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Acute respiratory distress syndrome



Respiratory system


Upper respiratory tract disorders
Lower respiratory tract disorders
Pleura and pleural space disorders
Pulmonary vascular disorders
Apnea and hypoventilation
Respiratory system pathology review

Acute respiratory distress syndrome


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High Yield Notes
7 pages

Acute respiratory distress syndrome

8 flashcards

USMLE® Step 1 style questions USMLE

3 questions

A 45-year-old man with a history of alcohol abuse is admitted for acute pancreatitis, and he becomes acutely short of breath on day two of his hospitalization. His temperature is 37°C (98.6°F), pulse is 108/min, respirations are 26/min, blood pressure is 110/94 mmHg, and oxygen saturation is 87% on room air. He is given supplemental O2 via non-invasive ventilation, but he later requires intubation due to persistent hypoxemia and concern for airway compromise. Chest x-ray demonstrates new bilateral opacities. His arterial blood gas on 100% FiO2 shows the following:  


Laboratory value  Result
Blood Gases, Serum 
pH  7.51 
 PCO2  23 mmHg 
 PO2  54 mm Hg 
Cardiac Enzymes, Serum 
Brain Natriuretic Peptide  (BNP)  <100 ng/dL (N = <100) 
 Troponin  <.03 ng/dL 
Which of the following physiologic parameters best confirms the diagnosis in this patient?

External References

Content Reviewers:

Vincent Waldman, PhD


Marisa Pedron

Acute Respiratory Distress Syndrome, or ARDS, is exactly what it sounds like.

‘Acute’ means that it happens rapidly.

‘Respiratory distress’ means that a person becomes unable to breathe and oxygenate their blood, and ‘syndrome’ means that it is a group of symptoms that may be caused by any number of underlying conditions.

In ARDS, the alveoli and the capillaries that surround them - the site of gas exchange in the lungs - are damaged by an inflammatory process like pneumonia or sepsis.

Air enters the lungs through a series of airways that branch and narrow until they end in clusters of alveoli, which look kinda like a bunch of grapes.

The alveoli are covered in nets of capillaries that allow gas exchange into and out of the blood.

Gas exchange happens efficiently between alveoli and capillaries because each of their walls is only one cell thick!

Capillaries are lined with a single layer of endothelial cells and alveoli are lined with a single layer of epithelial cells.

These cell layers are fused to one another by the basement membrane and surrounding the alveoli and blood vessels is connective tissue made up of mostly proteins and water - in a space called the interstitial space.

The alveolar epithelial cells—called pneumocytes—come in two types.

The vast majority are type I pneumocytes, which are thin and have a large surface area, a shape that allows oxygen and carbon dioxide to pass through them easily.

There are also type II pneumocytes scattered around which are smaller and thicker, and are important because they make surfactant, an oily secretion that coats the alveoli.

The alveoli are so tiny that their walls end up being really close together.

Surface tension from water molecules lining the alveolar walls can easily attract one another, and pull the walls together, making the alveoli collapse.

Surfactant contains various phospholipids and is a bit like a droplet of oil that coats the inside of the alveoli, blocking the surface tension, so that the alveoli stay open.

In addition to the pneumocytes, there are alveolar macrophages, which are also called dust cells because they consume dust and dangerous particles before they enter the bloodstream.

The process of ARDS gets started when inflammatory molecules arrive in the lungs.

More specifically, these are cytokines like TNF-alpha and interleukin 1, that come through the bloodstream due to a systemic illness like a massive infection, or get released locally by alveolar macrophages in response to a lung injury.

Whatever the source, these cytokines cause capillary endothelial cells to secrete inflammatory molecules, and express adhesion molecules on their surface that help circulating immune cells to adhere or stick to them.

Neutrophils—some of the first responders of the immune response—then stick to the endothelium and migrate out of the capillary and into the alveoli.

These neutrophils launch into inflammatory mode, releasing proteases, enzymes that digest protein, reactive oxygen molecules, that cause free radical damage, and cytokines, which perpetuate the cycle of inflammation.

As a result of this inflammation, a few important things happen. First, some inflammatory molecules are pro-coagulant, meaning they make the blood more likely to clot.

Second, the endothelium becomes leaky, allowing fluid to seep into the interstitium—causing pulmonary edema—and the fluid then seeps into the alveoli—causing an infiltrate to show up on a chest Xray.

Third, the pneumocytes themselves get injured and die, which means that type I pneumocytes don’t do a good job with facilitating gas exchange, and type II pneumocytes produce less surfactant.

Without surfactants there’s more surface tension within the alveoli and that makes them more likely to collapse.

Finally, dead cells and protein-rich fluid start to pile up in the alveolar space and over time it forms a waxy hyaline—or glassy-appearing—material: a telltale finding of ARDS.

Hyaline membranes can be seen lining the inside of alveolar walls, and that makes gas exchange even more difficult.


Acute respiratory distress syndrome (ARDS) is a life-threatening lung condition that results in non-compliant lungs and poor blood oxygenation. It is associated with diffuse alveolar and endothelial injury. ARDS can be caused by a number of things, including pneumonia, sepsis, and trauma. Symptoms include shortness of breath, rapid breathing, and blue lips and fingernails.

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