Respiratory Ards
Chapter 11
ARDS
INTRODUCTION
Acute respiratory distress syndrome (ARDS) - lung inflammation seen at the level of the alveolar capillary membrane with increased vascular permeability.
ARDS results in: bilateral pulmonary edema and atelectasis despite no evidence of left heart failure (e.g., normal pulmonary capillary wedge pressure (PCWP).
ARDS is present when the ALI results in such severe hypoxia that at the PaO2/FIO2 ratio is 200 mm Hg or less.
Approximately 10% to 15% of intensive care patients meet the criteria for ARDS in the typical ICU.
ARDS is often accompanied by multiple organ system failure.
When ARDS was first described, its mortality rate was approximately 90% and the majority of deaths were due to respiratory failure.
Currently, the mortality rate is 35% to 40% and the cause of death is frequently due to nonrespiratory problems.
ETIOLOGY
The most common clinical problems associated with the onset of ALI and ARDS are sepsis, severe trauma, multiple transfusions, aspiration, severe pneumonia, and smoke inhalation.
PATHOPHYSIOLOGY
ARDS affects lung mechanics, gas exchange, and the pulmonary vasculature of both lungs.
Although both lungs are affected, the degree of lung involvement varies throughout each lung.
Alveolar flooding and atelectasis procedure uneven pathological changes in the lung and areas of perfusion without ventilation (shunt).
Ventilation-perfusion (V/Q) mismatch is present in both lungs.
These abnormalities cause hypoxemia that responds poorly to supplemental oxygen administration. (refractory hypoxemia)
Causes of ALI and ARDS * Sepsis * Pneumonia * Major Trauma * Pulmonary aspiration and near drowning * Burns * Inhalation of noxious fumes * Fat embolism * Massive blood transfusion * Amniotic fluid embolism * Air embolism * Eclampsia * Poisoning * Radiation
CLINCIAL FEATURES
The clinical findings in the patient with ARDS vary according to the underlying cause
ARDS
INTRODUCTION
Acute respiratory distress syndrome (ARDS) - lung inflammation seen at the level of the alveolar capillary membrane with increased vascular permeability.
ARDS results in: bilateral pulmonary edema and atelectasis despite no evidence of left heart failure (e.g., normal pulmonary capillary wedge pressure (PCWP).
ARDS is present when the ALI results in such severe hypoxia that at the PaO2/FIO2 ratio is 200 mm Hg or less.
Approximately 10% to 15% of intensive care patients meet the criteria for ARDS in the typical ICU.
ARDS is often accompanied by multiple organ system failure.
When ARDS was first described, its mortality rate was approximately 90% and the majority of deaths were due to respiratory failure.
Currently, the mortality rate is 35% to 40% and the cause of death is frequently due to nonrespiratory problems.
ETIOLOGY
The most common clinical problems associated with the onset of ALI and ARDS are sepsis, severe trauma, multiple transfusions, aspiration, severe pneumonia, and smoke inhalation.
PATHOPHYSIOLOGY
ARDS affects lung mechanics, gas exchange, and the pulmonary vasculature of both lungs.
Although both lungs are affected, the degree of lung involvement varies throughout each lung.
Alveolar flooding and atelectasis procedure uneven pathological changes in the lung and areas of perfusion without ventilation (shunt).
Ventilation-perfusion (V/Q) mismatch is present in both lungs.
These abnormalities cause hypoxemia that responds poorly to supplemental oxygen administration. (refractory hypoxemia)
Causes of ALI and ARDS * Sepsis * Pneumonia * Major Trauma * Pulmonary aspiration and near drowning * Burns * Inhalation of noxious fumes * Fat embolism * Massive blood transfusion * Amniotic fluid embolism * Air embolism * Eclampsia * Poisoning * Radiation
CLINCIAL FEATURES
The clinical findings in the patient with ARDS vary according to the underlying cause