Acute respiratory distress syndrome (ARDS): Nursing

Acute Respiratory Distress Syndrome, or ARDS, is a type of severe respiratory condition characterized by severe lung inflammation and noncardiogenic pulmonary edema. As a result, there’s decreased lung compliance, leading to hypoxemia and respiratory failure.

Now, let’s quickly review the respiratory tract, which can be divided into two regions: the upper respiratory tract and lower respiratory tract. The upper respiratory tract includes the nose, nasal cavity, the oral cavity, pharynx, epiglottis, larynx, and the upper part of the trachea; while the lower respiratory tract includes the lower part of the trachea, and the lungs containing the bronchi, bronchioles, alveolar ducts, and finally the alveoli.

Alveoli are tiny air-filled sacs where most gas exchange occurs, so as we breathe, the inhaled oxygen moves from the alveolar sacs into the blood, while the carbon dioxide moves from the blood into the alveolar sacs to be exhaled. Now, the alveoli are lined by two types of alveolar epithelial cells, called pneumocytes. The vast majority are type I pneumocytes, which allow oxygen and carbon dioxide to pass through them. There are also type II pneumocytes scattered around which produce surfactant, an oily secretion that coats the alveoli and prevents their collapse.

Now, ARDS is not a primary lung disease, rather it arises as a complication of a systemic injury that causes widespread inflammation which results in damage to the alveolar-capillary membranes within the lung. So, the most common underlying cause of ARDS is sepsis, which causes inflammation in response to an infection. This infection is most often bacterial, but some cases can be associated with viral infections, such as COVID-19. But other injuries include trauma, severe burns, near-drowning, acute pancreatitis, massive blood transfusions, aspiration of gastric contents, and toxic smoke inhalation, as well as vaping-related injury. The list basically includes any serious injury that directly or indirectly affects the entire body.

Risk factors for developing ARDS include tube feeding, difficulty swallowing, a poor gag reflex, or a serious infection, as well as smoking or vaping.

Alright, so the pathology of ARDS begins when a pulmonary or systemic injury triggers a severe inflammatory response in the lungs, which in turn causes damage to the alveolar epithelium and capillary endothelium. As a result, the capillaries become permeable to larger molecules like proteins, which leak into the alveoli, pulling water with them. The end result is noncardiogenic pulmonary edema.

Meanwhile, damaged type II pneumocytes stop producing surfactant, causing alveolar collapse. These collapsed, fluid-filled alveoli cannot participate in gas exchange, causing non-aerated, stiff, and non-compliant lungs. This leads to ventilation-perfusion mismatch and shunting, where blood doesn't become oxygenated as it moves through the lungs. This results in acute, refractory hypoxemia, meaning that the client’s oxygenation does not improve even when they receive higher concentrations of oxygen; and ultimately, clients develop complications like respiratory failure.

Clients with ARDS often present with short, shallow, and rapid breathing, as well as intercostal and substernal retraction during inspiration. In severe cases, they may also experience shortness of breath, cyanosis, and refractory hypoxemia. Additionally, clients can develop hemodynamic instability, which presents as hypotension, tachycardia, or arrhythmias. During auscultation of the chest, there are diffuse crackles which is the sound of collapsed alveoli popping open with inspiration.

Diagnosis of ARDS involves the client’s history and physical assessment, followed by a chest X-ray, which shows opacities or “white out” in both lungs, which is due to the massive pulmonary edema. An arterial blood gas test is often also used to measure the lowered partial pressure of arterial oxygen or PaO2 and calculate the P/F ratio.

The P/F ratio is the partial pressure of oxygen in the arterial blood, or PaO2, divided by the percent of oxygen in the inspired air, also called the fraction of inspired oxygen or FiO2. In ARDS, the PF ratio is below 300 mmHg, and the lower this ratio gets, the more severe the ARDS is. And that PaO2 doesn’t rise even if we give extra FiO2, because blood passing by edematous alveoli simply isn’t participating in gas exchange. Finally, a bronchoscopy or transtracheal aspiration might be performed to obtain sputum cultures and check for a lung infection.

Treatment of ARDS depends on the underlying condition, so clients with a bacterial infection generally require antibiotics, while diuretics can be administered to reduce edema. But because the alveoli are damaged, supportive care for breathing is really important, usually in the form of mechanical ventilation with positive end-expiratory pressure or PEEP. This is where the pressure in the lungs is kept slightly above atmospheric pressure, even after exhalation, because that helps prevent the alveoli from collapsing. So, PEEP is set at 5 cm H2O and increased in increments of 3 to 5 mm H2O until oxygenation is adequate. A low tidal volume of about 4 to 8 mL/kg is used to prevent over-inflation of the damaged alveoli. Also, when possible, the FiO2 is set to 60% or less.