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STEP Pathology > deck_5326617 > Flashcards

deck_5326617 Flashcards

1
Q

How can ARDS be defined?

A

respiratory distress with stiff lungs (i.e. decreased compliance) and diffuse alveolar damage with ACUTE onset

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2
Q

How would ARDS present upon chest radiograph?

A

new bilateral, diffuse, patchy or homogeneous pulmonary infiltrates

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3
Q

How would ARDS present upon cardiac exam?

A

no apparent cardiogenic cause of pulmonary edema (exudate is protein rich due to increase vascular permeability)

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4
Q

How would mild ARDS present upon exam of PaO2/fractional inspired oxygen ratio?

A

less than 300 mmHg

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5
Q

How would moderate ARDS present upon exam of PaO2/fractional inspired oxygen ratio?

A

less than 200 mmHg (severe is less than 100)

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6
Q

What is the most common pre-disposing factor that leads to ALI/ARDS?

A

sepsis (20-40% of sepsis patients will develop sepsis)

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7
Q

T or F. Acute lung injury can be viewed as an early manifestation of a generalized inflammatory response with endothelial dysfunction and is therefore frequently associated with the development of multiple organ dysfunction syndrome (MODS)

A

T. Predisone helps

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8
Q

What is the cardinal feature of ALI?

A

non-cardiogenic pulmonary edema

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9
Q

Why does non-cardiogenic pulmonary edema occur in ALI?

A

generalized increase in vascular permeability caused by the microcirculatory changes and release of inflammatory mediators ANDThe pulmonary epithelium is also damaged in the early stages, reducing surfactant production and lowering the threshold for alveolar flooding.

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10
Q

What is another common feature of ALI/ARDS?

A

pulmonary HTN

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11
Q

Why does pulmonary HTN occur?

A

1) mechanical compression due to edema 2) local activation of micro-clots3) hypoxic vasoconstriction in response to decreased diffusion

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12
Q

Describe the intra-alveolar exudate seen in ALI/ARDS?

A

it is rich in platelets, fibrin, and fibrinogen/CFs

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13
Q

How can the exudate affect the lungs?

A

-may inactivate surfactant and stimulate inflammation-promotes migration of fibroblasts into the air spaces

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14
Q

What are some of the side-effects of lung tissue repair following injury?

A

interstitial fibrosis progresses, with loss of elastic tissue and damage to vasculature, couple with emphysema

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15
Q

What are some physiologic changes that accompany ALI/ARDS?

A

-shunt and dead-space increase-compliance decreases-diffusion limitations increase

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16
Q

What is the first sign of ALI?

A

unexplained tachypnea, followed by hypoxemia

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17
Q

Other signs of ALI?

A

fine crackles in both lung fields

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18
Q

What is an air bronchogram?

A

A tubular outline of an airway made visible by filling of the surrounding alveoli by fluid or inflammatory exudates.

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19
Q

Chest radiograph developments in ALI?

A

-bilateral diffuse shadowing-eventually air bronchograms-no cardiac enlargement

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20
Q

What is on the DDX of ALI?

A

-Cardiac failure-lung fibrosis

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21
Q

How should pulmonary edema be addressed in ALI?

A

limit left ventricular HTN with fluid restriction, diuretics, and lastly haemofiltration

22
Q

What other supportive measures should be taken in ALI?

A

When the patient is changed from the supine to the prone position, lung densities in the dependent region are redistributed and shunt fraction is reduced. Not great evidence for this

23
Q

How does being in the prone position affect gas exchange?

A

More uniform alveolar ventilation, caudal movement of the diaphragm, redistribution of perfusion and recruitment of collapsed alveoli

24
Q

Treatment for ALI?

A

-Inhaled NO can improve V/Q and reduce pulmonary HTN-Aerosolized prostacyclin (variable) or surfactant (best response in neonatal RDS)-Steroids (does not appear to improve outcomes)

25
Q

T or F. One criteria of ARDS is lack of evidence of volume evidence

A

T.

26
Q

What are some causes of direct lung injury?

A

-Pneumonia/aspiration of gastric contents-Pulmonary contusion/penetration-Fat emboli (long bone fracture)-Near drowning

27
Q

What are some causes of indirect lung injury?

A

-Sepsis-Drug overdose (opiods)-Cardiopulmonary bypass-Acute pancreatitis-Transfusion (TRALI)

28
Q

What are the stages of ARDS? Timeframes?

A

-Exudative (acute)- 0-4 days-Proliferative- 4-8 days-Fibrotic- 8+ days-Recovery timeframes not set in stone

29
Q

T or F. Some ARDS patients can completely recover

A

T. With only mild reduction in FRC

30
Q

What are the negative predictors of outcome for ARDS?

A

-chronic liver disease-non-pulmonary organ dysfunction-sepsis-older

31
Q

What is a hyaline membrane?

A

an increased thickness basement membrane

32
Q

What causes of the fibrotic phase?

A

deposits of pro collagen which mature into collagen

33
Q

What are the components of a lung injury score?

A

-CXR-PaO2/FiO2-PEEP-Respiratory compliance (lower compliance gets a higher score)all on a scale of 1-4

34
Q

What scale is used for judging lung injury?

A

Add all and divide by 4 and -mild-moderate: 1-2.5-severe: 2.5-4can also look at changes to judge prognosis

35
Q

A patient with pneumonia is undergoing mechanical ventilation following ARDS onset. Currently on 100% O2 and PEEP=5. O2 Sat is at 75%. What should be done to improve oxygenation?

A

Do NOT want to increase tidal volume, move the patient supine, or use a pulmonary vasoconstrictor,want to increase PEEP to apply a steady pressure to open atelectatic alveolar and increasing FRC by redistributing lung water

36
Q

What is PEEP?

A

Positive end-expiratory pressure

37
Q

Should PEEP be positive or negative?

A

End-expiratory pressure impedes ability to exhale. Humans have a little bit of PEEP (aka resistance of air to come out) so our lungs don’t collapse when we exhale. Zero PEEP is BAD (aka ZEEP)!!

38
Q

What helps in reducing mortality in ARDS patients?

A

deployment of a lower tidal volume than normal (6cc/kg BW)

39
Q

How does NO help in hypoxemia?

A

increases PERFUSION to help V/Q ratio, not diffusion

40
Q

The incidence of pneumothorax usually occurs when with ARDS?

A

after/during two weeks (subcutaneous interstitial emphysema results from micro-necrosis and causes pneumothorax)if it was all due to ventilation pressure, it should come earlier on

41
Q

Death in ARDS is usually due to _______.

A

Multi-organ failure

42
Q

T or F. Proning a patient helps in ARDS

A

T. Redistributes lung water and recruits alveoli

43
Q

What other treatments help in ARDS?

A

-Apply PEEP-Recruitment Maneuver -Increase mean airway pressure WITHOUT over distention of lungs-NO via endotracheal tube-APRV (Airway Pressure Release Ventilation)

44
Q

Does increasing inspiratory time help in ARDS?

A

Yes

45
Q

36 y/o FM with acute onset dyspnea, L sided pleuritic chest pain, and purulent sputum since last night

A

Pneumonia

46
Q

AIDS with pneumonia. Whats the most likely cause?

A

??

47
Q

T or F. SHUNT physiology is seen in ARDS

A

T.

48
Q

How does PEEP work in ARDS?

A

by recruiting collapsed alveoli and re-distributed lung water to improve oxygenation

49
Q

How does low tidal volume decrease mortality in ARDS?

A

stretch can cause inflammation (more preventative than curative)

50
Q

T or F. Surfactant helps in ARDS

A

F. NO benefit

51
Q

Difference between peak and plateau pressure

A

Peak pressure adds flow pressures to alveolar pressures (often higher than plateau pressures)

STEP Pathology (80 decks)

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