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BRS Physio > Respiratory Physiology > Flashcards

Respiratory Physiology Flashcards

1
Q

Volume of air inspired or expired with each NORMAL breath

A

Tidal Volume

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2
Q

Volume that can be inspired above the tidal volume (used with exercise)

A

inspiratory reserve volume

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3
Q

volume that can be exhaled after expiration of tidal volume

A

expiratory reserve volume

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4
Q

volume in the lungs after maximal expiration

A

residual volume (not measured with spirometry)

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5
Q

Anatomic Dead Space

A

volume of conducting airways, ~150mL

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6
Q

Physiologic Dead Space

A

volume of lungs that doesn’t participate in gas exchange
Vd = Vt*[(PaCO2 - PeCO2)/PaCO2]
Vt is tidal volume
PaCO2 is pCO2 of alveolar gas or arterial blood
PeCO2 is pCO2 of expired air

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7
Q

Minute ventilation

A

tidal volume * breaths/min

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8
Q

Alveolar ventilation

A

(tidal vol - dead space) - breaths/min

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9
Q

volume remaining in lungs after tidal volume expiration

A

functional residual capacity (not measured by spirometry)

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10
Q

Volume of air that can be forcibly expired after a maximal inspiration

A

forced vital capacity

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11
Q

volume of air that can be expired in the 1st second of forced max expiration

A

FEV1, normal 80% of FVC

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12
Q

FEV1/FVC in obstructive lung disease

A

FEV1 is reduced more than FVC so it is DECREASED

ex. asthma

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13
Q

FEV1/FVC in restrictive lung disease

A

FEV1 and FVC are reduced so it is NORMAL or INCREASED

ex. fibrosis

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14
Q

external intercostals and accessory muscles

A

used during exercise and respiratory distress for inspiration

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15
Q

Abdominal muscle and internal intercostals

A

expiratory muscles in exercise or airway resistance like asthma

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16
Q

the distensibility of the lungs and chest wall, is inversely related to elastance

A

compliance of respiratory system

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17
Q

alveolar pressure - intrapleural pressure

A

transmural pressure of lung

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18
Q

hysteresis

A

inflation of a lung follows a different curve than deflation

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19
Q

At FRC, collapsing force of chest wall and expanding force of lung pressures are:

A

equal and opposite, thus the lung-chest wall system neither wants to collapse or expand

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20
Q

Pneumothorax

A

air is introduced into the intrapleural space, intrapleural pressure becomes equal with atmospheric pressure and lung collapses while chest wall expands

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21
Q

disease with increased lung compliance and lungs expand

A

emphysema, higher FRC

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22
Q

disease where lung compliance is decreased and tendency for lungs to collapse is increased

A

fibrosis, lower FRC

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23
Q

small alveoli

A

high colapsing pressures, need higher amounts of surfactant

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24
Q

LaPlace Law on Alveoli

A

P = (2T)/r
P is collapsing pressure (pressure to alveoli open)
T is surface tension
r is radius

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25
Q

dipalmitoyl phosphatidylcholine

A

main component of surfactant used to reduce surface tension, increases compliance, esp in small alveoli
starts being produced at week 24

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26
Q

Major site of airway resistance

A

medium-sized bronchi (not small airways because of parallel arrangement)

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27
Q

At rest before inspiration begins

  • alveolar pressure
  • intrapleural pressure
  • Lung Volume
A

Alveolar pressure - atm pressure, said to be zero
intrapleural pressure is negative
lung volume is FRC

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28
Q

During Inspiration

  • alveolar pressure
  • intrapleural pressure
  • Lung Volume
A

As lung lung increases, alveolar pressure will decrease to less than atm pressure (negative) allowing air to enter
intrapleural pressure becomes more negative
lung volume FRC + TV

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29
Q

During expiration

  • alveolar pressure
  • intrapleural pressure
  • Lung Volume
A

alveolar pressure greater than atm pressure (more positive) so air flows out of lungs
intrapleural pressure is returns to normal (negative) unless it is forced expiration then it is (+) to squeeze out air
lung volume returns to FRC

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30
Q

pursed lips

A

COPD, to prevent airway collapse

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31
Q

decreased FEV1/FVC

A

COPD and asthma, also have increased FRC

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32
Q

pink puffers

A

emphysema, have mild hypoxemia and normocapnia

air trapping so barrel chested

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33
Q

blue bloaters

A

primarily bronchitis, severe hypoxemia with cyanosis, can’t maintain alveolar ventilation so hypercapnia

34
Q

decrease lung compliance in which inspiration is impaired

A

fibrosis, a restrictive lung disease

FEV1/FVC is normal or increased

35
Q

dry inspired air partial pressure of O2

A

160mmHg

36
Q

humidified inspired air partial pressure of O2

A

150mmHg
this is because partial pressure of H2O is 47mmHg
so 760-47 = 713mmHg
713mmHg*0.21 = 150mmHg

37
Q

Ferrous state

A

Fe2+ binds oxygen

38
Q

Ferric State

A

Methemoglobin, Fe3+, doesn’t bind O2

39
Q

O2 affinity to fetal Hb

A

higher than adult. left shift

allows fetus to take mother’s oxygen

40
Q

pO2 of 100mmHg (arterial blood)

A

Hb is 100% saturated, O2 is bound to all 4 heme groups

41
Q

pO2 40mmHg (mixed venous blood)

A

Hb is 75% saturated, O2 is bound to 3 of 4 heme groups

42
Q

pO2 25mmHg

A

Hb is 50% saturated, O2 is bound to 2 of 4 heme groups

43
Q

Positive cooperativity

A

change of affinity of Hb as each successive O2 binds to heme site, affinity for 4th O2 molecule is highest

44
Q

Right shift of Hb-O2 curve

A

affinity for oxygen is decrease, P50 is increased
increase in pCO2 or decreases in pH (during exercise)
increase in temperature (durin exercise)
increase in 2,3-DPG

45
Q

living at a high altitude

A

increase in 2,3-DPG as adaptation to chronic hypoxemia

Right shift of Hb-O2 curve

46
Q

Left shift of Hb-O2 curve

A

affinity for oxygen is increase, P50 is decreased
decreased pCO2, increased pH, decreased temperature, decreased 2,3-DPG (esp HbF)
CO poisoning

47
Q

A-a gradient

A

difference between alveolar (A) and arterial (a) pO2

normal is <10mmHg

48
Q

Causes of increased A-a gradient (>10mmHg)

A

diffusion defect like fibrosis, V/Q defect, right-to-left shint

49
Q

decreased O2 delivery to the tissues

A

hypoxia

50
Q

major form of CO2 in the blood

A

HCO3-

51
Q

Pulmonary blood flow when patient is supine

A

nearly uniform throughout lung

52
Q

Pulmonary blood flow if standing

A

lowest at apex and highest at base

53
Q

Zone 1 of lung (apex)

A

Alveolar pressure > arterial pressure > venous pressure

high alveolar pressure may compress capillaries and decrease blood flow

54
Q

Zone 2 of lung (middle)

A

arterial pressure > alveolar pressure> venous pressure

blood flow is driven by difference between arterial pressure and alveolar pressure

55
Q

Zone 3 of lung (base)

A

arterial pressure> venous pressure > alveolar pressure

blood flow is driven by difference between arterial pressure and venous pressure

56
Q

hypoxia in lungs

A

vasoconstriction to get blood to more oxygenated areas of the lung

57
Q

fetal respiratory resistance

A

high from generalized hypoxemia until first breath

58
Q

Right-to-left shunt

A

tetralogy of Fallot
decrease in arterial pO2
admixture of venous blood with arterial blood

59
Q

Left-to-right shunt

A

patent ductus arteriosis

pO2 will be elevated on right side of heart because mixture of arterial blood with venous blood

60
Q

V/Q ratio

A

ventilation/perfusion, ~0.8
arterial pO2 is 100mmHg
arterial pCO2 is 40mmHg

61
Q

V/Q at apex of lung

A

higher V/Q, pO2 is highest and pCO2 is lowest because more gas exchange
blood flow loest, ventilation lower

62
Q

V/Q at base of lung

A

lower V/Q, pO2 is lowest and pCO2 is highest because there is less gas exchange
bloof flow highest, higher ventilation

63
Q

Shunt

A

Airway blocked, blood flow is normal
V/Q is zero
increased A-a gradient

64
Q

Dead Space

A

Blood flow is blocked, ventilation is normal
V/Q is infinite
Ex. pulmonary embolism

65
Q

Input to dorsal respiratory group

A

vagus - from peropheral chemoreceptors and mechanoreceptors in lung
glossopharyngeal - from peripheral chemoreceptors

66
Q

Output from dorsal respiratory group

A

via phrenic nerve t othe diaphragm

67
Q

primarily responsible for inspiration and generates the basic rhythm for breathing

A

Dorsal respiratory group

68
Q

Primarily responsible for expiration

A

ventral respiratory group, not active in normal or quiet breathing

69
Q

stimulates inspiration, produces a deep and prolonged inspiratory gasp

A

Apneustic center in LOWER pons

70
Q

inhibits inspiration, regulates inspiratory colume and respiratory rate

A

pneumotaxic center in UPPER pons

71
Q

breathing under voluntary control

A

cerebral cortex

72
Q

Central chemoreceptors in the medulla

A

sensitive to pH
decrease in pH of the CSF produces hyperventilation
CO2 crosses BBB, combines with H2O and makes H+ and HCO3 in CSF

73
Q

Peripheral chemoreceptors in carotid and aortic bodies

A

pO2 <60mmHg will cause an increase in breathing rate

pCO2 can increase breathing and increases in arterial H+

74
Q

Hering-Breuer Reflex

A

Lung stretch receptors in smooth muscle of airways, stimulated by distention of lungs to decrease breathing frequency

75
Q

J receptors

A

juxtacapillary receptors, located in alveolar walls close to capillaries
engorgement of pulmonary capillaries, like in left heart failure, stimulates the J receptors, cause rapid, shallow breathing

76
Q

joint and muscle receptors

A

activated during movement of the limbs

involved in the early stimulation of breathing during exercise

77
Q

Exercise and ventilatory rate

A

during exercise, there is an increase in ventilatory rate that matches the increase in O2 consumption and CO2 production by the body.

78
Q

changes in pO2 and pCO2 during exercise

A

mean values for pO2 and pCO2 do not change during exercise

79
Q

Adaptation to high altitudes

A

alveolar pO2 is decreased
hypoxemia stimulates the peripheral chemoreceptors (hyperventilation, respiratory alkalosis)
increase erythropoietin, increase 2,3-DPG, pulmonary vasoconstriction

80
Q

Snack that smiles back

A

Goldfish

BRS Physio (7 decks)

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