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.


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.

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.

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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).

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 (image) 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 image 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 image 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.

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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).

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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.

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.

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.

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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.