32 - Instruments and Techniques of Video-Assisted Thoracic Surgery
Editors: Shields, Thomas W.; LoCicero, Joseph; Ponn, Ronald B.; Rusch, Valerie W.
Title: General Thoracic Surgery, 6th Edition
Copyright 2005 Lippincott Williams & Wilkins
> Table of Contents > Volume I - The Lung, Pleura, Diaphragm, and Chest Wall > Section VIII - Postoperative Management of the General Thoracic Surgical Patient > Chapter 40 - Mechanical Ventilation of the Surgical Patient
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Chapter 40
Mechanical Ventilation of the Surgical Patient
Lucinda Miller
Kenneth J. Woodside
Akhil Bidani
Joseph B. Zwischenberger
During the latter quarter of the last century, great advances have been made in postoperative ventilatory assistance and ventilatory assistance of the critically ill patient. Multiple alternative methods of ventilatory support have been developed in an effort to decrease complications, minimize patient work of breathing, and improve patient outcomes. Because of the bewildering number of options available, understanding the basic principles, advantages, and disadvantages associated with each choice of ventilatory support is necessary to critically evaluate application and reported outcomes.
POSTOPERATIVE PULMONARY PATHOPHYSIOLOGY
Pulmonary function and resultant gas exchange deteriorate after any major surgical procedure, particularly after pulmonary resections. Latimer and associates (1971) found that the highest rates of postoperative pulmonary complications occurred with thoracic and upper abdominal procedures. Atelectasis occurs when the closing volume of the airways exceeds the expiratory reserve volume in the early postoperative period. At special risk are the elderly and smokers, whose closing volume is already elevated. Obese patients already have a diminished expiratory reserve volume. Patients with chronic obstructive lung disease exhibit problems with expiratory reserve volume and closing volume.
Postoperatively, minute ventilation is often preserved; the components of respiratory mechanics are considerably altered. Churchill and McNeil (1927) reported that vital capacity (VC) is reduced by 50% to 75% in the first 24 hours. On average, tidal volume is diminished by 20% and functional residual capacity by 35% in thoracic and upper abdominal procedures. Normally, a return to preoperative levels is observed in 7 to 14 days. Due to the decline in tidal volume, minute ventilation is maintained by compensatory increases in respiratory rate.
Several other mechanisms contribute to a postoperative decrease in lung volume and compliance. A major increase in extravascular lung water results not only in decreased compliance of the lung but also in diffusion barrier and subsequent hypoxemia. The increases in lung water may result from fluid overload, left ventricular failure, or impairment of the permeability characteristics of the pulmonary capillary membrane (so-called low-pressure pulmonary edema). As Prys-Roberts and colleagues (1967) point out, such may occur even in the absence of the characteristic radiographic changes of pulmonary edema. Low-pressure pulmonary edema is often associated with adult respiratory distress syndrome (ARDS) and may occur after shock, sepsis, aspiration, and multiple blood transfusions, all of which may be present after major surgical procedures. After pulmonary surgery, these abnormalities may be exaggerated by two factors. First, the ipsilateral lung may have undergone operative trauma and contusion. In addition, intraoperative collapse and reexpansion may result in fluid extravasation from the pulmonary capillary bed. Second, pulmonary artery pressure may increase transiently after resection of pulmonary tissue, particularly after pneumonectomy. Capillary pressure (Pc) is largely determined by both left atrial pressure (Pla) and pulmonary artery pressure (Ppa), as shown in the equation Pc = Pla + 0.4(Ppa - Pla). Therefore, any increase in pulmonary artery pressure particularly if complicated by excessive fluid administration results in additional fluid movement into the alveolar and interstitial spaces.
This accumulation of extravascular lung water may affect regional ventilation not only by subsequent alveolar flooding but also by augmenting airway closure via peribronchial cuffing. Atelectasis and decreased compliance alter regional ventilation and, in the end, adversely affect ventilation-perfusion ([V with dot above]/[Q with dot above]) matching with resulting hypoxemia. Hypercarbia is usually a late-appearing abnormality, often signifying that the patient is tiring and may soon require mechanical assistance. Indeed, unless pain is particularly severe or the patient is oversedated, hypocarbia is typical after surgery because the respiratory rate increases as a function of anxiety, pain, and hypoxemia.
Several postoperative cardiovascular changes may further alter [V with dot above]/[Q with dot above] matching. A decrease in cardiac output
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resulting from hypovolemia, sepsis, or an increase in left ventricular afterload may affect the degree of regional pulmonary artery perfusion and further aggravate impaired [V with dot above]/[Q with dot above] matching. Increases in right ventricular filling pressure caused by pulmonary hypertension (which may result from excision of lung tissue) may further impair left ventricular function by shifting the intraventricular septum and adversely affecting left ventricular filling.
GOALS OF VENTILATORY ASSISTANCE
The primary goal of mechanical ventilatory support is to provide adequate pulmonary gas exchange. The need for mechanical ventilatory support may be manifested by primary CO2 retention (ventilatory failure) or inadequate arterial oxygenation (oxygenation failure). Secondary goals of mechanical ventilatory assistance are to provide rest for fatigued ventilatory muscles, to avoid ventilator-associated lung injury and the complications associated with positive pressure ventilation, and to allow healing of parenchymal lung injury. The type of mechanical ventilatory support provided a particular patient depends on the mechanism, severity, and expected duration of the respiratory failure illustrated in Fig. 40-1. Comorbidities and specific clinical objectives for each patient are important in determining the type and level of mechanical ventilatory support as outlined in Table 40-1.
The spontaneously breathing individual has an intact ventilatory control system that includes feedback from peripheral and central chemoreceptors and mechanoreceptors from the lung and chest wall. Inspiratory muscle contraction, primarily of the diaphragm, generates negative intrathoracic pressure and inspiratory flow into the lungs. Exhalation is usually a passive process, occurring when the ventilatory control system signals relaxation of the inspiratory muscles. However, exhalation becomes an active process when there are high minute ventilation requirements, and is then aided by the contraction of expiratory muscles. The relative amounts of time spent during inspiration and expiration are determined by the magnitude of the respiratory drive and interactions among stimuli received from other receptors.
In patients receiving ventilatory support, the vital role of feedback to the ventilatory control system is supplanted by the open-loop physician-dependent ventilatory settings. The physician controls most aspects of the ventilator supported breath, among these are the tidal volume (VT), respiratory rate, duration of inspiratory flow, and the inspiration-expiration ratio (I:E ratio). However, multiple studies have demonstrated that, while mechanical ventilation is indispensable in the support of the critically ill patient, ventilator technology can induce a number of adverse effects. Application of exogenous pressure to the lung, whether positive or negative, can damage lung parenchyma and exacerbate preexisting lung injury. Positive pressure
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ventilation may also induce a systemic inflammatory response and multiorgan failure.
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Fig. 40-1. Modalities of respiratory failure. CPAP, continuous positive airway pressure; PEEP, positive end expiratory pressure. From Bidani A, et al: Mechanical ventilatory assistance. In Pearson FG, et al (eds): Thoracic Surgery. 2nd Ed. Oxford: Churchill Livingstone, 2002, pp. 155 188. With permission. |
Table 40-1. Goals of Mechanical Ventilatory Assistance | ||
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INDICATIONS FOR VENTILATORY ASSISTANCE
When executed cautiously and judiciously, ventilatory assistance can come close to replacing the normal functions of the lungs and chest bellows and can support gas exchange and lung inflation while minimizing lung injury. General indications for the institution of ventilatory assistance can be classified into several broad categories and are listed in Table 40-2.
Postoperative Indications for Support
The decision to initiate or continue mechanical ventilation is usually based on an assessment of gas exchange, impending respiratory failure, and the patient's ability to protect the airway. Many patients have indwelling arterial lines placed by the anesthesia staff to facilitate management of one-lung anesthesia techniques. Arterial blood can and should be sampled early to assess both Pao2 and Paco2. However, oxygenation can be adequately assessed noninvasively through pulse oximetry as long as peripheral perfusion is satisfactory.
Table 40-2. Indications for Ventilatory Assistance | ||
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One must recognize the clinical signs of impending respiratory muscle fatigue to initiate corrective measures before respiratory fatigue is reflected in abnormal arterial blood gas values. Such recognition requires bedside assessment of the patient, rather than laboratory data. Mental acuity and awareness are the most important indicators. In the early postoperative period, the patient's level of consciousness may be impaired from inadequate reversal of anesthesia or other complications, such as postoperative cerebral vascular accident and narcotic overdosage, which may also result in central nervous system (CNS) depression sufficient to cause an inability to protect the airway. At such times, micro- or macroaspiration may occur. Unless rapid reversal with naloxone hydrochloride is achieved, early intubation is advisable. The patient who is able to converse in sentences is certainly able to generate an adequate tidal volume. Respiratory muscle paradox is an early and reliable sign of established muscle fatigue, and is easily assessed by placing a hand on the chest and the abdomen during inspiration and expiration. Normally, the chest and abdomen expand together when the patient inhales because diaphragmatic descent displaces abdominal viscera. In established fatigue, the diaphragm moves paradoxically upward during inspiration, resulting in the abdominal hand moving inward while the chest expands.
Postoperative respiratory failure can occur in one of three situations. Most problems in the immediate postoperative period are related to ventilatory failure due to inadequate reversal of anesthesia, narcotic overdosage, perioperative aspiration, or airway obstruction secondary to laryngeal edema. Shapiro and associates (1977) defined acute ventilatory failure as a Paco2 determination of greater than 50 mm Hg and a pH of less than 7.30. Once reintubation has been accomplished, radiographic examination of the chest is necessary to evaluate inciting complications from aspiration, fluid overload, inadequate pulmonary reserve, or major atelectasis.
For the patient who does well in the initial postoperative period, continued monitoring of oxygen saturation is important as long as he or she requires supplemental oxygen. The need for continued blood gas analysis may be indicated by the following: (a) a preoperative elevation of Paco2, (b) a postoperative elevation of Paco2, and (c) unreliable or inconsistent oximetric saturation readings.
Inadequate Alveolar Ventilation
The adequacy of alveolar ventilation is reflected by the Paco2. An elevated Paco2 indicates alveolar hypoventilation (see Fig. 40-1). When alveolar hypoventilation occurs rapidly enough to produce a significant respiratory acidosis (pH <7.30), acute ventilatory failure is present. On the other hand, long-standing or slowly developing alveolar hypoventilation will manifest as a compensated respiratory acidosis [chronic ventilatory failure as occurs in chronic obstructive pulmonary disease (COPD)] that can be well
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tolerated and does not necessitate ventilatory assistance. Based in part on the studies of Zwillich (1974) and Plant (2000) and their colleagues, an arterial pH of less than 7.30 is a good indicator for ventilatory assistance, because these patients have a higher rate of morbidity and mortality. Although arterial blood pH is a more accurate indicator of acute ventilatory failure than is Paco2, trends in both Paco2 and arterial pH may be equally important. Worsening acute respiratory acidosis occurring over minutes or hours should be an indication for ventilatory assistance irrespective of the actual value of arterial pH. Patients with alveolar hypoventilation and respiratory acidosis are now commonly treated with noninvasive mechanical ventilation to avert endotracheal intubation. Despite the reduction in intubation rates in this subset of patients, in their report on noninvasive positive pressure ventilation (NIPPV) in acute respiratory failure, the attendees of the American College of Chest Physicians (ACCP)-sponsored International Consensus Conferences in Intensive Care Medicine (2001b) recommended that all patients with an acute worsening of respiratory acidosis should be in a monitored setting, so that invasive ventilatory assistance can be instituted prior to hemodynamic compromise.
Diminished or Unstable Ventilatory Drive
Diminished ventilatory drive in relation to metabolic needs is manifested by a decreased respiratory rate or frank apnea, and is an independent indication for ventilatory assistance if it cannot be reversed immediately. Although hypoxic or hypercapnic drive cannot be readily measured at the bedside, the finding of respiratory acidosis in the absence of airway or neuromuscular disease suggests that one or both of these may be impaired (see Fig. 40-1). In addition, a risk exists for sudden apnea or life-threatening hypoventilation in the initial hours following closed head injury, drug overdose, or massive cerebrovascular accident. Ventilatory support is often appropriate in such circumstances, even in the absence of hypercapnia.
Severe Hypoxemia
Hypoxemia of mild to moderate severity can usually be managed by the administration of supplemental oxygen via a face mask. With more severe hypoxemia from right to left shunting of blood flow, [V with dot above]/[Q with dot above] mismatching, or markedly reduced mixed venous Po2 (see Fig. 40-1), mechanical ventilation is necessary. Assessing the efficacy of oxygenation requires knowledge of Pao2 and Paco2 in arterial blood and the inspired fraction of oxygen (Fio2). The alveolar-arterial oxygen gradient (A-a ratio) is one of several calculated indices used to assess oxygenation. The alveolar gas equation is used to calculate the alveolar oxygen tension (Pao2):
where Patm is the atmospheric pressure in mm Hg and PH2Ois the partial pressure of H2O. The respiratory quotient, R, is equal to 0.8 at steady-state conditions but may vary depending on the protein, fat, and carbohydrate ingested. The A-a gradient is obtained by subtracting the measured arterial oxygen tension from the calculated alveolar oxygen tension. The normal A-a gradient varies with age and inspired fraction of oxygen. While breathing room air, the normal A-a gradient is 7 to 14. The ratio of Pao2 to Fio2 is also used to assess the efficacy of oxygenation. The normal value for Pao2 to Fio2 is 300 to 500, whereas a value of less than 250 is indicative of a clinically significant gas exchange derangement. For example, a patient with a Pao2 of 90 mm Hg while breathing an FIO2 of 0.30 would have a Pao2 to fio2 of 300. None of these quantitative measures of hypoxemia according to Tobin (1994) has been prospectively evaluated as independent criteria for the institution of ventilatory assistance. Mechanical ventilatory assistance in these patients improves oxygenation by at least three mechanisms: delivery of a high fractional inspired O2 to the airway, decreased work of breathing, and use of positive end-expiratory pressure, allowing recruitment of collapsed alveolar units and thereby improving [V with dot above]/[Q with dot above] matching.
Inadequate Lung Expansion
Even if alveolar ventilation is adequate as assessed by Paco2, inadequate lung expansion may lead to the development of atelectasis or pneumonia. Inadequate lung expansion may occur during general anesthesia, after upper abdominal or thoracic surgery, following trauma, or in the setting of acute restrictive pulmonary disease. In addition, morbid obesity frequently results in inadequate lung expansion. Spontaneous VC is probably the most practical method of assessment. Tobin and Yang (1990) found that rapid shallow breathing, as commonly assessed by the ratio of spontaneous respiratory rate to spontaneous tidal volume (VT) during assessment for weaning, is also a good indicator of inadequate pulmonary expansion.
Inadequate ventilatory muscle function can lead to inadequate lung expansion, loss of lung compliance, atelectasis, and pneumonia. Maximum voluntary ventilation is a useful measure of ventilatory muscle function, although VC and maximum inspiratory pressure (PImax) are more readily assessed. Sequential determinations of these functions can be extremely helpful in following the progression of ventilatory muscle weakness in neuromuscular disorders such as Guillain-Barr syndrome. Tobin (1994) recommended that ventilatory assistance is indicated when the VC declines to 10 to 15 mL/kg, or the PImax declines to 20 to 25 cm H2O, rather than waiting for acute respiratory acidosis to develop.
Excessive Work of Breathing
According to Tobin (1994), a respiratory rate in the mid-thirties (breaths per minute) or higher (rapid, shallow
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breathing) in an acutely ill patient suggests that the work of breathing exceeds that which can be sustained by the patient. Healthy individuals may be able to maintain minute ventilation twice that of normal indefinitely. However, in the setting of acute illness or underlying pulmonary disease when the resting ventilation required to maintain a normal Paco2 exceeds 10 to 15 L/min, inadequate lung expansion, acute respiratory acidosis, and respiratory failure are likely. The minute ventilation required to maintain a normal Paco2 is determined by CO2 production and the ratio of dead space to alveolar ventilation. Although these factors are rarely measured directly in patients who are not intubated, consideration should be given to factors that might be expected to increase one or both of them in the acutely ill patient.
Mixed forms of respiratory failure are seen in some well-defined clinical scenarios. First, it can occur when there is preexisting CO2 retention, and excessive oxygen administration may remove the hypoxic drive for breathing that has become a compensatory mechanism in patients with chronic hypercarbia. Too often, the goals of oxygen administration are poorly defined, and physicians assume that a high Pao2 value provides a margin of safety. A saturation of more than 95% may actually depress respiratory effort in these patients, leading to an exacerbation of CO2 retention and the onset of an acute respiratory acidosis wherein hypoxemia is a late feature. Second, in cases of mental obtundation, arterial oxygen desaturation may result in an inability to respond with an increased respiratory effort, and CO2 retention complicates the hypoxia. Third, when respiratory muscle fatigue comes on quickly because of malnutrition or associated chronic disease, both depression of oxygenation and elevation of CO2 levels occurs, particularly in the patient recovering from prolonged ventilatory support after severe lung injury. Finally, the development of a pulmonary embolus in a patient receiving mechanical ventilatory assistance is a classic example of the mixed picture. The pathophysiology of pulmonary embolism involves an increase in dead space because the vascular supply to well-ventilated alveoli is obstructed. In the spontaneously ventilated patient, reflex hyperventilation usually leads to hypocarbia. In the ventilated-controlled patient, however, such a reflex increase in minute ventilation does not occur, depending on the ventilator mode and the presence or absence of paralysis, and therefore hypercarbia develops.
DETERMINANTS OF VENTILATOR-INITIATED BREATH
Ventilatory modes are defined by the manner in which the goals of mechanical ventilation are met. As defined by a variety of reports from the ACCP Consensus Conference on Mechanical Ventilation (1993), as well as by Bersten and Oh (1997), Chatburn and Primiano (2001), Hubmayr (1994), Pierson (1999), Pilbeam (1997), and Sassoon (1992), the physical principles underlying the different ventilatory modes and breath characteristics relate to manipulation of pressure, volume, flow, trigger, and time cycle.
Breath Duration and Type
Each breath is composed of four phases: inspiratory phase, change from inspiration to expiration, expiratory phase, and change from expiration to inspiration. In order to appreciate the differences among these breaths and phases of each breath, it is important to understand the concepts of control variables and phase variables (Table 40-3). A control variable is the variable that the ventilator manipulates to initiate inspiration. Specific control variables are pressure, volume, flow, and duration (time). Phase variables are measured and used by the ventilator to initiate each phase of the ventilatory cycle: trigger, limit, and cycle. The trigger variable initiates inspiration. The limit variable is the pressure, flow, or volume target that is set by the physician and cannot be exceeded during inspiration. When the limit variable (i.e., the target) is reached, inspiration is terminated. The cycle variable is the pressure, volume, flow, or time target that is reached to signal the termination of inspiration.
The various modes of mechanical ventilation are classified according to the combination of control variables and phase variables used by the ventilator to deliver the positive pressure breath. Depending on the distribution of the workload between the patient and the ventilator, four different breath types can be provided during mechanical ventilation: mandatory, assisted, supported, and spontaneous. A mandatory breath is triggered, limited, and cycled off by the ventilator, with the ventilator performing all of the work of breathing. An assisted breath is triggered by the patient, and is limited and cycled off by the ventilator. The patient does only the work of initiating the breath, while the ventilator does the rest. A supported breath is triggered by the patient, limited by the ventilator, and cycled off by the patient. The patient does the work of initiating the breath, and then interacts with the ventilator to perform a variable amount of the remaining work as determined by the physician settings. A spontaneous breath is triggered, limited, and cycled off by the patient. The patient performs all of the ventilatory work.
Table 40-3. Breath Types Defined by Machine versus Patient Control | ||||||||||||||||||||
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Initiation (Trigger)
A ventilator breath may be initiated by the machine (machine-triggered, controlled breath) or by the patient (patient-triggered, assisted breath). In a controlled breath, inspiration is triggered at a time set by the ventilator, regardless of the patient's effort and respiratory cycle. In an assisted breath, inspiration is triggered when the patient generates a negative airway pressure below a preset threshold (usually 2 cm H2O), termed the sensitivity. In an assisted breath, the ventilator rate is dependent on the patient rate, unless efforts are too feeble to reach the sensitivity threshold.
Limit (Target)
The limit, or target, for each breath is commonly used to define the primary ventilator mode. A preset tidal volume or airway pressure is the usual limiting variable. In the volume-limited mode, the ventilator delivers a preset tidal volume at a set flow for a set time until the breath is achieved. The peak airway pressure that results is variable, and depends on the peak flow, tubing and airway resistance, as well as lung and chest wall compliance. In the pressure-limited mode, the ventilator delivers a variable (often decelerating) flow to maintain the preset airway pressure limit. The tidal volume that results is variable and also depends on the peak flow, tubing and airway resistance, and lung and chest wall compliance.
Cycle Off
The phase variable measured and used by the ventilator to cycle from inspiration to expiration defines the cycle-off function. Tidal volume, airway pressure, elapsed time, or inspiratory flow rate (IFR) may be used to initiate the transition from inspiration to expiration. The breath may be cycled to expiration as soon as the preset tidal volume or airway pressure has been achieved (volume-cycled, pressure-cycled, respectively). The breath may cycle off to expiration when the patient's IFR declines to about 25% of the peak flow rate (flow-cycled), as occurs in pressure support ventilation (PSV). The inspiratory time can be prolonged by the addition of a phase of zero flow, called an inspiratory pause, and the breath cycles off once the predetermined time has elapsed (time-cycled).
OPTIONS IN VENTILATORY ASSISTANCE
Ventilatory support has been viewed as largely supportive, but patient-ventilator dynamics are increasingly recognized as contributing to complications and outcomes.
Invasive Versus Noninvasive Ventilatory Assistance
Ventilatory assistance may be provided invasively via an artificial airway, that is, endotracheal tube or tracheostomy [invasive ventilatory assistance (IVA)], or via the use of tight-fitting nasal or facial masks (NIPPV). A recent review by the invitees to the ACCP-sponsored International Consensus Conferences in Intensive Care Medicine (2001b) concluded that NIPPV is associated with decreased incidence of nosocomial pneumonia, shorter duration of ventilator assistance, shorter duration of intensive care unit (ICU) stay, and improved morbidity and mortality when compared with IVA in selected groups of patients.
Pressure- Versus Volume-Targeted Ventilation
The fundamental difference between pressure and volume-targeted ventilation is implicit. The AARC Consensus Conference on the Essentials of Mechanical Ventilation (1992) pointed out that pressure-targeted modes guarantee pressure at the expense of variability in tidal volume, while volume-targeted modes guarantee flow and consequently tidal volume, within a preset inspiratory time, at the expense of airway pressure variability with changes in airway impedance. When pressure-control is used, the targeted inspiratory pressure and the inspiratory time must be selected with consideration of the desired tidal volume. If volume-cycled ventilation is used, one may select either a tidal volume and flow delivery pattern (waveform and peak flow) or a flow delivery pattern and minimum minute ventilation.
Volume-targeted modes provide a preset volume, unless a specified pressure limit is exceeded. Pierson (1999) and Hess and Kacmarek (1996) showed that major advantages with volume-targeted ventilation include the capacity to deliver a predictable VT, the flexibility of flow and volume adjustments, and the guarantee of a preset minute ventilation. In volume-targeted ventilation, alterations in airway resistance or lung compliance will alter airway pressures, but will not affect minute ventilation. Volume cycling suffers from some important disadvantages. Volume-cycled modes cannot ventilate effectively and consistently unless the airway is well sealed. Gas leaks through an endotracheal tube cuff or a face mask will diminish the VT delivered to the patient. Furthermore, once IFR is set, the inflation time of the machine is fixed and remains unresponsive to the patient's respiratory pattern. Perhaps most importantly, with changes in the patient's airway resistance or lung compliance, excessive alveolar pressure may be required to deliver the desired VT. With volume-targeted modes, if the patient's lungs become less compliant, the tidal volume and overall ventilation stay the same while the airway pressures increase. Increased airway pressure leads to ventilator-induced lung injury, overt barotrauma, and compromised cardiac function. With pressure-targeted modes, if the overall compliance of the system decreases, peak airway pressure would stay the same and the delivered tidal volume would decrease, resulting in worsening respiratory acidosis, atelectasis, and gas exchange.
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MODES OF VENTILATORY ASSISTANCE
There are many classifications of common ventilator modes, as shown in Table 40-4. It is convenient to divide these into volume-targeted and pressure-targeted modes, as demonstrated in Figs. 40-2 and 40-3.
Volume-Targeted Modes
Volume-Controlled Ventilation
This mode is also referred to as controlled mechanical ventilation. All breaths are initiated at a set time (machine-triggered, controlled breaths) and delivered with a preset flow pattern to achieve a set tidal volume (volume limited). The ventilator cycles off to expiration once the tidal volume has been delivered (volume-cycled), unless an inspiratory pause is added for a predetermined time (time-cycled). Minute ventilation (VE) is determined solely by the ventilator. The airway pressure alarm limit is usually set to 60 cm H2O. If it is exceeded, which occurs with coughing, bronchospasm, or stiff lungs, an alarm sounds and the ventilator cycles to expiration without delivering the entire preset tidal volume. Volume-controlled ventilation (VCV) is useful in patients who are anesthetized, heavily sedated, paralyzed, or who have severe neuromuscular disorders, and performs most of the work of breathing.
Volume-Assisted Ventilation
This mode is also referred to as assisted mechanical ventilation. In this mode, the ventilator delivers a breath when the patient triggers the machine by a spontaneous inspiratory effort or automatically if the patient fails to make an effort within a predetermined time frame. The tidal volume, the backup rate, the sensitivity, and the IFR are manually set. Although tidal volume is set in this mode, the volume delivered may be markedly decreased in patients with abnormal pulmonary mechanics or with volume compression in the ventilator tubing. All breaths are initiated by patient inspiratory effort above threshold (patient-triggered, assisted breaths). When a breath is triggered, the full preset tidal volume is delivered and the patient cannot breathe
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spontaneously between machine breaths. The minute ventilation (VE) is determined by the product of the machine-delivered tidal volume and the patient's respiratory rate. Patient work of breathing is greater than with VCV, but is still largely provided by the ventilator. Volume-assisted ventilation (VAV) mandates spontaneous ventilation and is contraindicated in patients with heavy sedation, muscle relaxation, or in patients too weak to trigger a ventilator breath. This mode can be hazardous in patients with central hyperventilation syndromes. Also, patients who are anxious can trigger the ventilator too frequently, leading to extremely high VE and resulting in acute respiratory alkalosis and arrhythmias.
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Fig. 40-2. Idealized airway pressure, alveolar pressure, and flow tracings during volume-cycled ventilation (with constant inspiratory flow) and pressure-cycled ventilation. From Marcy TW, Marini JJ: Control mode ventilation and assist/control ventilation. In Stock MC, Perel A (eds): Mechanical Ventilatory Support. Philadelphia: Lippincott Williams&Wilkins, 1997. With permission. |
Table 40-4. Modes of Mechanical Ventilation | ||||||||||||||||||||||||||||||||||||||||||||||||
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Fig. 40-3. Patterns of airflow, airway pressure, and lung volume during mechanical ventilation. Gas flow (cycle ) is initiated by either patient effort (-P) or set time cycle. Inspiratory flow ceases (limit ) when a preset volume, pressure, or flow is achieved. CMV, continuous mechanical ventilation; IMV, intermittent mandatory ventilation; PCIRV, pressure-controlled inverted-ratio ventilation; PCV, pressure control ventilation; PEEP, positive end-expiratory pressure; PS, pressure support. From Bartlett RH: Respiratory physiology and pathophysiology. In Bartlett RH (ed): Critical Care Physiology. Boston: Little, Brown, 1996. With permission. |
Volume Assist-Controlled Ventilation
This mode is also referred to by Pierson (1999) as assist-control ventilation. Volume assist-controlled ventilation (VACV) is a combination of VAV and VCV. A minimum ventilator rate is set, but patient-triggered breaths are allowed if the spontaneous rate exceeds the controlled rate. This mode can thereby prevent hypoventilation but, like VAV, exacerbate hyperventilation. The sensitivity to inspiratory effort can be adjusted to require a small or large negative pressure deflection below the set level of end-expiratory pressure to initiate the machine's inspiratory phase. Many of the latest generation ventilators can be flow triggered, initiating a breath when a flow deficit is sensed in the expiratory limb of the circuit relative to the inspiratory limb during the exhalation period. Both may be effective. As a safety mechanism, Marcy and Marini (1997) set a backup rate so that if the patient does not initiate a breath within the number of seconds dictated by that frequency, a machine cycle is initiated automatically.
Intermittent Mandatory Ventilation
In this mode, the patient receives periodic positive pressure breaths from the ventilator at a preset volume and rate. Sassoon and associates (1994) note that spontaneous breathing is also permitted, unlike the situation with VACV. Spontaneous breathing is usually achieved through the use of a demand valve, which can result in a considerable increase in the work of breathing. This mode is essentially
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VCV imposed on spontaneous ventilation. At an operator-set frequency, the intermittent mandatory ventilation (IMV) rate, the ventilator provides a positive pressure breath to the patient regardless of the phase of the patient's cycle that is identical to a VCV breath (machine-triggered, volume-limited, volume- or time-cycled). However, an additional circuit provides a continuous gas flow that allows the patient to breathe spontaneously between machine breaths. Total VE is the sum of machine VE and patient VE. Theoretically, the degree of respiratory muscle rest is proportional to the number of breaths received from the ventilator. However, Tobin (1994) noted that patients may have difficulty in adapting to the intermittent nature of ventilatory assistance. Instead, respiratory center output appears to be consistent and does not adjust to breath-to-breath changes in inspiratory load. Consequently, as noted by Brochard (1994) and Tobin (1994), IMV can result in increased work of breathing and contribute to the development of respiratory muscle fatigue.
Synchronous Intermittent Mandatory Ventilation
Sassoon and colleagues (1994) defined synchronous intermittent mandatory ventilation (SIMV) as a modification of IMV in which the patient is allowed to trigger a breath in a manner analogous to volume-assisted ventilation. However, if the patient does not breathe within an allotted time (i.e., 6 seconds if the IMV rate is set at 10 breaths/min), the ventilator delivers a mandatory or volume-controlled breath. Thus, SIMV may be thought of as volume assist-controlled ventilation superimposed on spontaneous ventilation.
Comparison Among Volume-Targeted Modes
Since the introduction of SIMV to adult ventilation 20 years ago, a debate has raged over whether SIMV or VACV is more beneficial. If the ventilator rate is set high enough that the patient's ventilation needs are met, and the patient is not dyspneic, then VACV and SIMV are essentially equivalent and the ventilator is providing full ventilatory support. The differences occur when the patient wants more ventilation than the ventilator provides, either by the backup rate in the VACV mode or by the mandatory rate in the SIMV mode. In VACV, the patient can increase the ventilator's output by triggering breaths more frequently than the set backup rate. Depending on the set triggering sensitivity and the IFR, the patient is required to do a variable amount of work to get this extra ventilation. Under ideal circumstances, the patient triggers an additional breath, which is delivered immediately and fast enough to satisfy the patient with little work done over and above full ventilatory support. A fundamental hypothesis underlying SIMV is that patients should do some breathing work in order to maintain ventilatory muscle tone. Implementing the SIMV hypothesis means that the mandatory rate should be low so that the patient contributes a substantial portion of the total minute ventilation. With SIMV, when the patient wants a higher minute ventilation than that provided by the set-volume mandatory breaths, the patient must generate spontaneous breaths that are unassisted by the ventilator. Because this may require substantial effort to breathe through the endotracheal tube, the spontaneous breaths generated by patients on SIMV tend to be small in comparison with the mandatory breaths. A number of techniques have been introduced to reduce the effort, including continuous flow, flow-by, and inspiratory pressure support.
Pressure-Targeted Modes
Pressure Support Ventilation
This mode allows the physician to set a level of pressure to boost each breath. The machine attempts to maintain airway pressure at a preset level until the patient's IFR decreases below a threshold value, typically 25% of the peak flow. The tidal volume is determined by the preset level of pressure support, patient effort, and pulmonary mechanics. This mode is a unique, patient-triggered, pressure-limited, flow-cycled mode that can allow close tracking of the patient's ventilatory effort and facilitates withdrawal of ventilation. PSV provides the greatest patient ventilator interaction of any of the conventionally used ventilatory modes. Once initiated, there is a rapid flow of fresh gas until the airway pressure limit is achieved. Thereafter, the inspiratory flow adjusts via microprocessor circuitry to keep the airway pressure constant. The patient can continue to inhale actively and increase the delivered tidal volume above that provided by the ventilator alone. When the patient's IFR declines to 25% of the peak flow rate, the ventilator cycles off into expiration. The actual tidal volume delivered for a given level of PSV depends on patient effort, airway resistance, and chest wall and lung compliance.
Advantages of Pressure Support Ventilation
Pressure support provides ventilatory assistance that ranges from minimal support to full ventilation. Because the depth, length, and flow profile of each breath is influenced by the patient, well-adjusted PSV tends to be more comfortable for the patient. PSV has its widest application as a weaning mode. Pressure support is also valuable in offsetting the resistive work required to breathe spontaneously through an endotracheal tube, as during continuous positive airway pressure (CPAP) or SIMV. The pressure support level should be adjusted to maintain an adequate tidal volume at an acceptable frequency (<30 breaths/min). In theory, as noted by Brochard (1994) and Pierson (1999), PSV can provide sufficient support to perform the entire work of breathing if set to meet or exceed the average inspiratory pressure requirement of the patient.
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Problems with Pressure Support Ventilation
Pressure support ventilation requires the ventilatory cycle to be patient initiated and cannot adjust to changes in pulmonary resistance and compliance. Therefore, PSV is not an ideal mode for patients with unstable ventilatory drive or highly variable thoracic impedance. Furthermore, because a true square-wave of airway pressure tends to deteriorate as ventilatory demands increase, the tidal volume resulting from PSV tends to be frequency dependent. Brochard (1994) and Pierson (1999) emphasized that pressure support is a spontaneous breathing mode (if the patient does not breathe, nothing happens). Pressure support is often combined with SIMV during partial ventilatory support, so that each spontaneous breath receives a positive-pressure assist.
Pressure-Controlled Ventilation
This is a machine-triggered, pressure-limited, and time-cycled mode intended for patients with acute respiratory failure, severe hypoxemia, and poor lung compliance. Immediately after initiation of the breath, flow rapidly achieves the preset pressure limit. For example, pressure-controlled ventilation (PCV) of 25 cm H2O added to 10 cm H2O positive end-expiratory pressure (PEEP) achieves a peak airway pressure of 35 cm H2O. Thereafter, flow decelerates to zero with an inspiratory pause that sustains airway pressure at the limit for the defined inspiratory time after which it cycles off. This allows precise definition of inspiratory and expiratory ratios. In PCV, maximal pressure is controlled, but tidal volume is a complex function of applied pressure and its rate of approach to target pressure, available inspiratory time, and the impedance to breathing [compliance, inspiratory and expiratory resistance, and self-controlled positive end-expiratory pressure (auto-PEEP)]. Marini (1994) defined pressure-controlled inverse-ratio ventilation (PC-IRV) as prolongation of inspiratory time such that the I:E ratio is greater than 1:1.
Advantages of Pressure-Controlled Ventilation
Limiting airway pressure may decrease the risk for volutrauma/barotrauma. Precise control of IFR, inspiratory time, and mean airway pressure allows IRV, which enhances alveolar inflation, recruitment and oxygenation, and may decrease supplemental oxygen requirements. High-flow, pressure-targeted ventilation compensates well for small air leaks and is appropriate for use with leaking or uncuffed endotracheal tubes. Pressure-targeted ventilation is also an appropriate choice for spontaneously breathing patients with high inspiratory flow demands because it can deliver flow with a decelerating flow profile. Marini (1994) and Nahum and Marini (1996) noted that decelerating flow profiles also tend to improve the distribution of ventilation in a lung with heterogeneous mechanical properties (i.e., widely varying time constants). Apart from an application in limiting the lung's exposure to high airway pressure and barotrauma, pressure-targeted modes can also be helpful in adult patients in whom the airway cannot be completely sealed (e.g., bronchopleural fistula).
Disadvantages of Pressure-Controlled Ventilation
Pressure-controlled ventilation and PC-IRV modes evoke patient discomfort, usually requiring heavy sedation. Increased mean airway pressure may impair cardiac filling, although transmission of high airway pressures to the vasculature may be attenuated by lung stiffness. Inverse I:E ratio may result in inadequate expiratory time, air trapping, breath stacking, and the development of auto-PEEP (intrinsic PEEP). This auto-PEEP, in turn, may lead to hypercapnia, impaired cardiac filling, and spontaneous pneumothorax.
Combined Modes
In certain situations, according to Pierson (1999), it is desirable to adjust midinspiratory flow in response to changing patient needs, or alternatively, to restrict pressure but ensure the delivery of a specified tidal volume. Advances in computer microprocessor technology have led to such combination modes.
Pressure-Regulated Volume Control
This mode satisfies a target tidal volume with the lowest inspiratory pressure within the predetermined inspiratory time as noted by the American Association for Respiratory Consensus Group (AARC) (1995). Inflation pressure is continuously regulated in response to changes in inflation impedance to satisfy the preset tidal volume. If a satisfactory tidal volume is achieved by spontaneous patient effort, no ventilatory assistance is provided.
Volume Support
In this mode, Hess and Kacmarek (1996) note that the flow-cycled pressure support is adjusted (up or down) to achieve the primary minute ventilation target, while guaranteeing a minimum tidal volume. When breathing frequency declines, the tidal volume may increase by as much as 50% over a baseline minimum to satisfy a target minute ventilation.
Volume-Assured Pressure Support
In this mode, Kacmarek and Hess (1994) and Pierson (1999) pointed out that a fixed level of pressure support is supplemented by gas from a backup source if the PSV is insufficient to meet a target tidal volume.
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High-Frequency Ventilation
High-frequency ventilation, with 150 to 300 breaths/min, delivers respiratory tidal volumes (1 to 3 mL/kg) averaging significantly less than anatomic dead space. Because of the reduced tidal volumes, peak inspiratory pressures (PIPs) during high-frequency ventilation are less than those in conventional ventilation. High-frequency oscillatory ventilation uses a reciprocating piston, diaphragm, or bellows to generate a sinusoidal respiratory waveform during the breathing cycle. Improvements in oxygenation can be attributed to the static inflation (up to 30 cm H2O). High-frequency jet ventilation consists of the intermittent delivery of gas through a small-bore cannula within the airway in short bursts. Respiratory rates are commonly in the range of 100 to 200 breaths/min. Furthermore, the expiratory phase of the cycle is passive, dependent on the chest wall and lung compliance. The primary use is as a rescue therapy in adults with acute respiratory failure related hypoxemia in the face of high PEEP or a significant air leak.
VENTILATOR SETTINGS
Many investigators, including Hubmayr (1994), Kacmarek (1992), Nahum and Marini (1996), Pierson (1999), Tobin and Dantzker (1988), and Wood and Hall (1993), have stated that the initial settings are estimated on the basis of the patient's size and clinical condition and are generally altered after obtaining arterial blood gas readings or other laboratory information. Depending on the stability of the patient's clinical state, the settings should be assessed repeatedly and adjustment made accordingly.
Fractional Inspired Oxygen Concentration
Immediately after intubation, it is generally prudent to administer higher levels of oxygen until adequate arterial oxygenation has been confirmed with later adjustment guided by pulse oximetry or blood gases. Many predictive equations have been created to aid in the selection of a satisfactory Fio2, but Tobin (1994) noted that none are sufficiently rigorous to substitute for a trial-and-error approach. The risk for oxygen toxicity is minimized by using the lowest Fio2 that achieves satisfactory arterial oxygenation. The usual goal is a Pao2 of approximately 60 mm Hg or arterial oxygen saturation (Sao2) of 90%. Higher values do not substantially enhance oxygen delivery or tissue oxygenation. The response to a change in Fio2 depends on the underlying pathophysiology. Nelson (1993) noted that right-to-left shunts do not respond as well to increases in Fio2 as do hypoventilation or [V with dot above]/[Q with dot above] mismatch. Studies by Durbin and Wallace (1993) and Jenkinson (1993) demonstrated that exposure to an Fio2 of 0.95 for up to 24 hours probably does not pose a significant clinical risk, although prolonged exposure to this concentration is clearly toxic. An Fio2 of 0.5 is generally considered safe for several weeks, if necessary in the management of hypoxemia. For Fio2 values between 0.5 and 1, the duration of safe exposure before the onset of toxicity is unknown, but severe hypoxemia is more a threat in critically ill patients than potential oxygen toxicity. An Fio2 of 1.00 causes nitrogen washout and promotes atelectasis, so should be avoided.
Tidal Volume
It was customary according to Marini and Kelsen (1992) and Marini (1993) to use tidal volumes that are two to three times higher than normal during mechanical ventilation (10 to 15 mL/kg). This approach, often referred to as traditional ventilation in the literature, has been successfully challenged in animal and human trials by Kacmarek and Chiche (1998), as well as by Dreyfuss (1988), Parker (1993), and Tsuno (1990) and their co-workers, showing that alveolar overdistention can produce pulmonary epithelial, endothelial, and basement membrane injuries that are associated with increased microvascular permeability and lung rupture. Amato and co-workers (1995, 1998) reported improved survival in ARDS patients using a lung-protective strategy (tidal volume of 6 8 m/kg and adequate positive end-expiratory pressure to ensure alveolar recruitment) compared with ARDS patients managed using traditional ventilator management. The ARDS Network reported on the Assessment of Low Tidal Volume and Elevated End-Expiratory Volume to Obviate Lung Injury (ALVEOLI) trial (2002), which confirmed the benefit of a strategy that lowers tidal volumes to 5 to 7 mL/kg of ideal body weight and limits plateau pressures in patients with ARDS. While one would ideally titrate delivered volume based on monitoring of alveolar volume, this is not feasible in practice. A reasonable substitute is to monitor alveolar pressure, which can be estimated from the plateau in airway pressure and can be measured by briefly occluding the ventilatory circuit at end inspiration in a relaxed patient. The pressure-volume curve of a normal lung shows that the lung is maximally distended at a transpulmonary pressure of 30 to 35 cm H2O; higher pressures cause overdistention. Therefore, Gattinoni and associates (1994), Marini and Kelsen (1992), and Slutsky (1993) recommended that plateau pressure be maintained at less than 35 cm H2O. As additional experimental data become available from Brochard and colleagues W(1998), as well as by Hudson (1998), and Kacmarek and Chiche (1998), even lower plateau pressure may be considered a desirable target. Reduction in plateau pressure often requires a reduction in tidal volume and can result in an increase in arterial carbon dioxide tension (Paco2), a strategy termed by one of us (AB) (1994) and Hickling (1994) and respective co-workers, as well as by Tuxen (1994) as permissive hypercapnia or controlled hypoventilation. In addition to the potential adverse effects of hypercapnia, such as increased intracranial pressure (ICP), depressed myocardial contractility, pulmonary hypertension, and decreased renal blood flow, reductions in tidal volume may
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have other unwanted effects. Decreases in the volume of aerated lung, increases in shunt, and worsening of oxygenation may also be consequences of low tidal volume ventilation. One means of minimizing loss of lung volume and improving oxygenation is through the application of PEEP.
Ventilatory Rate
According to Hubmayr (1994), selection of the ventilatory rate depends on the mode of ventilatory support. With volume assist-controlled ventilation, the backup rate should be approximately 4 breaths/min less than the patient's spontaneous rate. These settings ensure that the ventilator will supply an adequate volume should the patient have a sudden decrease in respiratory center output. Because there may be a substantial difference between the machine backup rate and the patient's spontaneous rate, Hubmayr (1994) noted that this mode may promote breathing patterns with inverse inspiratory-expiratory time ratios, which can be very uncomfortable. With IMV, the ventilator rate is usually set at a high initial value (15 to 20 breaths/min) and then reduced as tolerated. In patients with obstructive lung disease, the rate may be set low (8 to 12 breaths/min) to allow a prolonged expiratory phase and to reduce the risk for auto-PEEP and dynamic hyperinflation. With PSV, the ventilatory rate is not set; the patient determines the respiratory rate.
Sensitivity Setting
In the assist-control, SIMV, and pressure support modes, the patient must lower the airway pressure below a preset threshold in order to trigger the ventilator, with the sensitivity usually set at -1 to -2 cm H2O. However, with a poorly responsive demand valve, Sassoon (1992) noted that the actual pressure generated by the patient may be considerably greater. If the trigger setting is too sensitive, the ventilator may be triggered by the small changes in flow or pressure that are not caused by inspiratory efforts. The result is frequent cycling (autocycling) and severe respiratory alkalosis.
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Fig. 40-4. Airway pressure waveforms during assist-control ventilation (VACV). With no patient effort, a convex inspiratory pattern is present, but with increasing patient inspiratory effort and inadequate inspiratory airflow, a concave pressure waveform is noted. From Tobin MJ: Mechanical ventilation. N Engl J Med 330:1056, 1994. With permission. |
Kacmarek and Hess (1994) showed that flow triggering appears to involve less patient work than pressure triggering. Some patients, especially those with COPD and high minute ventilation, develop air trapping and have a positive alveolar pressure at end expiration (auto-PEEP). Auto-PEEP makes ventilator triggering more difficulty according to Hubmayr (1994), since the patient needs to generate a negative pressure equal in magnitude to the level of auto-PEEP in addition to the set sensitivity. This increased pressure requirement according to Tobin (1994) is one of the factors that accounts for the patient who is unable to trigger the ventilator, despite making obvious respiratory efforts.
Inspiratory Flow Rate
The IFR may be independently adjusted or may be determined by alteration of the tidal volume, ventilator rate, and the I:E ratio. Generally, an IFR of approximately 60 L/min achieves optimum gas exchange. However, higher IFRs of 80 to 100 L/min may be preferred in patients with COPD. Laghi and co-workers (2001) demonstrated that, although patients with COPD respond to decreases in inflation time with tachypnea, expiratory time was increased by 10% and intrinsic PEEP was decreased by 9%. Connors and associates (1981) and Tobin (1994) attributed decreases in intrinsic PEEP to the reduction in I:E ratio and associated prolongation of expiration, allowing regions of air trapping to empty more completely. If the flow rate is insufficient to meet a patient's ventilatory demands, Tobin (1994) stated that the patient will pull against their pulmonary impedance and the ventilator, with consequent increase in the work of breathing. Ideally, according to Sassoon (1991), the airway pressure waveform should demonstrate a smooth rise and convex appearance during inspiration when adjusting the flow rate and trigger sensitivity. In contrast, Marcy and Marini (1997), Marini and colleagues (1985), and Sassoon (1991) noted that a prolonged negative phase with excessive scalloping of the tracing signifies unsatisfactory sensitivity and flow settings, as illustrated in Fig. 40-4.
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Positive End-Expiratory Pressure
PEEP is the elevation in alveolar pressure above atmospheric pressure present in the lung at the end of expiration. PEEP can be supplied by the ventilator through a tight-fitting face mask or endotracheal tube. PEEP may also result from incomplete alveolar emptying in patients with airflow limitations (auto-PEEP). No other area of ventilatory management has aroused as much controversy as PEEP, yet among Albert (1985), Romano (1985), Hudson (1988), Kacmarek and Pierson (1988), Rossi and Ranieri (1994), and Dries and Marini (2002), there is still no consensus. PEEP is most often used in three clinical settings: hypoxemic respiratory, acute pulmonary edema, and COPD to overcome the effects of auto-PEEP.
Some investigators, such as Albert (1985), Horton and Cheney (1975), and Suter and associates (1975), consider PEEP to have no application other than to ameliorate life-threatening hypoxemia and decrease exposure to a potentially toxic Fio2. With this approach, one strives for a satisfactory Pao2 with the lowest level of PEEP. Others like Pepe and colleagues (1984) have reported that early use of PEEP may modify the natural course of acute lung injury (ALI) and ARDS and may prevent its development but this has not been demonstrated in patients at risk for developing ARDS. In patients with ARDS, Malo and co-workers (1984) noted that PEEP usually produces a significant improvement in Pao2, primarily due to a reduction in intrapulmonary shunt resulting from opening of atelectatic regions (alveolar recruitment) and by redistribution of lung water from the alveoli to the perivascular interstitial space. Malbouisson and coinvestigators (2001) showed in computed tomographic (CT) scans of the chest of patients with ARDS that the degree of improvement in Pao2 correlates with the degree of PEEP-induced alveolar recruitment. Provided this improvement in Pao2 is not offset by a decrease in cardiac output, supplemental PEEP is indicated in these patients. Moreover, Pepe and associates (1984) postulated that oxygen requirements can be reduced.
The addition of PEEP also influences lung mechanics. Patients with ALI commonly have a decreased end-expiratory lung volume, and thus, tidal breathing occurs on the low flat portion of the pressure-volume curve. By shifting tidal breathing to a more compliant portion of the curve, Marini and colleagues (1985) and Marini (1993) found that PEEP can decrease the work of breathing and may prevent the cyclic alveolar recruitment/derecruitment that has been associated with ventilator-induced lung injury. In addition to the injury induced by high inflation pressures, Muscedere and associates (1994) and Rossi and Ranieri (1994) noted that mechanical ventilation at a low end-expiratory lung volume aggravates lung injury in experimental animal models, probably from the shear stress associated with repeated closing and opening of lung units. According to Rossi and Ranieri (1994) the debate continues as to the level of PEEP required to maintain alveolar opening, but most likely 2 cm H2O above the lower inflexion point
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(Pflex on the pressure-volume curve of the respiratory system shown in Fig. 40-5) is adequate. Clearly, PEEP may have both beneficial and detrimental effects, depending on the clinical situation (Table 40-5). The ongoing ALVEOLI trial is investigating outcome with and without PEEP, but has so far failed to find improved outcomes with PEEP.
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Fig. 40-5. Pulmonary pressure-volume curve of a patient with acute lung injury. Top. The lower inflection point is typically 12 to 18 cm H2O and the upper inflection point 26 to 32 cm H2O. Bottom. The goal of protective ventilation strategies is to ventilate the lung in the zone between recruitment and derecruitment and the zone of overdistention. Positive end-expiratory pressure is set just above the lower inflection point and the pressure limit (Pmax) just below the upper inflection point; both high- and low-volume injury are avoided. From Pinhu L, et al: Ventilator-associated lung injury. Lancet 361:332, 2003. With permission. |
Table 40-5. Beneficial and Detrimental Effects of Positive End-Expiratory Pressure (PEEP) | ||||||||||||||
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In obstructive lung disease, PEEP serves a different function than in ALI. The purpose of PEEP is not to increase lung volume (which is already excessive), but to decrease the muscular effort required to trigger the ventilator in the presence of dynamic hyperinflation and auto-PEEP. Patients with auto-PEEP may have difficulty triggering the ventilator. The patient must typically generate a negative pressure of -2 cm H2O in order to trigger a breath. The presence of a positive end-expiratory pressure of 5 cm H2O requires that the patient generate -7 cm H2O inspiratory pressure to trigger the ventilator breath. The addition of external PEEP (to a level not exceeding the level of auto-PEEP) can help to counteract this difficulty. A PEEP of 5 cm H2O applied by the ventilator results in an equal pressure at the airway opening and at the alveolus. Therefore, as Tobin and Lodato (1989) showed, the patient is only required to generate a negative inspiratory pressure of -2 cm H2O, and the work of breathing is decreased.
PEEP should be initiated with small stepwise increments of 3 to 5 cm H2O, with evaluation of the response to each change. Several alternative approaches have been suggested to determine the optimum level of PEEP, but none has been shown to be clearly superior. The best PEEP is achieved when the Fio2 can be reduced to an acceptable level without compromising tissue oxygen delivery. A methodical approach also is required when PEEP is being reduced or discontinued. Pepe and co-workers (1984), Tobin (1994), and Rossi and Ranieri (1994) noted that abrupt cessation may produce hypoxemia that takes hours or days to reverse or requires reinstitution of PEEP at a higher level than that used before its suspension.
COMPLICATIONS OF VENTILATORY ASSISTANCE
A host of complications delineated on Table 40-6 can occur while patients are receiving ventilatory assistance, often confounded by the underlying illness, its severity, and the intensive care environment.
Airway Problems
Heffner (1990) noted that complications can occur during intubation (e.g., trauma, right main-stem bronchus intubation, hypoxia), while the tube is in place (e.g., laryngeal injury, tracheal injury, hemorrhage, infection), at the time of extubation (e.g., laryngoedema, aspiration), or subsequently (e.g., hoarseness, laryngeal stenosis, tracheal stenosis). According to George and collaborators (1998), sinusitis is a common complication of intubation that predisposes the patient to the development of nosocomial pneumonia. Nasotracheal intubation is associated with a higher incidence of sinus opacification than orotracheal intubation, 96% versus 23% following 1 week of intubation. However, Rouby and associates (1994) noted that sinus opacification is not synonymous with infectious sinusitis. According to Souweine (2000), 70% of intubated patients with sinus opacification by CT had infectious sinusitis confirmed by sinus aspirate. However, aggressive treatment of maxillary sinusitis is needed to decrease the risk
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for nosocomial pneumonia. In those patients with sinus opacification and fever, nasotracheal and nasogastric tubes should be removed and replaced orally to allow drainage of the sinuses.
Table 40-6. Complications of Mechanical Ventilation | ||
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Intracuff pressures should be monitored and kept in the range of 18 to 25 cm H2O. Pressures exceeding 25 cm H2O are associated with an increased likelihood of mucosal necrosis and subsequent tracheal stenosis. However, Heffner (1990) and Rello and colleagues (1996) pointed out that lower pressures (<18 cm H2O) may allow aspiration of oropharyngeal secretions around the cuff and an increased risk for nosocomial pneumonia.
Right main-stem bronchus intubation, as most frequently occurs in emergent intubation, can result in hyperinflation of the right lung with subsequent alveolar rupture and tension pneumothorax. Left lung atelectasis is also a potential complication of a right main-stem intubation. Because physical examination is an unreliable method for determining correct positioning of the endotracheal tube, a postintubation chest radiograph or endoscopic evaluation should be performed to ensure that the endotracheal tube is at least 4 cm above the carina.
Ventilation-Perfusion Mismatch
Positive pressure ventilation often results in worsening of [V with dot above]/[Q with dot above] mismatch and according to Pierson (1999) may result in impairment of oxygen uptake in the lung. Gravitational forces favor perfusion to the dependent lung zones, but gas delivered by positive pressure ventilation follows the path of least resistance; ventilation is greatest in the apices in the semiupright patient or substernal in the supine patient. During spontaneous breathing, Tobin (1994) noted that the diaphragm actively ventilates dependent lung zones, but with paralysis and heavy sedation, the diaphragm is pushed passively cephalad by the abdominal viscera into the dependent lung zones, further impairing ventilation of these regions.
Impairment of Alveolar Ventilation
High airway pressures, particularly in the presence of hypovolemia, may result in dynamic compression of perfused pulmonary capillaries, thereby converting functioning alveolar-capillary units to physiologic dead space. If minute ventilation is fixed (i.e., the patient cannot increase respiratory rate due to sedation or paralysis) alveolar ventilation may decrease due the increased dead space fraction. Thus, during positive pressure ventilatory support, intravascular volume needs to be carefully assessed and repleted. Otherwise, increased alveolar dead space can increase the ventilatory requirement, which may lead to the development of hypercapnia and respiratory acidosis if not met.
Circulatory Impairment
Zimmermann and co-workers (1982), Strieter and Lynch (1988), and Pierson (1990) all noted that increased intrathoracic pressure decreases venous return, cardiac output, and renal blood flow. Measured intravascular central pressure and cardiac preload appear to increase, but effective transmural pressures decline, because there is increased intrapleural pressure. Circulatory effects are directly proportional to the elevation of intrathoracic pressure, and according to Harken and coinvestigators (1974) are further exacerbated by hypovolemia. Michard and associates (1999) noted that the hemodynamic effects of positive pressure ventilation and volume loading in hypovolemic patients can be assessed by changes in the arterial pulse pressure during the respiratory cycle. The adverse circulatory effects of mechanical ventilation are less pronounced in stiff, noncompliant lungs, which attenuate the transmission of intraalveolar pressure to the intravascular space. Mean intrathoracic pressures tend to be lower with partial than with full ventilatory support; the more the patient breathes spontaneously, the less the tendency will be to compromise cardiac output. On the other hand, patients who actively fight the ventilator may experience severe circulatory compromise regardless of ventilator mode. PEEP of greater than 10 cm H2O may compress the pulmonary capillary bed, increase right ventricular afterload and pressure, shift the intraventricular septum, and impede left ventricular filling according to Bishop (1991) and Jardin (1981) and their colleagues, as well as Zimmermann (1982).
Renal and Hepatic Dysfunction
Strieter and Lynch (1988), Pierson (1990), and Bennett and Vender (1997) showed that reductions in portal flow have been associated with the use of PEEP in patients receiving ventilatory assistance, which can potentially lead to hepatic dysfunction. Doherty and Sladen (1989) also documented reductions in renal blood flow.
Intracranial Pressure
Intracranial pressure may increase, but Pierson (1990) demonstrated that as cerebrospinal fluid pressure rises equally in the closed cranium, the distending pressure across the brain should not increase. The increase in ICP may be minimized in the head-up position. Furthermore, high intrathoracic pressure may impede venous return from the head and increase ICP, thereby exacerbating neurologic injury. This increase can impair cerebral perfusion in patients with head injury causing loss of cerebral autoregulation.
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Gastric Distention
According to Strieter and Lynch (1988), patients receiving mechanical ventilation, particularly those with low lung-chest wall compliance, may develop gastric or intestinal distention with air. The mechanism is believed to be due to an air leak around the cuff of the endotracheal tube, resulting in increased esophageal pressures that can overcome the resistance of the lower esophageal sphincter. This problem can be alleviated by passage of a small-bore nasogastric tube.
Prolonged Muscle Weakness
Prolonged muscle weakness following the long-term use of muscle relaxants and paralytics during mechanical ventilation can substantially increase a patient's requirement for intensive care and rehabilitation. Hansen-Flaschen (1993) and Shapiro (1993) and their co-workers initially reported on patients with status asthmaticus who were treated with sedation and paralysis in conjunction with high doses of corticosteroids. However, both Hansen-Flaschen (1993) and Segredo (1992) and their associates showed that myopathy, elevation of serum creatine phosphokinase, or both also occur in patients with other diagnoses who receive muscle relaxants. Subsequent studies by Helliwell (1991), Leijten (1995), and Bernard (2002) and their collaborators have identified the use of aminoglycosides, renal failure, female gender, and duration of mechanical intubation to be risk factors for ICU-paresis. Neuromuscular dysfunction acquired in the ICU has also been reported by Leijten and associates (1996) to occur in patients with sepsis and multiorgan dysfunction.
Acid-Base Problems
Acid-base disturbances from suboptimal ventilator adjustment can become clinically relevant. Patients with underlying chronic ventilatory insufficiency (e.g., compensated CO2 retention) are particularly prone to acute respiratory alkalosis. Failure to appreciate a patient's elevated baseline arterial Pco2, coupled with management that results in a normal Pco2 of 40 mm Hg, can acutely produce a dangerous posthypercapnic metabolic alkalosis in such patients. Furthermore, Pierson (1999) noted that severe alkalosis can result in cardiac arrhythmias and other potentially fatal sequelae.
Air Trapping, Dynamic Hyperinflation, and Auto-PEEP
Pepe and Marini (1982) and Benson and Pierson (1988), as well as Tobin (1990) and Lodato and Tobin (1991), emphasized that understanding dynamic hyperinflation is central to avoiding complications, performing accurate hemodynamic monitoring, and preventing unnecessary patient discomfort. In the presence of expiratory airflow obstruction (e.g., in COPD or asthma), or when minute ventilation exceeds 15 to 20 L/min, Leatherman (1996) showed that exhalation of a delivered mechanical breath may not be complete by the time the next breath is given. When this happens, as shown in Fig. 40-6, both overall lung volume and alveolar pressure remain increased at end expiration,
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resulting in the same physiologic effects as excessive externally applied PEEP (i.e., hyperinflation and decreased cardiac ou3put). Auto-PEEP is common, occurring to some degree in one third or more of all patients with acute respiratory failure, and according to Pepe and Marini (1982) and Pierson (1999) is physiologically important in perhaps half of these.
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Fig. 40-6. A. Schematic diagram of an asthmatic patient exhibiting significant residual flow at end expiration. B.The esophageal pressure (Poes), an estimate of intrapleural pressure, shows the degree of pressure change required to overcome intrinsic pressure (PEEPi) and initiate inspiratory flow. C.A progressive increase in lung volume (breath stacking) occurs if expiratory time is insufficient to allow complete exhalation of the tidal volume. From Phipps P, Garrard CS: The pulmonary physician in critical care. Acute severe asthma in the intensive care unit. Thorax 58:81, 2003. With permission. |
Auto-PEEP cannot be read from the ventilator's airway pressure manometer during routine operation; one of several special maneuvers must be performed to detect it. The usual method is via an end-expiratory pause, demonstrated in Fig. 40-7. This permits brief equalization of pressures, from alveolus to central airways to inspiratory circuit, and allows the auto-PEEP value to be read on the pressure manometer. To reduce auto-PEEP, overall expiratory time must be increased in order to permit more complete exhalation. Airway obstruction (e.g., bronchospasm or secretions) should be treated aggressively. Tobin (1994) described maneuvers that increase expiratory time, regardless of the ventilator mode, including the reduction of the respiratory rate, increases in the IFR, and the use of low-compressible-volume ventilator circuits.
As a consequence of auto-PEEP, the patient must develop a greater negative pleural (alveolar) pressure to overcome the auto-PEEP to generate a negative pressure at the proximal airway and trigger the inspiratory cycle of the ventilator, greatly increasing the patient's work of breathing. A logical approach to evaluate and reduce dynamic hyperinflation and auto-PEEP is shown in Table 40-7.
Nosocomial Pneumonia
Pneumonia is the leading cause of death from hospital-acquired infections, with the majority of hospital-acquired pneumonia occurring in patients outside the ICU. However, intubation significantly increases the risk for nosocomial pneumonia by 6- to 21-fold according to Tablan and collaborators (1994) of the Centers for Disease Control and Prevention (CDC), with up to half of all episodes of ventilator-associated pneumonia (VAP) occurring within the first 3 days. The risk for VAP in those receiving invasive mechanical ventilation according to Cook and associates (1998) is 3% per day in the first 5 days, 2% per day on days 5 to 10,
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and 1% per day on days 10 to 15. Impaired host defenses, virulent organisms, and endotracheal tubes that bypass the protective mechanisms of the upper airway predispose the mechanically ventilated patient to pneumonia development. Aspiration of gastric contents and oropharyngeal secretions that pool around the endotracheal tube cuff are a major cause of VAP. Furthermore, the supine position leads to microaspiration of gastric contents and increased incidence of VAP. Based on these observations, Drakulovik and colleagues (1999) suggested that the head should be elevated (~30 degrees) unless contraindicated. Alterations in gastric pH due to illness, medications, or enteric feeds predispose the patient to development of VAP. Elevated gastric pH allows abnormal polymicrobial colonization of the gastric fluid. A randomized controlled trial comparing three strategies for stress ulcer prophylaxis and incidence of VAP showed that the rate of VAP was lower in the group of patients treated with sucralfate. Even in those patients wit3 a gastric pH greater than 4, sucralfate was associated with a decreased incidence of VAP when compared with other regimens, leading Prod'hom and co-workers (1994) to conclude that sucralfate may possess intrinsic antimicrobial activity.
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Fig. 40-7. (A)Relationship between alveolar, central airway, and ventilator circuit pressure under normal conditions; (B)in the presence of a severe dynamic airway obstruction, with expiratory port open; (C)and in the presence of severe dynamic airflow obstruction, with the expiratory port occluded. Self-controlled positive end-expiratory pressure (auto-PEEP) is identified by creating an end-expiratory hold, allowing alveolar, central, and ventilatory pressures to equilibrate. Note that during expiratory hold, following equilibration, auto-PEEP is read on the system manometer. From Pepe PE, Marini JJ: Occult positive end-expiratory pressure in mechanically ventilated patients with airflow obstruction: the auto-PEEP effect. Am Rev Respir Dis 126:166, 1982. With permission. |
Table 40-7. Steps for Reducing Dynamic Hyperinflation and Self-Controlled Positive End-Expiratory Pressure (auto-PEEP) | ||
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Multiple other risk factors exist for VAP. Craven and colleagues (1984), as well as Craven and Steger (1989), demonstrated that the ventilator circuit is usually contaminated by organisms commensal to the patient and is a common cause of VAP. However, frequent changes of ventilator tubing and reintubation are associated with an increased risk for VAP. Tablan and coinvestigators (1994) wrote that the CDC currently recommends that ventilator tubing be changed no more frequently than every 48 hours, whereas some investigators suggest that weekly or less frequent changes are advisable.
Ventilator-associated pneumonia reflects the vulnerability of critically ill patients to their own oropharyngeal and gut organisms, and to infection spread by improper hand washing and other physical contact. Pierson (1999) showed that prophylactic antimicrobial agents administered systemically are ineffective in preventing pneumonia and can promote infection with resistant organisms. Topical oropharyngeal agents and systemic antibiotics have gained popularity, but have not yet been sufficiently validated to warrant widespread use. Several strategies that have demonstrated efficacy in reducing the incidence of VAP include infection surveillance, strict hand-washing protocols, elevating the head of the bed, continuous suctioning of supraglottic secretions, and noninvasive ventilation.
Deteriorating Oxygenation in the Ventilated Patient
Deteriorating oxygenation during mechanical ventilation should initiate a systematic search for specific causes rather than simply increases in inspired oxygen fraction or PEEP. Glauser and colleagues (1988) described that the possible causes for worsening oxygenation fall into several categories. The problem could be with the ventilator and its circuitry. The patient's primary disease process could be worsening, or a new medical problem may have developed, including pneumothorax, acute lobar atelectasis, pulmonary edema from fluid overload, nosocomial pneumonia, sepsis, aspiration of gastric contents, retained secretions, or bronchospasm. A decline in cardiac output can also cause worsening oxygenation in a patient with significant intrapulmonary right-to-left shunt. Interventions and procedures, including the effects of airway sectioning, chest physical therapy, or changes in body position, can also lead to a decline in oxygenation, especially in patients with heterogeneously distributed pulmonary involvement. Bronchoscopy, thoracentesis, and hemodialysis can also lead to a decline in oxygenation. Finally, a number of drugs administered to patients undergoing mechanical ventilation can interfere with arterial oxygenation, such as vasodilators (which can increase right-to-left shunt), -blockers (which can depress cardiac output and induce bronchospasm), and bronchodilators (which can alter [V with dot above]/[Q with dot above] ratios).
Ventilator-Associated Lung Injury
Barotrauma
Pierson (1988, 1998) noted that the term barotrauma currently applies both to extraalveolar air (classical barotrauma) and parenchymal lung damage that may be caused by ventilatory support. Figure 40-8 demonstrates that the clinical manifestations of extraalveolar air encountered during ventilatory support are pneumothorax, pneumomediastinum, and subcutaneous emphysema, any of which can
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indicate a potential tension pneumothorax. Air embolism also can occur during mechanical ventilation, but is uncommon. These forms of barotrauma generally result from alveolar rupture into the interstitium of an adjacent bronchovascular sheath, with subsequent dissection to the mediastinum or pleura. Direct alveolar rupture into the pleural space most commonly results from direct puncture of the visceral pleura during central line placement or other procedures. Barotrauma is more likely to occur in the presence of pulmonary hyperinflation, which may develop in obstructive lung disease, a unilateral or localized process such as lobar pneumonia or atelectasis, or when a diffuse acute pathologic process is unevenly distributed, as is typical in ARDS. Animal studies by Dreyfuss and associates (1988) showed that high airway pressures without concomitantly increased inflation volume did not result in alveolar rupture. Conversely, high inflation volumes produced parenchymal lung injury even when pulmonary pressures were zero. Despite the evidence that volume, rather than pressure, is responsible for alveolar rupture, Gammon and co-workers W(1995) challenged that no controlled study has shown that barotrauma is more frequent with the use of volume-targeted rather than pressure-targeted ventilation in humans. Pierson (1988) noted that barotrauma or pneumothorax is more likely when tidal volumes of greater than 12 mL/kg or high levels of PEEP are used. In a retrospective analysis of 718 patients from the ARDS Network trial, high levels of PEEP were associated with increased risk for barotrauma. However, Eisner and colleagues (2002) showed that mean airway pressure, plateau pressure, and driving pressure (plateau pressure minus PEEP) were not predictive of subsequent barotrauma.
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Fig. 40-8. Pathogenesis of the various clinical manifestations of extraalveolar air flowing alveolar rupture during mechanical ventilation. From Pierson DJ: Complications associated with mechanical ventilation. Crit Care Clin 6:771, 1990, With permission. |
Volutrauma
Over the past decade, there has been a reevaluation of the paradigm of maintaining normocapnia in mechanically ventilated patients. Bendixen and collaborators noted in 1963 that traditional ventilatory support for respiratory failure utilized volume-controlled mechanical ventilation using supraphysiologic tidal volumes (10 to 15 mL/kg), because high lung volumes minimized atelectasis and prevented deterioration in oxygenation in patients undergoing anesthesia. This strategy often required high airway pressures to deliver these volumes and maintain normocapnia in patients with severe lung injury. In fact, the original description of ARDS by Ashbaugh and associates (1967) included high inspiratory ventilator pressures as part of the definition. Considerable animal and human data suggest that the conventional tidal volumes of 10 to 15 mL/kg are associated with alveolar overdistention, leading to volutrauma and ventilator-associated lung injury. Webb and Tierney (1974) were the first investigators to recognize ventilator-induced parenchymal lung injury as separate from the previously recognized
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forms of barotrauma. Rats ventilated at high airway pressures (45 cm H2O) developed alveolar edema, hypoxemia, and decreased lung compliance, with death occurring within 1 hour. They theorized that the interstitial edema was from pulmonary interdependence and that the alveolar edema was from depletion or inactivation of surfactant. Dreyfuss and colleagues (1988) likewise showed that application of high inflation pressure ventilation in rats resulted in a high permeability edema of the lung after only 20 minutes, with histologic findings similar to those seen in human ARDS. To discern whether high alveolar pressure or alveolar overdistention was the causative factor in the observed pulmonary edema, they subjected rats to five ventilatory modes: (a) control group (low pressure low volume positive pressure ventilation), (b) high pressure high volume (HiP-LoV) group, (c) high pressure low volume group achieved by thoracoabdominal strapping, (d) low pressure high volume group achieved by iron lung ventilation, and (e) high pressure high volume group with 10 cm H2O PEEP added. No significant difference between the control and the HiP-LoV group was seen. However, the lungs from the groups ventilated with high volumes developed severe high permeability edema, regardless of whether positive or negative pressure was the generating force. This study strongly suggested that alveolar overdistention was more important in ventilator-associated lung injury than high alveolar pressure. Hernandez and co-workers (1989) similarly found that chest wall restriction limited high airway pressure induced lung injury in immature rabbits. Tsuno and coinvestigators (1990) analyzed the histopathologic changes in baby pig lungs after mechanical ventilation at high peak airway pressures. After ventilation at a PIP of 40 cm H2O for 22 11 hours, one group of pigs was killed and the lungs examined. Alveolar hemorrhage, alveolar neutrophil infiltration, alveolar macrophage and type II pneumocyte proliferation, interstitial congestion and thickening, interstitial lymphocyte infiltration, emphysematous change, and hyaline membrane formation were noted. Bachofen and Weibel (1982), Tomashefski (1990), and Croce and associates (1999) showed that similar histopathologic changes appear in the early stages of ARDS. Another group of pigs continued on mechanical ventilation for an additional 3 to 6 days using conventional ventilatory parameters (VT 15 mL/kg; PIP 30 cm H2O; Paco2 40 mm Hg), and developed prominent organized alveolar exudates consistent with late ARDS. Dreyfuss and colleagues (1988) presented a control group ventilated at a PIP of 18 cm H2O that showed no histopathologic change in the lung. These results suggest a clear association between alveolar overdistention and lung injury similar to that seen in ARDS. However, the exact mechanism of injury remains unclear.
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Fig. 40-9. The interface between collapsed and consolidated lung (A) and overdistended lung units (B) is heterogeneous and unstable. This region is prone to cyclic recruitment and derecruitment with asymmetric stretch of the lung units (C) immediately apposed to regions of collapsed lung. From Pinhu L, et al: Ventilator-associated lung injury. Lancet 361:332, 2003. With permission. |
Atelectotrauma
Adjacent alveoli share walls such that the forces acting on one are transmitted to all. In healthy lung, alveoli expand uniformly with similar transalveolar pressures. In ARDS, a heterogeneous distribution of consolidation (Fig. 40-9) results in alveolar collapse and overdistended lung units result in traction forces at the interface between collapsed and overdistended lung parenchyma. In addition to
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lung injury induced by overdistention of alveoli, lung injury also results from the repeated cycles of alveolar opening (recruitment) and closing (derecruitment) that occur with each ventilator breath (atelectotrauma). However, PEEP has been associated with a reduction in ventilator-induced lung injury, probably because it interrupts this cycle. In animal models, lung injury was more severe in those animals ventilated without PEEP, leading Dreyfuss and associates (1988) to suggest that forces generated by repeated recruitment and derecruitment of lung units may be responsible for parenchymal damage. Hudson (1998) proposed that PEEP acting as a pneumatic stent prevents alveolar collapse at end expiration and minimizes the shear forces associated with repeated opening and closing of collapsed alveolar units.
Biotrauma
In patients with ARDS, Artigas (2002) noted that the histopathologic severity of lung injury is not predictive of outcome. However, multiple studies have shown improved survival in those ARDS patients receiving a lung protective ventilation strategy. Ranieri and co-workers (1999, 2000) found that concentrations of plasma and bronchoalveolar cytokines are significantly lower in patients receiving a protective ventilation strategy as compared with those receiving conventional mechanical ventilation. Patients ventilated with low tidal volumes also had significantly less organ dysfunction than the group receiving conventional mechanical ventilation. Similarly, the ARDS Network (2000) study demonstrated lower plasma concentrations of interleukin-6 in a group of patients treated with protective ventilation. Figure 40-10 demonstrates these findings, suggesting that mechanical ventilation may induce a systemic inflammatory response that may contribute to and exacerbate lung injury and multiorgan failure, and may be associated with poorer outcomes.
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Fig. 40-10. Ventilated patients are susceptible to pneumonia and lung injury (VALI). Inflammatory mediators generated in the lung are released into the systemic circulation causing generalized inflammation (SIRS). Patients with adult respiratory distress syndrome are at high risk for pneumothorax and pneumomediastinum. High intrathoracic pressure can contribute to poor organ perfusion and oxygen delivery (DO2) by decreasing cardiac output (CO). From Pinhu L, et al: Ventilator-associated lung injury. Lancet 361:332, 2003. With permission. |
NONINVASIVE POSITIVE-PRESSURE VENTILATION
Mask CPAP therapy for obstructive sleep apnea was the springboard for the development of NIPPV for patients with chronic ventilatory failure. NIPPV was first applied to patients with neuromuscular disorders and chest wall disease, but has been successfully used in patients with COPD. More recently, the attendees of the International Consensus Conference on Non-invasive Mechanical Ventilation (2000) extended the indications for NIPPV as a safe and effective means of ventilatory support in acute respiratory failure of diverse etiology to include asthma, pulmonary edema secondary to congestive heart failure, and pneumonia.
NIPPV provides a ventilator-assisted breath without the need for tracheal intubation. Positive pressure, with or without PEEP, is transmitted to the airways via a nasal mask or face mask, with exhalation achieved by passive lung recoil. The success of NIPPV is dependent on the patient's ability to cooperate, synchronize breathing with the ventilator, clear secretions, and protect the airway. Although readily achieved in the conscious, cooperative patient, problems arise in uncooperative, obtunded, or sleeping patients. Hypercapnic COPD patients with lethargy caused by narcosis are a possible exception. Mental status in most hypercapnic COPD patients is expected to improve within 15 to 30 minutes of initiation of NIPPV. However, patients must be closely monitored for deterioration or worsening gas exchange.
NIPPV can avoid intubation in selected COPD patients, with most series reporting success rates of 60% to 80%. In a randomized controlled trial, Kramer and co-workers (1995) showed a reduction in the percentage of patients requiring intubation from 73% in the control group to 26% in the NIPPV group. In the subset of patients with COPD, the intubation rate decreased from 67% in the control group to 9% in patients treated with NIPPV. In a trial of 85 patients
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with acute respiratory failure secondary to COPD, Brochard and co-workers (1995) found an almost identical reduction in intubation rates (74% in controls to 24% in NIPPV; p <0.001). Patients treated with NIPPV also benefited from a lower complication rate, shorter duration of hospital stay, and lower mortality rate.
Patients requiring invasive mechanical ventilation for severe exacerbations of COPD frequently undergo prolonged mechanical ventilation and protracted weaning protocols. Based on evidence from randomized controlled trials and observational studies by Nava (1998) and Girault (1999) and their associates, NIPPV is now widely accepted as a first-line intervention in patients presenting with COPD exacerbation that does not require emergent intubation. However, experience with NIPPV as an adjunct to weaning is sparse and data to support extubation to NIPPV in weaning protocols for other forms of acute respiratory failure according to Keenan and colleagues (2002) are currently lacking. Wide acceptance of the routine use of NIPPV in place of conventional weaning protocols depends on the demonstration that outcome variables, such as time on the ventilator, morbidity, mortality, and lengths of ICU and hospital stays, are improved by NIPPV.
Studies of the efficacy of NIPPV by Antonelli and colleagues (1998) and Antonelli and Conti (2000), as well as by Martin and co-workers (2000) in patients with acute respiratory failure from causes other than COPD have shown similar trends toward decreased ventilator days, duration of ICU stay, and decreased incidence of nosocomial pneumonia. However, studies by Kramer (1995), Wysocki (1995), Antonelli (1998), and Confalonieri (1999) and their associates showed that patients with hypoxemic respiratory failure, such as that caused by severe pneumonia or ARDS, fared worse than those with hypercapnia requiring invasive ventilation more frequently than the subset of patients with hypercapnic respiratory failure. Benhamou (1992), Meduri (1994), and Masip (2000) and their colleagues, as well as Mehta and Hill (2001), found subgroups of patients with hypoxic respiratory failure who may benefit from NIPPV, including patients with acute pulmonary edema and asthma exacerbations, postoperative patients with brief deteriorations following extubation, and those with acute respiratory failure who decline intubation. According to Hill (1993, 1999) and Meyer and Hill (1994), patient selection is crucial in the use of NIPPV in acute respiratory failure. Table 40-8 shows the indications and Table 40-9 the contraindications for NIPPV. In addition to those requiring immediate intubation, patients with compromised upper airway function should be excluded according to Hill (1999), such as those at risk for aspiration due to swallowing dysfunction and those unable to clear secretions due to excessive production or impaired cough. Patients with unstable medical conditions, such as shock, uncontrolled arrhythmias, acute cardiac ischemia, or uncontrolled gastrointestinal bleeding, should be treated using invasive positive pressure ventilation (IPPV). Patients with anatomic abnormalities or injuries that interfere with interface fitting are also poor candidates for NIPPV. In addition, uncooperative, agitated patients who are continually removing the mask cannot benefit from NIPPV. More severe forms of respiratory failure that will require prolonged periods of ventilatory support, such as severe status asthmaticus, complicated pneumonias, or ARDS, should also be managed using invasive PPV.
Table 40-8. Characteristics of Patients Successfully Treated with Noninvasive Positive-Pressure Ventilation | ||
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Technique
Hill (1999) noted that a well-fitting and comfortable nasal mask or full face mask is crucial to the success of NIPPV. Success rates of studies using different masks are
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comparable, so mask selection depends mainly on practitioner and patient preference. Nasal masks have the advantage of leaving the mouth uncovered, allowing for speech and eating during use, and perhaps enhancing patient tolerance. However, air leak through the mouth is common during nasal ventilation, a problem that may be alleviated by switching to full face masks. Air leaking can also occur with the full face mask, if there is an inadequate seal over the chin.
Table 40-9. Contraindications to Noninvasive Positive Pressure Ventilation | ||
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Ventilator Selection
Standard critical care ventilators may be adapted to deliver NIPPV in either the pressure support or volume control modes. Confalonieri (1994) and Kramer (1995) and their associates note that portable pressure support devices have seen increasing use in the acute setting. These ventilators are compact, highly portable, and less costly than standard critical care ventilators. They cycle between high inspiratory positive airway pressure (IPAP) and the lower expiratory positive airway pressure (EPAP) settings as determined by a sensitive flow triggering or time cycling, closely resembling pressure support modes on standard ventilators. However, these devices deliver lower maximal pressures (20 to 30 cm H2O) and have less sophisticated alarms than standard critical care ventilators, and should only be used in more stable patients in closely monitored settings.
Settings
Low initial pressures facilitate patient acceptance of NIPPV. Typical starting pressure support settings are 4 to 10 cm H2O and PEEP of 2 to 4 cm H2O (8 to 12 cm H2O for IPAP and 2 to 4 cm H2O for EPAP). For volume ventilation, initial tidal volumes range from 8 to 10 mL/kg. The ventilator is set in the spontaneous tidal volume (S/T) or VACV mode to allow patient triggering. Oxygen cannula inspiratory flow is titrated to maintain the desired oxygen saturation. The patient is then coached to relax and let the device assist breathing. As patients adapt, the IPAP or tidal volume is gradually increased to obtain the largest exhaled tidal volume (>7 mL/kg), a respiratory rate of less than 25 breaths/min, and patient comfort. The invitees to the ACCP-sponsored International Consensus Conferences in Intensive Care Medicine (2001b) stated that EPAP can be increased if oxygenation remains inadequate. Meduri (1991) and Soo Hoo (1994) and their collaborators noted that successfully managed patients rapidly synchronize their breathing with the device and have a reduction in respiratory rate, heart rate, and Paco2 within the first few hours of initiation. Roughly half of NIPPV studies used pressure-limited ventilation while the other half used volume-controlled ventilatory modes via nasal or full face masks. In comparison studies, Vitacca and coinvestigators (1993) found that PSV was as effective as assist-controlled ventilation in reducing the work of breathing and improving gas exchange but was better tolerated. In a direct comparison of the two modes, Vitacca and associates (1993) found similar success rates, but higher comfort ratings and lower complication rates among patients using the pressure support mode.
Problems
In properly selected patients, NIPPV is safe and well tolerated. As many as 10% to 25% of patients fail to tolerate the nasal mask or face mask despite adjustments in strap tension, repositioning, and trials of different sizes and types of interfaces. Some air leaking through the mouth with nasal masks or around the face mask is inevitable. Pressure support type devices compensate for air leaks by maintaining inspiratory airflow during leaking; tidal volumes on volume-limited ventilators are increased to compensate. To reduce air leaking through the mouth, patients are coached to keep the mouth closed. Also, chin straps or full-face masks may be used. Soo Hoo and associates (1994) found that patients who fail NIPPV have larger mouth leaks than those who succeed. Erythema, pain, or ulceration on the bridge of the nose related to nasal mask pressure is commonly encountered, but minimizing strap tension and using artificial skins can ameliorate these irritations. Patients may also complain of excessive air pressure leading to ear or sinus pain, or dryness or irritation of the eyes or mouth related to air leaking. Pneumothoraces and painful gastric insufflation are unusual, probably because inflation pressures are low compared with those used with invasive ventilation. Likewise, barotrauma or adverse hemodynamic effects caused by NIPPV are unusual. Lack of patient cooperation interferes with efficacy, and may be ameliorated by judicious use of sedation, such as low doses of benzodiazepines. Unremitting agitation should be considered an indication for intubation. Aspiration has been reported by Meduri and co-workers (1991), but should be unusual if patients with swallowing dysfunction and those patients who have problems clearing secretions are excluded. Progressive hypoventilation occurs in a small minority of patients, usually necessitating intubation.
ALTERNATIVE MEANS OF RESPIRATORY SUPPORT
Due to the morbidity associated with ventilatory support in patients with severe respiratory failure, there has been an increased impetus for developing alternative means of providing respiratory support, allowing lung rest and presumably facilitating lung healing. Slutsky (1985), Kolobow (1988), and Bartlett (1990), as well as Lewandowski (1992) and Pesenti (1997) and their colleagues, and Alpard and one of us (JBZ) (1998) and one of us (JBZ) and associates (1999)
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all used the premise that oxygenator technology for partial or total gas exchange (O2 or CO2), with or without cardiac support accomplishes lung rest that facilitates repair and avoids the barotrauma or volutrauma of ventilator management. The basic technique involves a permeable membrane gas exchanger, either extracorporeal or intracorporeal, with or with the use of a pump. Large vessel cannulation is typically needed in patients with extracorporeal support. The circuit orientation can be venovenous; venoarterial, as with extracorporeal membrane oxygenation (ECMO); or arteriovenous, as with arteriovenous CO2 removal (AVCO2R).
Extracorporeal membrane oxygenation, a modification of cardiopulmonary bypass, decreases the mortality of neonatal respiratory distress syndrome and is capable of total gas exchange. Kolla (1997) and Lewandowski (1997) and their collaborators demonstrated that adult ECMO has demonstrated improved survival in selected patients. Tracy and co-workers (1995) reported that the Extracorporeal Life Support Organization database on all adults with severe respiratory failure demonstrated a cumulative short-term survival rate of 47%.
Gattinoni (1978) and Kolobow (1978) and their associates introduced the use of extracorporeal CO2 removal (ECCO2R) in both animals and humans, where the focus was on CO2 removal to facilitate reduction in ventilatory support. CO2 removal was accomplished via extracorporeal circulation through the membrane lung, while oxygenation was maintained by simple diffusion or apneic oxygenation as O2 was supplied via constant flow to alveoli maintained with PEEP. Gattinoni and colleagues (1986) demonstrated a decrease in mortality in patients managed with ECCO2R and low-frequency, pressure-limited ventilation. Morris and colleagues (1994), however, compared conventional ventilation with PC-IRV, with or without ECCO2R in 40 ARDS patients. No significant difference in survival was found between groups, with rates of 42% and 33%, respectively. Of note, the majority of patients were hypercapnic on randomization, and although mean peak airway pressures were significantly lower in the new therapy group, they remained elevated (57.8 vs. 49.5 cm H2O). The improvement in survival seen with current techniques of venovenous and venoarterial ECMO and ECCO2R like those reported by Lewandowski and associates (1997) have since been duplicated at various centers worldwide with an overall survival rate of 46% in patients thought to have 90% mortality rate.
As an alternative to the complexities of extracorporeal devices, Mortensen and Berry (1989) proposed the use of an intravenous gas exchange device in patients with acute respiratory failure. The IVOX intravenacaval gas exchange device developed by Cardiopulmonics Inc. (Salt Lake City, UT, U.S.A.) consists of multiple hollow fibers that are positioned under fluoroscopy into the vena cava via a surgical venotomy in the common femoral vein. Oxygen is drawn through the lumen of each hollow fiber at subatmospheric pressure to prevent gas embolism, and gas exchange with free-flowing venous blood takes place across the fiber wall. Available in membrane surface areas from 0.21 to 0.52 m2, one of us (JBZ) and colleagues (1994) anticipated that IVOX would result in clinically significant improvement in gas exchange with fewer complications than those associated with extracorporeal circuits. Clinical studies reported by Conrad and co-workers (1994) demonstrated transfer rates for O2 and CO2 of 40 to 70 mL/min, or approximately 25% to 30% of metabolic demand. Based on measurements of CO2 transfer by different sizes of IVOX in an ovine model, Tao and colleagues (1996) have calculated that the membrane surface area required to excrete 150 mL/min CO2 with a vena cava blood flow of 4 L/min at normocapnia (Paco2= 40 mm Hg) is approximately 1.8 m2, considerably greater than the largest size (size 10) IVOX (0.52 m2). One of us (AB) and associates (1996) found that high levels of hypercapnia (Paco2 = 100 mm Hg) can reduce the required surface area by 80% to 0.49 m2. Permissive hypercapnia and active blood mixing have been incorporated in other intracorporeal devices, such as the intravenous membrane oxygenator designed by the University of Pittsburgh group and reported by Federspiel and colleagues W(1997).
AVCO2R is achieved with a simple percutaneous arteriovenous shunt that eliminates a substantial portion of ECMO-related components, reducing the extent of exposure to foreign surfaces and eliminating the pump. The procedure described by Awad (1991), Young (1992), and Brunston (1996, 1997) and their collaborators involves cannulation of the femoral artery and vein, with a membrane oxygenator interposed in the circuit. Blood flows spontaneously through the oxygenator because of the pressure gradient between the artery and vein. The circuit is essentially identical to that used for continuous arteriovenous hemofiltration. The difference is the use of a gas exchange device (membrane oxygenator) in place of a hemofilter, and a larger arterial cannula (approximately 12F) to accommodate blood flows of about 1 L. There are many theoretical advantages to this approach over venovenous ECCO2R. The first is the use of a small, highly efficient, low-resistance fiber membrane oxygenator, allowing the use of a much smaller priming volume (<300 mL). Using a mathematical model, Conrad and co-workers (1998) found that shunt flows of 10% to 15% of the cardiac output can support total CO2 removal at levels of Paco2 that are physiologically tolerable. In a sheep model of smoke inhalation injury, one of us (JBZ) and associates (1999) noted that AVCO2R facilitated significant reductions in ventilator settings without compromising systemic Pao2 or Paco2, while removing 96% of CO2 metabolic production. AVCO2R is currently undergoing clinical trials.
MONITORING OF PATIENTS RECEIVING VENTILATORY ASSISTANCE
Close monitoring of airway mechanics and gas exchange as described by Rossi and co-workers (1998) is necessary
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to evaluate the physiologic state of the patient, as well as the need and nature of interventions to correct either inadequate gas exchange or abnormalities in airway mechanics. Secondarily, these measurements provide insight into the pathophysiology of the patient's illness.
Basic Concepts in Airway Mechanics
Under static conditions in intubated, completely relaxed patients, Hess and Kacmarek (1996) and Alex and Tobin (1999) noted that airway pressure is equal to the elastic recoil pressure (lung + chest wall) of the respiratory system. It is important to recognize that the chest wall includes the rib cage and the diaphragm. The pressure required to inflate the lung by a certain volume ( V) is the corresponding change in transpulmonary pressure ( PL= Palv Ppl, where Palv is the alveolar pressure and Ppl is the pleural pressure). Lung compliance (CL), the inverse of lung elastance (EL), is defined as the pressure required to change the lung volume (CL = V/ PL). Under passive conditions, the pressure required to simultaneously distend the chest wall by the same V is given by the average change in intrathoracic pressure (~, PL). The compliance of the relaxed chest wall is given by CW = V/ Ppl. The lung and chest wall are arranged in series, and thus the pressure required to distend the respiratory system may be expressed in terms of an overall elastance of the respiratory system (ERS = EL + ECW). Expressed in terms of the compliance of the respiratory system (CRS), 1/CRS= 1/CL+1/CCWor CRS = (CL)(CW)/ (CL+CW).
Based on this equation, changes in the elastance of the chest wall can have independent and significant effects on the compliance of the respiratory system. Alex and Tobin (1999) noted that the lung and chest wall display different pressure-volume relationships. The overall pressure-volume relationship of the overall respiratory system is sigmoid in shape (see Fig. 40-5), and overall compliance (CRS) is greatest over the midvolume change. At both extremes of lung volumes, CRS is low because the pressure-volume curve of the lung becomes flat as the lung gets fully inflated, or the pressure-volume curve of the chest wall becomes flat as the thoracic volume is reduced. High lung volumes can occur during mechanical ventilation as a result of large tidal volumes, dynamic hyperinflation, or inappropriately high levels of PEEP. Hess and Kacmarek (1996) show that at low lung volumes, reduced CRS may be secondary to obesity or abdominal distention (Table 40-10).
Table 40-10. Causes of Decreased Compliance and Increased Airway Resistance in Patients Receiving Ventilatory Assistance | ||||||||||||||||||
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In 1990, Tobin found that the slope of the pressure-volume curve of the respiratory system may be altered by abnormalities in either the lung or the chestwall. Elastic recoil of the lung is decreased in emphysema (increased CL), while lung recoil is increased with pulmonary edema or interstitial fibrosis (decreased CL). Increased stiffness of the chest wall (decreased CCW) can be seen in patients with kyphoscoliosis, obesity, or massive ascites. Lung compliance also depends on the number of alveolar units available to accept the tidal volume. As the chest expands, the number of recruited alveolar units tend to increase, increasing CRS. The reverse phenomenon, derecruitment, demonstrated in Fig. 40-5, occurs during tidal lung deflation, producing hysteresis of the static pressure-volume curve of the respiratory system.
Airway Pressure
The time course of the airway pressure depends on the inspiratory flow pattern. If a constant flow pattern is chosen, there will be a linear increase in airway pressure during inspiration. With a decelerating inspiratory flow pattern, the inspiratory pressure waveform will be convex. The PIP varies directly with inspiratory airway resistance, end-inspiratory flow, tidal volume, PEEP, and respiratory system compliance. Depending on the inspiratory flow waveform, Tobin (1990) and Alex and Tobin (1999) noted that PIP may not occur at end inspiration. Typical airway pressure waveforms during mechanical ventilation are shown in Figs. 40-2 and 40-3.
Alex and Tobin (1999) stated that an end-inspiratory pause of 0.5 to 2 seconds allows equilibration between proximal airway pressure and alveolar pressure. During the end-inspiratory pause, there is no flow, and a pressure plateau develops as proximal airway pressure equilibrates with alveolar pressure. The proximal airway pressure during the inspiratory pressure shown in Fig. 40-11 is referred to as plateau pressure and represents peak alveolar pressure. The difference between PIP and peak alveolar pressure is due to the inspiratory resistance of the respiratory system (airway resistance + endotracheal tube resistance), and the difference between peak alveolar pressure and total PEEP is due to the elastic properties of the respiratory system (i.e., lung + chest wall compliance).
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During pressure-targeted ventilation, Hess and Kacmarek (1996) showed that PIP and peak alveolar pressure may be equal. With pressure-targeted ventilation, inspiratory flow decreases during inspiration and is often followed by a period of zero flow at end-inspiration. During this period of no flow, proximal airway pressure should equal peak alveolar pressure (see Fig. 40-11). Based on the above considerations, PIP should be lower during pressure-targeted ventilation than during volume-targeted ventilation. With volume-targeted ventilation, PIP will be greater than peak alveolar pressure due to the presence of end-inspiratory flow. With pressure-targeted ventilation, PIP will equal alveolar pressure if end-inspiratory flow is zero. With all factors held constant (e.g., tidal volume, lung impedance, PEEP), peak alveolar pressure is identical for volume-targeted and pressure-targeted ventilation.
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Fig. 40-11. Relationship between tidal volume and airway pressure in a patient receiving mechanical ventilation. The inspiratory plateau in the volume tracing is achieved by using inspiratory hold or by occluding the expiratory port long enough (1 to 2 seconds) to allow airway pressure to reach a constant value. This pressure is referred to as the plateau pressure and represents the elastic recoil pressure of the total respiratory system at end-inflation volume. PEEP, positive end-expiratory pressure. From Tobin MJ, Danzker DR: Ventilatory support: who, when, how? In Miller TA (ed): Physiological Basis of Modern Surgical Care. St. Louis: Mosby-Year Book, 1988. With permission. |
Static Compliance
According to Hess and Kacmarek (1996) and Alex and Tobin (1999), the difference between plateau pressure (Pplat) and total PEEP [(PEEP)tot] is determined by the combined static compliance of the lung and chest wall. The static compliance can be calculated from CRS= VT/[Pplat (PEEP)tot], where (PEEP)tot includes any auto-PEEP that is present. The tidal volume is the actual tidal volume delivered to the patient and should be corrected for the effects of volume compressed in the circuit. Tobin (1990) posited that Pplat should be determined from an end-inspiratory pause in a relaxed or sedated patient (i.e., the patient should not have any active inspiratory effort) that is long enough to produce equilibration between proximal airway pressure and alveolar pressure. Alterations in overall respiratory system compliance (Fig. 40-12) result in changes in the slope of the pressure-versus-volume curve.
Airway Resistance
Hess and Kacmarek (1996) reported that the difference between PIP and Pplat is determined by inspiratory resistance and end-inspiratory flow. During constant-flow volume-targeted ventilation, inspiratory resistance (RI) can be approximated by RI = (PIP Pplat)/VI, where VI is the inspiratory flow. Expiratory resistance may be approximated by RE= [Pplat (PEEP)tot]/VEmax, where VEmax is the peak expiratory flow. Inspiratory resistance is typically smaller than the expiratory resistance, because of the increased airway diameter during inspiration and the added impedance of the endotracheal tube. Some causes of increased airway resistance are listed in Table 40-10. During mechanical ventilation, MacIntyre and Grooper (1995) and Marini (1998) noted that the resistance of the endotracheal tube (Ret) in series with the resistance of the respiratory system (RRS) is implicitly included in the measured overall resistance (Rtot) (during both inspiration and expiration), such that RRS= Rtot Ret. The effect of increased airway resistance on the pressure-versus-volume curve is shown in Fig. 40-13.
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Fig. 40-12. Pressure-volume loop during passive mechanical ventilation. The slope of the line connecting the points-of-zero flow at the beginning of inspiration to the point-of-zero flow at the beginning of expiration represents the lung plus chest wall compliance. A shift of the pressure-volume loop to the right represents a decrease in lung compliance. From Hess DR, Kacmarek RM (eds): Essentials of Mechanical Ventilation. New York: McGraw-Hill, 1996. With permission. |
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Fig. 40-13. The area under the dynamic pressure-volume loop is a measure of the resistive work. An increase in airway resistance causes an increase in the area within the pressure-volume loop. From Hess DR, Kacmarek RM (eds): Essentials of Mechanical Ventilation. New York: McGraw-Hill, 1996. With permission. |
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Mean Airway Pressure
Many of the beneficial and deleterious effects of mechanical ventilation are a function of the mean airway pressure. Factors affecting mean airway pressure according to Hess and Kacmarek (1996) are PIP, PEEP, I:E ratio, respiratory rate, and the inspiratory pressure waveform. Increments in inspiratory time cause an increase in airway pressure, whereas an increase in expiratory time reduces airway pressure.
Waveform Analysis: Flow-Volume and Pressure-Volume Loops
Bardoczky and d'Hollander (1992) and Rahoof and Khan (1998), as well as Waugh (1999) and Henning (1977) and their associates, described the difference between pressure-versus-time and flow-versus-time waveforms (see Figs 40-2 and 40-3) and the pressure-versus-volume and flow-versus-volume loops for mechanically ventilated breaths (Figs. 40-12, 40-13, 40-14 40-15). The presence of a lower inflection point on the pressure-versus-volume curve (see Fig. 40-5) in the early stages of inspiration implies alveolar recruitment and may be used to guide the use of PEEP. The presence of an upper deflection point may help to recognize alveolar overdistention (see Fig. 40-5). Changes in the slope of the line connecting points of zero flow on the pressure-volume loop (see Fig. 40-12) can provide a visual clue to a change in the overall respiratory system static compliance. The area under the dynamic pressure-volume loop (see Fig. 40-13) provides information on airway resistance. Flow-versus-volume loops (see Figs. 40-14 and 40-15) may be used to detect expiratory or inspiratory airflow obstruction, assess quantitative response to bronchodilators, and detect the presence of auto-PEEP. Additional monitoring packages are available on most ventilators which combine information obtained from an esophageal catheter (for estimation of
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pleural pressure) to produce breath-by-breath information on several aspects of respiratory mechanics, including the work of breathing, pressure time product, dynamic compliance, mean airway resistance and other measures of pulmonary mechanics.
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Fig. 40-14. Recognition of air trapping and self-controlled end-expiratory pressure (auto-PEEP) from the flow-volume loop during mechanical ventilation. In the presence of auto-PEEP, expiratory flow does not reach zero prior to the initiation of inspiratory flow. From Waugh JB, Deshpande VM, Harwood RJ: Rapid Interpretation of Ventilator Waveforms. Englewood Cliffs, NJ: Prentice-Hall, 1999. With permission. |
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Fig. 40-15. Idealized flow-volume loop during mechanical ventilation, before and after bronchodilator administration. Inspiratory flow is limited because of the fixed endotracheal tube resistance. Before bronchodilator administration, the expiratory flow versus exhaled-volume loop is biphasic or scooped owing to increased expiratory airflow resistance. Following bronchodilator administration, there is an increment in the peak expiratory flow as well as straightening of the expiratory flow loop, indicating improvement in expiratory airflow obstruction. From Bidani A, et al: Mechanical ventilatory assistance. In Pearson FG, et al (eds): Thoracic Surgery. Oxford: Churchill Livingston, 2002. With permission. |
Gas Exchange Indices
Arterial Oxygenation
The a/A ratio (Pao2/Pao2) is relatively stable with changes in inspired oxygen concentration and the level of alveolar ventilation, and as reported by Nelson (1993) and Wood and Hall (1993) is the preferred method of following the efficacy of arterial oxygenation in mechanically ventilated subjects. The Pac2 is estimated using the ideal alveolar gas equation: (Pac2 = [PB + Pplat PAH2O] Fio2 Paco2/RQ). Generally, the barometric pressure, PB, is assumed to be 760 mm Hg, Pplat ignored, the water vapor pressure (PAH2O) is assumed to be 47.0 mm Hg, and the respiratory quotient (RQ) assumed to be 0.8. Alternatively, the P/F ratio (Pao2/Fio2) may be used, since it is easier to calculate than the a/A ratio. The Pac2/Fio2 ratio is affected by changes in Paco2 but appears to correlate well with the extent of pulmonary shunt.
Oxygen Delivery Index
The oxygen delivery index (ODI) is calculated as follows: ODI = (CI)([O2]a), where CI is cardiac index and [O2]a is the arterial oxygen content.
Oxygen Utilization Coefficient
The oxygen utilization coefficient (OUC), also called O2 extraction ratio, is defined as follows: OUC = ([D with dot above]o2)/(CO [O2]a). OUC may be estimated from Sao2 (via pulse oximetry) and Svo2 (via mixed-venous blood oximetry), OUC = (Sao2 Svo2)/Sao2. This index quantitates the oxygen consumption relative to the peripheral oxygen delivery. According to Nelson (1993), OUC greater than 0.35 indicates an excessively high oxygen extraction to satisfy the patient's metabolic need.
Mixed Venous Oxyhemoglobin Saturation
Mixed venous blood oxyhemoglobin saturation (Svo2) reflects the relative balance between oxygen consumption ([D with dot above]o2) and peripheral oxygen delivery ([V with dot above]o2 = (CO) ([O2]a). It is defined as: Svo2 = 1 ([D with dot above]o2/[V with dot above]o2). The four primary determinants of Svo2 are Sao2, hemoglobin concentration (Hb), cardiac output, and oxygen consumption ([D with dot above]o2). Svo2 is a sensitive, but nonspecific, indicator of the imbalance between [D with dot above]o2 and [V with dot above]o2, affected more by low-extraction, high-flow tissues (such as the kidney) than by high-extraction low-flow vascular beds (such as the myocardium).
Intrapulmonary Shunt
The intrapulmonary shunt (QS/QT) fraction is estimated from a simplified two-compartment model in which part of the blood reaching the left side of the circulation is completely oxygenated by passage through ventilated lung units that are perfused (i.e., with [V with dot above]/[Q with dot above] = 1), and part of the blood is mixed venous blood that passes from the right side of the circulation to the left without exposure to ventilated alveoli (i.e., with [V with dot above]/[Q with dot above] = 0). Nelson (1993) estimated the shunt from the equation: QS/QT = ([O2]c [O2]a)/([O2]c [O2]v). Blood oxygen content is estimated from the general equation [O2] = 1.34 [Hb] So2. This calculation ignores the concentration of physically dissolved oxygen. End-capillary oxyhemoglobin saturation (Sco2) is assumed to be 100%. Arterial oxygen saturation is measured while the patient is transiently switched to 0.90 Fio2. Contrary to previous practice, 1.00 Fio2 is best avoided, because it tends to promote absorption atelectasis in very low [V with dot above]/[Q with dot above] units ([V with dot above]/[Q with dot above] <0.01). The intrapulmonary shunt fraction is the gold standard for clinical assessment of lung oxygenation function, but requires placement of a Swan-Ganz catheter for mixed venous oxyhemoglobin saturation determination.
Ventilation-Perfusion Index
The ventilation-perfusion index (VQI) as noted by Nelson (1993) is an approximation of QS/QT that can be performed on a continuous basis using combined arterial and mixed venous oximetry, and is calculated as VQI = (1 Sao2)/(1 Svo2). The VQI reflects QS/QT when arterial saturation is reduced. In the presence of high intrapulmonary shunts, Nelson (1993) showed that when Sao2 is less than 1, the VQI reasonably approximates QS/QT.
Dead Space Ventilation
Dead space ventilation (VD/VT) is that fraction of the minute ventilation that does not participate in alveolar gas exchange, and Nelson (1993) reported that it is a measure of the efficiency of ventilation. It may be estimated from the Bohr Equation, VD/VT = (Paco2 Peco2)/Paco2, based on the arterial blood Pco2 and mixed expired Pco2 (PeCO2). The collection of expired gas in a large collection bag to estimate mixed expired Pco2is laborious and requires meticulous attention to detail.
PRACTICAL GUIDELINES FOR VENTILATOR MANAGEMENT
Regardless of the specific issues associated with each of the following settings, the following general principles are
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important according to Tobin (2001) when providing ventilatory assistance: (a) limit plateau pressure (<30 to 35 cm H2O); (b) watch for and avoid the unintentional development of auto-PEEP; (c) limit tidal volumes to 6 to 8 mL/kg of ideal body weight; and (d) use the lowest Fio2 necessary to maintain arterial Po2 of 60 mm Hg. Some details of disease-specific ventilatory management are shown in Table 40-11.
Table 40-11. Recommended Ventilatory Settings | ||
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Routine Ventilatory Assistance
Many patients who require a period of invasive mechanical ventilation have relatively normal underlying lung function. What may be referred to as routine ventilatory support is encountered most frequently in the postoperative period or in the setting of short-term loss of spontaneous ventilation, such as with a drug overdose. In such
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settings, a volume-targeted mode, such as VACV, is simplest and most reliable, and usually requires fewer adjustments than pressure-targeted ventilation. According to Pierson (1999), 5 cm H2O of PEEP can counteract the modest decline in functional residual capacity that may occur with endotracheal intubation, although this is probably unnecessary in most patients.
Chronic Obstructive Pulmonary Disease
Decompensation in patients with COPD according to Schmidt and Hall (1989) is primarily caused by increased work of breathing. Tobin (1994) reports that signs of ventilatory muscle fatigue and weakness, such as rapid shallow breathing, use of accessory muscles, and abdominal paradox, are usually present. The most common problem is pulmonary hyperinflation present at baseline, which worsens during times of acute exacerbation. The three main goals of ventilatory support in patients who have acutely exacerbated COPD are to rest the ventilatory muscles, avoid further dynamic hyperinflation, and avoid acute alkalemia. NIPPV should be considered a first-line intervention in the early phases of acute exacerbation of COPD. Prospective, randomized studies by Bott (1993), Brochard (1995), Kramer (1995), Wysocki (1995), and Keenan (1997) and their coinvestigators demonstrated decreased rates of intubation in those COPD patients treated with NIPPV when compared with conventional care. Brochard (1995), Kramer (1995), and Wysocki (1995) and their colleagues, as well as Wunderink and Hill (1997), all reported decreases in mortality, ICU and hospital lengths of stay, and rates of nosocomial pneumonia. Potential predictors for success according to the International Consensus Conference on Non-invasive Mechanical Ventilation (2000) include moderate acidemia (pH >7.15 but <7.35) and moderate hypercarbia (Pco2 >45 but <95 mm Hg). Improvements in pH and Pco2 in the first one half to two hours as noted by Vitacca (1993), Soo Hoo (1994), and Meduri (1996) and their associates as well as by Kacmarek (1999) are often predictive of success. According to Anton and colleagues (2000), patients exhibiting agitation, altered mental status, inability to tolerate the mask, worsening hypoxia or hemodynamic instability should be considered to have failed NIPPV. The expedient implementation of invasive mechanical ventilation is crucial for those patients who fail NIPPV.
Because the majority of COPD patients are placed on mechanical ventilation after days or weeks of progressive deterioration, the goal is to rest both the patient and the respiratory muscles. Tidal volumes in the range of 5 to 8 mL/kg, rapid inspiratory flow (e.g., 80 to 100 L/min), and low respiratory rates serve to maximize expiratory time and avoid air trapping. Patients with COPD typically have an underlying compensated respiratory acidosis. Excessive ventilation risks not only dynamic hyperinflation with circulatory impairment and barotrauma but severe respiratory alkalosis.
Mechanical Ventilation of Patients with Severe Asthma
The most important factor in the decision to intubate a patient with asthma is not any absolute numerical value of Pao2, respiratory rate, or pulsus paradoxus, but is based on an overall clinical assessment of the patient's mental status, degree of respiratory distress, and hemodynamic stability. According to Tuxen (1996), mechanical ventilation of patients with severe asthma continues to be associated with high rates of morbidity (hypotension 23%, pulmonary barotrauma 12%) and mortality (overall 12%). Much of this morbidity and 20% to 35% of the mortality is probably from unrecognized or undertreated dynamic pulmonary hyperinflation (DHI), with auto-PEEP arising during mechanical ventilation. Darioli and Perret (1984) reported on several uncontrolled studies suggesting that controlled hypoventilation results in a lower mortality than conventional mechanical ventilation in patients with acute severe asthma who require ventilator support.
Current recommendations for mechanical ventilation include sedation, with or without transient initial paralysis, using an initial VT of 6 to 8 mL/kg, respiratory rate 10 to 12 breaths/min, and IFR (VI) of 60 L/min. Ventilation should then be adjusted based on DHI, and not Paco2. Excessive DHI may reduce venous return to the heart and impede cardiac output. Tuxen (1994) pointed out that any unexplained hypotension, apparent cardiac tamponade or electromechanical dissociation occurring during mechanical ventilation of a patient with severe airflow obstruction should first be evaluated by discontinuation of mechanical ventilation to allow deflation of the hyperinflated lungs and restoration of venous return before any other delaying or potentially harmful diagnostic or therapeutic procedures are attempted.
Acute Lung Injury/Adult Respiratory Distress Syndrome
Patients with ARDS have decreased pulmonary compliance, increased airways resistance, and increased dead space. Through the work of Hinson and Marini (1992), Bone (1993), Koleff and Schuster (1995), Pierson (1995), Schuster (1995), and Matthay (1996), our approach to mechanical ventilation of ARDS has changed as our understanding of ARDS has evolved. Previously, ARDS was viewed as a homogeneous disease in which alveolar compliance was uniformly decreased. The goal of mechanical ventilation was to deliver a normal tidal volume to each individual alveolus during inspiration and to prevent collapse of the alveolus during expiration. Thus, the approach was to use tidal volumes appropriate for normal patients (12 mL/kg)
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and to use PEEP to recruit collapsed alveoli and maintain alveolar expansion during expiration (Fig. 40-16). Because patients with ARDS have extremely low compliance at these tidal volumes, this approach resulted in extremely high inspiratory pressures. In addition, since dead space is markedly increased in ARDS, and patients frequently developed auto-PEEP as a consequence of high respiratory rates and inadequate time for exhalation.
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Fig. 40-16. Respiratory pressure-volume curve and the effects of traditional as compared with protective ventilation in a 70-kg patient with the acute respiratory distress syndrome. The lower and upper inflection points of the inspiratory pressure-volume curve (center panel) are at 14 and 26 cm of water, respectively. With conventional ventilation at a tidal volume of 12 mL per kilogram of body weight and zero end-expiratory pressure (left panel), alveoli collapse at the end of expiration. The generation of shear forces during the subsequent mechanical inflation may tear the alveolar lining, and attaining and end-inspiratory volume higher than the upper inflection point causes alveolar overdistention. With protective ventilation at a tidal volume of 6 mL per kilogram of body weight (right panel), the end-inspiratory volume remains below the upper inflection point; the addition of positive end-expiratory pressure at 2 cm of water above the lower inflection point may prevent alveolar collapse at the end of expiration and provide protection against the development of shear forces during mechanical ventilation. From Tobin MJ: Advances in mechanical ventilation. N Engl J Med 344:1986, 2001. With permission. |
Two concepts have directed recent changes in the management of ARDS: heterogeneity of lung injury in ARDS and ventilator-induced lung injury. Although chest radiographs may show a homogeneous increase in lung density in ARDS, CT scans of the chest demonstrate remarkable variability in density from region to region. Ventilation-perfusion distributions measured by multiple inert gas elimination technique demonstrate the entire range from complete shunt to normal to dead space units, and histologic examination demonstrates extreme variability in injury among adjacent lung areas. The diminished compliance of the lung in ARDS is therefore primarily explained by a reduced number of normal alveoli rather than by a normal number of poorly compliant alveoli. Accordingly, Gattinoni (1987, 1988, 1994) has popularized the baby lung concept whereby the patient with ARDS is considered to have a severely diminished volume of normal lung with no effective ventilation in the remainder of the lung. Appropriate ventilation requires the use of tidal volumes appropriate for smaller lungs, rather than for adult-sized lungs. The recognition of heterogeneity of lung units has additional implications for mechanical ventilation in ARDS. As a result of heterogeneous injury, some alveoli are consolidated and unavailable for gas exchange, while some lung units are collapsed and available to be recruited with the application of positive pressure ventilation or the addition of PEEP (see Fig. 40-9). The less affected alveoli preferentially receive the majority of the positive pressure breath, and may become overdistended, resulting in further parenchymal injury. Low tidal volume ventilation (6 to 8 mL/kg of ideal
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body weight), is a protective ventilation strategy in which the alveolar units contributing to gas exchange are not overdistended and damaged as a result of ventilator-induced sheer forces.
Hickling (1990), Marini (1993), and Pierson (1995) have helped to evolve new lung-protective strategies of ventilator management where the overall goal is to support gas exchange at an acceptable level while avoiding ventilator-induced lung injury. These principles are best illustrated on a pressure-volume curve corresponding to an ARDS patient (see Fig. 40-5). Static lung compliance increases as recruitable areas of atelectasis open (at the lower inflection point). At higher inflation pressures, compliance decreases as overdistention of individual lung units occurs (at the upper inflection point). The invitees to the ACCP-sponsored International Consensus Conferences in Intensive Care Medicine (1999) noted that lung injury occurs in lungs that are inflated at volumes below the lower inflection point as well as above the upper inflection point. Some advocate the use of PEEP above the lower inflection point to prevent collapse of recruitable lung units on expiration and the cyclical opening and closing of alveoli with respiration, while maintaining low tidal volumes to prevent overdistention. This is referred to as the open lung approach. With this technique, as described by Marini and Kelsen (1992) and Pierson (1995), a minimum level of PEEP is required to avoid alveolar derecruitment, and tidal volume must be kept small so that the end-inspiratory plateau pressure does not exceed that at the upper inflection point. By constructing a pressure-volume curve, the upper and lower inflection points can be determined for each patient. However, static pressure-volume curves are difficult to perform, may not reveal a definitive inflection points, and are of unproven benefit. Because an alveolar distending pressure of 30 to 35 cm H2O is the injury threshold in animal studies such as those by Marini and Kelsen (1992) and Pierson (1995), efforts should be made to keep the plateau pressure below 30 to 35 cm H2O. In most patients, the use of 8 to 15 cm PEEP and a tidal volume of 5 to 8 mL/kg will accomplish the goals of ventilation.
These concepts have led to the application of PC-IRV in ARDS. During PCV, the peak airway pressure is maintained throughout the duration of inspiration, allowing inflation of all lung units to a degree dependent primarily on compliance. Thus, lung units that are not inflated during conventional VCV may be inflated during PCV, a process called alveolar recruitment. These recruited lung units are then maintained open by the addition of an appropriate level of PEEP. The combination of a low level of PEEP and a moderate but constant level of inspiratory pressure during PCV results in an elevated mean airway pressure at a lower peak pressure than occurs during VCV. However, significant controversy exists regarding whether PCV, usually with IRV, actually produces any additional benefit over VCV.
The potential benefits of PC-IRV, such as decreased lung injury and improved gas exchange, must outweigh the potential hazards, including decreased tidal volume and decreased cardiac output. In general, the use of PC-IRV requires deep sedation and possibly chemical paralysis of the patient, frequent evaluation of intrinsic PEEP, tidal volume and mean airway pressure, and invasive hemodynamic monitoring to determine adverse affects of increased mean airway pressure and intrinsic PEEP. In treating patients who have severe ARDS, one may have to accept permissive hypoxemia as well as permissive hypercapnia. Although the goal is to maintain Pao2 in the normal range, this may not be attainable in some patients without the use of potentially injurious levels of PEEP. A Pao2 of 50 to 55 mm Hg is usually well tolerated, if hemoglobin concentration and cardiac function are adequate.
Patient Positioning
According to Gattinoni and associates (1994) and Tobin (1994), many diseases affect the lung in a nonhomogeneous manner. Gattinoni and colleagues (1986) reported that CT scans of patients with ARDS demonstrated heterogeneous airspace disease, with the majority of airspace consolidation localized to the dependent regions of the lung. Prone positioning has been shown to improve oxygenation in approximately 50% of patients with ARDS by Gattinoni and co-workers (1994), allowing reductions of Fio2 and PEEP. Prone positioning improves oxygenation by decreasing blood flow through atelectatic and consolidated lung, resulting in a decreased shunt fraction and improved [V with dot above]/[Q with dot above] matching, particularly in the supradiaphragmatic regions. Albert and Hubmayr (2000) have demonstrated that the compressive effects of the heart on the lung parenchyma are attenuated in the prone position. Furthermore, transition of the patient from the supine to the prone position is often accompanied by mobilization and drainage of airway secretions.
Although multiple studies have demonstrated improvement in oxygenation with prone positioning, a recent large prospective trial by Gattinoni and coinvestigators (2001) to evaluate the effect of prophylactic routine prone positioning on survival in patients with ALI/ARDS failed to show an improvement in mortality. Posthoc analysis indicated that mortality was reduced in the subset of patients with the worst gas exchange (Pao2/Fio2 <88) and in those with Simplified Acute Physiology II scores higher than 49. The likelihood of response to prone positioning is generally higher early in the course of ARDS, and patients may derive benefit only hours after repositioning has occurred. Although the hemodynamic parameters tend to remain unchanged, hypotension, desaturation, and cardiac arrhythmias may occur in the transition from supine to prone positions.
Unilateral/Asymmetric Lung Disease
Patients who have lobar pneumonia, lobar or whole-lung atelectasis, or other markedly asymmetric pulmonary involvement
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present a special problem in ventilatory assistance, particularly in the presence of severe hypoxemia. Applying PEEP as in Fig. 40-5 can worsen rather than improve arterial oxygenation in such instances according to Pierson (1995). Use of a double-lumen endotracheal tube with two ventilators may be necessary to individually address each lung.
Flail Chest
Several studies demonstrate that the clinical course and outcome of flail chest injury are determined mainly by the underlying pulmonary injury rather than the flail segment. Patients who sustain multiple rib fractures without associated lung contusion or pneumonia generally recover uneventfully, while flail chest in the setting of ALI typically follows the course of that illness, with little separate contribution from the chest wall instability. Ventilator management of patients who have a flail chest injury is essentially that used to manage the underlying pulmonary condition. In addition, attention must be directed to pain control. Intercostal nerve blocks or administration of epidural narcotics can greatly aid in pain control and ventilator weaning in such patients.
WEANING FROM VENTILATORY ASSISTANCE
Discontinuation of mechanical ventilation is usually easily accomplished in patients requiring short-term ventilator support. In the setting of acute illness, failure of the ventilatory and gas exchange capabilities of the lung as reported by Hall and Wood (1987), MacIntyre and Stock (1990), Yang and Tobin (1991), and Tobin (1994) is often multifactorial, and liberating such patients from the ventilator can represent a major clinical challenge (with as much as 40% of hospitalization spent weaning). If weaning is delayed unnecessarily, the patient remains at risk for ventilator-associated complications. If performed prematurely, severe cardiopulmonary decompensation may occur.
Before attempting to wean the patient from the ventilator, the disease process that compromised the patient's pulmonary function should be stable or improving and there should be no evidence of hemodynamic instability. If extubation is anticipated, clinical evaluation of the patient's ability to protect the upper airway and to cough needs to be verified. When ventilatory support has been required for 1 to 2 weeks or longer in the setting of acute illness, Pierson (1999) reported that nonrespiratory factors become increasingly relevant because patients with prolonged acute respiratory failure typically develop multisystem dysfunction. Weaning therefore depends on the balance between ventilatory demand and the patient's capabilities. Occasionally the minute ventilation required to keep the patient's arterial Pco2in the normal range is too high (e.g., 16 to 18 L/min instead of the expected 10 L/min). In such cases, at least one of two possible physiologic derangements may be present: hypermetabolism (increased CO2production) or inefficient ventilation [increased dead space ventilation (VD/VT)]. Causes of hypermetabolism include fever, sepsis, excessive skeletal muscle activity (e.g., increased work of breathing, shivering, or agitation), or overzealous caloric supplementation, especially with carbohydrate calories. Inefficient ventilation is a hallmark of severe obstructive lung disease and is also a characteristic feature of late ARDS. Bedside measurement of both CO2production and VD/VT may be helpful in identifying the cause or causes of excessive minute ventilation requirements. According to Pierson (1999), elevated CO2production may be caused by fever, thyrotoxicosis, excessive parenteral nutrition, or a generalized catabolic state. Elevated dead space ventilation, manifested as increased VD/VT, may be from hypovolemia, excessive airway pressures, or pulmonary vascular disease.
Neurologic factors may also contribute to prolonged mechanical ventilation. A failure of the central respiratory pattern generator in the brainstem can result from structural defects, metabolic derangements from electrolyte abnormalities, or drug-induced sedation. All sedatives, tranquilizers, and hypnotics depress ventilatory drive or compromise ventilatory muscle function. Neuromuscular blockers such as vecuronium and pancuronium can cause muscle weakness and prolong weaning in two ways. As noted by Hansen-Flaschen (1993), clearance of these agents may be prolonged for days in the presence of renal insufficiency, and a myopathy, often seen with concurrent corticosteroids, can produce muscle weakness that lasts for multiple weeks. In addition, aminoglycoside antibiotics can also produce neuromuscular abnormalities that may prolong ventilatory support.
Predicting Weaning Outcome
Evidence-based guidelines for weaning and discontinuation of ventilator support have been issued after the collaborative efforts of the American College of Chest Physicians, the American College of Critical Care Medicine, and the American Association for Respiratory Care in 2001. A review of the literature found over 400 putative weaning predictors. Many were of no use in predicting weaning results, and few had been studied in more than 50 patients. Table 40-12 provides a list of the indexes most often used to predict the outcome of a weaning trial.
Gas Exchange
Discontinuation of ventilator support is not advisable in a patient with persistent hypoxemia, as manifested by a Pao2of less than 55 mm Hg while on an Fio2of greater than 0.40. A number of indexes derived from arterial blood gas (ABG) measurements have been proposed by Tobin and Yang (1990) and Tobin and Alex (1994) as predictors of weaning
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outcome, but have not consistently been shown to be helpful. Additionally, none of the ABG criteria listed in Table 40-10 have been subjected to prospective investigation.
Table 40-12. Variables Used to Predict Successful Weaning from Mechanical Ventilation | ||
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Maximum Inspiratory Pressure
Maximum inspiratory pressure (Pimax), provides a global assessment of the strength of all the inspiratory muscles. In a classic study, Sahn and Lakshminarayan (1973) found that a Pimax value of -30 cm H2O or less predicted successful weaning, whereas a Pimax value higher than -20 cm H2O predicted weaning failure. However, subsequent studies by Fiastro and associates (1988) and Tobin (1994) found that Pimax has limited power in predicting weaning outcome. Recently, data pooled from studies of weaning predictors and reported in the ACCP conference on weaning and discontinuing ventilatory support (2001a) suggest that an inspiratory pressure0.1/Pimax ratio of less than 0.3 was predictive of successful unassisted breathing and extubation, with a pooled likelihood ratio of 16.3 (95% CI, 2.35 to 113).
Vital Capacity
Vital capacity is the largest volume of gas that a patient is able to exhale after a maximal inspiration. A value of 10 mL/kg has been suggested by Tobin and Alex (1994) as being essential to sustain spontaneous ventilation; the implication is that a VC of greater than 10 to 15 mL/kg could predict weaning success. However, Tahvanainen and co-workers (1983) found that a VC of greater than 10 mL/kg was falsely positive in 18% of patients and falsely negative in 50%.
Thoracic Compliance
A decrease in static thoracic compliance is associated with disorders of the thoracic cage or a reduction in the number of functioning lung units (e.g., pneumonia, pneumothorax, or pulmonary edema). According to Tobin and Yang (1990) and Tobin and Alex (1994), successful weaning outcome is considered unlikely in patients with an effective thoracic compliance of less than 25 mL/cm H2O because the resistive load would increase the work of breathing and make it difficult to sustain the level of ventilation necessary for adequate gas exchange. An index termed effective dynamic compliance is obtained by dividing the tidal volume by the difference of peak airway pressure and total PEEP, and has been proposed as being useful to assess the overall impedance of the respiratory system.
Minute Ventilation and Maximum Voluntary Ventilation
The relationship between minute ventilation and arterial blood Paco2 provides a good indication of the demands placed on the respiratory system. A high minute ventilation in the presence of hypercapnia indicates the presence of either increased CO2 production or a high dead space fraction (VD/VT). Maximum voluntary ventilation is the volume of air that can be inhaled or exhaled with maximum effort over 1 minute. Tobin and Alex (1994) reported that a minute ventilation of less than 10 L/min is the conventionally accepted benchmark to predict successful weaning.
Airway Occlusion Pressure
Airway occlusion pressure is theoretically proportional to the respiratory drive. Airway occlusion pressure is determined by the airway pressure generated at 0.1 second (P0.1) after initiating an inspiratory effort against an occluded airway. Using the data of Hererra (1985) and Sassoon (1987) and their co-workers, with subsequent data reported by Montgomery and associates (1987), Tobin and Yang (1990) estimated that the use of P0.1 of less than or equal to 4.2 cm H2O as a predictor of weaning success was associated with a 44% false-positive rate and a 50% false-negative rate, whereas a P0.1 of less than 6 cm H2O was associated with a 46% false-positive rate and a 33% false-negative rate.
Rib Cage/Abdominal Motion
The chest wall has two compartments, the rib cage and abdomen, and assessment of their relative motion can help in the detection of respiratory dysfunction and distress. Asynchronous and paradoxic motion of the rib cage and abdomen can be assessed using an index of the maximum compartmental amplitude to VT ratio, which relates the total extension of both the rib cage and abdomen to VT. A high value suggests that weaning is unlikely to be successful.
Rapid Shallow Breathing
Patients who fail a weaning trial develop an immediate increase in respiratory frequency and a decrease in tidal
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volume (VT) following discontinuation of ventilator support. Measurements of frequency (f) and VT are combined into an index of rapid shallow breathing (the f/VT ratio). An f/VT value of 105 breaths/min per liter best differentiated patients who were successfully weaned. The predictive power of this value was then prospectively assessed, with positive and negative predictive values of 0.78 and 0.95, respectively. Many consider the f/VT ratio to be the current best single parameter for prediction of weaning success.
Integrative Indexes
Weaning failure is commonly multifactorial in origin, so it is not surprising that an index that assesses a single function may be unreliable. Accordingly, an index that integrates a number of physiologic functions would be expected to have greater predictive accuracy. The CROP index as suggested by Yang and Tobin (1991) incorporates a measure of pulmonary gas exchange and an assessment of the demands placed on the respiratory system and the capacity of the respiratory muscles to handle them: CROP index = (Cdyn)(Pimax)(Pao2/Pac2)/respiratory rate, where Cdyn is dynamic compliance, and Pao2/Pac2 is the a/A ratio and a measure of gas exchange. Successful weaning is reliably suggested by a CROP index of greater than 13, whereas difficult weaning frequently occurs with a CROP index between 11 and 13, and unsuccessful weaning attempts with a CROP index of less than 11. When prospectively examined, Yang and Tobin (1991) found this index had positive and negative predictive values of 0.71 and 0.70, respectively.
The pressure-time index (PTI) reported by Jabour and co-workers (1991) is an estimate of the efficiency of gas exchange (the minute ventilation needed to bring Paco2to 40 mm Hg, or VE40) and tidal volume during spontaneous breathing. Integrative index = PTI (VE40/(VT)sb), where (VT)sb is the tidal volume during spontaneous breathing. This integrative index had a positive predictive value of 0.96 and a negative predictive value of 0.95.
Methods of Weaning
Numerous techniques are used for weaning, as outlined in Table 40-13, with variable success rates. However, the removal of an artificial airway from a patient should be based on assessments of airway patency, the ability of the patient to protect the airway and gas exchange. Therefore, careful assessment must be performed even in the healthiest patient.
Abrupt Discontinuation
Not all patients require stepwise reduction in ventilator support or formal discontinuation assessments. Prakash and colleagues (1982) showed that patients requiring brief periods of ventilatory assistance can resume spontaneous respiration with little difficulty, including immediately following surgery.
Table 40-13. Different Strategies Used in Weaning Following Short-Term Ventilatory Support | ||||||||||
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T-piece Weaning
The patient is disconnected from the ventilator and receives supplemental oxygen through a T-tube system that is connected to the endotracheal tube. It is most often used to assess a patient's ability to tolerate unassisted breathing prior to extubation. If the patient does not develop signs of intolerance, extubation is performed without any further weaning. Alternatively, T-piece trials of spontaneous breathing may be interposed with resumption of mechanical ventilation and gradual increases in the duration of the trial.
Intermittent Mandatory Ventilation
IMV involves a gradual reduction in the amount of support being provided by the ventilator as an increased amount of respiratory work is performed by the patient. When IMV is used for weaning, a stepwise reduction in ventilator-assisted breaths, usually in steps of 1 to 3 breaths/min, requires the patient to generate a stepwise increase in the number of spontaneous breaths. Unfortunately, the patient performs the same amount of work during an assisted breath as during a spontaneous breath, as shown by Marini and associates (1988), largely due to the inability of the respiratory center to adapt to intermittent ventilatory support. Tobin (2000) suggests that IMV weaning may result in respiratory muscle fatigue and may be responsible for the poor performance of IMV when compared with other weaning strategies.
Pressure-Support Ventilation Weaning
As the amount of pressure support is decreased, the patient is responsible for generating more of the minute ventilation. Patients tolerating low level (e.g., 5 to 8 cm H2O) support are considered ready for extubation. However, the resistance posed by an endotracheal tube varies with the diameter and flow, and even when these are constant, resistance will vary as a result of tube deformation and adherent secretion. Brochard and co-workers(1991) demonstrated that the level of PSV necessary to eliminate imposed work varied considerably (3 to 14 cm H2O) from patient to patient. Likewise, Nathan and co-workers (1993) could not define a level of PSV that predicted respiratory work following extubation.
Relative Efficacy of Weaning Techniques
Two large, randomized controlled trails reported by Brochard (1994) and Esteban (1995) and their coinvestigators compared the three commonly used strategies for the stepwise reduction in mechanical support: multiple daily T-piece trials, PSV, and SIMV. The Brochard and co-workers study (1994) found that weaning time was significantly shorter with PSV (mean 5.7 3.7 days) than the combination of the IMV and T-piece groups (mean 9.9 8.2 days, p <0.05). Later, Esteban and colleagues (1995) conducted a similar investigation, but included a fourth arm (once daily T-piece breathing). The study concluded that a once-daily T-piece trial of spontaneous breathing led to extubation about three times quicker than IMV and about twice as quick as PSV. Both studies favored T-piece trial and PSV weaning strategies to SIMV when duration of mechanical ventilation was the end point. However, the trend in favor of PSV was greater in the Brochard study.
The majority of patients can be weaned easily from mechanical ventilation, but a substantial minority have considerable difficulty, as outlined in Table 40-14. The major determinants of weaning outcome include the adequacy of pulmonary gas exchange, respiratory muscle function, and psychological problems. Many of the physiologic indexes that have been used to predict weaning outcome are inaccurate. A number of techniques can be used for weaning. Of these, a once-daily trial of spontaneous breathing is usually the most expeditious.
Table 40-14. Causes of Difficulty in Weaning | ||||||||||||||||||||||||
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