Approach to the Use of the Mechanical Ventilator

Transcription

1 7 MECHANICAL VENTILATION Matthew J. Sena, M.D., and Avery B. Nathens, M.D., Ph.D., M.P.H., F.A.C.S. 7 MECHANICAL VENTILATION 1 Approach to the Use of the Mechanical Ventilator Patients requiring mechanical ventilation account for a large percentage of admissions to medical and surgical intensive care units. The initial indications for mechanical ventilation can be divided into two main categories: (1) airway instability necessitating endotracheal intubation (as a consequence of operation, brain trauma, or intoxication) and (2) primary respiratory failure from any of several diverse causes, including the acute respiratory distress syndrome (ARDS), trauma, cardiogenic pulmonary edema, and exacerbation of chronic obstructive pulmonary disease (COPD). 1 In the first category, ventilator management is relatively straightforward, and support is temporary, maintained only until the patient s airway is stabilized. In the second category, a prolonged period of mechanical ventilation (> 2 to 3 days) is frequently required.the majority of ventilated ICU patients fall into this second group, 1 and it is these patients in whom specific attention should be paid to the cause of respiratory failure and the goals of therapy. The ventilator mode and settings can then be appropriately tailored to minimize lung injury and facilitate resolution of the underlying disease. Proper use of a mechanical ventilator requires a solid understanding of normal and abnormal pulmonary mechanics, gas exchange, and the relation between systemic oxygen delivery and consumption. Mechanical ventilators, along with currently available noninvasive and invasive monitoring devices, allow support of critically ill patients while the acute physiologic derangements that led to respiratory failure resolve. In addition, specific ventilator strategies geared toward minimizing further lung injury and expediting the process of liberation from the ventilator not only yield improved support of patients with respiratory failure but also appear to have an impact on outcome. Ventilator terminology has become increasingly complex as the technology has advanced, but the basic principles of management remain unchanged: to facilitate gas exchange for tissue oxygen delivery, to provide ventilation for removal of carbon dioxide, and to minimize the detrimental effects of both endotracheal intubation and mechanical ventilation. With these priorities in mind, the clinician can use an evidence-based approach to ventilator management as a component of multimodal therapy to improve patient outcome in the ICU. Such management includes use of a lung-protective strategy for patients with acute lung injury (ALI) or ARDS, performance of daily spontaneous breathing trials (SBTs) to identify patients who are ready for liberation from the ventilator, and, when possible, consideration of a nurse-driven or respiratory therapist driven protocol to minimize delays in extubation. Newer therapies have been developed that offer attractive alternatives to conventional modes of ventilation. Most such therapies are of unproven efficacy, and must therefore be employed with caution in clinical settings. Nonetheless, they provide the clinician with more options for treating patients with advanced respiratory failure and should be considered in extreme cases. Ventilation and Oxygenation An essential concept in mechanical ventilation is the distinction between two key processes, ventilation and oxygenation. The primary purpose of ventilation is to excrete carbon dioxide. The minute ventilation (V E) is the total amount of gas exhaled per minute, computed as the product of the rate and the tidal volume (V T ). Minute ventilation has two components, alveolar ventilation (V A) and dead space ventilation (V D). Under normal conditions, approximately two thirds of V E reaches the alveoli and takes part in gas exchange (V A); the remaining third moves in and out of the conducting airways and nonperfused alveoli (V D).Thus, the ratio of dead space to tidal volume (V D /V T ) is normally The amount of CO 2 excreted is directly related to the amount of alveolar ventilation and inversely proportional to the partial pressure of CO 2 in the alveoli (P A CO 2 ). During spontaneous breathing, V E is regulated by the brain stem respiratory center. The brain stem respiratory center responds primarily to changes in plasma ph and in the partial pressure of CO 2 in arterial blood (P a CO 2 ). In the face of normal CO 2 production (~ 200 ml/min) and normal minute ventilation (6 L/min), alveolar ventilation amounts to approximately 4 L/min and corresponds to a P a CO 2 of 40 mm Hg. In a patient requiring mechanical ventilation,v E is at least partially determined by the mode and settings of the ventilator. Respiratory rate and tidal volume can be set independently, and the mode of ventilation can be set to allow additional spontaneous breathing if necessary. In most cases, the primary goal is maintenance of a near-normal P a CO 2. The physician must be cognizant of factors that might increase CO 2 production (e.g., fever, sepsis, injury, and overfeeding) or V D (e.g., lung injury, ARDS, and massive pulmonary embolism), any of which would increase the V E requirements in a ventilated patient. Oxygenation refers to the equilibrium between oxygen in the pulmonary capillary blood and oxygen in inflated alveoli. The oxygen tension gradient between the alveoli and the capillaries favors the transfer of oxygen into the blood. Although the partial pressure of oxygen in arterial blood (P a O 2 ) is partially dependent on ventilation, it depends less on adequate alveolar ventilation than on the appropriate matching of pulmonary blood flow to well-inflated alveoli, a process referred to as ventilation-perfusion (V / Q ) matching. V / Q matching can be affected by many factors, including patient position, airway pressure, pulmonary parenchymal disease, and small-airway disease. The efficiency of V / Q matching, and thus of oxygenation, can be evaluated by measuring the P a O 2 at a known value of the fraction (concentration) of inspired oxygen (F I O 2 ). Under normal circumstances, oxygenation is very efficient, with P a O 2 values approaching 90% of P A O 2. Its efficiency can be assessed by calculating the alveolar-arterial oxygen gradient (i.e., P A O 2 P a O 2 ). Under normal conditions, P a O 2 is approximately 90 mm Hg.To determine P A O 2, the following formula is employed:

2 7 MECHANICAL VENTILATION 2 Mechanical ventilation is initiated Initial ventilator settings are as follows (depending on clinical scenario): F I O2 = 0.5; PEEP = 5 cm H 2 O; respiratory rate = breaths/min; V T = 8 10 ml/kg predicted body weight. Measure S a O2. S a O2 < 90% Approach to Use of the Mechanical Ventilator Increase F I O2 in stepwise manner to keep S a O2 90%. Increase PEEP by 2 5 cm H 2 O. Continue increasing PEEP by 2 5 cm H 2 O to maximum of 20 cm H 2 O if S a O2 < 90% despite F I O Identify and treat cause of respiratory failure. Look for evidence of acute lung injury. Evidence of ALI is present Utilize low tidal volume (lung-protective) ventilation: Reduce V T to 6 ml/kg. Increase RR to up to 35 breaths/min to achieve ph > 7.20 and P ~ a CO2 = mm Hg. (Traumatic brain injury is a relative contraindication to this approach. Patients without intracranial hemorrhage but with intracranial pressure monitors may be considered if P a CO2 is normal and S a O2 > 95%.) Attempt to determine best PEEP through clinical or invasive assessment of DO2. Measure S a O2. S a O2 < 90% S a O2 90% Diagnose and treat associated conditions: Pneumothorax Hydrothorax/hemothorax Asynchrony (increase sedation; consider NMBA) Consider adjunctive measures: Nitric oxide Prone positioning HFOV ECLS P stat > 30 cm H 2 O Measure P stat. Reduce V T in stepwise manner to 4 ml/kg to keep P stat 30 cm H 2 O. (In patients with morbid obesity or ascites, P stat may reflect transdiaphragmatic pressure rather than transpulmonary pressure. The lung-protective approach should be maintained, but consideration should be given to allowing a higher P stat before lowering V T significantly below 6 ml/kg.) When lung compliance improves, begin increasing V T to 6 ml/kg while maintaining P stat 30 cm H 2 O. P stat 30 cm H 2 O Continue lung-protective ventilation strategy until P a O2/F I O2 ratio 300 or patient meets criteria for SBT.

3 7 MECHANICAL VENTILATION 3 S a O2 90% Adjust RR to keep P a CO2 = ~ mm Hg, unless severe bronchospasm or COPD is present. Evidence of ALI is absent Continue support until gas exchange improves. As hypoxemia resolves, Reduce F I O2 as tolerated: 0.5 to keep S a O2 90% Reduce PEEP to 8 cm H 2 O (in steps of 2 5 cm H 2 O). Perform daily assessment for liberation from ventilator. Determine whether patient meets criteria for SBT. Patient passes SBT Assess stability of airway. Patient fails SBT Determine cause of failure and attempt to correct it. Resume completely supported ventilation for 24 hr, then reattempt SBT. Patient passes SBT on subsequent attempt Assess stability of airway. Patient persistently fails SBT Consider tracheostomy. Airway is stable Extubate patient. Airway is unstable Consider tracheostomy. Resume daily SBTs with CPAP or tracheostomy collar. For patients with prolonged ventilator dependence ( 2 wk), consider Planned, gradual reduction of pressure support (PSV wean) or Planned, gradual increases in duration of SBT (2 12 hr) until patient s endurance improves.

4 7 MECHANICAL VENTILATION 4 P A O 2 = [F I O 2 (barometric pressure P H2 O) P a CO 2 /RQ] where RQ represents the respiratory quotient and P H2O represents the partial pressure of water vapor at sea level. Normally, at sea level, barometric pressure is approximately 760 mm Hg, F I O 2 is 0.21, P H2 O is 47 mm Hg, P a CO 2 is 40 mm Hg, and RQ is 0.8. Accordingly, P A O 2 = [0.21(760 47) 40/0.8] P A O P A O P A O 2 P a O Thus, the alveolar-arterial gradient under these conditions is approximately 10 mm Hg, which falls within the standard range of 8 to 12 mm Hg. A shorthand method of quantifying the degree of hypoxemia is to calculate the P a O 2 /F I O 2 ratio (also referred to as the P/F ratio), which is simply an assessment of the efficiency of gas exchange. At sea level, with the patient breathing room air, P/F 100/ Unlike regulation of V E, adjustment of the rate or V T generally has little effect on P a O 2, except at extremely low levels of ventilation. Greater effects on arterial oxygenation are achieved through adjustment of either F I O 2 or mean airway pressure (P aw ), both of which can be readily manipulated with a mechanical ventilator. Ventilator Modes Current mechanical ventilators possess a wide, and potentially confusing, array of modes, settings, and capabilities. All of them, however, control three variables: trigger, limit, and cycle. The trigger variable is the signal that serves to initiate the inspiratory phase. This signal occurs as a result of patient effort that leads to a change in either flow or pressure within the ventilator circuit. Flow-triggered ventilators deliver a continuous flow of gas across the inspiratory and expiratory limbs of the ventilator circuit and initiate the inspiratory phase when patient effort results in a change in this flow. The required change can be as little as 0.1 L/min; the sensitivity of the trigger is decreased by increasing the required flow change and therefore increasing the patient effort necessary to begin inspiration. Pressure-triggered ventilators initiate the inspiratory phase when a patient s spontaneous effort results in a change in pressure. At the most sensitive setting, a pressure change of approximately 1 cm H 2 O is required; at the least sensitive setting, a change of 15 cm H 2 O is required. Finally, a time trigger is used to start the inspiratory phase in mandatory ventilation modes, as well as in assisted modes. The limit variable is the maximal set inspiratory pressure or flow. Pressure-controlled ventilation (PCV) and pressure-support ventilation (PSV) are both modes of pressure-limited ventilation. Because volume is the product of flow and time, volume-controlled ventilation is actually flow-limited ventilation during the inspiratory phase with the inspiratory time set independently. The cycling variable is the factor that terminates the inspiratory cycle (i.e., time, flow, pressure, or volume). To add more confusion, each breath can be considered as a mandatory breath (which is time triggered), a spontaneous breath (which is patient initiated), or a combination of the two. PRESSURE-LIMITED VERSUS VOLUME-LIMITED VENTILATION Pressure-support ventilation is the simplest form of pressurelimited ventilation and, by definition, is a purely spontaneous mode of ventilatory support. In PSV, the patient triggers a breath through an inspiratory effort, which leads to the delivery of a breath at a variable flow rate to meet a preset pressure. As the lung inflates, compliance decreases and flow decreases to maintain a constant inspiratory pressure. The result is a descending flow curve that is similar to air flow in unassisted breathing. Cycling in this mode occurs when flow declines to a specified percentage of the maximal flow rate (approximately 5% of the peak flow rate in some ventilator models) [see Figure 1]. When inspiratory flow ceases, the patient exhales passively. Pressure-controlled ventilation is related to PSV in that flow descends in amplitude during the inspiratory cycle. It differs from PSV primarily in that the inspiratory time is set by the ventilator, not by the patient. PCV is generally used in the assist-control mode, which allows full support of patient-initiated breaths in addition to ventilator-initiated breaths (which are time triggered). It can also be used in conjunction with the intermittent mandatory ventilation (IMV) mode in newer ventilator models.the largest drawback of PCV is that V T can change as lung compliance changes, necessitating frequent adjustments to ensure adequate V E. For example, as the lung becomes less compliant with increasing pulmonary edema, V T will decrease, as will V E. This problem can be addressed by using another form of pressurelimited ventilation, known as pressure-regulated volume control (PRVC) [see Combined Modes of Ventilation, below]. Volume-controlled ventilation (VCV) is delivered at a set frequency (in the IMV or the assist-control mode) or may be patient initiated (in the assist-control mode). After the ventilator is triggered, a fixed flow of gas is generated for a specific time, thus providing a preset inspiratory volume (volume = flow time). Volume-limited ventilation is generally easier to regulate than pressure-limited ventilation, but it may be less comfortable for awake patients, because the flow curve is a square wave, which is markedly different from the normal inspiratory flow pattern in nonventilated patients. MANDATORY VERSUS SPONTANEOUS VENTILATION There are several modes of ventilation that provide mandatory ventilator support with or without patient-triggered ventilation. For example, assist-control ventilation ensures delivery of a minimum (mandatory) set V E but also allows additional patient-triggered (spontaneous) breaths. Each breath, regardless of the trigger, is completely supported, so that either a fixed volume (with VCV) or a fixed pressure (with PCV) is provided for a preset inspiratory time. Full support can be provided by increasing the mandatory rate. If the patient has respiratory drive, V E might be increased by adding spontaneous breaths.the major drawback of this approach is that agitated patients may become hyperventilated and may manifest respiratory alkalosis if not sedated. The IMV mode allows only the preset number of breaths to be supported. In most cases, breaths are synchronized with the patient s effort (so-called synchronized IMV [SIMV]) if spontaneous respiration is occurring. Patient efforts at inspiration above the preset frequency are not supported with gas flow from the ventilator unless pressure support is added. In the past, IMV was frequently used as a weaning mode: by gradually decreasing the set frequency, patients gradually assumed a greater role in their own respirations.today, however, it is not frequently employed for this purpose and plays only a limited role in weaning patients from the ventilator. INSPIRATORY TIME, FLOW, RESPIRATORY RATE, AND INSPIRATORY-EXPIRATORY RATIO Inspiratory time, flow, respiratory rate, and inspiratory-expira-

5 7 MECHANICAL VENTILATION 5 Volume-Limited (Flow-Limited) Ventilation Pressure-Limited Ventilation Flow (ml/sec) 1, Volume-Controlled (Assist Control, Time Trigger) Square Flow Wave, Variable Pressure Volume-Controlled (Assist Control, Patient Trigger) Pressure-Controlled (Assist Control, Time Trigger) Decelerating Flow Wave, Constant Pressure Pressure-Support Expiratory Phase Begins 800 1,200 Spontaneous Effort 30 Pressure (cm H 2 O) Ventilator Trigger Set to 2 cm H 2 O Pressure Deflection of 2 cm H 2 O Inspiratory Time Determined by Patient = 1.2 sec PS = 10 cm H 2 O Tidal Volume (ml) 1, V T = 600 ml Time (sec) Time (sec) Trigger variable Time RR set at 15 breaths/min Inspiratory time = 1 sec; thus, I/E = 1:3 Patient (pressure in this case, but may be flow) Sensitivity set at 2 cm H 2 O Time RR set at 15 breaths/min Inspiratory time = 1 sec; thus, I/E = 1:3 Patient (pressure in this case, but may be flow) Sensitivity set at 2 cm H 2 O Limit variable Flow Square wave, 600 ml/sec Flow Square wave, 600 ml/sec Pressure P = 10 cm H 2 O above PEEP Pressure P = 10 cm H 2 O above PEEP Cycling variable Volume or time Volume = flow time; thus, 600 ml = 600 ml/sec 1 sec inspiratory time Volume or time Volume = flow time; thus, 600 ml = 600 ml/sec 1 sec inspiratory time Time Flow (determined by patient s lung compliance) Gas flow ceases when flow rate reaches 5% of peak value Figure 1 Shown are flow, pressure, and volume profiles in volume-limited and pressure-limited ventilation modes. tory (I/E) ratio are all closely related. In most patients, they can be preset to mimic the normal respiratory cycle.the normal I/E ratio is approximately 1:3. With the respiratory rate set at 15 breaths/ min, the inspiratory time is 1 second, with 3 seconds of expiratory time.the flow rate can then be manipulated so as to achieve a desired tidal volume (in VCV) or can be adjusted automatically by the ventilator so as to achieve a certain pressure (in PCV). Manipulation of these variables can be useful in certain conditions, such as a high level of intrinsic positive end-expiratory pressure (PEEP) [see Discussion, Special Problems in Ventilator Management, Chronic Obstructive Pulmonary Disease, below]. In the past, manipulation of the I/E ratio has been used to treat severe hypoxemia [see Alternative Modes of Ventilation and Adjunctive Therapies, Inverse-Ratio Ventilation, below]. AIRWAY PRESSURES, LUNG INJURY, AND OXYGENATION The flow of gas through the ventilator circuit produces pressure both at the level of the endotracheal tube and across the alveolar surface. These pressures, though related, have different implications for the assessment and treatment of pulmonary dysfunction [see Figure 2]. Peak inspiratory pressure (PIP) is the pressure measured in the ventilator circuit during maximal gas flow; it primarily represents the interaction between the inspiratory flow rate and airway resistance. Mean airway pressure is the area under the pressure-time curve divided by the time required for a complete respiratory cycle. Because the normal respiratory cycle is dominated by the expiratory phase, P aw is determined primarily by PEEP. P aw is important in that it has a direct effect on alveolar recruitment and gas exchange; it also is the major determinant of

6 7 MECHANICAL VENTILATION 6 Pressure (cm H 2 O) PIP P stat PEEP Time (sec) Figure 2 Shown are measured ventilator pressures during a single machine-triggered volume breath during VCV. (PEEP positive end-expiratory pressure; PIP peak inspiratory pressure; (P stat static pressure measured during a 0.5 sec inspiratory pause) intrathoracic pressure and thus is the parameter to follow when there is concern about the cardiovascular sequelae of higher ventilatory pressures. Static pressure (P stat ) is measured in the ventilator circuit during a 1-second pause at the end of inspiration. P stat is generally considered to be the pressure distending the alveoli, on the assumption that intrathoracic pressure is equivalent to atmospheric pressure; this distending pressure is also referred to as transpulmonary pressure. Limitation of P stat plays an important role in minimizing ventilator-induced lung injury [see Discussion, Special Problems in Ventilator Management, Acute Lung Injury and Acute Respiratory Distress Syndrome, below]. COMBINED MODES OF VENTILATION Many newer modes of ventilation are hybrids, incorporating combinations of pressure control and volume control and combinations of spontaneous and mandatory breathing. One such mode is pressure-regulated volume control. PRVC is a variant of PCV but has the ability to prevent significant changes in V T if lung compliance changes. The ventilator accomplishes this by continuously evaluating changes in delivered V T at a given pressure over several respiratory cycles and adjusting the pressure accordingly.the operator can preset the inspiratory pressure limit to prevent barotrauma. Another hybrid mode is mandatory minute ventilation, which is a form of assisted VCV. In the assist mode, the patient may trigger a complete volume-cycled breath.the operator sets a specific V E, rather than a specific rate and V T. In this way, the operator can ensure adequate CO 2 removal in patients with variable respiratory drive. In general, these combined modes are of limited utility in ventilator management. The overwhelming majority of patients can be managed with simple PCV or VCV or, if they have adequate respiratory drive, with PSV. Use of the Mechanical Ventilator in Respiratory Failure After endotracheal intubation, the initial ventilator settings should be determined by assessing the cause and severity of the patient s respiratory failure. After an initial stabilization period of approximately 30 minutes, blood gas values should be obtained and the ventilator adjusted accordingly. Certain patients specifically, those with profound hypoxemia may require an immediate increase in F I O 2, PEEP, or both; such increases should not be postponed to await blood gas results. F I O 2 and PEEP can be manipulated on the basis of information from pulse oximetry, so that there is less need for frequent arterial blood gas assessment. Further treatment should be prioritized on the basis of the underlying problem of oxygenation or ventilation. OXYGENATION The purpose of ensuring adequate arterial oxygenation is ultimately to maintain adequate delivery of oxygen to the tissues. A P a O 2 higher than 60 mm Hg generally results in an arterial hemoglobin saturation (S a O 2 ) of 90% or greater and is sufficient for most patients, provided that the other components of oxygen delivery are normal or nearly so. An adequate P a O 2 can be obtained by altering either F I O 2 or P aw. Increasing the F I O 2 is the simplest maneuver, but it is not necessarily the correct adjustment in patients with pulmonary dysfunction. Nonetheless, it should be tried first, while other options are being considered. Generally, a moderate increase in F I O 2 (to 0.6) has minimal adverse consequences. The desired and immediate effect is to increase the gradient for oxygen diffusion across the alveolar and pulmonary capillary membranes. In normal lungs, this increased gradient results in a proportional increase in P a O 2. If an intrapulmonary shunt is present, however, increasing F I O 2 has little effect on P a O 2. Often, an effort to increase F I O 2 is combined with some measure aimed at increasing P aw, the idea being that a smaller increase in F I O 2 will then be required to produce the desired effect. Although a high F I O 2 (> 0.6) has few negative consequences in the short term, prolonged maintenance of F I O 2 at this level can Effective Compliance O 2 Delivery P a O Cardiac Output Arterial Content Venous O 2 Content PEEP (cm H 2 O) Figure 3 Shown are measurements for determining the optimal PEEP. The objective is to maximize the ratio of oxygen delivery to oxygen consumption, which is determined by measuring mixed venous saturation. Here, the best PEEP is 10 cm H 2 O, even though the P a O 2 and the arterial oxygen content are higher at higher levels of PEEP.

7 7 MECHANICAL VENTILATION 7 Volume (L) Normal ARDS Normal FRC Expiratory Inspiratory A A P B C Expiratory V D Inspiratory C,D Overdistention Lower Inflection Point (P flex, Derecruitment) PEEP Set at 12 cm H 2 O (P flex + 2 cm H 2 O) Pressure (cm H 2 O) B Figure 4 Depicted is a static volume-pressure curve. A A represents normal tidal ventilation in a normal lung, with a PEEP of 5 cm H 2 O and a tidal volume of 10 ml/kg 70 kg = 700 ml. C stat = V/ P = 700 ml 5 cm H 2 O/kg = 2 ml/cm H 2 O 70 kg. B B represents normal tidal ventilation in a lung from an ARDS patient, with a PEEP of 5 cm H 2 O and a tidal volume of 10 ml/kg 70 kg = 700 ml. C stat = cm H 2 O 70 kg = 0.45 ml/cm H 2 O/kg. C C represents a low tidal volume, lung-protective ventilation strategy, with a PEEP of 5 cm H 2 O and a tidal volume of 6 ml/kg 70 kg = 420 ml. C stat = cm H 2 O 70 kg = 0.35 ml/cm H 2 O/kg. D D represents a low tidal volume, lung-protective ventilation strategy, with a PEEP of 12 cm H 2 O (best PEEP), which is above P flex. The tidal volume is 6 ml/kg 70 kg = 420 ml. C stat = cm H 2 O 70 kg = 0.60 ml/cm H 2 O/kg. The low tidal volume strategy prevents the overdistention that occurs at higher tidal volumes, whereas the higher PEEP level prevents the derecruitment that can occur at lower volumes. Although low tidal volume ventilation strategies have been demonstrated to improve outcome in ARDS, higher PEEP levels, though theoretically attractive, have not been shown to be efficacious. result in nitrogen washout, resorption atelectasis, and an increased pulmonary shunt fraction, with consequent exacerbation of hypoxemia. The simplest way of increasing P aw is to increase PEEP. The purpose of PEEP is to prevent loss of functional residual capacity (FRC), defined as the volume maintained in the lungs at the end of expiration. In normal persons, FRC is maintained by a balance between the negative intrapleural pressure and the elastic recoil of the lung. Negative intrapleural pressure is affected by patient position. The upright position yields a greater negative intrapleural pressure than the supine position, because of the weight of the abdominal viscera, which literally pull down on the diaphragm. In the supine position, this pull is absent, and FRC may be as much as 25% lower in normal persons in the supine position. 2,3 This decrease is even more pronounced in patients with ascites or abdominal distention and especially in patients with intra-abdominal hypertension. 4 In a normal alert patient, the loss of FRC can be reversed with changes in position or intermittent sigh breaths throughout the respiratory cycle, and there will be minimal net impact on pulmonary physiology. In a supine ventilated patient, the loss of FRC results in progressive atelectasis, intrapulmonary shunting, and hypoxemia. Accordingly, small amounts of PEEP (5 10 cm H 2 O) should be delivered to help restore FRC to levels adequate for maintaining normal gas exchange and preventing hypoxemia in patients without significant pulmonary dysfunction. In patients with pulmonary dysfunction, FRC is lost through alveolar collapse. This collapse occurs by several means for example, through extrinsic pressure (see above) or through some combination of blood, pus, or secretions that results in occlusion of small airways. In these settings, increasing PEEP improves V / Q matching by recruiting these collapsed alveoli and thereby bringing about improved gas exchange and P a O 2. Unfortunately, the increased intrathoracic pressure that may develop when PEEP is increased can have detrimental effects on cardiac output. Because the overall goal is to improve tissue oxygen delivery (not just P a O 2 ), assessment of the net effect of an increase in PEEP should take into consideration the effect on oxygen delivery (ḊO 2 ). The amount of PEEP necessary to maximize ḊO 2 in a given patient is referred to as best PEEP and generally corresponds to the PEEP setting that results in maximal static lung compliance. 5 PEEP levels above this point may increase arterial oxygen content (C a O 2 ) but typically impair cardiac output and result in decreased ḊO 2 [see Figure 3]. The improvement in lung compliance achieved by increasing PEEP levels in patients with pulmonary dysfunction can be demonstrated by using a static or low-flow volume-pressure curve to determine the lower inflection point (P flex ) [see Figure 4]. P flex corresponds to the point at which recruitable alveoli open and become available for tidal ventilation and gas exchange. Setting PEEP slightly higher (+2 cm H 2 O) allows tidal ventilation over the range of maximal lung compliance and prevents the repetitive end-expiratory derecruitment that may be associated with ventilator-induced lung injury. 6 Although this approach is theoretically attractive, determining P flex is technically cumbersome and may not be tolerated by the sickest patients. In practice, F I O 2 and PEEP are manipulated simultaneously, with the specifics depending on the cause of arterial hypoxemia and on an empirical determination of best PEEP. Best PEEP is determined by means of stepwise increases in PEEP coupled with serial assessments of arterial oxygenation and cardiovascular function. At high levels of PEEP (> 15 cm H 2 O), consideration should be given to using a pulmonary arterial catheter for assessment of ḊO 2 and mixed venous oxygen saturation (S v O 2 ). If an increase in PEEP results in a drop in either S v O 2 or ḊO 2, then the increase was detrimental to the goal of improving tissue oxygenation. As a rule, the maximal PEEP level that may provide benefit rarely exceeds 20 cm H 2 O. 7 Above this level, it is fairly common for detrimental effects on cardiovascular function to predominate and ḊO 2 to decline. 8 The initial settings for F I O 2 and PEEP depend on the clinical scenario. Patients intubated for postoperative airway protection may require an F I O 2 of 0.3 and a PEEP of 5 cm H 2 O. In contrast, multiply injured patients who have been resuscitated may require an F I O 2 of 1.0 and a PEEP of 15 cm H 2 O. In either case, early evaluation of arterial blood gas concentrations can guide further manipulations. Alternatively, oxygen saturation and end-tidal CO 2

8 7 MECHANICAL VENTILATION 8 values may be followed noninvasively with pulse oximetry and capnography. Sudden decreases in P a O 2 (or S a O 2 ) should be treated by first increasing F I O 2 and then increasing PEEP.These measures should be followed by attempts to ascertain the cause of the acute change. A first assessment including suctioning, arterial blood gas measurements, and a chest radiograph should be carried out immediately, with particular attention to rapidly reversible causes (e.g., mucous plugging, pneumothorax, a large hemothorax or hydrothorax, and cardiogenic pulmonary edema). A more detailed assessment should then follow to look for other possible causes (e.g., pulmonary embolism, worsening ARDS, aspiration pneumonitis, and pneumonia). It must be kept in mind that in many cases, the etiology is multifactorial, and that in the treatment of profound hypoxemia, it is important to address any and all correctable abnormalities, even when the potential gain is small. For example, in a patient with no pulmonary reserve, drainage of a large hydrothorax may yield a significant improvement in oxygenation, whereas in a patient with near-normal pulmonary function, this measure would have little, if any, effect. In a minority of cases, a mismatch between patient effort and ventilatory support can result in increased work of breathing, progressive respiratory muscle fatigue, and, on rare occasions, arterial desaturation. This situation, referred to as patient-ventilator asynchrony, occurs as a consequence of the ventilator s failure to match the patient s respiratory drive and pulmonary mechanics. It only occurs during spontaneous breathing modes and may be secondary to a problem in the inspiratory trigger (inspiratory asynchrony), the expiratory trigger (expiratory asynchrony), or the flow rate (flow asynchrony). 9 In these cases, direct patient observation often suffices to establish the diagnosis. Therapy is aimed at improving the patient-ventilator interaction and may involve changing the mode of ventilation (e.g., from VCV or PCV to PSV), the trigger setting (e.g., from pressure to flow), the inspiratory gas flow (either the rate or the waveform), or the cycling variable (time, flow, or pressure). Alternatively, in severe cases that result in hypoxemia, it may be necessary to increase sedation to the point where spontaneous respiratory efforts are eliminated. Neuromuscular blocking agents should only be considered if other measures have failed and hypoxemia is worsening. Generally, use of these agents should be avoided in critically ill patients when possible, because their administration has been associated with significant complications. 10 VENTILATION Adequate CO 2 elimination can be achieved with either PCV or VCV; the two methods can be used to achieve the same end points, and neither has any overwhelming advantage over the other. Accordingly, it is reasonable to choose between them on the basis of individual or institutional experience, simply for ease of management. The initial settings should include a V T of 8 to 10 ml/kg predicted body weight 11 and a set respiratory rate of 12 to 15 breaths/min. In general, the assist mode is preferable, because it allows the patient to regulate P a CO 2 while still receiving completely supported ventilation. If PCV is preferred, the inspiratory pressure can be adjusted at the bedside to achieve a V T of 8 to 10 ml/kg. In either case, if the V D /V T ratio is nearly normal, the resultant alveolar ventilation should be sufficient to eliminate all of the metabolically produced CO 2 and maintain a P a CO 2 of 40 mm Hg. After approximately 30 minutes, blood gases should be measured and the respiratory rate adjusted accordingly. In a patient with adequate respiratory drive, PSV is a reasonable choice. In the past, it was largely considered a weaning mode. Table 1 Criteria for Liberation from Mechanical Ventilation Patient criteria for spontaneous breathing trial (SBT) to assess readiness for liberation from mechanical ventilator Resolution or stabilization of underlying disease process No evidence of residual pharmacologic neuromuscular blockade Spontaneous respiratory efforts Hemodynamic stability (no recent increase in pressor or inotrope requirements) Ventilator settings as follows: F I O PEEP 8 cm H 2 O P a O 2 > 75 mm Hg Minute ventilation < 15 L/min ph Patient criteria to assess readiness for extubation Suctioning required less often than every 4 hr Good spontaneous cough Endotracheal tube cuff leak* No recent upper airway obstruction or stridor No recent reintubation for bronchial hygiene Criteria for a failed SBT Respiratory rate > 35 breaths/min for 5 min S a O 2 < 90% for 30 sec HR > 140 beats/min, or 20% increase or decrease from baseline Systolic BP > 180 mm Hg or < 90 mm Hg Sustained evidence of increased work of breathing (e.g., retractions, accessory muscle use) Cardiac instability or dysrhythmias ph 7.32 *Absence of a cuff leak is not an absolute contraindication to extubation. Each patient s risk for postextubation upper airway obstruction should be assessed individually. If extubation has recently failed because of airway obstruction, patient should be assessed and the underlying cause addressed (if possible) before extubation is reattempted. Appropriate adjunctive measures (e.g., racemic epinephrine or heliumoxygen) should be available before patient is extubated. If any of these criteria are met, SBT should be terminated and the patient placed back on previous ventilator settings for 24 hr. Currently, however, it is considered to be best suited for patients in whom the acute physiologic derangements leading to respiratory failure are resolving but who are not ready to be liberated from the ventilator.the main difference from past applications of PSV is that in current practice, pressure support is not intentionally decreased over time [see Liberation from Mechanical Ventilation, below]; instead, the patient is completely supported while daily assessments of the patient s readiness for extubation are made. A potential advantage of PSV is enhanced patient comfort. This is a particularly important consideration when the patient s overall condition is improving and minimization of sedation may allow earlier extubation. In the pressure-support mode, the patient determines the respiratory rate, inspiratory time, and V E. In a patient with normal lung compliance, pressure support of between 5 and 10 cm H 2 O is usually sufficient and should result in a V T of at least 600 ml. Pressure support may be increased as needed for patient comfort and should be titrated to keep the respiratory rate below 25 breaths/min. When pressures higher than 20 cm H 2 O are required, most physicians elect to support the patient in the assist mode until pulmonary compliance improves. If P a CO 2 is elevated despite a V E of 100 ml kg -1 min -1 (6 7 L/min), then the metabolic production of CO 2 is excessively high,

9 7 MECHANICAL VENTILATION 9 alveolar ventilation is an inappropriately low percentage of V T (increased V D /V T ), or both. To increase ventilation, the first step should be to increase the respiratory rate in a stepwise fashion to 20 to 25 breaths/min. In addition, the use of low-compliance ventilator tubing should be considered to minimize dead space in the ventilator circuit. If the P a CO 2 is still elevated, V D and total CO 2 production can be measured directly by using a metabolic cart. If CO 2 production is higher than normal (130 ml m -2 min -1 ), it can be decreased by reducing muscular activity or seizures, controlling hypermetabolic states (if possible), and minimizing the exogenous carbohydrate load. If the P a CO 2 is still elevated after all of these measures have been taken, the respiratory rate may be increased to 30 breaths/min or higher. It should be kept in mind, however, that the efficiency of ventilation decreases as the respiratory rate increases. This loss of efficiency occurs because the percentage of V E used for gas exchange decreases as the respiratory rate increases because in the face of a fixed volume of dead space, there may be inadequate time for alveolar emptying during expiration. In addition, steps may be taken to increase V T, though significant increases may worsen ventilator-induced lung injury through either barotrauma or volutrauma [see Discussion, Special Problems in Ventilator Management, Acute Lung Injury and Acute Respiratory Distress Syndrome, below]. The importance of maintaining a normal P a CO 2 is often overstated. Allowing P a CO 2 to climb above 40 mm Hg has no intrinsic detrimental effects in the absence of increased intracranial pressure, and it is not uncommon to permit the P a CO 2 to rise to avert the adverse consequences of high tidal volumes and the ventilatory pressures required to generate these volumes. This approach, referred to as permissive hypercapnia, is safe as long as ph remains above Over time, ph will increase with compensatory increases in renal bicarbonate preservation, provided that renal function is normal. Liberation from Mechanical Ventilation As the patient s condition improves, it is useful to distinguish between the need for continued endotracheal intubation and the ongoing requirement for mechanical ventilation. The need for endotracheal intubation requires an assessment of airway stability and is relatively straightforward (see below). Deciding when pulmonary function and respiratory muscle reserve are adequate for unassisted breathing is considerably more complex. The latter is what has traditionally been referred to as weaning from mechanical ventilation. The term weaning implies a planned, gradual reduction in ventilator support whereby the patient assumes more and more of the work of breathing that had been performed by the ventilator.this is an inaccurate description of the actual process, which essentially involves assessment of a patient s ability to sustain independent ventilation and adequate gas exchange. Although the amount of support provided does decline as the patient improves, this decline is patient driven and is different from the physician-driven reduction of support historically used to wean the patient from the ventilator gradually. 12 Multiple indices have been devised for determining a patient s readiness for unassisted breathing, with variable degrees of success. Perhaps the optimal method might involve an algorithm that incorporates clinical data, ventilator-derived data, and laboratory data to determine the timing and likelihood of successful liberation from the ventilator. A randomized trial from 1995 compared four different weaning methods: (1) daily 2-hour SBTs, (2) twice-daily 2-hour SBTs, (3) gradual reduction of pressure support, and (4) gradual reduction of the IMV rate.the two SBT methods were superior in predicting successful extubation. 13 In a follow-up study, the investigators reported that a 30-minute SBT was as effective as a 2-hour SBT, and the shorter duration is now preferred for most patients. 14 Other traditional parameters used to predict the end of the need for mechanical ventilation are respiratory rate, rapidshallow breathing index (RSBI; calculated as frequency divided by V T ), V T, vital capacity, pressure-time product, and negative inspiratory force.these variables are useful adjuncts in the assessment of a patient s readiness to undergo an SBT, but they are not highly accurate in predicting the likelihood of successful extubation when used alone. 15 It is not necessary for the acute process to have resolved completely before an SBT can be performed, provided that other predetermined criteria are met [see Table 1].To await normalization of the P/F ratio or resolution of the chest x-ray abnormality would result in a needless delay in extubation should the patient successfully complete the SBT. Unnecessary prolongation of mechanical ventilation heightens the risk of ventilator-associated pneumonia [see 7:17 Postoperative and Ventilator-Associated Pneumonia], increases sedation requirements, postpones mobilization, and delays discharge from the ICU. 16 SPONTANEOUS BREATHING TRIAL SBTs should be performed on a daily basis once the acute respiratory process has resolved and the patient is hemodynamically normal [see Table 1]. PEEP should be set at 5 cm H 2 O, with or without an additional 5 cm H 2 O of pressure support (if the endotracheal tube is less than 7.0 mm in diameter).the F I O 2 should be set to a value approximately 10% greater than required while the patient is fully supported, and the patient should be allowed to breathe spontaneously for 30 to 120 minutes. At the conclusion of the SBT, blood gas values should be obtained, and the patient should be placed back on the ventilator at the previous settings. At all times, the patient s vital signs should be monitored for evidence of increased work of breathing. Criteria for a failed SBT include (1) significant changes in the respiratory rate, (2) evidence of increased work of breathing, (3) significant dysrhythmia, and (4) hemodynamic instability [see Table 1]. In addition, the arterial blood gas values should be evaluated for evidence of worsening hypoxemia or hypercarbia, though it should be kept in mind that a normal P a CO 2 is less important if the ph is within the normal range. If the patient successfully completes the SBT, extubation should be attempted. There are few reasons to continue mechanical ventilation in this situation. If it is suggested that the patient remain intubated, one should ask whether a further delay in extubation would improve the chances of success, and if so, how. Among the reasons frequently cited for continuing intubation are altered mental status and inability to protect the airway, a potentially technically difficult reintubation, the presence of an unstable injury to the cervical spine, the likelihood of return trips to the operating room, and the need for frequent suctioning. Each of these reasons must be balanced against the inherent risks of continued intubation, and a clear plan should be developed outlining how postponing extubation will alter the situation for the better. The patient with traumatic brain injury (TBI) presents a unique problem, for two reasons. First, the patient is often unable

10 7 MECHANICAL VENTILATION 10 to maintain an adequate airway. Second, the patient is often unable to clear upper and lower airway secretions adequately and thus is at risk for continued aspiration and pneumonia. In patients whose mental status is altered but who are expected to recover quickly, the risk imposed by 1 or 2 additional days of intubation is relatively small, and delaying extubation to wait for mental status to clear can be justified. In TBI patients whose recovery is anticipated to take months (if it happens at all), the options are early tracheostomy [see Tracheostomy, below] and attempted extubation. Ultimately, the choice between these two options should be made on a case-by-case basis. Although tracheostomy is often preferred, these patients can frequently be extubated without significant sequelae. 17 Failed SBT When a patient fails an SBT, the first priority is to determine the reason for the failure. Initially, it is important to distinguish between patients who fail to meet the extubation criteria for unrelated reasons (e.g., agitation or cerebral storming in a TBI patient) and those who truly are not ready to be liberated from the ventilator. Direct observation of the patient during the SBT, if feasible, may provide insight into the failed attempt. The next step is to attempt to identify the specific cause of the failure. In these situations, a thorough knowledge of the patient s history is important, with special attention paid to age, comorbid conditions, reasons for and duration of mechanical ventilation, other indices of critical illness, and nutritional status [see Table 2]. Failure is frequently multifactorial, and actions to improve one or more of these factors should be undertaken to alter the outcome of the next SBT. After a failed attempt, it is best to provide a stable, nonfatiguing form of respiratory support (e.g., PSV) until the following day, thus allowing the patient a period of rest. Patients who persistently fail SBTs are typically classified as exhibiting failure to wean. Comorbid conditions, including congestive heart failure, chronic lung disease, and renal or hepatic insufficiency, should be treated medically to the extent possible before further trials are attempted. The excess sodium and water frequently administered to critically ill patients can have negative effects on pulmonary mechanics, making liberation from the ventilator more difficult. Hydrostatic pulmonary edema, chest wall or visceral edema, and pleural effusions can have a greater impact on patients recovering from critical illness, who may be malnourished and deconditioned. General measures to facilitate weaning include judicious use of diuretics, upright positioning, correction of electrolyte abnormalities (in particular, low serum potassium or phosphate levels), and, in some cases, drainage of hydrothoraces. In addition, attention should be given to providing appropriate nutritional support while avoiding excessive carbohydrate administration (which can increase CO 2 production). Physical therapy should begin as soon as possible to prevent further muscle atrophy. In addition to these general measures, consideration should be given to performing a tracheostomy. Although there is disagreement about the optimal timing and method of tracheostomy in this setting (see below), it is obvious that this measure can greatly facilitate attempts to discontinue mechanical ventilation by eliminating the risks associated with extubation. When the tracheostomy is in place and all general measures have been considered, SBTs should resume. A very small percentage of patients are unable to tolerate the sudden reduction in support that occurs when they are treated with continuous positive airway pressure (CPAP) or a tracheostomy collar. These patients, who are often severely deconditioned after having been mechanically ventilated for several Table 2 Causes of Failed Spontaneous Breathing Trials Cause of Failure Anxiety/agitation Infection (pulmonary or extrapulmonary) Electrolyte abnormalities (low K +, low PO - 4 ) Pulmonary edema/cardiac ischemia Deconditioning/malnutrition Neuromuscular disease (critical illness polyneuropathy, myasthenia gravis) Increased intra-abdominal pressure (obesity, abdominal distention) Hypothyroidism Large hydrothoraces (rarely primary cause but may increase work of breathing in patients with marginal reserve) Excessive auto-peep (COPD, asthma) Excessive minute ventilation requirements: CO 2 production Metabolic acidosis Treatment Judicious use of benzodiazepines ± haloperidol Diagnosis and treatment of causative infection Correction of electrolyte concentrations Administration of diuretics ± nitrates Aggressive nutritional support (via enteral route whenever possible) Physical therapy Aggressive bronchopulmonary hygiene Specific treatment of myasthenia gravis (pyridostigmine, steroids, plasmapheresis) Early consideration of tracheostomy Semirecumbent positioning Nasogastric decompression Thyroid replacement Initiation of diuresis ± thoracentesis Bronchodilator therapy I.V. sedation to prevent agitation and air trapping Reduction of carbohydrate intake Treatment of underlying cause (e.g., lactate production or renal failure) Consideration of HCO 3 - replacement if wasting is present (e.g., with renal tubular acidosis or pancreatic fistula) weeks or longer, may benefit from a more gradual reduction in ventilatory support. In these cases, the term weaning is probably an accurate description of the process. A planned gradual reduction in support may be better tolerated with scheduled decreases in pressure support or, alternatively, with gradual increases in the duration of periods of unassisted breathing. In the setting of chronic ventilator dependence, neither method is necessarily superior to the other.what is important is that the patient should never be allowed to continue until exhaustion during the weaning process. Formulating a well-defined plan for weaning is more important than choosing a particular weaning method. One approach is to use a daily workout calendar similar to those used for athletic training, so that the details of the plan are clear and easily understandable by the patient, the family, the nursing staff, the respiratory staff, and the ICU team. Finally, both patients and families should be counseled to expect weaning to last a long time. PROTOCOL-BASED VENTILATOR MANAGEMENT Once respiratory failure has resolved, the patient s readiness for extubation is assessed. Traditionally, this assessment has been made by the physician. Unfortunately, both physician factors and