or homogeneous) infiltrates consistent with pulmonary edema
	No clinical evidence of left atrial hypertension

PART I: VENTILATOR SETUP AND ADJUSTMENT

1. Calculate predicted body weight (PBW)

	Males = 50 + 2.3 [height (inches) - 60]
	Females = 45.5 + 2.3 [height (inches) -60]

	Select any ventilator mode
	Set ventilator settings to achieve initial VT = 8 ml/kg PBW
	Reduce VT by 1 ml/kg at intervals ≤ 2 hours until VT = 6ml/kg PBW.
	Set initial rate to approximate baseline minute ventilation (not > 35 bpm).
	Adjust VT and RR to achieve pH and plateau pressure goals below.

OXYGENATION GOAL: PaO2 55-80 mmHg or SpO2 88-95%

Use a minimum PEEP of 5 cm H2O. Consider use of incremental FiO2/PEEP combinations such as shown below (not required) to achieve goal.

PLATEAU PRESSURE GOAL: ≤ 30 cm H2O

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 = 4 ml/kg).

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.

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.

I: E RATIO GOAL: Recommend that duration of inspiration be < duration of expiration.

PART II: WEANING:

A. Conduct a SPONTANEOUS BREATHING TRIAL daily when:

	FiO2 ≤ 0.40 and PEEP ≤ 8
	PEEP and FiO2 ≤ values of previous day.
	Patient has acceptable spontaneous breathing efforts. (May decrease vent rate by 50% for 5 minutes to detect effort.)
	Systolic BP ≥ 90 mmHg without vasopressor support.
	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.
	SpO2 ≥ 90: and/or PaO2 ≥ 60 mmHg
	Spontaneous VT ≥ 4 ml/kg PBW
	RR ≤ 35/min
	pH ≥ 7.3
	No respiratory distress (distress= 2 or more)

	HR > 120% of baseline
	Marked accessory muscle use
	Abdominal paradox
	Diaphoresis
	Marked dyspnea

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

Definition of UNASSISTED BREATHING

(Different from the spontaneous breathing criteria as PS is not allowed)

1.Extubated with face mask, nasal prong oxygen, or room air, OR

2.T-tube breathing, OR

3.Tracheostomy mask breathing, OR

4.CPAP less than or equal to 5 cm H20 without pressure support or IMV assistance.

Ref:

1. The 1. NHLBI ARDS Network, Lower Tidal Volume / Higher PEEP Reference Card

2. EMCrit Blog: EMCrit Lecture – Dominating the Vent: Part I

3. Critical Care Medicine Tutorials

Mechanical Ventilation in ARDS: 2014 Update

PulmCCM Updates

Introduction

People with acute respiratory distress syndrome (ARDS) are by definition severely hypoxemic, and nearly all require invasive mechanical ventilation. Yet mechanical ventilation itself can further injure damaged lungs (so-called ventilator-induced lung injury); minimizing any additional damage while maintaining adequate gas exchange (“compatible with life”) is the central goal of mechanical ventilation in ARDS and acute lung injury, its less-severe form.

Benefits of Low Tidal Volume Ventilation in ARDS:

Low tidal volume ventilation (LTVV) reduces the damaging, excessive stretch of lung tissue and alveoli (so-called volutrauma), and is the standard of care for people with ARDS requiring mechanical ventilation.

The meta-analyses including ten randomized trials total, have convinced most intensivist physicians that using low tidal volumes improves survival for people with ARDS. Taken together, the trials suggest that a strategy of low tidal volume ventilation (6-8 mL/kg ideal body weight) reduces absolute mortality by about 7-9%, as compared to using >= 10 mL/kg tidal volumes (~42% mortality in control groups vs. ~34% in the LTVV groups).

How to Use Low Tidal Volume Ventilation in ARDS:

The protocol from the ARMA trial can serve as a guide to performing low tidal volume ventilation for mechanically ventilated patients with ARDS:

	Start in any ventilator mode with initial tidal volumes of 8 mL/kg predicted body weight in kg, calculated by: [2.3 *(height in inches - 60) + 45.5 for women or + 50 for men].
	Set the respiratory rate up to 35 breaths/min to deliver the expected minute ventilation requirement (generally, 7-9 L /min)
	Set positive end-expiratory pressure (PEEP) to at least 5 cm H2O (but much higher is probably better), and FiO2 to maintain an arterial oxygen saturation (SaO2) of 88-95% (paO2 55-80 mm Hg). Titrate FiO2 to below 70% when feasible (though ARDSNet does not specify this).
	Over a period of less than 4 hours, reduce tidal volumes to 7 mL/kg, and then to 6 mL/kg.

Ventilator adjustments are then made with the primary goal of keeping plateau pressure (measured during an inspiratory hold of 0.5 sec) less than 30 cm H2O, and preferably as low as possible, while keeping blood gas parameters “compatible with life.” High plateau pressures vastly elevate the risk for harmful alveolar distension (a.k.a. ventilator-associated lung injury, volutrauma). If plateau pressures remain elevated after following the above protocol, further strategies should be tried:

	Further reduce tidal volume, to as low as 4 mL/kg by 1 mL/kg stepwise increments.
	Sedate the patient (heavily, if necessary) to minimize ventilator-patient dyssynchrony.
	Consider other mechanisms for the increased plateau pressure besides the stiff, noncompliant lungs of ARDS.

As a last resort, neuromuscular blockade can be employed to reduce plateau pressure by eliminating patient effort, muscle tone and dyssynchrony. However, this approach has unquantified risks of long-term neuromuscular weakness and disability.

Permissive Hypercapnia in ARDS:

This single-minded focus on reducing plateau pressures derives from the likely survival benefit from low tidal volume ventilation and low plateau pressures observed in clinical trials (or if you prefer, the harmful effects seen from using “normal” or physiologic tidal volumes with resulting high plateau pressures in those trials).

Achieving these low plateau pressures usually requires tidal volumes low enough to result in hypoventilation, with resulting elevations in pCO2 and respiratory acidemia that can be severe and to the treating physician, anxiety-provoking. This approach, “permissive hypercapnia,” represents a paradigm shift from previous eras, in which achieving normal blood gas values was the main goal of mechanical ventilation.

How “permissive” can one be? Mechanically ventilated patients with ARDS appear to tolerate very low blood pH and very high pCO2s without any adverse sequelae (defying physicians’ anxieties based on intuition, training and medical lore):

	Current consensus suggests it is safe to allow pH to fall to at least 7.20.
	The actual pCO2 is of little importance.
	When pH falls below 7.20, many physicians choose to administer sodium bicarbonate, Carbicarb, or THAM to maintain blood pH between 7.15 – 7.20.
	However, it is unknown whether such correction of acidemia is helpful, harmful, or neither (good evidence is lacking for any of these hypotheses).

Conditions in which permissive hypercapnia for ARDS could theoretically be harmful include cerebral edema, mass lesions or seizures; active coronary artery disease; arrhythmias; hypovolemia; GI bleeding, and possibly others. These are hypothetical harms based on pathophysiology and not outcomes data, while the harm of ventilator induced lung injury and the benefits of a protective ventilator strategy in ARDS are real and known. The potential risks of hypercapnia in such patients must be weighed against the risks of ARDS, and therapy individualized.

Limitations in Use of Plateau Pressure for ARDS:

Patients with reduced chest wall compliance — most commonly due to obesity — may have higher plateau pressures at baseline and during ARDS than non-obese patients. It is possible that in some obese patients, titrating tidal volumes to plateau pressures < 30 cm H2O may be inadequate and result in worsened hypoventilation. There are no recommendations to treat obese patients with ALI / ARDS differently than non-obese patients with regard to mechanical ventilation. Esophageal manometry is considered superior to plateau pressures through its measurement of transpulmonary pressure, considered a more precise measure of potentially injurious pressures in the lung. Because it is invasive and the probes are prone to migration, esophageal manometry is not widely used.

Prone Positioning in ARDS:

Prone positioning (face-down) improves gas exchange and has long been used as an adjunctive or salvage therapy for severe or refractory ARDS. Prone positioning is gaining credibility as a new standard of care for ARDS after a multicenter trial published in 2013, demonstrated a dramatic near-50% relative risk reduction, and a 17% absolute risk reduction for mortality. Patients were kept in prone position for 16 hours a day in that trial, which was conducted at 27 European centers highly experienced with prone positioning for ARDS. The benefits of prone positioning have not yet been replicated in a large U.S. trial, but a meta-analysis of 6 randomized trials also concluded prone positioning saves lives in ARDS when added to a lung-protective ventilatory strategy.

High vs. Low PEEP in ARDS:

A strategy employing higher PEEP along with low tidal volume ventilation should be considered for patients receiving mechanical ventilation for ARDS. This suggestion is based on a 2010 meta-analysis of 3 randomized trials (n=2,229) testing higher vs. lower PEEP in patients with acute lung injury or ARDS, in which ARDS patients receiving higher PEEP had a strong trend toward improved survival.

However, patients with milder acute lung injury (paO2/FiO2 ratio > 200) receiving higher PEEP had a strong trend toward harm in that same meta-analysis. Higher PEEP can conceivably cause ventilator-induced lung injury by increasing plateau pressures, or cause pneumothorax or decreased cardiac output. These adverse effects were not noted in the largest ARDSNet trial (2004) testing high vs. low PEEP.

Predicting Survival and Outcomes After ARDS:

In a 2012 retrospective analysis in JAMA including data from over 4,400 patients with ARDS enrolled in randomized trials, only the severity of hypoxemia (low PaO2/FiO2 ratio) was predictive of mortality. Commonly used clinical parameters of severity (static compliance, degree of PEEP, and extent of opacities on chest X-ray) were not predictive of outcome. A “high risk” patient profile with a 52% mortality was identified post hoc, comprised of severe ARDS (PaO2/FiO2 ratio < 100) with either a high corrected expired volume >= 13 L/min, or a low static compliance < 20 mL/cm H2O. Reviews of ARDS outcomes suggest that most people who survive ARDS recover pulmonary function, but may remain impaired for months or years in other domains, both physically and psychologically.

Alternative / Rescue Ventilator Modes & ECMO in ARDS:

Some patients with severe ARDS develop severe hypoxemia or hypercarbia with acidemia despite optimal treatment with low-tidal volume mechanical ventilation. In these situations, alternative, salvage or “rescue” ventilator strategies are often employed. Their common goal is to maintain high airway pressures to maximize alveolar recruitment and oxygenation, while minimizing alveolar stretch or shear stress. The most commonly used alternative ventilatory strategies are high-frequency oscillatory ventilation (HFOV) or airway pressure release ventilation (APRV or “bilevel”). HFOV is not appropriate as a first-line treatment for ARDS.

SOURCE:

Mechanical Ventilation in ARDS: 2014 Update: PulmCCM Updates.

Further Reading:

1. ARMA Trial (N Engl J Med)- Ventilation with Lower Tidal Volumes as Compared with Traditional Tidal Volumes for Acute Lung Injury and the Acute Respiratory Distress Syndrome. N Engl J Med 2000; 342:1301-1308May 4, 2000.

2. Meta-analysis: ventilation strategies and outcomes of the acute respiratory distress syndrome and acute lung injury. Ann Intern Med. 2009 Oct 20;151(8):566-76.

3. Ventilation with lower tidal volumes versus traditional tidal volumes in adults for acute lung injury and acute respiratory distress syndrome. Cochrane Database Syst Rev. 2004;(2):CD003844.

ISA KANYAKUMARI

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