Ventilatory Weaning and Extubation

Tobins review of the weaning meta-analysis and MAs in general (Crit Care Med 2008;36:1)

Weaning from Mechanical Ventilation

Most patients fail weaning because of excessive respiratory loads leading to muscle fatigue.

weaning can be complicated by many factors associated with long-term CMV that cause respiratory pump failure, such as sedation overhang, sleep deprivation, psychological factors, malnutrition, bronchoconstriction, and neuromuscular problems

Predictors of successful weaning

Frequency/V_T

increased time to wean in a study when added to SBTs (Crit Care Med 2006;34:2530)

PaO2/FiO2

PEEP

Cough with suctioning

Maximum Inspiratory Pressure (P_IMAX)

if less than -30 predictive of successful wean if greater than -20, predictive of unsuccessful wean

Leak Volume on Cuff Deflation

after extubation, ~5% of patients develop laryngeal edema. Absence of a leak with cuff deflation is predictive of laryngeal edema. Look for at least 110 cc of leak averaged over three lowest volumes.

weaning parameters

Methods of Weaning

Once daily T-piece trials should probably be the standard, ~30 minutes with failures placed back on full support.

When evaluating IMV vs PSV vs spont breathing trials, the latter won handily NEJM 1995;332:345-50)

Tobin's Analysis of Rapid Shallow

Reintubation Following Unsuccessful Weaning

10-20% of successfully weaned patients will require reintubation within 24 hours

Upper airway obstruction, excess secretions, respiratory failure, CHF, encephalopathy are among the reasons

Extubation

Extubation over airway exchange cath seems to ease reintubation in patients. (Anesth Analg 2007;105)

Steroids

Extubation: good method for extubating patient with known difficult airway (patient may not breathe adequately after extubation; reintubation may not be possible) over jet stylet, tube changer, or airway exchange catheter; use tube changer to give patient 1 to 3 puffs per minute from jet ventilator while determining if he or she able to respire; if patient not ventilating adequately, use laryngoscope to slide new endotracheal tube into place over tube changer

Emergency Department Extubation

Post-Extubation Complications

Extubated patients are prone to aspiration because of vocal cord dysfunction for at least 8 hours after tube removal

Delayed sequelae are seen when ulcerations from the tube heal and cause laryngeal or tracheal stenosis. High volume low pressure cuffs have sharply decreased the incidence of stenosis

consider extubation under these conditions— awake and responsive, adequate cough reflex, hemodynamically stable, minimal bleeding, normothermic (not shivering), adequate renal function, and weaning parameters met

can get negative pressure pulmonary edema from struggling against closed or swollen glottis

prospective study included 76 patients with endotracheal intubation for more than 12 h. The leak, in percent, was defined as the difference between expired tidal volume measured just before extubation, in volume-controlled mode, with the cuff inflated and then deflated. A gas leak around the endotracheal tube greater than 15.5% can be used as a screening test to limit the risk of re-intubation for laryngeal edema. (Intensive Care Med. 2002 Sep;28(9):1267-72.) Leak test is only 80% sensitivie

Work of Breathing

Work can be defined as the force needed to effect a change. For instance, if one were to push a chair from one side of the room to the other, the amount of work necessary for this action could be determined by measuring how much pressure was applied to the chair and how far the chair is moved. Thus, work in this example would be calculated as force x distance. WOB can be expressed in a similar format, with force being expressed as the pressure that is required to effect a change in volume and similarly could be expressed as pressure x volume, where pressure is the effort or force generated by the respiratory muscles or ventilator, and volume is the amount of gas exchanged as a result of the force applied.

The work load placed on the respiratory muscles is minimal during quiet breathing, accounting for approximately 5% of the total body oxygen consumption.^[1] Even under stress, a normal individual will be able to increase their ventilation with only a moderate increase in total work. This is testimony to the amazing configuration of the respiratory apparatus.

For the patient receiving mechanical ventilation, the work necessary for effective ventilation can be visualized as either physiologic work or imposed work (Table 1).

Table 1. Classifications of Work

Total Work of Breathing = Physiologic + Imposed

Physiologic Work of Breathing = Elastic + Nonelastic

Imposed Work of Breathing = Ventilator Demand Valve + Circuit + Artificial Airway

Physiologic Work of Breathing

Much of what we know about the about the WOB originates from the early works of Otis and coworkers.^[2] They partitioned the WOB into those forces required to overcome the elastic resistance and the frictional resistance of the lungs, chest wall, and airways. The elastic component is primarily influenced by inward recoil of the lungs and the outward recoil of the chest wall. Elastic work is performed primarily during inspiration to expand the lungs and chest wall, which creates a pressure gradient to move gas into the lungs. Factors that contribute to the elastic WOB include the compliance "stiffness" of the pulmonary tissue, inward recoil pressure of the chest wall, and resistance offered by the abdominal cavity. Patients who have an underlying disorder that results in decreased lung or chest wall compliance will require more work to effect a given change in tidal volume. Included in this group are those with decreased compliance secondary to pulmonary infiltrates, fibrotic parenchymal disorders, atelectasis, and abdominal distention.

Energy to overcome the frictional forces during quiet or active breathing is primarily directed at overcoming flow resistance created in the airways. This frictional component is often referred to as the nonelastic WOB. Nonelastic work loads are generated in the airways as gas flows through them during inspiration and expiration. Typically referred to as airways resistance, this work load is primarily influenced by the caliber and configuration of the airways. Acute chances in airway resistance may occur with accumulation of airway secretions, constriction of airway smooth muscle, edema, and inflammation of airway mucosal lining as seen during an asthma attack. Additionally, aspiration of foreign bodies or narrowing of the airway from extralumunal compression also increases the nonelastic WOB. Chronic changes in airway caliber are frequently seen in patients with chronic obstructive pulmonary disease (COPD), especially those diagnosed with chronic bronchitis. In these patients, the airway loses some of its natural rigidity, through repeated infections, and may partially collapse.

In normal individuals, approximately two thirds of the total WOB can be attributed to elastic forces and the remaining one third to nonelastic (frictional) forces (Table 2).^[3] The majority of the physiologic WOB is performed during inspiration due to the natural recoil properties of the lung and chest wall that provide energy for exhalation. However, patients with COPD may experience an increased WOB during exhalation. These patients present a different challenge when considering their ventilatory workloads. While inspiratory work loads may be normal or even reduced, it is expiratory work that becomes elevated. Normally, the inherent elastic recoil of lungs performs the greatest portion of expiratory work; thus, the respiratory muscles are thought to be in a resting state during this period. However, with a loss of elasticity, as seen in pulmonary emphysema, this natural recoil effort is compromised and the patient is required to use their respiratory muscles to aid in exhalation. In addition to a loss of pulmonary elasticity, these patients often experience an increase in resistive work during normal or forced exhalation as pleural pressure increases, causing the airways to narrow. The viscosity of gas, especially during mechanical ventilation, is not a major determinant in the WOB. However, special gas mixtures containing helium have been used to specifically reduce airways resistance.

Table 2. Physiologic Force Factors

Elastic Work Forces	Resistive Work Forces
Thoracic elastance	Airway resistance
Lung elastance	Gas viscosity

Imposed Work of Breathing

The imposed WOB refers to the forces required from the patient to initiate and terminate gas flow from the ventilation (Table 3). This "imposed" work is in addition to physiologic work and is affected by the response of ventilator's demand valve to patient trigger effort (sensitivity), the matching of inspiratory flow to patient demand (synchrony), and resistance from the artificial airway.

Table 3. Imposed Work of Breathing Factors

1. Response of ventilator to patient effort

a. Sensitivity -- trigger effort

b. Synchrony -- matching of ventilator flow to patient demand

2. Frictional resistance from the artificial airway (nonelastic imposed work).

Sensitivity refers to the effort required from the patient to signal the ventilator for delivery of a mandatory breath. This effort, usually referred to as trigger effort, can either be in the form of a drop in pressure "pressure trigger" or from a change in measured flow "flow trigger" in the ventilator circuit. In early ventilators, prior to microprocessor technology, the primary method of triggering was accomplished through a pressure signal. These ventilators, and even early microprocessor models, had demand valves that often were not responsive to patient effort and thus created an increase in the WOB. With the advent of current microprocessor technology, demand valve sensitivity is rarely seen as a problem; however, controversy remains over the merits of pressure triggering vs flow triggering.

While sensitivity issues are related to patient effort required to signal the ventilator to initiate a breath, patient-ventilator synchrony is related to the matching of flow from the ventilator to the patient's inspiratory demand. At the onset of a patient-initiated effort, the ventilator must provide flow sufficient to meet the patient's inspiratory needs. If the flow delivery system of the ventilator, either by design or from the selection of a particular breath type, is not able to meet the patient's demand, patient-ventilator dysynchrony often occurs. Here, the patient is demanding more output from the ventilator, at the onset of a breath, than it can provide, and a sense of air hunger is often experienced. The patient gets "out of synch" with the ventilator and often tries to override the ventilator's gas flow delivery system. This may lead to increased effort and frustration from the patient. Several investigators have suggested that selection of ventilator breath types that allow for variable flow (ie, pressure control breaths) may avoid flow dysynchrony.^[4] This benefit may be partially off-set, however, if lung protective ventilation strategies are used.^[5]

The work required to initiate and sustain gas flow from most modern microprocessor-based ventilators is negligible and can be adjusted through selection of trigger modes, either pressure or flow, and selection of breath types. However, even more critical is the imposed WOB created by artificial airways. Care is required in the selection of a properly sized artificial airway and also in maintaining its patency with appropriate bronchial hygiene procedure. Inadvertent narrowing of an endotracheal or tracheotomy tube, from accumulated secretions or compression, will result in a profound increase in patient work.

Bronchial hygiene procedures that are frequently used to minimize the WOB include airway suctioning, aerosol treatments, and secretion mobilization with chest physical therapy or percussive breathing maneuvers. These therapies are directed at improving lung compliance and reducing airway resistance. Positioning the patients to optimize respiratory muscle function can also be used to reduce the WOB.^[8]

Pressure Support Ventilation

PSV is a patient assist maneuver that is applied to spontaneous breaths during mechanical ventilation. Pressure support assists the patient's effort through a preset pressure level applied during inspiration. At the onset of a spontaneous breath, the ventilator delivers flow to the patient sufficient to achieve the prescribed pressure level. As airway pressure is maintained, flow gradually decelerates in response to the patient's decreasing inspiratory demand, and then at a predetermined point of minimal flow, spontaneous inspiration is terminated and expiration begins. By assisting the patient's inspiratory effort with a preset level of pressure, PSV can be used to overcome both elastic and nonelastic WOB. Lower levels of PSV are envisioned as assisting the patient in flow-resistive work (nonelastic) associated with the imposed WOB from the artificial airway. As the level of PSV is increased, not only is the nonelastic work load decreased but elastic work load is also reduced.^[9] Although some practitioners have advocated using a level of PSV that performs all of the WOB, PSV primarily is used to overcome artificial airway resistance and to partially assist the patient's elastic work. Adjusting the level of PSV is a topic of continued interest, even after 15 plus years of clinical use. Many clinicians initiate PSV using a predetermined minimal setting (eg, 5 cm H₂O) while others adjust PSV to achieve a minimal spontaneous tidal volume based on ideal body weight (eg, 5-8 mL/kg ideal body weight). Establishing a spontaneous tidal volume with PSV is partially based on the work of Otis and coworkers.^[2] Based on the patient's underlying lung pathology, either primary restrictive or obstructive, a least WOB point is determined. For obstructive patients, this would generally equate to spontaneous tidal volumes of approximately 7-8 mL/kg ideal body weight, while restrictive patients have least WOB points at tidal volumes closer to 4-5 mL/kg ideal body weight. In either situation, the goal is to assist the patient in generating a tidal volume and thus adopting a concomitant spontaneous rate that results in a desirable level of ventilatory work.

Pressure support adjustment: adjust PSV to achieve the desired tidal volume-breathing frequency combination based on the patient's least work of breathing point.

In older-generation ventilators, the rise to the preset PSV pressure and the level of flow that terminated each inspiration was preset and usually not adjustable. As will be discussed in the next sections, these criteria can now be adjusted to fit individual patient needs.

Rise Time

Rise time (RT) refers to the time required by the ventilator to achieve the preset pressure during a pressure breath including PSV or pressure control ventilation (PCV). RT can be envisioned as a means to adjust the attack rate at which the ventilator establishes a preset pressure (Figure 2) and indirectly control peak flow. Several investigators have suggested using RT to adjust flow delivery to establish a more synchronous interaction between ventilator and patient. By establishing a peak flow that is synchronous with the patient's ventilatory pattern and underlying lung disease, WOB can be optimized.^[10] Take, for instance, a patient with COPD who has significant airway remolding with increased airway resistance (increased nonelastic work). A breathing pattern that favors lower initial flow rates may result in less flow turbulence and improved gas distribution to those lung units distal to partially obstructed airways. In this situation, a lower RT may be preferred. For those patients with restrictive disorders, a breathing pattern of smaller tidal volumes and faster rates often results in the least amount of energy expenditure during spontaneous ventilation as previously discussed. This pattern necessitates that the ventilator provide fast initial peak flows to satisfy the patient's demand. Setting a faster RT for these patients may lead to improved patient-ventilator synchrony and reduce WOB levels.^[11] Figure 2: Changes in peak flow at various rise time settings.

Figure 2. Changes in peak flow at various rise time settings.

Expiratory Sensitivity -- Flow Termination

The cycling from inspiration to expiration on a spontaneous breath is activated once flow has decelerated to percent of initial peak flow. Prior to the current generation of mechanical ventilators, the flow termination point was preset by many manufacturers at 25% of peak flow. Thus, if the initial peak flow on a spontaneous breath was 100 LPM, inspiration would proceed until flow from the ventilator decelerated to 25% of its initial level, or in this example 25 LPM (Figure 3). The deceleration in flow, from the ventilator, is in direct response to patient demand. As patient demands decrease, flow decelerates, and at a given point inspiration is terminated. In a perfect situation, the termination of inspiration would coincide with patient effort. Having an exact match between the ventilator and patient's neural drive would avoid under or over shooting flow delivery and result in a synchronous transition between inspiration and expiration. Figure 3: Expiratory sensitivity (Esens).

Figure 3: Expiratory sensitivity (Esens).

Figure 3. Expiratory sensitivity (Esens).

While today's ventilators lack the sophistication to exactly match flow termination with the patient's neural respiratory drive, many of them do allow for the setting of a flow termination point using expiratory sensitivity (Esens). This feature provides a means to adjust the termination of spontaneous inspiration based on a percent of peak flow. Again, assume that a patient has a peak spontaneous flow of 100 LPM (Figure 3). At an Esens of 25%, inspiration would last until flow decelerated to 25 LPM, which in this example resulted in a spontaneous inspiratory time of 0.60 seconds (used for descriptive purposes only). If the Esens was set to 50%, and the patient again has an initial peak flow of 100 LPM, the breath would terminate when flow decelerated to 50% or 50 LPM, which would decrease spontaneous inspiratory time to 0.30 seconds. Or if a longer spontaneous inspiratory time is desirable, then Esens would be set at 10% and inspiration would continue until flow has decelerated down to 10 LPM (10% of 100 LPM), resulting in a longer spontaneous inspiratory time. In each of these hypothetical situations, spontaneous inspiratory time was selectively altered by adjusting Esens.

Selective use of various flow termination points has been studied by several investigators in patients with COPD.^[12] Imagine a patient with emphysema who is on PSV and CPAP. Due to the nature of the patient's airway disease, expiratory flows are diminished and at times may never decrease to the set Esens level. The patient may have to forcefully end spontaneous inspiration by contracting their expiratory muscles, to increase the signal to the ventilator to end spontaneous inspiration, which may lead to further air trapping and autoPEEP. Several strategies could correct this problem, including a resetting of the flow termination point by increasing the Esens level. For those patients with restrictive lung disorders, a lengthening of spontaneous inspiratory time may be desirable to increase tidal volume at any given level of pressure support. Here, a decrease in Esens may prove useful.^[13]

Adjusting PSV, RT, or Esens is at the present time not an exact science. Consideration of the patient's underlying cardiopulmonary disease, any acute situations that may influence the neurologic drive for ventilation, and conditions that alter or impair respiratory muscle function must all be taken into account when determining the most appropriate setting for maneuvers. Monitoring spontaneous breathing frequency and tidal volume may be useful in determining if the rise in pressure matches the elastic and nonelastic properties of a patient's pulmonary system. At the "optimal" setting for these strategies, spontaneous tidal volume should be in normal range (5-8 mL/kg ideal body weight), with obstructive patients favoring the higher end of this range and conversely restrictive patients in the lower end of this range. Tidal breathing in this range should result in a spontaneous breathing frequency that results in the lowest WOB for each patient type (Table 5). However, care should be taken when adjusting RT or Esens to assess patient-ventilator synchrony. This may be accomplished by observing the retraction of the inspiratory muscles, in the case of RT, or expiratory muscles, when using Esens, to ensure that the patient is not "fighting" the ventilator. Using the advanced graphic features on modern ventilators affords clinicians the opportunity to observe patient-ventilator synchrony.^[10]

Table 5. Obstructive vs Restrictive

Patient Type	Pressure Support	Rise Time	Esens (flow termination)
Obstructive	7-8 mL/kg IBW tidal volume	Lower setting to reduce turbulence	Higher setting to avoid air trapping
Restrictive	4-5 mL/kg IBW tidal volume	Higher setting to match increased drive	Lower setting to increase VT

Esens = expiratory sensitivity; IBW = ideal body weight; VT = tidal volume

Automatic Tube Compensation

As previously mentioned, PSV allows for a preset level of pressure to be applied during each spontaneous breath. Critical to using PSV is determining the appropriate level of pressure that is set by the operator. Pressure settings may range from minimal settings sufficient to provide spontaneous tidal volumes based on a least WOB point or may be set such that the level of PSV provides tidal volumes similar to those used for mandatory breaths. Regardless of the initial level of PSV, the goal is to reduce PSV to a minimal setting prior to ventilator discontinuance. A minimal setting for PSV is often defined as that level of support that is sufficient in overcoming only imposed WOB from the artificial airway, while encouraging the patient to perform the remaining WOB (elastic work). Determining a minimal PSV level that accomplishes this has challenged practitioners since the inception of PSV, and there is often confusion on what pressure should be used to achieve these outcomes. Using too high of a PSV level may mask a problem and the patient could develop respiratory muscle fatigue once the ventilator is discontinued. On the other hand, too low of a "minimal" setting may result in the patient exhibiting an undesirable ventilator pattern while on the ventilator, and discontinuance from the ventilator may be delayed.

Automatic tube compensation (ATC), or what is sometimes referred to as tube compensation (TC), provides a partial solution to this dilemma. TC allows the ventilator to autoregulate the PSV level based on the resistance of the artificial airway. Pressure support is adjusted, by ventilator, throughout each spontaneous inspiratory period in response to changes in airway resistance. While the mechanism for accomplishing this differs between various ventilator manufacturers, the basic premise is that once the fixed diameter and an approximation of the tube length is known, the ventilator can determine artificial airways resistance. Based on a now known endotracheal or tracheotomy tube resistance factor, the ventilator calculates a "targeted" carinal pressure, with carinal pressure being pressure at the distal end of the artificial airway. TC attempts to minimize the difference between the proximal and carinal pressures, thus "erasing" the presence of the imposed WOB from the artificial airway. At the onset of the spontaneous breath, flow is delivered from the ventilator through the airway and PSV is applied to create a constant carinal pressure. Pressure is then regulated proportional to the inspiratory flow during each spontaneous breath. This "automatic" titration of PSV occurs within minimum and maximum limits set on the ventilator to avoid pressure "runaways". As with traditional PSV, the breath can be tailored using RT and Esens to match flow delivery and inspiratory time to the patient's underlying lung disease. The efficiency of ATC has been demonstrated by several investigators.^[14] While these studies show a dramatic decrease in the imposed WOB with ATC, factors such as kinking of the tube and accumulation of secretion within the airway may reduce the effectiveness of this maneuver.^[15]

Tube compensation takes the guesswork out of setting a "minimal" level of pressure support.

TC may provide another method to assess certain patients for extubation. Patients who would typically be placed on a set level of "minimal" PSV or removed from the ventilator and placed on supplementary oxygen may benefit from ATC. In this situation, ATC takes the guess work out of selecting a "minimal level of PSV" and negates the need to take the patient off of the ventilator so they may be assessed for extubation. In a sense, ATC can be seen as a form of "electronic extubation" providing the practitioner with a glimpse of how the patient will respond if extubated, while avoiding the hazards and complications of premature extubation and the need for immediate reintubation.

Bailey Maneuver

Only two components of a semiquantitative assessment of the need for airway care were associated with successful extubation: spontaneous cough (P = 0.01) and suctioning frequency (P = 0.001).

start solumedrol 20 mg 12 hrs before extubation and every four hours thereafter until tube removal

The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production.

Prophylactic steroid therapy to reduce the occurrence of postextubation laryngeal edema is controversial. Only a limited number of prospective trials involve adults in an intensive care unit. The purpose of this study was to ascertain whether administration of multiple doses of dexamethasone to critically ill, intubated patients reduces or prevents the occurrence of postextubation airway obstruction. Another specific objective of our study was to investigate whether an after-effect (i.e., a transient lingering benefit) exists 24 hours after the discontinuation of dexamethasone.

A randomized, placebo-controlled, double-blind trial was conducted in an adult medical intensive care unit of a tertiary care hospital. 86 patients who had been intubated for more than 48 hours with a cuff leak volume < 110 mL and met weaning criteria were randomly assigned to receive either dexamethasone (5 mg; n = 43) or placebo (normal saline; n = 43) every 6 hours for a total of four doses on the day preceding extubation. Cuff leak volume was measured before the first injection, one hour after each injection and 24 hours after the 4th injection. Extubation was carried out 24 hours after the last injection. Postextubation obstruction (defined as the presence of stridor) was recorded within 48 hours of extubation.

Administration of dexamethasone during the 24-hour period preceding extubation resulted in a statistically significant increase in the cuff leak volume (p < 0.05). The significant increase of CLV and change of CLV relative to baseline tidal volume (%) was not only throughout the treatment period, but also 24 hours after the last dexamethasone injection. The incidence of postextubation stridor was significantly lower in the dexamethasone group than in placebo group (10% [4/40] versus 27.5% [11/40], p =0.037), whereas there was no significant difference in reintubation rate between the two groups (2.5% [1/40] versus 5% [2/40], p =0.561).

Prophylactic administration of multiple-dose dexamethasone is effective in reducing the incidence of postextubation stridor in the adult patients at high risk for postextubation laryngeal edema. The after-effect of dexamethasone may validate the reduced incidence of postextubation stridor in delay of extubation within 24 hours after multiple doses dexamethasone. Trial Registration: NCT00452062

(Chest. 2007; 131:1742-1746)
Postobstructive Pulmonary Edema A Case for Hydrostatic Mechanisms

Measurement of the edema fluid/plasma protein ratio and the presence of net alveolar fluid clearance in 10 patients with postobstructive pulmonary edema supports a hydrostatic mechanism for edema fluid formation. The predominantly fast rates of alveolar fluid clearance may explain the rapid resolution of clinical postobstructive pulmonary edema that is typically described.