Acute Respiratory Distress Syndrome
Acute respiratory distress syndrome (ARDS; previously calledadult respiratory distress syndrome) is a clinical syndrome char-acterized by a sudden and progressive pulmonary edema, in-creasing bilateral infiltrates on chest x-ray, hypoxemia refractory to oxygen supplementation, and reduced lung compliance. These signs occur in the absence of left-sided heart failure. Patients with ARDS usually require mechanical ventilation with a higher-than-normal airway pressure. A wide range of factors are associated with the development of ARDS (Chart 23-6), including direct injury to the lungs (eg, smoke inhalation) or indirect insult to the lungs (eg, shock). ARDS has been associated with a mortality rate as high as 50% to 60%. The major cause of death in ARDS is nonpulmonary multiple-system organ failure, often with sepsis.
ARDS occurs as a result of an inflammatory trigger that initiates the release of cellular and chemical mediators, causing injury to the alveolar capillary membrane. This results in leakage of fluid into the alveolar interstitial spaces and alterations in the capillary bed.
Severe ventilation–perfusion mismatching occurs in ARDS. Alveoli collapse because of the inflammatory infiltrate, blood, fluid, and surfactant dysfunction. Small airways are narrowed be-cause of interstitial fluid and bronchial obstruction. The lung com-pliance becomes markedly decreased (stiff lungs), and the result is a characteristic decrease in functional residual capacity and severe hypoxemia. The blood returning to the lung for gas exchange is pumped through the nonventilated, nonfunctioning areas of the lung, causing a shunt to develop. This means that blood is inter-facing with nonfunctioning alveoli and gas exchange is markedly impaired, resulting in severe, refractory hypoxemia. Figure 23-6 shows the sequence of pathophysiologic events leading to ARDS.
Clinically, the acute phase of ARDS is marked by a rapid onset of severe dyspnea that usually occurs 12 to 48 hours after the ini-tiating event. A characteristic feature is arterial hypoxemia that does not respond to supplemental oxygen. On chest x-ray, the findings are similar to those seen with cardiogenic pulmonary edema and present as bilateral infiltrates that quickly worsen. The acute lung injury then progresses to fibrosing alveolitis with per-sistent, severe hypoxemia. The patient also has increased alveolar dead space (ventilation to alveoli, but poor perfusion) and de-creased pulmonary compliance (“stiff lungs,” which are difficult to ventilate). Clinically, a patient is thought to be in the recovery phase if the hypoxemia gradually resolves, the chest x-ray im-proves, and the lungs become more compliant (Ware & Matthay, 2000).
Intercostal retractions and crackles, as the fluid begins to leak into the alveolar interstitial space, are evident on physical examination. A diagnosis of ARDS may be made based on the following criteria: a history of systemic or pulmonary risk factors, acute onset of respiratory distress, bilateral pulmonary infiltrates, clinical absence of left-sided heart failure, and a ratio of partial pressure of oxygen of arterial blood to fraction of inspired oxygen (PaO2/FiO2) less than 200 mm Hg (severe refractory hypoxemia).
The primary focus in the management of ARDS includes identi-fication and treatment of the underlying condition. Aggressive, supportive care must be provided to compensate for the severe respiratory dysfunction. This supportive therapy almost always includes intubation and mechanical ventilation. In addition, circulatory support, adequate fluid volume, and nutritional support are important. Supplemental oxygen is used as the pa-tient begins the initial spiral of hypoxemia. As the hypoxemia progresses, intubation and mechanical ventilation are insti-tuted. The concentration of oxygen and ventilator settings and modes are determined by the patient’s status. This is monitored by arterial blood gas analysis, pulse oximetry, and bedside pul-monary function testing.
Positive end-expiratory pressure (PEEP) is a critical part of the treatment of ARDS. PEEP usually improves oxygenation, but it does not influence the natural history of the syndrome. Use of PEEP helps to increase functional residual capacity and reverse alveolar collapse by keeping the alveoli open, resulting in im-proved arterial oxygenation and a reduction in the severity of the ventilation–perfusion imbalance. By using PEEP, a lower FiO2 may be required. The goal is a PaO2 greater than 60 mm Hg or an oxygen saturation level of greater than 90% at the lowest pos-sible FiO2.
Systemic hypotension may occur in ARDS as a result of hypovolemia secondary to leakage of fluid into the interstitial spaces and depressed cardiac output from high levels of PEEP therapy. Hypovolemia must be carefully treated without causing further overload. Intravenous crystalloid solutions are adminis-tered, with careful monitoring of pulmonary status. Inotropic or vasopressor agents may be required. Pulmonary artery pressure catheters are used to monitor the patient’s fluid status and the severe and progressive pulmonary hypertension sometimes ob-served in ARDS.
Numerous pharmacologic treatments are under investigation to stop the cascade of events leading to ARDS. These include human recombinant interleukin-1 receptor antagonist, neu-trophil inhibitors, pulmonary-specific vasodilators, surfactant re-placement therapy, antisepsis agents, antioxidant therapy, and corticosteroids late in the course of ARDS (Ware & Matthay, 2000).
Adequate nutritional support is vital in the treatment of ARDS. Patients with ARDS require 35 to 45 kcal/kg per day to meet caloric requirements. Enteral feeding is the first consideration; however, parenteral nutrition also may be required.
The patient with ARDS is critically ill and requires close moni-toring because the condition could quickly change to a life-threatening situation.
In addition to implementing the medical plan of care, the nurse considers other needs of the patient. Positioning is impor-tant. The nurse should turn the patient frequently to improve ventilation and perfusion in the lungs and enhance secretion drainage. However, the nurse must closely monitor the patient for deterioration in oxygenation with changes in position. Oxy-genation in the ARDS patient is sometimes improved in the prone position and may be used in special circumstances; studies to assess the benefits and problems of such positioning are ongo-ing (Curley, 2000; Marion, 2001).
The patient is extremely anxious and agitated because of the increasing hypoxemia and dyspnea. The nurse should explain all procedures and provide care in a calm, reassuring manner. It is important to reduce the patient’s anxiety because anxiety pre-vents rest and increases oxygen expenditure. Rest is essential to reduce oxygen consumption, thereby reducing oxygen needs.
If the patient is intubated and receiving mechanical ventilation with PEEP, several considerations must be addressed. PEEP, which causes increased end-expiratory pressure, is an unnatural pattern of breathing and feels strange to the patient. The patient may be anxious and “fight” the ventilator. Nursing assessment is important to assess for problems with ventilation that may be causing the anxiety reaction: tube blockage by kinking or retained secretions; other acute respiratory problems (eg, pneumothorax, pain); a sudden drop in the oxygen level; the patient’s level of dys-pnea; or ventilator malfunction. In some cases, sedation may be required to decrease the patient’s oxygen consumption, allow the ventilator to provide full support of ventilation, and decrease the patient’s anxiety. Possible sedatives are lorazepam (Ativan), midazolam (Versed), haloperidol (Haldol), propofol (Diprivan), and short-acting barbiturates.
If the PEEP level cannot be maintained despite the use of sedatives, neuromuscular blocking agents, such as pancuronium (Pavulon), vecuronium (Norcuron), atracurium (Tracrium), and rocuronium (Zemuron), may be given to paralyze the patient. This allows the patient to be ventilated more easily. With paral-ysis, the patient appears unconscious, loses motor function, and cannot breathe, talk, or blink independently. However, the pa-tient retains sensation and is awake and able to hear. The nurse must reassure the patient that the paralysis is a result of the med-ication and is temporary. Paralysis should be used for the short-est possible time and never without adequate sedation.
Use of paralytic agents has many dangers and side effects. The nurse must be sure the patient does not become disconnected from the ventilator, because respiratory muscles are paralyzed and the patient will be apneic. Consequently, the nurse ensures that the patient is closely monitored at all times. All ventilator and pa-tient alarms should be on at all times. Eye care is important as well because the patient cannot blink, increasing the risk of corneal abrasions. Neuromuscular blockers predispose patients to the de-velopment of deep venous thrombi, muscle atrophy, and skin breakdown. Nursing assessment is essential to minimize the com-plications related to neuromuscular blockade. The patient may have discomfort or pain but cannot communicate these sensations.Analgesia is usually administered concurrently with neuromus-cular blocking agents. The nurse must anticipate the patient’s needs regarding pain and comfort. The nurse checks the patient’s position to ensure it is comfortable and in normal alignment and talks to, and not about, the patient while in the patient’s presence.
In addition, it is important for the nurse to describe the pur-pose and effects of the paralytic agents to the family. This expe-rience can be very frightening to family members if they are unaware that these agents have been administered.
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