Acute Respiratory Distress Syndrome, or ARDS, can develop suddenly and make it hard for your lungs to deliver enough oxygen to your body. It often appears in people who are already very sick or injured, such as those with severe infections, pneumonia, or significant trauma.
ARDS happens when fluid builds up in the tiny air sacs of the lungs, making it difficult to breathe and reducing oxygen flow to vital organs.
We often see ARDS progress quickly, which is why early recognition and treatment are so important. You might notice symptoms like rapid breathing, shortness of breath, or low oxygen levels that don’t improve with regular oxygen therapy.
In many cases, care in an intensive care unit and the use of a ventilator are needed to help the lungs heal.
Acute respiratory distress syndrome (ARDS) is a severe form of respiratory failure that develops quickly after lung injury or illness. It limits how much oxygen reaches the blood and can occur in people who were previously healthy or already critically ill.
Early recognition and supportive care are key to improving outcomes.
ARDS describes sudden, widespread inflammation in the lungs that causes fluid to leak into the air sacs. The Berlin Definition provides a clear framework for diagnosis based on timing, imaging, cause, and oxygen levels.
We diagnose ARDS when respiratory failure begins within 7 days of a known trigger, such as pneumonia, sepsis, or trauma. Chest imaging must show bilateral opacities not explained by heart failure or fluid overload.
The PaO₂/FiO₂ ratio helps measure severity:
| Severity | PaO₂/FiO₂ (mm Hg) | Mortality (approx.) |
| Mild | 201–300 | ~35% |
| Moderate | 101–200 | ~40% |
| Severe | ≤100 | ~45% |
These criteria help us identify ARDS early and guide oxygen and ventilation strategies.
In ARDS, the small air sacs in the lungs, called alveoli, become damaged and leaky. Fluid and inflammatory cells fill these spaces, reducing the lungs’ ability to move oxygen into the blood.
This leads to hypoxemia, or low blood oxygen levels. The alveoli may collapse or stiffen, making breathing difficult even with mechanical support.
The lungs lose compliance, meaning they require higher pressure to expand. This can worsen inflammation if not managed carefully.
We often use low tidal volume ventilation and prone positioning to protect the lungs and improve oxygen exchange.
Acute lung injury (ALI) and ARDS describe a similar process but differ in severity. Both involve noncardiogenic pulmonary edema and inflammation caused by infection, trauma, or other insults.
Under the Berlin Definition, ALI is no longer a separate diagnosis. What was once called ALI now falls under mild ARDS with a PaO₂/FiO₂ ratio between 201 and 300 mm Hg.
The change simplified classification and improved consistency in research and treatment.
Acute Respiratory Distress Syndrome (ARDS) develops when injury or illness damages the lungs, causing fluid to leak into the air sacs. This damage can result from direct harm to the lungs or from conditions that affect the body more broadly, leading to inflammation and fluid buildup.
Direct causes involve injury or infection that primarily affects the lungs. Pneumonia is the most common cause, as infection inflames lung tissue and fills air sacs with fluid.
Aspiration of stomach contents can also injure the lungs, introducing acid and bacteria that trigger inflammation—inhalation injuries, such as smoke or chemical exposure, damage airway linings and alveoli.
Near drowning introduces contaminated water into the lungs, disrupting gas exchange and causing inflammation. Chest trauma from accidents or medical procedures can bruise lung tissue or collapse air sacs.
COVID‑19 and other severe viral infections directly attack lung cells, leading to widespread inflammation and impaired oxygen transfer. These direct injuries compromise the alveolar–capillary barrier, allowing fluid to leak into air spaces and making breathing difficult.
Indirect causes result from conditions outside the lungs that trigger widespread inflammation. Sepsis, a severe bloodstream infection, is the leading indirect cause.
It releases inflammatory chemicals that weaken lung blood vessels, causing fluid leakage. Pancreatitis can release digestive enzymes and inflammatory mediators that damage lung tissue.
Severe trauma, burns, and massive blood transfusions may also provoke systemic inflammation that harms the lungs. Drug overdose and reactions to certain medications, such as chemotherapy or immunotherapy, can lead to lung injury.
Cardiopulmonary bypass and reperfusion injury after restoring blood flow may also contribute by generating oxidative stress. In each case, the lungs are affected secondarily, but the resulting inflammation and fluid buildup mirror direct injury patterns.
Certain factors increase our likelihood of developing ARDS when exposed to these triggers. Heavy alcohol use and cigarette smoking weaken the lungs and immune system, making them more prone to injury.
Older adults and people with chronic illnesses, such as liver disease or diabetes, face higher risk because their bodies respond poorly to stress and infection.
Multiple transfusions, prolonged mechanical ventilation, and severe systemic infections further raise the risk. People with poor overall health or reduced lung reserve may experience more severe symptoms and slower recovery.
| Risk Factor | Effect on ARDS Risk |
| Heavy alcohol use | Increases lung inflammation and infection risk |
| Cigarette smoking | Damages airway lining and impairs healing |
| Sepsis or trauma | Triggers systemic inflammation |
| Multiple transfusions | Can cause transfusion-related lung injury |
ARDS develops when widespread inflammation injures the lungs, disrupting the regular exchange of oxygen and carbon dioxide. This process damages the alveoli and capillaries, causes fluid buildup, and progresses through predictable stages that affect breathing and oxygen delivery.
We recognize that ARDS begins with injury to the alveolar–capillary barrier, which includes both the thin alveolar epithelium and the capillary endothelium. These layers usually keep air and blood separate while allowing gas exchange.
When inflammation or infection activates immune cells, they release cytokines and enzymes that harm these cells. This damage increases permeability, allowing proteins and inflammatory fluid to leak into the air sacs.
The type I alveolar cells, which cover most of the surface area, often die or detach. Type II cells, responsible for surfactant production, may also be impaired, reducing surfactant levels.
Without enough surfactant, alveoli collapse more easily, decreasing lung compliance and worsening oxygen exchange. As the injury continues, the lungs become stiff and require higher pressure to inflate.
These mechanical changes make ventilation difficult and can further aggravate the injury if not carefully managed.
In ARDS, fluid accumulates in the lungs due to increased capillary permeability, not from heart failure. This is what defines it as noncardiogenic pulmonary edema.
The damaged barrier allows protein-rich plasma to leak into the interstitial and alveolar spaces. This flooding reduces the amount of air that can reach the alveoli and dilutes or inactivates surfactant.
As alveoli fill with fluid, oxygen cannot move efficiently into the blood, resulting in severe hypoxemia. The lungs may appear heavy and consolidated on imaging, with diffuse bilateral opacities.
This process also triggers microvascular thrombosis, which increases dead space and further limits oxygen exchange. Managing fluid balance and maintaining adequate oxygenation are critical to prevent worsening edema and respiratory failure.
We typically describe ARDS progression in three overlapping phases: exudative, proliferative, and fibrotic.
| Phase | Main Features | Approximate Timeframe |
| Exudative | Alveolar flooding, inflammation, and diffuse alveolar damage | First 7 days |
| Proliferative | Repair of epithelium, reabsorption of edema, and fibroblast activity | Days 7–21 |
| Fibrotic | Collagen deposition, lung scarring, and decreased compliance | After 3 weeks |
In the exudative phase, inflammation dominates and gas exchange worsens. The proliferative phase involves partial recovery as cells begin to repair the lining.
If the injury persists, the fibrotic phase can lead to lasting stiffness and reduced lung function.
Acute Respiratory Distress Syndrome (ARDS) causes a rapid decline in lung function that affects oxygen delivery throughout the body. We often see a pattern that begins with mild breathing problems and can quickly progress to severe respiratory failure if not treated promptly.
In the early stages, patients may notice shortness of breath and rapid breathing that worsen over hours or days. These symptoms often appear after an illness or injury such as pneumonia, sepsis, or trauma.
We may also observe fatigue, mild chest pain, or a feeling of not getting enough air. Oxygen levels start to drop, which can make the skin appear pale or slightly bluish.
Typical early signs include:
Some patients experience a low-grade fever or a mild cough.
As ARDS progresses, symptoms become more intense and life-threatening. Breathing becomes very difficult, and oxygen levels fall sharply despite supplemental oxygen.
We often see severe shortness of breath, cyanosis (bluish lips or fingertips), and confusion from low oxygen in the brain. The heart may respond with tachycardia (fast heartbeat) and low blood pressure as the body struggles to maintain oxygen supply.
Severe indicators may include:
| Symptom | Description |
| Cyanosis | Blue tint to lips, nails, or skin |
| Tachycardia | Heart rate above 100 beats per minute |
| Low blood pressure | Systolic pressure under 90 mmHg |
| Confusion or agitation | From reduced oxygen to the brain |
At this stage, patients often require mechanical ventilation to maintain adequate oxygen levels.
During a physical exam, we listen to the lungs and often hear crackles or rales, which sound like bubbling or popping. These noises come from fluid in the air sacs.
We check oxygen saturation, heart rate, and blood pressure carefully. Low oxygen levels, fast heartbeat, and low blood pressure are typical findings.
The skin may appear cool or bluish, especially around the mouth and fingertips. In severe cases, we may see labored breathing with the use of chest and neck muscles.
These findings help us confirm the severity of lung injury and guide immediate treatment decisions.
We identify acute respiratory distress syndrome (ARDS) through a combination of clinical findings, imaging studies, and laboratory measures that confirm lung injury and impaired oxygen exchange. Accurate diagnosis helps us guide treatment and rule out other causes of respiratory failure such as heart failure or fluid overload.
We diagnose ARDS using the Berlin definition, which focuses on the timing, imaging, and severity of hypoxemia. Symptoms must begin or worsen within one week of a known clinical event, such as pneumonia or sepsis.
Patients show acute respiratory failure not fully explained by cardiac causes. We assess oxygenation using the PaO₂/FiO₂ ratio:
Mechanical ventilation with positive end-expiratory pressure (PEEP ≥5 cm H₂O) is usually required for accurate measurement. We also monitor plateau pressure to limit ventilator-induced injury.
Chest imaging confirms lung injury and helps exclude other conditions. We typically start with a chest X-ray, which shows bilateral opacities not due to effusion, nodules, or lung collapse.
These opacities reflect fluid-filled or collapsed alveoli. When findings are unclear, we use a computed tomography (CT) scan for more detail.
A CT scan can reveal diffuse alveolar damage, areas of consolidation, and dependent lung collapse.
Table: Common Imaging Findings in ARDS
| Test | Key Findings | Purpose |
| Chest X-ray | Bilateral infiltrates | Initial screening |
| CT scan | Ground-glass opacities, consolidation | Assess extent and distribution |
| Echocardiogram | Normal left heart function | Rule out cardiac causes |
We use blood tests to evaluate oxygenation, inflammation, and possible triggers such as infection or sepsis. Arterial blood gas (ABG) testing provides the PaO₂/FiO₂ ratio, which quantifies oxygen impairment.
An echocardiogram helps exclude left ventricular failure as the cause of pulmonary edema. Additional tests, like complete blood count and metabolic panels, identify infections or organ dysfunction.
We may measure lung compliance and plateau pressure during ventilation to assess stiffness and guide ventilator settings. Elevated plateau pressures suggest reduced lung elasticity, a hallmark of ARDS.
We focus on stabilizing breathing, improving oxygen levels, and preventing further lung injury. Care usually takes place in the intensive care unit (ICU) and often requires mechanical support, close monitoring, and coordinated medical care.
Most patients with ARDS need mechanical ventilation to maintain oxygen levels. We use low tidal volume ventilation to reduce stress on the lungs and lower the risk of ventilator-induced injury.
Typical settings aim for about 6 mL/kg of ideal body weight. We adjust positive end-expiratory pressure (PEEP) to keep air sacs open and improve oxygen exchange.
PEEP levels vary based on lung compliance and oxygen response. Prone positioning, or turning the patient onto their stomach, often improves oxygenation by redistributing blood flow and reducing lung compression.
We apply this for several hours a day in moderate to severe cases. Sedation and, at times, temporary neuromuscular blockers help patients tolerate the ventilator and reduce asynchrony between breathing efforts and machine cycles.
There is no single drug that cures ARDS, but we use several treatments to support recovery. Antibiotics treat or prevent infections that may have triggered the condition.
Diuretics help control fluid buildup in the lungs, while careful fluid management prevents overload. We provide sedation to maintain comfort and reduce anxiety during ventilation.
When needed, we use vasopressors to stabilize blood pressure. Nutritional support, often through a feeding tube, helps maintain strength and healing.
Our team also prevents complications like blood clots, pressure injuries, and secondary infections. Frequent repositioning, early mobility when possible, and deep vein thrombosis prophylaxis are standard parts of care.
If standard ventilation fails to maintain oxygen levels, we consider advanced options. Extracorporeal membrane oxygenation (ECMO) temporarily replaces lung function by circulating blood through an external oxygenator, allowing the lungs to rest.
We may use inhaled pulmonary vasodilators, such as nitric oxide, to improve oxygen delivery in select cases. Corticosteroids can reduce inflammation in certain patients, though their benefit varies.
Other adjunctive measures include recruitment maneuvers to reopen collapsed lung areas and conservative fluid strategies to limit pulmonary edema. These therapies require careful monitoring to balance oxygenation with the risk of further lung damage.
ARDS can lead to serious complications during hospitalization and lasting effects after recovery. These issues often involve the lungs, muscles, and other organs, and they can affect both survival and quality of life.
During the acute phase, respiratory failure is the most immediate concern. Patients often require mechanical ventilation to maintain oxygen levels due to severe hypoxemia.
This treatment, while lifesaving, can cause ventilator-related injuries such as barotrauma or pneumonia. Infection is another significant risk.
The use of invasive lines and prolonged ICU stays increases the chance of sepsis or septic shock, which can worsen organ damage. Other short-term problems include kidney injury, low blood pressure, and blood clots from immobility.
Many patients also experience delirium or confusion caused by critical illness and medications.
| Common Short-Term Complications | Description |
| Respiratory failure | Requires mechanical ventilation |
| Infection or sepsis | May lead to septic shock |
| Kidney injury | Often due to low blood flow or medications |
| Delirium | Temporary confusion or agitation |
| Blood clots | Caused by immobility in the ICU |
Even after hospital discharge, many survivors face lasting effects. Muscle weakness and fatigue are common due to prolonged bed rest and inflammation.
Some develop critical illness neuropathy or myopathy, which slows physical recovery. Lung function usually improves within a year, but mild scarring or reduced capacity may remain.
Breathing issues can persist, especially after severe or COVID-19–related ARDS. Cognitive and emotional challenges, such as memory problems, anxiety, or depression, may continue for months.
These symptoms are part of post–intensive care syndrome (PICS) and can affect daily activities and work. Ongoing rehabilitation, including physical therapy and mental health support, helps improve strength and quality of life.
ARDS severity—classified as mild, moderate, or severe based on oxygenation levels—strongly influences outcomes. Patients with severe hypoxemia face higher mortality and longer recovery times.
Survival rates have improved with better ventilation strategies and critical care practices.
However, those who survive severe ARDS often experience reduced exercise tolerance and slower return to normal function.
Age, underlying health, and complications like septic shock or multi-organ failure also affect prognosis.
Early recognition, lung-protective ventilation, and coordinated post-discharge care improve the chances of long-term recovery.
Acute Respiratory Distress Syndrome (ARDS) is a severe yet treatable lung condition that requires timely recognition and advanced medical care. By understanding its symptoms—such as rapid breathing, low oxygen levels, and sudden respiratory distress—patients and families can act quickly to seek the care that makes a difference. Early intervention in a critical care setting, supported by expert pulmonologists, can help stabilize breathing, restore oxygen flow, and prevent long-term lung damage. Beyond emergency treatment, pulmonary rehabilitation and close follow-up care are essential for full recovery and rebuilding lung strength. With proactive monitoring and guidance, patients can improve their outcomes and regain their quality of life.
Get the specialized care your lungs deserve.
At Gwinnett Pulmonary & Sleep, our board-certified pulmonologists provide expert diagnosis and advanced treatment for ARDS and other serious lung conditions. From hospital-based management to long-term recovery support, we deliver compassionate, comprehensive care tailored to every patient.
Book your appointment today at gwinnettlung.com or call 770-995-0630 to schedule your consultation.
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