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As332-03.tex

Crit Care Nurs QVol. 27, No. 4, pp. 325–335 c 2004 Lippincott Williams & Wilkins, Inc.
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 an
overview 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 radiologic
descriptors 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 issues
presented offer opportunities for further study. Key words: adult respiratory distress syndrome,
ARDS, high-frequency ventilation, nitric oxide, outcomes

EPIDEMIOLOGY/INCIDENCE
tory distress syndrome, to distinguish it fromthe infant respiratory distress syndrome. The Acute respiratory distress syndrome (ARDS) was introduced into the medical literature by ence on ARDS decided that there should be a Ashbaugh and colleagues in 1967, when they return to the original term acute rather than described 12 patients who developed a res- adult, since the syndrome is not limited to piratory distress syndrome which was mani- fested by acute onset of hypoxemia, tachyp- diffuse alveolar infiltrates on chest x-ray.1 Of lung injury (ALI) and ARDS.2,3 Both are acute these 12 patients, 7 had severe trauma, 4 had in onset, last for days to weeks, are char- viral infections, and 1 had acute pancreatitis.
acterized by arterial hypoxemia resistant to The mortality rate was 58% (7 of 12 patients).
oxygen therapy alone, and display diffuse ra- Case reports dating back to World War I and diologic infiltrates. Both definitions include a World War II revealed that trauma and sepsis pulmonary artery wedge pressure (PAWP) of may affect pulmonary function. However, it became more evident during the Vietnam era, sured, or no clinical evidence of left atrial hy- as patients who previously would have died pertension. The difference in definition be- were resuscitated with advanced medical care tween ALI and ARDS is related to oxygenation, and went on to develop the above pulmonary defined as PaO2/FiO2 ≤ 300 mm Hg for ALI cri- manifestations. Their 1967 paper was the first teria, and PaO2/FiO2 ≤ 200 mm Hg for ARDS to define the ARDS. In the following years, this syndrome was referred to as the adult respira- tory distress syndrome was introduced intothe literature, there have been thousandsof publications addressing all aspects of From the Suburban Lung Associates, Elk Grove ARDS. It is estimated that there are 150,000 Village, Ill (Ms Kane); and the Suburban Lung cases of ARDS in the United States annually.4 Associates, Winfield, Ill (Ms Galanes). Incidence of ARDS throughout the world has Corresponding author: Cynthia Kane, MS, RN, APRN, been variable, ranging from 1.5 to 13.4 cases/ Suburban Lung Associates, 801 Biesterfield Rd, Elk 100,000/year.5–8 Only one of these studies Grove Village, IL 60007 (e-mail: cindy.kane@sublung.
com).
addresses incidence using the ALI and ARDS CRITICAL CARE NURSING QUARTERLY/OCTOBER–DECEMBER 2004 PATHOPHYSIOLOGY
European Consensus Conference. Furtherstudies defining incidence using the new fined by physiologic and radiologic criteria Mortality rate for ARDS is between 40% and 60% and has remained in this range with lit- alveolar-capillary membrane composite oc- tle change over the last 30 years despite ex- curs within hours to days of a predispos- tensive research and literature devoted to it.9 ing insult.17 The National Heart, Lung, and In 1995, Krafft reported that the standard for outcome in ARDS should be a mortality group consensus is that ARDS is a systemic syndrome.17,18 Systemic responses to stress promise with a decline in mortality,10,11 and involve neural, endocrine, pro and antiin- flammatory mechanisms that are adaptive or use of permissive hypercapnea and low tidal Specifically, cells of the alveolar-capillary membrane as well as those of the immune andhemostatic systems are targets of damage, and ETIOLOGY/PRECIPITATORS
The alveolar-capillary barrier comprises the There are a number of clinical conditions that result in systemic inflammation leading lar endothelium. As endothelial permeabil- to the lung injury process with ARDS. The ity increases, protein-rich edema fills the air spaces.17 Resultant damage to epithelial on ARDS recommended categorizing the risk type 2 cells causes surfactant production to factors into direct and indirect categories.2,3 decrease.19 Further disruption of alveolar/ The direct-injury risk factors include aspira- epithelial integrity leads to increased perme- tion, diffuse pulmonary infection (eg, bac- ability and alveolar flooding of edema. In addi- terial, viral, or pneumocystis infection etc), tion, neutrophils adhere to the damaged cap- near-drowning, toxic fume inhalation, and illary membrane and transfer into alveolar air lung contusion. The indirect injury risk fac- tors include sepsis syndrome with or without Alveolar macrophages secrete cytokines; in- hypotension or evidence of infection outside terleukins 1, 6, 8, and 10; and tumor necro- the lung; severe nonthoracic trauma; hyper- sis factor alpha (TNF-α).18 These act locally to transfusion for emergency resuscitation; and advance chemotaxis and activate neutrophils, ARDS increases when sustained hypotension creasing contractility. Alveolar epithelial cells occurs.2,3 In 1995, Hudson et al found that produce cytokines in response to stimuli such the highest incidence of ARDS occurred in pa- as lung stretch, which is exacerbated by me- tients with sepsis syndrome (43%) and those chanical ventilation forces. The degree of alve- olar epithelial injury is an important predictor (40%).14 Garber et al showed a strong cause- of outcomes.17 Lung stretch induces local and effect relationship for increased incidence of systemic cytokine release. These mechanical- ARDS with sepsis, aspiration, trauma, and mul- ventilation–based mediators, endotoxins, and tiple transfusions.15 Other inciting factors in- bacteria, may also translocate into systemic clude cardiopulmonary bypass, fat embolism, circulation.17,18 Genetic factors may be re- pancreatitis, and drug overdose.2,3,14 Inciden- sponsible for its onset, as significantly smaller tally, it is also noted that the incidence of subsets of patients in any ARDS trigger group ARDS in severe acute respiratory syndrome go on to develop this severe inflammatory Adult Respiratory Distress Syndrome The first phase is the acute or exudative silhouette. Infiltrates are generally focal, and phase, with rapid onset of respiratory fail- may be very similar to those of severe car- ure, bilateral infiltrates, and refractory hy- poxemia. Diffuse alveolar damage occurs and serial chest radiographs often show rapid progresses rapidly. This occurs in context of progression of dependent bilateral infiltrates capillary injury and disruption of the alveo- progressing to diffuse interstitial infiltrates lar capillary membrane. Other complications include mechanical-ventilation–induced baro- demonstrated that alveolar consolidation and Later phase changes include a subgroup of atelectasis occur most often in dependent patients who progress to fibrosing alveolitis lung zones; other areas may be relatively complicated by alveolar tissue necrosis.17 Pul- spared.24 However, even areas that appear rel- monary hypertension may be severe17,18,20; atively radiologically spared may have substan- however, in many patients radiographic and tial inflammation present.23 Bugedo found pulmonary function tests return to normal.
improved aeration of poorly aerated and non-aerated tissue by 16% and 33%, respectively, EVALUATION OF ARDS
per CT during recruitment measures.25 Radio-logic follow-up should be closely monitored, Clinical examination
as some patients show progression to fibros- ing alveolitis with linear opacities consistent supporting data, but little definitive diagnos- tic clarity. ARDS usually develops within 24 to 48 hours of initial injury or insult,18,20 plicating factor, which has been reported to and clarification of clinical examination find- occur in 10% to 13% of ARDS cases, and is ings over a short duration may be difficult.
not clearly related to levels of positive end- Dyspnea with tachypnea generally presents expiratory pressure or airway pressure.17,18,23 first, and patients may be in considerable respiratory distress.20 This often is accompa- with higher level plateau pressures.17,18 nied by shallow inspiratory effort, as compli- ance decreases. Tissue perfusion alterations ment has been evaluated by use of positron emission tomography (PET) scans. Although mottled, or cyanotic. Auscultation will reveal initial data has been promising, barriers exist characteristic findings associated with the related to availability and some difficulty clar- predisposing cause, and may include crack- ifying pulmonary edema due to left heart fail- les, decreased sounds, or wheeze. As ARDS progresses and both compliance and pro-inflammatory changes worsen, lung sounds Blood gas analysis
may become significantly decreased, with ar-eas of consolidation and pneumonia.17,20 Ap- Arterial blood gas (ABG) analysis is key to plication of end-expiratory pressure compli- evaluation of patients with suspected ARDS.
cates assessment. In addition, if the patient is being managed on oscillating ventilation or of proportion to chest x-ray. Pulmonary right high-frequency ventilation, accuracy of aus- to left shunting because of infiltrates and at- electatic areas contribute to worsening hy-poxemia, which is resistant to increasing FiO2.
Initial presentation of respiratory alkalosis Radiologic evaluation
Chest radiographs usually show diffuse bi- PaCO2 and elevated pH is an early indication of lateral infiltrates, but with a normal cardiac progression of diffuse alveolar compromise.27 CRITICAL CARE NURSING QUARTERLY/OCTOBER–DECEMBER 2004 in tissue perfusion. Generally, patients with ence defines ARDS as PaO2/FiO2 < 200, bilat- ARDS do better when kept on the dry side.20 eral infiltrates, and PAWP ≤ 18 mm Hg, or no Complications such as acute cor pulmonale clinical evidence of left atrial hypertension.18 may be minimized by protective ventilation.30 This may be preceded by acute lung injury In addition, recruitment maneuvers may be with a PaO2/FiO2 ratio of less than 300. After associated with hypotension, but this is not treatment is initiated, the goal FiO2 is less than 60%, as hyperoxia can lead to excessive oxi-dant production, protein oxidant damage, and Late-phase clinical evaluation
Clinical manifestations of the fibroprolifer- ative phase include fever, leukocytosis, dif- treatment ensues, current recommendations fuse alveolar infiltrates on chest radiograph, include low tidal volumes. Significant airway and persistent inflammatory mediators in the trauma decreases when there is no recurrent serum.17,18 Associated physiologic manifesta- opening and closing of alveoli, which tradi- tions include worsening of pulmonary com- tionally occurs with higher tidal volumes.12 pliance, abnormal gas exchange, increased A consequence of this volume-related avoid- dead space ventilation, pulmonary hyperten- tilation. This in turn increases the PCO2,which then lowers the pH. Although aci- TREATMENT AND COURSE
dosis increases the significant inflammatoryprocess, the negative effects of barotraumas/ Identification and treatment
volutrauma are lessened because of this lower of precipitator
tidal volume. The net result has been linked to Multiple organ failure is listed as the most common cause of death in patients withARDS.7 ARDS is often associated with a sys- Cardiogenic issues
temic inflammation leading to multiple organ Hypoxemic issues, which continue after ap- failure. Treatment of the inciting clinical dis- plication of support, suggest further cardio- order is important in the initial management logic evaluation. When there is doubt about of ARDS. The diagnostic evaluation should be the presence of heart failure, right heart guided by the patient’s history. Evaluation of catheterization is helpful. Typically, PAWP a septic source should be done early in pa- is low (<18 mm Hg) in ARDS, and high tients deemed septic, looking at pulmonary (>20 mm Hg) in heart failure.18 Compromise and extrapulmonary sites of infection. Intra- in intravascular volume along with positive abdominal sepsis should be considered early end-expiratory pressure (PEEP) results in de- in patients with sepsis syndrome who exhibit creased cardiac output.29 Sepsis and diuretic acute lung injury of uncertain etiology.
therapy contribute to relative volume deple- Several reports have listed that the high- tion. Despite significant fluid loads within est incidence of ARDS is associated with sep- the pulmonary bed, blood volume issues are sis syndrome and that these patients also critical. Tissue perfusion and oxygen delivery reflect adequacy of the cardiopulmonary sta- prognosis than lung injury induced by other tus. If this is not maintained, or is interrupted, mechanisms.7,14 Early evaluation and specific poor perfusion contributes further to multi- medical or surgical treatment of the source of ple organ failure. The range of volume man- sepsis can enhance the chance of survival.
agement is narrow, as both overhydration and aggressive diuresis cause significant variation tein C for appropriate patients will reduce Adult Respiratory Distress Syndrome mortality in patients with severe sepsis.33 For hypercapnia.37,38 Permissive hypercapnia is other insults, such as aspiration or multiple an effective strategy for limiting the ventila- transfusions, care should be focused on pre- tory pressures by allowing PaCO2 to rise.34 It is vention of recurrence. Optimal supportive generally felt that with permissive hypercap- care is recommended for all acute lung in- nia, PaCO2 may be kept in the range of 60 to juries with ARDS due to various causes.
100, and the pH maintained at more than orequal to 7.25 without deleterious effects.
To prevent ventilator-associated injury to VENTILATION
the lungs, plateau pressures need to be mon-itored with attempts to maintain them at Mechanical ventilation is the mainstay of can be achieved by permissive hypercapnia, quate oxygenation and to stabilize ventilation pressure-controlled ventilation, and pressure- (Table 1). Initially, with any form of res- limited volume cycled ventilation. Another piratory failure, standard ventilatory strate- protective ventilation strategy includes an gies may be utilized, using flow-controlled “open lung”technique in which PEEP is main- volume-cycled ventilation, with a tidal volume tained at a level above where alveoli collapse, (TV) of 10 to15 mL/kg. In recent years, it has and the distending pressure and volume is become more evident that the standard ven- limited (TV < 6 mL/kg and driving pressures tilation for patients with ARDS is the use of small tidal volumes so as to be protective to permissive hypercapnia, and use of pressure- the lungs and to prevent ventilator-associated lung injury.12,34–37 The Acute Respiratory Dis- PEEP can be used to increase end-expiratory crease in mortality and a decrease in venti- leads to improved gas exchange. When oxy- lator days by using a lower TV of 6 mL/kg genation requirements increase, a high FiO and a plateau pressure of less than or equal may be used for brief periods as a tempo- rizing measure, with aggressive efforts to at- in past studies that limited peak airway pres- sures and reduced overdistention of the lung (which is generally considered to be safe).
by using low tidal volumes and permissive PEEP can be increased in an attempt to recruitalveoli by opening previously collapsed alve- Table 1. Ventilator management goals in
oli and preventing further collapse.34,35 PEEP decreases intrapulmonary shunt, and there-fore improves arterial oxygenation. Potentialadverse effects of PEEP include a decrease in cardiac output, increase in dead space, in- crease in lung volume, and stretch during in- Plateau pressure ≤ 30 cm H2O (adjust TV as spiration. The lowest mean airway pressure that achieves an acceptable level of arterial oxygenation with a nontoxic FiO2 should be A retrospective review of 150 patients by Ensure adequate oxygenation (O2 saturation Page et al found that with protective venti- lation (plateau pressure < 30 cm H2O) anda low positive end-expiratory pressure (PEEP ∗TV indicates tidal volume; PEEP, positive end-expiratory < 10 cm H2O), there was a mortality of only 38%.40 In addition, the major factor associated CRITICAL CARE NURSING QUARTERLY/OCTOBER–DECEMBER 2004 with the probability of dying was the severity (HFPPV), which uses 60 to 100 breaths/min; of circulatory failure. Patients without circula- high-frequency jet ventilation (HFJV), which uses 100 to 300 breaths/min; and high-frequency oscillation (HFO), which uses up ALTERNATIVE VENTILATOR MODES
to 2400 breaths/min. Auscultation of lungsounds is altered with the small tidal volumes Other alternative ventilator modes for ARDS at the supra physiologic rate.42 Air movement include inverse ratio, high-frequency ventila- is difficult to assess. Therefore, continuous tion, extracorporeal membrane oxygenation monitoring of oxygen saturation is necessary (ECMO), and prone positioning. Inverse ratio to quickly address changes in oxygenation.
ventilation is a technique that changes the Frequent ABG analysis and daily chest radio- time of the respiratory cycle so that inspira- graphy is indicated. Patients are switched tion and expiration time are equal or reversed.
back to conventional ventilation when they Normal inspiratory to expiratory (I/E) ratio is 1:2 in a spontaneously breathing patient with normal airways. With inverse ratio ventilation, the I/E ratio changes to 1:1 or even 2:1. The 2 potential benefits are a reduction in peak in- patients.43,44 Mortality at 30 days was 37% spiratory pressure (PIP) and an improvement in the HFO group and 52% in the pressure- in oxygenation from the prolonged inspira- control ventilation group. Derdak recommen- tory time.34,35,37 However, patients do not tol- ded that a trial of HFO be considered when erate reversals of I/E ratio well, and require patients need more than 60% FiO2 and mean neuromuscular blockade to achieve this type higher, or PEEP is more than 15 cm H2O and There is renewed interest in high-frequency inspiratory plateau pressure cannot be main- ventilation in an attempt to reduce lung in- tained at less than or equal to 30 cm H2O.43,44 jury and improve clinical outcomes in ARDS.
Overall, more research needs to be under- Conventional ventilation with higher tidal taken to compare HFV and conventional lung- volumes is associated with potentiating or protective ventilation, as well as timing of the causing further lung injury. It is generally felt that the injuries occur from regional overdis- tension by excessive end-inspiratory lung (ECMO) is still in experimental stage, and volumes related to the uneven distribution as shown in past studies does not improve of ventilation, that injury occurs in the small survival.37 However, techniques and results and injury occurs with shear force at the a decrease in complications, and it may be margins between atelectatic lung units and appropriate to consider new studies utilizing aerated units.41 High-frequency ventilation ECMO. In addition, treatment protocols are being suggested for ARDS in which combined higher end-expiratory lung volumes with less treatment methods are utilized. Ullrich et al overdistension than conventional ventilation.
Also, the high respiratory rates allow the of airway pressure control, nitrous oxide maintenance of normal or near-normal PaCO2 inhalation, prone position, and early triage levels, despite the small tidal volumes.41 It of nonresponders to ECMO, and achieved an limits lung overdistension and prevents cyclic lung collapse by maintaining end-expiratory lung volume. The broad classifications of ing ventilation resulted in improved oxygena- tion and decreased shunt without an increase in distending pressures.45,46 Various studies Adult Respiratory Distress Syndrome patients.53 Nutritional support should be at- and oxygenation with use of prone position- tempted and the enteral route is preferable.
ing for 8 to 12 hours a day.45,46 McAuley et al Enteral feedings decrease the incidence of gas- showed progressive improvement in gas ex- tric colonization with gram-negative bacilli as change over an 18-hour period and suggest well as prevent stress ulcers.34 Enteral feed- further research to address the prone position ings may also have an effect on the host- for more prolonged periods.47 The improve- ment in oxygenation with prone positioning low-carbohydrate, high-fat enteral formula may be due to the redistribution of ventilation containing a combination of fish and bor- with improved dorsal ventilation, changes in age oils as well as antioxidants over a 4- to perfusion, and improvement in ventilation- 7-day period, and showed a significant re- duction in pulmonary neutrophil recruitment proves in approximately two thirds of patients and inflammation, a resultant improvement in who are positioned prone.46 Protocols for oxygenation, reduction in ventilator stay in prone positioning are needed to prevent com- the ICU, and a reduction in organ failure.54 plications such as development of skin pres- Further nutritional studies are recommended.
sure sites, extubation, catheter removal, or Maintaining the elevation of head of bed at 30 worsening oxygenation.48–50 Although prone degrees can help prevent aspiration.
In ventilator management, it is necessary to maintain an appropriate level of sedation mechanical ventilation in past studies, there is to achieve patient-ventilator synchrony. Most significant improvement in oxygenation.45–47 patients need sedation or analgesia as well Further research is recommended utilizing to improve their comfort level. The use of paralytic agents or excessive and prolonged sedation should be limited because of thepotential for complications. Paralytic agents OTHER SUPPORTIVE MEASURES
may be needed to decrease oxygen consump-tion when a patient is very hypoxemic or has a reduced cardiovascular reserve. Seda- prevention of other complications, such as tion and paralysis may be needed for poorly nosocomial infections, through the use of ap- tolerated ventilator settings, such as inverse propriate techniques. The failure to resolve ratio ventilation. These agents should be used and prevent secondary infections is a factor for the shortest period possible, and the pa- in mortality.34 Bronchodilators can be use- tient should be monitored closely to limit ful in patients with bronchospasm or with the depth of induced paralysis. In addition, a markedly increased airflow resistance, to de- train-of-four monitoring to guide the depth of crease peak and plateau pressures and to im- paralysis is the recommended standard of care prove PaO2.51 Also, they may increase the se- for patients receiving neuromuscular block- cretion of surfactant and may even exert an ing agents. This helps to achieve the minimum anti-inflammatory effect in the lungs.52 Hemo- dose of paralytic agent necessary for achiev- dynamic stability must be maintained for ad- equate organ perfusion. Changes in bodyposition help to facilitate bronchial hygiene DEVELOPING TREATMENT OPTIONS
and improved gas exchange, as well as tominimize skin breakdown. Daily management Nitric oxide in its inhaled form is a potent should also include prophylaxis for deep vein selective pulmonary vasodilator that does not thrombosis as well as stress ulcer prophylaxis.
cause systemic vasodilation. It can improve Sucralfate has been shown to be useful in arterial oxygenation in patients with ARDS.
preventing late-onset pneumonia in ventilated However, in studies examining the effects CRITICAL CARE NURSING QUARTERLY/OCTOBER–DECEMBER 2004 of inhaled nitric oxide, there was no effect Mild restrictive patterns are most common.
on mortality or the duration of mechanical Pulmonary function results are not clearly re- ventilation.55 It may still be useful in patients lated to severity and duration of ARDS.60 In with refractory hypoxemia, but not for rou- one report of post-ARDS functional status, tine treatment of ARDS. Further studies are timed 6-minute walks were used to evaluate endurance and desaturation. Just 1% of pa- Corticosteroids are not useful in the acute tients showed desaturation to 88% with exer- cise at 1 year post-ARDS.59 Poor functional ca- been suggested as a treatment in the fibropro- pacity may be related to muscle weakness and liferative phase of ARDS when administered to patients after 7 days of respiratory failure.56 Prolonged administration to these patients re- survivors reveals significant impairment at the sulted in associated improvement in lung in- time of hospital discharge. Reasoning, judg- jury and reduced mortality. Further investiga- ment, and memory were all lower at the 3-year tion is suggested regarding timing and dura- follow-up as well.61 Patients also reported in- creased incidence of hallucinations, paranoia, depressed mood, and personality changes in carbon-associated ventilation (partial liquid) follow-up.58 Age-related changes are a diffi- cult variable to control for, and incidence of along with other experimental approaches, ARDS increases 10-fold from the ages of 55 such as surfactant administration with alter- native delivery techniques to optimize distri- higher duration of ventilation days and signifi- bution, still need further investigation.34,35,57 cantly higher mortality; with prolonged func- Also under study are lipid mediators (pros- tional recovery time likely linked to underly- platelet-activating factor inhibitors and recep- tor antagonists, antiadhesion molecules, and decline in the past several decades.64,65 Early clinical detection is difficult, as there are fewmeasurable predictable variables that corre- OUTCOMES
late initial presentation with eventual mortal-ity. The use of low tidal volumes and per- ARDS still has significant associated mor- missive hypercapnia have shown promise in tality outcomes.58 Cause of death is most continuing to decrease mortality. Timely nurs- ing assessment and intervention regarding re- multiple organ failure. Since the predisposing sponse to treatment is essential. Research con- factors are variable, the subsets of survivors tinues to be focused on multiple avenues of often are not similar in diagnosis or age.59 treatment options in an attempt to improve Pulmonary function tests are often reported outcomes. Supportive care issues are an im- in follow-up as showing almost complete re- portant factor in functional outcomes. Critical turn to normal airflows; however, persistently care nurses have a valuable role in treatment decreased diffusion capacities are common.59 REFERENCES
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