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CVPR > cvpr first Respiratory physiology > Flashcards

cvpr first Respiratory physiology Flashcards

1
Q

Lung volumes vs capacities

A

A capacity is a sum of ≥ 2 physiologic volumes

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2
Q

What is inspiratory reserve volume

A

Air that can still be breathed in after normal inspiration

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3
Q

What is tidal volume?

A

Air that moves into lung with each quiet inspiration

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4
Q

Average tidal volume

A

≈ 500 mL

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5
Q

What is expiratory reserve volume

A

Air that can still be breathed out after normal expiration

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6
Q

What is residual volume

A

Air in lung at the end of maximal expiration RV and any lung capacity that includes RV cannot be measured by spirometry

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7
Q

What is inspiratory capacity

A

IRV + TV Air that can be breathed in after normal exhalation

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8
Q

What is functional residual capacity

A

Volume of gas in lungs after normal expiration

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9
Q

What is vital capacity

A

TV + IRV + ERV Maximum volume of gas that can be expired after a maximal inpiration

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10
Q

What is total lung capacity?

A

IRV + TV + ERV + RV Volume of gas present in lungs after maximal inspiration

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11
Q

Lung capacities figure

A

646

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12
Q

Equation to determination of physiologic dead space

A

VD = VT x (PaCO2 - PECO2) / (PaCO2)

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13
Q

What is VD?

A

Physiologic dead space = anatomic dead space (dead space of conducting airways) + alveolar dead space (unventilated or unperfused dead space)

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14
Q

VT =

A

tidal volume

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15
Q

PaCO2 =

A

arterial PCO2

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16
Q

PECO2

A

Expired PCO2

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17
Q

Mnemonic of determining physiologic dead space

A

Taco, Paco, Peco, Paco Refers to the order of the variables in the equation

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18
Q

Physiologic dead space

A

approximately equivalent to anatomic dead space in normal lungs May be greater than anatomic dead space in lung diseases with V/Q effects

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19
Q

Describe minute ventilation

A

Total volume of gas entering lungs per minute VE = VT x RR

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20
Q

Describe alveolar ventilation

A

Volume of gas that reaches alveoli each minute VA = (VT-VD) x RR

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21
Q

Normal respiratory volumes

A

RR: 12-20 breaths/min VT = 500 mL/breath VD = 150 mL/breath

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22
Q

Describe elastic recoil

A

Tendency for lungs to collapse inward and chest wall to spring outward

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23
Q

Describe lung and chestwall forces at FRC

A

Inward pull of lung is balanced by outward pull of chest wall and atmospheric system pressure

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24
Q

Describe airway and alveolar forces at FRC

A

Airway and alveolar pressures equal atmospheric pressure (called zero) and intrapleural pressure is negative (prevents atelectasis) The inward pull of the lung is balanced by the outward pull of the chest wall System pressure is atmmospheric PVR is at a minimum

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25
Q

Describe compliance

A

Change in lung volume for a change in pressure

Expressed as ΔV/ΔP

inversely proportional to wall stiffness

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26
Q

Describe high compliance

A

High-compliance = lung easier to fill

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27
Q

Describe low compliance

A

Low compliance = lung is more difficult to fill

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28
Q

What kind of things can cause high compliance

A

emphysema

normal aging

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29
Q

What kind of things can cause low compliance

4 listed

A
  • pulmonary fibrosis
  • pneumonia
  • NRDS
  • pulmonary edema
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30
Q

Surfactant effect on lung compliance

A

increases lung compliance and reduces lung recoil reducing the likelihood of alveolar collapse

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31
Q

Compliance is inversely proportionate to

A

inversely proportional to wall stiffness

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32
Q

What is hysteresis

A

Lung inflation curve follows a different curve than the lung deflation curve due to need to overcome surface tension forces in inflation

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33
Q

Respiratory system changes in the elderly

8 listed

A

↑ lung compliance

↓ chest wall compliance

↑ RV

↓ FVC and FEV

Normal TLC

↑ ventilation/perfusion mismatch (V/Q mismatch)

↑ A-a gradient

↓ respiratory muscle strength

34
Q

Describe hemoglobin

A

Hb is composed of 4 polypeptide subunits 2-α and 2-β and exists in 2 forms

Deoxygenated form has low affinity for O2 thus promoting release/unloading of O2

Oxygenated form has high affinity for O2 (300x) Hb exhibits positive cooperativity and negative allostery

↑Cl, H, CO2, 2,3-BPG and temperature favor deoxygenated form over oxygenated form (shifts dissociation curve → ↑O2 unloading

35
Q

Hemoglobin O2 binding properties

A

Exists in 2 forms:

Deoxygenated form has low-affinity for O2 thus promoting release/unloading of O2

Oxygenated form has a high-affinity for O2 (300x)

Hb exhibits positive cooperativity and negative allostery ↑Cl, H, CO2, 2,3-BPG and temperature favor deoxygenated form over oxygenated form (shifts dissociation curve → ↑O2 unloading

36
Q

Hb deoxygenated form is favored by?

5 listed

A

↑Cl-

↑H+

↑CO2

↑2,3-BPG

↑temperature

(shifts dissociation curve → ↑O2 unloading

37
Q

Hb oxygenated form is favored by?

5 listed

A

↓Cl-

↓H+,

↓CO2

↓2,3-BPG

↓temperature

(shifts dissociation curve ← ↑O2 binding

38
Q

Hb acid-base properties

A

acts as a buffer for H ions

39
Q

Hemoglobin structure

A

Hb is composed of 4 polypeptide subunits 2-α and 2-β

40
Q

Hemoglobin modifications

A

Lead to tissue hypoxia from ↓O2 saturation and ↓O2 content

41
Q

Methemoglobin

A

The oxidized form of Hb (ferric, Fe) does not bind O2 as readily as Fe but has

↑ affinity for cyanide

With methemoglobinemia, the hemoglobin can carry oxygen, but is not able to release it effectively to body tissues.

Fe binds O2 Iron in Hb is normally in a reduced state (ferrous Fe “just the 2 of us”)

42
Q

Causes of methemoglobinemia

A

Inherited

Type 1 (also called erythrocyte reductase deficiency) occurs when RBCs lack the enzyme.

Type 2 (also called generalized reductase deficiency) occurs when the enzyme doesn’t work in the body.

Acquired

Anesthetics such as benzocaine

Nitrobenzene

Certain antibiotics (including dapsone and chloroquine)

Nitrites (used as additives to prevent meat from spoiling)

43
Q

Treatment of methemoglobinemia

A

Methemoglobinemia can be treated with methylene blue and vitamin C

44
Q

Carboxyhemoglobin is caused by?

A

CO poisoning

45
Q

What is carboxyhemoglobin?

A

Form of Hb bound to CO in place of O2 (CO poisoning)

46
Q

Common causes of CO poisoning

A

May be caused by fires, car exhaust or gas heaters

47
Q

Presentation of CO poisoning

3 listed

A

CO poisoning can present with

  • headaches
  • dizziness
  • cherry red skin
48
Q

Treatment of CO poisoning

A

100% O2 and hyperbaric O2

49
Q

Causes of cyanide poisoning

A

Usually due to inhalation injury (eg fires)

50
Q

Presentation of cyanide poisoning

4 listed

A
  • Almond breath odor
  • Pink skin
  • Cyanosis
  • Rapidly fatal if untreated
51
Q

Treatment of cyanide poisoning

A

Treat with induced methemoglobinemia:

  1. First give nitrates (oxidize hemoglobin to methemoglobin, which can trap cyanide as cyanmethemoglobin),
  2. then thiosulfates (convert cyanide to thiocyanate which is excreted by the renal system)
52
Q

Describe the shape of the O2-Hb dissociation curve

A

Sigmoidal shape due to positive cooperativity (ie tetrameric hb molecule can bind 4O2 molecules and has higher affinity for each subsequent O2 molecule bound

53
Q

Shifting O2-Hb dissociation curve to the right leads to

A

↓ Hb affinity for O2 (facilitates unloading of O2 into tissues) → ↑P50 (higher Po2 required to maintain 50% saturation

54
Q

Elderly lung compliance

A

↑ lung compliance

55
Q

Shifting O2-Hb dissociation curve to the left leads to

A

↑ Hb affinity for O2 (facilitates Hb binding of O2)

↓ O2 unloading → renal hypoxia → ↑ EPO synthesis → compensatory erythrocytosis → ↓P50 (lower Po2 required to maintain 50% saturation)

56
Q

O2-Myoglobin dissociation curve shape

A

Myoglobin is monomeric and thus does not show positive cooperativity: curve lacks sigmoidal appearance

57
Q

Describe fetal Hb

A

Fetal Hb has higher affinity for O2 than adult Hb (due to low affinity for O2 than adult Hb (due to low affinity for 2, 3-BPG) So its dissociation curve is shifted left

58
Q

Describe left and right shifts of O2-Hb dissociation curves

59
Q

Oxygen content of the blood equation

A

O2 content = (1.34 x Hb x SaO2) + (0.003 x PaO2)

Hb = hemoglobin level

SaO2 = arterial O2 saturation

PaO2 = partial pressure of O2 in arterial blood

60
Q

Typical binding capacity of Hb

A

1 g Hb can bind 1.34 mL O2

61
Q

Typically amount of Hb in blood

A

normal Hb amount in blood is 15g/dL

62
Q

O2 binding capacity

A

20.1 mL O2/dL of blood

63
Q

Anemia Hb and O2 values

A

With ↓ Hb there is ↓O2 content of arterial blood but no change in O2 saturation and PaO2

64
Q

O2 delivery to tissues =

A

cardiac output x O2 content of blood

65
Q

Hb concentration in CO poisoning

66
Q

Hb concentration in Anemia

67
Q

Hb concentration in polycythemia

68
Q

CO poisoning and % O2 sat of Hb

A

↓ (CO competes with O2)

69
Q

Anemia and % O2 sat of Hb

70
Q

Polycythemia and % O2 sat of Hb

71
Q

CO poisoning dissolved O2 (PaO2)

72
Q

CO poisoning Total O2 content

73
Q

Anemia Dissolved O2 (PaO2)

74
Q

Anemia Total O2 content

75
Q

Polycythemia dissolved O2 (PaO2)

76
Q

Polycythemia Total O2 content

77
Q

Describe the pulmonary circulation

A

Normally a low-resistance, high-compliance system

78
Q

PaO2 and PaCO2 effects on pulmonary vasculature

A

Exert opposite effects on pulmonary and systemic vasculature

↓PaO2 causes hypoxic vasoconstriction that shifts blood away from poorly ventilated regions of lung to better ventilated regions of the lung

79
Q

What is anatomic deadspace?

A

anatomic dead space (dead space of conducting airways)

80
Q

What is alveolar dead space

A

alveolar dead space (unventilated or unperfused dead space)

81
Q

Effects of carboxyhemoglobin

A

↓ O2-binding capacity with left shift in O2Hb dissociation curve

↓O2 unloading in tissues CO binds competitively to Hb and with 200x greater affinity than O2

CO poisoning can present with headaches dizziness and cherry red skin May be caused by fires, car exhaust or gas heaters

82
Q

Effects of cyanide poisoning

A

Inhibits aerobic metabolism via complex IV inhibition → hypoxia unresponsive to supplemental O2 and ↑ aerobic metabolism

CVPR (93 decks)

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