Respiratory Sysytem and Gas Exchange part 2 (slides 50-) Flashcards Preview

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Flashcards in Respiratory Sysytem and Gas Exchange part 2 (slides 50-) Deck (42):
1

So, how much gas is exchanged every minute-Translation-What is "J"?
-Under normal resting conditions:
-ml of O2 exchanged every minute?
-ml of CO2 exchanged every minute?

-250 ml of O2 exchanged every minute
-200 ml of CO2 exchanged every minute
-They ARE NOT EQUAL!

2

First lesson about gas exchange?

The diffusion of each gas (O2 and CO2) is INDEPENDENT of one another

3

2 factors from alveolar gas exchange equation that depend directly on the structure of the alveolus?

Surface area and diffusion distance (thickness of alveolar barrier)

4

Alveolar gas exchange
-Equation and what is each variable?

J = ((S.A.) x D x (P1-P2))/distance
J: diffusion rate in ml/min
D:diffusion coefficient for each gas
(P1-P2): pressure gradient across alveolar membrane
S.A.:surface area available for diffusion
distance: diffusion distance (thickness of alveolar barrier)
***Equation is solved for each gas individually***

5

Alveoli

-Thin-walled structures
-In a typical section of lung tissue, most of the tissue sample will be composed of alveoli

6

Alveoli-Separated by?

-Alveoli are separated by interalveolar septa that consist of two simple squamous epithelial layers with an interstitium (non-fenestrated capillaries embedded in an elastic connective tissue) between them
-The structure of the walls enhances diffusion and gas exchange

7

The alveolar epithelium consists of two cell types lining the surface of the capillaries (terminal branches of the pulmonary artery) and the alveolar wall

Type I and type II alveolar cells

8

Type I alveolar cells

Represent about 40% of the alveolar epithelial cell population and cover 90% of the alveolar surface

9

Type II alveolar cells

-Represent about 60% of the alveolar epithelial cell population but cover only 10% of the surface
-Preferentially located at the angles formed by adjacent alveolar septa

10

Type II alveolar cell function?

Produce surfactant

11

Alveolar macrophages (dust cells)
-Part of?
-Where are they located?

-Part of the mononuclear phagocyte system
-Found along the alveolar surface, within the interstitium
-Often seen detached in alveolar lumen of histological sections

12

Alveolar macrophages (dust cells)
-Function?

-Remove debris that escapes mucus and cilia in the conducting portion of the system
-Many migrate to bronchi and are transported via ciliary action to pharynx to be swallowed or expectorated

13

Alveolar macrophages (dust cells)
-Can be indicative of what disease?
-Why?

-Called HEART FAILURE CELLS IN CONGESTIVE HEART FAILURE
-Left ventricle fails to keep pace with venous return from lungs
-Lungs become congested with blood
-RBCs pass into alveoli and are phagocytosed

14

In the diffusion rate equation (J), S.A. is the surface area available for diffusion
-This means that S.A. corresponds to?

-The number of alveoli in the lungs and the number of open pulmonary capillaries

15

As surface area increases, what happens to J?

As surface area increases, J (diffusion rate) increases

16

Emphysema-Caused by?

-Emphysema is caused by a permanent enlargement of the air spaces distal to the terminal bronchioles due to the progressive and irreversible destruction of elastic tissue of the alveolar walls

17

Emphysema
-Elastic tissue in the interalveolar wall can be destroyed by what enzyme?
-What type of cell releases this enzyme?

-Elastase released by neutrophils present in the alveolar lumen
-

18

Emphysema
-Elastase is neutralized by?

-Serum a1-antitrypsin (serum trypsin inhibitor) neutralizes elastase

19

Emphysema
-So what happens in the absence of of a1-antitrypsin?

Neutrophil elastase is free to break down elastin, which contributes to the elasticity of the lungs, resulting in respiratory complications such as emphysema, or COPD

20

Centriacinar emphysema

-Dilated respiratory bronchioles at the apex of the respiratory acinus, surrounded by dilated alveolar ducts and alveoli
-This form of emphysema is found in cigarette smokers

21

Panacinar emphysema

-Thin-walled air spaces of varying sizes are observed in the whole respiratory acinus
-The boundaries of alveoli, alveolar ducts, and respiratory bronchioles are lost by coalescence after destruction of the elastic wall
-This form of emphysema is frequent in individuals with an a1-antitrypsin deficiency

22

Structural landmark of emphysema?

Large air spaces (blebs)

23

What is mainly destroyed in centriacinar emphysema?

The respiratory bronchioles

24

What is mainly destroyed in panacinar emphysema?

Respiratory bronchioles, alveolar ducts, and alveoli

25

Blood-air barrier
-Refers to?

-Refers to the structures that O2 and CO2 must cross during gas exchange

26

Blood-air barrier
-It contains?

-It contains:
-Cytoplasm of squamous epithelial cells (type I alveolar cells or pneumocytes)
-Fused basal lamina of type I alveolar cells and capillary endothelial cells
-Cytoplasm of capillary epithelial cell

27

In the diffusion rate equation, what happens to J when distance is increased?

J (diffusion rate) decreases as distance (thickness of alveolar barrier) increases

28

Distance includes?

-Fluid layer
-Alveolar epithelium
-Interstitial space
-Blood vessel wall

29

Pathology of Pulmonary interstitial Fibrosis

The deposition of collagen within the interstitial spaces increases the diffusion distance and decreases the diffusion of the gases across the barrier

30

Acute Respiratory Distress Syndrome
-A form of?

-A form of pulmonary edema that causes acute respiratory failure

31

Acute Respiratory Distress Syndrome (ARDS)
-Results from?

-Results from increased permeability of the alveolocapillary membrane
-Results from an increase in the hydrostatic pressure in the alveolar capillaries (cardiogenic) or damage to the alveolar epithelial lining caused by bacterial endotoxins or trauma (noncardiogenic)

32

Acute Respiratory Distress Syndrome (ARDS)
-What happens as a result?

-**Fluid accumulates in the lung interstitium**, alveolar spaces, and small airways, causing the lung to stiffen
-This stiffening impairs ventilation, prohibiting adequate oxygenation of pulmonary capillary blood

33

ARDS
-Severe ARDS can cause?

Severe ARDS can cause intractable and fatal hypoxemia, but patients who recover may have little or no permanent lung damage

34

D: Diffusion coefficient for each gas
-Depends on?

-The solubility of the gas in water (in your body)
-CO2 is much more soluble than O2
-The molecular weight of the gas
-CO2 weighs more than O2

35

Pressure gradient
-Which gas has the larger pressure gradient-O2 or CO2?

O2 has the larger pressure gradient

36

DL O2
-Normal value at rest??

-Diffusion capacity of the lung for oxygen
-Normal value at rest = 21 ml O2/min/mmHg
-mmHg: avg gradient along alveolar capillary

37

Measuring the DL O2
-***What gas is used? Why?***
-***What is the correction factor?***

-Carbon monoxide is used to measure the DL O2
-Used because it binds to Hb so avidly that it doesn't dissolve in the plasma
-Correction factor: DL O2 = 1.23 x DL CO

38

Describe the diffusion capacity of the lung for CO2 and O2

How much of each gas crosses in 1 minute for every 1 mmHg gradient

39

Describe how we measure the diffusion capacity for Oxygen and be able to calculate DL O2

-Measured using carbon dioxide
-To convert from DL CO to DL O2, multiply by 1.23
-Calculates to about 21 ml O2/min/mmHg

40

Pneumocyte type I

Squamous alveolar epithelium

41

Pneumocyte type II

Surfactant secreting cells

42

***Why is surfactant important?***

-Surfactant changes the surface tension (T)
-It reduces T in the smallest alveoli more than in larger alveoli to account for the change in the radius between the two different sized alveoli