COVID-19 Resources – Acute Respiratory Distress Syndrome Pathophysiology & Management
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COVID 19 Acute Respiratory Distress Syndrome Slides
COVID 19 Acute Respiratory Distress Syndrome Notes
COVID-19 has left us with many unanswered questions about the care and treatment for our pandemic population.
In response to the rising questions and concerns, I have decided to create some educational videos that we can refer back to related to the care and treatment of our COVID-19 patients.
Let’s get started on understanding how hemodynamics and arterial blood gas results effect our COVID-19 population.
Acute Respiratory Distress Syndrome Pathophysiology
To understand how Acute Respiratory Distress Syndrome (ARDS) effects our COVID patients we must understand the pathophysiology of the lungs.
The lungs replicate an upside-down tree
This same structure exists in our airways and lungs
Airway divides into two parts:
The branches further divide into smaller branches ending with the alveolar sacs
The alveolar sacs are small grape like structures where oxygen and carbon dioxide are exchanged
Process of oxygenation
What is happening in ARDS?
The barrier between the alveoli and capillary bed is very thin because the oxygen must come down and diffuse into the bloodstream
When inflammation occurs in this space → problems occur
What happens in ARDS is a viral infection affects the lungs and the entire lung becomes inflamed (massive systemic inflammation) not in one area like in the example of a sprained ankle or in most pneumonias.
Acute Respiratory Distress Syndrome Pathophysiology
Injury reduces normal blood flow to the lungs, allowing platelets to cluster together. Serotonin, bradykinin, and histamine are released and cause inflammation and damage to the alveolar membrane and later increases capillary permeability.
This increase in capillary permeability causes fluid to shift into the interstitial space between the blood vessel and alveolar sac.
As capillary permeability increases, protein-rich fluid build-up begins to leak into the alveolar space and the sacs begin to fill with liquid causing pulmonary edema
Fluid in the alveoli and decreased blood flow begin to damage surfactant in the alveoli. This reduces the alveolar cell’s ability to produce more surfactant. Without surfactant, alveoli collapse, further impairing gas exchange.
The patient’s respiratory rate increases, but sufficient oxygen (O2) cannot cross the alveolar capillary membrane due to the fluid build up. Carbon dioxide (CO2); however, crosses more easily and is lost with every exhalation the patient takes. Both oxygen and carbon dioxide levels in the blood decreases leading the patient to initially have respiratory alkalosis.
Pulmonary edema worsens and the inflammation leads to fibrosis. These changes further impede gas exchange resulting in hypoxemia, respiratory acidosis and very stiff lungs.
If the patient becomes hypoxic, he or she can have a hard time breathing and more times then not the patient gets placed on the ventilator
Hypoxemia (low blood oxygen) causes the organs to suffer
Decreased oxygenation causes the body to shunt the remaining oxygen to the life sustaining organs (brain, heart, lungs)
The kidneys and liver initially take the hit due to the low oxygenation
If oxygenation does not improve, the life sustaining organs begin to decline leading to an increase in morbidities and mortalities
What have we learned about ARDS?
Acute Respiratory Distress Syndrome is a type of respiratory failure caused by leaking of fluid into the alveoli sacs from the capillary membranes due to increase permeability. ARDS is non-cardiogenic pulmonary edema.
A mnemonic to remember what happens during ARDS
Atelectasis
Refractory Hypoxemia
Decreased Lung compliance
Surfactant
Causes
Acute Respiratory Distress Syndrome Signs and Symptoms
Early signs
Later Signs
Acute Respiratory Distress Syndrome Diagnostics
Imaging
Chest x-ray – whited out, ground glass appearance throughout bilateral lungs fields
P:F Ratio
ARDS Severity | PaO2 / FiO2* | Mortality** |
Mild | 200 – 300 | 27% |
Moderate | 100 – 200 | 32% |
Severe | < 100 | 45% |
*on PEEP 5+; **observed in cohort |
Normal P:F Ratio
P:F Ratio = 476 (> 300)
Acute Respiratory Distress Syndrome Treatment
There is no way to speed up or slow down the inflammation process of ARDS
Maintain airway/function
Complications
Prone positioning
Fluid Management in ARDS
Inhaled pulmonary vasodilators
Steroids
Neuromuscular blockade
ECMO (Extracorporeal membrane oxygenation)