Crtt Care Nurs Q Vol. 27, No.

Crtt Care Nurs QVol. 27, No. 4, pp. 325-335© 2004 Uppincott Williams & Wilkins, Inc.

Adult Respiratory DistressSyndrome

Cynthia Kane, MS, RN, APRN; Susan Galanes, MS, RN, APRN

ARDS or acute respiratory distress syndrome continues to be a considerable critical care challenge.Mortality has not decreased significantly over the last more than 30 years. This article presents anoverview of origin, evaluation, and treatment of ARDS. Recent findings relative to onset and pre-cipitators of ARDS have led to changes in evaluation and treatment plans. Clinical and radiologicdescriptors in assessment of the patient with ARDS are discussed. Ventilatory modes and nurs-ing interventions to optimize patient outcomes are identified. The challenges of outcomes issuespresented offer opportunities for further study. Key words: adult respiratory distress syndrome,ARDS, high-frequency ventilation, nitric oxide, outcomes

EPIDEMIOLOGY/INCIDENCE

Acute respiratory distress syndrome (ARDS)was introduced into the medical literature byAshbaugh and colleagues in 1967, when theydescribed 12 patients who developed a res-piratory distress syndrome which was mani-fested by acute onset of hypoxemia, tachyp-nea, decreased pulmonary compliance, anddiffuse alveolar infiltrates on chest x-ray' Ofthese 12 patients, 7 had severe trauma, 4 hadviral infections, and 1 had acute pancreatitis.The mortality rate was 58% (7 of 12 patients).Case reports dating back to World War I andWorld War II revealed that trauma and sepsismay affect pulmonary function. However, itbecame more evident during the Vietnam era,as patients who previously would have diedwere resuscitated w ith advanced medical careand went on to develop the above pulmonarymanifestations. Their 1967 paper was the firstto define the ARDS. In the following years, thissyndrome w as referred to as the adult respLra-

From the Suburban Lung Associates, Elk GroveVillage, III (Ms Kane); and the Suburban LungAssociates, Winfield, III (Ms Galanes).

Corresponding author: Cynthia Kane, MS, RN, APRN,Suburban Lung Associates, 801 Biesterfield Rd, ElkGrove Village, IL 60007 (e-mail: cindy.kane®sublung.com).

tory distress syndrome, to distinguish it fromthe infant respiratory distress syndrome. The1992 American-European Consensus Confer-ence on ARDS decided that there should be areturn to the original term acute rather thanadult, since the syndrome is not limited toadults. '*

The American-European Consensus Confer-ence Committee on ARDS redefined acutelung injury (ALI) and ARDS. '* Both are acutein onset, last for days to w eeks, are char-acterized by arterial hypoxemia resistant tooxygen therapy alone, and display diffuse ra-diologic infiltrates. Both definitions include apulmonary artery w edge pressure (PAWP) ofless than or equal to 18 mm Hg when mea-sured, or no cUnical evidence of left atrial hy-pertension. The difference in definition be-tween ALI and ARDS is related to oxygenation,defined as PaO2/FiO2 < 300 mm Hg for ALI cri-teria, and PaO2/FiO2 < 200 mm Hg for ARDScriteria.

Since 1967 when the term acute respira-tory distress syndrome w as introduced intothe literature, there have been thousandsof publications addressing all aspects ofARDS. It is estimated that there are 150,000cases of ARDS in the United States annually.'*Incidence of ARDS throughout the w orld hasbeen variable, ranging from 1.5 to 13.4 cases/100,000/year.5-8 Qjjy ^^^ ^f these studiesaddresses incidence using the ALI and ARDS

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definitions set forth by the American-European Consensus Conference. Furtherstudies defining incidence using the newARDS criteria are needed.

Mortality rate for ARDS is between 40% and60% and has remained in this range with lit-tle change over the last 30 years despite ex-tensive research and literature devoted to it.In 1995, Krafft reported that the standardfor outcome in ARDS should be a mortalityof 50%. Recent reports are showing somepromise with a decline in mortality,'"" andsome of this decline has been due to theuse of permissive hypercapnea and low tidalvolumes.'^'"

ETIOLOGY/PRECIPITATORS

There are a number of clinical conditionsthat result in systemic inflammation leadingto the lung injury process with ARDS. TheAmerican-European Consensus Conferenceon ARDS recommended categorizing the riskfactors into direct and indirect categories.^''The direct-injury risk factors include aspira-tion, diffuse pulmonary infection (eg, bac-terial, viral, or pneumocystis infection etc),near-drowning, toxic fume inhalation, andlung contusion. The indirect injury risk fac-tors include sepsis syndrome with or withouthypotension or evidence of infection outsidethe lung; severe nonthoracic trauma; hyper-transfusion for emergency resuscitation; andcardiopulmonary bypass. The incidence ofARDS increases when sustained hypotensionoccurs.^-' In 1995, Hudson et al found thatthe highest incidence of ARDS occurred in pa-tients with sepsis syndrome (43%) and those•who had multiple emergency transfusions(40%).''' Garber et al showed a strong cause-effect relationship for increased incidence ofARDS with sepsis, aspiration, trauma, and mul-tiple transfusions.'^ Other inciting factors in-clude cardiopulmonary bypass, fat embolism,pancreatitis, and drug overdose.^''-''' Inciden-tally, it is also noted that the incidence ofARDS in severe acute respiratory syndrome(SARS) is listed at 25%.'^

PATHOPHYSIOLOGY

ARDS is a syndrome of lung injury de-fined by physiologic and radiologic criteriain which diffuse damage to cells and thealveolar<apillary membrane composite oc-curs within hours to days of a predispos-ing insult.'^ The National Heart, Lung, andBlood Institute (NHLBI) AU/ARDS workinggroup consensus is that ARDS is a systemicsyndrome.'^"'^ Systemic responses to stressinvolve neural, endocrine, pro and antiin-flammatory mechanisms that are adaptive orpathologic.

Specifically, cells of the alveolar-capillarymembrane as well as those of the immune andhemostatic systems are targets of damage, andmay effect injury in ARDS.

The alveolar-capillary barrier comprises themicrovascular endothelium and the alveo-lar endothelium. As endothelial permeabil-ity increases, protein-rich edema fills theair spaces." Resultant damage to epithelialtype 2 cells causes surfactant production todecrease.'^ Further disruption of alveolar/epithelial integrity leads to increased perme-abUity and alveolar flooding of edema. In addi-tion, neutrophils adhere to the damaged cap-illary membrane and transfer into alveolar airspaces.'''

Alveolar macrophages secrete cytokines; in-terleukins 1, 6, 8, and 10; and tumor necro-sis factor alpha (TNF-a). '* These act locally toadvance chemotaxis and activate neutrophils,further compromising oxygenation and de-creasing contractility. Alveolar epithelial cellsproduce cytokines in response to stimuli suchas lung stretch, which is exacerbated by me-chanical ventilation forces. The degree of alve-olar epithelial injury is an important predictorof outcomes." Lung stretch induces local andsystemic cytokine release. These mechanical-ventilation-based mediators, endotoxins, andbacteria, may also translocate into systemiccirculation.'^'^ Genetic factors may be re-sponsible for its onset, as significantly smallersubsets of patients in any ARDS trigger groupgo on to develop this severe inflammatoryprocess.'^

Adult Respiratory Distress Syndrome 327

The first phase is the acute or exudativephase, with rapid onset of respiratory fail-ure, bilateral infiltrates, and refractory hy-poxemia. Diffuse alveolar damage occurs andprogresses rapidly. This occurs in context ofcapillary injury and disruption of the alveo-lar capillary membrane. Other complicationsinclude mechanical-ventilation-induced baro-traumas and thrombotic considerations.'^

Later phase changes include a subgroup ofpatients who progress to fibrosing alveolitiscomplicated by alveolar tissue necrosis.'^ Pul-monary hypertension may be severe'^'^'^";how^ever, in many patients radiographic andpulmonary function tests return to normal.

EVALUATION OF ARDS

Clinical examination

Physical examination parameters providesupporting data, but little definitive diagnos-tic clarity. ARDS usually develops within 24to 48 hours of initial injury or insult,'^'^^and clarification of clinical examination find-ings over a short duration may be difficult.Dyspnea with tachypnea generally presentsfirst, and patients may be in considerablerespiratory distress.^" This often is accompa-nied by shallow^ inspiratory effort, as compli-ance decreases. Tissue perfusion alterationsmay be evidenced by the skin appearingmottled, or cyanotic. Auscultation will revealcharacteristic findings associated with thepredisposing cause, and may include crack-les, decreased sounds, or wheeze. As ARDSprogresses and both compliance and pro-inflammatory changes worsen, lung soundsmay become significantly decreased, with ar-eas of consolidation and pneumonia.'^•^'' Ap-plication of end-expiratory pressure compli-cates assessment. In addition, if the patientis being managed on oscillating ventilation orhigh-frequency ventilation, accuracy of aus-cultation is of limited utility.' '

Radiologic evaluationChest radiographs usually show diffuse bi-

lateral infiltrates, but with a normal cardiac

silhouette. Infiltrates are generally focal, andmay be very similar to those of severe car-diogenic pulmonary edema.^^ Changes inserial chest radiographs often show rapidprogression of dependent bilateral infiltratesprogressing to diffuse interstitial infiltratesthroughout.'^'

Computed tomographic (CT) scanning hasdemonstrated that alveolar consolidation andatelectasis occur most often in dependentlung zones; other areas may be relativelyspared. "* However, even areas that appear rel-atively radiologically spared may have substan-tial inflammation present.^' Bugedo foundimproved aeration of poorly aerated and non-aerated tissue by 16% and 33%, respectively,per CT during recruitment measures.^^ Radio-logic follow-up should be closely monitored,as some patients show progression to fibros-ing alveolitis w ith linear opacities consistentwith fibrosis.

Pneumothorax may be a significant com-plicating factor, which has been reported tooccur in 10% to 13% of ARDS cases, and isnot clearly related to levels of positive end-expiratory pressure or airway pressure.'^-'^'^^However, barotrauma has been associatedwith higher level plateau pressures.'^''^

Pulmonary vascular permeability develop-ment has been evaluated by use of positronemission tomography (PET) scans. Althoughinitial data has been promising, barriers existrelated to availability and some difficulty clar-ifying pulmonary edema due to left heart fail-ure comparative to ALI/ARDS. ^

Blood gas analysisArterial blood gas (ABG) analysis is key to

evaluation of patients w ith suspected ARDS.Hypoxemia is severe, and it may seem outof proportion to chest x-ray. Pulmonary rightto left shunting because of infiltrates and at-electatic areas contribute to worsening hy-poxemia, which is resistant to increasing FiO2.Initial presentation of respiratory alkalosiswith a very low PaO2 and normal or lowPacO2 and elevated pH is an early indication ofprogression of diffuse alveolar compromise.^^

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The American-European Consensus Confer-ence defines ARDS as PaO2/FiO2 < 200, bilat-eral infiltrates, and PAWP < 18 mm Hg, or noclinical evidence of left atrial hypertension.'^This may be preceded by acute lung injurywith a PaO2/FiO2 ratio of less than 300. Aftertreatment is initiated, the goal FiO2 is less than60%, as hyperoxia can lead to excessive oxi-dant production, protein oxidant damage, andcell death. i«

Carbon dioxide levels initially presentwithin normal or low-normal ranges. Oncetreatment ensues, current recommendationsinclude low tidal volumes. Significant airwaytrauma decreases when there is no recurrentopening and closing of alveoli, which tradi-tionally occurs with higher tidal volumes.'^A consequence of this volume-related avoid-ance of barotraumas is relative hypoven-tilation. This in turn increases the PCO2,which then low^ers the pH. Although aci-dosis increases the significant inflammatoryprocess, the negative effects of barotraumas/volutrauma are lessened because of this lowertidal volume. The net result has been linked todecreased mortality. ^

Cardlogenic issuesHypoxemic issues, w^hich continue after ap-

plication of support, suggest further cardio-logic evaluation. When there is doubt aboutthe presence of heart failure, right heartcatheterization is helpful. Typically, PAWPis lo^v (<18 mm Hg) in ARDS, and high(>20 mm Hg) in heart failure.'^ Compromisein intravascular volume along with positiveend-expiratory pressure (PEEP) results in de-creased cardiac output.^^ Sepsis and diuretictherapy contribute to relative volume deple-tion. Despite significant fluid loads withinthe pulmonary bed, blood volume issues arecritical. Tissue perfusion and oxygen deliveryreflect adequacy of the cardiopuknonary sta-tus. If this is not maintained, or is interrupted,poor perfusion contributes further to multi-ple organ failure. The range of volume man-agement is narrow, as both overhydration andaggressive diuresis cause significant variation

in tissue perfusion. Generally, patients withARDS do better w^hen kept on the dry side.^"Complications such as acute cor pulmonalemay be minimized by protective ventilation.'**In addition, recruitment maneuvers may beassociated with hypotension, but this is notsustained.''"'^

Late-phase clinical evaluation

Clinical manifestations of the fibroprolifer-ative phase include fever, leukocytosis, dif-fuse alveolar infiltrates on chest radiograph,and persistent inflammatory mediators in theserum.'^''® Associated physiologic manifesta-tions include worsening of pulmonary com-pliance, abnormal gas exchange, increaseddead space ventilation, pulmonary hyperten-sion, and lack of PEEP response.

TREATMENT AND COURSE

Identification and treatmentof precipitator

Multiple organ failure is listed as the mostcommon cause of death in patients withARDS. ARDS is often associated with a sys-temic inflammation leading to multiple organfailure. Treatment of the inciting cUnical dis-order is important in the initial managementof ARDS. The diagnostic evaluation should beguided by the patient's history. Evaluation ofa septic source should be done early in pa-tients deemed septic, looking at pulmonaryand extrapuknonary sites of infection. Intra-abdominal sepsis should be considered earlyin patients with sepsis syndrome w ho exhibitacute lung injury of uncertain etiology.

Several reports have listed that the high-est incidence of ARDS is associated with sep-sis syndrome and that these patients alsoexperience a higher mortality and worseprognosis than lung injury induced by othermechanisms.^''^ Early evaluation and specificmedical or surgical treatment of the source ofsepsis can enhance the chance of survival.

Use of recombinant human activated pro-tein C for appropriate patients will reduce

Adult Respiratory Distress Syndrome 329

mortality in patients with severe sepsis.'' Forother insults, such as aspiration or multipletransfusions, care should be focused on pre-vention of recurrence. Optimal supportivecare is recommended for all acute lung in-juries with ARDS due to various causes.

VENTILATION

Mechanical ventilation is the mainstay ofsupportive care in ARDS to provide ade-quate oxygenation and to stabilize ventilation(Table 1). Initially, with any form of res-piratory failure, standard ventilatory strate-gies may be utilized, using flow-controlledvolume-cycled ventilation, with a tidal volume(TV) of 10 tol5 mL/kg. In recent years, it hasbecome more evident that the standard ven-tilation for patients with ARDS is the use ofsmall tidal volumes so as to be protective tothe lungs and to prevent ventilator-associatedlung injury.'^'^"'^ The Acute Respiratory Dis-tress Syndrome Network Study found a de-crease in mortality and a decrease in venti-lator days by using a lower TV of 6 miykgand a plateau pressure of less than or equalto 30 cm YliO}^ This has also been show nin past studies that limited peak airway pres-sures and reduced overdistention of the lungby using low tidal volumes and permissive

Table 1. Ventilator management goals inARDS*

TV at 6 miykg (minimum 4 mL/kg andmaximum 8 mL/kg)

Plateau pressure < 30 cm H2O (adjust TV asnecessary)

Keep FiO2 < 60% (minimize O2 toxicity)Utilize PEEP at 5-15 cm H2O (recruit alveoU)Permissive hypercapnia (PacO2 60-100;

pH > 7.25)Ensure adequate oxygenation (O2 saturation

88%-95%)

•TV indicates tidal volume; PEEI> positive enil-expiiatoryptessiue.

hypercapnia.'^'^ Permissive hypercapnia isan effective strategy for limiting the ventila-tory pressures by allowing Paco2 to rise.'^ It isgenerally felt that with permissive hypercap-nia, PacO2 may be kept in the range of 60 to100, and the pH maintained at more than orequal to 7.25 without deleterious effects.

To prevent ventilator-associated injury tothe ltings, plateau pressures need to be mon-itored vifith attempts to maintain them atless than or equal to 30 cm H2O.''*"' Thiscan be achieved by permissive hypercapnia,pressure-controlled ventilation, and pressure-limited volume cycled ventilation. Anotherprotective ventilation strategy includes an"open lung" technique in which PEEP is main-tained at a level above where alveoli collapse,and the distending pressure and volume islimited (TV < 6 mL/kg and driving pressures< 20 cm of H2O above the PEEP value),permissive hypercapnia, and use of pressure-limited ventilation modes.'^

PEEP can be used to increase end-expiratorytransalveolar pressure and volume, w hichleads to improved gas exchange. When oxy-genation requirements increase, a high FiO2may be used for brief periods as a tempo-rizing measure, with aggressive efforts to at-tempt to decrease the FiO2 to 60% or lower(which is generally considered to be safe).PEEP can be increased in an attempt to recniitalveoli by opening previously collapsed alve-oli and preventing further collapse.'^" PEEPdecreases intrapulmonary shxint, and there-fore improves arterial oxygenation. Potentialadverse effects of PEEP include a decreasein cardiac output, increase in dead space, in-crease in lung volume, and stretch dtiring in-spiration. The low est mean airway pressurethat achieves an acceptable level of arterialoxygenation w ith a nontoxic FiO2 should beused.'^

A retrospective review of 150 patients byPage et al found that with protective venti-lation (plateau pressure < 30 cm H2O) anda low positive end-expiratory pressure (PEEP< 10 cm H2O), there was a mortality of only38%.*^ In addition, the major fector associated

330 CRITICAL CARE NURSING QUARTERLY/OCTOBER-DECEMBER 2004

with the probability of dying was the severityof circulatory failure. Patients without circula-tory failure had a 95% recovery rate/°

ALTERNATIVE VENTILATOR MODES

Other alternative ventilator modes for ARDSinclude inverse ratio, high-frequency ventila-tion, extracorporeal membrane oxygenation(ECMO), and prone positioning. Inverse ratioventilation is a technique that changes thetime of the respiratory cycle so that inspira-tion and expiration time are equal or reversed.Normal inspiratory to expiratory (I/E) ratio is1:2 in a spontaneously breathing patient withnormal airways. With inverse ratio ventilation,the I/E ratio changes to 1:1 or even 2:1. The 2potential benefits are a reduction in peak in-spiratory pressure O IP) and an improvementin oxygenation from the prolonged inspira-tory time. "*' ' ' However, patients do not tol-erate reversals of I/E ratio well, and requireneuromuscular blockade to achieve this typeof ventilation.

There is renewed interest in high-frequencyventilation in an attempt to reduce lung in-jury and improve clinical outcomes in ARDS.Conventional ventilation w ith higher tidalvolumes is associated with potentiating orcausing further lung injury. It is generally feltthat the injuries occur from regional overdis-tension by excessive end-inspiratory lungvolumes related to the uneven distributionof ventilation, that injury occurs in the smallairways w hen they snap open and close,and injury occurs with shear force at themargins between atelectatic lung units andaerated units.'" High-frequency ventilationuses very small tidal volumes and allowshigher end-expiratory lung volumes with lessoverdistension than conventional ventilation.Also, the high respiratory rates allow^ themaintenance of normal or near-normal Paco2levels, despite the small tidal volumes.'*' Itlimits lung overdistension and prevents cycliclung collapse by maintaining end-expiratorylung volume. The broad classifications ofhigh-frequency ventilation include high-frequency positive pressure ventilation

(HFPPV), which uses 60 to 100 breaths/min;high-frequency jet ventilation (HFJV), whichuses 100 to 300 breaths/min; and high-frequency oscillation (HFO), which uses upto 2400 breaths/min. Auscultation of lungsounds is altered with the small tidal volumesat the supra physiologic rate. ^ Air movementis difficult to assess. Therefore, continuousmonitoring of oxygen saturation is necessaryto quickly address changes in oxygenation.Frequent ABG analysis and daUy chest radio-graphy is indicated. Patients are switchedback to conventional ventilation when theyare able to tolerate lower mean airwaypressures.''^

Derdak compared HFO with a pressure-control ventilation strategy in 148 ARDSpatients.'*'''*'' Mortality at 30 days was 37%in the HFO group and 52% in the pressure-control ventilation group. Derdak recommen-ded that a trial of HFO be considered whenpatients need more than 60% FiO2 and meanairway pressure approaches 20 cm H2O orhigher, or PEEP is more than 15 cm H2O andinspiratory plateau pressure cannot be main-tained at less than or equal to 30 cm H2O.'''''''Overall, more research needs to be under-taken to compare HFV and conventional lung-protective ventilation, as w ell as timing of theuse of new ventilatory techniques.

Extracorporeal membrane oxygenation(ECMO) is still in experimental stage, andas shown in past studies does not improvesurvival.'^ How ever, techniques and resultshave improved in recent years leading toa decrease in complications, and it may beappropriate to consider new studies utilizingECMO. In addition, treatment protocols arebeing suggested for ARDS in which combinedtreatment methods are utilized. Ullrich et alutilized a combined treatment protocolof airway pressure control, nitrous oxideinhalation, prone position, and early triageof nonresponders to ECMO, and achieved an80% overall survival rate. ^

In some patients, prone positioning dur-ing ventilation resulted in improved oxygena-tion and decreased shunt w ithout an increasein distending pressures.'* ' ^ Various studies

Adult Respiratory Distress Syndrome 331

have shown improvements in gas exchangeand oxygenation with use of prone position-ing for 8 to 12 hours a day.'* '' McAuley et alshowed progressive improvement in gas ex-change over an 18-hour period and suggestfurther research to address the prone positionfor more prolonged periods.''^ The improve-ment in oxygenation w ith prone positioningmay be due to the redistribution of ventilationwith improved dorsal ventilation, changes inperfusion, and improvement in ventilation-perfusion (VQ) matching. Oxygenation im-proves in approximately two thirds of patientsw ho are positioned prone."*^ Protocols forprone positioning are needed to prevent com-plications such as development of skin pres-sure sites, extubation, catheter removal, orworsening oxygenation.'' "^" Although pronepositioning has not shown a decrease inpatient mortality or in the duration ofmechanical ventilation in past studies, there issignificant improvement in oxygenation.'*^"''Further research is recommended utilizingcombined methods of treatment to achieveimproved results.

OTHER SUPPORTIVE MEASURES

Supportive measures in ARDS include theprevention of other complications, such asnosocomial infections, through the use of ap-propriate techniques. The failure to resolveand prevent secondary infections is a factorin mortality.''' Bronchodilators can be use-ful in patients with bronchospasm or withmarkedly increased airflow resistance, to de-crease peak and plateau pressures and to im-prove PaO2. ' Also, they may increase the se-cretion of surfactant and may even exert ananti-inflammatory effect in the lungs. ^ Hemo-dynamic stability must be maintained for ad-equate organ perfusion. Changes in bodyposition help to facilitate bronchial hygieneand improved gas exchange, as well as tominimize skin breakdown. Daily managementshould also include prophylaxis for deep veinthrombosis as well as stress ulcer prophylaxis.Sucralfate has been shown to be useful inpreventing late-onset pneumonia in ventilated

patients.'' Nutritional support should be at-tempted and the enteral route is preferable.Enteral feedings decrease the incidence of gas-tric colonization w ith gram-negative bacilli aswell as prevent stress ulcers.''* Enteral feed-ings may also have an effect on the host-immune response. A recent study used alow-carbohydrate, high-fat enteral formulacontaining a combination of fish and bor-age oils as w ell as antioxidants over a 4- to7-day period, and show ed a significant re-duction in pulmonary neutrophil recruitmentand inflammation, a resultant improvement inoxygenation, reduction in ventilator stay inthe ICU, and a reduction in organ failure. '*Further nutritional studies are recommended.Maintaining the elevation of head of bed at 30degrees can help prevent aspiration.

In ventilator management, it is necessaryto maintain an appropriate level of sedationto achieve patient-ventilator synchrony. Mostpatients need sedation or analgesia as wellto improve their comfort level. The use ofparalytic agents or excessive and prolongedsedation should be limited because of thepotential for complications. Paralytic agentsmay be needed to decrease oxygen consump-tion when a patient is very hypoxemic orhas a reduced cardiovascular reserve. Seda-tion and paralysis may be needed for poorlytolerated ventilator settings, such as inverseratio ventilation. These agents should be usedfor the shortest period possible, and the pa-tient should be monitored closely to limitthe depth of induced paralysis. In addition, atrain-of-four monitoring to guide the depth ofparalysis is the recommended standard of carefor patients receiving neuromuscular block-ing agents. This helps to achieve the minimumdose of paralytic agent necessary for achiev-ing the desired effect.

DEVELOPING TREATMENT OPTIONS

Nitric oxide in its inhaled form is a potentselective pulmonary vasodilator that does notcause systemic vasodilation. It can improvearterial oxygenation in patients with ARDS.However, in studies examining the effects

332 CRITICAL CARE NURSING QUARTERLY/OCTOBER-DECEMBER 2004

of inhaled nitric oxide, there w as no effecton mortality or the duration of mechanicalventilation.^^ It may still be useful in patientswith refractory hypoxemia, but not for rou-tine treatment of ARDS. Further studies arerecommended.

Corticosteroids are not useful in the acutemanagement of ARDS; however, they havebeen suggested as a treatment in the fibropro-liferative phase of ARDS when administeredto patients after 7 days of respiratory failure.'^Prolonged administration to these patients re-sulted in associated improvement in lung in-jury and reduced mortality. Further investiga-tion is suggested regarding timing and dura-tion of therapy.

Tracheal gas insufflation and perfluoro-carbon-associated ventilation (partial liquid)show improvement in gas exchange, butalong with other experimental approaches,such as surfactant administration w ith alter-native delivery techniques to optimize distri-bution, still need further investigation.'''•^^•^^Also under study are lipid mediators (pros-taglandins), antioxidants, antiproteases,platelet-activating factor inhibitors and recep-tor antagonists, antiadhesion molecules, andgene therapy.'''•'^•'^

OUTCOMES

ARDS Still has significant associated mor-tality outcomes.'^ Cause of death is mostclosely linked to presence of sepsis andmultiple organ failure. Since the predisposingfactors are variable, the subsets of survivorsoften are not similar in diagnosis or age.'^Pulmonary function tests are often reportedin follow-up as showing almost complete re-turn to normal airflow s; how ever, persistentlydecreased diffusion capacities are common.^^

MUd restrictive patterns are most common.Pulmonary function results are not clearly re-lated to severity and duration of ARDS. " Inone report of post-ARDS functional status,timed 6-minute walks were used to evaluateendurance and desaturation. Just 1% of pa-tients showed desaturation to 88% with exer-cise at 1 year post-ARDS. ^ Poor functional ca-pacity may be related to muscle weakness andheterotopic ossification.

Cognitive and psychologic evaluation ofsurvivors reveals significant impairment at thetime of hospital discharge. Reasoning, judg-ment, and memory were all lower at the 3-yearfollow-up as well.''' Patients also reported in-creased incidence of hallucinations, paranoia,depressed mood, and personality changes infoUow-up. ^ Age-related changes are a diffi-cult variable to control for, and incidence ofARDS increases 10-fold from the ages of 55to 85 years.'' Those older than 70 had ahigher duration of ventilation days and signifi-cantly higher mortality; with prolonged func-tional recovery time likely linked to underly-ing cardio-neuro comorbidities.^'"*''

Mortality due to ARDS has shown minimaldecline in the past several decades. ''•'' Earlyclinical detection is difficult, as there are fewmeasurable predictable variables that corre-late initial presentation w ith eventual mortal-ity. The use of low tidal volumes and per-missive hypercapnia have shown promise incontinuing to decrease mortality. Timely nurs-ing assessment and intervention regarding re-sponse to treatment is essential. Research con-tinues to be focused on multiple avenues oftreatment options in an attempt to improveoutcomes. Supportive care issues are an im-portant factor in functional outcomes. Criticalcare nurses have a valuable role in treatmentand outcomes in patients with ARDS.

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