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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
Describe compliance
Change in lung volume for a change in pressure Expressed as ΔV/ΔP inversely proportional to wall stiffness
26
Describe high compliance
High-compliance = lung easier to fill
27
Describe low compliance
Low compliance = lung is more difficult to fill
28
What kind of things can cause high compliance
emphysema normal aging
29
What kind of things can cause low compliance 4 listed
* pulmonary fibrosis * pneumonia * NRDS * pulmonary edema
30
Surfactant effect on lung compliance
increases lung compliance and reduces lung recoil reducing the likelihood of alveolar collapse
31
Compliance is inversely proportionate to
inversely proportional to wall stiffness
32
What is hysteresis
Lung inflation curve follows a different curve than the lung deflation curve due to need to overcome surface tension forces in inflation
33
Respiratory system changes in the elderly 8 listed
↑ lung compliance ↓ chest wall compliance ↑ RV ↓ FVC and FEV Normal TLC ↑ ventilation/perfusion mismatch (V/Q mismatch) ↑ A-a gradient ↓ respiratory muscle strength
34
Describe hemoglobin
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
Hemoglobin O2 binding properties
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
Hb deoxygenated form is favored by? 5 listed
↑Cl- ↑H+ ↑CO2 ↑2,3-BPG ↑temperature (shifts dissociation curve → ↑O2 unloading
37
Hb oxygenated form is favored by? 5 listed
↓Cl- ↓H+, ↓CO2 ↓2,3-BPG ↓temperature (shifts dissociation curve ← ↑O2 binding
38
Hb acid-base properties
acts as a buffer for H ions
39
Hemoglobin structure
Hb is composed of 4 polypeptide subunits 2-α and 2-β
40
Hemoglobin modifications
Lead to tissue hypoxia from ↓O2 saturation and ↓O2 content
41
Methemoglobin
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
Causes of methemoglobinemia
**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
Treatment of methemoglobinemia
Methemoglobinemia can be treated with methylene blue and vitamin C
44
Carboxyhemoglobin is caused by?
CO poisoning
45
What is carboxyhemoglobin?
Form of Hb bound to CO in place of O2 (CO poisoning)
46
Common causes of CO poisoning
May be caused by fires, car exhaust or gas heaters
47
Presentation of CO poisoning 3 listed
CO poisoning can present with * headaches * dizziness * cherry red skin
48
Treatment of CO poisoning
100% O2 and hyperbaric O2
49
Causes of cyanide poisoning
Usually due to inhalation injury (eg fires)
50
Presentation of cyanide poisoning 4 listed
* Almond breath odor * Pink skin * Cyanosis * Rapidly fatal if untreated
51
Treatment of cyanide poisoning
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
Describe the shape of the O2-Hb dissociation curve
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
Shifting O2-Hb dissociation curve to the right leads to
↓ Hb affinity for O2 (facilitates unloading of O2 into tissues) → ↑P50 (higher Po2 required to maintain 50% saturation
54
Elderly lung compliance
↑ lung compliance
55
Shifting O2-Hb dissociation curve to the left leads to
↑ 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
O2-Myoglobin dissociation curve shape
Myoglobin is monomeric and thus does not show positive cooperativity: curve lacks sigmoidal appearance
57
Describe fetal Hb
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
Describe left and right shifts of O2-Hb dissociation curves
649
59
Oxygen content of the blood equation
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
Typical binding capacity of Hb
1 g Hb can bind 1.34 mL O2
61
Typically amount of Hb in blood
normal Hb amount in blood is 15g/dL
62
O2 binding capacity
20.1 mL O2/dL of blood
63
Anemia Hb and O2 values
With ↓ Hb there is ↓O2 content of arterial blood but no change in O2 saturation and PaO2
64
O2 delivery to tissues =
cardiac output x O2 content of blood
65
Hb concentration in CO poisoning
normal
66
Hb concentration in Anemia
↓
67
Hb concentration in polycythemia
↑
68
CO poisoning and % O2 sat of Hb
↓ (CO competes with O2)
69
Anemia and % O2 sat of Hb
Normal
70
Polycythemia and % O2 sat of Hb
Normal
71
CO poisoning dissolved O2 (PaO2)
Normal
72
CO poisoning Total O2 content
↓
73
Anemia Dissolved O2 (PaO2)
Normal
74
Anemia Total O2 content
↓
75
Polycythemia dissolved O2 (PaO2)
Normal
76
Polycythemia Total O2 content
↑
77
Describe the pulmonary circulation
Normally a low-resistance, high-compliance system
78
PaO2 and PaCO2 effects on pulmonary vasculature
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
What is anatomic deadspace?
anatomic dead space (dead space of conducting airways)
80
What is alveolar dead space
alveolar dead space (unventilated or unperfused dead space)
81
Effects of carboxyhemoglobin
↓ 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
Effects of cyanide poisoning
Inhibits aerobic metabolism via complex IV inhibition → hypoxia unresponsive to supplemental O2 and ↑ aerobic metabolism

CVPR (93 decks)

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