Resp: 20. Killeen : Acute Lung Injury

Front 1

what are the 3 clinical features of acute lung injury?

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Back 1

Bilateral radiographic infiltrates.

(PaO2/FiO2) between 201 and 300 mmHg - The PaO2 is measured in mmHg and the FiO2 is expressed as a decimal between 0.21 and 1.00

No clinical evidence for an elevated left atrial pressure. If measured, the pulmonary capillary wedge pressure is 18 mmHg or less. (aka no evidence of HF)

Front 2

what is the definition of Acute Respiratory Distress Syndrome (ARDS)

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Back 2

The definition of ARDS is the same as acute lung injury except that the hypoxia is worse, requiring a PaO2/FiO2 ratio of 200 mmHg or less.

Front 3

does the severity of the hypoxia with ARDS impact predictability on clinical course or survival?

Back 3

nope...

Front 4

typically develops over 4 to 48 hours and persists for days to weeks
Progressive hypoxemia despite increasing supplemental oxygen many times requiring mechanical ventilation.. this describes?

Back 4

Acute Respiratory Distress Syndrome (ARDS)

Front 5

how do you calculate FiO2

what is it normally?

Back 5

FiO2 = ((Liters of O2) x 3) + 21

33%

Front 6

Back 6

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Back 7

Front 8

Back 8

Front 9

what are 3 derangements in ARDS?

Back 9

Impaired gas exchange — Ventilation-perfusion mismatching and physiologic shunting are the major causes of hypoxemia

Decreased lung compliance — Decreased pulmonary compliance is one of the hallmarks of ARDS . The low compliance is due to the stiffness of poorly or non-aerated lung

Pulmonary hypertension — Pulmonary hypertension occurs in up to 25 percent of patients with ARDS subjected to mechanical ventilation. Contributing factors include hypoxic vasoconstriction and vascular compression by positive pressure ventilation

Front 10

why do you have impaired gas exchange with ARDS?

Back 10

Alveoli have a tendency to collapse – complete collapse can contribute to barotrauma via repeated re-inflation & collapse

Diffuse alveolar damage leads to destruction of type II pneumocytes
Loss of surfactant to atelectasis -> increased A-a gradient ->hypoxemia -> increased work of breathing and can result in muscle fatigue and failure

Front 11

how do you have decreased lung compliance in ARDS?

Back 11

Loss of surfactant makes opening and closing of airways more difficult by the increase in airway pressure due to loss of surfactant

Causes a more ‘stiff’ appearance of lung function

Not a hemogenous effect – alveoli have different levels of involvment

Front 12

how do you have pulmonary HT in ARDS?

Back 12

Pulmonary vasculature vasoconstricts with hypoxemia leading to increased pulmonary artery pressures and subsequent right ventricluar systolic pressure elevation
If severe enough, forward flow is reduced and cardiac output drops
Cardiac output is also affected by intrathoracic pressure of ventilator

Front 13

what is the A-a gradient?

what does a wider gap show?

Back 13

Difference between alveolar (A) oxygen content and arterial (a) oxygen content

Wider gap suggests poor diffusion of oxygen from the alveoli to the pulmonary arterial capillaries

Front 14

what should your difference in A-a be?

Back 14

Should not be any more than
Patient age/4 + 2.5

Front 15

what are the 3 stages in progression of ARDS?

Back 15

“exudative" stage, characterized by diffuse alveolar damage over the first week

"proliferative" stage, characterized by resolution of pulmonary edema and by proliferation of type II alveolar cells, squamous metaplasia, interstitial infiltration by myofibroblasts, and early deposition of collagen.

Some patients progress to a third "fibrotic" stage, characterized by obliteration of normal lung architecture, diffuse fibrosis, and cyst formation.

Front 16

what is treatment for Acute respiratory distress syndrome (ARDS)?

Back 16

mostly supportive

can give prolonged ventilation with high O2
Goal is to oxygenate while reducing barotrauma caused by increased pressure from tidal volume/lung expansion

Front 17

if ventillation continues for longer than 10-14 days of ARDS what should you do? "rule of thumb"

Back 17

tracheostomy

Front 18

diagnosis of ARDS is based on 3 things... what are they

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Back 18

CXR, PaO2/FiO2 and no clinical findings of CHF

Front 19

main treatment for ARDS

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Back 19

supportive

Front 20

what is the general mechanism of disease with ARDS?

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Back 20

Cytokine activation with damage to alveolar walls and type II pneumocytes with resultant loss of surfactant and further atelectasis and barotrauma.