ARDS Flashcards

1
Q

Definition of ARDS

A

Acute Respiratory Distress Syndrome: Acute onset of tachypnea, hypoxemia, panlobular infiltrates on chest radiography and loss of lung compliance.

Severe form of Acute Lung Injury

PaO2/FiO2 <=200 (but also consider lung function)

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2
Q

What is the most common cause of ARDS in hospitalized patients?

What are other causes of indirect lung injury causes associated with development of ARDS?

A

Sepsis (13%)

Severe trauma with shock
and multiple transfusions (massive- immune response)
Cardiopulmonary bypass
Drug overdose
Acute pancreatitis
Blood transfusions
Head trauma

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3
Q

What is the most common cause of community ARDS?

What are the other causes of direct lung injury associated with ARDS?

A

Pneumonia (35%)

Aspiration
Pulmonary contusion
Fat emboli
Near drowning
Inhalation injury
Reperfusion PE

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4
Q

What are the risk factors for ARDS?

A

Age, chronic alcohol abuse, metabolic acidosis,
severity of critical illness

Increases with >1 factor

Highest risk for trauma + sepsis

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5
Q

Mechanism of Injury in ARDS

A

Normal lung function requires that dry, patent alveoli be closely situated to appropriately perfused capillaries.
Injury>pro-inf. cytokines> PMN> toxic mediators>damage to the capillary endothelium and alveolar epithelium (permeability)
Protein escapes from vascular spaces>fluid follows >edema of intersitium and alveoli
>damage to surfactant>alveolar collapse

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6
Q

Pathophysiology of ARDS

A
  1. Lung injury: impaired gas exchange-V/Q mismatch.
  2. Non-cardiogenic exudate (with proteins causing more damage).
  3. Areas of low ventilation (V/Q–>0) and low perfusion (high V/Q- causing procoaguable state)
  4. High V/Q causes increased ventilation in order to keep arterial PCO2 low–>tachypnea/dyspnea
  5. Fluid filled lungs are stiffer, decreased compliance. Non homogenous, some well aerated some not which causes stress upon ventilation on weaker areas can cause pneumothorax.
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7
Q

What are the causes of pulmonary hypertension in ARDS?

A

Hypoxic vasoconstriction, shunt from atelectasis, vascular compression from fluid, pro-coagulation state (from low perfusion), parenchymal destruction etc.

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8
Q

Three phases of ARDS

A

Acute exudative phase:

Loss of epithelial integrity : both endothelial and alveolar. Increased permeability of the alveolar-capillary barrier. Diffuse alveolar damage with macrophages, erythrocytes, hyaline membranes and protein rich edema in the alveolar spaces. Epithelial injury disrupts normal fluid transport. Activation of pro inflammatory cytokines.
Damage to surfactant. Rapid onset of respiratory failure. Hypoxemia refractory to supplemental O2. Pulmonary edema on chest X ray. Alveolar filling, consolidation and atelectasis occur predominantly in dependent lung zones.

Proliferative Phase:

Days 7-21. Most patients recover in this phase. Many still experience dyspnea, tachypnea, and hypoxemia. Some develop progressive lung injury and early changes of lung fibrosis (collagen). Histology- organization of infiltrates, shift from neutrophil to ly-predominant infiltrate proliferation of type 2 pneumocytes along alveolar basement membrane (new surfactant).

Fibrotic Phase (if no resolution):

Extensive alveolar and interstitial fibrosis. Emphysema like changes, bullae>>>pneumothorax (10-13%). Intimal proliferation>>>pulmonary hypertension. Persistent hypoxemia. Increased alveolar dead space. Further decrease in lung compliance. Interstitial opacities and bullae on chest CT.

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9
Q

Differential Diagnoses with ARDS

A

Cardiogenic pulmonary edema, pneumonia, pulmonary hemorrhage, cancer.

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10
Q

Treatment for ARDS

A

Prevention or early treatment of nosocomial infections
Adequate nutrition (enteral!)
Prevention of GI bleeding
Prevention of thromboembolism

Mechanical Ventilation
Fluid Management-balance
Corticosteroids (Immune modulating)-maybe
Surfactant (children, not adults)
Nitric Oxide (vasodilation improved shunt and oxygenation)
Beta agonists

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11
Q

What are the important aspects of mechanical ventilation in ARDS?

A

Conventional, with PEEP
Inverse ratio ventilation
Prone ventilation
Lung protective ventilation (permissive hypercapnea- keep higher CO2 bc higher O2 creates more shear forces)
High frequency ventilation
Extracorporeal life support

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