Invasive Mechanical Ventilation

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Chapter 32 Invasive Mechanical Ventilation

The ancient Greek physician and philosopher Claudius Galen (129 to 210 CE) was the first to describe artificial ventilation of an animal. With the exception of a few historical anecdotes, mechanical ventilation did not become a widely used therapeutic intervention in clinical medicine until the outbreak of the poliomyelitis epidemic in Europe and the United States in the 1940s and 1950s, during which negative-pressure ventilators were made available to many of the patients with polio-related breathing impairment. Since then, there have been many developments in the technology of ventilators, and mechanical ventilation has become a commonly used, lifesaving procedure for patients with respiratory failure.

Ventilators initially were used in conjunction with neuromuscular blocking agents to provide controlled ventilation. Recognition that abolition of spontaneous breathing rapidly leads to deconditioning of the respiratory muscles stimulated the development of ventilatory strategies designed to deliver assistance in synchrony with the patient’s spontaneous breathing efforts. The first mode to allow a patient to initiate and terminate a predefined level of pressure support was introduced in the early 1980s, initiating a process that led to a growing awareness of the complexity and consequences of patient-ventilator interactions and more recently to the development of ventilatory modes that allow individualization of the assist on a breath-by-breath basis.

This chapter outlines the indications for and contraindications to invasive mechanical ventilation, illustrates the operation of various ventilatory modes, describes the essentials of mechanical ventilation in patients with obstructive and with restrictive pulmonary disease processes, and summarizes the potential complications of mechanical ventilation.

Indications and Contraindications

The goals of mechanical ventilation include decreasing the oxygen cost of breathing by unloading the respiratory muscles and maintaining adequate gas exchange, while minimizing potential complications associated with ventilation, including ventilation-induced lung injury (VILI), patient-ventilator asynchrony, hemodynamic compromise, and negative effects on other nonpulmonary organs. Mechanical ventilation is indicated when the patient is unable to maintain the function of their respiratory system as a result of underlying pulmonary disease, failure of the respiratory muscles, instability of the chest wall, increased metabolic demand, or the requirement for deep sedation or for neuromuscular blockade, and when noninvasive ventilation has failed or is contraindicated (e.g., in an unconscious patient, during surgery, with rapid progression of respiratory failure).

A number of methods can be used to monitor mechanical ventilation, including clinical assessment (e.g., respiratory pattern, auscultation, patient-ventilator interaction) and assessment of gas exchange (e.g., arterial blood gases, pulse oximetry, carbon dioxide tension in exhaled air). Monitoring the pressure waveforms and flow applied to the airways allows calculation of the variables of respiratory system mechanics; chest radiography or computed tomography helps assess the underlying disease process or some complications of mechanical ventilation (e.g., displacement of the endotracheal tube, pneumothorax); and monitoring the function of nonpulmonary organs (e.g., cardiac performance, central nervous system function, urinary output) may indicate adequacy of global and regional oxygen delivery. For safety reasons, virtually all ventilators contain adjustable alarm limits for the various functional components, such as upper and lower limits of applied ventilator pressure (i.e., pressure wave forms [PVENT]), ventilatory rate, tidal volume (VT), minute ventilation, and other variables.

Techniques

Modes of Invasive Mechanical Ventilation

Most mechanical ventilators are capable of delivering ventilation in a fully controlled manner, to assist spontaneous breathing, and to facilitate nonassisted spontaneous breathing (Figure 32-1). Normally, the means by which inhalation is terminated (cycled off) is used to classify the ventilatory modes. Common mechanisms to cycle off the inhalation include volume, pressure, airflow, and time. Initiation of an inhalation (i.e., trigger-on) can be based either on predefined time intervals or on systems in which the patient’s inspiratory effort has to exceed a specific threshold. Most frequently, pneumatic systems are used that require a predefined, adjustable change in pressure or airflow within the ventilator circuit to trigger the initiation of an inhalation by the ventilator. Alternative trigger-on and cycling-off methods, such as changes in pleural pressure (PPL) (as can be assessed by esophageal pressure [PES] measurements) or changes in the amplitude of the diaphragm electrical activity (Edi), are currently entering clinical practice.

Figure 32-1 Characteristics of available modes of mechanical ventilation including the method used to terminate (cycle-off) the inhalation and the method to initiate (trigger-on) the inhalation. The available modes include time-cycled, volume-targeted, or pressure-targeted (or -controlled) modes (volume-targeted” or “-controlled” ventilation [VCV], pressure-targeted” or “-controlled” ventilation [PCV]); modes combining controlled ventilation with assist to spontaneous breathing (synchronized intermittent mandatory ventilation [SIMV], pressure-regulated volume control [PRVC], volume support [VS], airway pressure release ventilation [APRV], bilevel positive airway pressure [BiPAP]); modes of pure assist to spontaneous breathing (pressure support [PSV], proportional assist ventilation [PAV], neurally adjusted ventilatory assist [NAVA]); and finally, modes that do not deliver assist to the patient but allow unrestricted breathing while delivering a constant pressure (continuous positive airway pressure [CPAP]). The work of breathing can completely or largely be taken over by the ventilator during controlled modes of ventilation, whereas during modes that assist spontaneous breathing, the load on the respiratory muscles is shared between the patient and the ventilator.

With volume-cycled ventilation, the ventilator delivers a predefined VT with a frequency that is either predefined or set by the patient’s inspiratory effort. The pressure used to deliver the VT depends on the mechanical properties of the two major components of the respiratory system (see also further on): (1) the resistance of the inspiratory limb of the ventilator circuit (including the endotracheal tube) and the central airways and (2) the compliance of the respiratory system, consisting of the lung and chest wall.

With pressure-cycled ventilation, the ventilator will stop delivering pressure as soon as a predefined pressure level is reached. With this system, the delivered VT depends on the respiratory system mechanics, and minute ventilation is not guaranteed.

With flow-cycled ventilation, the ventilator will cease delivery of pressure as soon as the airflow drops to a predefined level of its maximum. For example, with pressure support ventilation, a preset pressure is applied as soon as the patient’s effort exceeds the trigger-on threshold. The ventilator will stop delivering pressure when the inspiratory flow has decreased to a predetermined percentage of its peak value.

With time-cycled ventilation, the ventilator will deliver a predefined level of pressure for a predefined time.

Modes That Target Volume or Pressure

Controlled modes of ventilation (i.e., volume- or pressure-targeted or -controlled ventilation) normally are used when deep sedation or muscle paralysis is required (e.g., during surgery), when the patient is making no breathing efforts (e.g., after drug overdose), as a last resort when sufficient synchrony between the ventilator and the patient cannot be achieved, or when maximal reduction of the oxygen cost of breathing and complete unloading of the respiratory muscles from the work of inspiration are desired (e.g., respiratory muscle fatigue, severely altered mechanics of the respiratory system, or severely compromised oxygenation). Adaptation of the patient to controlled mechanical ventilation may require deep sedation and occasionally muscle paralysis.

Volume-Targeted (or -Controlled) Ventilation

With time-cycled, volume-targeted (i.e., volume-controlled) ventilation (VCV), VT is preset, and the minute ventilation is guaranteed by the ventilator, depending on the ventilatory rate. Triggering delivery of additional breaths with the preset VT occurs when the patient’s breathing efforts exceed a caregiver-defined trigger-on threshold. Volume assist-control (A/C) refers to a variation of VCV in which the patient initiates delivery of a fixed VT by the ventilator, whereas a VCV backup rate ensures that the patient receives a minimum minute ventilation. Parameters that can be modified with most of the ventilators are the rate of inspiratory flow or ratio of the inspiratory to expiratory times (I/E ratio), the inspiratory rise time, the duration of the end-inspiratory pause time, and with some ventilators, the flow pattern during inhalation (Figure 32-2). The effects of changes in these parameters on the pressure and flow waveforms are demonstrated in Figure 32-2, B and C.

Figure 32-2 A, Volume-targeted (or volume-controlled) ventilation (VCV) with a square-wave flow pattern. The delivered tidal volume (VT) is calculated by integrating the area under the flow curve, as indicated by the blue-shaded area. During the end-inspiratory pause, the inspiratory and expiratory valves of the ventilator are closed for a predefined time interval (expressed as a percentage of the entire breath period). Ideally, at the end of expiration, the full tidal volume applied during inhalation (minus that lost during gas exchange) has left the lung and the airflow is reduced to zero. This may not be the case in a patient with dynamic collapse of the airways during expiration (e.g., in a patient with chronic obstructive pulmonary disease), where dynamic hyperinflation of the lungs may result from incomplete exhalation of the applied VT and persistence of expiratory airflow is detectable at end expiration (dashed line). The inspiratory flow pattern can be varied with many of the modern ventilators to constant (square-wave), decelerating (ramp), or sinusoidal. B, Changes in the adjustable parameters with volume-controlled ventilation (VCV) result in characteristic changes of the pressure and volume waveforms. The plotted curves demonstrate isolated changes in parameters, under conditions in which all other ventilatory parameters, as well as the mechanical characteristics of the respiratory system, are assumed to remain unchanged. The area under the inspiratory flow curve reflects the tidal volume (VT). A, Baseline conditions. B, An increase in VT results in an increase in the maximum inspiratory flow and hence in an increased peak airway pressure and end-inspiratory plateau pressure. C, Decreasing the I/E ratio results in a prolongation of expiration, while the maximum inspiratory flow and hence the peak airway pressure both increase. D, An increase in the I/E ratio has the exact opposite effect. E, A reduction in the inspiratory pause time reduces the maximum inspiratory flow and hence the peak airway pressure, while the plateau pressure and the inspiratory and expiratory times remain unchanged. F, When the time to reach the maximum inspiratory flow (inspiratory rise time) is shortened, the maximum inspiratory flow and the peak airway pressure will both decrease, whereas prolongation of the inspiratory rise time, G, has the opposite effect. In both situations, the end-inspiratory plateau pressure and the inspiratory and expiratory times do not change. C, Airway pressure tracings during volume-controlled ventilation. The shape of the airway pressure waveform may provide an indication of whether settings of inspiratory flow are adequate. A and B are normal waveforms: a, fast pressure increase; b, convex or straight pressure shoulder; c, peak pressure. The interrupted (C) or even concave (D) segments a and b of the pressure waveform indicate that the maximal inspiratory flow falls short of the patient’s actual demand. This may be the case in patients with high respiratory drive, such as in hypermetabolic states, sepsis, and delirium.

Pressure-Targeted (or -Controlled) Ventilation

With pressure-controlled ventilation (PCV), a maximum inspiratory pressure is targeted by the caregiver. The ventilator increases the pressure to this level during each breath. The flow pattern is decelerating; flow is high initially but decreases as the PVENT limit is approached. Inhalation is terminated when a predefined time limit or flow level is reached. The applied VT depends on the relative stiffness (elastance) of the respiratory system (e.g., VT is lower if pulmonary edema develops or if the patient contracts the abdominal or chest wall musculature) and on the resistance to airflow (e.g., VT will be lower if secretions markedly increase airway resistance). The adjustable parameters are the targeted PVENT, the inspiratory rise time, and, in some ventilators, the inspiratory time (Figure 32-3).

Figure 32-3 Pressure-targeted (or pressure-controlled) ventilation (PCV). Delivery of the predefined pressure level is initiated after a trajectory defined by the preset ventilatory rate. Additional triggering-on also is possible when the patient’s effort exceeds a predefined trigger-on threshold. The delivered tidal volume (VT) is calculated as the time integral of the flow curve. The inspiratory rise time defines how quickly the maximal airflow is reached. Inspiration is terminated after a caregiver-specified time interval that results from choosing a ratio of inspiratory-to-expiratory times (I/E ratio) and a ventilatory rate or, alternately, from choosing an absolute inspiratory time.

Modes That Deliver Assistance to Spontaneous Breathing

Patients often are ventilated with volume- or pressure-targeted modes (i.e., controlled ventilation) in the early phase of the disease process, whereas modes delivering assistance to spontaneous breathing usually are applied later. Assistance to spontaneous breathing is used to prevent respiratory muscle atrophy as well as to maintain physiologic feedback and intrinsic defense mechanisms, such as the Hering-Breuer reflex, based on the hypothesis that integration rather than abolition may help to minimize VILI. This approach should be better suited than “caregiver-controlled” mechanical ventilation to accommodate the typically rapid changes in lung mechanics and metabolic demands in critically ill patients. Ventilatory modes in which patients breathe spontaneously early in the course of the acute lung injury (ALI) process may have certain advantages, such as improved pulmonary ventilation-perfusion (V/Q) matching (Figure 32-4), increased oxygenation, preserved cardiac function, reduced need for excessive sedation, prevention of ventilation-associated respiratory muscle dysfunction, and ventilation at lower mean airway pressure, compared with controlled modes of ventilation. Induction of respiratory muscle fatigue or failure secondary to increased work of breathing is a potential disadvantage, but this frequently can be minimized with use of the appropriate level of positive end-expiratory pressure (PEEP) and adjustment of inspiratory flow rates. Of interest, recent data suggest that early neuromuscular blockade for 48 hours in patients with ALI may decrease mortality (see further on).

Figure 32-4 Ventilation-perfusion () distribution during spontaneous breathing and during mechanical ventilation. In a classic article, Froese and Bryan demonstrated that with spontaneous breathing (in either an awake or sedated patient), dorsal excursions of the diaphragm were more pronounced than ventral excursion. The active diaphragm generates a greater negative pressure in the dorsal pleural space, thereby increasing the pressure gradient between the central airways and the pleural space (transpulmonary pressure); this promotes alveolar recruitment and ventilation of the dependent lung regions. Ventilation of dependent, usually well-perfused parts of the lungs, along with an increase in blood flow to previously minimally perfused or nonperfused areas, helps to convert shunt units to units with normal distribution, thereby increasing oxygen content of arterial blood, and to lower pulmonary vascular resistance. During application of positive-pressure ventilation with inactive or only minimally active inspiratory muscles (e.g., with neuromuscular blockade or with hyperventilation), gas is preferentially distributed toward the ventral regions of the lungs, where the impedance to airflow is lower than in the dependent, partially atelectatic regions. Generation of positive pressure in the dorsal pleura promotes collapse of alveoli in the dorsal lung regions and the mismatch becomes worse.

(Data from Froese AB, Bryan AC: Effects of anesthesia and paralysis on diaphragmatic mechanics in man, Anesthesiology 41:242–255, 1974; Warner DO, Warner MA, Ritman EL: Atelectasis and chest wall shape during halothane anesthesia, Anesthesiology 85:49–59, 1996; Hedenstierna G, Lichtwarck-Aschoff M: Interfacing spontaneous breathing and mechanical ventilation. New insights, Minerva Anestesiol 72:183–198, 2006; Oczenski W, editor: Atmen-Atemhifen, Stuttgart, Georg Thieme Verlag, 2006.)

Pressure Support Ventilation

Pressure support ventilation is patient-triggered and, normally, flow-cycled, allowing the patient to actively control the start of each breath. Once the patient’s inspiratory effort exceeds the trigger-on threshold, a caregiver-defined level of PVENT is delivered to the airways (Figure 32-5, A). After a high initial airflow that is required to rapidly approach the targeted pressure, the airflow progressively decreases. Once a predefined percentage of the maximum inspiratory flow is reached, the ventilator terminates inhalation and opens the expiratory valve. Parameters that can be adjusted with pressure support ventilation are the trigger-on threshold, the inspiratory rise time, and the pressure level (see Figure 32-5, B). To better match termination of the inhalation with the patient’s individual demand, the cycling-off airflow threshold can be varied in some ventilators.

Figure 32-5 A, Pressure support ventilation (PSV). The delivered tidal volume (VT) is calculated by integrating the area under the flow curve, as indicated by the blue-shaded area. The inspiratory rise time defines how fast the maximal airflow (100%) is achieved. Thereafter, the inspiratory airflow continuously decreases because, once the pressure target is reached, maintaining this level requires progressively less air to flow into the lungs. As soon as the cycling-off airflow threshold (i.e., a preset percentage of maximal air flow) is reached, the ventilator ceases to deliver inspiratory flow, and the expiratory valve is opened to allow passive exhalation. B, Changes in the parameters of pressure support ventilation result in characteristic changes of the pressure and volume curves. Panels A to D demonstrate isolated changes of parameters assuming that all other ventilatory parameters and the mechanical characteristics of the respiratory system remain unchanged. A, PSV breath with an inspiratory rise time of 0.20 second. B, After reducing the inspiratory rise time to its minimum, the peak inspiratory flow and consequently also the cycling-off airflow threshold are both reached earlier. Decreasing the inspiratory rise time results in a shorter inspiratory time, while the VT remains unchanged. Note that although the inspiratory rise time is decreased to 0 seconds, the peak inspiratory flow is reached with a small delay. C, Increasing the cycling-off airflow threshold from 30% to 50% similarly shortens the inspiratory time; however, VT decreases in this case. D, A combination of a maximal decrease in the inspiratory time and a moderate increase in the cycling-off airflow threshold shortens the inspiratory time, whereas the loss in VT is only minimal. Such an approach can be used to achieve a prolongation of the expiratory time in patients at risk for dynamic hyperinflation because of expiratory flow limitation (e.g., patients with COPD) (see also Figure 32-19). COPD, chronic obstructive pulmonary disease.

Analogous to all pressure-targeted ventilation modes, pressure support ventilation does not guarantee a specific VT or minute ventilation. Changes in VT and minute ventilation can be achieved by adjusting the level of pressure support and/or the cycling-off criteria.

Difficulties with Conventional Modes of Assistance to Spontaneous Breathing

It is sometimes assumed that assisting spontaneous breathing will decrease respiratory effort; however, unless the ventilator settings are selected to satisfy the patient’s demand, such a mode can actually result in the opposite. Ideally, assistance should be delivered in synchrony with and in proportion to the patient’s actual respiratory demand (i.e., both the timing and magnitude of the assist delivered by the ventilator are synchronized to the patient’s inspiratory effort).

Although important improvements have been made in the trigger-on characteristics and the cycling-off characteristics of ventilators, ideal synchrony between the ventilator and the patient has not been achieved with most modes of ventilation, and patient-ventilator asynchrony is common (Figure 32-6). Patient-ventilator asynchrony may result in increased inspiratory and expiratory muscle activity and may introduce an unnecessary burden, in terms of work of breathing, in patients whose respiratory muscles are already under stress. Technologies that allow delivery of assistance in proportion to the patient’s demand on a breath-by-breath basis have only recently been developed (e.g., proportional assist ventilation [PAV] and neurally adjusted ventilatory assist [NAVA], as described later on).

Figure 32-6 Examples of patient-ventilator asynchrony. A, Both the initiation and the termination of the assist delivered by the ventilator are delayed relative with the patient’s respiratory demand, as reflected by the electrical activity of the diaphragm (Edi). Note that the neural expiration normally starts at approximately 70% to 80% of the maximum Edi. B, The ventilator delivers assist in response to the breathing efforts 1 and 2, whereas effort 3 fails to trigger the ventilator. Wasted inspiratory efforts frequently occur when settings for the trigger threshold are inadequate, when excessive inspiratory efforts are required because of auto-PEEP, when delay in cycling-off is excessive, or when the respiratory muscles are too weak to translate a neural inspiratory effort into an effective breath. C, Auto triggering may occur when the generation of airflow or negative pressure in the expiratory limb of the ventilatory circuit is not related to an inspiratory effort (e.g., transmission of pressure oscillations because of cardiac activity, leaks in the ventilator circuit). Auto triggering often occurs when the trigger-on threshold is set at a level that is too sensitive. D, Short cycles. Delivery of assist by the ventilator is prematurely terminated and immediately resumed as the patient makes an inspiratory effort. For example, short cycles may occur when the airflow is impeded by a high resistance within the ventilator circuit (e.g., secretion in the endotracheal tube or in the trachea) or when the patient actively blocks inspiratory airflow that might be delivered in excess of the patient’s demand.

Variables that can be adjusted to improve synchrony between the patient and the ventilator include the trigger-on threshold, the inspiratory rise time or flow rate, and the cycling-off airflow threshold. The mechanisms used to initiate a breath (trigger-on) detect changes in airflow or pressure in the ventilatory circuit. Hence, negative deflections of short duration (pneumatic trigger mechanisms) may be detectable in the airway pressure and/or flow tracings when a breath is triggered by the patient’s effort. Delivery of the assistance is terminated either after a predefined time has elapsed (time-cycled) or after a prespecified cycling-off airflow threshold (flow-cycled) has been reached (see Figure 32-5). Rise time refers to the time required by the ventilator to increase the inspiratory airflow from zero to peak. As demonstrated in Figure 32-7, the rise time changes the slope of the increase in pressure during early inspiration. Generally, rise time (or the inspiratory flow pattern) should be set to ensure that air is delivered rapidly (fast increase in airway pressure) after initiation of a breath. By establishing an optimal inspiratory rise time, synchrony to the patient’s respiratory demand can be optimized and work of breathing can be reduced.

Figure 32-7 The rise time of the inspiratory flow is adjustable with most current ventilators. A, A pressure spike in early inspiration may indicate inspiratory flow in excess of the patient’s demand or an obstruction in the central airways including the tracheal tube. B, No deformation of the inspiratory pressure waveform is visible with a midrange rise time. C, A concave deformation of the inspiratory pressure waveform indicates that the patient is making an inspiratory effect, because demand is higher than the flow provided by the ventilator.

(Modified from Branson RD, Campell RS: Pressure support ventilation, patient ventilator synchrony and ventilator algorithms, Respir Care 43:1045–1047, 1998.)

The fact that conventional modes of ventilation always deliver a uniform, predefined level of assist but do not take into account the physiologic variability of the breathing pattern stimulated the development of the PAV and NAVA modes, which deliver pressure assistance in proportion to the patient’s demand.

Proportional Assist Ventilation

PAV, the first patient-triggered mode that adapted the level of assist to the patient’s inspiratory effort, was introduced in 1987. With PAV, the ventilator delivers positive pressure throughout inspiration in proportion to the inspiratory airflow and volume generated by the patient (Figure 32-8). The magnitude of unloading is based on measuring elastance and resistance of the respiratory system. Whereas with conventional modes of ventilation the VT or the delivered PVENT is relatively constant from breath to breath, with PAV only the relationship between delivered PVENT and the inspiratory effort of the patient is constant, whereas VT and the delivered PVENT become dependent variables. Although PAV requires that the patient always assume a portion of the respiratory work, this mode has been demonstrated to effectively unload the respiratory muscles.

Figure 32-8 Proportional assist ventilation (PAV) as volume assist. A, With PAV, the assist is delivered in proportion to inspiratory effort. The pressure delivered to the airways increases until the end of inspiration. B, An increase in volume assist results in a higher pressure delivered for the same tidal volume. Note that with PAV delivered as flow assist, the waveforms appear different, although the basic principles are very similar to those for delivery of PAV as volume assist.

(Modified from Oczenski W, editor: Atmen-Atemhilfen, Georg Thieme Verlag, 2006.)

Limitations of PAV include the necessity to determine elastance and resistance of the respiratory system (a task that is not easy to perform in spontaneously breathing patients) and the occurrence of runaway phenomena at high levels of assist.

Neurally Adjusted Ventilatory Assist

A relatively new strategy of mechanical ventilation, NAVA, uses the Edi to control the ventilator (Figure 32-9). Because breathing signals originate from the brain and reach the diaphragm by way of the phrenic nerves, Edi represents the neural respiratory effort with respect to both timing and amplitude. During NAVA, positive pressure is applied to the airway opening in direct proportion to the Edi amplitude, so defining a target pressure or volume is not required. The patient’s respiratory control mechanisms, including feedback from mechanoreceptors and chemoreceptors, adjust the Edi and thereby regulate the pressure and delivered volume. Animal data and a number of clinical studies suggest that NAVA is applicable in the ICU environment, efficiently delivers assistance synchronous to the subject’s demand, unloads the respiratory muscles, maintains gas exchange, and preserves cardiac performance during invasive ventilation and also during noninvasive ventilation even with use of an excessively leaky interface. Simultaneous measurement of the Edi (which reflects the patient’s neurally generated effort) and the delivered assist allows monitoring the patient’s ability to translate a neural effort into ventilation, referred to as neuroventilatory efficiency. NAVA does not require measurement of respiratory system mechanics, and runaway phenomena are unlikely to occur.

Figure 32-9 A, With neurally adjusted ventilatory assist (NAVA), the electrical activity of the diaphragm (Edi) is derived by use of an array of electrodes mounted on a nasogastric tube. The signals from each electrode pair on the array are differentially amplified, filtered, and multiplied by a proportionality factor (NAVA level) before the signal is used to control the pressure generated by the ventilator. Hence, with NAVA, the pressure delivered to the patient is synchronous and (virtually) instantaneously proportional to the patient’s Edi. B, Neuromechanical coupling and control of the ventilator. Chain of steps necessary to transform central respiratory drive into an inspiration (neuromechanical coupling) that ultimately results in delivery of assist by the ventilator (neuroventilator coupling). The current technology requires transmission of the electrical excitation into a contraction of the respiratory muscles (e.g., the diaphragm) and in generation of a pneumatic signal (pressure or flow at the airway opening) that is sufficient in magnitude to exceed the trigger-on threshold of a sensor within the ventilator. With NAVA, the Edi is used to control the ventilator. Hence, with NAVA, control of the ventilator is independent of the force generated by the respiratory muscles and also is independent of leaks in the ventilator circuit.

(A and B, Modified from Sinderby C, Navalesi P, Beck J, et al: Neural control of mechanical ventilation in respiratory failure, Nat Med 5:1433–1436, 1999.)

PAV and NAVA both depend on presence of an intact respiratory drive. Although the concept of delivering assistance in proportion to the patient’s demand is appealing, and although data from experimental and clinical studies are promising, these modes need to be tested in clinical trials to better define their indications and limitations.

Combined Modes

Airway Pressure Release Ventilation

With airway pressure release ventilation (APRV) (Figure 32-10), the pressure in the ventilator circuit alternates between a high and a lower level (normally the higher pressure level is of longer duration than the lower pressure level) and spontaneous breathing is allowed in any phase of the cycle. The high- and low-pressure levels, the rate of change between the two levels, the respiratory system compliance, and the airway resistance to flow are the main determinants of the “mechanical ventilation” portion with APRV, whereas the complementary “spontaneous breathing” portion mainly depends on the patient’s respiratory drive. In contrast with continuous positive airway pressure (CPAP), APRV interrupts PVENT briefly to augment spontaneous minute ventilation and thereby increases alveolar ventilation and CO₂ removal without increasing the work of breathing. Spontaneous efforts during APRV are not actively assisted except for those breaths that happen to occur during the change from the lower to the upper pressure level. Total minute ventilation with APRV is the sum of the mechanical, pressure-controlled ventilation and the complementary spontaneous breathing. APRV without spontaneous breathing is essentially the same as PCV.

Figure 32-10 With airway pressure release ventilation (APRV), two levels of continuous positive airway pressure (CPAP) are delivered by the ventilator. The higher pressure level is maintained until the inspiratory time (TI) has elapsed; the pressure is then changed to the lower pressure level, usually for a short period of time (TE, typically 0.5 to 1.5 second), before the high-pressure level is resumed. The duration of TI and TE is defined by the caregiver. Spontaneous breathing is allowed in any phase of the cycle. Because the pressure release periods are of short duration, a residual expiratory positive airway pressure (intrinsic PEEP) will be maintained in the lung compartments with a high time constant (slow passive exhalation), preventing end-expiratory collapse of these lung regions. While preventing end-expiratory collapse of the lungs, this helps improve oxygenation as a result of a better match between ventilation and perfusion, and periodic release of the airway pressure assists in removal of carbon dioxide.

APRV has a number of interesting features. First, APRV overcomes shortcomings inherent in many modes of assisted spontaneous breathing related to triggering-on and cycling-off the ventilator by simply avoiding inspiratory and expiratory valves in the ventilator circuit. However, the time-cycled release and reestablishment of the high PVENT is not synchronized to the patient’s breathing efforts, so patient-ventilator asynchrony may result. Second, the application of CPAP recruits some atelectatic areas, increases lung volume, and allows spontaneous breathing to occur on a portion of the pressure-volume curve where impedance to airflow is low and only a small transpulmonary pressure change is required to produce the VT. Third, APRV maintains PVENT at high levels for a prolonged period. Because alveoli are continually recruited along the inspiratory limb of the pressure-volume curve, recruitment may be more efficient with APRV than with shorter-application positive pressure (e.g., with pressure support ventilation).

Bilevel Positive Airway Pressure Ventilation

With BiPAP ventilation, two levels of continuous positive pressure are used, as with APRV, and unrestricted spontaneous breathing is allowed on both pressure levels (Figure 32-11, A). As an additional option, assistance to spontaneous breathing efforts can be provided at the lower pressure level (see Figure 32-11, B), at the higher pressure level, or at both levels. The transition from the low-pressure to the high-pressure level is coordinated with the patient’s breathing effort. The designations Bi-Vent, DuoPAP, and Bi-level used by ventilator manufacturers are synonymous with BiPAP.

Figure 32-11 A, With bilevel positive airway pressure (BiPAP) ventilation, two levels of continuous positive airway pressure are delivered by the ventilator. The pressure levels and the relationship between inspiratory and expiratory times (TI and TE) are both defined by the caregiver. B, Delivery of assist to individual spontaneous breathing efforts is optional; this modality can be combined with BiPAP to compensate for the additional inspiratory work imposed by the flow resistance of the endotracheal tube. Of note, changes between the lower and the higher pressure levels are synchronized to the patient’s efforts. The major difference between BiPAP and airway pressure release ventilation (APRV) is the longer duration at the low-pressure level with BiPAP, with a higher probability of derecruitment of lung regions.

(Modified from Oczenski W, editor: Atmen-Atemhifen, Stuttgart, Georg Thieme Verlag, 2006.)

Despite the theoretical advantages of APRV and BiPAP, trials showing clinically relevant benefits are currently lacking. Further work is needed before these modes can be recommended for specific patient conditions or phases in the process of mechanical ventilation.

Synchronized Intermittent Mandatory Ventilation

Synchronized intermittent mandatory ventilation (SIMV) combines volume- or pressure-targeted breaths at a caregiver-defined rate (mandatory breaths) with unassisted spontaneous breathing (Figure 32-12). Because ideally the mandatory breaths should be synchronized to the patient’s own breathing effort, SIMV requires that the ventilator settings for the trigger-on threshold be adequate for this purpose.

Figure 32-12 Synchronized intermittent mandatory ventilation (SIMV) with unassisted spontaneous breathing between two volume-targeted breaths. Within a short period before starting the next mandatory breath, a trigger window allows synchronization of the controlled breath to the patient’s breathing effort. When the patient’s breathing effort does not exceed the trigger-on threshold during this trigger window, the ventilator will deliver a mandatory breath (either volume- or pressure-targeted as defined by the caregiver) after the maximal time interval for intermittent mandatory ventilation (IMV) has elapsed. This time interval is defined by the preset rate for IMV. PEEP, positive end-expiratory pressure.

(Modified from Oczenski W, editor: Atmen-Atemhifen, Stuttgart, Georg Thieme Verlag, 2006.)

The main differences between SIMV and BiPAP are that SIMV does not allow spontaneous breathing during the mandatory breaths, whereas spontaneous breathing is possible during all phases with BiPAP, and that with SIMV, all mandatory breaths are volume- or pressure-targeted, whereas BiPAP provides only pressure-targeted breaths. Despite its name, concerns similar to those with all pneumatically triggered modes of mechanical ventilation, regarding the delivery of ventilator assistance in synchrony and in proportion to the patient’s demand, apply for SIMV as well.

Pressure-Regulated Volume Control and Volume Support

Pressure-regulated volume control (PRVC) and volume support (VS) use either pressure-targeted ventilation (for PRVC) or pressure support ventilation (for VS) to achieve a predefined VT. Basically, both modes first deliver a test breath at a low-pressure level, measure the achieved VT, and calculate the necessary adjustments in the inspiratory pressure to achieve the targeted VT in the subsequent breath. The same procedure is repeated for every breath. It has been suggested that these modes may be useful in weaning the patient from the ventilator on the basis of the rationale that the stronger the respiratory muscles (e.g., the higher the share of the VT produced by the inspiratory effort of the patient), the lower the level of assistance needed by the ventilator. The major concern with both PRVC and VS is that if the patient’s breathing efforts increase because of an increased respiratory demand (e.g., hypoxemia, fever, increased metabolism), the level of assistance will paradoxically decrease. Also, spontaneous breathing patterns in critically ill patients often are highly variable, and the required VT may vary on a breath-by-breath basis. Again, PRVC and VS are designed such that the level of assist paradoxically decreases during periods of high demand, and vice versa.

Modes That Facilitate Spontaneous Breathing

Continuous Positive Airway Pressure

With CPAP, a caregiver-defined level of positive pressure is maintained by the ventilator while the patient is breathing spontaneously (Figure 32-13). Of note, because the patient’s breathing efforts are not assisted with CPAP, the patient must have adequate respiratory drive and adequate respiratory muscle function. CPAP helps to increase and maintain the functional residual capacity (FRC) and thereby to increase the lung units available for gas exchange (reduction of intrapulmonary right-to-left shunt), prevent end-expiratory airway collapse, and counter the effects of auto-PEEP or intrinsic PEEP.

Figure 32-13 With continuous positive airway pressure (CPAP), a caregiver-defined level of pressure within the ventilatory circuit is maintained. Changes in the airway pressure with inspiration and expiration are constantly compensated for by pressure generated by the ventilator. PEEP, positive end-expiratory pressure.

Positive End-Expiratory Pressure

PEEP refers to the airway pressure (relative to atmospheric pressure) at the end of a breath. PEEP can be applied with most ventilation modes. Patients with respiratory failure from asthma or chronic obstructive pulmonary disease (COPD) who require mechanical ventilation have increases in FRC and in alveolar pressure at the end of exhalation that exceeds atmospheric pressure (i.e., auto-PEEP or intrinsic PEEP), thereby increasing the inspiratory work of breathing. Applying PEEP counters the effect of auto-PEEP on work of breathing. Patients with the acute respiratory distress syndrome (ARDS), acute lung injury (ALI), or hypoxemic respiratory failure from obesity have a reduced FRC that leads to alveolar and/or airway collapse. In these patients, PEEP is used to restore FRC, to recruit regions with collapsed alveoli or airways, to prevent derecruitment of open alveoli, to redistribute fluid within the lung, and to make dependent lung regions available for ventilation. All of these effects can improve the match between ventilation and perfusion, improve oxygen saturation, and decrease the need for high fractions of inspired oxygen. PEEP also has been used in patients with flail chest to stabilize the chest wall.

All of the aforementioned beneficial effects of PEEP are lost and adverse or even harmful effects may occur when excessive levels of PEEP are used. For example, excessive PEEP may increase dead space by over-distending alveoli and concomitantly decreasing alveolar capillary blood flow or may add to the hyperinflation of the lungs in patients with COPD or asthma. High levels of PEEP may reduce pulmonary blood flow by impeding venous return, thereby increasing pulmonary vascular resistance (i.e., decreasing cardiac output in the face of constant pulmonary arterial and venous pressure translates to an increased pulmonary vascular resistance). If pulmonary vascular pressures are kept constant relative to the level of PEEP, however (as will be the case unless cardiac output decreases), the effect of increasing lung volume on pulmonary vascular resistance is small. Of note, the effects of PEEP on cardiac performance are more pronounced during hypovolemia and can partially be reversed by ensuring adequate intravascular fluid volume.

In the past, PEEP was used mainly to increase oxygenation, thereby improving oxygen transport; however, there has been a change in the rationale underlying the use of PEEP, with a greater focus on its use to minimize cyclic air space opening and closing (i.e., atelectrauma) and hence to decrease ventilator-induced lung injury, rather than simply to improve oxygenation.

Given the current lack of tools to monitor both alveolar overdistention and collapse, and given the heterogeneity of the distribution of most disease processes within the lung, identification of the “best PEEP?” level is not straightforward in clinical practice. In fact, the gravitational gradient in pleural pressure and end-expiratory lung volume that exists in both normal subjects and patients requiring mechanical ventilation implies that there cannot be a single level of PEEP that is “best” for all regions of the lung. Pending further clarification on how to set PEEP, a pragmatic approach for daily clinical practice in patients with ALI is to adhere to the algorithm used in the large Acute Respiratory Distress Syndrome Network (ARDSNet) trial (Table 32-1) and to carefully observe the effect of changes in PEEP on parameters such as blood oxygenation, cardiac performance, and expiratory flow limitation. Of note, in patients with stiff chest walls (e.g., massive ascites), higher levels of PEEP are warranted.

Table 32-1 Combinations of Inspiratory Oxygen Fraction (FIO₂) and Positive End-Expiratory Pressure (PEEP) in Patients with Acute Lung Injury or Acute Respiratory Distress Syndrome to Achieve Oxygenation Goals *

FIO₂	PEEP (cm H₂O)
0.3	5
0.4	5
0.4	8
0.5	8
0.5	10
0.6	10
0.7	10
0.7	12
0.7	14
0.8	14
0.9	14
0.9	16
0.9	18
1.0	18
1.0	20
1.0	22
1.0	24

* Partial pressure of arterial oxygen (PaO₂) of 55 to 80 mm Hg or oxyhemoglobin saturation measured by pulse oximetry (SpO₂) of 88% to 95%.

Modified from Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network, N Engl J Med 342:1301–1308, 2000.

Principles of Respiratory System Mechanics Relevant to Mechanical Ventilation

Adjusting ventilator parameters to the patient’s individual condition and interpreting pressure and airflow tracings requires an understanding of the fundamental principles of respiratory system mechanics in ventilated patients. Although these general principles apply to the entire respiratory system, regional inhomogeneities (e.g., lower end-expiratory lung volumes, airway closure, and/or atelectasis in dependent regions) and regional differences in disease processes result in ventilation is never distributed uniformly within the lungs in mechanically ventilated patients. The compliance of a specific alveolar region and the resistance of the associated airways ultimately determine the portion of the VT received by a particular lung region.

Airway Resistance and Lung Elastance

To a simplified approximation, the patient-ventilator unit can be considered as an in-series mechanical system that consists of a resistive element (ventilator and endotracheal tubing + central airways) and an elastic element (lung-thorax compartment). During inflation, the pressure applied to the tube inlet (PVENT) is equal to the sum of the pressure required to overcome the resistive elements (PRESIST) and the pressure required to distend the lung and chest wall (PELAST). The flow through the resistive element is a function of the difference in pressure between the tube inlet and the tube outlet (PRESIST) and the resistance of the tubing system (i.e., flow [L/min] = PRESIST [cm H₂O]/resistance [cm H₂O × min/L]). For example, forcing air at a low flow rate through a large-bore tube requires less pressure than if a high flow is applied to a small bore tube. Because PRESIST is used to overcome the resistive element, only PELAST is applied across the respiratory system (i.e., the lungs and the chest wall). Figure 32-14 demonstrates the relationship between PVENT and the pressure within the central airways (PAW) throughout a respiratory cycle.

Figure 32-14 A, During inspiration, the ventilator generates pressure (PVENT) to force a predefined volume of air (VT) in a predefined time into the lungs of the patient. The pressure loss over the total resistance of the endotracheal tube and of the central airways (PRESIST) defines what proportion of the PVENT reaches the central airways (PAW). B, Because the pressure within the respiratory system and the central airways equilibrates when the inspiratory and expiratory valves are closed, assessment of the respiratory system elastance (ERS) is possible during an end-inspiratory hold. For a given VT, the ERS defines the plateau pressure (PPLAT) at the end of inspiration. Note that because of the inhomogeneity of the time constants among different lung regions, the duration of the end-inspiratory plateau (normally approximately 10% of the breath cycle) often is too short for sufficient equilibration of the pressure across all lung regions. Hence, an end-inspiratory hold of longer duration (e.g., longer than 5 seconds) is necessary to adequately assess respiratory system mechanics. C, The expiration is passive (not actively supported by the ventilator) and driven only by the elastic recoil of the lungs and the chest wall. PEEP, positive end-expiratory pressure.

PELAST is made up of two components: the pressure required to distend the lung and the pressure required to distend the chest wall (which includes both the ribcage and the diaphragm, along with the abdomen). The elastance (1/Compliance = applied pressure [PELAST] divided by the applied VT) of the chest wall (ECW) and that of the lung (EL) are mechanically in series, and their sum equals the elastance of the entire respiratory system (ERS). In clinical practice, PVENT measured either at the airway opening or in the ventilator circuit is considered to be the “driving pressure,” and PVENT typically is used to assess the propensity for induction of VILI. Such an approach has important shortcomings, however, and may yield misleading results. PVENT is referenced to ambient pressure and therefore reflects the pressure gradient across the entire respiratory system (i.e., across both the lung and the chest wall). The key variable defining the degree of lung distention and the propensity for induction of VILI, however, is only the pressure across the lung (i.e., the transpulmonary pressure [PL]).

The relative stiffness (or elastance) of the lung and the chest wall define what proportion of PAW is used to distend the chest wall and what proportion is used to distend the lung (Figure 32-15). For example, if the elastance of the chest wall is twice that of the lung, then two thirds of PAW is used to distend the chest wall and only one third is used to distend the lung. The fractions EL/ERS and ECW/ERS determine how PAW is apportioned between the lung (PL = PAW × EL/ERS) and the chest wall (PCW = PAW × ECW/ERS). Predicting PL on the basis of PAW without information on the elastance of the lung and the chest wall is not possible. Furthermore, lung and chest wall elastance vary among individuals and may also change over time during critical illness (e.g., with accumulation of edema or ascites). Although calculating the elastance of the entire respiratory system (ERS) is relatively easy (ERS = PVENT/VT), calculating the elastance of the lung and the chest wall separately is unfortunately not straightforward and requires knowledge of PL. Figure 32-16 illustrates the intrabreath changes in PL during unassisted spontaneous breathing and during volume-targeted ventilation.

Figure 32-15 The total respiratory system elastance (ERS) equals the sum of its components: ERS = elastance of the lungs (EL) + elastance of the chest wall (ECW). The same ERS may arise from a high EL and a low ECW elastance (A) or from identical EL and ECW (B).

(Modified from Gattinoni L, Chiumello D, Carlesso E, Valenza F: Bench-to-bedside review: chest wall elastance in acute lung injury/acute respiratory distress syndrome patients, Crit Care 8:350–355, 2004.)

Figure 32-16 Transpulmonary pressure (PL). The pressure applied to the lungs (i.e., PL) equals the intrapulmonary pressure minus the intrapleural pressure: PL = PAW − PPL. The changes of PL from inspiration to expiration, and hence the propensity for development for ventilator-induced lung injury (VILI), are greater with volume-controlled mechanical ventilation than with spontaneous breathing.

(Modified from Oczenski W, editor: Atmen-Atemhilfen, Stuttgart, Georg Thieme Verlag, 2006.)

PL equals the difference between the alveolar pressure (PALV) and the pleural pressure (PPL). Because PVENT closely approximates PALV during an end-inspiratory and end-expiratory airway occlusion, PL can be calculated as PL = PVENT − PPL after performance of an appropriate maneuver to occlude the airways. Because direct measurement of PPL is invasive, and because the pressure in the lower third of the esophagus closely approximates that in the adjacent pleura, measurement of Pes (by means of inflatable latex balloons) can be used to estimate PPL. Hence, PL can be estimated as PL = PVENT − Pes (with a number of caveats, such as the effect of mediastinal weight on Pes in a supine patient, gravitational gradients, and spatial heterogeneity of PPL). Accordingly, approximation of PPL from measured Pes is not widely used currently in routine clinical practice.

Patients with ALI or ARDS may demonstrate an increase in ERS that is mainly attributed to an alteration in the EL. Some studies suggest, however, that the increase in EL results from presence of fluid filling a large portion of the lung such that the tidal volume delivered now expands the ventilated lung to a higher end-inspiratory lung volume (requiring a higher distending pressure, which is reflected in a greater EL). An increase in ERS also could be due to an increase in ECW. Of note, the chest wall in this context comprises not only the thoracic cage but also its caudal boundary, the diaphragmatic-abdominal compartment. ECW is increased in patients with severe obesity, chest wall injury, surgical dressings, and ascites and after major abdominal surgery. For example, in a patient with ALI associated with abdominal surgery, ECW may increase when intraabdominal hypertension (e.g., bowel edema, ascites) develops, even when the lung mechanics are normal. With the assumption that PVENT remains unchanged in the patient described previously, the pressure distending the lung actually decreases, because a greater share of PVENT is used to distend the chest wall (i.e., to displace the diaphragm toward the abdomen). Thus, arbitrarily limiting PVENT to a specific uniform value may not be necessary to prevent VILI in patients with high ECW but may potentially even cause harm by leading to marked reductions in tidal volume, insufficient ventilation, and severe hypoxemia.

Practical Approach to Ventilating Patients with Obstructive Airway Disease

An increase in airway resistance leading to expiratory airflow limitation and gas trapping is the major pathophysiologic abnormality in patients with asthma or COPD. With healthy lungs, the elastic recoil forces are sufficient to promote passive exhalation until FRC is reached. Partial loss of the elastic lung recoil in patients with COPD further aggravates this problem. Patients with limitation of expiratory airflow often activate expiratory muscles in an attempt to force the inspired volume through the partially collapsed or constricted central airways.

Dynamic Hyperinflation and Auto-Peep

Dynamic hyperinflation occurs when expiratory flow has not emptied alveoli to their resting FRC values by the end of exhalation. The residual positive pressure within the lungs referenced to atmospheric pressure or to PEEP applied through a ventilator is referred to as auto-PEEP (or intrinsic PEEP). Although auto-PEEP usually implies dynamic hyperinflation, the two are not synonymous, because lung volume at end-expiration can be normal when expiratory muscles are highly activated. The presence of auto-PEEP results in the underestimation of mean pressure within the lung as measured by PVENT, and hence in misinterpretation, if assessment of lung mechanics is solely based on PVENT.

Classically, dynamic hyperinflation is present in patients with COPD, in whom the unstable airways collapse during exhalation (Figure 32-17), and in patients with asthma, in whom increased bronchomotor tone impedes exhalation. Exacerbation of the disease process such as bronchospasm in asthma or bronchitis with thickening of the mucosa in COPD worsens the condition. Of note, auto-PEEP also may develop in patients with more restrictive disease processes such as ARDS, in which intrapulmonary time constants are widely inhomogeneous, or when low VT settings at high ventilatory rates are used. A narrow-diameter or kinked endotracheal tube, inspissated secretions, an obstructed filter in the expiratory limb of the ventilatory circuit, a highly variable respiratory rate, or tachypnea will further predispose the respiratory system to development of auto-PEEP.

Figure 32-17 A, Ideally there is no airflow at the end of the expiration, and hence alveolar pressure (PALV) is in equilibrium with the pressure in the ventilator (PVENT), and the respiratory system has returned to its functional residual capacity (FRC). Unstable airways collapse during passive or during forced expiration when the pressure surrounding the airways exceeds the intraluminal pressure, resulting in expiratory flow limitation. Consequently, air may be trapped within the lung, and a pressure gradient between the alveoli (PALV) and the ventilator circuit (PVENT) may be established (auto-PEEP) if the expiratory phase is too short to allow complete exhalation. B, Application of extrinsic PEEP partially counters the collapse of the airways, reduces the resistance to expiratory airflow, and may help with triggering of the ventilator by the patient. Note that peak and plateau pressure did not change, because extrinsic PEEP partially replaced auto-PEEP without adding to it. Note that expiratory flow may be impeded when an extrinsic PEEP level in excess of the auto-PEEP level is used. PEEP, positive end-expiratory pressure.

Persistent airflow at the end of exhalation, especially in combination with consistent failure to trigger the ventilator with inspiratory efforts, should heighten clinical suspicion for the presence of dynamic hyperinflation. Measurement of auto-PEEP requires equilibration of the pressure across the entire lung during occlusion of the expiratory valve at end-expiration (Figure 32-18), ideally performed during muscle paralysis (but paralysis usually should not be undertaken solely to make this measurement). Measurement of auto-PEEP during spontaneous breathing is difficult and often unreliable, because the inspiratory and expiratory efforts interfere with the procedure, and studies have shown that expiratory muscle contraction can occur. These contractions may be difficult to detect clinically.

Figure 32-18 Expiratory hold technique to estimate the level of auto-PEEP. The exhalation valve is closed during an expiratory hold. When the expiratory flow equals zero, airway pressure rises to the auto-PEEP level. After reopening of the expiratory valve, flow continues, and the additional exhaled volume equals the volume of trapped gas. Of note, inspiratory and expiratory muscle activity interferes with the measurement of intrinsic PEEP. PEEP, positive end-expiratory pressure.

(Modified from MacIntyre NR: Intrinsic PEEP, Prob Respir Care 4:45, 1991.)

Dynamic hyperinflation can markedly increase the oxygen cost of breathing in a spontaneously breathing patient (Figure 32-19). Because the compliance of the respiratory system is lower at high lung volumes, more energy is required to expand the lungs. Furthermore, with dynamic hyperinflation the patient needs to produce large pleural pressure swings to overcome the auto-PEEP before pressure in the ventilator circuit decreases below the applied PEEP level and before pneumatic trigger systems located in the ventilator can be excited. Because generation of force by the inspiratory muscles is impaired during hyperinflation (decreased resting length of the diaphragm requires a higher-than-normal respiratory drive to lower pleural pressure), triggering the ventilator becomes challenging for patients with COPD and especially for those who have weakness or fatigue of the respiratory muscles—both of these conditions are difficult to distinguish from the effects of trying to inhale while breathing at a lung volume near total lung capacity (TLC).

Figure 32-19 A, Demonstration of delivery of assist with pressure support ventilation (PSV) in a patient with expiratory flow limitation resulting in dynamic hyperinflation. There is substantial asynchrony (delayed triggering-on and cycling-off) between the assist delivered by the ventilator and the patient’s (neural) respiratory demand, as reflected by the electrical activity of the diaphragm (Edi). The high amplitudes for the Edi and for esophageal pressure (Pes) deflections indicate that the inspiratory muscles are highly active during delivery of pressure by the ventilator, whereas the high amplitudes for the expiratory muscle activity and for the gastric pressure (Pga) deflections indicate that the patient uses his expiratory muscles to counter delivery of pressure by the ventilator during neural expiration. B, After optimizing the trigger-on threshold, delivery of assist starts earlier (requiring less inspiratory effort) and also ceases earlier (requiring less activation of the expiratory muscles). C, Adjusting the level of extrinsic PEEP to compensate for auto-PEEP allows earlier detection of the inspiratory effort by the ventilator (see Figure 32-21) and helps to further reduce the inspiratory workload. D, Increasing the cycling-off airflow threshold results in earlier termination of the assist. Hence, expiratory muscle activity can be reduced. Note that the ventilator inspiratory time, as well as the delivered tidal volume (VT), decreases when the cycling-off airflow threshold is increased, whereas the expiratory time increases (provided the respiratory rate remains unchanged). E, When the inspiratory rise time is reduced, the peak inspiratory flow and thus the cycling-off airflow threshold both are reached earlier, and the inspiratory time is further shortened. After completion of all steps as demonstrated here (B to E), ventilator assist is delivered in synchrony with the patient’s neural respiratory demand, and unloading of the inspiratory muscles is achieved as reflected by minimization of the amplitudes for Edi and for Pes deflections. Expiration is driven only by the elastic recoil of the lung and the chest wall, as reflected by minimization of the amplitudes for expiratory muscle activity and for Pga deflections. PEEP, positive end-expiratory pressure.

Dynamic hyperinflation increases resistance of the inferior vena cava and increases pleural and juxtacardiac pressures, thereby impeding venous return to the right atrium, leading in turn to a decrease in cardiac output. Recognition that auto-PEEP and not cardiac dysfunction is the main cause of impaired cardiac performance under such circumstances is important, because treatment strategies are markedly different.

Inappropriate settings during mechanical ventilation can worsen dynamic hyperinflation, especially when high ventilatory rates and/or high VT settings resulting in excessive minute ventilation are used, when the assist is delivered asynchronous to the patient’s demand (Figure 32-20), or when PEEP levels higher than those needed to counterbalance auto-PEEP are used.

Figure 32-20 Adjustment of ventilatory parameters with volume-targeted ventilation in a patient with expiratory flow limitation and dynamic hyperinflation. A, Baseline condition with persistent flow at end-expiration. B, Shortening the inspiratory phase by reduction of the inspiratory-expiratory times relationship allows longer expiration provided the ventilatory rate remains unchanged. A higher maximal inspiratory airflow and hence a higher peak pressure during inspiration are required to force the same tidal volume (VT) into the lungs in a shorter period of time. Of note, a high inspiratory flow may result in a moderate increase in the respiratory rate, which will necessitate careful monitoring of the net effect on the duration of the expiration. C and D, Decreasing the inspiratory rise time (here, from 5% to 0% of the respiratory cycle) while shortening the time of the inspiratory pause at end-inspiration (here from 10% to 5% of the respiratory cycle) allows more time to deliver the tidal volume and hence results in lower maximal flow and lower peak pressure. E, Increasing the extrinsic PEEP partially counteracts the dynamic collapse of airways during expiration and diminishes the impedance to expiratory flow. PEEP, Positive end-expiratory pressure.

The first approach to minimizing dynamic hyperinflation in a patient with obstructive airway disease is to decrease the resistance in the expiratory airways by removing any mechanical obstruction and by treating bronchospasm and airway inflammation. The most effective and abrupt way to decrease auto-PEEP is to reduce minute ventilation, although this may lead to an increase in an already elevated arterial PCO₂ (PaCO₂). Alternatively, adding extrinsic PEEP (Figure 32-21) will decrease the work of breathing, thereby reducing CO₂ production and lowering the PaCO₂ even if alveolar ventilation is unchanged. Because patients with COPD with chronically elevated PaCO₂ levels retain sufficient bicarbonate to normalize arterial pH, minute ventilation should not be adjusted to maintain a normal PaCO₂. In addition, the inspiratory phase should be shortened (thereby allowing maximum time for exhalation), as demonstrated in Figures 32-19 and 32-20. Of note, the variability in the duration of the expiratory phase and, hence, in the expired volume per breath increases when switching from a controlled mode of ventilation to a mode that delivers assistance to spontaneous breathing. This may result in modification of the degree of dynamic hyperinflation on a breath-by-breath basis and can induce patient-ventilator asynchrony because of wasted inspiratory efforts, especially when high levels of assist are used (see Figure 32-6).

Figure 32-21 A and B, Without auto-PEEP, a small inspiratory effort is required by the patient to exceed the predefined trigger-on threshold (here, 1 to 2 cm H₂O below extrinsic PEEP). C, In the presence of auto-PEEP, the patient first needs to lower alveolar pressure to overcome auto-PEEP before the pressure in the ventilator circuit can be reduced sufficiently to exceed the trigger threshold below extrinsic PEEP. D, Applying extrinsic PEEP brings the trigger threshold closer to the alveolar pressure level at end-expiration. Now only a small inspiratory effort is required to exceed the trigger-on threshold. PEEP, positive end-expiratory pressure.

(Modified from Howman SF: Mechanical ventilation: a review and update for clinicians, Hosp Physician 35:26–36, 1999.)

The principles of a ventilatory strategy in acute asthma are very similar to those described for COPD—that is, adjusting the ventilatory rate to low frequencies and using low VT while accepting hypercapnic acidosis. A pH as low as 7.20 normally is well tolerated in these patients, and such an approach helps minimize hyperinflation.

Practical Approach to Ventilating Patients with Restrictive Pulmonary Disease

A decrease in lung compliance and in FRC is the major pathophysiologic abnormality in patients with restrictive pulmonary disease processes such as pulmonary fibrosis, interstitial pneumonias, sarcoidosis, bronchiolitis obliterans organizing pneumonia, and those with ALI and ARDS.

The challenge in ventilating patients with restrictive diseases is to provide adequate oxygenation, while at the same time not causing further lung injury. Although mechanical ventilation clearly leads to improved survival in patients with ALI or ARDS, its ability to improve survival in patients with other restrictive processes (particularly idiopathic pulmonary fibrosis) is limited at best. The required approach is one of maintaining adequate oxygenation while trying not to overinflate the lung at end-inhalation (see later).

Complications of Mechanical Ventilation

Complications and side effects of intubation or of invasive mechanical ventilation include upper airway trauma (e.g., vocal cord injury), aspiration of gastric contents, barotrauma (e.g., pneumothorax or pneumomediastinum), disruption of normal host defense mechanisms, reduction in the ability to heat and humidify inspired gases, local tracheal ischemia induced by the cuff of the endotracheal tube, impairment of communication and of swallowing, and the perceived need by health care providers for sedatives and occasionally neuromuscular blocking drugs. Although use of a cuffed endotracheal tube helps prevent gross aspiration, pharyngeal secretions that pool at the top of the cuff may still seep into the lungs, increasing the probability of development of nosocomial pneumonia. An endotracheal tube greatly impairs the patient’s inherent cough mechanisms by preventing closure of the glottis.

Mechanical ventilation itself can induce or aggravate lung injury that is clinically, functionally, and histologically indistinguishable from ALI or ARDS. Also, applying positive pressure to the airways may adversely affect cardiac performance and result in hemodynamic compromise.

Ventilator-Induced Lung Injury

Diseased lungs are more susceptible than healthy lungs to the development of VILI. VILI also can initiate and propagate cascades (e.g., upregulation of a systemic inflammatory response) that ultimately culminate in multiple system organ failure (MSOF) (Figure 32-22). A ventilatory strategy that uses low VT and limited PVENT is not only protective to the lung but also has the potential to reduce the incidence of MSOF. Exposure to excessive mechanical stresses can result in damage to lung tissue and cell integrity from either of two primary factors: (1) overdistention of the lung (i.e., volutrauma) and (2) repetitive air space recruitment and derecruitment (atelectrauma). The critical feature defining induction of VILI secondary to volutrauma seems to be the degree of regional lung distention, rather than the absolute PVENT reached. High pressures per se in the respiratory system do not necessarily result in VILI. For example, trumpet players repeatedly generate very high airway pressures (more than 150 cm H₂O) without incurring lung damage, because no excessive lung distention occurs.

Figure 32-22 Postulated mechanisms whereby mechanical ventilation may contribute to multiple system organ failure (MSOF). mΦ, macrophages.

(Modified from Slutsky AS, Tremblay LN: Multiple system organ failure. Is mechanical ventilation a contributing factor? Am J Respir Crit Care Med 157:1721–1725, 1998.)

Alveolar overdistention and shear forces can stimulate lung and immune cells to produce and release inflammatory cytokines and chemokines—that is, biotrauma. Biotrauma encompasses the release of numerous biologic (including inflammatory) mediators into the pulmonary interstitial and alveolar spaces. Concomitant disruption of lung tissue and cell integrity and disruption of lung epithelial and endothelial barriers facilitates the spillover of lung-derived inflammatory mediators, endotoxin, and even bacteria into the bloodstream, resulting in initiation, exacerbation, or propagation of a systemic inflammatory response. In view of the vast aerated surface area of the lung, it is conceivable that release of even small quantities of inflammatory mediators per cell could lead to a large quantity of mediators that could potentially enter the circulation.

The typically heterogeneous distribution of disease in patients with ALI or ARDS puts them at a high risk for VILI, because the consolidated lung regions are susceptible to atelectrauma and the better or normally aerated regions are prone to volutrauma. Barotrauma and volutrauma are likely to occur when volumes and pressures meant for the entire lung (e.g., a VT of approximately 10 mL/kg) are forced into only a small portion of functional lung (the “baby lung”). In addition, shear forces at the interface between the open and closed lung units result in atelectrauma when PEEP levels insufficient to prevent end-expiratory alveolar collapse are used. Hence, ideally, a ventilatory strategy in patients with ALI or ARDS should prevent both alveolar overdistention during lung inflation and alveolar collapse at the end of lung deflation.

Strategies to Prevent Ventilator-Induced Lung Injury in Clinical Practice

Although mechanical ventilation is only one of multiple factors contributing to the pathogenesis of multiple organ dysfunction syndrome (MODS), clinical trials have clearly shown that lung-protective mechanical ventilation decreases mortality among patients with ARDS.

The large ARDSNet study demonstrated that a VT of 6 mL/kg predicted body weight (PBW) was associated with decreased mortality compared with use of 12 mL/kg PBW in patients with ALI. It is important in applying this approach to base VT on the PBW, not on measured body weight. For a male patient, PBW = 50 + 0.91 × (cm of height − 152.4); for a female patient, PBW = 45.5 + 0.91 × (cm of height − 152.4). The VT should be lowered if necessary to reduce PPLAT to less than 30 cm H₂O. Some investigators suggest that a ventilatory strategy that keeps PPLAT below 30 cm H₂O is sufficient to ensure lung protection. However, a safe upper limit of PPLAT in patients with ALI or ARDS is not known. A recent post hoc analysis demonstrated that lowering PPLAT even further to values less than 30 cm H₂O could potentially decrease mortality.

The beneficial effects of using relatively low VT, and possibly also higher levels of PEEP, probably are related to the two main components—reduction of VILI and prevention of nonpulmonary organ dysfunction—as suggested by many preclinical and smaller clinical studies. In support of this mechanism, a recent large clinical study by Mascia and colleagues demonstrated that a lung-protective ventilatory strategy using VT of 6 to 8 mL/kg PBW combined with higher levels of PEEP prevented the decline of pulmonary function in brain-dead organ donors and roughly doubled the number of lungs available for transplantation. Another recent large clinical study demonstrated that pharmacologic neuromuscular blockade for 48 hours early in the course of ARDS resulted in both better survival and less time spent on the ventilator, compared with the use of placebo. Possible mechanisms by which neuromuscular blockade might lead to improved outcome are summarized in Figure 32-23.

Figure 32-23 Possible mechanisms by which use of neuromuscular blocking agents (NMBAs) may lead to improved survival in patients with the acute respiratory distress syndrome (ARDS). Before induction of paralysis (top), increased respiratory drive from multiple causes can lead to increased tidal volumes (VT) and patient-ventilator asynchrony, all of which can potentially worsen various forms of ventilator-induced lung injury (VILI). VILI combined with impaired cardiac performance and consequent decrease in oxygen delivery to vital organs may lead to increased organ dysfunction and ultimately death. After paralysis is obtained (bottom), lower VT and improved patient-ventilator synchrony allow for better lung-protective ventilation, less VILI, and less impairment of cardiac performance. VILI also may be lessened by reduced pulmonary blood flow from decreased oxygen consumption. NMBAs also may indirectly improve arterial oxygenation by decreased muscular oxygen consumption and by improving the distribution of ventilation relative to perfusion (). Finally, NMBAs may have direct antiinflammatory effects.

(From Slutsky AS: Neuromuscular blocking agents in ARDS, N Engl J Med 363:1176–1180, 2010.)

In a number of studies, the investigators used permissive hypercapnia (i.e., allowing the PaCO₂ to increase if necessary to maintain a sufficiently low VT) in the absence of any specific contraindications (e.g., increased intracranial pressure). The concept is that the detrimental effects of the acute hypercapnia are less than the use of higher VT. How to treat the accompanying respiratory acidosis is still a matter of debate, but decreases in pH to approximately 7.20 to 7.25 usually are well tolerated and probably do not have to be addressed unless detrimental physiologic consequences of the acidosis develop.

How to adjust PEEP in patients with ARDS continues to be widely debated. Three recent large studies on higher versus lower PEEP levels in patients with ALI and ARDS, as well as two metaanalyses, found that random application of either higher or lower levels of PEEP in an unselected population does not significantly improve outcome. However, both metaanalyses suggested that in the subgroup of patients with severe, hypoxemic ARDS (as opposed to those without ARDS), higher levels of PEEP might be associated with a reduction in mortality. Some workers have suggested that in the aforementioned clinical studies, a potentially beneficial effect of higher PEEP in some (“lung-recruitable”) patients might have been negated by a detrimental effect occurring in others (i.e., “non–lung-recruitable”). In fact, a cohort study recently demonstrated that the effect of PEEP on lung recruitment is closely associated with the percentage of potentially recruitable lung as determined by computed tomography.

Pending further clarification of how to define optimal PEEP levels in individual patients, a pragmatic approach for daily clinical practice is to adhere to the algorithm used in the large ARDSNet trial (see Table 32-1). Determining optimal ventilator setting in an individual patient with ALI or ARDS is always a continuous, iterative process of evaluation, intervention, and reevaluation that must take into account changes in the disease process over time.

Ventilator-Induced Diaphragm Dysfunction

Acquired neuromuscular disorders, referred to as critical illness polyneuromyopathy (CIPM), are frequently encountered in critically ill patients. The inability of the patient to resume the entire work of breathing due to reduced respiratory muscle strength and endurance, with consequent difficulties in weaning from mechanical ventilation, is a hallmark of the syndrome and may be the first symptom to alert the clinician of the disorder. In fact, many patients who experience weaning failure display diaphragmatic weakness as manifested by reduced pressure generation by the diaphragm after supramaximal magnetic stimulation of the phrenic nerves.

It has been suggested that in addition to the well-established risk factors for CIPM (i.e., corticosteroids, neuromuscular blocking agents, severe sepsis, MODS and severe pulmonary diseases), the use of controlled modes of mechanical ventilation may be another factor that contributes to the development of respiratory muscle weakness. For example, two recent studies demonstrated that about 1 to 3 days of complete diaphragm inactivity in brain-dead organ donors (i.e., in absence of any spontaneous muscle activity) associated with mechanical ventilation resulted in a roughly 50% reduction in the cross-sectional areas of diaphragm muscle fibers and in a marked decrease in diaphragm force generation during phrenic nerve stimulation. By contrast, the early and preferential use of ventilation modes that assist spontaneous breathing (i.e. the work of breathing is shared between the ventilator and the patient) has been suggested to help prevent or delay the development of respiratory muscle weakness. However, how much such assistance would adequately meet the patient’s demand and would thus prevent both respiratory muscle disuse atrophy and fatigue has not been established.

Lung Recruitment

Recruitment maneuvers can decrease the heterogeneities present in the lung, improve gas exchange, and potentially mitigate VILI by reducing cyclic air space opening and closing. Recruitment refers to the process of reopening collapsed alveoli by transiently increasing PVENT. This can be accomplished by maintaining a static PVENT of 40 cm H₂O for 40 seconds or by increasing PEEP transiently. Although animal studies seem to indicate that recruitment maneuvers are effective in decreasing VILI, human data indicating improved clinical outcomes are not available. This may be because recruitment maneuvers are likely to be effective in patients who have “recruitable” lungs, and none of the studies to date have stratified patients on the basis of lung recruitability. If recruitment maneuvers are used, it is important to monitor for adverse effects such as hypotension, barotraumas, and arrhythmias.

Alternative Approaches to Lung Recruitment

Prone positioning and high-frequency ventilation (HFV) represent alternative ways of attaining lung recruitment.

Placing patients with ARDS in a prone position improves PaO₂ in approximately 70% of patients and also may decrease VILI by improving the homogeneity of end-expiratory lung volume. Recent large clinical trials have been unable to confirm a specific survival benefit for prone positioning in diverse populations of patients with ALI and ARDS. However, posttrial studies and metaanalyses indicate that the subgroup of patients with severe hypoxemia, defined by baseline PaO₂/FIO₂ below 100 mm Hg, but not in patients with less severe hypoxemia, may indeed benefit from prone positioning. The optimal duration of prone positioning has not been established. In clinical practice, an empirical trial of such positioning may be attempted when severely impaired oxygenation fails to respond to usual measures, including sedation, recruiting maneuvers, and high PEEP; during such trials, every possible effort should be made to prevent misadventures associated with postural changes (e.g., displacement of endovascular lines or of the endotracheal tube).

HFV encompasses a number of ventilatory modes, including high-frequency positive-pressure ventilation (HFPPV), high-frequency jet ventilation (HFJV), high-frequency flow interruption (HFFI), and high-frequency oscillatory ventilation (HFOV), all of which use substantially higher ventilatory frequencies (i.e., in the range of 1 to 25 Hz) and much lower VT than with conventional modes (Figure 32-24). During HFV, the VT typically is less than the dead space. Gas transport is accomplished by various aspects of convection and diffusion. With HFV, a high mean PVENT is used to recruit alveoli and maintain lung volume above FRC. Thus, in contrast with controlled modes of ventilation, HFV maintains lung volume at a relatively constant level and uses very small VT to accomplish ventilation. Intermittent sighs or sustained inflations are optionally used to recruit collapsed lung regions and to avoid atelectasis.

Figure 32-24 With high-frequency ventilation (HFV), extremely small tidal volumes (typically 1 to 3 mL/kg) are applied at very high ventilatory rates (typically 60 to 1500/minute, equivalent to 1 to 25 Hz). HFV allows maintenance of a relatively high mean airway pressure, whereas tidal excursions, and hence alveolar recruitment and derecruitment, are minimized. HFV can be applied either with a constant mean airway pressure (A) or alternating between lower and higher mean airway pressures (B).

HFV is a potentially interesting ventilatory approach in patients with ARDS, because the small VT and the small pressure excursions allow the use of a relatively high mean PVENT without overdistending the lungs or allowing cyclic collapse to occur. Recent clinical studies in infants and adults with ARDS suggest that HFV may be as effective as conventional mechanical ventilatory support, but no studies have demonstrated that it reduces mortality.

Weaning from Mechanical Ventilation

“Weaning” often is used interchangeably with “liberation” from mechanical ventilation and refers to the transition from full ventilatory support to resumption of unassisted spontaneous breathing by the patient.

All mechanically ventilated patients should be allowed to progress to spontaneous breathing at the earliest possible time, because unnecessary prolongation of ventilation is associated with increased risk for adverse effects such as ventilation-associated pneumonia, VILI, or perhaps respiratory muscle atrophy. On the other hand, premature discontinuation of ventilatory support in a patient not yet ready to assume the entire work of breathing also entails potential harm, including complications related to reintubation. Conventional weaning predictors measure the patient’s ability to breathe without assistance but do not assess the ability to clear respiratory tract secretions or to protect the lower airways from aspiration.

Initiation of weaning requires that the patient can and will trigger the ventilator, a prerequisite that often can be achieved only when the level of sedation is reduced or when the PaCO₂ is allowed to increase by reducing the minute ventilation. It is not surprising that “protocolized” interruption of sedation on a daily basis reduces the total time spent on mechanical ventilation.

Good clinical judgment in this regard is essential: Only patients with a reasonable likelihood of being able to breathe on their own are suitable candidates for attempts at weaning. Although measuring a variety of physiologic variables may help guide this decision, the process often entails a “trial and error” component. Careful monitoring of the patient’s comfort, gas exchange, respiratory mechanics, and hemodynamics during a trial of spontaneous breathing is mandatory. The protocol-based use of spontaneous breathing trials (SBTs) is recommended to identify patients who are likely to be able to breathe spontaneously without assistance (Figure 32-25). Criteria to initiate an SBT as recently recommended by a consensus conference are summarized in Box 32-1 (for details, see the cited source paper authored by MacIntyre and co-workers), but each patient must be evaluated for specific factors that might modify the recommendation or mandate an alternate approach.

Figure 32-25 Example of a protocol for gradual reduction in the assist level during weaning.

(Modified from Jakob SM, Lubszky S, Friolet R, et al: Sedation and weaning from mechanical ventilation: effects of process optimization outside a clinical trial, J Crit Care 22:219–228, 2007.)

Box 32-1

Criteria for Initiation of a Spontaneous Breathing Trial *

Evidence of some reversal of the underlying cause of respiratory failure

Adequate oxygenation: PaO₂/FIO₂ ratio ≥150-200, required PEEP ≤5-8 cm H₂O, FIO₂ ≤0.4-0.5, and pH ≥7.25

Hemodynamic stability as defined by the absence of active myocardial ischemia and the absence of clinically significant hypotension—that is, a condition requiring no vasopressor therapy or therapy with only low-dose vasopressors (e.g., dopamine or dobutamine given at a dose of less than 5 µg/kg/minute).

The patient is able to initiate an inspiratory effort.

The decision to use these criteria for initiation of a spontaneous breathing trial must be individualized.

PaO₂/FIO₂, ratio of arterial partial pressure of oxygen to fraction of inspired oxygen; PEEP, positive end-expiratory pressure.

Modified from MacIntyre NR, Cook DJ, Ely EW Jr, et al: Evidence-based guidelines for weaning and discontinuing ventilatory support: a collective task force facilitated by the American College of Chest Physicians; the American Association for Respiratory Care; and the American College of Critical Care Medicine, Chest 120(suppl):375–395, 2001.

^* Some patients in whom not all of these criteria are satisfied (e.g., patients with chronic hypoxemia values below the thresholds cited) may be ready for attempts to discontinue mechanical ventilation.

A formal SBT often is not required after short-term ventilation (e.g., in patients ventilated for less than 24 hours as, for example, in the postoperative period), whereas an SBT should be performed on a daily basis during a daily interruption of sedation in those patients who meet certain criteria (see Box 32-1). Conventionally, an SBT is performed with use of a minimal level of assist (i.e., 0 to 7 cm H₂O, preferably 0 cm H₂O), an FIO₂ of 0.5, and a PEEP level of 5 to 7.5 cm H₂O. An initial brief period of spontaneous breathing can be used to assess the advisability of continuing on to a formal SBT. The criteria used to assess the patient’s readiness to continue tolerance during SBTs are the respiratory pattern, the adequacy of gas exchange, hemodynamic stability, and subjective comfort. Tolerating an SBT for 30 to 120 minutes warrants discontinuation of the ventilator. Removal of the artificial airway is a separate consideration and is based on assessing airway patency and the ability of the patient to protect the airway.

When an SBT fails, the cause should be determined. Once reversible causes for failure are corrected, and if the patient still meets the criteria listed in Box 32-1, subsequent SBTs should be performed at least every 24 hours. Patients who fail an SBT should receive a stable, nonfatiguing, comfortable form of ventilatory support. Anesthesia and sedation strategies and ventilator management aimed at early extubation should be used in postsurgical patients. Weaning protocols designed for nonphysician health care professionals should be developed and implemented by intensive care units (ICUs). Protocols aimed at optimizing sedation also should be developed and implemented.

Failure to Wean from Mechanical Ventilation

A number of factors may be involved in failure to wean a patient from mechanical ventilation, including mismatch between respiratory muscle strength and endurance and the respiratory load (e.g., with CIPM), altered mechanical properties of the respiratory system (e.g., with restrictive or obstructive pulmonary diseases or obesity), inability of the patient to sufficiently clear secretions and to maintain patency of the airways, or presence of a neuropsychological disorder (e.g., delirium, anxiety).

A frequently underrecognized predisposing factor in unsuccessful weaning is cardiac failure after removal of positive-pressure delivery during mechanical ventilation. A combination of several mechanisms may be involved and may result in either preferential right or left ventricular failure, or both. Consequences include myocardial ischemia in predisposed patients, arterial hypotension, cardiogenic pulmonary edema, and a mismatch between increased work of breathing and global oxygen delivery. Right ventricular failure most frequently results from increased right ventricular load due either to increased return of venous blood to the right ventricle or to increased pulmonary vascular resistance secondary to hypoxemia, hypercapnia, pulmonary edema, elevated intrinsic PEEP, or a combination of these factors. Left ventricular failure may be related to increased afterload (e.g., as a result of removing the positive intrathoracic pressure or arterial hypertension), to impaired filling due to right ventricular distention (interventricular dependence), or to diastolic dysfunction, which may be worsened by arterial hypertension or by catecholamines discharged during a stressful SBT or extubation period. In patients in whom cardiac dysfunction is suspected during weaning from mechanical ventilation, close monitoring (e.g., pulmonary artery pressure, pulmonary capillary wedge pressure, cardiac stroke volume, mixed venous oxygen saturation using a pulmonary artery catheter, or echocardiography) may be helpful to differentiate the mechanisms involved and to closely monitor the effect of therapeutic interventions.

Tracheotomy should be considered after an initial period of stabilization on the ventilator when it becomes apparent that the patient will require prolonged ventilator assistance. Unless there is evidence for clearly irreversible disease (e.g., high spinal cord injury or advanced amyotrophic lateral sclerosis), a patient requiring prolonged mechanical ventilatory support for respiratory failure should not be considered permanently ventilator-dependent until 3 months of weaning attempts have failed. Weaning strategies in patients requiring prolonged mechanical ventilation should be slow-paced and should include gradual lengthening of SBTs.

Controversies and Pitfalls

Better understanding of the potential harm of mechanical ventilation, of the interaction between the patient and the ventilator, and of the importance of optimizing treatment processes associated with mechanical ventilation (e.g., sedation and weaning protocols) has fostered the development of many technical and conceptual improvements in recent years. Nevertheless, further advances are required in numerous areas, including the development of ventilatory strategies that individualize ventilation to the specific patient at a specific point in time and that minimize VILI and its systemic consequences, improvement of alternative approaches to protecting the lung during mechanical ventilation, improving patient-ventilator interactions, and prevention of respiratory muscle deconditioning during mechanical ventilation. Current controversies include the precise role of recruitment maneuvers and ways to individualize PEEP levels, as well as the indications for invasive versus noninvasive ventilation.

Although further research is likely to provide new insights, an important challenge for researchers and clinicians alike is to identify elements of the current knowledge that can be incorporated into daily clinical management to improve outcomes for patients who require ventilatory assistance. In general, a protocolized approach is more likely to result in lasting improvement in care for ventilated patients. Implementing such protocols requires adequate resources, and institutions must make a commitment not only to develop protocols but also to the iterative process of implementation, reassessment, and refinement.

Web Resources

Guidelines/Protocols

http://ardsnet.org. —provides information on completed and on future research projects related to various aspects of ARDS

http://www.ccmtutorials.com/rs/mv/index.htm. —provides an illustrative tutorial on mechanical ventilation

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FIO₂	PEEP (cm H₂O)
0.3	5
0.4	5
0.4	8
0.5	8
0.5	10
0.6	10
0.7	10
0.7	12
0.7	14
0.8	14
0.9	14
0.9	16
0.9	18
1.0	18
1.0	20
1.0	22
1.0	24

FIO₂	PEEP (cm H₂O)
0.3	5
0.4	5
0.4	8
0.5	8
0.5	10
0.6	10
0.7	10
0.7	12
0.7	14
0.8	14
0.9	14
0.9	16
0.9	18
1.0	18
1.0	20
1.0	22
1.0	24

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FIO₂	PEEP (cm H₂O)
0.3	5
0.4	5
0.4	8
0.5	8
0.5	10
0.6	10
0.7	10
0.7	12
0.7	14
0.8	14
0.9	14
0.9	16
0.9	18
1.0	18
1.0	20
1.0	22
1.0	24