|Acute Respiratory Distress Syndrome (ARDS)|
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 For 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.
Causes For ARDS
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.
Nursing Assessment Nursing Care Plans for Acute Respiratory Distress Syndrome (ARDS)
ARDS showed that, in patients with ALI (acute lung injury), elevated levels of PAI-1 (plasminogen activator inhibitor-1) in pulmonary oedema fluid and in plasma are associated with a higher mortality rate and fewer days of assisted ventilation. Recently, Ware LB et al. showed that protein C levels were lower in ALI/ARDS patients than in normal subjects and were associated with worse clinical outcomes, including death, fewer ventilator-free days, and more non-pulmonary organ failures, even when only those patients without sepsis were analyzed. Levels of thrombomodulin in the pulmonary edema fluid of patients with ALI/ARDS were more than ten-fold higher than in normal plasma and two-fold higher than in ALI/ARDS plasma. Higher thrombomodulin levels in edema fluid were associated with worse clinical outcomes. Decreasing circulating protein C and increased circulating thrombomodulin are markers of the pro-thrombotic, anti fibrinolytic state. 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)
Nursing diagnosis Nursing Care Plans for Acute Respiratory Distress Syndrome (ARDS)
Common nursing diagnosis found in Nursing Care Plans for Acute Respiratory Distress Syndrome (ARDS)
- Ineffective airway clearance
- Ineffective breathing pattern
- Activity intolerance
- Anxiety (specify level: mild, moderate, severe, panic)
- Disturbed gas exchange
- Risk for aspiration
Nursing interventions Nursing Care Plans for Acute Respiratory Distress Syndrome (ARDS)
Common nursing diagnosis fond in Nursing Care Plans for Acute Respiratory Distress Syndrome ARDS is; Ineffective airway clearance, Ineffective breathing pattern, Activity intolerance, Anxiety (specify level: mild, moderate, severe, panic), Disturbed gas exchange, Risk for aspiration
Below is Nursing interventions Nursing Care Plans for Acute Respiratory Distress Syndrome (ARDS) with Nursing diagnosis Ineffective airway clearance
Ineffective airway clearance
• Maintain airway patency.
• Expectorate/clear secretions readily.
• Demonstrate absence/reduction of congestion with breath sounds clear, respirations noiseless, improved oxygen exchange (e.g., absence of cyanosis, ABG results within client norms).
• Verbalize understanding of cause(s) and therapeutic management regimen.
• Demonstrate behaviors to improve or maintain clear airway.
• Identify potential complications and how to initiate appropriate preventive or corrective actions.
• Position head midline with flexion appropriate for age/condition to open or maintain open airway in at-rest or compromised individual.
• Assist with appropriate testing (e.g. pulmonary function/ sleep studies) to identify causative/precipitating factors.
• Suction nasal/tracheal/oral porn to clear airway when secretions are blocking airway.
• Elevate head of the bed/change position every 2 hours to take advantage of gravity decreasing pressure on the diaphragm and enhancing drainage of/ventilation to different lung segments (pulmonary toilet).
• Monitor infant/child for feeding intolerance, abdominal distention, and emotional stressors that may compromise airway.
• Insert oral airway as appropriate to maintain anatomic position of tongue and natural airway.
• Assist with procedures (tracheotomy) to clear and maintain open airway.
• Keep environment allergen free (e.g., dust, feather pillows, smoke) according to individual situation.
• Encourage deep-breathing and coughing exercises; splint chest/incision to maximize effort.
• Administer analgesics to improve cough when pain is inhibiting effort. (Caution: Overmedication can depress respirations and cough effort.) Monitor for signs/symptoms of congestive heart failure (crackles, edema, weight gain).
• Encourage/provide warm versus cold liquids as appropriate.
• Provide supplemental humidification, if needed (ultrasonic nebulizer, room humidifier).
• Perform/assist client with postural drainage and percussion as indicated if not contraindicated by condition, such as asthma.
• Assist with respiratory treatments (intermittent positive pressure breathing—IPPB, incentive spirometer).
• Support reduction/cessation of smoking to improve lung function.
• Discourage use of oil-based products around nose to prevent aspiration into lungs.
• An auscultative breath sounds and assesses air movement to ascertain status and note progress.
• Monitor vital signs, noting blood pressure/pulse changes.
• Observe for signs of respiratory distress (increased rate, restlessness/ anxiety, use of accessory muscles for breathing).
• Evaluate changes in sleep pattern, noting insomnia or daytime somnolence.
• Document response to drug therapy and/or development of adverse side effects or interactions with antimicrobials, steroids, expectorants, bronchodilators.
• Observe for signs/symptoms of infection (e.g., increased dyspnea with onset of fever, change in sputum color, amount, or character) to identify infectious process/promote timely intervention.
• Obtain sputum specimen, preferably before antimicrobial therapy is initiated, to verify appropriateness of therapy.
• Monitor/document serial chest x-rays/ABGs/pulse oximetry readings.
• Observe for improvement in symptoms.
• Client’s response to interventions/teaching and actions performed.
• Attainment/progress toward desired outcome(s).
· Modifications to care plan.