Bio261 Lecture 18 Q's- Respiratory System

Front 1

What is the role of the conducting zone?

Back 1

-The conducting zone warms and humidifies the incoming gases. It also is the primary location of mucus production, which lines the passageways and serves to trap bacteria, viruses, and other pathogens. The epithelial cells of the conducting zone then move these trapped pathogens out of the body through cilliary action.

Front 2

Does gas exchange take place here?

Back 2

-NO

Front 3

How do we measure the concentration of gas molecules?

Back 3

-The concentration of gas molecules is measured by the amount of pressure that the gas exerts in a confined space. In a mixture of gases, such as our atmosphere, the individual concentrations of each type of gas is called the partial pressure of that gas, i.e. the partial pressure of oxygen, which is written as PO2.

Front 4

Across what membranes does respiratory exchange occur?

Back 4

-Respiratory exchange occurs in the alveolar sacs; and the exchange must diffuse through the Type I alveolar cells that line the alveolar sacs and the endothelial cells that line the capillaries.

Front 5

What gasses are involved and by what means are they transported?

Back 5

-The primary gasses that are exchanged are oxygen and carbon dioxide, they are transported by simple (passive) diffusion.

Front 6

Where is surfactant found and what is its function?

Back 6

-Surfactant is found in the thin liquid "film" which covers the inside of the alveolar sacs. It acts to decrease surface tension. (According to Laplace's law, the inside pressure is P = 2T/r (where T = tension and r is radius).

-Surfactant ensures that the alveolar sacs maintain a constant pressure as they change in size with inspiration and expiration. The pressure stays constant because as the radius decreases, the surfactant concentration increases and this reduces surface tension, so the effects counter one another and pressure stays constant.)

Front 7

Why do premature infants have difficulty breathing?

Back 7

-Premature infants have difficulty breathing because their lungs have not begun to produce surfactant, this means that with each breath they must re-inflate the lungs, which is both difficult and requires lots of energy

Front 8

The contraction of what muscles expands the lungs?

Back 8

-The muscles which expand the lungs are the diaphragm and the external intercostal muscles, during deep inhalation, the sternocleidomastoid and scalene muscles can also be involved.

Front 9

What type of gradient is created when the lungs expand?

Back 9

-When the lungs expand, a gas pressure gradient is formed

Front 10

What causes air to enter the lungs during inhalation?

Back 10

- the intrapulmonary pressure becomes < atmospheric pressure, so air is drawn into the lungs.

Front 11

What causes air to leave the lungs during exhalation?

Back 11

- During normal breathing, when the diaphragm muscles and external intercostal muscles relax, the volume of the lung is decreased to its pre-inhalation volume. This means that now the intrapulmonary pressure is > atmospheric pressure, so air is pushed out of the lungs.

Front 12

How does Boyle's law relate to ventilation?

Back 12

-Boyles's law describes the relationship between pressure and volume - it states that as volume increases in a closed container, the pressure will decrease, conversely, when the volume decreases in a closed container, the pressure will increase. Our lungs are like containers that are open to the "outside" world, so when we change the volume of our thoracic cavity, for a moment there is a change in pressure, which will allow air to move in or out of the lungs.

Front 13

Where is the pleural cavity?

Back 13

-The pleural cavity is the space within the pleural sac. There are two pleural sacs, one around each lobe (side) of the lung.

Front 14

What is in it?

Back 14

-There is a very small amount of fluid in the cavity (about 3ml or 3cc).

Front 15

How does the pressure in the pleural cavity compare with the pressure in the intrapulmonary space?

Back 15

-The pressure in the intrapleural space (within the pleural cavity) is always lower than the intrapulmonary space (the space within the lung tissue - alveolar spaces), and even when the intrapulmonary space in below atmospheric pressure, the intrapleural space is still below atmospheric pressure.

Front 16

What does the transmural pressure do?

Back 16

-The transmural pressure is the pressure gradient across the intrapleural space (it is produced because the pleural cavity is a sealed cavity. Both the parietal pleural membrane (next to the thoracic cavity) and the visceral pleural membrane (next to the lungs) are constantly trying to pull in opposite directions, but since the pleural cavity is sealed, the more the thoracic cavity is expanded, the greater the pressure becomes to hold the pleura together.

(For example if you fill a syringe with liquid, then put your finger over the end to plug it and try to pull on the plunger, the more you pull, the more it will resist, and it will snap quickly back into place when you stop pulling on it.) The pleural membranes behave in the same way. While the thoracic cavity is expanding, the visceral pleura is trying to pull in the direction to collapse the lungs, the liquid in the middle of the sealed cavity, creates a stronger pressure, and prevents the lungs from collapsing and also stretches the lungs in the process.)

Front 17

What is a pneumothorax?

Back 17

- refers to any puncture in the pleural sac (for instance a knife wound or a fractured rib). When this occurs, the intrapleural pressure quickly equalizes with the atmospheric pressure and air rushes into the pleural cavity, the lung is no longer held close to the wall of the thoracic cavity and easily collapses like a deflated balloon.

Front 18

When are abdominal muscles involved in breathing?

Back 18

-Abdominal muscles may become involved during exhalation, generally not during normal quiet breathing but when air is being forced out of the lungs.

Front 19

What factors provide resistance when breathing?

Back 19

- The factors that provide resistance to breathing are the compliance (or stretch ability), elasticity (tendency to return to normal size after being stretched), and surface tension of the lung tissue.

Front 20

What is the term for air left in the lungs after a maximum exhalation?

Back 20

-The air left in the lungs after a maximum exhalation is called the residual volume (it is composed of both the anatomical dead space air in the trachea and all the bronchi passageways (~150 ml) and the air that remains in the respiratory zone (recall the alveolar sacs do NOT collapse, so that means that air remains in the alveolar space).

Front 21

What is the term for the maximum volume of air that can be moved in and out of the lungs during breathing?

Back 21

-The maximum volume of air that can be moved in and out of the lungs is referred to as the vital capacity.

Front 22

What is the term for the volume of air moved in and out of the lungs during relaxed breathing?

Back 22

-The term for the volume of air moved in and out of the lungs during relaxed breathing is tidal volume.

Front 23

To what does the term dead space refer?

Back 23

-The term dead space refers to the major bronchial passageways that are continually open and provide for passage of gases from the outside atmosphere to the alveolar sacs. Since there is no gas exchange here but there is always gas present, it is referred to as the dead space.

Front 24

Why is it more efficient to increase the volume of breaths, than the frequency of breaths during exercise?

Back 24

-Mathematically we can show that it is more efficient to increase the volume of breath, rather that the frequency of breaths taken during exercise.

Since air is moving in both directions using the same "pipes", we can describe the amount of "new" air reaching the alveolar sacs as:

New air = ventilation rate (breaths per minute or bpm) x (tidal volume - dead space) Normally this would be: 12bpm x (500ml - 150ml) = 4200 ml/min. During exercise if you increased the breaths per minute, your breathing would be shallow and so you would also decrease the tidal volume, so with a higher frequency of breathing: 20 bpm x (300ml-150ml) = 3000 ml/min.

However, if you take deeper breaths (in essence an increase in tidal volume) at the same rate, then: 12 bpm x (750ml - 150ml) = 7200 ml/min. So it is more efficient to increase the volume (or depth) of breathing, than the frequency.

Front 25

To what does COPD refer?

Back 25

-COPD is chronic obstructive pulmonary disease. The most common symptom of COPD is dyspnea, which is a feeling of shortness of breath. COPD can have a number of causes, for instance asthma and emphysema.

Front 26

What are the symptoms, causes and physiological results of emphysema and asthma?

Back 26

In emphysema, there is a progressive destruction of the alveolar sacs, which results in fewer and fewer functional gas exchange sites. This decreases the ability to allow for adequate diffusion of O2 to the blood stream and so you have oxygen poor blood.

-In asthma, inflammation occurs, which causes both an increase in mucus secretions and vasoconstriction of the bronchioles. Together, this decreases and/or inhibits the flow of gasses into the alveolar sacs, again this will severely limit the amount of diffusion of O2 into the blood stream and so the blood is oxygen poor. -

Front 27

How do you distinguish between a restrictive pulmonary disease and an obstructive pulmonary disease?

Back 27

- The easiest way to determine whether a patient has a restrictive or an obstructive pulmonary disease is to perform a forced expiratory volume, 1-second test (FEV1). Only in the obstructive type of pulmonary disease is there a decrease in the rate at which air can be exhaled from the lungs.

-So if the FEV1 test is at about 80%, the patient has a restrictive pulmonary disease, and if the patient has a FEV1 of significantly less that 80%, then it is an obstructive type pulmonary disease.

Front 28

Ventillation

Back 28

-moves air in and out of lungs for gas exchange

Front 29

Gas exchange

Back 29

-gases moving from capillary beds to alveolar sacs and vice versa

Front 30

O2 utilization

Back 30

-cellular respiration

Front 31

External respiration

Back 31

-gas exchange w/ blood

Front 32

Internal respiration

Back 32

-gas exchange b/n blood and tissues, & O2 use by tissues

Front 33

Diaphragm

Back 33

- dome-shaped sheet of skeletal muscle that creates the thoracic cavity

Front 34

Thoracic cavity

Back 34

-contains heart, large BVs, trachea, esophagus, thymus & lungs

Front 35

Peritoneal cavity

Back 35

-below the diaphragm

-contains liver, pancreas, GI tract, spleen & GI tract

Front 36

Intrapleural space

Back 36

-thin fluid layer b/n visceral pleura and parietal pleura

Front 37

Visceral pleura

Back 37

-covering lungs

Front 38

Parietal pleura

Back 38

-lining thoracic cavity walls

Front 39

Pharynx

Back 39

-throat

-serves as a common passageway for both the respiratory and the digestive systems

Front 40

Larynx

Back 40

-voice box

-located at entrance of trachea

Front 41

Esophagus

Back 41

-tube through which food passes to the stomach

Front 42

Trachea

Back 42

-windpipe

-air is conducted through here to the lungs

Front 43

Bronchus

Back 43

-within each lung, continue to branch into progressively narrower, shorter and more numerous airways

Front 44

Bronchioles

Back 44

-the smaller branches of bronchi

Front 45

Terminal bronchioles

Back 45

-part of gas exchange

Front 46

Respiratory bronchioles

Back 46

-last part of conducting zone

Front 47

Alveolar sacs

Back 47

-where gases are exchanged b/n air and blood

Front 48

Conducting zone

Back 48

-warms inspired air, humidifies it and cleans it with mucus lining

Front 49

Type I alveolar cells

Back 49

-thin wall-forming cells

Front 50

Type II alveolar cells

Back 50

-pulmonary surfactant secretion by these cells

-cover about 5% of the alveolar surface epithelium

-

Front 51

Surfactant

Back 51

-Surface acing agents

-consists of phospholipids secreted by type II alveolar cells

-Lowers ST by getting b/n water molecules, reducing their ability to attract each other via hydrogen bonding

-prevents ST from collapsing alveoli!

Front 52

Boyle's law

Back 52

P1V1 = P2V2

-natural properties of gases

Front 53

Inspiration

Back 53

-inhalation; thoracic cavity expands

Front 54

Expiration

Back 54

-exhalation; thoracic cavity volume decreases

Front 55

External intercostals

Back 55

-used during inspiration

Front 56

Internal intercostals

Back 56

-used during expiratoin

Front 57

Scalenes

Back 57

-used during inspiration

Front 58

Sternocleidomastoid

Back 58

-used during inspiration

Front 59

Intrapulmonary Pressure

Back 59

-about -3mmHg during inspiration

-about +3 mmHg during expiration

(intra-alveolar pressure)

Front 60

Transpulmonary Pressure

Back 60

intrapulmonary - intrapleural pressure

-keeps lungs inflated

Front 61

Transmural pressure gradient

Back 61

-pushes out on the lungs, stratching or distending them.

-forces the lungs to expand to fill the thoracic cavity, no matter its size; as the cavity enlarges, so do the lungs.

Front 62

Compliance

Back 62

-how easily lung expands w/pressure

-change in lung volume per change in transpulmonary pressure (change in V/ change in P)

-reduced by factors that cause resistance to distension

Front 63

Elasticity

Back 63

-the tendency to return to initial size after distension

-due to high content of elastin proteins

-elastic tension increases during inspiration & is reduced by recoil during expiration

Front 64

Surface tension

Back 64

-lungs secrete & absorb fluid, normally leaving a thin film of fluid on alveolar surface

-film causes surface tension b/c water molecules are attracted to other water molecules

Front 65

Fibrosis

Back 65

-the thickening and scarring of connective tissue, usually as a result of injury

Front 66

Cystic fibrosis

Back 66

-defect in CFTR gene (cystic fibrosis transmembrane conductance regulatory gene) = chloride channel

Front 67

Law of Laplace

Back 67

-states that pressure in alveolus is directly proportional to ST; & inversely to radius of alveoli

Front 68

RDS - respiratory distress syndrome

Back 68

-premies are often born w/immature surfactant system and have trouble inflating lungs

Front 69

ARDS - acute RDS

Back 69

-in adults, caused by septic shock, which decreases compliance and surfactant secretion

Front 70

Pneumothorax

Back 70

-air in the chest

-abnormal condition of air entering the pleural cavity

Front 71

Spirometry

Back 71

-a method that measures volumes of air moved during inspiration and expiration

Front 72

Anatomical dead space

Back 72

-150 ml

-air in conducting zone where no gas exchange occurs

Front 73

Tidal volume

Back 73

-500 ml

-the volume of air entering or leaving the lungs during a single breath

Front 74

Inspiratory reserve volume

Back 74

-3100 ml

-the extra volume of air that can be maximally inspired over and above the typical resting tidal volume.

-accomplished by maximal contraction

Front 75

Expiratory reserve volume

Back 75

-1200 ml

-the extra volume of air that can be actively expired by maximally contracting the expiratory muscles beyond that normally passively expired at the end of a typical resting tidal volume

Front 76

Residual volume

Back 76

-made up of space in alveoli and the "anatomical dead space" or conducting zone.

-1200 ml

-the min volume of air remaining in the lungs even after a maximal expiration.

-not directly measured by a spirometer, b/c this volume of air does not move into and out of the lungs

Front 77

Total lung capacity

Back 77

-6000 ml

-the max volume of air that the lungs can hold

(TLC = VC + RV)

Front 78

Vital Capacity

Back 78

-4800 ml

-the max volume of air that can be moved out during a single breath following a maximal inspiration.

(VC = IRV + TV + ERV)

-reps the max volume change possible w/in the lungs

Front 79

Restrictive pulmonary disease

Back 79

-decreased lung compliance

-reduced inspiratory volume; a reduced vital capacity but w/normal forced vital capacity

e.g., pulmonary fibrosis, respiratory distress syndrome

Front 80

Obstructive pulmonary disease

Back 80

-increased airway resistance- can be related to loss of elasticity

-reduced airway flow (reduced diameter); there is a normal vital capacity but expiration is slowed down.

-COPD Chronic obstructive pulmonary diseases--emphysema, asthma, pulmonary edema

Front 81

FEV1 - forced expiratory volume

Back 81

-measure the rate of expiration to diagnose respiratory problems

-the volume of air that can be expired during the first second of expiration in a VC determination

Front 82

Dyspnea

Back 82

-difficult/labored breathing

Front 83

Asthma

Back 83

-bronchiolar constriction increases airway resistance

Front 84

Emphysema

Back 84

-loss of lung tissue decreases elastic recoil of lung

Front 85

COPD - chronic obstructive pulmonary disease

Back 85

-includes emphysema, asthma and pulmonary edema

Front 86

Atelectasis

Back 86

-partial or complete collapse of the lung