Respiratory Physiology

Front 1

Tidal volume

Back 1

Volume of air that enters and leaves the lung in a single cycle. 500ml

Front 2

Functional residual capacity

Back 2

Amount of air in the lungs after passive expiration. 2,700ml

Front 3

Inspiratory capacity

Back 3

Maximal volume of gas inspired from FRC. 4,000ml

Front 4

Inspiratory reserve volume

Back 4

Air that can be inhaled after normal inspiration. 3,500ml

Front 5

Expiratory reserve volume

Back 5

Air that can be expired after a normal expiration. 1,500ml

Front 6

Residual volume

Back 6

Air in the lungs after maximal expiration. 1,200ml

Front 7

Vital capacity

Back 7

Maximal air that can expired after maximal inspiration. 5,500ml

Front 8

Total lung capacity

Back 8

Air in the lungs after maximal inspiration. 6,700ml

Front 9

Total ventilation

Back 9

Total ventilation = Tidal volume X respiratory rate.

Front 10

Dead space

Back 10

Regions that contain air but do not exchange O2 and CO2

Front 11

Anatomic dead space

Back 11

Conducting zones. Approximately equal to person't weight in pounds.

Front 12

Alveolar dead space

Back 12

Alveoli with air but without blood flow

Front 13

Physiologic dead space

Back 13

Anatomic dead space plus alveolar dead space

Front 14

Alveolar ventilation

Back 14

Tidal volume - anatomic dead space X respiratory rate.

Front 15

Lung recoil

Back 15

Force that collapses the lung. As the lung enlarges, recoil increases and vice versa.

Front 16

Intrapleural pressure

Back 16

Normally -5 cmH2O. Force that expands the lung. The more negative, the more lung expansion.

Front 17

Lung mechanics before inspiration

Back 17

Glotis is open but no air is flowing - alveolar pressure = 0. Intrapleural pressure and lung recoil are equal but opposite. Gravity decreases intrapleural pressure at the apex and increases it at the bases. Apex alveoli are more distended.

Front 18

Lung mechanics during inspiration

Back 18

Diaphragm contracts, intrapleural pressure becomes more negative. Expansion of alveoli makes alveolar pressure negative causing air to flow into the lungs.

Front 19

Lung mechanics at the end of inspiration

Back 19

Intrapleural pressure and recoil are the same but opposite. Alveolar pressure returns to zero and air stops flowing in.

Front 20

Lung mechanics during expiration

Back 20

Diaphragm relaxes, intrapleural pressure increases, lung recoil collpases the lung. Alveoli compress tha air and alveolar pressure becomes positive and air flows out of the lungs until alveolar pressure is back to zero. Lung recoil and intrapleural pressure become equal but opposite.

Front 21

Assisted control mode ventilation

Back 21

Inspiration is initiated by the patient or the machine if no signal is detected.

Front 22

Positive end-expiratory pressure

Back 22

Does not allow intraalveolar pressure to return to zero at the end of expiration. The larger lung volume prevents atelectasis.

Front 23

What is lung compliacnce?

Back 23

It's the change in volume with a change in pressure. Increased compliance means more air flows in with a given change in pressure. Decreased compliance means the opposite. The steeper the slope of the lung inflation curve, the greater the compliance. Emphysema = very compliant; fibrosis = not compliant.

Front 24

Components of lung recoil

Back 24

1) the tissue's collagen and elastin fibers and 2) the surface tension (greatest component)

Front 25

Functions of surfactant

Back 25

Lowers lung recoil and increases compliance (↓ surface tension) more in small alveoli than large alveoli; reduces capillary filtration forces reducing tendency to develop edema.

Front 26

Pathophysiology of respiratory distress syndrome

Back 26

Low surfactant --> ↑ recoil, ↓ compliance (a greater change in intrapleural pressure is necessary to inflate the lungs); alveoli collapse (atelectasis); more negative intrapleural pressures promote capillary filtration (pulmonary edema)

Front 27

Airway resistance

Back 27

R = 1/r4; first and second bronchi have less radius than alveoli, therefore more resistance. Ach increases resistance (bronchoconstriction), catecholamines decrease resistance (bronchodilation)

Front 28

Effect of lung volume on airway resistance

Back 28

↑ lung volume --> ↑ radius --> ↓ resistance. The more negative the intrapleural pressure, the less resistance

Front 29

Lung volumes in obstructive disease

Back 29

↑ TLC, ↑ RV, ↑ FRC, ↓ FEV1, ↓ FVC, ↓ FEV1/FVC

Front 30

Lung volumes in restrictive disease

Back 30

↓ TLC, ↓ RV, ↓ FRC, ↓ FEV1, ↓ FEV, ↑ FEV1/FVC

Front 31

Pressure of alveolar O2 and CO2

Back 31

PAO2 = 100mmHg; PACO2 = 40mmHg

Front 32

Pressure of venous pulmonary capillary O2 and CO2

Back 32

PvO2 = 40mmHg; PvCO2 = 47mmHg

Front 33

Pressure of arterial pulmonary capillary O2 and CO2

Back 33

PO2 = 100mmHg; PCO2 = 40mmHg

Front 34

Which factors affect PCO2?

Back 34

Metabolic CO2 production and alveolar ventilation

Front 35

Relationship between alveolar ventilation and PACO2

Back 35

Inversely proportional. Hyperventilation decreases PACO2; hypoventilation increases PACO2.

Front 36

Relationship between PAO2 and PACO2

Back 36

↓ PACO2 --> ↑ PAO2 (hyperventilation); ↑ PACO2 --> ↓ PAO2 (hypoventilation)

Front 37

Which factors affect PAO2?

Back 37

Atmospheric pressure, oxygen concentration of inspired air and PACO2

Front 38

What determines oxygen content?

Back 38

Hemoglobin concentration. 1.34ml O2 combines with each gram of hemoglobin.

Front 39

Amount of dissolved oxygen in the blood

Back 39

0.3 volumes %; 0.3ml per 100ml of blood. Determines PO2 which acts to keep oxygen bound to Hb

Front 40

What determines oxygen attachment to hemoglobin?

Back 40

PO2 and the affinity of the individual attachment sites. The higher the affinity, the less PO2 is needed to keep it attached

Front 41

What determines PO2?

Back 41

Amount of oxygen dissolved in plasma. Normally 0.3 volumes %.

Front 42

Site 4 of hemoglobin

Back 42

Oxygen is attached at 100mmHg. Least affinity, last site to be saturated.

Front 43

Site 3 of hemoglobin

Back 43

Oxygen is attached at 40mmHg. More affinity than site 4, less affinity than site 2.

Front 44

Site 2 of hemoglobin

Back 44

Oxygen is attached at 26mmHg which is p50. More affinity, second site to be saturated.

Front 45

Site 1 of hemoglobin

Back 45

Oxygen remains attached under physiologic conditions. Highest affinity, first site to be saturated.

Front 46

Factors that shift oxygen dissociation curve to the right

Back 46

↑ CO2, ↑ 2,3BPG, fever, acidosis

Front 47

Factors that shift oxygen dissociation curve to the left

Back 47

↓ CO2, ↓ 2,3BPG, hypothermia, alkalosis, HbF, methemoglobin, carbon monoxide, stored blood

Front 48

How is CO2 carried in the blood?

Back 48

5% dissolved; 5% attached to Hb (carbamino compounds); 90% as bicarbonate.

Front 49

Main drive for ventilation

Back 49

H+ ions from dissociated H2CO3 which stimulate central chemoreceptors. H2CO3 is proportional to PCO2 of CSF

Front 50

Central chemoreceptors

Back 50

Sense [H+] which is proportional to PCO2 and H2CO3 of the CSF (not systemic)

Front 51

Peripheral chemoreceptors

Back 51

Carotid bodies (afferents via IX), aortic bodies (afferents via X). Monitor PO2 and [H+/CO2]

Front 52

Main drive for ventilation in severe hypoxemia

Back 52

Peripheral chemoreceptors sense PaO2 (dissolved oxygen) once PaO2 falls to 50-60mmHg.

Front 53

Ventilatory response to chronic hypoventilation

Back 53

Peripheral chemoreceptors are the main drive for ventilation eventhough PaCO2 is increased.

Front 54

Ventilatory response to anemia

Back 54

PaO2 and PACO2 are normal, therefore neither peripheral nor central chemoreceptors respond.

Front 55

Central control of ventilation

Back 55

Apneustic center in the caudal pons promotes prolonged inspiration. Pneumotaxic center in the rostral pons inhibits apneustic center. Efferents are from the medulla to the phrenic nerve (C1-C3) to the diaphragm

Front 56

Differences in ventilation between the base and the apex of the lung

Back 56

Base intrapleural pressure is -2.5, alveoli are compliant and small with a small volume of air but are underventilated due to too much blood flow; Apex pressure is -10, alveoli are large and stiff and contain a large volume of air but are overventilated due to limited blood flow

Front 57

Differences in blood flow between the base and the apex of the lung

Back 57

Blood vessels of the apex are less distended, have more resistance and receive less blood flow. Blood vessels of the base are more distended, have less resistance and receive more blood flow

Front 58

Ventilation/perfussion relationship at the base of the lungs

Back 58

Blood flow is higher than ventilation, the relationship is less than 0.8; the bases are underventilated, ↑ shunts

Front 59

Ventilation/perfussion relationship at the apex of the lungs

Back 59

Blood flow is lower than ventilation, the relationship is more than 0.8; the apex are overventilated, ↑ dead space

Front 60

What does a ventilation/perfussion relationship under and over 0.8 mean?

Back 60

Under 0.8 (at the bases) lungs are underventilated and less gas exchange takes place, therefore PACO2 and end-capillary PCO2 will be higher and PAO2 and end-capillary PO2 will be lower.

Front 61

What is hypoxic vasoconstriction?

Back 61

A decrease in PAO2 causes vasoconstriction and shunting of blood through that segment.

Front 62

What is the effect of a thrombus in a pulmonary artery?

Back 62

Blood flow decreases, therefore ↑ Va/Q --> ↓ PACO2, ↑ PAO2

Front 63

What is the effect of a foreign object occluding a terminal bronchi?

Back 63

Ventilation decreases, therefore ↓ Va/Q --> ↑ PACO2, ↓ PAO2

Front 64

What constitutes a pulmonary shunt?

Back 64

Regions of the lung where blood is not ventilated. Low Va/Q relationship.

Front 65

What constitutes alveolar dead space?

Back 65

Regions of the lung where there's no blood flow in spite of ventilation. High Va/Q relantionship

Front 66

Va/Q > 0.8

Back 66

Represents alveolar dead space. Can be reversed with supplemental O2

Front 67

Va/Q < 0.8

Back 67

Represents a pulmonary shunt. Cannot be reversed with supplemental O2

Front 68

What is the normal A-a gradient?

Back 68

5-10 mmHg

Front 69

Hypoventilation

Back 69

↓ PAO2 but diffusion and A-a gradient are normal. Perfusion-limited defect.

Front 70

What is a perfussion-limited defect?

Back 70

There's a lung problem but A-a gradient is normal

Front 71

What is a diffusion-limited defect?

Back 71

There's a lung problem where A-a gradient is below normal, therefore diffusion isn't normal

Front 72

Diffusion impairment lung defect

Back 72

Due to structural problem (↑ thickness or ↓ surface area). A-a gradient is more than normal. Supplemental oxygen compensates structural deficit but increased A-a gradient remains. Fibrosis, emphysema.

Front 73

Diffusion capacity of the lung

Back 73

Its measured with CO because it's a diffusion-limited gas. Structural problems decrease CO uptake. It's an index of surface area and membrane thickness.

Front 74

Pulmonary right-left shunt

Back 74

↓ Va/Q. Ther is an increased A-a gradient that is unresponsive to supplemental O2. Atelectasis or ARDS.

Front 75

PO2 in atrial septal defect

Back 75

↑ Right atrial PO2, ↑ right ventricular PO2, ↑ pulmonary artery PO2, ↑ pulmonary blood flow and pressure

Front 76

PO2 in ventricular septal defect

Back 76

No change in right atrial PO2, ↑ right ventricular PO2, ↑ pulmonary artery PO2, ↑ pulmonary flow and pressure

Front 77

PO2 in patent ductus arteriosus

Back 77

No change in right atrial PO2 nor right ventricular PO2, ↑ pulmonary artery PO2, ↑ pulmonary flow and pressure