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Acute Respiratory Distress Syndrome

By: Amanda and Tymonee
by

Tymonee Stanley

on 22 March 2011

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Transcript of Acute Respiratory Distress Syndrome

Acute Respiratory Distress Syndrome Pathogenesis Definition:
ARDS is acute onset of refractory hypoxemia in association with bilateral lung infiltrates on a chest X-ray in the absence of left atrial hypertension, but in the presence of a clinical condition known to cause the syndrome. Etiology:
Why do some very sick or seriously injured patients develop ARDS? It is unclear. However....
Many conditions or factors that can cause ARDS and can be classified as Direct Lung injury
Indirect Lung Injury
Radiological Oxygenation Exclusion No clinical evidence that the following are responsible for the infiltrates Heart failure
Fluid overload
Chronic lung disease Also Known As: Adult respiratory distress syndrome Increased-permeability pulmonary edema Non-cardiac pulmonary edema Example:
Normal: PaO2 = 95 mmHg & FiO2 = .21
PaO2: FiO2 ratio = 95/.21 = 452 ARDS: PaO2 = 60 mmHg & FiO2 = .70
PaO2:FiO2 ratio = 60/.70 = 86 New
Bilateral
Diffuse
Patchy
pulmonary infiltrates on chest X-ray Conditions that can directly injure the lungs: Pneumonia
harmful fumes or smoke
aspiration
near drowning
positive pressure ventilation Conditions that can indirectly injure the lungs Sepsis
Septic shock
Trauma
Many blood transfusions
Injury to the chest or head
Pancreatitis
Fat emolism
Drug overdose Incidence: Acute Lung Injury (ALI)
vs
Acute Repiratory Distress Syndrome (ARDS)
ARDS is an extreme
manifestation of ALI ALI is defined by a less severe gas-exchange abnormality than ARDS.

ARDS: P:F ratio criteria is </= 200
ALI: P:F ratio criteria is </= 300 ARDS used to be called:
Stiff lung
Shock lung
Wet Lung Starling's Law of the Lung -Three factors that affect the movement of water between cavities in the body... weight of H2O 1. Hydrostatic pressure -force generated by water Osmotic pressure force exerted by solutes Condition: Incidence of ARDS (%)

Sepsis Syndrome 29
Pneumonia 38
Extra pulmonary source 15

Septic Shock 37
Pulmonary source 48
Extra pulmonary source 25

Trauma 12 to 18
Blood transfusion 29
Gastrointetinal aspiration 22 to 38
3. Membrane characteristics affects the ability of water and solute to move between compartments Net Hydrostatic pressure:
the difference between the hydrostatic pressure in the capillary and the hydrostatic pressure in the instertial tissue
water flows OUT of the cavity with the greater hydrostatic pressure Capillary Interstitial Tissue Moves out Net Osmotic Pressure:
difference between the osmotic pressures in the capillary and interstitial tissue
water will flow INTO the cavity with high osmotic pressure Capillary Interstitial Tissue Moves into Starling's Law is the mathematical representation of the movement of water between capillaries and the interstital tissue

Net Filtration Pressure =
net hydrostatic pressure - net osmotic pressure Positive Net Filtration Pressure:
net hydrostatic pressure is greater than net osmotic pressure
water will move from the capillaries into the interstitial tissue capillaries interstitial tissue Negative Net Filtration Pressure:
net osmotic pressure is greater than net hydrostatic pressure
water will move from the interstitial tissue into the capillaries interstitial tissue capillary moves INTO move INTO leakage of increased amounts of water and protein into the intersitial tissue
-exudative effusion plays a major role in ARDS increased membrane permeability
-caused by direct injury
-due to inflammation
or infection Phases of ARDS Three phases of ARDS:
exudative phase

proliferative phase

fibrotic phase occurs around 24 hours after onset of symptoms
lasts about 1 week Main sites of injury: -vascular endothelium:
results in increased capillary permeability
influx of protein-rich fluid into the alveolar space -alveolar epithelium:
promotes pulmonary edema formation
pattern of injury is labeled as diffuse alveolar damage Injury to alveolar cells -Type I cells (makes up 90% of an alveoli
results in increase entry of fluid into the alveoli
allows fluid to flood the alveolar space -Type II cells:
produce surfactant and to proliferation and differentiation into type I cell after cellular injury
decreased production of surfactant
resulting in decreased compliance and alveolar collapse Please note:
if normal repair process in the lung is interfered with, there may be development of permanent fibrosis -Hyaline membrane: -formation becomes prominent in the alveolar spaces
-composed of:
fibrin: formed by intra-alveolar activation of the coagulation system
plasma protein: arrived from the inflammatory exudate that deposited in the alveolar space Neutrophils & Cytokines:
also aid in the diffuse alveolar damage
activated by immune response
increase alveolar damage due to inflammation -begins as early as 3 days into the course of ARDS
-last 7 to 21 days after initial injury -reparative process
type II cells replicate in attempt to replace the damged type I cells flooding into the alveoli is decreased
development of fibroblast in the parenchyma only occurs in patients with prolonged illness -decrease amounts of neutrophils, lymphocytes, and macrophages
-total lung collagen increases
fibroblastic response does not aid in repairing the parenchyma
significant scar tissue -lung becomes densely fibrotic
depends on the severety of damage -pulmonary vasculature:
extensive remodeling
compromise of the lumen of the capillaries Respiratory Consequences -Hypoxemia: -severe hypoxemia
resistant to supplemental oxygen
increase in alveolar-arterial difference in partial pressure of oxygen -due to widespread flooding or collapse of the alveoli

and in return...... Large right-to-left intrapulmonary shunt -Deadspace ventilation:
increased due to areas in the lungs that are being ventilated, but that area may be poorly perfused due to injury to the capillary -Surfactant production:
surfactant is inactive
unable to prevent atelectasis -FRC & Compliance:
significantly decreased
Severe V/Q Mismatch Hemodynamic & Cardiac Consequences -Pulmonary artery pressure:
increased
-Pulmonary vascular resistance:
increased
-PCWP:
must be </= 18
-ECG:
should be considered
suggest pulmonary edema is from a non-cardiogenic origin due to smaller lumen size of vessels caused by:
hypoxemia
decreased lumen size of the vessels
increased interstitial pressure due to fluid overload to help differentiate whether the pulmonary edema is from a cardiogenic our non-cardiogenic origin Now, let's determine on where water will flow between plasma and interstitial tissue P:F ratio can be used to help
quantify refactory hypoxemia
PaO2:FiO2 ratio of </= 200 ALI is defined by a less severe
gas-exchange abnormality than ARDS Oxygenation:
PaO2:FiO2 ratio of </= 300

Example:
Normal: PaO2=95 mmHg & FiO2=.21
PaO2:FiO2 ratio = 95/.21 = 452

ALI: PaO2=78 mmHg & FiO2=.30
PaO2:FiO2 ratio = 78/.3=260

ARDS: PaO2=60 mmHg & FiO2=.70
PaO2:FiO2 ratio = 60/.70=86 In fact, ALI was created to identify patients who are early in the course of their ARDS.

Both present with poor systemic oxygenation with ALI being less severe. influenced by the underlying clinical condition Before the development of the definition in 1994:
about 7.5 cases per 100,000 population 1st study to use the definition:
13.5 cases per 100,000 population Currenlty:
190,600 cases per year incidence increases with a higher age
associated with 74,500 deaths ARDS is defined by acute onset of refractory hypoxemia in association with bilateral lung infiltrates on a chest x-ray in the absence of left atrial hypertension, but in the presence of a clinical condition known to cause the syndrome. ALI is defined by acute onset of refractory hypoxemia in association with bilateral lung infiltrates on a chest x-ray in the absence of left atrial hypertension, but in the presence of a clinical condition known to cause the syndrome.
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