acute respiratory distress syndrome(redirected from Acute respiratory distress)
ARDS is characterized clinically by dyspnea, tachypnea, tachycardia, cyanosis, and hypoxemia. PaO2/FIO2 remains low (below 2 cc) even with oxygen therapy at high oxygen concentrations. The lung compliance is decreased so that the lung is stiffer and more difficult to ventilate. Chest radiographs show signs of bilateral interstitial and alveolar edema. Cardiac filling pressures are normal, and the pulmonary capillary wedge pressure is below 18 torr.
Most authorities consider that the syndrome has three phases or stages that characterize its progression: the exudative stage, the fibroproliferative or proliferative stage, and the resolution or recovery stage. The exudative stage comes first, two to four days after onset of lung injury, and is distinguished by the accumulation of excessive fluid in the alveoli with entrance of protein and inflammatory cells from the alveolar capillaries into the air spaces. The fibroproliferative stage comes second and is characterized by an increase in connective tissue and other structural elements in the lungs in response to the initial injury. It begins between the first and third weeks after the initial injury and may last up to ten weeks. Microscopic examination reveals lung tissue that appears densely cellular. The patient is at risk for pneumonia, sepsis, and pneumothorax at this time. The third stage is the resolution or recovery stage. During this stage the lung reorganizes and recovers, although it continues to show signs of fibrosis. Lung function may continue to improve for as long as six to twelve months or even longer, depending on the precipitating condition and severity of the injury. It is important to remember that there are often different levels of pulmonary recovery in patients with ARDS.
Some authorities refer to a fourth phase or stage of ARDS, the period after the resolution or recovery stage. Some patients continue to experience health problems caused by the acute illness, such as coughing, limited exercise tolerance, and fatigue. Anxiety, depression, and flashback memories of the critical illness may also occur and be similar to posttraumatic stress disorder.
This is the major cause of death in neonates and survivors have a high risk for chronic neurologic complications. No one factor is known to cause the condition; however, prematurity and interrupted development of the surfactant system is thought to be the major causative factor. Surfactant is secreted by the epithelial cells of the alveoli. It acts as a detergent, decreasing the surface tension of fluids that line the alveoli and bronchioles and allowing for uniform expansion of the lung and maintenance of lung expansion. When there is an inadequate amount of surfactant, a great deal of effort is required to re-expand the alveoli with air; thus the newborn must struggle for each breath. Insufficient expansion of the alveoli results in partial or complete collapse of the lung (atelectasis). This in turn produces hypoxemia and elevated serum carbon dioxide levels.
The hypoxemia causes metabolic acidosis from increased production of lactic acid and respiratory acidosis due to the hypercapnia. The lowered pH constricts pulmonary blood vessels and inhibits intake of oxygen, thus producing more hypoxemia and interfering with the transport of substances necessary for the production of the sorely needed surfactant.
To improve respiratory function, intubation, suctioning of the air passages, and continuous positive airway pressure via nasal prongs are commonly used, as well as instillation of artificial surfactant. Monitoring is conducted using transcutaneous oxygen monitoring or a pulse oximeter. To optimize breathing effort and facilitate air exchange, the newborn is positioned on the back with a shoulder support to keep the neck slightly extended, or on the side with the head supported. Because of the drying effect of oxygen therapy and the prohibition of oral fluids, mouth care must be given frequently to prevent drying and cracking of the lips and oral mucosa.
Early symptoms include dyspnea, wheezing, and apprehension; cyanosis is rarely present. As the condition worsens the patient becomes drowsy and mentally confused and may slip into a coma. blood gas analysis is an important tool in diagnosing respiratory failure and assessing effectiveness of treatment. The condition is a medical emergency that can rapidly progress to irreversible cardiopulmonary failure and death. Treatment is concerned with improving ventilation and oxygenation of tissues, restoring and maintaining fluid balance and acid-base balance, and stabilizing cardiac function.
a·dult res·pi·ra·to·ry dis·tress syn·drome (ARDS),
acute respiratory distress syndrome
a·dult res·pi·ra·to·ry dis·tress syn·drome(ARDS) (ă-dŭlt' res'pir-ă-tōr-ē dis-tres' sin'drōm)
Synonym(s): acute respiratory distress syndrome, wet lung (2) , white lung.
Acute Respiratory Distress Syndrome
|Mean LOS:||5.2 days|
|Description:||MEDICAL: Pulmonary Edema and Respiratory Failure|
|Mean LOS:||14.6 days|
|Description:||MEDICAL: Respiratory System Diagnosis with Ventilator Support 96+ Hours|
|Mean LOS:||7 days|
|Description:||MEDICAL: Respiratory System Diagnosis with Ventilator Support < 96 Hours|
|Mean LOS:||34.5 days|
|Description:||SURGICAL: Tracheostomy with MV 96+ Hours or Primary Diagnosis Except for Face, Mouth, and Neck with Major Operating Room|
The term adult 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.
ARDS, the most severe form of acute lung injury, 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 intra-alveolar 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.
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.
There may be genetic factors that influence both susceptibility and progression of ARDS. Survivors are more likely than nonsurvivors to have certain alleles of the genes that code for angiotensin-converting enzyme (ACE) and interleukin (IL)-6.
Gender, ethnic/racial, and life span considerations
ARDS can occur equally across genders and at any age, including during childhood, to those who have been subjected to severe physiological stresses such as sepsis, burns, or trauma. Ethnicity and race have no known effects on the risk for ARDS.
Global health considerations
People who live in developing nations without well-developed emergency medical systems may not survive the initial insult, and therefore ARDS may not occur. If critical care is not available to manage ARDS, mortality will be very high. In Europe, investigators have reported an incidence of 17.9 cases per 100,000 individuals for acute lung injury and 13.5 cases per 100,000 individuals for ARDS.
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 nailbeds, 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 and 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, and 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.
General Comments: The diagnosis of ARDS can be controversial and is one of exclusion. There are no specific markers that identify alveolar-capillary membrane damage. Early in ARDS, the pH is elevated and the Paco2 is decreased because of hyperventilation. In the later stages, the Paco2 is elevated and the pH is decreased. Other supporting tests include pulmonary function tests, pulse oximetry, and pulmonary capillary wedge pressure.
|Test||Normal Result||Abnormality With Condition||Explanation|
|Chest x-ray||Clear lung fields||Diffuse bilateral infiltrates without cardiomegaly or pulmonary vascular redistribution||Findings reflect noncardiogenic pulmonary edema|
|Arterial blood gases (ABGs)||Pao2 80–100 mm Hg; Paco2 35–45 mm Hg; SaO2 > 95%||Pao2 < 80 mm Hg; Paco2 varies; SaO2 < 95%||Poor gas exchange leads to hypoxemia and, as respiratory failure progresses, to hypercapnea|
Primary nursing diagnosis
DiagnosisImpaired gas exchange related to increased alveolar-capillary permeability, interstitial edema, and decreased lung compliance
OutcomesRespiratory status: Gas exchange; Respiratory status: Ventilation; Comfort level; Anxiety control
InterventionsAirway insertion and stabilization; Airway management; Respiratory monitoring; Oxygen therapy; Mechanical ventilation; Anxiety reduction
Planning and implementation
mechanical ventilation.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 reestablish 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.
General Comments: Use of genetically engineered surfactant has been studied in ARDS but has not demonstrated the success that has occurred in premature infants with surfactant deficiency. Although high- and low-dose corticosteroids have been used in ARDS, studies have not demonstrated improvement in patient outcomes and their use remains controversial. Simvastatin, a hydroxymethylglutaryl-coenzyme A reductase inhibitor, may improve oxygenation and respiratory mechanics in some patients. If the patient is difficult to ventilate, she or he may receive skeletal muscle relaxants such as cisatracurium (Nimbex) or vecuronium (Norcuron), which are neuromuscular-blocking agents that paralyze the patient’s skeletal muscles. These medications are used only when the patient’s gas exchange is so poor as to threaten his or her life. Neuromuscular-blocking agents paralyze the patient without affecting mental status, so the patient requires sedation to counteract the accompanying fear and anxiety that occur when the patient is unable to move.
|Medication or Drug Class||Dosage||Description||Rationale|
|Nitric oxide||Inhalation route; dosage varied||Pulmonary vascular vasodilator||Decreases pulmonary vascular resistance with increased perfusion to ventilated areas; no long-term outcome benefit has been observed, but it may improve oxygenation temporarily|
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. Prone position may improve oxygenation in selected patients. If the patient’s condition allows, get the patient out of bed for brief periods, even if he or she is intubated and on a ventilator. 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 are likely to 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.
Evidence-Based Practice and Health Policy
Schmidt, M., Zogheib, E., Roze, H., Repesse, X., Lebreton, G., Luyt, C., …Combes, A. (2013). The PRESERVE mortality risk score and analysis of long-term outcomes after extracorporeal membrane oxygenation for severe acute respiratory distress syndrome. Intensive Care Medicine, 39(10), 1704–1713.
- Mortality rates for ARDS exceed 50%, and those who survive experience persistent physical, functional, and psychological impairments.
- Mechanical ventilation with extracorporeal membrane oxygenation (ECMO) has been proposed as protective against ventilator-induced lung injury; however, identifying patients who would most benefit in the long term from this highly specialized and costly intervention is encouraged.
- Investigators of one study among 140 ARDS patients who received ECMO developed an algorithm to predict death for severe ARDS posttreatment with ECMO (PRESERVE) using eight pre-ECMO parameters including age, body mass index, immunocompromised status, prone positioning, days of mechanical ventilation, sepsis-related organ failure assessment, plateau pressure, and positive end-expiratory pressure.
- The PRESERVE algorithm predicted survival probabilities of 97%, 79%, 54%, and 16% for score ranges from 0 to 2, 3 to 4, 5 to 6, and ≥ 7, respectively (p < 0.001) for ARDS patients who received ECMO.
- Respiratory status of the patient: respiratory rate, breath sounds, and the use of accessory muscles; ABG levels; pulse oximeter and chest x-ray results
- Response to treatment, mechanical ventilation, immobility, and bedrest
- Presence of any complications (depends on the precipitating condition leading to ARDS)