Acute respiratory distress syndrome (ARDS) is an acute and persistent lung disease characterized by an arterial hypoxemia (PaO2/FiO2<200 mmHg), resistant to oxygen therapy and bilateral infiltrates on chest X ray’ (Lucangelo et al). Brunner and Suddarth defined ARDS is a clinical syndrome characterized by a sudden and progressive pulmonary edema, increasing 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.
Pathophysiology of Acute Respiratory Distress Syndrome ARDS
Inflammatory damage to the alveoli, either by locally produced pro-inflammatory mediators, or remotely produced and arriving via the pulmonary artery. The change in pulmonary capillary permeability allows fluid and protein leakage into the alveolar spaces with pulmonary infiltrates. The alveolar surfactant is diluted with loss of its stabilizing effect, resulting in diffuse alveolar collapse and stiff lungs.
In general, ARDS has two different pathogeneses: a direct ‘pulmonary’ insult to the lung cell or an indirect ‘‘extrapulmonary’ insult resulting in a systemic inflammatory response. ARDS is a progressive disease, with different stages, different mediators, and both inflammatory and anti-inflammatory activity (cellular and humoural). At the beginning of the inflammatory response, changes occur in the alveolar capillary barrier, including the formation of a protein-rich fluid, alteration of surfactant and migration into the lung of neutrophils, lymphocytes and macrophages. Plasma factors, such as complement, and mediators generated by the cells, such as cytokines, oxidants and leucotrienes, are secreted inappropriately and at high levels. Resolution of the disease starts with a decrease in the levels of inflammatory mediators, the migration of fibroblasts into the lung, collagen deposition and the re-absorption of oedema fluid.
In the acute phase of ARDS, damage to the alveolar capillary barrier, including an increase in its permeability, causes the accumulation of a protein-rich fluid. The degree of injury to the epithelium and endothelium influences both the severity of lung injury and the clinical outcome. The protein-rich fluid may gradually become organised, producing the characteristic hyaline membrane that further destroys the alveolar structure.
In the early phases of ARDS, there is an intense alveolar inflammatory process that is characterized by the local accumulation and activation of neutrophils and macrophages. These cells, in turn, release oxidants and inflammatory mediators. The lung per se has a large reservoir of alveolar and interstitial macrophages, both of which come from blood monocytes. Alveolar macrophages release oxygen metabolites, cytokines, hormones, proteases and anti-proteases, all of which are fundamental for normal lung homeostasis and have the ability to eliminate microorganisms. According to an animal model of lung injury, there is an initial accumulation of neutrophils and then macrophages, which is followed by resolution of the inflammatory process. During phagocytosis, macrophages produce oxygen radicals and proteases, which eliminate most particulate matter and microorganism from the distal airways, thus keeping the alveoli ‘clean’. Similar to macrophages, neutrophils secrete several enzymes, such as hydrolases, myeloperoxidate, lysozyme and neutral proteases, which can cause further damage to the injured lung. In the presence of lung injury there is also breakdown of alveolar cells, with the subsequent release of nuclear debris and membrane damage and thus activation of the complement pathway.
Trauma is the most common cause of ARDS, possibly because trauma-related factors, such as fat emboli, sepsis, shock, pulmonary contusions, and multiple transfusions, increase the likelihood of microemboli developing.
There are many causes of pro-inflammatory mediator release sufficient to cause ARDS, and there may be more than one present. Common causes in order of prevalence:
- Sepsis/pneumonia; secondary risk factors for developing ARDS, when septic, are alcoholism and cigarette smoking
- Gastric aspiration (even if on a proton pump inhibitor, indicating that a low pH is not the only damaging component)
- Trauma/burns, via sepsis, lung trauma, smoke inhalation, fat emboli, and possibly direct effects of large amounts of necrotic tissue.
Complications for Acute Respiratory Distress Syndrome (ARDS)
Severe ARDS can lead to metabolic and respiratory acidosis and ensuing cardiac arrest.
Treatment for Acute Respiratory Distress Syndrome ARDS
The primary focus in the management of ARDS includes identification 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 patient begins the initial spiral of hypoxemia. As the hypoxemia progresses, intubation and mechanical ventilation are instituted. 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 pulmonary 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 improved 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 possible FiO2.
Numerous pharmacologic treatments are under investigation to stop the cascade of events leading to ARDS. These include pulmonary-specific vasodilators, surfactant replacement therapy, antisepsis agents, antioxidant therapy, and corticosteroids.
Nursing Care Plans for Acute Respiratory Distress Syndrome (ARDS)