ARDS Flashcards

1
Q

Acute respiratory distress syndrome (ARDS) is a clinical syndrome leading to respiratory failure. What is the diagnostic criteria:

A

severe dyspnea of rapid onset =ACUTE
hypoxemia
diffuse pulmonary Infiltrates (bilateral alveolar infiltrates)
Pao2/fio2 <200mmhg
No evidence of increased left atrial pressure

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2
Q

ARDS DIRECT LUNG INJURIES

A
Pneumonia
Aspiration of gastric lavage
Pulmonary contusion 
Near drowning
Toxic inhalation injury
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3
Q

Value of MILD ARDS

A

Pao2/fio2 200-300mmhg

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4
Q

Chest radiograph of ARDS

A

Bilateral opacities consistent With PULMONARY EDEMA

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5
Q

Value on severe ARDS

A

Pao2/fio2 <100mmhg

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6
Q

Last diagnostic criteria of ARDS

A

Absence of left atrial hypertension

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7
Q

ARDS severity of Pao2/fio2 100-200 mmHg

A

moderate ARDS

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8
Q

most frequently reported surgical conditions in ARDS are

A

pulmonary contusion,
multiple bone fractures,
and
chest wall trauma/flail chest,

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9
Q

Trauma patients with an Acute Physiology and Chronic Health Evaluation(APACHE) II score ≥ ___ have a 2.5-fold increased risk ofdeveloping ARDS.

A

≥ 16

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10
Q

In this phase, alveolar capillary endothelial cells and type I pneumocytes (alveolar epithelial cells) are injured,with consequent loss of the normally tight alveolar barrier to fluid and macromolecules

A

Exudative phase

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11
Q

Chest X-ray in exudative phase 1

A

Alveolar and interstitial opacities ≥ 3/4 of the lung fields

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12
Q

What phase:

  • recruitment of leukocytes (especiallyneutrophils) into the pulmonary interstitium and alveoli
  • dysfunctional pulmonary surfactant to form hyaline membrane whorls
A

Exudative phase

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13
Q

in addition to severe hypoxemia, _____ secondary to an increase in pulmonary dead space can beprominent in early ARDS.

A

hypercapnia

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14
Q

This phase of ARDS usually lasts from day7 to day 21. Most patients recover rapidly and are liberated from mechanical ventilation during this phase. Despite this improvement,many patients still experience dyspnea, tachypnea, and hypoxemia

A

Proliferative phase

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15
Q

In proliferative phase, Histologically, the first signs of resolution are often evident in this phase, with the initiation of lung repair, the organization of alveolar exudates, and a shift from neutrophil- to

A

lymphocyte-predominant pulmonary infiltrates

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16
Q

These specialized epithelial cells synthesized new pulmonary surfactant and differentiate into type I pneumocytes.

A

type II pneumocytes.

17
Q

Histologically, the alveolar edema and inflammatory exudates of earlier phases convert to extensive alveolar-duct and interstitial fibrosis. Marked disruption of acinar architecture leads to emphysema-like changes, with large bullae

A

Fibrotic phase 3-4 weeks

18
Q

Consequences of fibrotic phase

A

Increased risk for pneumothorax
Decreased lung compliance
Increase pulmonary dead space

19
Q

Experimental models have demonstrated that ventilator-induced lung injury can arise from at least two principal mechanisms:

A
  1. “volutrauma” from repeated alveolar over distention from excess tidal volume
    and
  2. “atelectrauma” from recurrent alveolar collapse
20
Q

Minimizing Ventilator-Induced Lung Injury by using

A
  1. low VT ventilation (6 mL/kg of predicted body weight)
  2. plateau pressure ≤30 cm H2O

(measured on the ventilator after a 0.5-s pause after inspiration)

21
Q

What is used to prevent alveolar collapse to minimize atelectrauma by setting to minimize Fio2 (inspired O2 percentage) and provide adequate Pao2 (arterial partial pressure of O2) without causing alveolar overdistention.

A

positive end-expiratorypressure (PEEP)

22
Q

a recent trial demonstrated a significant reduction in 28-day mortality (32.8 to 16%) for patients with severe ARDS (Pao2/Fio2 <150 mmHg).

A

prone positioning

23
Q

Not recommended in ARDS therapy (grade D recommendation)

A

Glucocorticoids
Surfactant replacement therapy
High frequency ventilation
Anti-inflammatory therapy

24
Q

ARDS Grade B recommendation based on supportive but limited studies

A
Minimized left atrial filling pressures
High-PEEP or “open lung”
Prone position
ECMO (extracorporeal membrane oxygenation)
Early neuromuscular blockade
25
Q

The only class A recommendation with strong clinical evidence for ARDS therapy

A

LOW TIDAL VOLUME

26
Q

ARDS alternative therapy Class C

A

Recruitment maneuvers

Inhaled vasodilator

27
Q

Initial management of ARDS

A
Tidal volume ≤ 6 ml/kg
Plateau pressure ≤ 30 cmH2O
RR ≤ 35 bpm
FIO2 ≤ 0.6
pH ≥ 7.30
SpO2 88 – 95%
MAP ≥ 65 mmHg 
Avoid hypoperfusion