Transcript for Acute respiratory distress syndrome
Acute respiratory distress syndrome
The main site of injury in ARDS is the alveolar-capillary membrane.
Now, any damage to the alveolar epithelium or the capillary endothelium increases the permeability of the alveolar-capillary membrane, causing fluid to move into the alveoli.
Oxygen and carbon dioxide have to travel across this fluid, so it acts as a barrier against normal gas exchange.
The fluid also dilutes out the surfactant molecules coating the alveoli, and as a result the alveoli are less able to remain open and compliant, so they become stiff.
If the injury continues, the alveoli eventually collapse.
Now, the pulmonary edema from ARDS causes the same problems as pulmonary edema from congestive heart failure, but because the triggering events are different, the term non-cardiogenic pulmonary edema is often used for ARDS.
Now, ARDS is not a primary lung disease, rather it arises as a complication of a systemic injury that causes widespread inflammation which results in damage to the alveolar-capillary membranes within the lung.
The most common underlying systemic cause of ARDS is sepsis, which causes systemic inflammation in response to an infection.
But other insults include trauma, severe burns, near-drowning, disseminated intravascular coagulation or DIC, acute pancreatitis, massive blood transfusions, aspiration of gastric contents, and toxic smoke inhalation.
The list basically includes any serious injury that directly or indirectly affects the entire body.
So, as you would guess, individuals with ARDS are very sick, and have severe shortness of breath, tachypnea, hypoxemia, and diffuse crackles on auscultation of the chest. At that point, it’s important to look for an underlying cause, like a pneumonia, urinary tract infection, or an infected intravenous line - all of which might result in sepsis.
Other clues might include epigastric abdominal pain radiating to the back along with a history of an alcohol binge or gallstones which indicate acute pancreatitis.
It’s equally important to make sure that the signs of pulmonary edema are not due to heart failure.
An elevated jugular venous pressure, an S3 heart sound, orthopnea and paroxysmal nocturnal dyspnea - all clue towards heart failure, and these findings are not present in ARDS.
ARDS is clinically diagnosed by fulfilling the following criteria: the symptoms developed within 1 week of the suspected injury, a chest x-ray shows diffuse bilateral opacities, the symptoms are not fully explained by congestive heart failure, and the ratio of the partial pressure of oxygen in the arteries or PaO2, to the fraction of inspired oxygen, or FiO2 is less than 300 mmHg.
The first two criteria are usually straightforward.
For criterion 3, there are some ways to help objectively determine whether congestive heart failure is contributing to the pulmonary edema.
First, you can measure the serum brain-natriuretic peptide, or BNP levels, which are elevated in congestive heart failure.
Second, you can do an echocardiogram, which would show an ejection fraction below 55% in systolic heart failure, and abnormal relaxation of the myocardium in diastolic heart failure.
Third, you can insert a Swan-Ganz catheter and measure the pulmonary capillary wedge pressure, or PCWP, which is a reflection of the pulmonary venous or the left atrial pressure.
The PCWP is increased in heart failure, typically over 18 mmHg.
The PCWP increases because blood backs up into the atria and subsequently into the pulmonary veins, increasing the hydrostatic pressure in those veins.
In ARDS, BNP levels, the ejection fraction and myocardial relaxation, and PCWP are all normal.
Now, measurement of the PCWP is the most accurate in differentiating ARDS from heart failure, but it’s not routinely done because it’s invasive.
For criteria 4, an arterial blood gas or ABG is needed to calculate the PaO2 to the FiO2 ratio.
The PaO2 is measured in millimeters of mercury, while the FiO2 is measured as a decimal between 0.21, which is the FiO2 of the atmospheric air, and 1, which is the maximum FiO2 you can artificially give an individual.
In ARDS, the edema in the alveoli prevents adequate ventilation, and some blood ends up in the left atrium without being oxygenated.
As a result, giving extra FiO2, doesn’t fully correct the hypoxemia, because blood passing by edematous alveoli simply aren’t participating in gas exchange. This means that the PaO2 doesn’t rise in accordance with FiO2, which decreases the PaO2 to FiO2 ratio, and the more alveoli are affected, the lower the ratio.