Resp 05: Atelectasis And Ards

Front 1

What are the characteristics of the R bronchus?

Back 1

- Wider
- Shorter
- Steeper
- 2 cm

Front 2

What are the characteristics of the L bronchus?

Back 2

- Narrower
- Longer
- More horizontal
- 5 cm

Front 3

Which bronchi is an inhaled foreign body more likely to enter? Why?

Back 3

Right Bronchus:
- Wider
- Shorter
- Steeper
- 2 cm

Front 4

Which part of the respiratory system is lined w/ respiratory epithelium? What kind of epithelium?

Back 4

- Lines airways proximal to the respiratory bronchioles
- Pseudostratified ciliated columnar epithelium

Front 5

What is the acinus?

Back 5

Airway structures distal to the terminal bronchiole:
- Respiratory Bronchiole
- Alveolar Duct
- Alveolus

Front 6

What are the L & R arrows pointing at?

Back 6

L: Normal Alveoli
R: Alveolar Septa

Front 7

What kind of cells cover 95% of the alveolar surface

Back 7

Type 1 Pneumocytes

Front 8

What is the function of Type 2 Pneumocytes?

Back 8

- Produce surfactant
- Repair alveolar epithelium

Front 9

Describe the continuity of the alveolar septum?

Back 9

- Fenestrated
- Pores of Kohn
- Important for exchange of substances

Front 10

What is Atelectasis?

Back 10

State in which the lung, in whole or in part, is COLLAPSED or without air; loss of lung volume d/t inadequate expansion of air-spaces

Front 11

What are the types of Atelectasis?

Back 11

1. Resorptive
2. Compressive
3. Loss of Surfactant (neonatal)
4. Contraction

Front 12

What are the acquired forms of Atelectasis?

Back 12

- Resorptive
- Compressive
- Contraction

Front 13

What kind of Atelectasis is the consequence of COMPLETE airway obstruction?

Back 13

Resorption Atelectasis

Front 14

What causes Resorption Atelectasis?

Back 14

Complete Airway Obstruction:
- Mucus/mucopurulent plug following surgery
- Aspiration of foreign materials
- Bronchial asthma, bronchitis, bronchiectasis
- Bronchial neoplasms (caveat - total obstruction)

Front 15

Where does the obstruction occur in Resorption Atelectasis?

Back 15

Complete Airway Obstruction occurs in bronchi, subsegmental bronchi, or bronchioles

Front 16

What are the consequences of Resorption Atelectasis?

Back 16

- 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

Front 17

What are the clinical findings of Resorption Atelectasis?

Back 17

* Fever and dyspnea w/in 24-36 hours of collapse
- Ipsilateral deviation of trachea
- Ipsilateral diaphragmatic elevation
- Absent breath sounds and absent vocal vibratory sensation (tactile fremitus)
- Collapsed lung does not expand on inspiration

Front 18

What is the most common cause of fever 24-36 hours after surgery?

Back 18

Resorption Atelectasis

Front 19

What kind of Atelectasis is caused by air or fluid accumulation in the pleural cavity, causing collapse of the underlying lung?

Back 19

Compression Atelectasis

Front 20

What causes Compression Atelectasis?

Back 20

Air or fluid accumulation in pleural cavity, increases pressure and collapses underlying lung

Front 21

What are some examples of Compression Atelectasis?

Back 21

- Tension Pneumothorax
- Pleural Effusion

Front 22

What are the clinical findings of Compression Atelectasis?

Back 22

- Trachea and mediastinum shift AWAY from atelectatic lung (contralateral side)

Front 23

What is happening in these lungs?

Back 23

Compression Atelectasis d/t Pneumothorax:
- Note that R lung has a darker / lucent appearance because of presence of air occupying almost entire pleural space
- R lung is next to mediastinum
- Deviation of trachea to contralateral side

Front 24

What is happening in these lungs?

Back 24

Compression Atelectasis d/t Pleural Effusion
- Lung should be taking up entire space
- Pleural Effusion filled entire space, but was drained before doing autopsy

Front 25

What happens to the alveoli during Compression Atelectasis?

Back 25

Alveoli collapse into slit-like spaces

Front 26

What is the cause of Neonatal Atelectasis?

Back 26

Loss of Surfactant

Front 27

What are the components of Surfactant?

Back 27

Lipids:
- Phosphatidylcholine (Lecithin)
- Phosphatidylglycerol

Proteins:
- Surfactant proteins A and D
- Surfactant proteins B and C

Front 28

What is the function of the proteins in Surfactant?

Back 28

- A and D: innate immunity
- B and C: reduces surface tension at air liquid barrier in alveoli

Front 29

Where is Surfactant stored?

Back 29

Lamellar bodies

Front 30

What is the function of Surfactant?

Back 30

- Reduces surface tension in small airways
- Prevents collapse of airways on expiration

Front 31

What modulates the synthesis of surfactant?

Back 31

- ↑ by cortisol and thyroxine
- ↓ by insulin

Front 32

What can cause Neonatal Atelectasis?

Back 32

Decreased surfactant in fetal lungs:
- Prematurity
- Maternal diabetes (fetal hyperglycemia stimulates insulin release)
- C-section (labor and vaginal delivery ↑ stress related cortisol secretion which ↑ surfactant production)

Front 33

What is happening in this image?

Back 33

Neonatal Atelectasis: collapsed alveoli are lined by hyaline membranes

Front 34

What happens to the alveoli during Neonatal Atelectasis?

Back 34

Collapsed alveoli are lined by hyaline membranes

Front 35

What are the clinical findings of Neonatal Atelectasis?

Back 35

- Respiratory distress w/in a few hours after birth
- Hypoxemia → Respiratory Acidosis
- Ground glass appearance (opacified and pale) on chest x-ray

Front 36

What are the complications of Neonatal Atelectasis?

Back 36

- Intraventricular hemorrhage
- PDA (persistent hypoxemia)
- Necrotizing enterocolitis (intestinal ischemia)
- Hypoglycemia (excessive insulin release)
- O2 therapy damages lungs (bronchopulmonary dysplasia) and may cause cataracts (blindness)

Front 37

What are the complications of O2 therapy in Neonatal Atelectasis?

Back 37

- Damages lungs (bronchopulmonary dysplasia)
- Cataracts (blindness)

Front 38

Why does Neonatal Atelectasis cause Hyaline Membranes to form on the alveoli?

Back 38

- Prematurity leads to reduced surfactant synthesis, storage, and release
- Causes increased alveolar surface tension
- Leads to atelectasis: uneven perfusion and hypoventilation
- Causes hypoxemia and CO2 retention
- Leads to acidosis, pulmonary vasoconstriction, and pulmonary hypoperfusion
- Leads to endothelial and epithelial damage which causes plasma to leak into alveoli
- Causes fibrin and necrotic cells to accumulate within alveoli forming a Hyaline Membrane

Front 39

What type of Atelectasis is caused by fibrotic changes in lung or pleura, which prevents full expansion?

Back 39

Contraction Atelectasis

Front 40

What happens in Contraction Atelectasis?

Back 40

- Fibrotic changes in lung parenchyma or pleura
- Prevents full expansion
- Not reversible

Front 41

What part of the lung is damaged in Acute Lung injury?

Back 41

Endothelium or Epithelium

Front 42

Is there a genetic predisposition to Acute Lung injury?

Back 42

- There are both non-heritable and heritable forms
- The response and survival of heritable forms depends on multiple loci on different chromosomes

Front 43

What are the chemical mediators of Acute Lung injury?

Back 43

- Cytokines, oxidants, growth factors
- TNF; IL-1, -6, -10; TGF-β

Front 44

What are the manifestations of Acute Lung injury?

Back 44

- Mild form: pulmonary edema
- Severe form: diffuse alveolar damage (acute respiratory distress syndrome)

Front 45

What are the features of the mild form of Acute Lung Injury?

Back 45

* Pulmonary Edema
- Microvascular or alveolar injury → increase in capillary permeability

Front 46

What causes pulmonary edema in acute lung injury?

Back 46

Alterations in Starling forces:
- ↑ Hydrostatic P in pulmonary capillaries
- ↓ Oncotic P

Front 47

What can cause increased hydrostatic pressure in pulmonary capillaries? Outcome?

Back 47

- L sided heart failure
- Volume overload
- Mitral stenosis
- Hemodynamic disturbances - cardiogenic pulmonary edema

Leads to pulmonary edema

Front 48

What can cause decreased oncotic pressure in pulmonary capillaries? Outcome?

Back 48

- Nephrotic syndrome
- Liver cirrhosis

Leads to pulmonary edema

Front 49

What are the features of pulmonary edema in acute lung injury?

Back 49

- Transudate (low in proteins)
- Edema fluid accumulation in alveoli w/ heart failure cells and brown induration

Front 50

What can cause increased capillary permeability / pulmonary edema in acute lung injury?

Back 50

Microvascular or Alveolar Injury:
- Infections
- Aspiration
- Drugs, shock, trauma
- High altitude

Front 51

What causes Acute Respiratory Distress Syndrome?

Back 51

Non-cardiogenic pulmonary edema resulting from acute alveolar-capillary damage:
- Direct lung injury
- Indirect lung injury (systemic diseases)

Front 52

What are the risks for Acute Respiratory Distress Syndrome?

Back 52

* Gram negative sepsis (40%)
* Gastric Aspiration (30%)
* Severe trauma (10%)
* Pulmonary infections (diffuse)
(these account for >50% of causes)

- Heroin
- Smoke inhalation

Front 53

What are the clinical findings of Acute Respiratory Distress Syndrome?

Back 53

- Dyspnea
- Severe hypoxemia NOT responsive to O2 therapy
- Respiratory acidosis

Front 54

What does this x-ray show?

Back 54

- White-out appearance (like a snow storm)
- Represents severe and advanced Acute Respiratory Distress Syndrome (ARDS)

Front 55

What is the pathogenesis of Acute Respiratory Distress Syndrome?

Back 55

- Acute injury to alveolar epithelium or endothelium
- Alveolar macrophages and other cells release cytokines → neutrophil chemotaxis → transmigration of neutrophils into alveoli → leakage of protein (fibrin) rich exudate → form hyaline membrane
- Damage to pneumocytes causes surfactant deficiency leading to atelectasis
- Progressive interstitial fibrosis

Front 56

What tries to repair damage in Acute Respiratory Distress Syndrome?

Back 56

Type 2 Pneumocytes

Front 57

What is the prognosis for Acute Respiratory Distress Syndrome?

Back 57

Poor ~60% mortality rate

Front 58

What is seen in this image?

Back 58

Hyaline Membrane in Acute Respiratory Distress Syndrome

Front 59

What is seen in this image?

Back 59

Hyperplastic Type 2 Pneumocytes, trying to repair damage

Front 60

What are the stages of Acute Respiratory Distress Syndrome? What happens in each stage? Timeline?

Back 60

Exudative Stage (days 0-7)
- Edema (peaks day 1)
- Hyaline Membrane formation (peaks day 4)

Proliferative Stage (days 7-14)
- Interstitial Inflammation (peaks day 11)
- Interstitial Fibrosis (peaks day 14)
- Interstitial inflammation and fibrosis begin during exudative stage

Front 61

Case: 60 yo woman develops pneumonia complicated by septicemia. 3 wks later develops multiple organ failure. Abx led to sputum and blood cultures lacking growth of organisms. Requires intubation w/ mechanical ventilation and becomes more difficult to maintain SaO2. Chest x-ray shows increasing opacifications of all lung fields.

What is the pathologic process most likely to be present in her lungs?

Back 61

Diffuse hyaline membrane formation