COVID-19 Resources – Acute Respiratory Distress Syndrome Pathophysiology & Management -

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

•The tree starts with a tree trunk → trunk branches off → branches continue to branch → ends with the leaves

•The leaves capture the sun’s rays → creates photosynthesis → helps the tree live

This same structure exists in our airways and lungs

Airway divides into two parts:

•Right mainstem bronchus

•Divides into the right upper lobe, right middle lobe and right lower lobe

•Left mainstem bronchus

•Divides into the left upper lobe and left lower lobe

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

•Approximately 600 million alveoli in the lungs

Process of oxygenation

•Deoxygenated blood comes from the pulmonary artery to the capillary beds surrounding the alveoli sacs

•Oxygen crosses the capillary beds for transportation via the red blood cells

•The red blood cell’s main job is to pick up the oxygen that comes into the alveoli in exchange for the carbon dioxide the deoxygenated blood picked up from the tissues

•Oxygenated blood continues through the pulmonary vein and is pumped out to the body

•This well-versed dance between oxygen and carbon dioxide continues when our lungs and body are healthy and able to maintain 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

•For example, if you fall and sprain your ankle, inflammation occurs at the site were your ankle is sprained and that inflammation causes leaking of fluid into the tissue space

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.

•The lung goes insane with inflammation and the thin, healthy barrier becomes large with inflammation and fluid begins to enter the interstitial space

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

•Protein helps regulate water so as protein rich fluid build up in the alveolar space more water will be pulled into the sac causing more problems

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

•Indirect (source not from the lungs)

•Sepsis (primarily gram-negative)***

•Blood transfusion (multiple)

•Inflammation of the pancreas (pancreatitis)

•Drug overdose

•Direct (source is from the lungs)

•Pneumonia

•Aspiration of gastric contents

•Inhalation Injury

•Near Drowning

•Embolism

Acute Respiratory Distress Syndrome Signs and Symptoms

Early signs

•The beginning, rarely noticeable, normal lungs sounds to random crackles

•Fluid is building up in the interstitial space

•Difficulty breathing with increased respiratory rate

•Low oxygen, low carbon dioxide causing respiratory alkalosis

Later Signs

•Full respiratory failure

•Refractory hypoxemia

•Cyanosis

•Mental status changes (tired, confused, restlessness)

•Increased heart rate (stressed from low oxygen)

•Retractions

•Crackles throughout the lungs

•Once the fluid reaches the alveolar sacs, you may begin to hear crackles from the pulmonary edema

Acute Respiratory Distress Syndrome Diagnostics

Imaging

Chest x-ray – whited out, ground glass appearance throughout bilateral lungs fields

P:F Ratio

•Calculated by PaO2 (divided by) FiO2

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

•Breathing on Room Air = 0.21

•PaO2 = 100

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

•The ventilator helps breathe for the patient and provide better oxygenation until the inflammation lessens and the fluid begins to decrease in the alveolar sacs

•Once this occurs, the thick barrier will once again become thin allowing the barrier to do what it does naturally and diffuse oxygen into the bloodstream

Maintain airway/function

•Mechanical ventilation with higher levels of PEEP and low tidal volumes

•Higher PEEP is needed to get those collapsed sacs open

•Low tidal volumes 6 ml/kg

•Goal is to reduce barotrauma

Complications

•High PEEP pressures can lead to

•Increase in intrathoracic pressure

•Compresses the heart

•Decreased cardiac output (monitor for hypotension)

•Pneumothorax (the entire lung collapse)

•Subcutaneous emphysema