Care of postoperative patients with adult respiratory distress syndrome

Care of Postoperative Patients With Adult Respiratory Distress Syndrome CYNTHIA

REED,

BSN,

RN,

RRT

Providing care to the postanesthesia patient requires precise and continual assessment in conjunction with prompt and aggressive intervention. This article discusses the cause, pathology, diagnosis, and management of adult respiratory distress syndrome in the PACU. 0 1996 by American Society of PeriAnesthesia Nurses.

DULT respiratory distress syndrome (ARDS) is not a specific disease; it is a life-threatening form of acute respiratory failure that is a result of illness or injury that may not initially involve the lungs.’ Patients at risk of developing ARDS include those presenting with sepsis, aspiration of gastric contents, multiple trauma, multiple organ failure, post-cardiac bypass, and recipients of multiple transfusions.2.3,4 Clearly, many of the patients receiving care in the PACU are at risk to develop ARDS. Prompt diagnosis and intervention by the nurse is the first step in management. There are an estimated 150,000 cases of APDS each year. Even with prompt medical intervention, mortality rates remain between 50% to 60%.5

A

PULMONARY

PHYSIOLOGY

The function of the lung is to remove carbon dioxide and oxygenate the circulating arterial Cynthia Reed, BSN, W, RRT, is a Newborn Intensive Care Uait Staff Nurse at the University of New Mexico Health Sciences Center, Albuquerque, NM. Address correspondence to Cynthia Reed, BSN, RN, RRT, c/o Kim Litwack, lJniversi@ of New Mexico Health Sciences Center, College of Nursing, Albuquerque, NM 87131-1061 0 1994 by American Society of PeriAnesthesia Nurses. 1089-9472/96/1106-0008$03.00/0

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blood. Adequate oxygenation on a cellular level is required to generate adenosine triphosphate (ATP) and maintain life. Delivery of oxygen to the tissues can be viewed as being facilitated by the following three processes: perfusion, ventilation, and exchange.2 Perfusion applies to the blood flow that transports oxygen and carbon dioxide between body tissues and alveoli. Perfusion is affected by the functioning of the heart, blood vessels, pressures and flow within the blood vessels, and the quantity and capability of the red blood cells to carry oxygen. Ventilation applies to the mechanics of inspiration and expiration, and is affected by lung compliance, chest wall resistance, and the efficiency of the respiratory muscles. Exchange applies to the diffusion of oxygen and carbon dioxide at the alveolar-capillary membrane and at the tissues. Exchange is affected by the permeability, integrity, thickness, and surface area at the alveolar-capillary membrane. It is also influenced by the ventilation to perfusion ratio of the alveoli (V/Q), the pressure gradients and solubility of the gases on either side of the alveolar-capillary membrane, and the affinity between hemoglobin and oxygen. When all processes are functioning,

of Per;AnesHxs;a

Nursing,

Voi 11, No 6 (December),

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ADULT

RESPIRATORY

DISTRESS

SYNDROME

the supply and demand for oxygen are in equilibrium.* Nearly 100 years ago, Starling delineated the forces that regulate the movement of the fluid across the alveolar-capillary membrane. There is normally a delicate balance within the lung between the capillary colloid oncotic pressure, the capillary hydrostatic pressure, interstitial colloid oncotic pressure, and the interstitial hydrostatic pressure. These factors, in conjunction with the permeability of the capillary endothelial cells and the flow through the pulmonary lymphatics, are instrumental in maintaining the fluid balance in the pulmonary capillaries and, consequently, in the alveoli.637,s Pulmonary edema develops when the pulmonary vessels lose the capability of holding plasma within the vascular tree. As permeability is lost, a protein-rich exudate gathers within the lung. This is referred to as noncardiogenic pulmonary edema because the pathology is either systemic or pulmonary in origin.’ In ARDS, there is injury to the lung parenchymal cells at the alveolarcapillary membrane, a form of noncardiogenic pulmonary edema develops and the exchange processes are altered. PATHOPHYSIOLOGY OF ADULT RESPIRATORY DISTRESS SYNDROME

In the last 25 years, terms such as wet lung, shock lung, white lung, and pump lung have been used to describe the syndrome now known as ARDS.‘,5 In 1967, Ashbaugh et al9 described 12 patients with hypoxia, tachypnea, and loss of pulmonary compliance all following various precipitating conditions such as trauma, lung infection, and aspiration. They noted the occurrence of surfactant abnormalities in ARDS patients. In 1971, Petty and Ashbaugh” went on to define ARDS as a condition of respiratory distress occurring after a precipitating event (excluding chronic lung disease and cardiogenic pulmonary edema). Their definition included a loss of pulmonary compliance, refractory hypoxemia, and diffuse pulmonary infiltrates on chest radiograph.” In 1988, Murray et al” expanded the definition by developing a method of scoring acute lung injury to assist with quantifying the severity of ARDS and to develop a methodology to determine prognosis. The acute lung injury scoring method eval-

41 I Table

I.

Predisposing

Conditions

to ARDS

Sepsis Aspiration of gastric contents Multiple organ failure Postcardiac Recipients

bypass of multiple

Prolonged Pneumonia

surgery

transfusions

Cardioversion Oxygen toxicity Eclampsia Increased intracranial Pancreatitis Disseminated

pressure

intravascular

coagulopathy

uates and attaches a numerical value to the four following components: the degree of hypoxemia, lung consolidation on chest radiograph, positive end-expiratory pressure {PEEP) levels needed to achieve adequate oxygenation, and ventilated lung compliance. The higher the score, the more severe the ARDS.” ARDS can affect children as well as adults, and not all patients with acute lung injury will develop ARDS, but all patients with ARDS have had an acute lung injury. The American-European Consensus Conference on ARDS has recommended changing the name from “adult” to “acute” respiratory distress syndrome.5 It is apparent that as medical advancements are made, the definition, management, and outcome of patients with ARDS will continue to evolve. In the PACU, emphasis should be placed on prompt assessment and intervention, as 80% of patients that develop ARDS do so within the first 24 hours after the precipitating event.5 The two most common conditions associated with the occurrence of ARDS are gastric acid aspiration and sepsis. As seen in Table 1, numerous factors can predispose a patient to developing ARDS.‘%2.6 Although the exact pathogenesis of ARDS is unknown at this time, the progression from noncardiogenic pulmonary edema to ARDS has been attributed to an uncontrolled inflammatory process at the pulmonary endothelium triggered by an initial insult. Neutrophils and alveolar macrophages have been identified within the alveoli 24 hours after the onset of ARDS and are thought to release or stimulate the release of toxic mediators, oxygen free radicals. and proteases within

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412 Table

2. The Four

Phases

of Adult

Respiratory

Distress

REED

Syndrome

Pathogenesis Phase I

Direct

or indirect

Occurs

injury

12 to 24 hours

Phase IV

Phase Ill

Phase II

after

injury

Massive

fluid

leakage

into

Alveoli

lack surfactant

alveoli Lasts 6-48 hours

L

Worsening

J pulmonary

Decreased

lung compliance

edema

Damage to pulmonary surfactant

L Systemic

release

of chemical

Alveolar

collapse

L

L

Increasing

V/Q mismatch

Refractory

hypoxemia

Decreasing

L compliance

Decreasing

Worsening

L hypoxemia

Inflammation

Mechanical

ventilation

mediators Cellular

release

of toxic

by-

J hypoventilation

Alveolar

L compliance

products L injury

Microvascular Interstitial

J V/Q mismatch

Increased

L edema

J L

L Hypoxemia

usually

Fibrosis

indicated V/Q mismatch

develops

Pulmonary

hypertension

Signs and Symptoms Phase I

l l

Clear breath Tachypnea

l

Mild respiratory Normal PaO*

l

Normal

l

sounds

PAOP

l l

alkalosis

l

l l l

Fine raies or crackles Tachycardia Tachypnea Dyspnea Decreased PaOz Irregular patchy infiltrates chest

I-THE INITIAL

0 Coarse rales or crackles Decreasing PaO* l Extensive infiltration and

INSULT

The initial insult includes a period that lasts 6 to 48 hours. Injury to the lung by direct or indirect causes will prompt a release of mediators that in turn activate the release of toxic cell by-products. These toxic by-products result in pansystemic microvascular injury and fluid leakage into the interstitial spaces. At this phase, the capillary endothelium has been disrupted and interstitial edema

Phase IV

l

Decreased

l

volumes Stiff lungs

l

consolidation radiograph on

on chest

l

l

radiograph

the lung parenchyma which results in an increased permeability defect and endothelial damage. “J~J~X The clinical course of ARDS can be divided into four phases (Table 2). PHASE

Phase ill

Phase II

l

lung

Metabolic respiratory Decreasing

and acidosis PaOz

Extensive on chest

atelectasis radiograph

ensues. The patient may present with unexplained tachypnea and clear breath sounds. Clinical signs include a mild respiratory alkalosis secondary to hyperventilation and a normal PaO?. A V/Q mismatch is developing but may be difficult to assess. Normal pulmonary artery occlusion pressure (PAOP) of less than 18 mm Hg will be-evident and rules out cardiogenic pulmonary edema.‘.59’4 PHASE

II-THE

BEGINNING OF RESPIRATORY DIFFICULTY

Phase II occurs within 12 to 24 hours after injury. The leakage of fluid continues and the lungs become stiff and begin to lose compliance.

ADULT

RESPIRATORY

DISTRESS

SYNDROME

‘The increase in alveolar fluid and the decrease in compliance causes alveolar hypoventilation and a resultant hypoxemia. The PaOZ will fall and the V/Q mismatch will increase. The patient will exhibit restlessness, tachycardia, tachypnea, dyspnea, and fine rales or crackles in the dependent portions of the lungs. Chest radiographs will show irregular patchy infiltrates.2Z5,‘4 PHASE

III-PROGRESSIVE PULMONARY INSUFFICIENCY

Massive leakage of fluid into the alveoli continues and perfusion without ventilation (shunt) increases. Surfactant in the alveoli is damaged by the excess fluid, and the compliance and Pa02 continues to decrease. The patient will have rhonchi and coarse rales or crackles on auscultation of the chest. Mechanical ventilation is often required at this point to maintain adequate oxygenation and provide ventilatory support. Chest films will show extensive infiltration and consolidation.*,5.14

PHASE

IV-HYPOXIA

AND

HYPERCAPNIA

The alveoli now lack surfactant and collapse. The increasing shunt causes severe hypoxemia unresponsive to an increase in Fi02, and the PaCO* increases. Inflammation occurs and leads to fibrosis, further decreased compliance, impaired gas exchange, and decreased lung volumes. Chest radiographs show alveolar collapse with extensive atelectasis. At this point of the disease process, pulmonary hypertension may occur.2,5.‘4 PATHOPHYSIOLOGY OF INFANT RESPIRATORY DISTRESS SYNDROME

Although the term ARDS is known by most practitioners, note should be given to the diagnosis of infant respiratory distress syndrome (IRDS). IRDS is frequently precipitated by prematurity with the major causative factor being a deficiency of pulmonary surfactant. The incidence of IRDS is inversely proportional to the infant’s gestational age, and has the highest occurrence in infants of less than 30 weeks gestational age and/or a birth weight less than 1,200 grams. IRDS is one of the leading causes of morbidity and mortality in the neonatal population.‘5 Premature lungs cannot provide adequate gas

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exchange secondary to a limited number of terminal alveoli, an undeveloped pulmonary capillary network, and a lack of or a decrease in the production of pulmonary surfactant. Surfactant is a lipid protein complex produced by type II alveolar cells at approximately 28 weeks gestation. Surfactant adjusts the alveolar surface tension and enables the alveoli to remain open at low volumes. Without surfactant, the alveoli collapse during expiration. The ensuing atelectasis can result in pulmonary hypertension, a right-to-left shunt, a patent ductus arteriosus, metabolic acidosis, hypoxia, hypercapnia, and a respiratory acidosis. The infant will exhibit symptoms of increased respiratory distress. A few hours after birth, hyaline membranes begin to form in the air spaces and the infant’s lungs become noncompliant. Even with ventilatory support, the infant may be difficult to stabilize.‘5,16 Treatment modalities include ventilatory support, surfactant replacement, and the use of nitric oxide @~0)~15,16,~7-18 NO is a potent selective pulmonary vasodilator. Continual low dose administration (18 ppm) of NO via endotracheal tube (ETT) has been proven effective in treating pulmonary hypertension and improving ventilation and perfusion in infants and children.” The treatment of choice for the IRDS population is surfactant replacement. Administration of surfactant will lower alveolar surface tension and increase lung compliance thereby decreasing intrapulmonary shunting.‘*-‘6X17 Products available for clinical use are either prepared from bovine lungs (Survanta, Ross Laboratories, Columbus, OH) or synthetically manufactured (Exosurf, Burroughs Wellcome, Research Triangle Park, NC).16 Surfactant replacement therapy is delivered topically to the lung tissue via instillation through the endotracheal tube. Studies suggest that exogenous surfactant reduces the risk of barotrauma and decreases the development of bronchopulmonary dysplasia.15.16 As these infants are rarely, if ever, seen in the post anesthesia care unit, the remaining discussion will focus on ARDS. NURSING PRIORITIES RESPIRATORY DISTRESS

IN ADULT SYNDROME

The over-riding goal of patient care is to maximize the delivery of oxygen sufficient to relieve

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hypoxemia. Therefore, patient monitoring will include continuous pulse oximetry monitoring to measure the percent of hemoglobin in the blood bound with oxygen (SpOZ).’ Oxygen delivery via face mask may prove inadequate, and frequently endotracheal intubation will be required to maintain an airway and provide support for the ensuing respiratory distress. Assistance with ETT insertion can be facilitated by having an ambubag with a PEEP valve readily available, an appropriate size face mask, extra endotracheal tubes, stylettes and laryngoscopes, a 5 or 10 mL syringe to inflate the ETT cuff, and adhesive tape for securing the tube. Auscultation immediately after intubation is essential to evaluate for bilateral equal breath sounds that will assist in confirming correct ETT placement, and to prevent barotrauma that can occur from a right or left mainstem bronchus intubation. A chest radiograph may also be repeated to confirm ETT placement. Recent studies of ARDS pathology show that the lung damage caused by ARDS is not uniform as was previously thought. This implies that with the conventional methods of ventilation, inflating the lungs with normal volumes of 10 to 15 mL/ kg is overdistending and damaging the healthy compliant portions of the lungs. This knowledge has led to a change in traditional ventilator management to strategies that now use low tidal volume ventilation or pressure control ventilation (PCV) to limit peak inspiratoty pressures (PIP) and prevent barotrauma. Permissive hypercapnia is being used in conjunction with the low volume ventilation strategy for the management of ARDS patients. High levels of PaCOZ can be tolerated by the patient if precautions are taken to prevent an intracellular acidosis by buffering with bicarbonate administration or managing the patient to achieve gradual retention of CO? which will result in a compensated respiratory acidosis.“3i9,‘o PEEP is used to reinflate atelectatic alveoli thus facilitating gas exchange at the alveolar-capillary membrane and improving oxygenation. PEEP has also been found to prevent collapse of unstable lung units at the end of expiration.20,21 The PEEP levels required to facilitate gas exchange during ARDS depends on the severity of the disease process. Levels of PEEP can be classified as follows: mild, less than 10 cmH20;

CYNTHIA

REED

moderate, 10 to 20 cmHZO; and severe, 25 to 40 cmH*O (rarely used). Optimal PEEP is defined as the amount of PEEP required to keep the PaOZ greater than 60 mm Hg and the fraction of inspired oxygen (Fi02) less than 50%.2’ Recent guidelines for ARDS patients places appropriate PEEP levels in the range of 7 to 15 cmHZO with a recommended maximum of 20 cmHZO PEEP.” Improvement in oxygenation facilitated by PEEP may allow for decreases in the FiO* needed to correct life-threatening hypoxemia, result in an acceptable SpOZ, establish an adequate Pa02 on arterial blood gas samples, and subsequently reduce the risk for oxygen toxicity that can result after long periods of high FiOZ administration.2i A patient on PEEP is at risk for barotrauma or a tension pneumothorax. The following three components must be present for barotrauma to occur: lung injury, overdistention of the alveoli, and pressure. Because the acute lung injury in ARDS is patchy and heterogeneous, the overdistention of an alveolar unit may occur with any level of PEEP, consequently, it is important to administer PEEP at the lowest therapeutic level possible.2’ Frequent chest auscultation by the nurse and readily available supplies for chest tube insertion are essential. A tension pneumothorax is a result of damage to the lung tissue integrity and formation of a one-way valve that allows gas to enter the pleural space but not exit.* This results in a significant increase of pressure within the pleural space. A patient presenting with a tension pneumothorax may exhibit signs of distress such as tachypnea, increased work of breathing, and decreased or absent breath sounds on the affected side.2’ Initially, tachycardia will be present that progresses quickly to bradycardia as cardiovascular compromise develops. Absence of expiratory movement of the chest wall on the affected side will be observed. Shifting of the mediastinum and/or trachea to the unaffected side may occur in severe cases. The peak airway pressures on the ventilator will increase with each breath and vital signs will deteriorate rapidly secondary to the pressure gradients forcing more gas into the pleural space.‘,” Rapid decompression of the chest may be necessary before definitive diagnosis can be made by radiograph. This is accomplished by the insertion of an 18 gauge needle into the anterior wall of the chest

ADULT

RESPIRATORY

DISTRESS

SYNDROME

at the second or third intercostal space at the nipple line. To avoid penetrating the vessels that perfuse the intercostals, the needle should be inserted over the lower rib.” Decompression may resolve the pneumothorax or further treatment may require insertion of a chest tube placed to suction with a water seal. Decreased cardiac output can also be a side effect of increased levels of PEEP. It is caused by decreased venous return secondary to increased intrathoracic pressure.” A fall in cardiac output will result in a decrease in blood pressure and tissue perfusion. Cardiac output may be monitored via a pulmonary artery catheter with the normal cardiac output range being 4 to 8 L/M.3 Patients may require inotropic support with dopamine and/or dobutamine if cardiac output decreases to levels that compromise cerebral and systemic perfusion. Severe pulmonary hypertension is also a complication of ARDS. Prostaglandin E1 (PGE1) is a vasodilator with anti-inflammatory properties that will decrease systemic and pulmonary vascular resistance, increase cardiac output, and consequently increase oxygen delivery. The potent hemodynamic effects of PGE1 are useful in managing specific ARDS patients with severe pulmonary hypertension and the resultant impairment in cardiac function.4,17 RESEARCH

INTO THE MANAGEMENT OF ARDS

New approaches to managing ARDS include various ventilator strategies such as volume control, volume control inverse ratio ventilation, pressure control inverse ratio ventilation, highfrequency jet ventilation, and tracheal gas insufflation. Several controlled trials are currently being conducted but results are inconclusive.53’9,20 Pharmacological investigations include the use of surfactant as a treatment for patients with ARDS. The efficacy of surfactant administration by instillation through the ETT or by aerosolization for the treatment of ARDS patients is currently under investigation. Problems associated with treatment include high volume instilled doses (4 mL/kg via ETT) and high costs per dose. Data indicates that while surfactant abnormalities exist, a surfactant-deficient state is not the primary pathogenic factor in ARDS as it is in

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IRDS.17~22The use of anti-inflammatory agents such as corticosteroids have been trialed in attempt to reduce the alveolar-capillary permeability defect, but results are inconclusive.‘* Extracorporeal therapies used to oxygenate and/or remove carbon dioxide have been trialed in adults, but results have not supported clinical application for the treatment of ARDS.183’9 Studies are currently being conducted to evaluate the effectiveness of nitric oxide administration as a treatment modality for ARDS.17.‘8,zz Intravascular oxygenation via a hollow-fiber membrane oxygenator placed within the vena cava is currently being trialed under Food and Drug Administration supervision. Results indicate the method is safe but clinical effectiveness has not been established.23 Attending to the emotional needs of the patient is very important. Feelings of confusion, anxiety, and fear can all be a result of hypoxemia. The nurse can easily provide reassurance and continual explanations of care, in addition to administering anxiolytics to decrease the fear, anxiety and additional oxygen demands initiated by these emotionsz4 Management of precipitating causes can slow the progression of ARDS and decrease the amount of respiratory distress the patient experiences. A brief physical examination and review of the patient chart may show risk factors and possible underlying pathologies that can lead to ARDS. Practical initial diagnostic tools include a chest radiograph, an arterial blood gas, and an electrocardiogram. Insertion of a pulmonary artery catheter may be indicated if septic shock or ARDS is suspected. The catheter will measure the PAOP to evaluate pulmonary hypertension, cardiac output to monitor for levels of optimal PEEP, and also assist in evaluating the effectiveness of other therapies.z5 Care of the patient with ARDS will extend beyond PACU time, requiring transport of the patient to an intensive care unit. Patients with ARDS may not tolerate handbagging for long periods of time so a dedicated elevator for transport should be used to avoid delays. A PEEP valve must be placed on the resuscitation bag before handbagging via endotracheal tube or face mask. If the patient does not tolerate handbagging the use of long extension cords for the

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ventilator may be recruited to ensure safe transport to the intensive care unit. NURSING

DIAGNOSES

Knowledge of the patient3 history, risk factors, and the ensuing pathophysiology of ARDS will assist the nurse in making accurate diagnoses that will provide a strong foundation for comprehensive care.24 The following nursing diagnoses, approved by the Norm American Nursing Diagnosis Association (NANDA), may be helpful when delineating a plan of care for the patient with ARDS.26 The following nursing diagnoses are listed alphabetically, not in order of priority: Communication, impaired Fatigue Fear Fluid volume excess

REED

Gas exchange, impaired Knowledge deficit Pain Powerlessness Thought processes, altered CONCLUSION

Providing comprehensive nursing care to the postanesthesia patient requires a large knowledge base that includes normal lung physiology and the cascade of events that lead to ARDS. Postoperative patients with risk factors and/or the signs and symptoms of ARDS present a clinical emergency and a professional challenge to the nurse. The comprehensive assessment skills and prompt intervention provided by the PACU nurse are essential to insure a continuing decrease in morbidity and mortality.

REFERENCES 1. Hunter FC, Mitchell S: Managing ARDS. RN 7:52-58, 1993 2. Shekleton ME, Litwack K Critical Care Nursing of the Surgical Patient. Philadelphia, PA, Saunders, 1991, pp 12, 100-112 3. Litwack K: Post Anesthesia Care Nursing (ed 2). St. Louis, MO, Mosby-Year Book, 1995, pp 294-295, 402 4. Hudson LD: The prediction and prevention of ARDS. Respir Care 2:1161-1173, 1990 5. Jones MA, Hoffman LA, Delgado E: ARDS revisited. Nursing 12:34-43, 1994 6. Drain CB: The Post Anesthesia Care Unit: A Critical Care Approach to Post Anesthesia Nursing (ed 3). Philadelphia, PA, Saunders, 1994, pp 119 7. Angerio AD, Kot PA Pathophysiology of pulmonary edema. Crit Care Nurs Q 17:21-26, 1994 8 Kacmarek RM: The Essentials of Respiratory Therapy (ed 2). St Louis, MO, Mosby-Year Book, 1985, pp 318-323 9. Ashbaugh DG, Bigelow DB, Petty TL, et al: Acute respiratory distress in adults. Lancet 2:319-323, 1967 10. Petty TL, Ashbaugh DC: The adult respiratory distress syndrome. Chest 3:233-239, 1971 11. Murray JF, Matthay MA, Lute JM, et al: An expanded definition of Adult Respiratory Distress Syndrome. Am Rev Respir Dis 138720.723, 1988 12. Chapman MJ: Adult respiratory distress syndromeAn update. Anaestb Intensive Care 22:255-266, 1994 13. Vollman KM: Adult respiratory distress syndrome: Mediators on the run. Crit Care Nurs Clin North Am 2:341356, 1994 14. Hammer J: Challenging diagnosis: Adult respiratory distress syndrome. Crit Care Nurse 10:46-51, 1995

15. Sinski A, Corbo J: Surfactant replacement in adults and children with ARDS-an effective therapy? Crit Care Nurse 12:55-59, 1994 16. Steinberg KP: Surfactant therapy in the adult respiratory distress syndrome. Respir Care, 38:365-372, 1993 17. Atkins PJ, Egloff ME, Wilm DC: Respiratory consequences of multisystem crisis: The adult respiratory distress syndrome. Crit Care Nurse 4:27-38, 1994 18 Craig J, Mullins D: Nitric oxide inhalation in infants and children: Physiologic and clinical implications. Am J Crit Care 6:450, 1995 19. East TM: The magic bullets in the war on ARDS: Aggressive therapy for oxygenation failure. Respir Care, 38690-702, 1993 20. Marini JJ: New options for the ventilatory management of acute lung injury. New Horiz 4:489-503, 1993 21. Pierson DJ, Kacmarek RM: Foundations of Respiratory Care. New York, NY, Churchill-Livingstone, 1992, pp 726-729, 899 22. Hudson LD: Pharmacologic approaches to respiratory failure. Respir Care, 38:754-763, 1993 23. Ravenscraft SA: Tracheal gas insufflation. Adjunct to conventional mechanical ventilation. Respir Care, 41:105111, 1996 24. Roberts SL, White B: Common nursing diagnoses for pulmonary alveolar edema patients. Dimensions Crit Care Nurs 11:13-27, 1992 25. Allison RC: Initial treatment of pulmonary edema: A physiological approach. Am J Med Sci 302:385-391, 1991 26. Carpenito LJ: Nursing Diagnosis: Application to Clinical Practice (ed 6), Philadelphia, PA, Lippincott, 1995