Physiology- Exam 3

Front 1

Tidal Volume (TV)

Back 1

Is tje volume inspired with each breath

Front 2

Inspiratory reserve volume (IRV)

Back 2

Is the volume that can be inspired over and above the tidal volume. THis is used during exercise.

Front 3

Expiratory reserve volume (ERV)

Back 3

is the volume that remains in the lungs after a maximal expiration. CANNOT be measured by spirometry

Front 4

Anatomic dead space

Back 4

is the volume of the conducting airways. Is normally approximately 150.

Front 5

Inspiratory Capacity

Back 5

is the sum of tidal volume and IRV

Front 6

Inspiratory capacity (IC)

Back 6

TV + IRV

Front 7

Functional residual capacity(FRC)

Back 7

ERV + RV
Is the volume remaing in the lungs after a tidal volume is expired. It includes RV, so CANNOT be measured by spirometry

Front 8

Vital Capacity (VC) or forced vital capacity (FVC)

Back 8

TV + IRV + ERV
Is the volume of air that can be forcibly expired after a maximal inspiration

Front 9

Total Lung Capacity (TLC)

Back 9

TV + IRV + ERV + RV

Front 10

Forced expiratory volume (FEV1)

Back 10

Volume of air that can expired in the first second of a forced maximal expiration

Front 11

FEV1

Back 11

Is normally 80% of forced vital capacity
FEV1/FVC=0.8

Front 12

FEV1/FVC is Decreased

Back 12

During obstruction (like asthma)
FEV1 is reduced MORE than FVC so that FEV1/FVC is decreased

Front 13

FEV1/FVC Increased or Normal

Back 13

In restrictive lung disease (fibrosis), both FEV1 and FVC are reduced FEV1/FVC normal or is increased

Front 14

Compliance of respiratory system

Back 14

Describes the distensibility of the lungs and chest wall. Is inversely related to elastance, which depends on the amount of elastic tissue.

Front 15

Emphysema

Back 15

Lung Compliance is INCREASED and tendency of the lungs to collapse is decreased. Therefore, at the original FRC, the tendency of the lungs to collapse is less than the tendency of the chest wall to expand. = Increased FRC. Increased TLC. Increased Compliance. Decreased FEV1. Decreased FVC. Decreased FEV1/FVC.

Front 16

Fibrosis

Back 16

Lung compliance is decreased and the tendency of the lungs to collapse is increased. Therefore, at the original FRC, the tendency of the lungs to collapse is GREATER than the tendency of the chest wall to expand. = Decreased FRC. Increased or normal FEV1/FVC ratio. Decrease FVC. Decrease FEV1.

Front 17

P=T/r

Back 17

Creates a collapsing pressure that is directly proportional to surface tension and inversely proportional to alveolar radius

Front 18

Large alveolus

Back 18

Increase radius, Decrease P, and Decrease tendency to collapse

Front 19

Small alveolus

Back 19

Decrease radius, Increase P and Increase tendency to collapse

Front 20

Surfactant

Back 20

Lines the alveoli, Reduces Surface Tension (T). Prevents small alveoli from collapsing and increases compliance.

Front 21

Airflow

Back 21

Is driven by, and is directly proportional to, the pressure difference between the mouth and the alveoli

Front 22

Airflow
Q=Change in P/R

Back 22

Is inversely proportional to airway resistance; thus the higher the airway resistance, the lower the airflow.

Front 23

At rest- before inspiration begins and before expiration

Back 23

Alveolar pressure is zero, intrapleural pressure is negative, and no air flow

Front 24

During inspiration

Back 24

Volume increases because of pressure gradient between atmosphere and alveoli. Intrapeural pressure becomes mroe negative. At peak of inspiration,lung volume is the FRC plue one TV

Front 25

During expiration

Back 25

Alveolar pressure becomes greater than atmospheric pressure (becomes positive), Air flows out of lungs,

Front 26

Asthma

Back 26

Obstructive Disease. Expiration impaired. Decreased FVC. Decreased FEV1. Decreased FEV1/FVC. Increased FRC (air that should have been expired is not, leading to air trapping)

Front 27

COPD

Back 27

Obstructive- Emphysema. Increased lung compliance. Expiration impaired. Decreased FVC. Decreased FEV1. Decreased FEV1/FVC. Increased FRC (air that should have been expired is not, leading to air trapping)

Front 28

Fibrosis

Back 28

Restrictive. Decreased lung compliance. Inspiration impaired. Decreases in all lung volumes (TV,IRV,ERV,RV), FEV1 Decreased less than FVC, FEV1/FEC is increased or Normal

Front 29

Ventilation

Back 29

Frequency X Depth of breathing

Front 30

Perfusion

Back 30

Blood Flow- cardiac output of right ventricle

Front 31

Bronchospasm and intraluminal secretions

Back 31

Decrease effective diameter. Increase resistance=Decrease Flow.

Front 32

Inspiration

Back 32

ACTIVE phase. Lungs expand passively due to decreased intrapleural pressure. Air flows in to equalize pressure.

Front 33

Expiration

Back 33

PASSIVE phase. Chest wall muscles relax. Pleural and alveolar pressures increase. Air flows out lung.

Front 34

PO2

Back 34

160- Dry Inspired Air
150- Humidified Tracheal
102- Alveolar Air
90- Systemic Arterial Blood
40- Mixed Venous Blood

Front 35

PCO2

Back 35

0- Dry Inspired Air
0- Humidified Air
40- Alveolar Air
40- Systemic Arterial Blood
46- Mixed Venous Blood

Front 36

Fraction of O2 in air

Back 36

21%- Constant
PB (760) X .21%=150mmHg

Front 37

Pulmonary Artery

Back 37

O2- 40
CO2- 46

Front 38

Pulmonary Veins

Back 38

O2- 102
CO2- 40

Front 39

Alveoli

Back 39

O2- 102
CO2-40

Front 40

Pulmonary Compliance decreased by:

Back 40

HighLung Volume, Fibrotic disease, Decreased surfactant, vascular congestion

Front 41

Pulmonary compliance is increased by:

Back 41

destruction of elastic tissue (emphysema)

Front 42

Total ventilation

Back 42

tidal volume X Respiratory Rate

Front 43

Alveolar ventilation

Back 43

(tidal volume-anatomic dead space) X respiratory rate

Front 44

Dead Space Ventilation

Back 44

Anatomic dead space x respiratory rate

Front 45

More effective method to increase alveolar ventilation

Back 45

Increasing depth

Front 46

Alveolar Ventilation

Back 46

PaCO2=VCO2/VA

Front 47

PaCO2=VCO2/VA

Back 47

As metabolism goes up, PaCO2 goes up. Alveolar ventilation increases, PaCO2 decreases.

Front 48

Exercise

Back 48

Alveolar ventilation and VCO2 goes up together and PaCO2 stays the same

Front 49

Hypoventilation

Back 49

PaCO2 is High. Alveolar is decreased.

Front 50

Hyperventilation

Back 50

PaCO2 is Low. Alveolar is increased.

Front 51

Advantages of Surfactant

Back 51

1.Decreases muscular effort needed to expand the lungs.
2. Lowers elastic recoil and thus helps prevent alveolar collapse.
3. Stabilizes alveoli that tend to deflate at different rates.

Front 52

Regional Hypoxia

Back 52

Vasoconstrict at the hypoxia region, blood flow reduced. Shunt blood away from that areas, so it can go the alveoli with normal oxygen levels.

Front 53

Normal V/Q

Back 53

0.8
(Normally so that mean you have more perfusion and less ventilation)

Front 54

Blood Flow in the lung

Back 54

Blood flow is lowest at the apex and highest at the base becasue of gravity.

Front 55

Ventilation in the lung

Back 55

Ventilation is also lowest at the apex and higher at the base, but the regional differences for ventilation are not as great as for perfusion.

Front 56

V/Q Ratio

Back 56

Highest at apex. Lowest at base.

Front 57

At Apex

Back 57

Highest V/Q, PO2 highest. PCO2 lowest because more gas exchange. Ventilation lower. Blood flow lowest.

Front 58

At Base

Back 58

Lowest V/Q, PO2 is lowest and PCO2 is highest becasue of less gas exchange. Ventilation Higher. Blood Flow Highest.

Front 59

V/Q ratio airway obstruction

Back 59

Ventilation zero. Blood flow normal. V/Q zero. No gas exchange. Perfused but not ventilated. PO2 and PCO2 of pulmonary capillary blood/systemic will approach their values in mixed venous blood.
PA02-0 PACO2-0 V/Q-0 Pa02-40 PaCO2-46

Front 60

V/Q ratio Pulmonary embolism

Back 60

Blood flow Zero. Ventilation normal. V/Q infinite (Dead Space). No gas exchange. Ventilation but not perfused. PO2 and PCO2 of alveolar gas approach values in inspired air.
PAO2-150 PACO2-0 PaO2-0 PaCO2-0

Front 61

P(A-a)O2 Gradient

Back 61

Commonly used to identify a defect in pulmonary gas exchange. Measure PaO2 and PaCO2 and calculate PAO2.

Front 62

PAO2=PIO2- (PACO2/R)
*No calculation but understand)

Back 62

Normal Gradient no higher than 12-15mmHg
Can be increased by: diffusion impairment and V/Q mismatch

Front 63

A-a Gradient

Back 63

High is abnormal. Something is wrong from 02 getting from alveoli to artery.

Front 64

Rightward Shift

Back 64

Metabolic by-products affect Hgb affinity
Favors unloading of O2
Increase H+, PCO2 (Decrease pH) = Bohr effect
Increase Temperature
Increase 2,3 DPG (glycolysis in rbc)
Increase P50 (Decrease O2 sat at given PO2)
Decrease Hgb affinity - more unloading of O2 at given PO2

Front 65

Leftward Shift

Back 65

Decrease H+, PCO2 (Increase pH)
Decrease Temperature
Decrease 2,3 DPG presence of fetal hemoglobin
Decrease P50 (Increase O2 sat at given PO2)
Increase affinity of Hgb for O2

Front 66

Disease that causes a Left Shift

Back 66

CO poisoning

Front 67

Disease that causes a Right Shift

Back 67

Exercise (increase temp) and Living at high altitude (increase in 2,3 DPG)

Front 68

O2 Content

Back 68

(O2 on Hb) + (O2 in plasma)
O2 Content= Hb x 1.34 x %Saturation

Front 69

O2 carrying capacity of Hb

Back 69

1.34 ml/gm

Front 70

O2 carrying capacity of blood

Back 70

1.34 X g of HB normally
~15g/dL x 1.34ml/g= ~20ml/dL

Front 71

O2 Saturation

Back 71

% of Hb that is boung (% of max content)

Front 72

Anemia

Back 72

Low Hg. Normal PO2 and Saturation, but CONTENT is lower because of low hemoglobin.

Front 73

Decrease Hb by 50%

Back 73

Decrease O2 content with normal PO2.
Venous PO2=26mmHg vs 40mmHg (Normal)

Front 74

CO Poision

Back 74

Acute decrease O2 carrying capacity
Normal PO2 and Hb concentration
Large Decrease venoud P02 (decrease unloading)

Front 75

Transport CO2

Back 75

Dissolved, HCOs- inplasma &RBC, Carbaminohemoglobin

Front 76

Central Chemoreceptors

Back 76

Located at medulla. Sensitive to PCO2 and pH.
Decrease pH. Increase PCO2.= Increased Breathing Rate

Front 77

Peripheral Chemoreceptors

Back 77

Carotid and aortic. Sensitive to PaO2, PaCO2, and pH.
Decrease P02. Increased PCO2. Decreased pH.= Increased Breathing Rate

Front 78

Most Important Chemical controller

Back 78

CO2 is most important controller.

Front 79

Normal PACO2 Values

Back 79

40mmHg at 5 L/min
Hyperventilation- Lower PCO2
Hypoventilation- Raises PCO2

Front 80

When PaCO2 is increased

Back 80

chemoreceptors sense the increase and provoke an inreased ventilation to blow off the excess CO2 (negative feedback control)
**PaCO2 determines the “drive to breathe” and thus, determines alveolar ventilation as a reflex response.

Front 81

Factors affecting CO2 control

Back 81

Basal level of PaCO2
Arousal state
Affected by PO2
Hyperventilation effect
Hypoventilation effect

Front 82

Factors affecting O2 control

Back 82

Basal level of PaO2
NOT O2 CONTENT
Affected by PaCO2

Front 83

Exercise

Back 83

Increase in ventilatory rate that matches the increase in O2 consumption and CO2 production by the body. Mean values for arterial PO2 and PCO2 do not change. Pulmonary blood flow increases.

Front 84

Exercise Response

Back 84

O2 consuption-Increase
CO2 productin- increase
Ventilation rate- Increases
Arterial PO2 and PCO2-No Change
Arterial pH No change w/moderate exercise..Decresae in strenuous
Venous PCO2- Increase
Pulm blood flow- Increase
V/Q ratio-Evenly distributed in lung

Front 85

High Altitude

Back 85

Alveolar PO2-Increase
Arterial PO2-Decrease
Ventilation Rate- Increase (hyperventilation)
Arterial pH-Increase (alkalosis)
[Hb]- increase
2,3 DPG- Increase
Shift to Right, dec affinity
Pulm vascular resistance- Inc(hypoxic vasoconstriction)