ARDS is one of the most important—and intimidating—topics in critical care, so we thought it was the perfect time to reboot one of our most comprehensive episodes. Whether you’re hearing it for the first time or need a refresher on the latest evidence and core principles, this episode is packed with practical pearls that still hold up today.
On this week’s episode, Cyrus & Nick tackle one of their biggest challenges yet: Acute Respiratory Distress Syndrome, more commonly known as ARDS.***WARNING*** this is no shorty! We cover all things ARDS from pathophysiology, diagnosis, treatments and things NOT to do. Dare we say, this is the definitive FOAM-ARDS experience for anyone and everyone who cares for people suffering from ARDS. Give it a listen and as always, send us your feedback!!
What is ARDS?
Acute respiratory distress syndrome (ARDS) is an acute diffuse lung inflammation characterized by poor oxygenation and reduced compliance.
ARDS is a common cause of respiratory failure – and mortality – in people with critical illness.
ARDS has many causes:
Direct lung injury: e.g Pneumonia, Aspiration, Near-drowning) and in particular lung infections like pneumonia influenza, COVID, etc
Indirect lung injury: e.g. Septic shock, cardiac arrest, drug overdose, pancreatitis, transfusions, etc
You can think of ARDS as a final common pathway where many different insults can lead to a common pathway of lung inflammation; like how septic shock can be caused by infection with different organisms at different sites.
Pathophysiology of ARDS
An insult leads to inflammation-mediated disruptions in alveolar-capillary permeability.
This causes fluid to spill out into the alveolar space, resulting in edema. The collection of proteinacious fluid in the alveoli leads to alveolar collapse/derecruitment. This causes the characteristic reduction in compliance.
Simultaneously we get impaired gas exchange due to shunting and ventilation-perfusion mismatch.
We also frequently get a rise in pulmonary vascular resistance as blood redirected away from collapsed areas.
For more about understanding hypoxemia, see our earlier episode:
Exudative phase – occurs within the first 7 days, and is characterized by damage to the lung’s alveolar epithelium and vascular endothelium, which leads to fluid, protein, and red blood cells leaking into the lungs.
Proliferative phase – begins 2–7 days after the initial lung injury. It’s characterized by the proliferation of type 2 pneumocytes, the development of early fibrosis, and the thickening of the alveolar capillaries.
Fibrotic phase – This phase is not reached by all patients, but in those who do, it’s characterized by the development of scar tissue in the lungs. It’s associated with increased collagen deposition, prolonged ventilation-perfusion mismatching, and further diminishment of lung compliance.
ARDS is a heterogeneous disease, and many authors have argued that there are ‘sub-phenotypes’ that benefit from personalized therapies:
Fluid responsive patients with ARDS – arguing for a liberal vs conservative fluid strategy
“Recruitable lung” e.g patients who respond well to PEEP –
Those who have a “hyper-inflammatory” phenotype such as those with COVID-19 as the cause for their ARDS – potentially those who benefit most from anti-inflammatory medications (e.g. corticosteroids).
In a recent publication by Siuba and colleagues they took this concept one step further and demonstrated a high PEEP strategy in those who have less of an inflammatory response and lower severity of illness actually have increased mortality when a high PEEP strategy is implemented.
Acute onset: Symptoms must appear within one week after some insult.
Bilateral opacitieson imaging: typically chest radiography or CT – must show bilateral opacities. POCUS can also be used.
Edema origin is not primarily cardiac: Edema must not be fully explained by cardiac failure or fluid overload. Cardiac causes can be present, but must be judged to not be a
Hypoxemia is present – usually defined by the P/F ratio. The P/F ratio or PaO2/FiO2 ratio is also how we grade the severity of ARDS in the US, though in resource limited settings SpO2/FiO2 can be used.
It is important to understand that this is broad pragmatic definition, meant to be as inclusive as possible. The definition has been changed several times, each time becoming slightly broader.
Earlier definitions required the patient to be intubated. (The current definition allows HFNC or NIPPV).
Earlier definitions required arterial blood gas to confirm hypoxemia (the current definition allows S/F ratio).
Earlier definitions used PCWP to exclude cardiac causes. (The current definition does not)
Does it matter that the definition of ARDS is broad?
On one hand it really doesn’t – the definition of ARDS is largely a research tool, which is important for studies, but less important for clinicians at the bedside.
But on the other hand, it probably is good to have a broad flexible definition for one reason:
ARDS has high mortality and morbidity
There are several highly effective treatments; but they are applied inconsistently and often too late in someones course.
Simply asking “could this person have ARDS” potentially triggers life-saving interventions, much like how “could this person be septic does”
For that reason having a broader more inclusive definition is probably a good thing.
Disease vs Syndrome, Diffuse Alveolar Damage, and Pseudo-ARDS
What does it mean to be a “syndrome” instead of a “disease”
Many diseases are defined by what cells look like under a microscope or even what mutations are present. But ARDS is defined more loosely, based on clinical criteria.
As a result ARDS is a heterogeneous group of patients – some with severe disease and others with more mild disease, who are all lumped together.
Diffuse alveolar damage (DAD) is the histological hallmark of ARDS. It’s acute phase with edema, hyaline membranes, and inflammation. It’s followed by an organizing phase with type II pneumocyte hyperplasia and fibrosis.
If we did lung biopsies – which we don’t because it would be incredibly morbid – only about half of the patients with ARDS have diffuse alveolar damage on pathology.
Does this mean we are getting the diagnosis wrong half the time? NO
It means that like many conditions in the ICU (AKI, sepsis, etc), ARDS is heterogeneous! There is a spectrum of disease present.
“Performing a lung biopsy in critical illness is like checking your credit score. The very act of checking makes it worse.”
— Nick
Even though we don’t focus on the pathological findings as much as the clinical findings, we DO often perform bronchoscopy with BAL. This is really important for a few reasons:
If the cause of ARDS is infectious, it helps us identify the microbe and tailor our therapy.
There are several conditions that are ARDS mimics – disease like acute eosinophilic pneumonia which can look like ARDS but require different treatment.
See an upcoming episode for more:
Pseudo-ARDS is loosely defined as ARDS that improves very rapidly with treatment and does not follow the expected course of several weeks.
Is this a misdiagnosis like cardiogenic pulmonary edema? Possibly
Does it matter? Maybe Not. ARDS vs pseudo-ARDS is a bit of a distinction without a meaningful difference. If someone meets criteria for ARDS, treat them accordingly. If they get better fast, great! Whether it was ARDS or something like ARDS doesn’t really matter
Start here at 34:15
The 11 P’s of Treatment
Protective ventilation
PEEP
Prone positioning
Prednisone (really dexamethasone)
Paralytics (really neuromuscular blockers)
Prostacyclins (inhaled EPO and inhaled nitric oxide)
