Acute Respiratory Distress Syndrome Flashcards

(28 cards)

1
Q

Definition of ARDS: clinical syndrome of

A
  1. Severe dyspnea of rapid onset
  2. Hypoxemia
  3. Diffuse pulmonary infiltrates leading to respiratory failure
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2
Q

Medical illness associated with development of ARDS

A

MC: penumonia (80%)
2nd: sepsis (40-60%)

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3
Q

Surgical conditions associated with ARDS

A

Pulmonary contusion
Multiple bone fractures
Chest wall trauma/flail chest

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4
Q

Clinical variables associated with development of ARDS

A

Older age
Chronic alcohol abuse
Pancreatitis
Pneumonia
Sepsis (40-60%)
Severity of critical illness

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5
Q

Three phases of ARDS

A

Exudative phase
Proliferative phase
Fibrotic phase

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6
Q

Exudative phase

A

Injured cells: alveolar capillary endothelial cells & Type I pneumocytes (alveolar epithelial cells)

Edema fluid rich in protein
(+) Inflam cytokines (IL1,IL8, TNF) and leukotriene B4

Plasma protein+dysfunctional pulmonary surfactant=hyaline membrane whorl

Alveolar edema: in dependent portion (diminished aeration)->collapse of dependent lung-> decreased lung compliance ->intrapulmonary shunting and hypoxemia ->dyspnea

Microvascular occlusion-> dec pulmonary arterial blood flow ->inc dead space ->pulmonary hypertension

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7
Q

Prominent findings in early ARDS (Exudative phase)

A

Severe hypoxemia
Hypercapnia

**Secondary to increase in pulmonary dead space

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8
Q

Differential diagnosis of ARDS

A

Cardiogenic pulmonary edema
Bilateral pneumonia
Alveolar hemorrhage

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9
Q

Proliferative phase

A

Occur in day 7 to 21
Patients liberated from MV

Fate of patients
1. Develop progressive lung injury
2. Resolution of symptoms

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10
Q

First signs of Resolution in ARDS (Seen in proliferative phase)

A

Initiation of lung repair
Organization of alveolar exudates
Shift from neutophil to lymphocyte-predominant pulmonary infiltrates (type II pneumocytes)

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11
Q

Fibrotic phase

A

After 3-4 weeks

Alveolar edema and inflammatory exudates convert to alveolar duct and interstitial fibrosis

Hallmarks: disruption of acinar architecture ->emphysema like changes with large bullae

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12
Q

Marker associated with increased mortality risk

A

Lung biopsy evidence for pulmonary fibrosis in ANY phase of ARDS

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13
Q

General principles in the treatment of ARDS

A
  1. recognition and treatment of underlying medical disorders (pneumonia, sepsis, aspiration, trauma)
  2. Minimization of uneccesary procedures
  3. Bundled care for ICU patients (prophy for DVT, GI bleeding, aspiration, excerssive sedation, prolonged MV, central venous catheter infections)
  4. Prompt recognition of nosocomial infections
  5. Adequate nutrition vua enteral route
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14
Q

2 Principal mechanisms for lung injury

A
  1. Volutrauma (overdistention from excess tital volume) and barotrauma (increased alveolar pressures)
  2. Atelectrauma (from recurrent alevolar collapse)
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15
Q

Chest CT findings of ARDS

A

Principally involving dependent portions of the lung with relative sparing of other regions

**Compliance differs in affected vs normal areas->attempts to fully inflate consolidated lungs–>overdistention and injury to the more normal areas

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16
Q

Ventilator induced injury: seen particularly with high tidal volume ventilation

A

High tidal volume ventilation

17
Q

Strategies to prevent ARDS during ventilation

A

low VT ventilation (6 ml/kg of PBW)
Plateau pressue at <=30 cm H20
PEEP adjusted to minimize FIo2

Mortality rate is lower by 31%

18
Q

Causes for reduced lung compliance

A

1.Presence of alveolar and interstitial fluid
2. Loss of surfactant

19
Q

Best PEEP

A
  1. Able to promote alveolar recruitment
  2. Minimize alveolar overdistentionand hemodynamic instability
  3. Provide adequate PaO2 while minimizing Fio2
20
Q

Prone positioning

A

Reduction in 28 day mortality for patients with severe ARDS PAO2/Fio2 <150 mmg HG

21
Q

Recruitment maneuvers

A
  1. Increase PEEP to high levels to recruit atelectatic lung
  2. Alternate modes of MV (airway pressure release ventilation and high frequency oscillatory ventilation)
  3. Lung-replacement therapy with extracorporeal membrane oxygenation (ECMO)
22
Q

Fluid management

Increased pulmonary vascular permeability ->leading to intersitial and alveolar edema fluid rich in protein

***CENTRAL FEATURE IN ARDS

A

Agressive attempts to reduce left atrial filing pressures with fluid restriction and diuresis

this is limited by hypotension and hypoperfusion

23
Q

True or false

current evidence does not support the routine use of glucocorticoids in the care of ARDS patients

24
Q

Mortality in ARDS is attributable to

A

Non pulmonary causes

Sepsis and nonpulmonary organ failure >80% of deaths

25
Major risk factors for ARDS mortality: nonpulmonary
1.Advanced age >75 2.Preexisting organ dysfunction: chronic liver disease, chronic alcohol abuse, chronic immunosuppression **Direct lung injury (pneumonia, pulmonary contusion, aspiration) have higher mortality rates as compared to indirect causes Surical and trauma patients with ARDS have higher survival rate than other ARDS patients
26
Increasing severity of ARDs: predicts mortality
Predicting ARDS mortality from other parameters of lung injury includes 1. PEEP >=10 cm H20 2. Respiratory system compliance <= 40 ml/cm H20 3.Extent of alveolar infiltrates on chest radiography 4. Corrected expired volume per minute >=10L/min (surrogate measure of dead space)
27
Recovery of maximal lung function: within 6 months
Recovery of lung function is strongly associated with 1. Extent of lung injury in early ARDS Factors associated with less recovery of pulmonary function 1. Low static respiratory compliance 2. High levels of required PEEP 3. longer duration of MV 4. jigh lung injury scores
28
Severity of ARDS: oxygenation
Mild: 200 mmHg