Increased Work of Breathing

The mechanical breathing workload during passive ventilation can be quantified as the product of mean inflation pressure and minute ventilation. The mean inflation pressure (Pm) is approximated in a modification of the equation of motion of the respiratory system:

In this equation R = resistance; VT is tidal volume; C is respiratory system compliance (the inverse of elastance); and PEEPi is auto-PEEP, the positive end-expiratory alveolar pressure in excess of set PEEP because of dynamic hyperinflation (Fig. 10.1).

Increased resistance to airflow is responsible (directly or indirectly) for many of the physiologic disturbances that typify this disease. Flow resistance, an important determinant of Pm, is increased by structural and functional narrowing of the airway. Structural changes include a reduced number of airway channels, as well as narrowed cross-sectional airway caliber. In this already narrowed tapering network of tubes, the additional reduction of airway caliber caused by mucosal edema, functional compression, increased bronchomotor tone, or secretion accumulation noticeably increases the work of breathing because resistance relates linearly to the airway length but inversely to the fourth power of airway radius. For similar reasons, resistance within these critically narrowed airways is highly volume dependent, so that loss of lung volume is accompanied by loss of elastic recoil tension, reduction of cross-sectional area, tendency for expiratory airway collapse, and major increases in the frictional workload.1,2

Although each factor just enumerated contributes to AO, functional compression of the airway during exhalation is of overriding importance in many patients with components of emphysema or vigorous expiratory effort. Loss of elastic recoil encourages collapse of these narrowed bronchi as their transluminal distending pressure gradients decline (or reverse) during the course of exhalation. In most patients who require mechanical ventilatory support, dynamic airway collapse occurs even during tidal breathing, so the average airway resistance is often several times higher during exhalation than during the inspiratory phase of ventilation. This compressive mechanism underlies the phenomenon of air trapping and such hyperinflation-related consequences as loss of inspiratory power and reduced compliance of the respiratory system.

Dynamic Hyperinflation (Air Trapping)

Expiration is normally a passive process that uses elastic energy stored during inflation to drive expiratory airflow. If the energy potential stored during inflation is insufficient to return the system to a relaxed equilibrium before the next inspiration begins, flow continues throughout expiration and alveolar pressure remains positive at end expiration, exceeding the clinician-selected PEEP value (Fig. 10.2).^3–9 This positive distending pressure within the alveoli increases the driving pressure for expiratory airflow and increases lung volume, thereby helping to overcome airflow resistance. Unfortunately, such hyperinflation also places the expiratory musculature at a mechanical disadvantage. Furthermore, because the hyperinflating end-expiratory alveolar pressure encourages deflation, it must first be counterbalanced by positive pressure applied to the central airway or by negative pleural pressure before inspiration can begin.^10,11 Thus PEEPi adds to the other components of the equation of motion to elevate the mean inflation pressure and inspiratory work of breathing. The process of air trapping contributes to an increase in the respiratory work of breathing in at least two other ways. Hyperinflation drives the respiratory system upward toward the least compliant portion of the pressure-volume relationship, incurring increased elastic work per liter of ventilation (see Fig. 10.1). At these higher volumes the lung approaches its elastic limit as the recoil tension of the distended rib cage becomes expiratory rather than inspiratory in nature. Finally, hyperinflation tends to convert more of the well-perfused (“zone 3”) lung into less-well-perfused tissue, thereby increasing ventilatory deadspace and the minute ventilation requirement.

Generally, the resistance increase in patients with chronic AO and many of those with severe asthma concentrates within small airways.¹ Yet for certain asthmatic patients, the central airways and larynx contribute impressively to total resistance, accounting for the helpfulness of helium-oxygen (heliox) mixtures in some (but not all) patients during exacerbated asthma.¹² According to some reports, heliox helps to reduce air trapping in patients with COPD as well. Although there is some concern regarding the generalizability and accuracy of such observations, several mechanisms can be invoked, even if the primary site of expiratory obstruction is too peripheral for helium to reduce resistance there. These mechanisms include reduced inspiratory turbulence, faster expiratory flow in non–flow-limited channels with increased wave speed, modestly decreased CO₂ production, and perhaps reduced associated gas trapping.

Of note, dynamically positive end-expiratory alveolar pressure can also exist without hyperinflation, provided that airway collapse does not occur. In these instances expiratory muscle contraction increases pleural pressure, alveolar pressure, and the speed of expiratory airflow, obviating the need for hyperinflation to complete exhalation in the allotted time. Such mechanisms are employed by normal subjects during heavy exercise or when faced with major respiratory workloads. Indeed, many untrained normal subjects expire to positions below the equilibrium point of the respiratory system when exposed to PEEP. In this way the respiratory muscles can begin contraction from a mechanically advantageous position, and the expiratory muscles can share in the ventilatory work. Using this strategy, PEEP actually provides a boost to inspiration, experienced early in the cycle when the expiratory muscles relax. This “work-sharing” strategy, although effective for a normal individual, cannot be implemented by patients who experience dynamic airway collapse during tidal breathing. Because forceful expiratory efforts succeed not only in raising alveolar pressure but also in intensifying dynamic airway collapse, flow rate is determined strictly by lung volume and is not accelerated by expiratory muscle activity after the first third of expiration has been completed.

When dynamic collapse occurs during tidal respiration and breathing requirements are high, there is little alternative to hyperinflation, CO₂ retention, or both. At the chosen level of minute ventilation, maintaining the lower lung volume may be either too energy costly or physically impossible. For this reason, many patients with severe obstruction do not or cannot decrease their lung volumes when recumbent. Such considerations may help to explain the dyspnea experienced by most patients with severe AO on assuming horizontal positions. For the same recumbent angle, the lateral position allows slightly more decompression than does the supine position because lung volume influences airway caliber, airway resistance, and tendency for collapse as the lung deflates.¹³ Patients with obesity have a lower resting lung volume and therefore exhibit higher airway resistance and tendency for dependent atelectasis and symptoms when airways are narrowed by bronchoconstriction or disease. Likewise, patients with acute respiratory distress syndrome have higher than normal airway resistance in dependent zones.

In fact, the distribution of gas trapping varies regionally throughout any diseased lung, depending on the local mechanical properties of the airways. Therefore, at the end of the expiratory cycle some zones remain patent, and some have sealed much earlier in the deflation cycle (see Fig. 10.2). Consequently, the end-expiratory value of auto-PEEP detected at the airway opening may not reflect the magnitude of gas trapping.¹⁴ Clues to the presence of regional closure are often seen when the airway is occluded at end expiration; the auto-PEEP value shows an atypically slow rise to its final value as quasi-occluded small airways decompress into the common airway. In such cases, PEEP often eliminates this characteristic. During volume-controlled ventilation, plateau pressure tracks hyperinflation more reliably than direct measurements of PEEPi.

In some patients, especially those who passively receive ventilatory support, the problems presented by air trapping and dynamic hyperinflation are as much cardiovascular as pulmonary in nature. A relatively high fraction of the resulting positive alveolar pressure is transmitted to the pleural space, where it impedes venous return and confuses interpretation of hemodynamic pressure measurements made with pulmonary artery catheters (Fig. 10.3). Lung distention also adds to pulmonary vascular resistance, exacerbating the tendencies of patients with cor pulmonale toward low cardiac output and hypotension. Marked respiratory variation of systolic and pulse pressures during passive inflation indicates phasically adverse cardiac loading and strongly implies the possibility of dynamic hyperinflation (Fig. 10.4).

Increased Minute Ventilation Requirement

Ventilation-perfusion () mismatching is widespread in patients with severe AO, reducing the efficiency of carbon dioxide elimination.¹ It is not uncommon for the resting minute ventilation requirement to exceed 12 L per minute (twice the normal value) in patients with exacerbated asthma or extensive emphysema and strong chemical drives to breathe. Not only do such increases in ventilation requirement act as a linear cofactor in the work of the breathing equation already discussed, but the high minute ventilation requirement itself increases most components of inspiratory pressure: flow, elastance (the reciprocal of compliance), tidal volume, and auto-PEEP. It is not surprising, therefore, that enormous increases in the oxygen consumption rate of the ventilatory muscles have been observed in patients with obstructive lung disease. During exacerbations, the oxygen consumed by ventilation and the metabolic demands associated with heightened vigilance, agitation, or anxiety may double the total body oxygen consumption observed during fully supported breathing. The prevalent combination of impaired matching, hypoventilation, and diffusion impairment result in arterial oxygen desaturation that generally responds well to modest supplementation of inspired oxygen.

Reduced Mechanical Efficiency

In patients with exacerbated COPD or decompensated asthma, the oxygen consumed in the ventilatory task is disproportionate to the amount of mechanical work actually performed. The muscles of the hyperinflated ventilatory system are inefficiently aligned, force-length relationships of the shortened end-inspiratory fibers are suboptimal, and normally efficient coordination among the various muscles of the ventilatory group is often disrupted.14–16 The energy cost of breathing, therefore, is greatly increased for the pressure and mechanical work actually generated by the breathing effort.

Interactions of Pressure-Targeted Modes with Auto-PEEP

Pressure-targeted modes of ventilation, exemplified by pressure control, airway pressure release ventilation (APRV), and pressure support, have become increasingly popular to employ in the care of intubated patients, as well as in those receiving noninvasive ventilation by facemask. Because the development of auto-PEEP reduces the pressure difference between airway opening and alveolus that drives inspiration, it has a powerful influence on ventilation efficacy (Fig. 10.5). As already described, auto-PEEP varies not only with airway mechanics but also with the pattern of breathing and minute ventilation. For a fixed value of applied airway pressure, inspiratory tidal volume in patients with AO will be more sensitive to the frequency and the inspiratory time fraction (an expression of the inspiratory-to-expiratory [I : E] ratio) than are normal subjects or those with restrictive disease¹⁸ (Fig. 10.6). Faster breathing frequencies, for example, allow auto-PEEP to build, and this auto-PEEP must first be counterbalanced for inspiratory airflow to begin. If the patient is passive or the amount of inspiratory muscle force remains constant, delivered tidal volume falls as the auto-PEEP builds.

This auto-PEEP/driving pressure interaction may result in an intriguing phenomenon resembling chaotic respiration during noninvasive ventilation with a leaky mask interface.¹⁹ The coupled PEEPi and tidal volume form a “feed-forward” system in which a building auto-PEEP of one cycle adversely influences the tidal volume of the next one. But this smaller tidal volume also reduces the auto-PEEP that follows that restricted cycle, which in turn allows the subsequent breath—the third in the cycle—to have a larger effective driving pressure and tidal volume, and the cycling variation continues. This may account for some of the wide variability in breathing rhythm often observed in these patients.²⁰ If the mask leak volume is a function of the I : E ratio, it can be shown mathematically and experimentally that fractal and chaotic tidal volume delivery may occur, even when the patient’s effort and mechanics remain unchanged (Fig. 10.7).¹⁹ The consequences for comfort and sleep efficiency are likely to be significant, but clinical data are lacking on these issues at this time.

Principle 1: Provide adequate support to rest the ventilatory muscles, while avoiding hypoxemia and profound acidemia.

    Poised on the edge of decompensation, the ventilatory muscles must be rested adequately before withdrawal of machine support can be considered. Rest may allow recovery of energy reserves and restore the balance between ventilatory capability and demand. Indeed, benefits may accrue to muscle rest, even when it occurs intermittently on a chronic basis. Sufficient oxygen and mechanical support must be provided to achieve this goal, to permit restorative sleep, and to avoid significant hypoxemia (arterial oxygen saturation < 85%) and acidemia (pH < 7.2)—derangements that increase pulmonary vascular resistance; stimulate vigorous breathing; and inhibit mental, cardiac, and skeletal muscle functions.

Principle 2: Do not overventilate.

    Profound respiratory acidosis and hypoxemia accentuate pulmonary hypertension, impair the right ventricle, and should be reversed. Nevertheless, although it is important to provide adequate ventilation and to reverse hypoxemia, overventilation is detrimental on several counts. Rapid reduction in the alveolar CO₂ tension tends to cause bronchoconstriction and impair neuromuscular and cardiovascular function. Furthermore, excess ventilation exacerbates dynamic hyperinflation and auto-PEEP, whereas moderate PaCO₂ elevations are generally well tolerated.²⁷ Generally, it is a mistake to depress the PaCO₂ below the level that the patient chronically maintains. Such a strategy may temporarily reset chemical drives, effectively increasing respiratory workload intensity once spontaneous breathing resumes. If PaCO₂ falls sufficiently, the patient will not maintain unassisted breathing without intolerable effort, potentially delaying discontinuation of mechanical breathing assistance.

Principle 3: Minimize minute ventilation requirement.

    Because hyperinflation, mean inflation pressure, and the adverse cardiovascular consequences of mechanical ventilation are intimately linked to the minute ventilation requirement, ventilatory deadspace and CO₂ output must be minimized and both metabolic acidosis and iatrogenic hyperventilation avoided or addressed.

Principle 4: Minimize the risk of barotrauma.

    The predisposition of patients with severe AO to barotrauma must be combated by intelligent choices for tidal volume, ventilation frequency, PEEP, and machine settings of trigger sensitivity and flow. Reduction of the minute ventilation requirement decreases the mean or peak alveolar pressures, or both, reducing the incidence of barotrauma. The relative contributions of mean alveolar pressure, PEEP, dynamic cycling pressure, and peak static (plateau) ventilatory pressure to the risk of barotrauma are not clear. Based on epidemiologic evidence, however, peak airway inflation pressures in a passively inflated lung should be kept below 40 cm H₂O whenever possible. Selecting a tidal volume at the low end of the recommended range (6 to 8 mL/kg of ideal body weight) is probably best. The question of optimal flow setting is of no small importance: auto-PEEP and mean alveolar pressure are reduced by selection of relatively rapid flow settings when minute ventilation is high. Overall ventilation-perfusion matching may improve as well. Higher peak dynamic airway pressures engendered by these rapid flows are not entirely without risk, however; units served by low resistance pathways are in jeopardy from associated overdistention. For the same tidal inspiratory time, a constant (“square”) flow waveform often serves better than a decelerating one. The risk of barotrauma can also be minimized by maintaining the lungs free of infection and the airways clear of secretions.

Principle 5: Maintain effective bronchial hygiene.

    Secretion retention may dramatically increase airflow resistance and effectively seal off entire banks of functional alveoli, preventing their participation in ventilation. Thickened central airway secretions are a particular risk during mechanical ventilation, whether invasive or noninvasive (Fig. 10.8).²⁸ Apart from raising the end-inspiratory pressure, the resulting dynamic hyperinflation can detrimentally affect cardiovascular function, work of breathing, and ventilatory capability. In addition to effective suctioning, bronchodilators, adequate hydration, corticosteroids, mucolytics, mucolubricants, and infection control, frequent repositioning, mobilization, and physiotherapy are fundamental to secretion management. Percussive ventilation or vibro-percussive vest treatments often complement mobilization effectively when tolerated. Tracheotomies not only reduce resistance and provide improved access to the lower airway but also eliminate the direct connection between the pharynx and trachea established by tracheal intubation.

Principle 6: Prevent panic reactions.

    In patients susceptible to dynamic airway collapse, an abrupt need to augment ventilation often precipitates a downward spiral in which the capability of the patient is overwhelmed by the imposed workload. Not only is minute ventilation increased during such episodes, but the resulting augmentation of dynamic hyperinflation impairs muscle strength and endurance. Respiratory acidosis, dyspnea, and anxiety result in an imbalance in the demand/capability relationship that creates a need for aggressive intervention. Anxiolytics, although hazardous to employ, may be extremely helpful in carefully selected circumstances.

Principle 7: Maintain appropriate nutrition, assure adequate hemoglobin concentration, and prevent obstipation.

    In stressed and often malnourished patients, the nature and quantity of nutritional support can make the difference between eventual compensation and continued ventilatory insufficiency. Although reasonable caution is advisable, anemia should be reversed and an adequate number of calories should be provided, via the enteral route whenever possible. Care must be taken to ensure that bowel motility is normal; patients with AO frequently develop breathing discomfort because of abdominal distention within a compartment bounded by a hyperinflation-depressed diaphragm.

Intubation

An understandable reluctance to initiate mechanical ventilation in patients with COPD or perennial asthma exists because ventilatory assistance may be needed for prolonged periods and because many such individuals are so chronically disabled as to be miserable or despondent at home—even when everything is going as well as possible from a physiologic viewpoint. The development of comfortable noninvasive systems, coupled with supportive trials and clinical experience, has given rise to the initial use of mask ventilation in those who are alert and can tolerate it. However, the most severely affected patients, especially those with copious, thick, and retained secretions, claustrophobia, anxiety, cardiovascular decompensation, or irreversible somnolence, continue to require intubation to stabilize their deteriorating conditions.²⁹

A mounting load of secretions audibly retained within the central airways generally indicates that the patient is too weak or breathless to expectorate and often portends an imminent crisis. Hence, when this sign arises and cannot be easily reversed, most physicians consider it to be strong evidence favoring intubation for secretion management and ventilation support. Overt disorganization of the breathing rhythm and gasping or ataxic respirations strongly suggest approaching exhaustion.

Initial Support

Machine Settings

As a general rule, ventilation should be adequately supported during this initial phase, but it is better to underventilate cautiously than to overventilate the patient. One reasonable approach is to use assisted flow-regulated volume-controlled mechanical ventilation, delivered with a square wave profile, with the backup rate set to provide about two thirds of the estimated minute ventilation requirement. Although the flow setting is adjusted empirically to coordinate the cycle lengths of the patient and the ventilator, an initial peak flow setting of approximately four to six times the minute ventilation requirement (depending on whether the flow profile is square or decelerating, respectively) usually suffices to meet expiratory time requirements and minimize auto-PEEP without imposing undue risks that attend extraordinarily high peak cycling pressures. Assuming a minute ventilation of 12 L per minute, a constant flow setting of about 60 L per minute is usually appropriate. This yields an I : E ratio of approximately 1 : 4, which is considerably shorter than customary in a patient with normal mechanics who breathes at this level of minute ventilation. Reducing the I : E ratio still further may not improve gas trapping noticeably, as terminal rates of airflow are predictably very low. On the other hand, increasing airflow carries a high pressure and work cost in patients with such severe AO. For similar reasons, a constant inspiratory flow is preferable to a decelerating one when flow-controlled, volume-cycled ventilation is in use. Pressure-targeted ventilation is a sensible choice only if it is monitored closely or adjusted automatically by the ventilator to maintain tidal volume in response to changing airflow impedance.

The triggering threshold of the ventilator is set to be as sensitive as possible, and the auto-PEEP level is estimated when feasible to do so. (Measurement typically requires passive inflation to allow predictable occlusion of the circuit at end-expiration.) If auto-PEEP exceeds 5 cm of water and expiratory flow is limited during tidal breathing (which is almost invariably the case during the initial phase), an uncomfortable patient who makes spontaneous breathing efforts may benefit from the addition of a low level of end-expiratory pressure to counterbalance auto-PEEP and reduce the breathing workload (Fig. 10.9). PEEP levels in excess of 15 cm H₂O may be necessary in some instances to reestablish patency of some air channels.

The plateau pressure is a better guide to the degree of hyperinflation than is the measured level of auto-PEEP, for reasons already given. First, most machines do not allow estimation of auto-PEEP in a patient who is spontaneously triggering the ventilator and varies the length of the respiratory cycle. On the other hand, a plateau pressure estimate is usually recordable during triggered, as well as during controlled, volume-cycled breathing. Just as importantly, the auto-PEEP estimated by central airway occlusion is simply the volume-weighted average of those airways that remain open at end expiration, which generally have shorter time constants and better mechanical properties than those that seal earlier in the expiratory period at higher pressure (see Fig. 10.2).

The flow tracing gives some indication of the underlying presence of gas trapping but does not indicate its severity. For example, a severely obstructed airway may be totally occluded and therefore unable to transmit its high pressure to the pressure sensor located within the machine circuitry. Similarly, a narrow airway may give rise to an almost imperceptible flow at end expiration. Several features of the flow tracing are of value: High-frequency variations of the flow tracing suggest the presence of retained airway secretions or water in the external tubing. An abrupt transition between the earliest part of expiration and what follows (“hockey sticking”) indicates a flow limitation during tidal breathing and the potential value of added PEEP if flow persists to the onset of the next breathing cycle (Fig. 10.10). Several signs appearing in the monitored airway pressure and flow signals have been reported that appear to be signatures of partial central airway occlusion, as by mucus plugging (see Fig. 10.8).²⁸

Support Phase Management

After the first hours of ventilatory support, rational management focuses not only on reversal of the underlying problems of infection, bronchospasm, secretion retention, and cardiac insufficiency but also on replenishing spent nutritional reserves and building endurance. It makes sense to support ventilation fully in patients intubated for ventilatory failure while fundamental pathologic processes and precipitating causes are being addressed—at least for the initial 24 to 48 hours. Because it is not known what intensity of ventilatory effort is best for patients with AO to undertake during the support phase of the illness, controversy exists as to the optimal mode of ventilation. During the support phase, the major ventilation objective as the acute problems causing deterioration are being addressed should be to provide sufficient breathing assistance to alleviate discomfort while not risking deconditioning of the ventilatory muscles. To this end, it is reasonable to use volume- or pressure-targeted assist-control (assisted mechanical ventilation) or synchronized intermittent mandatory ventilation (SIMV). In patients who are not deeply sedated and who breathe chaotically, the latter mode applied with pressure support sufficient to replicate the tidal volume of the mandated breaths may reduce the number of dyssynchronous “collisions” between the rhythms of patient and machine. Adequate sedation must be provided so as to assure comfort and reduce the minute ventilation requirement as other fundamental elements of ventilatory therapeutics are addressed (e.g., antibiotics, corticosteroids, regulation of intravascular volume, secretion expulsion or extraction, cardiovascular support). Assuring adequate oxygenation, ventilatory muscle rest, and restorative sleep deserve emphasis. Deep sedation and muscle relaxants, although occasionally necessary in achieving therapeutic objectives early in the ventilatory process, may prove detrimental when their use is prolonged unnecessarily. Not only does sedation present risks of muscle deconditioning and even neuromyopathy, but secretions tend to pool in dependent areas when breathing efforts and coughs are suppressed. As a general rule, deep sedation and paralysis should not be continued for longer than 40 to 72 hours after intubation.

Apart from improving expiratory resistance and reducing the minute ventilation requirement, another intervention aimed at reducing mean alveolar pressure and auto-PEEP is to modestly lengthen the available expiratory time (e.g., by increasing inspiratory flow rate). The flow rate should initially be set at approximately four times the minute ventilation requirement when using a constant inspiratory flow profile. Extending the expiratory time further is usually fruitless, unless minute ventilation is simultaneously reduced. Decelerating flow profiles are often poorly tolerated by the patient with severe AO who makes spontaneous efforts because the latter half of the inspiratory period may require higher flows than imposed by the tightly regulated and stereotyped flow waveform of the ventilator. Adjustments to the flow criterion off-switch that triggers expiration can help manage this problem during pressure-supported ventilation (Fig. 10.11).

PEEP and CPAP in Severe Airflow Obstruction

The deliberate use of PEEP in patients with AO has historically been considered undesirable, but there is now ample reason to believe that most of these patients benefit from the application of low levels of PEEP or continuous positive airway pressure (CPAP).5,10,11 When applied downstream of airways that collapse dynamically during the exhalation phase of tidal breathing, PEEP helps to improve the effective triggering responsiveness of the machine without significantly increasing the alveolar pressure or hyperinflation (Fig. 10.12). Most benefit is provided to patients receiving volume-controlled ventilation who do not experience proportionate increases of peak static or peak dynamic cycling pressures after PEEP application.^10,11,30 When using a fixed level of targeted pressure (pressure control or pressure support), tidal volume may increase after PEEP is applied. This occurs because the added PEEP counterbalances auto-PEEP to allow the applied inspiratory pressure to more effectively drive inspiratory flow. In effect, PEEP improves the pressure gradient that drives inspiratory flow and delivers tidal volume. (Should minute ventilation increase with PEEP application, total PEEP may also rise.) Applied PEEP may also help to keep airways more widely patent, and thereby improve secretion clearance. Finally, the application of the external PEEP may help to even the distribution of ventilation among multiple units with heterogeneous time constants (Fig. 10.13).

Newer Modes of Ventilation in Airflow Obstruction

Currently, the majority of ventilatory support of AO is still provided with modes of ventilation that are now decades old—flow-controlled, volume-cycled ventilation (“assist-control”); pressure assist control (pressure control, PCV); pressure support (PSV); and SIMV. When combined with PEEP/CPAP and an attentive provider, these time-tested options suffice for the majority of patients. Increasingly, however, practitioners have recognized the need to offload responsibility for minute-by-minute and even intrabreath adjustment of settings for flow and pressure delivery in response to changing conditions of mechanics or ventilatory demand. Patients with dyspnea generally need faster rise of pressure and flows to their target values, unimpeded inspiratory flow, and precise termination of the ventilator’s inspiratory phase so as to avoid collisions between the patient’s and the ventilator’s cycling rhythms. Once set, however, a specified flow pattern regulates the ventilator’s gas delivery, whereas pressure control caps airway pressure at the targeted value. Just as importantly, these time-cycled assist control modes (whether flow or pressure regulated) disregard the duty cycle rhythm variations of the patient’s own drive center; Therefore, asynchrony occurs commonly in these modes, and asynchrony may result not only in dyspnea but also in adverse outcomes.³¹ In either case the relative power contribution of the machine declines as effort increases and rises as patient effort declines. Appropriate moment-by-moment intracycle adjustment of flow or pressure is not an option with these “traditional” modes of ventilation. Logic dictates that better synchrony between patient and machine would require continuously monitored feedback and flexibility to adjust to the vagaries of patient need.

Of the newer modes of ventilation, four that have implications for AO have garnered considerable attention and have been incorporated into some of the latest equipment.

Weaning (“Liberation”) Phase

Protracted ventilator dependence is perhaps the most feared consequence of intubating patients with exacerbated COPD and perennial asthma. Not only are breathing workloads high, but the ability of the patient to sustain them is compromised by muscle weakness, hyperinflation, disadvantageous thoracic geometry, blunted ventilatory drive, and abnormal cardiovascular function. Rational management of the weaning patient with AO includes provision of adequate rest and nutritional support, enhancement of neuromuscular and cardiovascular function, and minimization of the breathing workload. Maintenance of positive mental attitude can greatly speed the weaning process.

Patients may fail to wean from mechanical ventilation for a wide variety of reasons. Among these are hypoxemia, cardiac arrhythmias, cardiovascular instability, and psychological dependence. However, imbalance between ventilatory capability and demand is perhaps the most common reason for failure to wean in patients with ventilatory failure either of itself or because it provokes one or more of the other factors just mentioned.37,38

Predicting Readiness for Spontaneous Breathing

In clinical practice a panel of indices has long been used to predict the outcome of the weaning trial. Most individual elements of these demand or capability panels can be classified as indicators of either one or the other, but not both. Some capability indicators depend on patient effort as well. Thus, a maximal inspiratory pressure measurement exceeding 30 cm H₂O and a minute ventilation requirement of less than 10 L per minute are standard components of the traditional predictive battery. Although minute ventilation has been criticized as unreliable when used alone, it is still a highly useful observation, particularly when referenced to blood gas measurements and integrated into an evaluation of other panel elements. When the patient is calm, a high degree of variation of minute ventilation suggests some degree of ventilatory reserve.³⁹ Because the product of minute ventilation and the average inspiratory pressure per breath are the main components of the breathing workload, minute ventilation must not be disregarded, even when more integrative indices are in use, such as the frequency-to–tidal volume ratio (rapid shallow breathing index, RSBI).⁴⁰ For example, a rising RSBI does not necessarily portend failure if minute ventilation rises as well. Published criteria for RSBI lose reliability in the presence of neuromuscular weakness, severe restriction, or chronic illness requiring ventilator support.³⁸

Numerous other weaning outcome indices have been suggested over the years, but none stands alone as infallible, including the RSBI. The most successful of these indicators reliably relate power requirement to the ability of the patient to sustain it. Certain physiologic measurements such as the P_0.1 (a measurable indicator of ventilatory drive now offered on some of the newest ventilators) have predictive appeal. These are not universally available, however, and cannot be relied on for definitive judgment in every case. Because many factors may limit the patient’s ability to be removed from the ventilator, more than one single indicator is usually necessary to observe. Alertness, degree of cardiovascular compensation, clinical trajectory over the preceding days, oxygenation status, secretion load, upper airway patency, coughing efficiency, and psychological well-being are as important as any single predictive measure based on mechanics and muscle strength. Successful weaning protocols take all such factors into account.37,38,40

Repeated failure to wean is often explained by cardiovascular factors such as ischemia and diastolic dysfunction. This is especially true when parameters based on ventilation appear favorable. Clues may appear in the form of cardiac dysrhythmias and an unfavorable excess of fluid intake over output. In part for such reasons, weaning protocols must be constructed carefully; failure to meet weaning criteria must be considered a cue to undertake a careful review of all potential factors that prevent success, not necessarily an indication to allow a bit more time with unchanging therapy.

Weaning Approaches

Periextubation Phase

In intubated patients suspected of upper airway obstruction, a cuff deflation test should be conducted before decannulating the airway. This is performed by elevating PEEP to 10 to 20 cm H₂O immediately in advance of deflation. An audible leak should be heard if the glottic space is not prohibitively tight. The sitting position, manipulation of head position and a temporary increase of PEEP may help break a “mucus seal” that otherwise prevents gas leakage. In questionable cases, advance preparations should be made for urgent intervention, should that prove necessary after tube extraction.

The immediate postextubation phase should be as carefully managed as the ventilated one. The first 24 hours off the ventilator are often difficult and tenuous, but in successful cases there should be progressive improvement. Coughing, deep breathing, adequate oxygenation, avoidance of arrhythmias, adequate bronchodilation and airstream hydration, maintenance of a clear central airway, and a mechanically efficient posture are crucial. Oral refeeding must be undertaken with extreme caution because swallowing difficulty in chronic dysfunction can persist days to weeks after extubation in patients who have been ventilated for lengthy periods. CPAP and intermittent noninvasive ventilation may be especially helpful in selected patients,⁴⁶ especially in the nighttime hours. Noninvasive ventilation maintains patency of an edematous upper airway and provides ventilation support during sleep. This is often important in patients who have received sedating medications or are sleep deprived. It must be used judiciously, however, and carefully applied. Ventilation by pressurized mask impedes secretion clearance, and if a humidifier is not used, mouth breathing during bilevel positive airway pressure (BiPAP) dries secretions and encourages displacement of oral material into the central airway. Therefore, it is common for patients who receive mask ventilation after extubation to require reintubation for clearance of thickened airway mucus.

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