Acute Respiratory Distress Syndrome (ARDS) Overview
Acute respiratory distress syndrome (ARDS) is sudden, life-threatening lung
failure. ARDS inflames the alveoli, causing them to fill with liquid and
collapse. Once the alveoli collapse, gas exchange ceases, and the body
becomes starved of oxygen. ARDS requires treatment with mechanical
ventilation or some other form of assisted breathing.
ARDS is a syndrome, not a specific disease. A variety of underlying conditions,
from blood-borne infections to major trauma, can cause the characteristic
inflammation and accumulation of fluid (edema) in the alveoli (see causes).
ARDS usually develops within 24 to 48 hours of the injury or illness. The
duration and intensity of the condition can vary considerably from patient to
patient. The mortality rate from ARDS ranges from 35—50%. In most cases,
death results from underlying disease or from complications of mechanical
ventilation. In patients who survive, normal lung function usually resumes
within 6 to 12 months.
Pathophysiology of ARDS
The respiratory system resembles an upside-down, hollow tree. Indeed, the
passageways leading from the mouth to the interior of the lungs are referred
to as the tracheobronchial tree. The parts of the body through which air
enters and exits the body (i.e., the mouth, nose, larynx, and trachea) make
up the "trunk" of the tree. The tubes that lead to the lungs (bronchi) and the
tiny tubes inside the lungs (bronchioles) are the tree's "branches" and
"twigs."Air moves through the respiratory system from the base of the trunk
to the tips of the twigs. Clustered at the tips of the trachiobronchial twigs are
tiny air sacs called alveoli, where inhaled oxygen passes into the blood
stream. This is where acute respiratory distress syndrome (ARDS) occurs.
Injury to the Alveoli
About 90% of the cells that make up the alveoli are very thin "type I epithelial
cells" across which actual gas exchange takes place. Oxygen normally diffuses
very easily through this layer of cells into the capillaries where it binds with
the hemoglobin in the red blood cells.
The alveolar epithelial cells normally form a very tight barrier around the
alveolar space, preventing any fluid from entering and disrupting gas
exchange. In ARDS, the alveolar epithelial barrier breaks, allowing flooding of
the alveolar space and making it difficult or impossible for oxygen to diffuse
into the capillaries.
ARDS also can affect the "type II alveolar cells". Type II cells are thicker,
square-shaped cells and the main function of these cells is to produce
surfactant. Surfactant plays an essential role in preventing the alveoli from
collapsing. The flooding through the broken type I cell barrier and the
diminished production of surfactant by the type II cells collapse the alveoli.
Alveolar damage is increased by the activity of immune system cells
(neutrophils) that rush to the site of injury, ironically, to help out. The activity
of these cells and the inflammation they cause create a cascade of further
injury that may extend into the capillaries as well.
Injury to the Alveolar Capillaries
If the original injury is in the alveolar capillaries that lie just beneath the
alveoli, chemical mediators (usually cytokines) that the immune system
releases in response, rush to the site of the injury, damaging and causing
inflammation to the cells that line the capillaries (i.e., the capillary
endothelium).
As a result, cells and fluid leak through the capillaries and into the alveolar
spaces; the capillaries become blocked with cellular debris and fibrin (i.e.,
protein that makes up blood clots); surfactant production ceases; and the
alveoli collapse.
Causes of acute respiratory distress syndrome include the following:
Serious infection in the blood or other tissues (called sepsis; accounts for
more than 30% of cases)
Severe chest trauma
Severe lung infection (e.g., bacterial or viral pneumonia)
Inhalation of vomited stomach contents
Inhalation of smoke or other toxic fumes
Fat embolis (globule of fat that blocks an artery)
Near drowning,Massive blood transfusion
Cardiopulmonary bypass surgery
Ingestion of certain drugs
Acute pancreatitis
Signs and Symptoms of Acute Respiratory Distress Syndrome (ARDS)
The symptoms of ARDS develop suddenly and include the following:
Dyspnea (audible, labored breathing, shortness of breath)
Tachypnea (abnormally rapid breathing)
Severe hypoxaemia (decreased oxygen concentration in the blood)
Pulmonary hypertension (high blood pressure in the pulmonary arteries)
Cyanosis (bluish discoloration of the skin due to poor oxygenation of the
blood)
Presence of abnormal deposits in the lungs (detected by chest x-rays)
Complications of ARDS
Complications of ARDS include the following:
Multiorgan failure (or multiple organ dysfunction syndrome): The same
inflammatory processes that injure the alveoli and capillary endothelial cells
can damage other organs, including the liver, kidney, brain, blood, and
immune system.
Irreversible pulmonary fibrosis (permanent scarring of lung tissue):
Pulmonary fibrosis can lead to prolonged mechanical ventilation and lung
dysfunction. Fibrosis decreases the abilities of the lungs to expand and
oxygen to cross the alveolar-capillary barrier.
Diagnosis of Acute Respiratory Distress Syndrome (ARDS)
ARDS is diagnosed primarily on the basis of the following clinical features:
Chest x-ray abnormalities (e.g., presence of fluid in the alveolar space of both
lungs; changes on x-ray may lag several hours behind functional changes
detected in arterial blood gas analysis)
 Abnormalities in the arterial blood gas analysis that reflect difficulties in
achieving sufficient oxygen levels in the blood
 Absence of clinical evidence of left atrial hypertension of other causes of
diffuse pulmonary infiltrates (e.g., congestive heart failure, pulmonary
hemorrhage)
 Abnormally low blood pressure in the pulmonary arteries
Treatment for Acute Respiratory Distress Syndrome (ARDS)
Treatment for ARDS is initiated as soon as possible to reduce the risk for
death and to help prevent additional damage to the lungs and other organs.
The goal is to treat the underlying condition and keep the patient alive and
breathing.
Mechanical Ventilation to Treat ARDS
In most cases, keeping the patient alive requires mechanical ventilation. With
ARDS, the breathing muscles (i.e., diaphragm and other muscles in the chest)
become fatigued very quickly and can stop working in their effort to get
oxygen into the body. The level of oxygen in the blood drops rapidly to
dangerously low levels, causing damage to vital organs and body processes. If
the oxygen level is not improved quickly and maintained at adequate levels,
damage (including severe brain damage) can be irreversible. Mechanical
ventilation keeps the level of oxygen at life-sustaining levels.
Once breathing is stabilized and blood is reoxygenated, the underlying
condition is treated. For example, if the condition is pneumonia or a septic
infection, the patient is treated with antibiotics.
Positive Pressure Ventilation to Treat ARDS
Mechanical ventilators deliver oxygen-rich air to the lungs and remove
carbon dioxide from the body. The technique, also known as positive
pressure ventilation, usually involves inserting an endotracheal tube into the
trachea through the mouth or nose. The endotracheal tube passes through
the upper airways, between the vocal cords, and into the trachea.
An inflatable balloon attached to the tube at the tracheal end prevents air
from escaping through the upper airways and out of the body. The end of the
tube outside of the body the is connected to a ventilator (machine that
forces air into the lungs by providing positive pressure).
Normally, people breathe spontaneously by contracting the large dome-
shaped muscle underneath the lungs (diaphragm). When the diaphragm
contracts during inhalation, the dome deflates, the volume of the chest
cavity increases, and negative pressure, or a partial vacuum, is created,
bringing air into the lungs. When the diaphragm relaxes during exhalation,
the dome rises, the volume of the chest cavity decreases, and air is pushed
out of the lungs.
Positive pressure ventilation does two things:
It pushes air into the lungs, relieving fatigued, nonfunctioning breathing
muscles.
It creates positive pressure in the alveoli, keeping them from collapsing and
pushing fluid out of the alveolar spaces.
How long does a patient with ARDS need mechanical ventilation support?
Positive pressure ventilation is maintained until the patient can breathe
independently at a normal rhythm. Some patients need support for only a
few days and others may require it for months.
Health care practitioners often refer to taking a person off mechanical
support as "weaning" them from the ventilator. Patients without a history of
lung disease are usually weaned fairly smoothly. Difficult weaning may
indicate complications, such as poor nutritional status, or an untreated or
new infection.