Nursing care plan acute respiratory distress syndrome with a nursing diagnosis of impaired gas exchange related to increased alveolar-capillary permeability, interstitial edema, and decreased lung compliance. Other nursing diagnoses were as follows: Ineffective Breathing Pattern, Impaired Gas Exchange, High Risk for Decreased Cardiac Output, High Risk for Injury: Barotrauma, Impaired Physical Mobility related factors,acute respiratory factor, High Risk for Impaired skin Integrity, and Knowledge Deficit.
Acute respiratory distress syndrome (ARDS) was first coined by Ashbaugh and Petty in 1971. Previously, terms such as stiff lung, wet lung, shock lung, adult hyaline-membrane disease, and others were used to describe this syndrome that occurs after catastrophic events such as major surgical procedures, serious injuries, or other critical illnesses. In 1992, the American- European Consensus Conference on ARDS recommended changing the name back to what Ashbaugh and Petty originally named it in 1967, acute respiratory distress syndrome, because this condition affects children, teenagers, and adults.
Acute respiratory distress syndrome (ARDS) is defined as noncardiogenic pulmonary edema that occurs despite low to normal pressures in the pulmonary capillaries. Many theories and hypotheses are currently under investigation. Patients with ARDS are characterized as having high-permeability pulmonary edema (HPPE) in contrast to cardiogenic pulmonary edema. In ARDS, the alveolar-capillary membrane is damaged, and both fluid and protein leak into the interstitial space and alveoli. Recent research has focused on possible mediators of the membrane damage, such as neutrophils, tumor necrosis factor (TNF), bacterial toxins, and oxygen free radicals, among others. The onset of symptoms generally occurs within 24 to 72 hours of the original injury or illness.
As ARDS progresses, patients exhibit decreased lung volumes and markedly decreased lung compliance. Type II pneumocytes, the cells responsible for surfactant production, are damaged. This deficiency is thought to be partly responsible for the alveolar collapse and the decrease in lung volumes that occur. In addition, fibroblasts proliferate in the alveolar wall, migrate into the intraalveolar fluid, and ultimately convert the exudate (fluid with high concentration of protein and cellular debris) into fibrous tissue. Refractory hypoxemia occurs as the lungs are perfused but not ventilated (a condition called capillary shunting) owing to the damage to the alveoli and developing fibrosis. As ARDS progresses, respiratory failure and cardiopulmonary arrest can develop.
Cause of Acute Respiratory Distress Syndrome
Various conditions can predispose a patient to ARDS, but they usually represent a sudden, catastrophic situation. These conditions can be classified into two categories: direct lung injury and indirect lung injury. Direct injury occurs from situations such as gastric aspiration, near drowning, chemical inhalation, and oxygen toxicity. Indirect injury occurs from mediators released during sepsis, multiple trauma, thermal injury, hypoperfusion or hemorrhagic shock, disseminated intravascular coagulation, drug overdose, and massive blood transfusions. The most common risk factor for ARDS is sepsis from an abdominal source. Approximately 150,000 new cases of ARDS occur each year. Mortality rates vary and have been estimated to be between 40% and 50%, but older patients and patients with severe infections have a higher rate. Survivors generally have almost normal lung function a year after the acute illness.
Physical examination and Assessment
The patient with ARDS appears in acute respiratory distress with a marked increase in the work of breathing that may lead to nasal flaring, the use of accessory muscles to breathe, and profound diaphoresis. The respiratory rate may be more than 30 to 40 breaths per minute. If ARDS has progressed, the patient may have a dusky appearance with cyanosis around the lips and nail beds, or the patient may be very pale. Hypoxemia usually leads to restlessness, confusion, agitation, and even combative behavior. Palpation of the peripheral pulses reveals rapid, sometimes thready, pulses. Blood pressure may be normal or elevated initially, then decreased in the later stages. Auscultation of the lungs differs, depending on the stage of ARDS. In the early stage, the lungs have decreased breath sounds. In the middle stages of ARDS, the patient may have basilar crackles or even coarse crackles. In the late stage of ARDS, if the disease has been left untreated, the patient may have bronchial breath sounds or little gas exchange with no breath sounds. If airway and breathing are not maintained, the patient becomes fatigued and apneic. When the patient is intubated and mechanically ventilated, the lungs may sound extremely congested, with wheezes and coarse crackles throughout.
Diagnosis involves excluding other causes of acute respiratory failure. A consensus conference has defined ARDS as having the following features: acute bilateral lung infiltrates; a ratio of PaO2 to inspired oxygen concentration (FiO2) of less than 200; no evidence of heart failure or volume overload.
Patients may exhibit anxiety and fear because of hypoxemia and the real threat of death. Feelings of social isolation and powerlessness can occur as the patient is placed on mechanical ventilation and is unable to verbalize.
Primary Nursing Diagnosis of this Nursing Care Plan: Impaired gas exchange related to increased alveolar-capillary permeability, interstitial edema, and decreased lung compliance
Nursing intervention and treatment
The treatment for ARDS is directed toward the underlying cause and maintaining gas exchange. To this end almost all patients with ARDS require endotracheal intubation and mechanical ventilation with a variety of positive-pressure modes. Common methods for mechanical ventilation include pressure-controlled ventilation with an inverse inspiratory-expiratory ratio. This mode alters the standard inspiratory-expiratory ratio of 1:2 to 1:3 by prolonging the inspiratory rate and changing the ratio to 1:1. It also controls the amount of pressure in each breath to stabilize the alveoli and to re-establish the functional residual capacity (FRC) to normal levels. If possible, the physician attempts to limit the fraction of inspired oxygen (FiO) to less than 0.50 (50%) to reduce complications from oxygen toxicity. Positive end-expiratory pressure (PEEP) is often added to the ventilator settings to increase the FRC and to augment gas exchange. Lung-protective, pressure-targeted ventilation, a method whereby controlled hypoventilation is allowed to occur, minimizes the detrimental effects of excessive airway pressures and has also been used in ARDS with positive outcomes.
To augment gas exchange, the patient needs endotracheal suctioning periodically. Prior to suctioning, hyperventilate and hyperoxygenate the patient to prevent the ill effects of suctioning, such as cardiac dysrhythmias or hypotension. Turn the patient as often as possible, even every hour, to increase ventilation and perfusion to all areas of the lung. If the patient has particularly poor gas exchange, consider a rocking bed that constantly changes the patient’s position. If the patient’s condition allows, even if the patient is intubated and on a ventilator, get the patient out of bed for brief periods. Evaluate the patient’s condition to determine if soft restraints are appropriate. Although restraints are frustrating for the patient, they may be necessary to reduce the risk of self-extubation.
If the patient requires medications for skeletal muscle paralysis, provide complete care and make sure the medical management includes sedation. Use artificial tears to moisten the patient’s eyes because the patient loses the blink reflex. Provide passive range-of-motion exercises every 8 hours to prevent contractures. Reposition the patient at least every 2 hours for comfort and adequate gas exchange, and to prevent skin breakdown. Provide complete hygiene, including mouth care, as needed. Assist the patient to conserve oxygen and limit oxygen consumption by spacing all activities, limiting interruptions to enhance rest, and providing a quiet environment.
The patient and family may be fearful and anxious. Acknowledge their fear without providing false reassurance. Explain the critical care environment and technology but emphasize the importance of the patient’s humanness over and above the technology. Maintain open communication among all involved. Answer all questions and provide methods for the patient and family to communicate, such as a magic slate or point board.