New Strategies for Mechanical Ventilation

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Lung Failure Across the Life Span

New Strategies for Mechanical Ventilation Lung Protective Ventilation Debra Wilmoth , RN , MSN

N urses have been caring for mechanically ventilated patients for 50 years, first with negativepressure ventilators (the iron lung) and now with positive-pressure ventilators. It is often difficult for medical personnel, and certainly for patients and their families, to realize that the mechanical ventilator is not a curative measure but a therapy that supports the body's physiologic functions, giving the lungs and the body time to heal. In fact, more and more data confirm that mechanical ventilation (MV) can be harmful, causing damage to the lungs and possibly acting as a source for sepsis and multiple organ dysfunction syndrome (MODS). Although research documents the iatrogenic damage of MV, there is no incontrovertible evidence describing the ultimate lung-protective ventilation (LPV) strategy. This article reviews the evidence base of LPV to assist the critical care nurse in using current management guidelines in patients with acute lung injury (ALI).

Complications of Mechanical Ventilation According to Tobin, 34 there are several objectives of MV, including improving gas exchange, relieving respiratory distress, and improving atelectasis and compliance; these usually take priority in patient management. He also mentions two additional ob-

From the Porter Medical Intensive Care Unit, University of Virginia Health System, Charlottesville, Virginia

jectives that are gaining popularity: avoiding complications and preventing further injury.34 Complications of MV include those related to the artificial airway, hemodynamic compromise, oxygen toxicity, barotrauma, and volutrauma. The reader is referred to basic critical care nursing texts for discussion of complications related to the artificial airway and hemodynamic compromise. Oxygen Toxicity

It has been recognized since 1945 that high fractions of inspired oxygen (F1o:z) can be harmful to the lungs. 6 The resultant injury is dependent on the level of F102 as well as on the length of exposure. 3' Oxygen free radicals are formed when normally protective antioxidants are overwhelmed by toxic oxygen concentrations; the oxygen free radicals cause an increase in shunt, alveolar-capillary leak, epithelial and endothelial damage, hyaline membrane formation, interstitial hemorrhage, fibrosis, decreased diffusing capacity, and atelectasis as a result of alveolar collapse. 6 Barotrauma and Volutrauma Barotrauma is the term that has historically been

used to describe alveolar air leaks induced by MV; pneumothorax is the most serious manifestation of barotrauma. The incidence of barotrauma in mechanically ventilated patients has been repotted to range from 5% to 15%. 38 Barotrauma is more likely to develop in patients with obstructive lung disease,37 who require MV and in the late stages of

CRITICAL CARE NURSING CLIN ICS OF NORTH AMERICA I Volume 11 I Number 4 /December 1999

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acute respiratory distress syndrome (ARDS) when fibrotic changes make the lungs more stiff and friable. It is thought that barotrauma is on the most severe end of a spectrum of diffuse lung injury that is caused by overdistension of alveoli with excessively large ventilating pressures and volumes. Gattinoni and associates 15 studied 84 patients with ARDS; 48.8% developed pneumothorax. Eighty-seven percent of these cases of pneumothorax developed in late ARDS (defined as ARDS lasting longer than 2 weeks), which is a significant increase over the incidence in either the early or intermediate ARDS group. In addition, mortality was significantly greater, and positive endexpiratory pressure (PEEP) was significantly lower in those patients who developed pneumothorax. There is a large body of experimental data that links the wider spectrum of ventilator-induced injury with overdistension of alveoli. This "volutrauma" is caused by overdistension, ripping, and stretching of the lung43 with high ventilating volumes and by the repeated opening and closing of alveoli with each respiratory cycle. The resultant damage, histologically similar to that in ARDS,20 includes an increase in endothelial and epithelial permeability with edema formation, depletion of surfactant, atelectasis, and microvascular hemorrhage. 38 Because the chest radiographs of ARDS patients are characterized by diffuse infiltrates, it was thought that the lung damage in ARDS was homogenous. Gattinoni et al1 6 have studied the lungs of ARDS patients using computed tomography and have shown that the ARDS lung is quite heterogeneous. As many as two thirds of all alveoli are collapsed and poorly compliant, and a smaller percentage of normally compliant alveoli receive the bulk of ventilation and are prone to overdistension. Although the lungs of any mechanically ventilated patient are at risk, there is an additive effect of ventilator-induced injury on the ARDS lung.

changes similar to those seen in early ARDS in an experimental group of pigs ventilated with a PIP of 40 cm of water compared with the control group, which was ventilated with a PIP of less than 18 cm of water. Hernandez et al1 7 showed that ventilatorinduced microvascular lung damage is the result of large volumes rather than high PIPs. Three groups of rabbits were ventilated with varying degrees of inspiratory volume limitation: closed-chest animals, animals encased in a full-body plaster cast, and animals with excised lungs with no limitation of VT. When a PIP of 15 cm of water was used, there was an 850% increase in the capillary filtration coefficient (a measure of permeability) in those lungs that had no volume limitation compared with no significant increase in the filtration coefficient in those lungs in which overdistension had been prevented with the full-body cast. Systemic Inflammation and Infection

Bronchoalveolar lavage fluid from rabbits subjected to injurious MV35 has been shown to contain inflammato1y mediators, most notably tumor necrosis factor-a and interleukin-I {3. The use of high volumes with no PEEP increased the tumor necrosis factor-a level by a factor of 56. In a study by Nahum et al, 27 Escherichia coli was instilled into the trachea of dogs. Those who were ventilated with high volumes and a low PEEP demonstrated a significantly greater incidence of E. colibacteremia than dogs ventilated with LPV strategies. It has been hypothesized that disruption of the alveolar-capillary interface may allow release of inflammatory mediators into the systemic circulation, contributing to the initiation of a systemic inflammatory response 35 and possibly MODS. 32 Indeed, the majority of deaths associated with ARDS are a result of MODS and not of respiratory failure. 10

Animal Data

Lung-Protective Ventilation Strategies

In a study published in 1974, Webb and Tierney41 showed that rats ventilated with 45 cm of water ventilating pressure (and no PEEP) developed alveolar and perivascular edema and severe hypoxemia and died within 1 hour. In a 1985 study,12 the alveoli of rats ventilated with a peak inspiratory pressure (PIP) of 45 cm of water and no PEEP for 20 minutes were flooded with a high-protein fluid. Kolobow and associates 22 found that sheep ventilated with a tidal volume (VT) of 50 to 70 mL/kg and a PIP of 50 cm of water developed severe respiratory failure with evidence of parenchymal consolidation at autopsy compared with a group of animals ventilated with a VT of 10 mL/kg and a PIP of 15 to 20 cm of water. Tsuno et al 36 found

LPV encompasses strategies believed to minimize the adverse effects of MV. One way to decrease these effects would be to obviate the need for MV. More and more interest is being devoted to noninvasive positive-pressure ventilation strategies19 as a replacement for MV in both chronic and acute respiratory failure. Once a patient is committed to invasive positive-pressure ventilation, LPV should be initiated from the outset in conjunction with a plan for weaning the patient as soon as physiologica.lly possible. The American-European Consensus Conference on ARDS recently agreed that despite an accumulating body of knowledge, there is currently no evidence base to recommend the "ideal" MV strat-

NEW STRATEGIES FOR MECHANICAL VENTILATION

egy, especially in ALI.4 The conference participants recommended that the goals of ventilator management should be to "ensure appropriate 0 2 delivery to vital organs along with sufficient C02 removal to maintain homeostasis, to relieve an intolerable breathing workload, and to avoid either extending lung damage or preventing tissue healing." 4 How can clinicians accomplish these goals? The literature4• 24 addresses three general objectives: (1) optimize oxygen supply and demand while minimizing F102, (2) minimize high airway pressures and volumes, and (3) recruit and prevent tidal collapse of alveoli. In addition, adjunctive and experimental methods may be considered when they are available. Minimize Fraction of Inspired Oxygen

Although there are no definitive data on which to base a recommendation for the "safe" upper level of F102, most experts agree that F102 should be limited to 0.50 to 0.65 or less4• 6• 10· 31 in order to obtain an oxygen saturation greater than 90% and a Pao2 of greater than 60 mm Hg. 30• 34 Optimize Oxygen Supply and Demand

In the setting of critical illness, metabolic needs are high, necessitating an enormous demand for oxygen by all body tissues, with resultant high levels of carbon dioxide production. Hypoxemia is frequently present, and it is difficult to maintain "normal" Pao2 levels, even with the use of toxic levels of F102• In addition, there is evidence that under certain conditions, the tissues are unable to extract an adequate amount of the oxygen delivered to them. It seems prudent to make every attempt to eliminate extraneous oxygen consumption and carbon dioxide production. Customary measures include control of fever; control of pain, agitation, and anxiety with the use of sedatives and analgesics; and appropriate nutrition.38 It is often necessary to use chemical paralysis in order to decrease the oxygen demand created by "fighting the ventilator" in response to uncomfortable ventilator modes or severe agitation. Adverse outcomes such as prolonged muscle weakness and myopathy may prolong ventilator weaning and rehabilitation, however. There is a trend toward maximization of sedation, reserving paralytics for shortterm use in those severely compromised patients who are resistant to other measures. 4 Clinicians attempt to maximize oxygen supply by manipulating the factors that contribute to oxygen delivery to tissues: oxygen content and cardiac output. Because oxygen binds to hemoglobin molecules, oxygen content may be improved by increasing hemoglobin. Van De Water39 recommends transfusing to a hemoglobin level not to exceed 15 g/dL, to avoid hyperviscosity. Optimizing intra-

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vascular volume and the use of dobutamine maximizes cardiac output when cardiac output is suboptimal.39 Fluid management is controversial. Judicious use of diuretics to lower the pulmonary wedge pressure may be beneficial in lowering the hydrostatic pressure in the lung already affected by increased permeability edema. 21 Another commonly used procedure that is thought to have a positive effect on oxygenation is the use of inverse ratio ventilation (IRV). The basic concept of IRV involves increasing the inspiratory time until it is equal to or greater than the expiratory time. It is thought that this maneuver may decrease shunt by recruiting alveoli and holding them open for a longer period of time in order to facilitate diffusion of oxygen. Despite a review by Shanholtz and Brower29 that indicates little evidence of an improvement in oxygenation with IRV, this ventilation strategy remains popular. More and more attention is being paid to the concept of alteration of the patient's position in an attempt to maximize oxygenation. The prone position is becoming popular as an adjunctive therapy, especially in the treatment of the patient with ARDS.40 Several studies have demonstrated an improvement in Pao2 and a decreased shunt in patients who were placed in the prone position. 1• 7• 13 In a study of 12 ARDS patients by Pappert et al,28 there was an overall increase in arterial oxygenation from 98.4 to 146.2 mm Hg. What is the mechanism for this improvement in oxygenation? As demonstrated by Gattinoni et al1 4 in computed tomography studies of ARDS patients, dependent alveoli are compressed and atelectatic. Lamm and associates23 found that turning the patient prone reverses the previously dependent alveoli to a nondependent position, generating enough transpulmonary pressure to exceed airway opening pressure and thus facilitating opening of the previously atelectatic alveoli. The result is a decrease in shunt; more oxygen is available for exchange with alveolar capillaries. Minimize Airway Pressures and Volumes

The bulk of LPV strategies involve recruitment of lung volume without overdistension of alveoli. Generally speaking, alveolar overdistension is reflective of alveolar volume and can be prevented by limiting ventilating pressures. This concept may be hard to understand until we remember the relationship between pressure and volume in the lung. If the patient is on a volume mode of ventilation, the desired VT is set, and the ventilator delivers that VT no matter what presure is required. Higher pressures are required to deliver volume to patients with increased airway resistance or stiff noncompliant lungs. On the pressure-volume curve of the lung, as pressure inside the lung increases, volume increases linearly to a point. Above this "upper

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Time Figure 1. Plateau pressure waveform; volume-cycled ventilator mode. Although the plateau pressure is generally read from the ventilator's manometer, it can also be visualized and measured using pressure waveform monitoring. Note the beginning of a typical volume-cycled waveform that is interrupted by a pause at end-inspiration and the plateau, until the pause is released. This plateau pressure would be measured at 31 cm of water.

inflexion point," further increases in pressure cause alveolar overdistension and a decrease in compliance. Based on this principle and the results of the animal studies discussed previously, most clinicians currently advocate a ventilation strategy that involves limiting lung volumes by limiting the plateau pressure. Plateau pressure (Fig. 1) is an estimate of alveolar pressure at end inspiration and can be easily measured at the bedside. The criteria for the measurement of plateau pressure are listed in Box 1 on this page.

Box 1 MEASUREMENT OF PLATEAU PRESSURE • The patient must be on a volume-cycled mode (intermittent mandatory ventilation or assist-control). • The patient cannot make spontaneous breathing efforts during measurement. • At the end of the inspiratory phase, apply an inspiratory hold. Most ventilators have an "inspiratory pause" or " inspiratory hold" button or switch for this purpose. • Watch the pressure manometer until the pressure stabilizes (plateaus). This takes only a few seconds. • Release the inspiratory hold and record the plateau pressure. • If the patient is on a pressure-cycled ventilator mode, ask the respiratory therapist to assist you in measuring the plateau pressure.

The target plateau pressure is 30 to 35 cm of water, 4•20•30 which corresponds to the alveolar pressure required to inflate the lungs to total lung capacity. In order to attain the target plateau pressure, the VT is usually limited.31, 38 What happens when the VT is reduced? Minute ventilation is a factor of VT and respiratory rate. If the VT is reduced without a compensatory increase in respiratory rate, minute ventilation falls. The Paco2 level rises, resulting in hypercapnia. For many years, it was believed that the goal of MV was to achieve and maintain normal levels of oxygen and carbon dioxide. This required the routine use of VT up to 15 mIJkg. Goals for desirable Pao2 and Paco2 levels have changed over the years. It is now common to allow carbon dioxide to rise gradually. This strategy is called "permissive hypercapnia" (PHC), 42 and some degree of PHC is practiced by many clinicians today. Permissive Hypercapnia

PHC is an LPV strategy in which the Paco2 level is allowed to rise as the result of the use of VTs as small as 5 mIJkg. As long as it is allowed to rise gradually, the absolute level of Paco2 is not as important as the pH. The pH may drop to as low as 7.20, at which point some clinicians administer sodium bicarbonate, although others do not. Although there is no concrete evidence and some controversy as to whether PHC is part of the ultimate answer to the prevention of volutrauma, one study by Hickling et al1 8 is often cited as a basis for its use. Hickling and his associates retro-

NEW STRATEGIES FOR MECHANICAL VENTILATION

spectively evaluated a group of 50 ARDS patients on the basis of three systems that score illness severity and predict mortality (AP ACHE II, lung injury score, Pao 2 : F10 2 [P: Fl ratio). In these patients, they employed a strategy of PHC, where PIP was usually maintained at less than 30 cm of water and always at less than 40 cm of water by reducing the VT to as low as 5 mL/kg. The actual mortality rate of this group was compared with the mortality rate predicted for the group using the three scoring systems. Although the study has been criticized for its lack of controls, Hickling's group showed lower mortality with the use of the PHC strategy. Based on APACHE II scores, the hospital mortality rate for this group of patients was predicted to be 39.6%; the group's actual mortality rate was 16%. 18 PHC is contraindicated in patients who have elevated intracranial pressure because of the vasodilatory effect of elevated Paco 2. There is some hyperdynamic effect associated with acute elevations in Paco 2; PHC should be used with caution in patients who have right or left ventricular dysfunction. 37 The action of exogenous catecholamines may be inhibited in an acidemic environment. In those patients who require high pressor doses for blood pressure support, the acidemia may need to be improved, requiring a reduction in the level of hypercapnia. Pressure Control Ventilation

The use of a pressure mode of ventilation in the treatment of ALI patients touts the ability to limit ventilating pressures with more laminar air flow, facilitating oxygenation. Despite a lack of evidence of its efficacy, pressure control ventilation, sometimes used in combination with IRV, is commonly employed. The reader is referred to a review by Bums9 for a more complete description of the pressure control ventilation mode. As is the case with any pressure mode, the VT is variable depending on airway resistance and lung compliance; nursing implications include the hourly monitoring of the VT. Because of the patient discomfort associated with this mode, especially when it is combined with IRV, sedation (and often, chemical paralysis) is required. High-Frequency Ventilation

High-frequency ventilation (HFV) has been touted as a mode that has the capability of limiting volutrauma. It uses small VTS (1-5 mL/kg) at rares of 60 to 3600 cycles per minute. The reader is referred to a review by Burns8 for a discussion of the application and nursing implications of HFV. Prospective clinical trials have failed to show any superiority of HFV over other ventilation strategies in ARDS patients. Cawley and associates 10 recommend that

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HFV continue to be studied and that it be considered investigational therapy at the present time. Extracorporeal Carbon Dioxide Removal

Extracorporeal carbon dioxide removal involves diverting blood from the body to an extracorporeal filter that removes carbon dioxide and supplies oxygen to the blood before it is returned to the body. This procedure is usually done in conjunction with a strategy of low-volume LPV. Marini 25 advocates limiting the use of extracorporeal carbon dioxide removal to severe or rapidly deteriorating patients at centers experienced in its use. Positive End-Expiratory Pressure

Perhaps the most important strategy in LPV is the use of levels of PEEP that are adequate to recruit marginal alveoli and keep them open at end expiration. The tidal opening and closing of alveoli has been implicated in damage to lung tissue caused by shear stress forces, especially at points of alveolar junction. In addition, it is thought that this opening and closing in some way inactivates surfactant. 24 Muscedere et al 26 demonstrated decreased compliance and progression of lung injury in rats ventilated with extremely low VTs from repeated opening and closing of alveoli, concluding that ". . . end-expiratory lung volume is an important determinant of the degree and site of lung injury during positive-pressure ventilation." In contrast to the earlier belief that high levels of PEEP would cause barotrauma, especially in the ARDS patient, it is now thought to be important to keep the lung "open" with the use of adequate PEEP early in the course of ARDS, decreasing PEEP levels during the fibrotic phase when most barotrauma occurs. In a randomized controlled clinical trial Amato et a!2 investigated the "open lung approach" to ventilation. The basis of this approach is to avoid overdistension of the lung by limiting pressures and volumes in conjunction with minimizing tidal collapse and reopening alveoli. The ideal or "best" PEEP level was identified by calculating the lower infection point (Pn.J on the pressure-volume curve and setting the PEEP at 2 cm of water above that level. The Pnex reflects that point at which an increase in pressure causes the volume to increase at a greater proportion than before and represents the volume and pressure at which the majority of recruitable alveoli have been opened. In those patients in whom a Pnex could not be demonstrated, the total PEEP was randomly set at a level of 16 cm of water, corresponding to the mean ideal PEEP level established by the authors in a previous study. The experimental group of patients with early ARDS was ventilated using a pressure-limited mode with a VT less than 6 mL/kg, peak pressures less than 40 cm of water, a respirato1y rate less

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than 30 breaths per minute, PHC, and a PEEP of 2 cm of water above Pnex or 16 cm of water. The control group was ventilated using the assistcontrol mode, a VT of 12 mVkg, a respiratory rate of 10 to 24 breaths per minute to keep Paco 2 less than 38 mm Hg, and a PEEP set initially at 5 cm water and increased according to F10 2 and hemodynamics. The following results were seen in the experimental group: (1) an improvement in compliance during the first week of MV, (2) an improvement in P : F ratio, (3) shorter periods of greater than 0.50 F10 2 requirement than in the control group, (4) a lower F10 2 on the day of death than in the control group, and (5) a higher weaning rate when adjusted for AP ACHE II score. There was no significant difference in mortality rates between the two groups. The authors point out that many LPV maneuvers were used in the experimental group in this study, making it difficult to differentiate the relative importance of each maneuver. Nevertheless, they conclude that the "strategy can markedly improve the lung function in patients with ARDS, increasing the chances of early weaning and lung recovery during mechanical ventilation." 2 A study in rats by Dreyfus and associates 11 demonstrated that the addition of 10 cm of water PEEP to highpressure and high-volume ventilation reduced the edema and prevented the alveolar flooding and epithelial lesions seen in a similar group of rats ventilated without the addition of PEEP. In a study published in 1998, Amato et al3 continued their earlier work by comparing two groups of ARDS patients. The control group was ventilated using a "conventional" approach (VT of 12 mVkg, volume-cycled mode, respiratory rate of 10 to 24 breaths per minute to maintain a Paco2 of 35 to 38 mm Hg independent of airway pressures, F102 <0.60, and minimum PEEP of 5 cm of water with incremental increases to maintain adequate oxygenation). The LPV group was ventilated using a VT of less than 6 ml/kg, pressurelimited mode, driving pressure (plateau pressure - PEEP) less than 20 cm of water and peak airway pressure less than 40 cm of water, respiratory rate less than 30 breaths per minute, and PEEP at 2 cm of water above Pnex (the maximum PEEP used was 24 cm of water) or 16 cm of water total PEEP when Pnex was not able to be determined. In addition, recruiting maneuvers meant to aerate alveoli and requiring extremely high opening pressures were employed in the experimental group. These recruiting maneuvers consisted of the "frequent" application of continuous positive airway pressures of 35 to 40 cm of water for 40 seconds, especially after any interruption in MV. The difference in survival rates between the groups was so significant that the study was stopped during the fifth interim analysis; after 28 days, 38% of the patients in the LPV group had died as opposed to 71% in the conventional MV group. In addition, a more favorable weaning rate was demonstrated in the experi-

mental group (66% vs 29% in the conventional MVgroup). An intriguing finding was that the rate of barotrauma was significantly higher (42%) in the conventional MV group, in which the lowest possible PEEP was used, compared with 7% in the experimental group, where higher than normal levels of PEEP were employed. This finding supports the hypothesis that levels of PEEP higher than those conventionally used may prevent lung injury instead of inducing barotrauma, at least when they are used early in ARDS. Stewart et al33 undertook a prospective study to determine the effect of limiting ventilating pressures and volumes on the mortality rate of patients with ARDS. The experimental group had a VT limited to 8 mL/kg with a PIP no greater than 30 cm of water. The control group had a VT of 10 to 15 mVkg with a PIP as high as 50 cm of water. The study showed no difference in in-hospital mortality rates between the two groups. The authors conclude that their results suggest that LPV strategies do not decrease m01tality. Nevertheless, two factors call this conclusion into question. First, even though the plateau pressure was not controlled in this study, the mean plateau pressure of patients in the control group was 28.5 cm of water. Second, the level of PEEP was not controlled in either group and was similar in both. Therefore, there was no comparison of the effect of prevention of alveolar collapse and tidal reopening, making a comparison with the results of Amato's group 3 difficult. As is the case with other LPV strategies, the ideal level of PEEP that can be recommended for use in the ARDS patient requires further study. Marini24 advocates maintaining the total PEEP at several cm above Pnex (in general, > 7 but < 20 cm of water). The American-European ARDS Consensus Conference recommends using PEEP levels that obliterate Pnex (total PEEP of 10 to 15 cm of water in most instances) in addition to utilizing periodic sigh breaths to prevent atelectasis .5

Implications for Nurses What can the bedside clinician do to assure that ventilator-induced lung damage is minimized? First, screen all mechanically ventilated patients every day for the development of ALI or ARDS as defined by the criteria developed by the AmericanEuropean Consensus Conference on ARDS. 5 A list of those diagnostic criteria is found in Box 2 on the next page. Although it is important to use LPV in all mechanically ventilated patients, it is certainly necessary to employ these strategies as early as possible in the evolution of ALI. It is helpful to trend the P : F ratio, measuring it daily to monitor an improvement or deterioration in the patient's lung function. The critical care nurse should monitor the ventilator mode and settings of each patient every shift.

NEW STRATEGIES FOR MECHANICAL VENTILATION

Box 2 DIAGNOSTIC CRITERIA FOR ACUTE LUNG INJURY AND ACUTE RESPIRATORY DISTRESS SYNDROME

Acute Lung Injury • Acute in onset • Bilateral infiltrates on chest radiograph • Pulmonary artery wedge pressure less than 18 mm Hg or no clinical evidence of left atrial hypertension • Pao2 : F10 2 ratio less than 300 mm Hg Acute Respiratory Distress Syndrome • Acute onset • Bilateral infiltrates on chest radiograph • Pulmonary artery wedge pressure less than 18 mm Hg or no clinical evidence of left atrial hypertension • Pao 2: F10 2 ratio less than 200 mm Hg Adapted from Bernard GR, Artigas A, Brigham KL, et al: The American-European Conference on ARDS: Definitions, mechanisms, relevant outcomes, and clinical trial coordination. Am J Respir Crit Care Med 149:818-824, 1994; with permission.

Settings to be monitored include F10 2, VT, respiratory rate, and total PEEP level. Monitor the plateau

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pressure every shift so that high plateau pressures (>35 cm of water) can be averted by applying LPV strategies. In patients with ARDS, it is helpful to measure daily trends in static compliance. The static compliance of the lung tells us how easy it is to distend the lung and the chest wall-in other words, the stiffness of the lungs. A lower compliance ( < 50 mL/cm of water) indicates greater shunt, because the lungs are unable to fully expand, limiting oxygen exchange across the alveolar-capillary membrane. To calculate static compliance, use the formula: VT + (plateau pressure - total PEEP) A compliance of less than 50 mL/cm of water with a decreasing trend correlates with a worsening shunt, indicating a deterioration in lung function. An improving trend indicates that lung function is improving. Finally, the critical care nurse should become familiar with the plethora of ongoing research in adjunctive and experimental therapies for ARDS as well as with new approaches to MV so that he or she is able to monitor changes in the patient's condition and suggest appropriate LPV strategies to the multidisciplinary team.

SUMMARY Although research is ongoing, and there are no definitive data to mandate the final answer to the question of which ventilation strategies result in the most optimal outcomes, the consensus of clinicans today suggests that we limit F10 2 to nontoxic levels, limit ventilating pressures and volumes, and use PEEP levels adequate to recruit alveoli and prevent tidal collapse. The critical care nurse must remain vigilant in his or her review of current literature to maintain knowledge of the current recommendations for optimal MV strategies.

ACKNOWLEDGMENT The author thanks Suzanne Burns, RN, MSN, RRT, CCRN, ACNP-CS, for her continued support, mentorship, friendship, and editing.

REFERENCES 1. Albert RK, Leasa D, Sanderson M, et al: The prone

position improves arterial oxygenation and reduces shunt in oleic-acid-induced acute lung injury. Am Rev Respir Dis 135:628-633, 1987 2. Amato MBP, Barbas CSV, Medeiros OM, et al: Beneficial effects of the "open lung approach" with low distending pressures in acute respiratory distress syndrome. American Journal of Respiratory Critical Care Medicine 152:1835-1846, 1995 3. Amato MBP, Barbas CSV, Medeiros OM, et al: Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome. N Engl J Med 338:347-354, 1998

4. Artigas A, Bernard GR, CarletJ, et al: The AmericanEuropean Consensus Conference on ARDS, part 2: Ventilatory, pharmacologic, supportive therapy, study design strategies and issues related to recovery and remodeling. Intensive Care Med 24:378-398, 1998 5. Bernard GR, Artigas A, Brigham KL, et al: The American-European Consensus Conference on ARDS: Definitions, mechanisms, relevant outcomes, and clinical trial coordination. American Journal of Respiratory Critical Care Medicine 149:818-824, 1994 6. Bezzant TB, Mortensen JD: Risks and hazards of mechanical ventilation: A collective review of published literature. Disease-a-Month 60:586-638, 1994 7. Blanch L, ManceboJ, Perez M, et al: Short-term effects of prone position in critically ill patients with acute respiratory distress syndrome. Intensive Care Med 23:1033-1039, 1997 8. Burns SM: Advances in ventilator therapy: Highfrequency, pressure support, and nocturnal nasal positive pressure ventilation. Focus on Critical Care 17:227-237. 1990

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