Sunday, July 19, 2015
Wednesday, August 11, 2010
ARDS
ARDS
Introduction
First described in 1967
The syndrome is often progressive, characterized by distinct stages with different clinical, histopathological, and radiographic manifestations.
Acute Phase
rapid onset of respiratory failure, arterial hypoxemia that is refractory to treatment with supplemental oxygen.
CXR is indistinguishable from those of cardiogenic pulmonary edema. Bilateral infiltrates may be patchy or asymmetric and may include pleural effusions.
Acute Phase
CT shows alveolar filling, consolidation, and atelectasis
Pathological findings include diffuse alveolar damage, with neutrophils, macrophages, erythrocytes, hyaline membranes, and protein-rich edema fluid in the alveolar spaces, capillary injury, and disruption of the alveolar epithelium
Fibrosis
Acute lung injury and the acute respiratory distress syndrome may resolve completely or progress to fibrosing alveolitis with persistent hypoxemia, increased alveolar dead space, and a further decrease in pulmonary compliance.
Pulmonary hypertension may lead to right ventricular failure.
CXR show linear opacities, consistent with the presence of evolving fibrosis.
Fibrosis
Pneumothorax may occur in 10 to 13 percent and is not clearly related to airway pressures or PEEP.
CT chest shows diffuse interstitial opacities and bullae
Histologically, there is fibrosis along with acute and chronic inflammatory cells and partial resolution of the pulmonary edema
Recovery Phase
gradual resolution of hypoxemia and improved lung compliance.
radiographic abnormalities resolve completely
Risk Factors
The commonly associated clinical disorders are those associated with direct injury and those that cause indirect lung injury in the setting of a systemic process
sepsis is associated with the highest risk approximately 40 %.
The presence of multiple predisposing disorders substantially increases the risk, as does the presence of secondary factors including chronic alcohol abuse, chronic lung disease, and a low serum pH
Outcomes
Until recently-mortality rate of 40-60%
The majority of deaths are attributable to sepsis or multiorgan dysfunction rather than primary respiratory causes
Recent reports suggest mortality may be decreasing. Possibly due to more effective treatments for sepsis, changes in the method of mechanical ventilation, and improvement in the supportive care of critically ill patients.
Outcomes
Poor outcome in patients with chronic liver disease, nonpulmonary organ dysfunction, sepsis, and advanced age.
Initial indexes of oxygenation and ventilation, including the ratio of the partial pressure of arterial oxygen to the fraction of inspired oxygen and the lung-injury score, do not predict outcome.
Failure to improve during the first week of treatment is a negative prognostic factor.
Outcomes
In those who survive, pulmonary function normalizes within 6 to 12 months
Residual impairment may include mild restriction, obstruction, impairment of DLCO, but usually asymptomatic.
Severe disease and prolonged mechanical ventilation are risk factors for persistent abnormalities
Survivors have a reduced health-related quality of life as well as pulmonary-disease–specific health-related quality of life.
Outcomes
Factors that increase risk of death: chronic liver disease, nonpulmonary organ dysfunction, sepsis, and advanced age.
Initial indexes of oxygenation and ventilation, including the ratio of the partial pressure of arterial oxygen to the fraction of inspired oxygen and the lung-injury score, do not predict outcome.
the failure of pulmonary function to improve during the first week of treatment is a negative prognostic factor.
Pathogenesis
Endothelial and Epithelial Injury
Characterized by the influx of protein-rich edema fluid into the air spaces as a consequence of increased permeability of the alveolar–capillary barrier.
The degree of alveolar epithelial injury is an important predictor of the outcome.
Treatment
Treat underlying cause
Provide adequate nutrition
Mechanical Ventilation:
ARDSnet protocol
Restrict Fluid
Surfactant Therapy
Inhaled Nitric Oxide and Other Vasodilators
Glucocorticoids and Other Antiinflammatory Agents
ARDSnet: Inclusion Criteria
1. PaO2/FiO2 ≤ 300 (corrected for altitude)
2. Bilateral (patchy, diffuse, or homogeneous) infiltrates consistent with pulmonary edema
3. No clinical evidence of left atrial hypertension
Vent Settings
1. Calculate predicted body weight (PBW)
2. Select any ventilator mode
3. Set ventilator settings to achieve initial VT = 8 ml/kg PBW
4. Reduce VT by 1 ml/kg at intervals ≤ 2 hours until VT = 6ml/kg PBW.
5. Set initial rate to approximate baseline minute ventilation (not > 35 bpm).
6. Adjust VT and RR to achieve pH and plateau pressure
OXYGENATION GOAL: PaO2 55-80 mmHg or SpO2 88-95%
Use a minimum PEEP of 5 cm H2O. Consider use of incremental FiO2/PEEP
PLATEAU PRESSURE GOAL: ≤ 30 cm H2O
Check Pplat (0.5 second inspiratory pause), at least q 4h and after each change in PEEP or VT.
If Pplat > 30 cm H2O: decrease VT by 1ml/kg steps (minimum = 4 ml/kg).
If Pplat < 25 cm H2O and VT< 6 ml/kg, increase VT by 1 ml/kg until Pplat > 25 cm H2O or VT = 6 ml/kg.
If Pplat < 30 and breath stacking or dys-synchrony occurs: may increase VT in 1ml/kg increments to 7 or 8 ml/kg if Pplat remains < 30 cm H2O.
pH GOAL: 7.30-7.45
Acidosis Management: (pH < 7.30)
If pH 7.15-7.30: Increase RR until pH > 7.30 or PaCO2 < 25 (Maximum set RR = 35).
.
If pH < 7.15: Increase RR to 35.
If pH remains < 7.15, VT may be increased in 1 ml/kg steps until pH > 7.15 (Pplat target of 30 may be exceeded).
May give NaHCO3
Alkalosis Management: (pH > 7.45) Decrease vent rate if possible.
I: E RATIO GOAL: Recommend that duration of inspiration be < duration of expiration.
Introduction
First described in 1967
The syndrome is often progressive, characterized by distinct stages with different clinical, histopathological, and radiographic manifestations.
Acute Phase
rapid onset of respiratory failure, arterial hypoxemia that is refractory to treatment with supplemental oxygen.
CXR is indistinguishable from those of cardiogenic pulmonary edema. Bilateral infiltrates may be patchy or asymmetric and may include pleural effusions.
Acute Phase
CT shows alveolar filling, consolidation, and atelectasis
Pathological findings include diffuse alveolar damage, with neutrophils, macrophages, erythrocytes, hyaline membranes, and protein-rich edema fluid in the alveolar spaces, capillary injury, and disruption of the alveolar epithelium
Fibrosis
Acute lung injury and the acute respiratory distress syndrome may resolve completely or progress to fibrosing alveolitis with persistent hypoxemia, increased alveolar dead space, and a further decrease in pulmonary compliance.
Pulmonary hypertension may lead to right ventricular failure.
CXR show linear opacities, consistent with the presence of evolving fibrosis.
Fibrosis
Pneumothorax may occur in 10 to 13 percent and is not clearly related to airway pressures or PEEP.
CT chest shows diffuse interstitial opacities and bullae
Histologically, there is fibrosis along with acute and chronic inflammatory cells and partial resolution of the pulmonary edema
Recovery Phase
gradual resolution of hypoxemia and improved lung compliance.
radiographic abnormalities resolve completely
Risk Factors
The commonly associated clinical disorders are those associated with direct injury and those that cause indirect lung injury in the setting of a systemic process
sepsis is associated with the highest risk approximately 40 %.
The presence of multiple predisposing disorders substantially increases the risk, as does the presence of secondary factors including chronic alcohol abuse, chronic lung disease, and a low serum pH
Outcomes
Until recently-mortality rate of 40-60%
The majority of deaths are attributable to sepsis or multiorgan dysfunction rather than primary respiratory causes
Recent reports suggest mortality may be decreasing. Possibly due to more effective treatments for sepsis, changes in the method of mechanical ventilation, and improvement in the supportive care of critically ill patients.
Outcomes
Poor outcome in patients with chronic liver disease, nonpulmonary organ dysfunction, sepsis, and advanced age.
Initial indexes of oxygenation and ventilation, including the ratio of the partial pressure of arterial oxygen to the fraction of inspired oxygen and the lung-injury score, do not predict outcome.
Failure to improve during the first week of treatment is a negative prognostic factor.
Outcomes
In those who survive, pulmonary function normalizes within 6 to 12 months
Residual impairment may include mild restriction, obstruction, impairment of DLCO, but usually asymptomatic.
Severe disease and prolonged mechanical ventilation are risk factors for persistent abnormalities
Survivors have a reduced health-related quality of life as well as pulmonary-disease–specific health-related quality of life.
Outcomes
Factors that increase risk of death: chronic liver disease, nonpulmonary organ dysfunction, sepsis, and advanced age.
Initial indexes of oxygenation and ventilation, including the ratio of the partial pressure of arterial oxygen to the fraction of inspired oxygen and the lung-injury score, do not predict outcome.
the failure of pulmonary function to improve during the first week of treatment is a negative prognostic factor.
Pathogenesis
Endothelial and Epithelial Injury
Characterized by the influx of protein-rich edema fluid into the air spaces as a consequence of increased permeability of the alveolar–capillary barrier.
The degree of alveolar epithelial injury is an important predictor of the outcome.
Treatment
Treat underlying cause
Provide adequate nutrition
Mechanical Ventilation:
ARDSnet protocol
Restrict Fluid
Surfactant Therapy
Inhaled Nitric Oxide and Other Vasodilators
Glucocorticoids and Other Antiinflammatory Agents
ARDSnet: Inclusion Criteria
1. PaO2/FiO2 ≤ 300 (corrected for altitude)
2. Bilateral (patchy, diffuse, or homogeneous) infiltrates consistent with pulmonary edema
3. No clinical evidence of left atrial hypertension
Vent Settings
1. Calculate predicted body weight (PBW)
2. Select any ventilator mode
3. Set ventilator settings to achieve initial VT = 8 ml/kg PBW
4. Reduce VT by 1 ml/kg at intervals ≤ 2 hours until VT = 6ml/kg PBW.
5. Set initial rate to approximate baseline minute ventilation (not > 35 bpm).
6. Adjust VT and RR to achieve pH and plateau pressure
OXYGENATION GOAL: PaO2 55-80 mmHg or SpO2 88-95%
Use a minimum PEEP of 5 cm H2O. Consider use of incremental FiO2/PEEP
PLATEAU PRESSURE GOAL: ≤ 30 cm H2O
Check Pplat (0.5 second inspiratory pause), at least q 4h and after each change in PEEP or VT.
If Pplat > 30 cm H2O: decrease VT by 1ml/kg steps (minimum = 4 ml/kg).
If Pplat < 25 cm H2O and VT< 6 ml/kg, increase VT by 1 ml/kg until Pplat > 25 cm H2O or VT = 6 ml/kg.
If Pplat < 30 and breath stacking or dys-synchrony occurs: may increase VT in 1ml/kg increments to 7 or 8 ml/kg if Pplat remains < 30 cm H2O.
pH GOAL: 7.30-7.45
Acidosis Management: (pH < 7.30)
If pH 7.15-7.30: Increase RR until pH > 7.30 or PaCO2 < 25 (Maximum set RR = 35).
.
If pH < 7.15: Increase RR to 35.
If pH remains < 7.15, VT may be increased in 1 ml/kg steps until pH > 7.15 (Pplat target of 30 may be exceeded).
May give NaHCO3
Alkalosis Management: (pH > 7.45) Decrease vent rate if possible.
I: E RATIO GOAL: Recommend that duration of inspiration be < duration of expiration.
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