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Pulmonology Final > Physio > Flashcards

Physio Flashcards

1
Q

Tidal Volume (Vt)

A

the normal inspired/expired volume during one breath

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2
Q

Inspiratory Reserve Volume (IRV)

A

The volume inspired above the tidal volume

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3
Q

Expiratory Reserve Volume (ERV)

A

The volume expired below the tidal volume

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4
Q

Residual Volume (RV)

A

The volume that is left in the lungs after the ERV (maximal expiration) *cannot be measured by spirometry

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5
Q

Anatomic Dead Space

A

The air in the conducting portions of the lungs. Conducting segments contain no alveoli and therefore do not participate in gas exchange. Typically arorund 150 ml. Use body weight to approximate.

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6
Q

Physiological Dead Space (Vd)

A

The volume of the lungs that does not participate in gas exchange. Includes anatomic dead space and alveolar dead space
Calculated by
Vd= Vt x ((PAco2 - PEco2)/PAco2)

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7
Q

Minute Ventilation

A

Tidal volume multiplied by respiratory rate

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8
Q

Alveolar Ventilation (VA)

A

VA is calculated by Taking tidal volume and subtracting the volume of dead space and then multiplying that amount by respiratory rate
VA=(Vt-Vd) x RR

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9
Q

Inspiratory Capacity

A

Vt + IRV

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10
Q

Functional Residual Capacity (FRC)

A

ERV + RV

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11
Q

Vital Capacity (VC or FVC)

A

IRV + ERV + Vt

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12
Q

Total Lung Capacity (TLC)

A

Vt + IRV + ERV + RV

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13
Q

FEV1

A

The forced expiration volume in 1 second. This amount is measured by having someone take a deep breath and blowing it out as quickly as possible. A person can typically blow out 80% of FVC in the first second.

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14
Q

FEV1/FVC ratio

A

The ratio of forced lung expiration. This ratio will change with obstructive and restrictive lung diseases

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15
Q

Decreased FEV1/FVC

A

Seen in Obstructive lung diseases such as asthma or COPD. In this case, both FVC and FEV1 are decreased. However FEV1 is decreased more so the ratio is decreased. (due to the increased amount of air trapped in the lungs= decrease in elasticity and impaired ability to expire quickly

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16
Q

Increased FEV1/FVC

A

Seen in Restrictive Lung diseases like Fibrosis. In actuality, FVC and FEV1 are reduced. However, FVC is reduced more than FEV1 so we see an increase in the ratio. This is due to restriction to inspiration and greater elasticity of the lungs. Increases the rate in which a person can expire.

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17
Q

Compliance

A

equal to volume divided by pressure

Describes the change in volume for a given change in pressure.

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18
Q

Hysteresis

A

Difference in inspiration vs expiration compliance curves, Due to the need to overcome surface tension forces when inflating the lungs

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19
Q

Pathological increase in compliance

A

Emphysema- At FRC, lung compliance is increased and the tendency of the lung to collapse is decreased. Therefore, the lung will seek a higher volume (Higher FRC) to rebalance these forces. Chest becomes barrel shaped, reflecting the increase in volume

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20
Q

Pathological decrease in compliance

A

Fibrosis- At FRC, lung compliance is decreased and the tendency of the lungs to collapse is increased. Therefore, the lung will seek a lower volume (lower FRC) to rebalance these forces.

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21
Q

Laplace’s Law

A

P=2T/r
P= collapsing pressure
T= surface tension
r= radius

With this is mind, large alveoli (large r) have low collapsing pressures. Small alveoli (small r) have high collapsing pressures.

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22
Q

Surface tension

A

results from the attractive forces between liquid molecules lining the alveoli at the air-liquid interface

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23
Q

Surfactant

A

reduces surface tension, increases compliance. Keeps small alveoli from collapsing. Synthesized by Type II alveolar cells.

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24
Q

Airflow (Q)

A

driven by and directly proportional to the pressure difference between the mouth and lungs. and inversely proportional to airway resistance.
Q= The change in pressure/resistance

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25
Q

Airway Resistance (R)

A

R=8nL/(Pi x r^4)

Just know that a small change in radius results in a large change in resistance

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26
Q

Bronchial smooth muscle

A

Contraction-> Parasympathetic stimulation, irritants, slow reacting substance of anaphylaxis (asthma)
Relaxation-> Sympathetic stimulation, sympathetic agonists (dilate airways via B2 receptors)

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27
Q

Lung Volume and Resistance

A

High volumes are associated with low airway resistance. Low volumes are associated with high airway resistance. (changes associated with changes in radius)

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28
Q

Asthma

A

Obstructive disease. Decreased FEV1/FVC. Increased FRC. Increased compliance

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29
Q

COPD

A

Obstructive Disease. Decreased FEV1/FVC. Increased FRC. Expiration is impaired. Increased compliance

Pink puffers- mild hypoxemia, normocapnia
Blue Bloaters- severe hypoxemia, hypercapnia.

30
Q

Fibrosis

A

Restrictive Disease. Increased FEV1/FVC. Decrease in all lung volumes Decreased compliance

31
Q

O2 dissolved in blood

A

PO2(partial pressure of O2 in blood- 100mmHg) x Solubility of O2 in blood (0.003 ml O2/ 100 mL/ mmHg) = 0.3ml O2/dL blood/100mmHg

32
Q

CO2 dissolved in blood

A

PCO2(partial pressure of CO2 in blood- 45mmHg) x Solubility of CO2 in blood (6ml CO2/dL blood/100mmHg) = 2.7mL CO2/dL blood/ 100mmHG

33
Q

Diffusion of gases

A

Ficks law- Vdot= DL x the change in partial pressure
Vdot= volume of gas transferred per minute
DL= lung diffusing capacity
The change in P=partial pressure difference of gas

This results in the diffusion rates of O2 and CO2 depend on the partial pressure differences across the membrane and the area available for diffusion

34
Q

Lung diffusing capacity (DL)

A

increases during exercise- more capillaries open thus more surface area
Decreases in emphysema due to decreased surface area, fibrosis and pulmonary edema due to increased diffusion distance

35
Q

When PO2 is 100mmHg. Hemoglobin is

A

100% saturated

36
Q

When PO2 is 40mmHg. Hemoglobin is

A

75% saturated

37
Q

When PO2 is 25mmHg. Hemoglobin is

A

50% saturated

38
Q

Factors that shift the hemoglobin-O2 dissociation curve

A

pH, temperature, DPG conc, PCO2

39
Q

Right shift of Hem-O2

A

Increase in PCO2, DPG, and temp. Decrease in pH (more acidic) P50 of dissociation curve is increased

40
Q

Left shift of Hem-O2

A

Decrease in PCO2, DPG, and temp. Increase in pH (more alkalotic) P50 of dissociation curve is decreased. CO poisoning

41
Q

Hypoxic hypoxia

A

In this form of hypoxia, the PaO2 is below normal because either the alveolar PO2 is reduced (e.g environmental reasons such as altitude) or the blood is unable to equilibrate fully with the alveolar air (e.g. as would occur in lung diseases with diffusion impairments such as emphysema or fibrosis).

42
Q

Anemic hypoxia

A

In this form of hypoxia, the lungs are in perfect working condition, but the oxygen carrying capacity of the blood has been reduced. Seen in CO poisioning

43
Q

Circulatory hypoxia

A

In this form of hypoxia the lungs are working just fine and the blood can carry sufficient oxygen. However, the tissue is not receiving sufficient oxygen because the heart cannot pump the blood to the tissue (or the arteries leading to the tissue have been blocked by clots etc…). Sickle cell anemia can lead to circulatory hypoxia as the cells sickle in the blood vessels and block them.

44
Q

Histotoxic hypoxia

A

In this form of hypoxia, there is no problem getting the oxygen to the tissue - the lungs, blood and circulatory system are all working just fine. However, the tissue is unable to use the oxygen. Cyanide leads to histotoxic hypoxia by poisoning the systems that utilize oxygen to create energy and preventing them from using the oxygen.

45
Q

Alveolar- arterial Gradient

A

A-a= PAO2-PaO2

46
Q

Alveolar gas equation

A

PAO2= PIO2- PACO2/R

47
Q

Erythropoietin

A

Growth factor synthesized in the kidneys in response to hypoxia. Decreased O2 delivery to kidneys causes increased production of hypoxia-inducible factor 1alpha

48
Q

CO2 transport as HCO3-

A

CO2 generated in tissues diffuses freely into plasma and then into RBC. Carbonic anhydrase in RBCs combines CO2 with water to from H2CO3. This dissociates into H+ and HCO3-. HCO3- leaves RBC in exchange for Cl-. (chloride shift) In the lungs, the reverse reaction takes place

49
Q

V/Q ratio

A

Ratio of alveolar ventilation to pulmonary blood flow. Good matching of the V/Q is critical in effective gas exchange

50
Q

V/Q ratio in airway obstruction

A

Airway is completely blocked. V/Q is zero. no gas exchange. therefore blood will approach values of mixed venous blood. 40 and 46 mmHg

51
Q

V/Q ratio in pulmonary embolism

A

no blood flow. V/Q is infinite aka dead space. no gas exchange. PO2 and PCO2 will approach atmospheric values 150 and 0 mmHg

52
Q

Dorsal Respiratory group

A

Medullary

Depth of breathing (tidal volume)

53
Q

Pre- Botzinger

A

Medullary

Generates Core rhythm

54
Q

Pontine Respiratory Group

A

Pons

Modifies inspiratory timing (activity->turns of inspiration)

55
Q

Ventral Respiratory Group

A

Medullary
Inspiration and Expiration
Depth

56
Q

Central Chemoreceptor

A

Located in the medulla

Stimulated by a decrease in pH or an Increase in pCO2

57
Q

Peripheral Chemoreceptor

A

Located in Carotid and Aortic bodies

Stimulated by a decrease in PO2 (less than 60mmHg), decrease in pH or an increase in PCO2

58
Q

Lung stretch receptors

A

located in the smooth muscle of the airways

when stimulated by distension of the lungs, they produce a reflex decrease in breathing frequency

59
Q

Irritant receptors

A

located between airway epithelial cells

are stimulated by noxious substances (dusts, pollen etc)

60
Q

J (juxtacapillary) receptors

A

located in the alveolar walls, close to capillaries

Stimulated by engorgement of the pulmonary capillaries from left heart failure. Results in rapid shallow breathing

61
Q

Joint and muscle receptors

A

activated by movement of limbs. Involved in early stimulation of breathing during exercise

62
Q

Alveolar Capillaries

A

Bring blood to participate in blood gas exchange. DO NOT supply the lung tissues. Come from the Right Ventricle

63
Q

Extra-Alveolar Capillaries

A

Bring blood to supply the lung tissues. Come from the Left ventricle.

64
Q

Nitric Oxide

A

made by the endothelium
causes smooth muscle relaxation and vasodilation
significant role in normal pulmonary blood flow

65
Q

Endothelin 1

A

made in the lungs
vasoconstrictor
seems to be a player in pathologic conditions. not present under normal circumstances

66
Q

Thromboxane A2

A

in the same category as Endothelin 1. Shouldnt be present in normal scenarios.

67
Q

Measuring DLO2

A

Use CO, conversion factor is 1.23

DLO2= 1.23 x DLCO

68
Q

Oxygen carrying capacity

A

Hemoglobin concentration x 1.34 mL O2/ g hb

69
Q

PIO2

A

PIO2= (barometric pressure - water vapor) x O2 partial pressure 21%

70
Q

Centriacinar Emphysema

A

Primarily the respiratory bronchiole (proximal and central part of the acinus is expanded), the distal acinus or alveoli are unchanged
Most common type of emphysema. Seen in cigarette smokers

71
Q

Panacinar Emphysema

A

Seen in alpha 1 antitrypsin deficiency. Affects the entire acinus. From the respiratory bronchiole to the alveoli. Due to the lack of inhibition of Elastase, which will break down elastic fibers in the lungs

Pulmonology Final (1 decks)

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