Atelectasis and Acute Respiratory Distress Syndrome (ARDS) Flashcards

(37 cards)

1
Q

what is atelectasis?

A

Atelectasis is defined as a state in which the lung, in whole or in part, is collapsed or without air.
– Loss of lung volume due to inadequate expansion of airspaces

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2
Q

Types of atelectasis

A

– Resorption
– Compression
– Loss of surfactant (neonatal) – Contraction

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3
Q

what causes resorption Atelectasis?

A

Consequence of complete airway obstruction
– Obstruction in bronchi, subsegmental bronchi or bronchioles
– Prevents air from reaching the alveoli
– Resorption of air trapped in distal airspaces through the pores of Kohn
– Lack of air in distal airspaces
– Collapse

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4
Q

what are possible causes of obstruction that can lead to respiration atelectasis?

A

Cause of obstruction:
–Mucus/mucopurulent plug following surgery
– Aspiration of foreign material
– Bronchial asthma, bronchitis,
bronchiectasis
– Bronchial neoplasms (caveat-total obstruction)

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5
Q

Clinical findings in resorption atelectasis

A
  • Fever and dyspnea – within 24-36 hours of collapse (commonest cause of fever 24-36 hrs following surgery)
  • Absent breath sounds and absent vocal vibratory sensation (tactile fremitus)
  • Collapsed lung does not expand on inspiration
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6
Q

what happens to the trachea and diaphragm with resorption atelectasis?

A
  • Ipsilateral deviation of trachea

* Ipsilateral diaphragmatic elevation

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7
Q

causes of compression atelectasis?

A

• Air or fluid accumulation in pleural cavity – increased pressure – collapses underlying lung

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8
Q

possible causes of compression atelectasis?

A
  • tension pneumotorax

- pleural effusion

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9
Q

what happens to the trachea with compression atelectasis?

A

• Trachea and mediastinum shift away from the atelectatic lung

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10
Q

what causes neonatal atelectasis?

A

loss of surfactant

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11
Q

what is surfactant made up of?

A

– Lipoprotein
• Phosphatidylcholine (lecithin)
• Phosphatidylglycerol
• Proteins
– Surfactant proteins (SP) A and D: innate immunity
– Surfactant proteins (SP) B and C: reduction of surface tension at air liquid barrier in alveoli

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12
Q

what cells synthesize surfactant? when does synthesis start?

A

– Synthesized by type 2 pneumocytes

• Synthesis begins by 28th week of gestation

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13
Q

where is surfactant stored?

A

• Stored in lamellar bodies

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14
Q

what is the role of surfactant?

A

Reduces surface tension in small airways and prevents collapse on expiration

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15
Q

what has an effect on surfactant synthesis?

A

hormones

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16
Q

which hormones have effects on surfactant synthesis and what are the effects?

A

– ↑ by cortisol and thyroxine

– ↓ by insulin

17
Q

what are causes of respiratory distress syndrome (RDS) in newborns?

A

• Decreased surfactant in fetal lungs
– Prematurity
– Maternal diabetes
» Fetal hyperglycemia stimulates insulin release
– Cesarean section
» Labor and vaginal delivery ↑es stress related cortisol secretion - ↑es surfactant production

18
Q

what lines collapsed alveoli in neonatal atelectasis?

A

hyaline membranes

19
Q

clinical findings of neonatal atelectasis?

A

– Respiratory distress within a few hours of birth
– Hypoxemia and respiratory acidosis
– “Ground glass appearance” on chest x-ray

20
Q

complications of neonatal atelectasis?

A

– Intraventricular hemorrhage
– Patent ductus arteriosus (persistent hypoxemia)
– Necrotizing enterocolitis (intestinal ischemia)
– Hypoglycemia (excessive insulin release)
– O2 therapy – damage to lungs (bronchopulmonary dysplasia) and cataracts (blindness)

21
Q

what causes contraction atelectasis?

A

fibrotic changes in lung

or pleura prevent full expansion (not reversible)

22
Q

damage where causes acute lung injury?

A

fibrotic changes in lung

or pleura prevent full expansion (not reversible)

23
Q

what can cause acute lung injury?

A

• Nonheritable AND heritable causes (response and survival depends on multiple loci on different chromosomes)

24
Q

what are mediators of acute lung injury?

A

• Mediators Cytokines, oxidants, growth factors– TNF; IL-1, 6 and 10; TGF-β.

25
manifestations of acute lung injury
• Manifestations–Pulmonary edema, Diffuse Alveolar Damage (Acute respiratory distress syndrome)
26
causes of pulmonary edema?
– Edema due to alterations in Starling pressure – Microvascular or alveolar injury – increase in capillary permeability – Undetermined origin – Therapy and outcome depend on underlying etiology
27
what changes in starling pressure can cause pulmonary edema?
• Increased hydrostatic pressure in pulmonary capillaries – Left sided heart failure, volume overload, mitral stenosis – Hemodynamic disturbances- cardiogenic pulmonary edema • Decreased oncotic pressure – Nephrotic syndrome, liver cirrhosis • Transudate • Edema fluid accumulation in alveoli with “heart failure” cells and “brown induration"
28
what microvascular or alveolar injuries (causing increase in capillary permeability) can cause pulmonary edema?
* Infections * Aspiration * Drugs, shock, trauma * High altitude
29
what is ARDS?
• Noncardiogenic pulmonary edema resulting from acute alveolar-capillary damage – Direct lung injury – Indirect lung injury (systemic diseases)
30
what are risks for ARDS?
* Gram negative sepsis (40%) * Aspiration (30%) * Severe trauma (10%) * Pulmonary infections, heroin, smoke inhalation
31
what four causes account for >50% of ARDS cases?
- sepsis - diffuse lung infections - gastric aspiration - physical injury/trauma
32
clinical findings in acute respiratory distress syndrome
– Dyspnea, severe hypoxemia NOT responsive to O2 therapy. | – Respiratory acidosis
33
pathogenesis and pathology of ARDS
– Acute injury to alveolar epithelial or endothelial cells – Alveolar macrophages and other cells release cytokines • Neutrophilic chemotaxis • Transmigration of neutrophils from capillaries into alveoli • Leakage of protein (fibrin) rich exudate forming hyaline membranes • Damage to pneumocytes causing surfactant deficiency leading to atelectasis – Repair by type 2 pneumocytes – Progressive interstitial fibrosis
34
prognosis of ARDS
Poor (~60%mortalityrate)
35
what happens to alveoli in ARDS?
- diffuse alveolar damage! - hyaline membranes - hyperplastic type 2 pneumocytes
36
main findings of the exudative state of ARDS?
- edema | - hyaline membranes (main one!!)
37
main findings of the proliferative state of ARDS
- interstitial infammation | - interstitial fibrosis