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).

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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.