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Physio Lec > Physio cont. > Flashcards

Physio cont. Flashcards

(143 cards)

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1
Q

Dead space origin

A

NO gas exchange in conductive zone

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2
Q

Dead space anatomically

A

volume of conductive zone

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3
Q

Dead space physiologic

A

Anatomic (volume conductive zone) + volume gas NOT equilibrating with blood

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4
Q

Effective ventilation

A

500-150=350ml

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5
Q

Mech relaxation diaphragm

A
  1. contraction diaphragm (goes downwards)
  2. increase volume chest cavity
  3. decrease pulmonary p.
  4. pulmonary < atmos
  5. air flows in
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6
Q

Muscle for normal breathing

A

Diaphagm - vertical movement
Intercoastal - sagittal plane (upwards, outwards)

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7
Q

Muscle for forced ventilation

A

Accessory musculature

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8
Q

Bronchial smooth muscles

A

NOT breathing muscle

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9
Q

Transmitter of breathing

A

acetylcholine

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10
Q

Receptor of breathing

A

nAch
in esophagus: upper 1/3 part skeletal m.

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11
Q

Inhibitors of breathing

A

curare (muslce relaxants)
only for nAchR

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12
Q

Atropin

A

NOT inhibit breathing muscle

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13
Q

Branching networks of airways zone

A

conducting
exchange zone

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14
Q

Conducting zone

A

NO gas exchange

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15
Q

Exchange zone

A

Large surface

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16
Q

Conducting system consists of

A

Trachea
1st bronchi
smaller bronchi

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17
Q

Bronchioles

A

in btw conducting system and exchange surface

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18
Q

Exchange surface

A

Alveoli

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19
Q

Bronchi division no.

A

aroung 12 times

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20
Q

Exchange surface

A

Large cross sectional area
small diameter

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21
Q

Dead space

A

NO gas exchange in conductive zone

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22
Q

Dead space physiologic

A

Anatomic + volume gas NOT equilibrating with blood (in exchange zone)

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23
Q

Long snorkel

A

increase dead space

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24
Q

Effective ventilation “formula”

A

normal inhale - dead space

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25
Effective ventilation values
500 -150= 350ml
26
Alveolar forces
Expanding forces Recoiling forces
27
Expanding forces
lung expands lung elastic tissue expands chest wall expands
28
Recoiling forces
lung recoil
29
Recoiling forces is by
surface tension
30
Surface tension (recoiling force) explaination
Molecules at 2 diff envi -> tend to interxs (clump up) -> decrease surface exposure -> forms surface tension
31
What helps surface tension
surfactant
32
Force on alveolar wall
Pressure pulmon. outwards aganist Pressure intrapleural inwards
33
Intrapleural pressure is
negative (subatmospheric)
34
What does neg intrapleural pressure mean
lower than pressure atmos.
35
Puncture wound in chest wall means, other name
puncture in intrapleural Traumatic pneumothorax
36
Hole in lungs means
hole in intrapulmon. Spontaneous pneumothorax
37
Effect of traumatic pneumothorax and spontaneous pneumothorax
loose neg intrapleural pressure aka intrapleural pressure increase - intrapulmon. pressure the same
38
Func surfactant
reduce surface tension prevent collapse small alveoli distribution air in alveoli prevent lungs collapse
39
Composition pulmon. surfactant
Dipalmitoylphosphatidylcholine (40%) Other phospholipids(40%) (phosphatidylcholine -85% ; phosphatidylglycerol -11%) Surfactant-associated proteins (5-10%) Other substances
40
Mechanism surfactant
counteracts radius effect
41
Effect of surface and intermolecular distance
Reduce surface reduces intermolecular distance
42
How surfactant helps in distribute air in alveoli
if NO surfactant: pressure from small alveoli -> flow to big alveoli YES surfactant: balance
43
Value total lung capacity
5.5L
44
Value func residual capacity +1L FRC1
3.5L
45
Value func residual capacity FRC aka vol. after normal exhale
2.5L
46
Residual volume
1.5L
47
Effect chest at total lung capacity
increase expanding force -> expand (-30-0mmHg)
48
Volume of chest at equilibrium
FRC+1L 3.5L
49
Effect lung at total lung capacity
tend to recoil b/c elastic tissue
50
Equilibrium of chest + lung at
FRC 2.5L (both chest+lungs -> 2 -> 2.5)
51
Tidal volume (L) during inspiration
increase
52
Tidal volume (L) during expiration
decrease
53
Intrapulmon. pressure inspiration
decrease (for pressure intra -> inspire -> decrease)
54
intrapulmon. pressure expiration
increase
55
Intrathoracal/ intrapleural pressure inspiration
decrease
56
Intrathoracal/ intrpleural pressure expiration
increase
57
Lung volume exchange in normal breathing
only 1/6 lung volume exchanged during normal breathing
58
TV
tidal volume
59
ERV
expiratory reserve volume
60
IRV
inspiratory reserve volume
61
RV
residual volume
62
VC /TLC
vital capacity
63
Vital capacity normal value
5.5 -6L
64
What is FVC
Forced vital capacity VC of deep inspiration + fast, forceful expiration (Fvc -> fast, forceful expiration)
65
What is FEV123
Forced expiratory volume volume exhaled air at 1st, 2nd, 3rd second of forceful expiration after deep inspiration
66
Tiffeneuas index
FEV1/FVC ratio
67
PIF PEF
Peak inspiration flow Peak expiration flow
68
Pulmon. ventillation/ minute ventillation/ alveolar ventillation
rate air enters/ leaves lungs
69
Formula pulmonary ventillation/ minute ventillation/ alveolar ventillation
TV * resp rate TV - death space
70
Whats work or breathing
total expenditure E need to breathe
71
Value range work of breathing
accounts 5% total body O2 consumption in rest
72
Work of breathing increase x50 in
increase meta illness
73
Components work of breathing
metabolic activity resp, accessory muscle (85%) thoracis compliance/ elastic resistance (10%) airway resistance/ non elastic resistance (<5%)
74
What is needed for increase ventilation
increase no. muscle/ muscle group
75
Stages metabolic activity resp muscle
1. inhalation: active ; exhalation: passive (quite breathing in rest, moderate physical activity) 2. both inhalation, exhalation active (hard exercise) 3. accessory muslce activated (extreme exercise) 4. support body position/ posture need to maintain minute ventilation
76
Compliance formula
C= delta V/ delta P
77
At high compliance
high surfactant
78
At low compliance
low surfactant
79
What does low compliance, low surfactant mean
high surface tension high recoiling
80
Compliance inhale < Compliance exhale
review notes
81
Restrictive disease
airway: free lung expansion limited aka reduced compliance, vital capacity
82
Intrinsic cause restrictive lung disease
Pulmon. fibrosis/ sarcoidosis Pneumoconiosis: long term exposure dust (asbestosis, silicosis) Pneumonia Acute resp distress syndrome ARDS: NO surfactant
83
Extrinsic cause restrictive lung disease
chest deform rheumatoid diseases reducing expansion of chest diseases restricting thoracic/ abdominal volume (obesity, hernia, ascites) pleural thickening, adhesino
84
Airway resistance mouth to trachea open mouth
35-40%
85
Airway resistance nasl breathing
40-50%
86
Airway resistance trachea to alveolar duct open mouth
60-65%
87
Airway resistance nasal breathing
50-60%
88
Importance of Reynolds no. in determining airway resistance
decrease dia -> decrease R increase longitudinal velocity -> increase R R=pvd/u
89
What happens to flow when increase ventilation
extends zone turbulent flow
90
Conducting zone composed of flow
turbulent transitional half laminar flow
91
Exchange zone composed flow
laminar flow
92
Cause of restrictive lung disease
reduced compliance
93
Cause of obstructuve lung disease
increase airway resistance
94
Conditions of obstructuve lung disease
mechanical airway obstruction (choking) bronchitis (acute/ chronic): hyperplasia, hypersecretion mucus glands asthma (immunologic or idiopathic) excessive mucus production inflammation smooth m. hyperplasia constriction
95
Clinical signs increase work breathing
nasal flaring gasping activation acesspry muscle tracheal tug scalene/ sternomastoid contraction suprasternal/ supraclavicular retraction abdominal muscle contraction paradox chest movements body posture
96
What effects work of breathing
(increase) airway resistance - NON elastic resistance (reduce) compliance - elastic resistance
97
Amount fresh air add to alveolar gas mixture during quite breathing
15%
98
Partial pressure O2 highest to lowest path
inspired air (> expire air ) -> alveolar air- > arteries -> [capillarires - veins]
99
Partial pressure CO2 highest to lowest path
[capillaried - veins] -> [arteries - alveolar air] -> expired air -> inspired air
100
Partial pressure O2 CO2 in arteries
O2: 95mmHg CO2: 40mmHg
101
Partial pressure O2 CO2 in alveolar air
O2: 100mmHg CO2: 40mmHg
102
Driving force for gas
partial pressure differences aka high gradient -> low gradient
103
pO2 trend air - alveoli - blood - tissue
(aabt) air - alveoli - blood - tissue decrease
104
pCO2 trend air - alveoli -blood - tissue
(aabt) air - alveoli - blood - tissue increase
105
Relationship between pO2 and alveolar ventilation
increase O2 utilization rate - increase alveolar ventilation
106
Relationship between pCO2 and alveolar ventillation
increase CO2 production rate - increase alveolar ventillation
107
Ventillation alveolar means
L/min Volume ventilation/ min
108
Ventillation alveolar formula
Va=(Vt-Vd) x Ventilation rate (Tidal volume - dead space)* ventillation rate
109
Rate of gas exchange
fast in pulmon. capillaries
110
Diffusion CO2 compares to O2
Diffusion CO2 > 20X O2
111
O2 saturation arterial blood
95-98%
112
Max O2 transport of blood limited by
blood hemoglobin conc pO2 envi Cardiac output alveolar ventillation (hyperventillatiom NO increase resting O2 saturation significantly)
113
Pathological aspects O2 transport
ventillation malfunc pathologic hemoglobin forms poisons: CO, cyanide
114
Types hypoxia (insuff O2 transport)
1. Hypoxemic 2. Hemoglobin related 3. Stagnant hypoxia 4. Hystotoxic hypoxia 5. Poisons
115
Hypoxemic hypoxia
reduced pO2 in blood
116
Cause of hypoxemic hypoxia
1. envi: high altitude/ reduce pO2 2. ventilation defect: resp control failure (dys central neurons, drug) 3. diffusion problems: reduced exchange surface/ diffusion rate
117
Hemoglobin related hypoxia
1. anemic hypoxia: reduced hemoglobin content 2. pathological hemoglobin forms (sickle cell disease) 3. poisons (CO)
118
Stagnant hypoxia
slow tissue perfusion b/c cardiovascular shock
119
Hystotoxic hypoxia
inhibition cellular resp (cyanid, pesticides/ rotenone, antimycin A) (hystoTOXIC -> inhibition by drugs)
120
Poisons hypoxia
CO binds 200X stronger
121
Types CO2 transport
Dissolved gas Carbamino compounds (mostly hemoglobin) Bicarbonate
122
CO2 transport percentage dissolved gas - free CO2
5%
123
CO2 transport percentage carbamino compounds - bind to hemoglobin
15%
124
CO2 transport percentage bicarbonate - CO2 -> HCO3-
80%
125
Water solubility of CO2
20X O2
126
Formation cabamino compounds from
hemoglobin but NOT exclusively
127
Equation formation carbamino compounds
CO2 + R-NH2 <-> R-NHCOOH
128
Name for formation bicarb in blood
chloride shift (hamburger shift) in RBC
129
Chloride shift
CO2 <-> CO2 + H20 <-> H2CO3 <-> H+ + HCO3- <-> Cl- (HCO3- exchange with Cl-)
130
Types interxn btw O2, CO2
Bohr effect Haldane effect
131
Bohr effect
acidosis -> decrease hemoglobin affinity for O2 23BPG binds Deo2 -> decrease O2 affinity
132
Haldane effect
hemoglobin binds O2 -> reduce affinity for CO2 (haldane - luke danes - nice -> binds O2 -> reduce affinity CO2)
133
Nitrogen gas
inert gas NOT metabolized
134
Lipid water partition coeff of N
lipid water partition high
135
Effect of lipi water partition coeff of N
1. N acc. in lipids especially at high pressure (>2bar) 2. Raoid decompression (aka >gas embolism) -> Caisson's disease (decompression sickness)
136
Partial pressure veins O2 CO2
O2: 40 CO2: 46
137
Partial pressure capillaries O2 CO2
O2: 40 CO2: 46
138
Partial pressure inspired air
O2: 158 CO2: 0.3
139
Partial pressure expired air
O2: 116 CO2: 32
140
Resistance pulmon vessel vs systemic
Resistance pulmon > Resistance systemic
141
Optimal load of muscle performance
optimal load = Fo/3 optimal loaf = 1/3max
142
vital capacity formula
insp reserve + tidal + exp reserve NO + residual
143

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