How Your Lungs Work

Front 1

How does the "Elastic Recoil" property of our lungs help us breathe?

Back 1

It helps us EXPIRE!

Elastic recoil drives normal expiration by compressing air in the lungs, which increases alveolar pressure and drives air out.

Front 2

What creates elastic recoil in the lungs?

Back 2

Two things:

1. Elastic tissue, which contracts as volume increases

2. Surfactant:
By lowering surface tension in the terminal conducting airways and in alveoli(by interfering with attraction among water molecules), surfactant keeps airways open (at the air-fluid interface).

Front 3

How does elastic recoil affect the ribs and chest wall while we are breathing?

Back 3

Elastic recoil of the chest wall is the tendency of the ribs and chest wall to expand outward.

Front 4

What creates "Lung Compliance" in the lungs?

Back 4

The "give" of elastic tissue. Compliance measures ease w/ which the lung expands.

Front 5

How does Emphasema affect Elastic Recoil and Lung Compliance?

Back 5

When elastic tissue is lost, elastic recol force is decreased and expiration in impaired. Compliance increases b/c there's less recoil force trying to collapse the lung.

Front 6

How do the Bronchi respond to diffuse lung injury?

Back 6

1. spasm (as in asthma)
2. mucus production (w/ infection, asthma, smokers)
3. Sustained inflammation (leading to fibrosis, scarring)
4. Metaplasia
5. Neoplasia

Front 7

How does the lung parenhyma respond to diffuse lung injury?

Back 7

1. Self-limited inflammation
2. Sustained inflammation (leading to fibrosis, scarring)
3. Capillary leak (seen in Adult Respiratory Distress Syndrome)--the alveoli are very delicate so capillaries within are highly susceptible to injury
4. Emphasema - loss of alveolar septal, elastic tissue that opposes lung expansion. This leads to permanent enlargemet of airspaces. Also, inflammation and fibrosis (minimal) destroys bronchiole walls.
5. Neoplasia

Front 8

What type of damage do Alveolar filling diseases cause? Give Ex.

Back 8

Air spaces become filled with liquid or cells and compliance is reduced.

Pneumonia or pulmonary edema

Front 9

What type of damage do Restrictive lung diseases cause?

Back 9

The alveolar spaces stay empty, but the walls (interstitium) become thickened and inelastic. The lung is smaller than normal b/c the stiffened walls restrict the ability to the lung to expand. As a consequence one cannot take a breath and becomes hypoxic.

Front 10

What type of damage do Restrictive lung diseases cause? Discuss Pulmonary interstitial fibrosis.

Back 10

Inhaled, blood-born toxin--> endo,epithelial injury--> alvolitis-->interstitial fibrosis (DECREASES LUNG COMPLIANCE)-->hypoxia

Front 11

What type of damage do Obstructive lung diseases cause? Discuss Emphysema.

Back 11

Emphasema - loss of alveolar septal, elastic tissue that opposes lung expansion. This leads to permanent enlargemet of airspaces.
The loss of elastic recoil causes the lungs to balloon out as we inspire and permanently increase in volume (BARREL CHEST).

With this loss of elastic recoil, airways eventually collapse, reistance increases, and expriation ends early, trapping air in the lungs.

Also, inflammation and fibrosis (minimal) destroys bronchiole walls so that the lung is departitioned, reducing area for gas exchange.

Front 12

What type of damage do Obstructive lung diseases cause? Discuss the obstructive mechanisms in Asthma and Chronic Bronchitis.

Back 12

Air can get in but not out d/t mucus plug, bronchospasm , and inflam edema, all of which increase airway resistance. The lung becomes overly expanded with trapped air.

Front 13

How does the CNS play a role in our breathing?

Back 13

Respiratory muscles acting on central commands generate airflow.

Front 14

What type of blood does the pulmonary artery pump into our lungs?

Back 14

Mixed venous blood.

Front 15

Alterations in what three factors result in abnormal blood flow?

Back 15

1. Ventilation
2. Perfusion (pulmonary circ)
3. Alveolar-capillary membrane integrity

Front 16

What factors shift the %O2 saturation vs. paO2 curve to the right? In what type of lung diseases would this happen?

Back 16

Increased C02, temperature
Decreased pH

Obstructive lung diseases prevent full expiration by trapping air and CO2 in the lungs.

Front 17

What factors shift the %O2 saturation vs. paO2 curve to the left? In what type of lung diseases would this happen?

Back 17

Decreased C02, temperature
Increased pH

Restrictive lung diseases comprimise gas exhange at the alveolar capillary membrane so that the tissues become hypoxic. Patients easily hyperventilate upon exertion.

Front 18

List two airway resistance formulas.

Back 18

R=8NL/(pie)r4

So resistance is related to viscocity(N) and channel radius (which clearly has a big impact).

Resistance is also equal to pressure difference/flow.

Front 19

What is the difference in airflow, gas density, and airway resistance in the upper and lower airways?

Back 19

In the upper airways, flow is turbulent (high airflow) d/t higher gas density, and large tube radius. The greatest resistance resides in the medium-sized bonchi and the second highest in the large.

True laminar flow occurs only in the smallest airways, in which air flows at different rates in concentric circles. Small airways have a high individual resistance, but are arranged in parallel, so resistance is low overall.

Airway resistance has an inverse relationship with lung volumes.

Front 20

Increased airway resistance is seen in what disease?

Back 20

Obstructive lung diseases: asmthma and COPD (both emphysema and chronic bronchitis are obstructive)

Front 21

Define and give the formula for alveolar ventilation.

Back 21

Volume of fresh air conducted to the alveoli. It is expressed as minute ventilation (tidal volume x respiratory rate)

Front 22

What is a normal value of minute ventilation? How is this value maintained?

Back 22

40 torr. The repiratory control center acts to keep mean arterial and alveolar pCO2 at this level.

Front 23

PaCO2 is directly proportional to what? Indirectly proportional to what?

Back 23

PaCO2 is directly proportional to CO2 production in the body and indirectly proportional to alveolar ventilation.

Front 24

How do you calculate the alveolar PAO2?

Back 24

PAO2=(PiO2-PaCO2)/ R

Where R= respiratory exchange ration of CO2 elimination to O2 uptake. R=0.8 in a health person

OR

PiO2 = Fi02 (Patm-PH20) - (PaCO2/R)

Front 25

How do you calculate the A-a diffusion gradient?

Back 25

First calculate the PA02.

Then,
A-a gradient = PA02-Pa02
Pa02 is normally 94 (ABG)

Normal range for an A-a gradient is 3-16mm Hg.

Front 26

What are some causes of an elevated A-a gradient?

Back 26

1) V-Q mismatch can be caused by restrictive lung diseases preventing normal diffusion. These diseases limit gast diffusion across the alveolar-capillary membrane, leading to hypoxemia and hyperventilation.

2) A right to left shunt.

3) An elevated A-a gradient may also occur in obstructive lung diseases such as asthma, which can prevent adequate ventilation of some areas of the lung and cause intrapulmonary shunting, so net that gas exhange decreases.

Front 27

What are some causes of hypoxemia with a normal A-a gradient?

Back 27

High altitude and alveolar hypoventilation.