Ventilation And Lung Mechanics

Front 1

Ventilation is

Back 1

exchange of air between external environment and the alveoli

Front 2

The equation for bulk flow of fluid is

Back 2

Flow (F) = Pressure gradient (DeltaP)/Resistance (R), where DeltaP is difference between atmospheric pressure (Patm) and alveolar pressure (Palv) and R is resistance to air flow in the airways

Front 3

All pressures in the respiratory system are given relative to

Back 3

atmospheric pressure

Front 4

The most important factor determining airway resistance is

Back 4

the diameter (or radius) of these passage, where resistance is inversely proportional to the 4th power of the radius.

Front 5

Under normal conditions, airway resistance is

Back 5

very low

Front 6

Boyle’s Law states that

Back 6

at constant temperature, the pressure exerted by a fixed number of gas molecules varies inversely with the volume of the container.

Front 7

Changes in alveolar pressure with the volume of the lungs changes

Back 7

the pressure gradient between the alveoli and the external environment.

Front 8

Air flows either into or out of the alveoli depending on

Back 8

the direction of the pressure gradient.

Front 9

Transpulmonary pressure is measured

Back 9

between the inside and outside of the lungs (not between the alveoli and the outside of the chest wall)

Front 10

The inside transpulmonary pressure is

Back 10

the pressure of the air in the alveoli

Front 11

The outside transpulmonary pressure is

Back 11

the pressure of the intrapleural fluid

Front 12

The equation for transpulmonary pressure is

Back 12

P(tp) = P(alv) – P(ip)

Front 13

Changes in transpulmonary pressure cause

Back 13

the changes in lung volume that ultimately result in air movement.

Front 14

At the end of expiration, the tendency for the lungs to expand because of the positive transpulmonary pressure is exactly balanced by

Back 14

the elastic recoil force of the chest wall.

Front 15

Intrapleural pressure is ______ with respect to atmospheric pressure.

Back 15

negative

Front 16

Inspiration is initiated by

Back 16

neutrally induced contraction of the diaphragm and inspiratory intercostal muscles between the ribs

Front 17

Inspiration results in ______ in the size (volume) of the thorax.

Back 17

increase

Front 18

Increase in volume of thorax during inspiration causes a ______ in intrapleural pressure.

Back 18

decrease

Front 19

Increase in volume of thorax during inspiration causes a ______ in transpulmonary pressure.

Back 19

increase

Front 20

Expansion of the lungs _____ the volume of the alveoli.

Back 20

increases

Front 21

By Boyle’s Law, when the alveoli volume increases, the alveolar pressure.

Back 21

decreases

Front 22

The decrease in alveolar pressure ______ the pressure gradient between alveoli and external environment and results in.

Back 22

increases (alveolar pressure less than atmospheric), movement of air into the lungs.

Front 23

The sequence of events for inspiration is

Back 23

1. Diaphragm and inspiratory intercostals contract, 2. Thorax expands, 3. P(ip) becomes more subatmospheric, 4. Transpulmonary pressure increases, 5. Lungs expand, 6. P(alv) becomes subatmospheric, 7. Air flows into alveoli.

Front 24

Expiration is initiated by

Back 24

relaxation of the diaphragm and inspiratory intercostal muscles.

Front 25

During expiration, chest volume decreases

Back 25

passively due to its elastic recoil after no longer being pulled outward

Front 26

During expiration, transpulmonary pressure

Back 26

decreases

Front 27

During expiration, the decrease in transpulmonary pressure results in

Back 27

a decrease in the volume of the lungs.

Front 28

During expiration, due to Boyle’s law, the pressure of air in the alveoli ________ due to.

Back 28

increases, volume of the alveoli decreasing

Front 29

During expiration, the increase in alveolar pressure

Back 29

increases the pressure gradient between the alveoli and external environment (alveolar pressure greater than atmospheric pressure) and air is expelled from the lungs.

Front 30

With normal quiet breathing, expiration is an entirely ________ process.

Back 30

passive

Front 31

The full sequence of events for expiration is

Back 31

1. Diaphgram and inspiratory intercostals stop contracting, 2. Chest wall recoils inward, 3. P(ip) moves back toward preinspiration value, 4. Transpulmonary pressure moves back toward preinspiration value, 5. Lungs recoil toward preinspiration size, 6. Air in alveoli becomes compressed, 7. P(alv) becomes greater than P(atm), 8. Air flows out of lungs.

Front 32

At the end of expiration, P(alv) and P(atm) are

Back 32

equal and there is no air flow

Front 33

At mid-inspiration, P(alv) and P(atm) are

Back 33

different due to chest wall expanding (lowers P(ip) amd makes P(tp) more positive) making P(alv) more negative and air flow inward.

Front 34

At end-inspiration, P(alv) and P(atm) are

Back 34

equal and there is no air flow due to chest wall no longer expanding or contracting (lung size is not changing and glottis is open to the atmosphere)

Front 35

At mid expiration, P(alv) and P(atm) are

Back 35

P(alv) greater than P(atm) and air is force out of lungs due to respiratory muscles relaxing and lungs and chest passively collapsing due to elastic recoil

Front 36

Lung compliance is

Back 36

the magnitude of the change in lung volume (DeltaV) produced by a given change in transpulmonary pressure

Front 37

Lung compliance equation is

Back 37

lung compliance (Cl) = Change in volume of lungs (deltaVl)/ change in transpulmonary pressure(Delta(P(alv)-P(ip))

Front 38

Low lung compliance means that

Back 38

a greater-than-normal transpulmonary pressure must be generated to produce a given amount of lung expansion.

Front 39

The determinants of lung compliance are

Back 39

1. Elasticity of pulmonary connective tissue, 2. Alveolar surface tension

Front 40

Elasticity of pulmonary connective tissue, a determinant of lung compliance, is compromised in patients with

Back 40

connective tissue disorders.

Front 41

Alveolar surface tension occurs at

Back 41

the interface between the air in the alveoli and the liquid matrix of the cells lining the alveoli.

Front 42

Surfactant is secreted by

Back 42

type II alveolar cells

Front 43

The function of surfactant is

Back 43

significantly reduces the surface tension forces within the alveoli to increase lung compliance.

Front 44

The effect of deep breaths is

Back 44

enhances the secretion of surfactant by stretching the Type II alveolar cells.

Front 45

Airway resistance is determined by

Back 45

physical, neural, and chemical factors

Front 46

Airway resistance is normally

Back 46

very low

Front 47

For airway resistance, small pressure gradients result in

Back 47

movement of large volumes of air.

Front 48

Airway resistance increases significantly in

Back 48

disease states.

Front 49

Physical factors determining airway resistance include

Back 49

transpulmonary pressure and lateral traction

Front 50

Transpulmonary pressure, a physical factor determining airway resistance, affects airway resistance by

Back 50

distending airways, particularly those without cartilage, and reduces resistance to air flow

Front 51

Lateral traction, a physical factor determining airway resistance, is

Back 51

the force exerted by elastic connective tissue fibers attached to exterior of airways to distend the airways.

Front 52

Neural factors determining airway resistance include

Back 52

epinephrine, leukotrines, neuroendocrine, and paracrine factors.

Front 53

Epinephrine, a neural factor determining airway resistance, affects airway resistance by

Back 53

relaxing airway smooth muscle (beta-adrenergic receptors) and reduces airway resistance

Front 54

Leukotrienes, a neural factor determining airway resistance, affects airway resistance by

Back 54

being produced during inflammatory processes and contracting airway smooth muscle to increase airway resistance.

Front 55

Asthma is a result of

Back 55

inflammation that causes airway smooth muscles to contract and increase airway resistance.

Front 56

Chronic obstructive pulmonary disease (COPD) causes

Back 56

difficulties with ventilation and oxygenation of blood

Front 57

COPD is not caused by

Back 57

increase in smooth muscle contraction

Front 58

Emphysema is a result of

Back 58

destruction of alveoli, enlargement of alveolar air spaces, and loss of pulmonary capillaries.

Front 59

The hypothesized cause of emphysema is

Back 59

lung produces proteolytic enzymes and elastic tissue is destroyed.

Front 60

Chronic bronchitis is the result of

Back 60

excessive mucus production in the bronchi and chronic inflammatory changes in small airways.

Front 61

The total lung volume can be divided into four mutually exclusive volumes

Back 61

1. Tidal volume, 2. Inspiratory reserve volume, 3. Expiratory reserve volume, 4. Residual volume.

Front 62

The lung tidal volume is

Back 62

the volume of air moved in and out of the lungs during quite breathing.

Front 63

The inspiratory reserve volume is

Back 63

the additional volume of air that can be inspired by maximum exertion of the inspiratory muscles following a normal inspiration.

Front 64

The expiratory reserve volume is

Back 64

the additional volume of air that can be exhaled by maximal contraction of the expiratory muscles following a normal expiration.

Front 65

The residual volume is

Back 65

the amount of air that is left in the lungs at the end of a maximal expiration.

Front 66

Lung capacities are defined as

Back 66

various combinations of individual lung volumes.

Front 67

The inspiratory capacity is

Back 67

the sum of the tidal volume and inspiratory reserve volume (represents the amount of air that can be inspired from the end of a normal expiration).

Front 68

The functional residual capacity is

Back 68

the sum of the expiratory reserve volume and the residual volume (represents the amount of air that remains in the lungs at the end of a normal expiration).

Front 69

The total lung volume is the sum of

Back 69

the inspiratory capacity and the functional residual capacity.

Front 70

The vital capacity is

Back 70

the total amount of air that can be inspired after performing a maximal expiration (the sum of the expiratory reserve volume, the tidal volume, and the inspiratory reserve volume).

Front 71

The total lung capacity is

Back 71

the total lung volume and sum of the four individual lung volumes.

Front 72

The forced expiratory volume in 1 second (FEV1) is

Back 72

the amount of air an individual can exhale in 1 second by maximum respiratory exertion following a maximal inspiration.

Front 73

The important clinical measurement for FEV1 is

Back 73

FEV1/Vital capacity (VC) ratio

Front 74

FEV1/VC ratio expresses

Back 74

the forced expiratory volume in 1 second a percentage of the vital capacity

Front 75

The normal value of FEV1/VC ratio is

Back 75

80%

Front 76

In obstructive lung disease, the FEV1/VC ratio is

Back 76

significantly less than 80% due to narrowing (obstruction) of respiratory airways.

Front 77

In restrictive lung diseases, the FEV1/VC ratio is

Back 77

is normal

Front 78

In restrictive lung diseases, the airway resistance is

Back 78

normal

Front 79

In restrictive lung diseases, the respiratory movements are

Back 79

impaired

Front 80

In restrictive lung diseases, the vital capacity is

Back 80

reduced

Front 81

Minute ventilation is

Back 81

the total amount of air moved into and out of the lungs over a 1 minute period

Front 82

Minute ventilation equation is

Back 82

minute ventilation (ml/min) = tital volume (ml/breath) x respiratory rate (breaths/min)

Front 83

Standard minute ventilation is

Back 83

5000 mL/min

Front 84

The conducting airways have a volume of approximately

Back 84

150 ml

Front 85

Anatomic dead space refers to

Back 85

conducting airway volume where no gas exchange occurs.

Front 86

Not all of the 500 mL of air inhaled on a normal breath goes to alveoli, because

Back 86

150 mL stays in conducting airways

Front 87

Alveolar ventilation is

Back 87

the amount of fresh air that moves into the alveoli during a 1 minute period

Front 88

Alveolar ventilation equation is

Back 88

alveolar ventilation (ml/min) = (tidal volume – dead space volume) (in ml/breath) x respiratory rate (breaths/min)

Front 89

Always use ________ to asses the efficacy of ventilation.

Back 89

alveolar ventilation

Front 90

Alveolar dead space is

Back 90

the volume of air contained in alveoli that have little or no blood supply.

Front 91

Physiologic dead space is

Back 91

the sum of anatomic dead space and alveolar dead space (total dead space)

Front 92

At the end of a quiet expiration, the air in the anatomic dead space has

Back 92

relatively high CO2 and low O2

Front 93

When you exhale, the first air that comes out is

Back 93

dead space air