Chapter 36. Management of the Ventilated Patient

• Effective preventive measures in ventilated patients include raising the head of the bed during enteral feeding, using measures to prevent venous thromboembolism, avoiding unnecessary changes of the ventilator circuit, and reducing the amount of sedation.
• Ventilator parameters should be determined by the pathophysiology underlying the particular form of respiratory failure; this approach facilitates stabilization and comfort of the patient on the ventilator, prevention of common complications, and early liberation from this supportive therapy.
• Although some patients may require sedation and muscle relaxation for initial stabilization on the ventilator, these agents should not be used to routinely adapt the patient to the machine; rather, ventilator adjustments should be used to stabilize and comfort the patient. This latter approach is facilitated by a careful analysis of airway pressure and flow waveforms.
• Whenever the adequacy of oxygen exchange is in question, the initial fraction of inspired oxygen (FiO2) should be 1.0; this will be diagnostic and therapeutic because failure to achieve full arterial hemoglobin saturation identifies a significant right-to-left shunt.
• Typical ventilator settings for the patient with normal lung mechanics and gas exchange include an FiO2 of 0.5, tidal volume of 8 to 12 mL/kg, and respiratory rate of 8 to 12 breaths/min; if mechanical ventilation has been instituted to rest fatigued respiratory muscles, deep sedation may be necessary to minimize respiratory muscle activity.
• The patient with severe airflow obstruction often develops hypoperfusion after institution of positive-pressure ventilation as a result of occult positive end-expiratory pressure (autoPEEP); this responds to temporary cessation of ventilation and vigorous volume resuscitation while measures are used to reduce airflow obstruction.
• The goals of ventilator management in severe airflow obstruction include a plateau airway pressure below 30 cm H2O, an autoPEEP below 10 cm H2O, or an end-inspired lung volume smaller than 20 mL/kg even if this results in hypercapnia; short expiratory times must be avoided.
• The patient with acute hypoxemic respiratory failure resulting from pulmonary edema benefits from lung-protective ventilation (6 mL/kg ideal body weight and rate approximately 30 breaths/min). The initial FiO2 of 1.0 can be lowered to nontoxic levels by raising PEEP, which is guided by pulse oximetry.

Too often, the management of the patient on a ventilator is guided by (a) a standard protocol applied to diverse patients regardless of the underlying pulmonary derangement or (b) mode-dominated thinking on the part of the physician, by which various microprocessor-controlled machine functions are hoped to have a salutary effect on patient outcome. This chapter offers an alternative approach, in which ventilator parameters are tailored to the patient's mechanical and gas exchange abnormalities. This facilitates early stabilization of the patient on the ventilator in such a way as to optimize carbon dioxide removal and oxygen delivery within the limits of abnormal neuromuscular function, lung mechanics, and gas exchange and limit complications of barotrauma, lung injury, and cardiovascular depression.

Other chapters of this book are complementary to the information presented here. The pathophysiology of respiratory failure is broadly reviewed in Chap. 31; monitoring the respiratory system is delineated in Chap. 32; noninvasive ventilation is covered in Chap. 33; ventilator-induced lung injury is discussed in Chap. 37; and several chapters (e.g., Chap. 38, “Acute Respiratory Distress Syndrome”; Chap. 39, “Acute-on-Chronic Respiratory Failure”; Chap. 40, “Status Asthmaticus”; Chap. 42, “Restrictive Disease of the Respiratory System”) discuss ventilatory support for specific problems.

The fundamental purpose of mechanical ventilation is to assist in elimination of carbon dioxide and inspiration of adequate oxygen when the patient is unable to do so or should not be allowed to do so. Such patients fall into two main groups: those in whom full rest of the respiratory muscles or permissive hypercapnia is indicated (e.g., during shock, severe acute pulmonary derangement, or with deep sedation or anesthesia) and those in whom some degree of respiratory muscle use is desired (e.g., to strengthen or improve the coordination of the respiratory muscles, to assess the ability of the patient to sustain the work of breathing, or to begin spontaneous ventilation). It is important for the intensivist to be explicit about whether the respiratory muscles should be rested or exercised because the details of ventilation (mode and settings) usually follow logically from this fundamental point.

We discuss the various conventional modes of ventilation practiced in most intensive care units (ICUs). If full rest of the respiratory muscles is desired, it is incumbent on the physician to ensure that this is achieved. Although some patients are fully passive while being ventilated (those with deep sedation, some forms of coma, metabolic alkalosis, sleep-disordered breathing), most patients will make active respiratory efforts, even on volume assist-control ventilation (ACV),1 at times performing extraordinary amounts of work. Unintended patient effort can be difficult to recognize but, aside from obvious patient effort, may be signaled by an inspiratory decrease in intrathoracic pressure (as noted on central venous or pulmonary artery pressure tracings or with an esophageal balloon), by triggering of the ventilator, or by a careful analysis of real-time flow and pressure waveforms, discussed more fully in Chap. 32. When there is evidence of unwanted patient effort, ventilator adjustments, psychological measures, pharmacologic sedation, and therapeutic paralysis can be useful, as discussed later in this chapter. Ventilator strategies to decrease the patient's work of breathing include increasing the minute ventilation to decrease arterial partial pressure of CO2 (PaCO2; although this may run counter to other goals of ventilation, especially in patients with acute respiratory distress syndrome [ARDS] or severe obstruction), increasing the inspiratory flow rate, and changing the mode to pressure-preset ventilation, as in pressure-support (PSV) or pressure-control (PCV) mode. Adjusting the ventilator to the patient's demand is described more fully below.

If some work of breathing on the patient's part is desired, this can be achieved through any of the existing ventilatory modes. The amount of work done may be highly variable, however, and depends on the specific mode, the settings chosen within each mode, and the interaction between the patient and the ventilator. A recurring question during the time when a patient can carry some of the work of breathing is, “Can this patient breathe without ventilatory assistance?” This issue is more fully developed in Chap. 44, “Liberation from Mechanical Ventilation.”

Choosing a ventilatory mode and settings appropriate for each patient depends not only on the physician's goals (rest versus exercise) but also on knowledge of the mechanical properties of the patient's respiratory system. Determining respiratory system mechanics is an integral part of ventilator management and a routine part of examination of the critically ill patient, discussed fully in Chap. 32 (“Ventilator Waveforms”) and reviewed extensively in the literature.2,3 The intensivist can combine clinical information, chest radiography, and respiratory system mechanical properties (as described in Chap. 32) to categorize the patient into one of four prototypes: (a) normal gas exchange and mechanics, (b) significant airflow obstruction (as in status asthmaticus or acute exacerbations of chronic obstructive pulmonary disease (COPD), (c) acute lung injury and ARDS, and (d) restriction of the lung or chest wall.

Appropriate initial ventilator settings and subsequent adjustments for each of these four states is discussed later in this chapter. We emphasize the use of pressure and flow waveforms to further adjust the ventilator to meet the physician's goals and maximize the patient's comfort. We discuss the role of sedation of the ventilated patient and describe how to respond to “crises” on the ventilator. This chapter concludes with a brief review of novel modes of ventilation, such as high-frequency ventilation, followed by a summary of preventive measures appropriate to all ventilated patients.

Mechanically ventilated patients are at risk of numerous complications related to the presence of the endotracheal tube, most notably ventilator-associated pneumonia (VAP), and complications of the sedatives and paralytics that are often given. Effective preventive measures are more fully discussed in Chaps. 4, 10, and 14, but are briefly summarized here.

Noninvasive ventilation should be used in appropriate candidates because this decreases the risk of VAP in COPD patients and perhaps those in an immunocompromised state.2,3 For intubated patients, the head of the bed should be elevated to 30 to 45 degrees during enteral feeding, a simple but effective step for decreasing the risk of VAP.4 Ventilator tubing should be changed only when the tubing is visibly soiled or malfunctioning, rather than on a time-based schedule.5 Heat and moisture exchangers should not be changed more than every 48 hours. Sedative use should be limited and patients should be allowed to wake up daily, as discussed below and in Chap. 14. Prophylaxis against venous thromboembolism is indicated in most patients. There is no consensus regarding the effectiveness of selective decontamination of the digestive tract, the use of lateral rotation therapy, or postpyloric placement of feeding tubes, so these measures should not be routinely applied.

Technologic innovations have provided a plethora of different modes by which a patient can be mechanically ventilated. Various modes have been developed with the hope of improving gas exchange, patient comfort, or speed of return to spontaneous ventilation. Aside from minor subtleties, nearly all modes allow full rest of the patient, on the one hand, or substantial exercise, on the other. Thus, in the great majority of patients, choice of mode is merely a matter of patient or physician preference. Noninvasive ventilation should be considered before intubation and ventilation in many patients who are hemodynamically stable and do not require an artificial airway, especially those with acute-on-chronic respiratory failure, postoperative respiratory failure, and cardiogenic pulmonary edema. Management of the patient ventilated noninvasively is discussed thoroughly in Chap. 33.

Pressure-Preset versus Volume-Preset Modes of Ventilation

The terminology describing modes of ventilation can be very confusing and may vary from one manufacturer to another. In this chapter, we refer to volume-preset modes as those in which the physician sets a desired tidal volume (Vt) that the ventilator delivers, using whatever pressure required, and pressure-preset modes, in which the physician sets a desired pressure that the ventilator maintains, delivering a volume that depends on the settings, respiratory mechanics, and patient effort. These two fundamental types of mode are compared in Table 36-1. Some modern modes (dual-control modes, see below) attempt to blend pressure and volume presets.

Historically, most adult patients have been ventilated using volume-preset modes (ACV and synchronized intermittent mandatory ventilation [SIMV]), but pressure-preset modes have several theoretical advantages. Few studies have compared these modes except with respect to comfort, a measure generally favoring pressure-preset modes.6,7 The only mode of ventilation shown to affect mortality rate was the application of ACV to patients with acute lung injury and ARDS when physiologic Vt is used (6 mL/kg ideal body weight [IBW] compared with 12 mL/kg), but pressure-preset modes were not employed in that trial.8

The differences between volume-preset and pressure-preset modes are fewer than is often appreciated, because volume and pressure are related through the mechanical properties of the patient's respiratory system, most notably the respiratory system compliance (Crs). For example, a passive patient with a static Crs of 50 mL/cm H2O ventilated on ACV at a Vt of 500 mL with no positive end-expiratory pressure will have a plateau airway pressure (Pplat; see Chap. 32) of about 10 cm H2O, whereas the same patient ventilated on PCV at 10 cm H2O can be expected to have a Vt close to 500 mL. The difference to the patient between these modes may be quite trivial, often amounting to small differences in inspiratory flow profile. Thus, although the physician's comfort level with volume-preset and pressure-preset modes may be very different, the modes can be similar because they are tied to each other through the patient's Crs.

Conventional Modes of Ventilation

In the following descriptions, each mode is first illustrated for a passive patient, such as after muscle paralysis, and then for the more common situation in which the patient plays an active role in ventilation. On some ventilators, Vt can be selected by the physician or respiratory therapist; on others, minute ventilation and respiratory rates (f) are chosen, secondarily determining the Vt. Similarly, on some machines, an inspiratory flow rate (V̇) is selected, whereas on others V̇ depends on the ratio of inspiratory time to total respiratory cycle time (Ti/Tt) and f, on an inspiratory-expiratory (I:E) ratio and f, or on rise time and other parameters.

Pressure-Preset Modes

In pressure-preset modes, a fixed inspiratory pressure (Pi) is applied to the patient, whatever the resulting Vt. Depending on the particular ventilator, the physician may have to specify the actual level of Pi or the increment in pressure over the expiratory pressure (PEEP). Ventilators designed primarily for noninvasive ventilation often require setting Pi and PEEP independently, whereas most ICU ventilators require setting the PEEP and an inspiratory pressure increment. For example, the following settings are identical: Pi = 20 cm H2O and PEEP = 5 cm H2O (noninvasive ventilator) versus pressure increment (e.g., “pressure-support” or “pressure-control”) = 15 cm H2O and PEEP = 5 cm H2O. In this chapter, we specify inspiratory (Pi) and expiratory (PEEP) pressures to avoid confusion.

In pressure-preset modes, the Vt is predictable (for the passive patient) when the Crs is known:

assuming time for equilibration between Pi and alveolar pressure (Pa) and the absence of autoPEEP (these assumptions are often not true in patients in the ICU: see below).

Compared with volume-preset modes, a potential advantage of pressure-preset ventilation is greater physician control over the peak airway pressure (Ppk; because Ppk = Pi) and the peak Pa, which could lessen the incidence of ventilator-induced lung injury (see Chap. 37). However, this same reduction in volutrauma risk should be attainable during volume-preset ventilation if a Vt appropriate to the lung derangement is chosen, as has been shown in patients with acute lung injury and ARDS.8 Nevertheless, pressure-preset modes make such a lung protection strategy easier to carry out by obviating repeated determinations of Pplat and periodic adjustment of Vt.

Pressure-preset modes also allow the patient greater control over inspiratory flow rate and therefore potentially increased comfort. A disadvantage of pressure-preset modes is that changes in respiratory system mechanics (e.g., increased airflow resistance or lung stiffness) or patient effort may decrease the minute ventilation, necessitating alarms for adequate ventilation. Further, the mechanics cannot be determined readily and partitioned as described in Chap. 32 without switching modes or inserting an esophageal balloon.

Pressure-Control Ventilation

In the passive patient, ventilation is determined by f, the inspiratory pressure increment (Pi − PEEP), the I:E, and Crs. In patients without severe obstruction given a sufficiently long Ti, there is equilibration between the ventilator-determined Pi and Pa, so that inspiratory flow ceases (Fig. 36-1A). In this situation, Vt is highly predictable, based on Pi(= Pa) and the mechanical properties of the respiratory system (Crs). In the presence of severe obstruction or if Ti is too short to allow equilibration between the ventilator and alveoli, Vt will decrease below the value predicted based on Pi and Crs (see Fig. 36-1A). One of the advantages of PCV is that it may facilitate ventilation with a lung protective strategy. For example, alveolar overdistention can be prevented by ensuring that Pa never exceeds some threshold value (this is often taken to be 30 cm H2O, but a truly safe level is unknown) by simply setting Pi (alternatively, PEEP + PSV) to the desired upper limit. During PCV, Ti and f are set by the physician and may not approximate the patient's desired Ti and f.

When the patient is active, the Vt reflects patient effort, and the patient may trigger additional breaths. When the patient makes inspiratory efforts synchronized with machine inspiration, the Vt is generally greater than that predicted from the Crs and Pi. However, dyssynchrony or expiratory effort during machine inspiration may decrease Vt below the value expected. Special care must be taken to adjust Ti to the individual patient (Fig. 36-2); otherwise, heavy sedation is typically needed. When unphysiologic settings are intentionally chosen, as when the physician desires an unusually long Ti (Ti longer than Te results in inverse ratio ventilation [IRV], described later), deep sedation or therapeutic paralysis is often given.

Pressure-Support Ventilation

The patient must trigger the ventilator to activate this mode, so PSV is not applied to passive patients. Ventilation is determined by Pi− PEEP, patient-determined f, patient effort, and the patient's mechanics. Once a breath is triggered, the ventilator attempts to maintain Pi by using whatever flow is necessary. Eventually, flow begins to decrease due to cessation of the patient's inspiratory effort or to increasing elastic recoil of the respiratory system as lung volume rises. The ventilator maintains Pi until inspiratory flow decreases an arbitrary amount (e.g., to 20% of initial flow) or below an absolute flow rate (depending on the ventilator).

It is useful to first consider what happens if the patient were to trigger the ventilator and then remain passive (an artificial situation). Vt would be determined by Pi and the (largely static) mechanical properties of the respiratory system, as during PCV (see Fig. 36-1B). More typically, the patient makes an effort throughout inspirations, in which case Vt is determined in part by the degree of effort (see Fig. 36-1B). At a constant minute ventilation, the patient's work of breathing can be increased by decreasing Pi or making the trigger less sensitive (Table 36-2) and can increase inadvertently if respiratory system mechanics change despite no change in ventilator settings. Respiratory system mechanical parameters cannot be determined readily on this mode because the ventilator and patient contributions to Vt and V̇ are not distinguishable from analysis of the ventilator airway opening pressure (Pao); accordingly, the important measurements of Pplat, Ppk minus Pplat, and autoPEEP are measured during a brief daily switch from PSV to ACV at the corresponding values of Vt, V̇, and I:E observed during PSV.

A potential advantage of PSV is improved patient comfort.6,7 An important caution about PSV is that it can account for a large fraction of total minute ventilation, even when set at rather low levels, as in patients with normal respiratory system mechanics. For example, in a patient with myasthenia gravis, 10 cm H2O of PSV may represent full mechanical ventilation. A “successful” spontaneous breathing trial with these settings should not be used to judge the patient's readiness for extubation.

Volume-Preset Modes

During volume-preset ventilation, a volume is delivered to the patient at the required pressure (within the limits of the high pressure alarm). The physician generally also sets a V̇ (indirectly determining the Ti) and f. In volume-preset modes, the Pplat is predictable (in a passive patient) when the Crs is known:

where PEEP includes autoPEEP.

Compared with pressure-preset modes, a potential advantage of volume-preset ventilation is greater control over the total minute ventilation because Vt does not depend on potentially changing patient effort or respiratory system mechanical properties. Another advantage of volume-preset modes was reported by ARDS Network Tidal Volume Trial, which demonstrated an advantage with respect to mortality rate when using ACV. Moreover, it is easy to characterize the respiratory system mechanics by measuring Ppk and Pplat, thereby simplifying follow-up of the patient's progress or response to therapies.

Assist Control Ventilation

The set parameters of the assist-control mode are the V̇, f, and Vt (on some ventilators, one must set the total minute ventilation and rate, thereby determining Vt and indirectly determining V̇). In the passive patient, the ventilator delivers f (f = 60 seconds/[Ti+ Te]) equal breaths per minute, and Vt or V̇ setting determine the Ti, Te, and the I:E. Pplat is related to the Vt and the Crs, whereas Ppk minus Pplat includes contributions from V̇ and inspiratory resistance (see Fig. 36-1C).

The active patient can trigger extra breaths by exerting an inspiratory effort exceeding the preset trigger sensitivity at the set Vt and V̇ and thereby change Ti, Te, and I:E and (potentially) create or increase autoPEEP. Typically, each patient will display a preferred rate for a given Vt and will trigger all breaths when the controlled ventilator frequency is set a few breaths per minute slower than the patient's rate; in this way, the control rate serves as an adequate support should the patient stop initiating breaths. When high inspiratory effort continues during the ventilator-delivered breath, the patient may trigger a second, superimposed (“stacked”) breath (and, rarely, a third breath). The total Vt of this breath is determined by the point in the first breath at which the second was triggered, so the total Vt can range from the set Vt to twice the Vt.

Typically, the patient performs inspiratory work during an assist-control breath.1,9 This may not be obvious despite careful examination of the patient unless measures of intrathoracic pressure (esophageal pressure and central venous pressure) are available, or the inspiratory pressure waveform is examined carefully (Chap 32). Effort at the end of the breath will affect the Ppk and Pplat, making determination of respiratory system mechanics unreliable. When the patient is assisting every breath, the work of breathing can be increased by increasing the magnitude of the trigger or by lowering Vt (which increases the rate of assisting; see Table 36-2). Decreasing f at the same Vt generally has no effect on the work of breathing (in contrast to SIMV, discussed below) when the patient is initiating all breaths.

Synchronized Intermittent Mandatory Ventilation

In the passive patient, intermittent mandatory ventilation (IMV) cannot be distinguished from controlled ventilation in the ACV mode. Ventilation is determined by the mandatory f, Vt, and V̇ values. However, if the patient is not truly passive, he or she may perform respiratory work during the mandatory breaths. More to the point of the SIMV mode, the patient can trigger additional breaths by decreasing Pao below the trigger threshold (see Fig. 36-1D). If this triggering effort comes in a brief, defined interval before the next mandatory breath is due, the ventilator will deliver the mandatory breath ahead of schedule to synchronize (SIMV) with the patient's inspiratory effort. If a breath is initiated outside the synchronization window, Vt, V̇, and I:E are determined by patient effort and respiratory system mechanics (see Fig. 36-1D), not by ventilator settings. The spontaneous breaths tend to be of small volume, as depicted in Fig. 36-1D, and are highly variable from breath to breath. The SIMV mode is often used to gradually augment the patient's work of breathing by lowering the mandatory breath f (or Vt), thereby driving the patient to breathe more rapidly to maintain adequate ventilation, but this approach appears to prolong “weaning”10,11 (see Table 36-2). Although this mode continues to be used widely, there is little rationale for it and SIMV is falling out of favor.

Mixed Modes

Some ventilators allow combinations of modes, most commonly SIMV plus PSV. There is little reason to use such a hybrid mode, although some physicians use the SIMV mode as a means to add sighs to PSV, an option not otherwise generally available. Because SIMV plus PSV guarantees some backup minute ventilation (which PSV does not), this mode combination may have value in occasional patients at high risk for abrupt deterioration in central drive.

Dual-Control Modes

The sophisticated microprocessors included with modern ventilators allow remarkably complex modes of ventilation. These modes typically try to meld the best features of volume- and pressure-preset modes. Some cause a switch of modes between breaths (e.g., pressure-regulated volume control [PRVC] and volume support) or within a breath (e.g., volume-assured pressure support). In general, these modes are complex, and their effects may vary greatly depending on the details of the patient's effort. None has been shown to be safer or more useful than more conventional modes. The greatest problem with such newer modes is that they are very complex, the algorithm describing their function is not usually understood by practitioners, and they change during a breath or from breath to breath, depending on patient effort, sometimes in ways that can provoke unanticipated effects.

Pressure-Regulated Volume Control

This is a pressure-preset mode with a set Ti (i.e., it is time cycled) in which the ventilator compares the Vt with a physician-set Vt and automatically and gradually adjusts Pi of subsequent breaths to deliver the desired Vt. A downside of PRVC is that, as patient effort increases, the ventilator decreases support. Proponents argue that this mode provides the benefits of pressure-preset modes and simultaneously guarantees Vt; whether this guarantee makes the mode better or worse for the patient is debated.

Volume Support

Volume support is a pressure-preset mode in which Pi is automatically changed to gradually bring Vt in line with the desired Vt over several breaths, differing from PRVC in that Ti is not set but rather depends on patient effort as in PSV. It is unknown whether this mode speeds or impedes weaning.

Volume-Assured Pressure Support

This mode begins as PSV, but, if a desired Vt is not met, the ventilator switches to ACV within the same breath to guarantee Vt. As with many dual-control modes, the physician delegates decision making to the ventilator. Complex adjustments and their potentially detrimental effects on the patient may come into play at any time of day or night, depending on changes in the mechanical properties of the respiratory system or changes in the patient's level of consciousness, comfort, or neuromuscular competence.

Continuous Positive Airway Pressure

Continuous positive airway pressure (CPAP) is not a mode of ventilation but a means of increasing functional residual capacity and allowing the patient to breathe spontaneously. This approach is frequently used when assessing the patient's ability to breathe without ventilatory assistance. Advantages of CPAP over T-piece breathing is that oxygenation may be increased, ventilator alarms (e.g., low minute ventilation and apnea) remain in place, the patient's spontaneous Vt and rate can be easily read from the ventilator panel, and the work of breathing is decreased if autoPEEP is present.12,13 Disadvantages include the loss of mobility and independence that comes with being tethered to the ventilator and the sometimes increased work of breathing attributed to triggering ventilator valves and driving flow through excess tubing and flow meters. A potentially misleading feature of some ventilators is that the display may show the mode as “CPAP” when it is “PSV.” This could lead health care providers to draw erroneous conclusions about the patient's ability to sustain spontaneous ventilation.

Effect of Inspiratory Flow Profile

With most ventilators, the physician can choose one of several inspiratory waveforms, most commonly square or decelerating. The rationale for the use of decelerating flow is the possible improvement in the distribution of ventilation and minimization of Ppk. This rationale works because maximal flow (and therefore flow-related pressure) occurs early in the breath when lung volume (and elastic recoil pressure) is minimal; in addition, near the end of the breath, lung volume is maximal but flow is minimal. However, an inescapable consequence of the overall lower V̇ (assuming equal peak inspiratory V̇ and a passive patient) is a shorter Te. Thus, in patients who have obstruction or high minute ventilations (those in whom a decelerating flow pattern will most decrease Ppk), autoPEEP is likely to be caused or increased (Fig. 36-3). Although the relative contributions of Ppk and PEEP (or autoPEEP) to barotrauma risk are not clearly defined, it seems likely that, in most patients, barotrauma risk will be worsened rather than improved with a decelerating profile. A sine waveform similarly lowers Ppk and shortens Te.

When a square waveform is used, the flow-related pressure near end inspiration is nearly the same as at the beginning of the breath and adds to the elastic recoil pressure to produce a higher Ppk than during sine wave or decelerating flow. However, this higher Ppk is largely borne by the robust proximal airways and not by the alveoli; by contrast, greater autoPEEP means greater Pa and risk of alveolar disruption. Because the peak pressure is visibly decreased by decelerating and sine wave profiles and increased autoPEEP is typically occult, such flow patterns can be insidiously threatening. Accordingly, we believe that there is little reason to use anything other than the conventional square wave inspiratory flow profile, except when IRV is desired (see below). When a decelerating flow profile is used, autoPEEP should be measured diligently and the hidden complexities of this phenomenon made clear to all caring for the patient.

A peak V̇ of 1 L/s (60 L/min) is a common initial setting, but this may require adjustment upward (for patient comfort or to lengthen Te) or downward (to create IRV). Increased V̇ may have a stimulatory effect on respiratory rate in active patients,14 paradoxically shortening Te, although the impact on respiratory rate and work of breathing after the first few seconds has not been studied. Decreasing the peak V̇ will decrease Ppk when there is significant resistance to airflow but, in this setting, will usually worsen autoPEEP, as described above. One often overlooked adverse consequence of setting peak V̇ at less than the patient wishes is that the patient will actively inspire against the ventilator, thereby increasing the respiratory work. This occurs frequently when patients having low ventilatory requirements are placed on volume-preset ventilators on which V̇ cannot be set directly but rather is determined by Vt and Ti (e.g., the Siemens 900C).

Triggered Sensitivity

In the ACV, SIMV, and PSV modes, the patient must decrease the Pao below a preset threshold to “trigger” the ventilator. In most situations this is straightforward because a more negative sensitivity increases the effort demanded of the patient. This can be used intentionally to increase the work of breathing when the goal is to strengthen the inspiratory muscles. In contrast, when autoPEEP is present, the patient must decrease Pa by the autoPEEP amount to have any effect on Pao and then by the trigger amount to initiate a breath. This can dramatically increase the required effort for breath initiation (Fig. 36-4). In several instances, we have seen physicians suspect machine malfunction and even change the ventilator when they are confronted with an obviously struggling patient seemingly unable to get a breath despite a “minimal” trigger threshold. The solution for this problem is to eliminate the cause for autoPEEP, sedate the patient, or use externally applied PEEP to counterbalance the autoPEEP (which only occasionally increases autoPEEP, risking barotrauma and hypotension)15–17 (see Chap. 39).

Flow-triggering systems (“flow-by”) have been used to further decrease the work of triggering the ventilator. In contrast to the usual approach, in which the patient must open a demand valve to receive ventilatory assistance, continuous-flow systems maintain a continuous high flow and then augment flow when the patient initiates a breath. These systems can decrease the work of breathing below that encountered when using conventional demand valves,18,19 in part by shortening the time to pressurization of the inspiratory circuit,20 but they do not solve the problem of triggering when autoPEEP is present.

Unconventional Ventilation Modes

Inverse Ratio Ventilation

IRV is defined as a mode in which the I:E is greater than 1. Like PEEP, it was introduced as an empirical variation to salvage lung oxygen exchange in patients with severe acute hypoxemic respiratory failure. There are two general ways to apply IRV: pressure-controlled IRV (PC-IRV), in which a preset airway pressure is delivered for a fixed period at an I:E greater than 1, or volume-controlled IRV (VC-IRV), in which a Vt is delivered at a slow (or decelerating) V̇ (or an end-inspiratory pause is inserted) to yield an I:E greater than 121 (Fig. 36-5). For PC-IRV, the physician must specify the inspiratory airway pressure, f, and I:E, and Vt and flow profile are determined by respiratory system impedance as discussed for PCV (see Fig. 36-5). Commonly, the initial Pi is 20 to 40 cm H2O (or 10 to 30 cm H2O above the PEEP), f is 20/min, and the I:E is 2:1 to 4:1. For VC-IRV, the operator selects a Vt, f, V̇ (typically a low value), flow profile, and, possibly, an end-inspiratory pause (see Fig. 36-5). The chosen values result in an I:E greater than 1:1 and as high as 5:1.

Compared with conventional modes of ventilation, lung oxygen exchange is often improved on IRV owing to increased mean Pa and volume consequent to the longer time above functional residual capacity (FRC)22,23 or owing to creation of autoPEEP.24,25 Conceivably, this decreases shunt as PEEP does by redistributing alveolar edema into the pulmonary interstitium.26 It is remotely possible that IRV causes better ventilation of lung units with long time constants, but these are so short in normal lungs27 (and shorter in ARDS) that such redistribution is unlikely to occur with slower flow and could not reduce shunt even if it did. Because autoPEEP is a common consequence of IRV, serial determination of its magnitude is essential for safe use of this mode. PC-IRV and VC-IRV generally require heavy sedation with or without muscle paralysis.

Airway Pressure-Release Ventilation

Airway pressure-release ventilation (APRV) consists of CPAP that is intermittently released to allow a brief expiratory interval.28 Conceptually, this mode is pressure-controlled IRV, during which the patient is allowed to initiate spontaneous breaths. It has been applied to patients with acute lung injury29,30 and has proved effective in maintaining oxygenation and assisting ventilation. A potential advantage of APRV is that mean Pa is lower than it would be during positive-pressure ventilation from the same amount of CPAP, possibly decreasing the risks of barotrauma and hemodynamic compromise. It has been claimed that the most important clinical advantage of APRV is that, compared with conventional ventilation, peak airway pressure can be decreased dramatically.29 In these studies, however, conventional positive-pressure ventilation was delivered by using excessive Vt (10 to 15 mL/kg).29,30 Disadvantages of APRV include hypoxemia due to the interruption of CPAP, atelectasis,30 and patient discomfort that sometimes mandates sedation. Another concern relates to the fact that, because the lung cycles tidally below rather than above the volume determined by CPAP, this mode probably encourages repeated recruitment and de-recruitment of flooded and collapsed alveoli. Although this point is controversial, the weight of evidence suggests that this may amplify ventilator-induced lung injury. Whether this mode provides any benefit over modern low-Vt ventilation remains to be shown.

Proportional-Assist Ventilation

Proportional-assist ventilation is intended only for spontaneously breathing patients. The goal of this novel mode is to attempt to normalize the relation between patient effort and the resulting ventilatory consequences.31,32 The ventilator adjusts Pi in proportion to patient effort throughout any given breath and from breath to breath. This allows the patient to modulate the breathing pattern and total ventilation. This is implemented by monitoring instantaneous V̇ and volume (V) of gas from the ventilator to the patient and changing the Pi as follows:

where f1 and f2 are selectable functions of volume (elastic assist) and flow (resistive assist), respectively, values that can be estimated from the patient's respiratory mechanics. Potential advantages of this method are greater patient comfort, lower Ppk, and enhancement of the patient's reflex and behavioral respiratory control mechanisms. In contrast, proportional-assist ventilation can amplify instabilities in the patient's breathing rhythm, as in the common instance of periodic (Cheyne-Stokes) respiration.

High-Frequency Ventilation

Several modes of ventilation have in common the use of Vt smaller than the dead space volume.33 Gas exchange does not occur through convection as during conventional ventilation but through bulk flow, Taylor diffusion, molecular diffusion, non-convective mixing, and possibly other mechanisms. These modes include high-frequency oscillatory ventilation and high-frequency jet ventilation. Theoretical benefits of high-frequency ventilation (HFV) include lower risk of barotrauma due to smaller tidal excursions, improved gas exchange through a more uniform distribution of ventilation, and improved healing of bronchopleural fistulas.34 Animal studies have suggested that HFV may be superior to lung protective ACV with respect to ventilator-induced lung injury, hemodynamic compromise, and inflammation.35,36 Delivered Vt is affected mostly by rate but also by I:E and frequency amplitude. In an animal model of severe lung injury, settings of 4 Hz, an I:E of 1:1, and a pressure amplitude of 60 cm H2O, the Vt was 4.4 mL/kg, a value approaching conventional Vt values.37 A substantial risk is that dynamic hyperinflation is the rule, and Pa is greatly underestimated by monitoring Pao.38 A controlled trial of HFV found no clinically relevant benefit, but the approach was shown to be safe, at least in the context of a clinical trial.39 Nevertheless, HFV is the natural extension of reducing the Vt as a means to prevent volutrauma, and there is renewed interest in this old technique.39a

Initial Ventilator Settings

Initial ventilator settings depend on the goals of ventilation (e.g., full respiratory muscle rest versus partial exercise), the patient's respiratory system mechanics, and minute ventilation requirements. Although each critically ill patient presents myriad challenges, it is possible to identify four subsets of ventilated patients: the patient with normal lung mechanics and gas exchange, the patient with predominant airflow obstruction, the patient with acute hypoxemic respiratory failure, and the patient with restrictive lung or chest wall disease. Specific recommendations regarding ventilator settings are detailed more fully in Chaps. 38, 39, 40, and 42 but are reviewed here briefly, in addition to guidelines for ventilating patients with normal respiratory system mechanics.

In all patients, the initial FiO2 should usually be 0.5 to 1.0 to ensure adequate oxygenation, although usually it can be decreased within minutes when guided by pulse oximetry and, in the appropriate setting, applying PEEP. In the first minutes after institution of mechanical ventilation, the physician should remain alert for several common problems, most notably, airway malposition, aspiration, and hypotension. Positive-pressure ventilation may decrease venous return and, hence, cardiac output, especially in patients with a low mean systemic pressure (e.g., hypovolemia, venodilating drugs, decreased sympathetic tone from sedating drugs, or neuromuscular disease) or a very high ventilation-related pleural pressure (e.g., chest wall restriction, large amounts of PEEP, or airway obstruction causing autoPEEP). If hypotension occurs, intravascular volume should be expanded rapidly while steps are taken to decrease the pleural pressure (a smaller Vt and less minute ventilation). Meanwhile, the FiO2 should be raised to 100%. If these steps do not rapidly restore the circulation, another complicating event (pneumothorax or myocardial ischemia) should be considered while the patient is taken off the ventilator and bagged manually to assess respiratory load and to observe the response of blood pressure to a brief suspension of positive-pressure ventilation.

The Patient with Normal Respiratory Mechanics and Gas Exchange

Patients with normal lung mechanics and gas exchange may require mechanical ventilation because of loss of the central drive to breathe (e.g., drug overdose or structural injury to the brain stem), because of neuromuscular weakness (e.g., high cervical cord injury, acute idiopathic myelitis, or myasthenia gravis), as an adjunctive therapy in the treatment of shock,40,41 or to achieve hyperventilation (e.g., in the treatment of elevated intracranial pressure after head trauma). After intubation, initial ventilator orders should be an FiO2 of 0.5 to 1.0, a Vt of 8 to 12 mL/kg, a respiratory rate of 8 to 12 breaths/min, and a V̇ of 50 to 60 L/min (Table 36-3). Alternatively, if the patient has sufficient drive and is not profoundly weak, PSV can be used. The level of pressure support is adjusted (usually to the range of 10 to 20 cm H2O above PEEP) to bring the respiratory rate down into the low 20s, usually corresponding to a Vt of about 500 mL. It is important to realize that PSV is mechanically supported but entirely spontaneous, with no machine “backup” unless mixed with a mode such as SIMV. Thus, hypoventilation may occur despite the use of PSV, if there is further deterioration of muscle strength or blunting of drive by disease or drugs. If gas exchange is entirely normal, the FiO2 likely can be decreased further based on pulse oximetry or arterial blood gas determinations. However, because right mainstem intubation, aspiration, and bronchospasm are relatively common complications of intubation, it is wise to initiate ventilation with the FiO2 at 0.5 or higher. Should hyperventilation be desired, the initial respiratory rate should be increased to the range of 16 to 20 breaths/min. The V̇ can be increased if the patient complains of air hunger, but 50 to 60 L/min is often sufficient.1 Even in most tachypneic patients with underlying lung disease and certainly in those individuals with normal lung mechanics, a V̇ greater than 60 L/min is rarely necessary or useful.

Soon after the initiation of ventilation, airway pressure and flow waveforms should be inspected for evidence of dyssynchrony between the patient and the ventilator or undesired patient effort (see Chap. 32). If the goal of ventilation is full rest, the patient's drive often can be suppressed by increasing the V̇, f, or Vt.42,43 The latter two changes may induce respiratory alkalemia. If such adjustments do not diminish breathing effort, despite normal blood gases, to an undetectable level, sedation may be necessary. If this does not abolish inspiratory efforts and full rest is essential (as in shock), muscle paralysis can be considered.

Measures to prevent atelectasis should include sighs (6 to 12 per hour at 1.5 to 2 times the Vt ) or small amounts of PEEP (5 to 7.5 cm H2O). This is particularly important in patients with neuromuscular diseases during protracted ventilation because atelectasis is common. In these patients, we use the upper limit of Vt (12 mL/kg). Three-point turning and chest physiotherapy are desirable in all patients unless other conditions preclude their use. Rotating beds may be effective in some patients for preventing atelectasis and pneumonia.44

Patients with Dominant Airflow Obstruction

Two general types of patients require mechanical ventilation for significant airflow obstruction; those with status asthmaticus (see Chap. 40) and those with exacerbations of chronic airflow obstruction (see Chap. 39). Rare alternative causes are inhalation injury or central airway lesions, such as tumor or foreign body, not bypassed with the endotracheal tube. In isolated upper airway injuries, assessment of the extent of damage is often possible by bronchoscopy shortly before or at the time of intubation. Bronchoscopy should not be performed routinely in patients with asthma.

Status Asthmaticus

Because the gas exchange abnormalities of airflow obstruction are largely limited to ventilation-perfusion mismatch, an FiO2 of 0.5 suffices in the vast majority of patients.45 Requirements for a higher FiO2 should prompt a search for an alveolar filling process or for lobar atelectasis. We have had success ventilating these patients with PSV by setting Pi at 25 to 30 cm H2O. Because these patients are typically anxious, we often give large doses of narcotics to suppress drive, an approach that, when combined with high-level PSV, often leads to an unusual but stable pattern of breathing, with a Vt larger than 900 mL and an f of 3 to 7. This approach appears to minimize autoPEEP by allowing such a long Te. Alternatively, ventilation can be initiated using the ACV mode with a normal Vt (5 to 7 mL/kg) and respiratory rate of 12 to 15 breaths/min (see Table 36-3). A peak flow of 60 L/min is recommended, and higher flow rates do little to increase Te. For example, if the Vt is 500 mL, the respiratory rate is 15 breaths/min, and the V̇ 60 L/min, the Te is 3.5 seconds. Raising V̇ (dramatically) to 120 L/min increases the Te to only 3.75 seconds, a trivial improvement. In contrast, a small reduction in respiratory rate to 14 breaths/min increases the Te to 3.8 seconds. This example emphasizes not only the relative lack of benefit of raising the flow rate but also the importance of minimizing minute ventilation when the goal is to reduce autoPEEP. If the patient is triggering the ventilator, it is essential that some PEEP be added to reduce the work of triggering. This does not generally worsen the hyperinflation as long as PEEP is not higher than about 85% of the autoPEEP.16,46–48 Ventilatory goals are to minimize alveolar overdistention (keep Pplat <30) and to minimize dynamic hyperinflation (keep autoPEEP <10 cm H2O or end-inspiratory lung volume <20 mL/kg), a strategy that largely prevents barotrauma.49 Reducing minute ventilation to achieve these goals generally causes the partial pressure of CO2 to rise above 40 mm Hg, often to 70 mm Hg or higher. Although this requires sedation, such permissive hypercapnia is quite well tolerated except in patients with increased intracranial pressure and perhaps in those with ventricular dysfunction or pulmonary hypertension.

Patients with status asthmaticus requiring mechanical ventilation are usually extremely anxious and distressed, especially when ventilated using a volume-preset mode. Deep sedation is usually necessary and supplemented in rare patients by therapeutic paralysis. The frequent occurrence of postparalytic myopathy in patients with asthma50–52 has led us to greatly decrease our use of paralytics, an approach facilitated by the use of high-level PSV.

Sighs are undesirable because they may lead to lung rupture. Because peak proximal airway pressure is so high in this patient group, upper-limit alarms of 75 cm H2O (and sometimes higher) are often required. Careful attention should be paid to the V̇ and flow profile. Changes in flow that have little effect in the patient without airflow obstruction can have a dramatic impact in obstructed patients. Specifically, reducing the inspiratory flow or changing to a decelerating flow profile reduces the airway pressures and the amount of ventilator alarming but, by prolonging inspiration, actually worsens autoPEEP. Although the ventilator looks “better,” the patient is worse, but this is only recognized if autoPEEP is regularly sought or if the expiratory flow profile is examined (see Fig. 36-3). Aggressive chest physiotherapy is advised because many patients mobilize mucous plugs during their recovery phase; often these plugs are so large and tenacious that they compromise endotracheal tube patency.

Acute‐on-Chronic Respiratory Failure

Acute-on-chronic respiratory failure is a term used to describe exacerbations of chronic ventilatory failure usually occurring in patients with COPD53 (see Chap. 39). Many of these patients are successfully (and preferably) ventilated noninvasively (see Chap. 33). When intubated, they are found to have relatively smaller increases in inspiratory resistance (compared with asthma), with their expiratory flow limitation arising largely from loss of elastic recoil.54 As a consequence, in the patient with COPD, peak airway pressures tend to be only modestly elevated (e.g., 30 cm H2O), but autoPEEP and its consequences are common.55 At the time of intubation, hypoperfusion is common, as manifested by tachycardia and relative hypotension, and typically responds to briefly ceasing ventilation combined with fluid loading.

Because most of these patients are ventilated after days to weeks of progressive deterioration, the goal is to rest the patient (and respiratory muscles) completely for 36 to 48 hours, although excessive rest and ventilatory support may contribute to atrophy and weakness of the diaphragm.56 Also, because the patient typically has an underlying compensated respiratory acidosis, excessive ventilation risks severe respiratory alkalosis and, over time, bicarbonate wasting by the kidney. The goals of rest and appropriate hypoventilation usually can be achieved with initial ventilator settings of a Vt of 5 to 7 mL/kg and a respiratory rate of 16 to 24 breaths/min, with an ACV mode set on minimal sensitivity (see Table 36-3). Because gas exchange abnormalities are primarily those of ventilation-perfusion mismatch, supplemental oxygen in the range of an FiO2 of 0.4 should achieve better than 90% saturation of arterial hemoglobin. Gas exchange abnormalities requiring an FiO2 greater than 0.5 should prompt a search for complicating alveolar filling processes, such as left ventricular failure with pulmonary edema, pneumonia, or lobar collapse. V̇ may be adjusted for patient comfort but usually is in the range of 50 to 60 L/min. Measures to prevent atelectasis and its complications (e.g., three-point turning, chest physiotherapy, or sighs) are necessary. PEEP should be used in this phase when the patient is triggering the ventilator because autoPEEP is universally present.

Most patients with COPD appear exhausted at the time when mechanical support is instituted and will sleep with minimal sedation. To the extent that muscle fatigue has played a role in a patient's functional decline, rest and sleep are desirable. Two days of such rest presumably will restore biochemical and functional changes associated with muscle fatigue, but 24 hours is probably not sufficient.57 Small numbers of patients are difficult to rest on the ventilator and they continue to demonstrate effortful breathing. Examination of airway pressure and flow waveforms can be very helpful in identifying this extra work and in suggesting strategies for improving the ventilator settings (Fig. 36-6). In many patients, this is the result of autoPEEP-induced triggering difficulty, as discussed in Chap. 32 and shown in Fig. 36-4.58 Frequently, adding extrinsic PEEP to nearly counterbalance the autoPEEP dramatically improves the patient's comfort.59 An alternative approach is to increase minute ventilation to drive down the partial pressure of CO2, but this will worsen autoPEEP and waste bicarbonate. This can be a difficult management problem. We advise a careful search for processes that might drive the patient to a respiratory rate higher than is desirable (e.g., hypoperfusion, pleural effusion or pain). If the patient continues to make significant inspiratory efforts—especially if these efforts are ineffective in actually triggering a machine breath or generating a Vt —judicious sedation is in order.

Once the patient improves and the respiratory muscles are rested, the patient should assume some of the work of breathing and be evaluated for liberation. During this phase, some extrinsic PEEP is typically useful to reduce the work of triggering.59

Patients with Acute Hypoxemic Respiratory Failure

Acute hypoxemic respiratory failure is caused by alveolar filling with blood, pus, or edema, the end results of which are impaired lung mechanics and gas exchange (see Chap. 31). The gas exchange impairment results from intrapulmonary shunt that is largely refractory to oxygen therapy. In ARDS (see Chap. 38), the significantly reduced FRC due to alveolar flooding and collapse leaves many fewer alveoli to accept the Vt , making the lung appear stiff and dramatically increasing the work of breathing. The ARDS lung should be viewed as a small lung rather than as a stiff lung. In line with this current conception of ARDS, it is clearly established that excessive distention of the ARDS lung compounds lung injury and may induce systemic inflammation.8,60 Ventilatory strategies have evolved markedly in the past decade and have changed clinical practice and generated tremendous excitement.

The goals of ventilation are to reduce shunt, avoid toxic concentrations of oxygen, and choose ventilator settings that do not amplify lung damage. The initial FiO2 should be 1.0 in view of the typically extreme hypoxemia (see Table 36-3). PEEP is indicated in patients with diffuse lung lesions but may not be helpful in patients with focal infiltrates, such as lobar pneumonia. In patients with ARDS, PEEP should be instituted immediately, beginning with 15 cm H2O, and then rapidly adjusted to the least PEEP necessary to produce an arterial saturation of 88% on an FiO2 no higher than 0.6 (the “least PEEP approach”). An alternative approach (the “open-lung approach”61) sets the PEEP at a value 2 cm H2O higher than the lower inflection point of the inflation pressure-volume curve (see Chap. 32), but this has not been shown to confer benefit. The Vt should be 6 mL/kg IBW on ACV because a higher Vt is associated with a higher mortality rate.8 Some have speculated that unstudied Vt values, such as 9 or 3 mL/kg IBW, might be even more beneficial than 6 mL/kg. It seems likely that there is a dose-response relation, with lower Vt values being superior, and this explains the resurgence in interest in HFV in which Vt can be very small. Nevertheless, because 6 mL/kg IBW has been conclusively shown to be safe and effective, this represents the standard of care to which other (potentially better, potentially worse) ventilator strategies should be compared. There is little doubt that lung protection can be achieved with pressure-preset ventilation, but safe settings are unknown. Some have extrapolated from the 30 cm H2O plateau pressure limit in the ARDS Network study that a Pi of 30 cm H2O ought to be safe; however, because the mean Pplat in those ventilated with 6 mL/kg IBW was only 26 cm H2O, 30 cm H2O may be too high. Whatever the mode, the respiratory rate should be set at 24 to 36 breaths/min as long as there is no autoPEEP. An occasional consequence of lung protective ventilation is hypercapnia. This approach of preferring hypercapnia to alveolar overdistention (“permissive hypercapnia”) is discussed further in Chaps. 37 and 40.61–63 Alternative modes of ventilation for ARDS, such as IRV, HFV, and tracheal gas insufflation, may have a role as salvage therapies but are of unproven benefit.

Once specimens have been collected from the airway for microbiologic and other studies, PEEP generally should not be disconnected to suction patients or to measure hemodynamic values because alveoli readily re-flood, provoking extreme hypoxemia. This supports multiple observations that PEEP does not reduce lung water but rather redistributes it into the lung interstitium to improve gas exchange.26 Several modified suction adapters are available to provide a route to the airway and maintain PEEP, although most tend to leak at PEEP levels above 15 cm H2O.

Sighs and other measures to prevent atelectasis are not necessary during the acute phases of acute hypoxemic respiratory failure, when PEEP levels are typically in excess of 10 cm H2O. It should be remembered that these patients are at risk of atelectasis as they improve and PEEP levels are lowered. This is probably due in part to surfactant deficiency during the recovery from diffuse alveolar damage and certainly will be aggravated by the use of small Vt.

The Patient with Restriction of the Lungs or Chest Wall

Several restrictive diseases of the lungs or chest wall can lead to respiratory failure, especially when there is a superimposed ventilatory challenge (e.g., pneumonia). These conditions are fully discussed in Chaps. 42 and 66 and include lung disease (e.g., advanced pulmonary fibrosis or late-stage ARDS), abdominal disease (e.g., massive ascites), and other chest wall abnormalities (e.g., kyphoscoliosis). We describe ventilator management.

Small Vt (5 to 7 mL/kg) and rapid rates (18 to 24 breaths/min) are especially important to minimize the hemodynamic consequences of positive-pressure ventilation and to reduce the likelihood of barotrauma (see Table 36-3). The FiO2 is usually determined by the degree of alveolar filling or collapse, if any. Rarely, we have encountered patients with enormous restrictive loads from intraabdominal catastrophes (e.g., massive intraperitoneal bleeding) who have a large intrapulmonary shunt but lack signs of alveolar flooding on the chest radiograph. We speculate that, in such patients, large numbers of alveolar units may be subserved by airways forced below their closing volume throughout tidal ventilation, so that these nonventilated alveoli comprise a large intrapulmonary shunt (see Chap. 42). Reversible contributors to restriction (e.g., circumferential burn eschar or tense ascites) should be identified and treated. Sitting the patient up in bed or on a chair may reduce the abdominal pressure, thereby easing the work of breathing.

The high Pa values typically generated in these patients may lead to increased physiologic dead space (when Pa exceeds the pulmonary artery pressure), especially when large Vt values are used. When the restrictive abnormality involves the chest wall (including the abdomen), the large ventilation-induced rise in pleural pressure has the potential to compromise cardiac output. This in turn will lower the mixed venous partial pressure of O2 and, in the setting of ventilation-perfusion mismatch or shunt, the arterial partial pressure of O2. If the physician responds to this decreasing arterial partial pressure of O2 by augmenting PEEP or increasing the minute ventilation, further circulatory compromise ensues. A potentially catastrophic cycle of worsening gas exchange, increasing ventilator settings, and progressive shock is begun. This circumstance must be recognized because treatment is to reduce dead space (e.g., by lowering minute ventilation or correcting hypovolemia).

Facilitating Patient Comfort and Communication

The Role of Sedation

Ideally, the mechanically ventilated patient should be alert, comfortable, and capable of communicating with the health care team. These desirable goals must be weighed against the need to heavily sedate and even therapeutically paralyze some patients with cardiovascular instability, severely compromised oxygen delivery to peripheral tissues, or severely deranged respiratory system mechanics.64

Much excessive sedation can be avoided by frequent communication, reassurance, and identification of sources of pain, anxiety, and agitation. Often, ventilator adjustment is more effective than drug therapy for calming the patient (see Table 36-1). Patients should be maximally alert during the day, with sedation limited to the evening, if possible. Short-acting benzodiazepines or haloperidol may facilitate sleep, thereby ensuring that the patient is maximally rested for efforts at spontaneous breathing during the day. Many patients must be deeply sedated to ensure comfort or to stabilize them hemodynamically during acute illness. A daily “wake up” during which sedatives are withheld until the patient awakens and is able to follow commands (or becomes agitated) is safe and effective in shortening time on the ventilator and in the ICU.65 We advocate such a wake up in essentially all patients, even those who are hemodynamically unstable and unlikely to be breathing spontaneously for days.

Whenever neuromuscular blockers are used, the agent should be withdrawn on a daily basis until neuromuscular function returns to prevent excessive drug accumulation.63 It also may be useful to monitor the degree of neuromuscular blockade with a nerve stimulator (aiming for a train-of-two out of four), although this has not been shown to decrease the incidence of postparalytic myopathy. In patients with impaired renal and hepatic function, continuous infusion of cis-atracurium is preferred because pancuronium may accumulate and lead to protracted paralysis. During muscle paralysis, careful assessment of the level of sedation is essential because individuals differ widely in their response to sedatives and narcotics.

When the patient is optimally alert, it is important that the caretakers provide brief, clear explanations of all interventions proposed, especially changes in ventilator settings, to evaluate the patient's perception of beneficial effect. This allows the patient to be a part of the decision making concerning the optimal ventilator settings.

Patient-Ventilator Synchrony

The initial ventilator settings should be reassessed promptly to assess their appropriateness for the individual patient. Such fine tuning of the ventilator often means the difference between a patient who rests on the ventilator or who continues to perform fatiguing efforts, who is calm yet awake, or who requires deep sedation or therapeutic paralysis. Assessing the patient-ventilator interaction requires substantial skill and experience. In part, the adequacy of ventilator settings is judged by the appearance of the patient (comfortable and resting versus diaphoretic and fighting) and arterial blood gas analysis. Tremendously valuable additional information comes from examination of waveforms, as elaborated in Chap. 32.

The intensivist should ensure that the patient and ventilator are synchronized, that is, that each attempt by the patient to trigger the ventilator generates a breath. The most common situation in which the patient fails to trigger breaths occurs in severe obstruction when autoPEEP is present (see Fig. 36-4). This is recognized at the bedside when the patient makes obvious efforts that fail to produce a breath. Using waveforms, these ineffective efforts cause a temporary slowing of expiratory flow, sometimes halting it completely (Fig. 36-7).

As an example, a patient was newly ventilated for septic shock and ARDS. His physicians found very high Pplat (38 cm H2O) on the following settings: ACV mode, Vt of 480 mL, an f of 28/min, and V̇ of 60 L/min. By reducing the V̇ to 30 L/min, Pplat was newly measured at 28 cm H2O, which the physicians interpreted as an improvement (Fig. 36-8). However, the airway pressure decreased only at the cost of greatly increased efforts on the patient's part, efforts that can consume a remarkable fraction of the cardiac output (>30% in animal models40,66,67). Moreover, the transpulmonary pressure remained excessive because the Vt was not reduced.

Response to “Crises” in the Ventilated Patient

A vast array of sudden and potentially catastrophic changes in clinical condition can occur in the course of mechanical ventilation (Table 36-4). We focus on high- and low-pressure alarms, worsened oxygenation, and hypercapnia. Whenever the function of the ventilator or the position and patency of the airway are in question, the patient should be removed from the ventilator and hand bagged with 100% oxygen. This point is extremely important because this maneuver immediately circumvents the ventilator (and any malfunction of it), provides the clinician with a direct assessment of respiratory system mechanics, and focuses attention on the patient and not on the machine.

High-Pressure Alarm

Aside from alarm or gauge malfunction, increased airway pressure indicates obstruction of the airway, obstruction to gas flow through the ventilator circuit, patient effort against the ventilator, or a change in the mechanics of the respiratory system. If manual bag ventilation is difficult, a suction catheter should be passed immediately through the endotracheal tube. If the catheter cannot be advanced 25 cm or farther, obstruction of the airway is likely. If repositioning of the head does not relieve kinking, and if the patient is not biting the airway, reintubation is necessary. If the patient is biting an endotracheal tube, a bite block should be placed; if this cannot be done, a short-acting neuromuscular blocking drug should be administered.

If the airway is patent but manual ventilation is difficult and the patient is struggling, a sedative should be given. If the patient can be easily ventilated (implicating vigorous respiratory muscle activity), the cause of the patient's distress should be sought. Possibilities include hypoxemia, hypercapnia, shock, or a new central nervous system process.

If ventilation remains difficult after deep sedation or muscle paralysis of a patient with a patent endotracheal tube, a new lower airway, pleural, lung, or chest wall process should be sought. Auscultation, palpation, and percussion often identify pneumothorax, collapse, or consolidation. Early portable chest radiography confirms these diagnoses or identifies an alternative cause of the crisis. Placing the patient back on the ventilator and measuring peak and plateau pressures and autoPEEP will further delineate the problem, as described above.

Low-Pressure Alarm

Low-pressure alarms signal machine malfunction, a leak, or inspiratory effort by the patient (usually obvious). Large persistent leaks can occur within the ventilator itself, in the inspiratory limb, at the connection to the Y adaptor and endotracheal tube, around the endotracheal tube cuff, or through a bronchopleural fistula. If normal resistance to ventilation is noted during manual ventilation, the problem lies with the ventilator or tubing. If hand bagging shows minimal resistance, an endotracheal tube cuff leak is likely. This can be confirmed by listening over the neck or by placing a hand over the mouth. A large bronchopleural fistula can be identified by inspection of the chest tube and pleural drainage system.

Worsened Oxygenation

When a patient develops hypoxemia, sufficient oxygen should be given immediately to return the saturation to 88%. However, this must be followed by a search for the cause of deterioration. Progression of the primary cause of respiratory failure (ARDS, pneumonia, or lung hemorrhage) will impair gas exchange, but this should not be assumed to be the case. Also possible is a new lesion (e.g., nosocomial pneumonia) that may be identified by physical examination or chest radiograph. However, a systematic approach is useful to identify the myriad (including nonpulmonary) causes of hypoxemia.

From a pathophysiologic perspective, new hypoxemia implies a reduced FiO2 (including ventilator malfunction), hypoventilation, ventilation-perfusion mismatching, shunt, or a decrease in the mixed venous oxygen saturation. Hypoventilation is usually obvious, being signaled by hypercapnia. Ventilation-perfusion mismatch typically causes mild hypoxemia that is easily corrected with supplemental oxygen. Bronchospasm, airway secretions, and airway plugging are common contributors in intubated patients. Inhaled bronchodilators may acutely worsen ventilation-perfusion relations,68 as will vasodilators.45 The combination of worsened ventilation-perfusion matching and an increase in dead space should prompt consideration of pulmonary embolism. Most often, when new hypoxemia develops in a mechanically ventilated patient, shunt or a decrease in mixed venous oxygenation can be found. A new shunt (e.g., pulmonary edema, pneumonia, or atelectasis) typically can be found on the chest radiograph, whereas mixed venous desaturation is detected by analyzing a venous blood sample or performing venous oximetry. The causes of venous desaturation include reduced cardiac output or hemoglobin concentration or increased systemic oxygen consumption. These nonpulmonary causes of hypoxemia are particularly common in patients with severe shunt lung disease and may herald life-threatening crises (e.g., pneumothorax).

Hypercapnia

A rising PaCO2 often elicits a change in the ventilator orders (increased frequency or Vt). However, a pathophysiologic approach is useful in this situation. From the equation for PaCO2:

where VCO2 is CO2 production, k is a constant, and Vd is the dead space, it can be seen that, in addition to a decrease in minute ventilation, rising CO2 production (e.g., fever, shivering, or agitation) or increasing dead space (e.g., hypovolemia, pulmonary embolism, PEEP) may account for new hypercapnia. Responding to hypercapnia by simply raising the minute ventilation is dangerous because causes of increased CO2 production and dead space may be important to diagnose in their own right. In addition, augmenting minute ventilation has the potential to (paradoxically) decrease alveolar ventilation if the increase in Vt or f worsens dead space (such as when autoPEEP is present). In this setting, the PaCO2 may rise when minute ventilation is increased and fall when minute ventilation is reduced. These issues are further discussed in Chap. 40.

Liberation of the Patient from Mechanical Ventilation

We refer to the discontinuation of mechanical ventilation not as weaning (which implies the withdrawal of a nurturing life-support system) but as liberation (connoting freedom from a confining, noxious, and dangerous circumstance69). Because liberation from the ventilator is fully discussed in Chap. 44, we make only a few points relevant to all ventilated patients. Patients recover the ability to breathe spontaneously because central drive is regained, neuromuscular competence is restored, and respiratory system load is reduced. Once these are achieved, the ventilator is no longer needed. Gradual adjustments of IMV rates or pressure-support levels that are too slow for the patient's needs simply serve to prolong the duration of mechanical ventilation, as shown in large trials of weaning strategies,10,11 and do not facilitate the recognition of evolving ventilatory failure.70 However, if drive, strength, and load are not repaired, no amount of ventilator technology will allow the patient to breathe on his or her own. Most often, when physicians believe they are “weaning” the patient, they are simply allowing time for their other therapies to treat the respiratory failure; ventilator changes are prescribed coincidentally but are irrelevant. Accordingly, effective liberation of each patient begins with intubation and stabilization on the ventilator, with the measurement of respiratory mechanics to assist in evaluating the reversible features of the patient's abnormally increased load; as soon as is clinically relevant, the respiratory muscle strength is evaluated for reversible causes of weakness.

Before an acceptable balance between neuromuscular competence and load is attained, different methods for exercising the patient may be useful because disuse causes muscles to weaken56 (see Table 36-3). These include T-piece sprints with which the patient is allowed to breathe without ventilatory assistance for progressively longer periods as ventilatory function improves. Alternatively, the pressure-support mode can be adjusted to allow a reasonably spontaneous Vt (e.g., 300 to 500 mL H2O) and respiratory rate (<30 breaths/min) but at a level that demands some work from the patient. The physician should be familiar with a number of different modes because patient preference can then dictate which is used in a particular circumstance. SIMV appears to prolong the period of ventilator dependency and should no longer be used for weaning. Aside from this, the method of exercise chosen is not clearly important and certainly secondary to the main goals of restoring drive, improving neuromuscular competence, and reducing load.

Of overriding importance is an approach that asks on a daily basis, “Can this patient breathe on his or her own?” In several studies of methods of weaning, 75% of patients assessed at entry into the trial were extubated successfully.10,11 The use of interdisciplinary weaning teams or respiratory therapist–driven protocols may expedite successful liberation by actively addressing this question each day.71,72

Conversion to a Tracheostomy

A tracheostomy provides easier tracheobronchial toilet, enhances communication, and is more comfortable for the patient than translaryngeal intubation (TLI). In contrast, endotracheal intubation is less invasive and, in the short run, less likely to cause complications. The timing of tracheostomy involves balancing its complications73 against the (typically) more delayed complications of TLI. The major complication of TLI is laryngeal damage with resulting postextubation upper airway obstruction or dysphonia.74 Injuries likely arise from abrasion and compression of laryngeal structures, with sequelae including posterior commissural stenosis, posterior cordal synechiae, arytenoid fixation, and subglottic stenosis. The precise contributions of insertion trauma, duration of TLI, and movement during ICU management to these injuries is not clear, but all are likely important. Some clinicians have suggested that women and patients with diabetes mellitus, rheumatoid arthritis, and ankylosing spondylitis are at increased risk of laryngeal injury during TLI. The incidence of cuff-induced injury to the trachea itself is probably similar between tracheostomy and TLI, at least in the critical care environment.75

Our own approach is to begin with TLI in most critically ill patients. Those with an immediate indication for tracheostomy, such as upper airway obstruction or severe sleep apnea, are scheduled for this procedure at the earliest opportunity. Patients who are extremely restless, have copious pulmonary secretions, or are likely to require more than 2 weeks of mechanical ventilation are also considered for early tracheostomy. All other patients are reassessed on a daily basis for these indications for tracheostomy. If extubation seems likely within the first 2 to 3 weeks, TLI is maintained. Occasionally, this approach provides TLI for 3 weeks or longer; however, even with soft cuffs and careful monitoring, the complications of this prolonged TLI begin to outweigh its advantages, and tracheostomy becomes indicated for its greater comfort and potential for enhanced communication. Percutaneous tracheostomy has several advantages in the critically ill patient. Performance of tracheostomy in the ICU provides a safely monitored environment for the procedure and obviates the risks of transporting the patient.

Extubation

Extubation after prolonged (>5 days) intubation should be approached cautiously. In addition to demonstrating freedom from mechanical ventilatory support, as discussed in Chap. 44, the patient must be capable of maintaining airway patency, have sufficient airway reflexes to avoid aspiration, and have adequate cough to mobilize secretions. Laryngeal injury causing postextubation upper airway obstruction should be anticipated.

The most common cause of postextubation stridor is posterior commissure edema, arising from direct mechanical injury to these soft tissues, and impaired vocal cord abduction. Before extubation, the degree of upper airway edema may be assessed by direct laryngoscopy or by deflating the tube cuff, obstructing its lumen, and measuring the amount of airflow around it. Alternatively, the airway can be inspected by fiberoptic laryngoscopy immediately after extubation. Despite these precautions, progressive airway edema with stridor will be encountered in 1% to 5% of patients after prolonged TLI. The initial management should include bag-mask ventilation synchronized to augment the patient's efforts. Noninvasive positive-pressure ventilation is generally considered to be useful, although one clinical trial showed no benefit,76 and another trial has called into use its general application for respiratory failure emerging shortly after extubation.76a Racemic epinephrine by inhalation and intravenous corticosteroids are usually recommended but have not been rigorously studied. A helium-oxygen gas mixture (heliox) also can be useful in this setting.77 Administration of this low-density gas mixture reduces the large pressure drop associated with turbulent flow across the obstruction, thus reducing the work of breathing. Heliox (21% oxygen and 79% helium) can be delivered by a mask connected to an H tank, supplemented by nasal cannula oxygen, to maintain an arterial hemoglobin saturation of 90%. Heliox and noninvasive positive-pressure ventilation should be used only to temporize while awaiting more definitive therapy of the critical airway narrowing.

If stridor fails to respond to initial measures or reemerges while on therapy, reintubation is usually necessary. The usual approach is to use a small endotracheal tube (6.0 or 6.5 mm) through the nasal route to minimize further injury to the posterior commissure. The managing team should be prepared to perform cricothyrotomy or tracheostomy, if necessary. After reintubation, edema resolves in most patients over 48 to 72 hours. During this time, corticosteroid therapy should be continued (e.g., dexamethasone 4 mg every 6 hours), and the airway should be viewed directly to confirm resolution of edema.

Extubation failure is a marker for prolonged ventilation and ICU stay, increased hospital costs and mortality rate, and greater likelihood of tracheostomy.78 Risk factors include age, longer duration of ventilation, continuous sedative infusion, and anemia.

Airway during Split-Lung Ventilation

The lungs may be separated for purposes of differential ventilation by two major means: blocking the bronchus of a lobe or whole lung while ventilating with a standard endotracheal tube or passing a double-lumen tube. Different devices have been used to obstruct a bronchus, but experience is greatest with the Fogarty embolectomy catheter. Double-lumen tubes carry the advantages of allowing each lung to be ventilated, collapsed, reexpanded, or inspected independently.

Split-lung ventilation is only rarely useful in the critical care unit, but occasionally its benefits are dramatic. Large bronchopleural fistulas severely compromise ventilation and may not respond to HFV.79 A double-lumen tube will maintain ventilation of the healthy lung and facilitate closure of the bronchopleural fistula.80 During massive hemoptysis, lung separation may be lifesaving by minimizing blood aspiration, maintaining airway patency, and tamponading the bleeding site while awaiting definitive therapy.81 Patients with focal causes of acute hypoxemic respiratory failure, such as lobar pneumonia or acute total atelectasis, may benefit from differential ventilation and application of PEEP.82

Complications with these devices are common because they are difficult to maintain in ideal position during a protracted period of respiratory failure and tend to directly injure the trachea and main bronchi. A clear protocol for airway assessment and repositioning should exist, and routine input from senior anesthesiology staff is required.