Exam I: Pulmonary Flashcards

1
Q

what are the key parts of respiration

A

ventilation-moving air into lungs

diffusion- exchange with blood at alveoli

transport- moving gases to tissues

transfusion/perfusion- gas exchange with tissues

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2
Q

what is the mucucilliary system (clearance)

A

cells with hairs lines upper and lower respiratory tract,
secrete a sticky mucus layer
spin the incoming air and trap viruses/bacteria in sticky layer
wash layer back to larynx to be killed by HCl in stomach

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3
Q

what saves us from constant PNA

A

coughing/sneezing
mucocilliary system
macrophages in alveolus

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4
Q

what happens in the conducting zone of the airway

A

transports and distributes air
warms and humidifies air
traps and clears harmful particles in mucus

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5
Q

what resp structures make up the conducting zone

A

trachea
bronchi
bronchioles
terminal bronchioles

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6
Q

what happens in the respiratory zone of the airway

A

exchange gas across alveolar capillary membrane

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7
Q

what structures make up the respiratory zone

A

respiratory bronchioles,
alveolar ducts,
alveolar sacs

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8
Q

what cells makes up the alveoli tissue

A

simple squamous epithelium

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9
Q

what tissues are present between gas in alveoli and gas in blood

A

epithelial cells of alveolus
endothelial cells of capillary
thin layer of fluid between

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10
Q

where is surfactant produced

A

type II alveolar cells

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11
Q

what structures are within the alveoli

A

type 2 alveolar cells- produce surfactant

basement membrane- structure of alveoli(type I alveolar cells)

elastin- recoil of alveoli

alveolar epithelium- where it makes contact with capillaries

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12
Q

what is role of surfactant

A

reduces surface tension

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13
Q

every alveolus has a __________ to prevent infection

A

macrophage

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14
Q

how many true ribs are there

A

7 pairs

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15
Q

how many false ribs are there

A

5 pairs (2 are floating)

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16
Q

how many floating ribs are there

A

2 pairs

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17
Q

inner intercostal and external intercostal muscles run in ___________ directions

A

opposite

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18
Q

what are the steps of inspiration

A

-diaphragm contracts
-sternocleidomastoid pulls sternum and 1st rib
-ribs elevated by scalenes, pec minor, and external intercostals
-rib cage turns out like bucket handle
causes an increase in volume and negative pressure

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19
Q

what are the steps of expiration

A

passive exp
elasticity of alveoulus

active exp
internal intercostals and abd muscle

causes a decrease in volume and positive pressure

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20
Q

Where is the visceral pleura?

A

on external lung surface

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21
Q

where is the parietal pleura

A

lines the thoracic cavity

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22
Q

what is between the visceral and parietal pleura

A

pleural cavity with thin layer of fluid

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23
Q

what is purpose of constant negative pressure in pleural cavity

A

suck lungs to rib cage

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24
Q

what law tells us about the relationship between pressure and volume

A

boyles law

inverse relationship

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25
Q

what law tells us about the relationship between volume and temp

A

charles law

direct relationship

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26
Q

what does pressure have to be for inspiration

A

at least 758 (ATM is 760)

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27
Q

what does pressure have to be for expiration

A

at least 761

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28
Q

what is the law of partial pressures

A

Daltons law

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29
Q

what is PO2 of venous blood

A

40mmhg

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30
Q

What is the PO2 of alveolar air?

A

105 mmhg

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31
Q

What is the PCO2 in the alveoli?

A

40 mmhg

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32
Q

what is PCO2 in the venous blood

A

46 mmhg

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33
Q

what is PO2 of atomoshpheric air

A

159

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34
Q

what causes diffusion process to occur between alveoli and capillaries

A

partial pressure difference

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35
Q

What is the PO2 of arterial blood?

A

100 mmhg

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36
Q

what is PCO2 of arterial blood

A

40

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37
Q

what is Paw

A

partial airway pressure

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38
Q

what is P A

A

alveolar pressure

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39
Q

what is Ppl

A

pleural pressure (pleural space)

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40
Q

what is Pta

A

Transairway pressure (tracheal wall)

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41
Q

what is PL

A

transpulmonary pressure

(pressure between alveoli sac and pleural cavity) (pressure within lung tissue)

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42
Q

what is Pl at rest

A

-5 cm H2O

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43
Q

Pta = ________ - __________

A

Paw (airway) - Ppl (pleural pressure)

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44
Q

Pl = _________ - ___________

A

P A (alveolar) - Ppl (pleural)
this is a negative pressure compared to ATM

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45
Q

what creates Ppl

A

elasticity of lungs

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46
Q

why do your lungs collapse in pneumothorax

A

no longer - pressure, becomes + so lungs collapse

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47
Q

Ppl ________ during inspiration and _________ during expiration

A

decreases

increases

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48
Q

P A _________ and returns to zero during inspiration and __________ then returns to zero during expiration

A

decreases

increases

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49
Q

when do we read peak tidal volume

A

end of inspiration

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50
Q

what are the 4 volumes we measure in lungs

A

inspiratory reserve volume
tidal volume
expiratory reserve volume
residual volume

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51
Q

what is total lung capacity formula?

A

inspiratory reserve volume

tidal volume

expiratory reserve volume

residual volume

or

vital capacity + residual volume

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52
Q

What is vital capacity formula?

A

inspiratory reserve volume + tidal volume + expiratory reserve volume

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53
Q

What is inspiratory capacity formula?

A

tidal volume + inspiratory reserve volume

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54
Q

what is functional residual capacity formula?

A

expiratory reserve volume + residual volume

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55
Q

what is normal tidal volume

A

500 ml

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56
Q

what is normal IRV (inspiratory reserve volume)

A

3100 ml

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57
Q

what is normal ERV (expiratory reserve volume)

A

1100 ml

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58
Q

what is normal RV (residual volume)

A

1200 ml

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59
Q

what is the definition of inspiratory capacity

A

The maximum amount of air that can be inspired after the expiration of a normal breath at rest

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60
Q

what is normal inspiratory capacity (IC)

A

3500 (TV + IRV)

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61
Q

What is FRC (functional residual capacity)?

A

Amount of air that Remains in lungs at the end of normal expiration

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62
Q

what is normal FRC

A

2400 (ERV + RV)

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63
Q

what is VC (vital capacity)

A

Maximum amount of air expelled from lungs after first filling the lungs to a max then expiring to a max
everything - residual volume

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64
Q

what is normal VC

A

4800 TV + IRV + ERV

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65
Q

What is TLC (total lung capacity)?

A

Maximum volume of air the lungs can hold

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66
Q

what is normal TLC

A

6000 (IC + FRC) (or all volumes)

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67
Q

what is FEV1

A

maximum forced expiratory volume in 1 second

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68
Q

what is FVC%

A

percentage of FVC forcibly exhaled in one second

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69
Q

what condition do we use FEV1 and FVC% tests for

A

COPD
bronchitis
emphysema

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70
Q

what factors influence VC

A

size (height)
environment

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71
Q

what factors change lung functions throughout life

A

lung damaging activities (smoking)
exercise
age

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72
Q

what is Minute ventilation (MV)

A

TV x RR
volume of air moved in a minute

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73
Q

what is anatomic dead space in lungs

A

volume of conducting zone that takes up space but does not exchange gas

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74
Q

where does stale air come from

A

anatomic dead space, air that is not exchanged

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75
Q

what causes alveolar dead space

A

inadequate perfusion of ventilated alveoli

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76
Q

what is antomical + alveolar dead space

A

physiologic dead space volume

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77
Q

what is normal amount of lung being used

A

1/3

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78
Q

T/F with alveolar dead space shallow/fast breathing is more effective than deep slow breathing

A

false, deep slow breathing allows for movement in dead spaces

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79
Q

how does hyperventilation affect PCO2

A

Decreased arterial PCO2 (increases pH)

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80
Q

how does hypoventilation affect PCO2

A

increased arterial PCO2, decreases pH

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81
Q

What is compliance of the lungs?

A

how much effort is required to stretch the lungs and chest wall

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82
Q

lung A has set pressure with low volume
lung B has same pressure with higher volume
which lung is more compliant

A

B

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83
Q

what condition has increased compliance but decreased recoil

A

emphysema

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84
Q

how does surfactant affect compliance

A

increases compliance

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85
Q

how do we measure lung compliance

A

spirometer

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86
Q

how does COPD affect lung compliance

A

increased compliance with decreased elasticity

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87
Q

How does ARDS affect lung compliance?

A

decreased compliance (less surfactant)

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88
Q

how does scarring affect lung compliance

A

decreases

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89
Q

how does pneumonia affect lung compliance

A

decreases

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90
Q

how do restrictive diseases affect lung compliance (asthma)

A

decreases

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91
Q

what is recoil direction of rib cage

A

inward

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92
Q

what is recoil direction of lungs

A

outward

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93
Q

where do opposing recoil of lungs and rib cage meet

A

FRC functional residual capacity

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94
Q

how does standing affect lung compliance

A

-top of lung stretched by gravity
-lower lung more compliant
-upper lung less compliant

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95
Q

what is purpose of surfactant

A
  • Reduces surface tension
  • Stops alveoli collapsing and sticking together
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96
Q

without surfactant compliance would ___________

A

decreases

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97
Q

what determines resistance in airway

A

radius

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98
Q

what leads to increased resistance in lungs

A

bronchoconstriction:
parasympathetic stimulation
environmental insults (smoke, cold)

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99
Q

what leads to decreased resistance in lungs

A

sympathetic stimulation
high CO2

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100
Q

where is turbulent airflow found

A

highest in smaller bronchi
increases in velocity

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101
Q

how does turbulence affect resistance

A

increases

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102
Q

how does lung volume affect resistance

A

increased lung volume decreased resistance

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103
Q

how does forced expiration affect airway pressures/resistance

A

compresses airway with positive pressure, increasing resistance

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104
Q

when does the lung have the most resistance

A

high and low volumes

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105
Q

what is the equal pressure point

A

point in the lung where pleural pressure is same as terminal bronchiole

during peak expiration, pressure is same inside and outside lung
lower pressure of conducting airway is protected by cartilage

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106
Q

what part of airway are we in after reaching EPP

A

conducting airway, protected by cartilage

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107
Q

how does emphysema affect EPP

A

EPP moves to smaller branches without cartilage, so air cannot be moved out

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108
Q

how does asthma (restrictive lung disorder) affect lung “work”

A

increases inspiratory work

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109
Q

how does emphysema (obstructive lung disease) affect lung “work”

A

increased expiratory work

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110
Q

why do pulmonary vessels need to be compliant

A

to accommodate stroke volume variations from R vent

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111
Q

what percent of CO goes through pulmonary circulation

A

100%

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112
Q

what is the purpose of pulmonary circulation

A

bring blood into contact with alveoli for gas exchange

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113
Q

what is inspired air
PO2
PCO2

A

159 mmhg (160?)
0.3 mmhg

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114
Q

what is alveolar air
PO2
PCO2

A

104 mmhg (102?)
40 mmhg

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115
Q

what is arterial blood
PO2
PCO2

A

95-105 (100) mmhg
40mmhg

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116
Q

what is tissue fluid
PO2
PCO2

A

40 mmhg
46 mmhg

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117
Q

what is venous blood
PO2
PCO2

A

40 mmhg
46 mmhg

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118
Q

what causes diffusion in lungs

A

concentration gradient/ partial pressure

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119
Q

what does the lung filtrate

A

emboli
thrombi
-small blockages in lungs are better than in heart, brain, kidneys

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120
Q

what is the fucntion of the lung for metabolism

A

formation of angiotensin 2 by ACE
inactivation of bradykinin, prostaglandins

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121
Q

what are the lungs a reservoir for

A

hemorrhagic shock

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122
Q

what are the three secondary functions of the lungs

A

filtration of embli/thrombi
metabolism
blood reservoir

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123
Q

what kind of blood is in pulmonary arteries

A

deoxygenated

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124
Q

what kind of blood is in pulmonary veins

A

oxygenated

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125
Q

where does bronchiole circulation come from

A

R lung -third post intercostal
L lung- aorta

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126
Q

what is function of pulmonary circulation

A

pick up O2 in lungs

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127
Q

what is function of bronchiole circulation

A

oxygenate lung tissue

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128
Q

how is pressure in pulmonary circulation when compared to systemic

A

low resistance, low pressure

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129
Q

pulmonary vessels have _______ smooth muscle

A

less

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130
Q

what is pressure of systolic and diastolic in pulmonary circulation

A

15/5

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131
Q

how does an increase in CO affect pulmonary resistance

A

decreases

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132
Q

what is lung recruitment

A

opening of more capillary beds to contact alveolar sacs
capillaries also dilate

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133
Q

what are the three ways lungs increase capacity

A

recruitment
distension
dilation

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134
Q

what is the purpose of recruitment

A

increased flow at low velocity allows for greater gas exchange

increased areas of capillaries available for gas exchange
lowers pressure and prevents pulmonary edema

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135
Q

how does a high lung volume (increased alveolar size) affect resistance

A

INSPIRATION
pleural pressures more negative, extra-alveolar vessels expand

expansion of alveolus compresses alveolar vessels, increasing resistance

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136
Q

how does a low lung volume affect resistance

A

exhalation
more positive pleural pressures compress extra-alveolar vessels

increases resistance

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137
Q

what is the time of lowest resistance in lungs

A

-FRC (functional residual capacity)
volume at rest after passive expiration
-least compression of blood vesses

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138
Q

how does hypoxia (low O2 tension) in alveoli affect pulmonary vessel resistance

A

causes pulmonary vasoconstriction

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139
Q

why does hypoxia of alveoli cause pulmonary vasoconstriction

A

maintain ventilation/perfusion balance
shunt blood to areas of higher oxygenation

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140
Q

how does generalized hypoxemia affect pulmonary vasculature

A

pulm vasoconstriction

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141
Q

what has a lower hydrostatic pressure, capillaries or alveoli

A

capillary

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142
Q

what creates pressures within the alveoli

A

air pressure (pushing out)
surface tension (pullin in)

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143
Q

what creates pressure within the pulmonary capillary

A

hydrostatic pressure (pushing out)
colloidal osmotic pressure (pulling in)

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144
Q

what fluids are around alveoli/capillary

A

interstitial fluid
lymph drainage

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145
Q

what is the normal net filtration pressure of capillary to interstitial space

A

+1 mmhg

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146
Q

a negative hydrostatic pressure of the interstitial fluid leads to a ____________ affect from the capillary

A

suction

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147
Q

what direction does fluid go between capillary, interstitial space, and alveoli

A

in normal conditions goes from capillary to interstitial fluid

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148
Q

where does excess fluid from interstitial space go

A

lymphatic system (has a pressure of -5 mmHg)

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149
Q

where does excess fluid from alveoli go

A

interstitial fluid

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150
Q

What is physiology of pulmonary edema?

A

pressure in pulmonary capillaries increases from L sided HF
pressure in interstitial space is greater than +5 mmHg,
fluid cant drain completely into lymphatics
fluid goes into alveoli
pulmonary edema

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151
Q

what condition causes pulmonary edema

A

L sided HF
damage to pulmonary membrane

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152
Q

what safety factors protect us from death r/t pulmonary edema

A

negative interstitial pressure
lymphatic pumping
decreased interstitial osmotic pressure

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153
Q

when standing up, the lung has more - pressure, the top of the lung is stretched, and compliance of lung is ____________ so more air goes to __________ part of lung because it is _________ compliant

A

decreased
lower
more

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154
Q

when standing which part of the lung has more perfusion and ventilation

A

base of the lung (gravity and compliance effects)

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155
Q

what is Zone 1 of lung

A

not normal
PA (alveoli) is greater than Pa (arteries)
alveoli compresses arteries

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156
Q

what is zone 2 of lung

A

Pa (arteries) > PA (alveoli) > Pv (venous)

flow limited by alveolar pressure, dialating venules will not increase flow

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157
Q

what is zone 3 of the lung

A

Pa >Pv>PA
blood flow is not determined by alveolar pressure

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158
Q

how does gravity affect V/Q

A

V/Q mismatch
perfusion higher in base of lung
V/Q low at base (excess blood in base)
V/Q high at apex (excess air at apex)

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159
Q

what is normal V/Q

A

1/1

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160
Q

how does airway obstruction affect V/Q ratio

A

low V/Q ratio

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161
Q

low V/Q is a ________ issue

A

ventilation

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162
Q

in a low V/Q ratio
PAO2 ______ normal
PACO2 ______ normal

A

less than
greater

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163
Q

in a high V/Q ratio
PAO2 ______ normal
PACO2 ______ normal

A

greater
less than

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164
Q

an arterial obstruction causes a _________ V/Q ratio which causes ___________

A

high
dead space

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165
Q

what diseases cause low V/Q ratio

A

COPD

bronchitis

asthma

emphesymea

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166
Q

what causes a high V/Q ratio

A

pulm embolism

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167
Q

Does FiO2 change with altitude?

A

no, PaO2 changes

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168
Q

PAO2 is

A

alveolar O2

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169
Q

paO2 is

A

arterial O2

170
Q

what causes drop of atmospheric O2 to alveolar O2

A

converted to water with CO2 to humidify air (turbinates)

171
Q

what are factors that affect diffusion

A

Ficks
thickness of membrane
surface area of membrane
diffusion coefficient
partial pressure difference

172
Q

how does PNA affect diffusion

A

thicker walls 2/2 edema = decreased diffusion

173
Q

CO2 diffuses _______ than O2

A

faster

174
Q

How much O2 is dissolved in plasma?

A

2%

175
Q

How much CO2 is dissolved in plasma?

A

10%

176
Q

what limits the diffusion of O2 and CO2 between capillaries and alveoli?

A

perfusion, not diffusion rate

177
Q

what medication can increase diffusion between capillaries and alveoli

A

N2O

178
Q

what percent of lungs do we usually use

A

30%

179
Q

what increases the diffusion capacity of respiratory membrane

A

exercise

180
Q

what happens inside lung to increase lung capacity to exchange O2 CO2

A

opening of dormant capillaries and increasing of diffusion capacities
(recruitment)

181
Q

amount of O2 and CO2 in tissues is equal to the amount of O2 and CO2 in ________________

A

venous blood

182
Q

how much O2 is carried on Hgb

A

98% (2% in plasma)

183
Q

what is the affinity of RBC for carbon monoxide

A

250x O2 affinity

184
Q

how does an increased metabolic rate affect PO2

A

decreases PO2

185
Q

how does a decreased metabolic rate affect PO2

A

increases PO2

186
Q

how does an increased metabolic rate affect CO2

A

increased

187
Q

how does a decreased metabolic rate affect CO2

A

decreased

188
Q

what factors affect Hgb affinity for O2

A

acidosis (H or CO2) = decreased affinity

pCO2 increased CO2 = decreased affinity

temp, increased temp = decreased affinity

DPG, increased DPG = decreased affinity

189
Q

what is DPG

A

2,3-diphosphoglycerate
released by hypoxic cells

190
Q

what does hgb decreased affinity for O2 mean

A

Hgb has a weaker hold, tissues receive O2 more easily, happens in response to increase metabolism or acidotic/hypoxic states

191
Q

what does SaO2 tell us

A

% of binding sites occupied by O2

192
Q

if a tissues has an unusually low PO2 Hgb gives up O2 __________ easily

A

more (decreased affinity for O2)

193
Q

how does anemia affect SaO2

A

SaO2 can read 100% but still hypoxia

194
Q

how does carbon monoxide affect SaO2

A

SaO2 can read 100% even in hypoxia

195
Q

what is it called when oxygen combines with Hbg

A

oxyhemoglobin

196
Q

what is a right shift in the oxyhemoglobin dissociation curve

A

decreased affinity for O2

197
Q

what is a left shift in the oxyhemoglobin dissociation curve

A

increased affinity for O2

198
Q

what processes cause a left shift in the oxyhemoglobin curve

A

alkalosis
decreased PCO2
decreased temp
low DPG
carboxyhemoglobin
Methemoglobin
abnormal hemoglobin

199
Q

what causes a right shift in oxyhemoglobin curve

A

acidosis
high PCO2
increased temp
high DPG
abnormal hemoglobin

200
Q

What is the Bohr effect?

A

shift in the oxyhemoglobin dissociation curve caused by changes in CO2 and H+ concentration in blood

201
Q

How is CO2 transported in the blood?

A

70% Bicarbonate
20% on Hgb
10% Plasma

202
Q

what catalyzes the process of CO2 and H2O forming H2CO3 (carbonic acid)

A

carbonic anhydrase

203
Q

What is the chloride shift?

A

HCO3- ions move out of red blood cells into the plasma down a concentration gradient.
To maintain the electrical balance, Cl- ions take their place.
AKA hamburger shift

204
Q

when Hgb is deoxygenated CO2 can bind to it, this creates

A

carbaminohemoglobin

205
Q

What is the Haldane effect?

A

increased O2 = decreased Hgb affinity for CO2 (arterial blood)
decreased O2 = increased Hgb affinity for CO2 (venous blood)

206
Q

blood can carry _______ CO2 than O2

A

more

207
Q

when oxygen is attached to Hgb what is given off?
what does this then attach to?
what does this become
what breaks it down
what is then diffused out of RBC

A

H+
HCO3 from Cl- exchange
carbonic acid
carbonic anhydrase breaks it into CO2 and H20
CO2 diffuses out

208
Q

What is pulmonary circulation?

A

circulation of deoxygenated blood between heart and lungs

209
Q

what is bronchiole circulation

A

oxygenated blood to provide lung tissues
L lung from aorta
R lung from 3rd posterior intercostal arteries

210
Q

where does deoxygenated blood from bronchiole circulation empty

A

pulmonary vein, so LA doesnt receive 100% saturated blood

211
Q

a decreased V/Q ratio is a __________ issue

A

ventilation

212
Q

an increased V/Q ratio is a _________ issue

A

perfusion

213
Q

what are causes of VQ mismatch

A

PE (decreased perfusion)
COPD (decreased ventilation)
diffusion block (fluid in lungs)
asthma (decreased ventilation)

214
Q

what has a greater impact on O2: ventilation or perfusion

A

ventilation

215
Q

what two ways is O2 transported

A

2% in plasma
98% in RBC (hgb)

216
Q

what are the 4 ways CO2 is transported

A

10% plasma
20% plasma bicarb
50% RBC bicarb
20% carbaminohemoglobin

217
Q

why is plasma conversion of CO2 to bicarb slow

A

no carbonic anhydrase

218
Q

why is plasma conversion of CO2 to bicarb fast

A

has carbonic anhydrase

219
Q

what happens to bicarb in RBC when it reaches the lungs

A

breathed off as CO2

220
Q

Where are peripheral chemoreceptors located?

A

carotid and aortic bodies

221
Q

Where are central chemoreceptors located?

A

medulla oblongata

222
Q

what are mechanoreceptors in the lungs sensitive to

A

stretch
J receptors
irritant (cough)

223
Q

where is an area of high concentration of irritant mechanoreceptors

A

carina

224
Q

what muscle are involved in inspiration

A

sternocleidomastoid- raises sternum
external intercostals- flips ribs out
diaphragm- pulls down

225
Q

what is end result of inspiratory muscle movement

A

increased (-) pressure
-5 (baseline) to -10 - -30

226
Q

What are chemoreceptors sensitive to?

A

CO2
H
O2

227
Q

inspiration has to be triggered by

A

muscles

228
Q

expiration is mostly

A

passive recoil

229
Q

what breathing control centers are in the Medulla

A

DRG (dorsal respiratory group)
VRG (ventral respiratory group)

230
Q

what breathing centers are in the PONs

A

pneumotactic center

231
Q

what does the DRG do

A

PURE inspiration
basic rhythm of quiet breathing

232
Q

what does the VRG do

A

increased ventilation over quiet/resting
increases Expiration and inspiration
using muscle for expiration

233
Q

what is the pneumotactic center responsible for

A

depth and rate of breathing

234
Q

T/F the pneumotactic center is dormant during quiet breathing

A

false

always active

235
Q

what triggers pneumotactic center

A

CO2

236
Q

T/F we dont need a trigger for inspiration

A

false
must trigger inspiratory muscle

237
Q

T/F we need a trigger for expiration

A

false

normally passive recoil

238
Q

what part of respiratory cycle does emphysema screw up

A

expiratory, loss of recoil of lungs

238
Q

when is electrical activity high in the diaphgram

A

inspiration (makes sense since this is contraction and expiration is relaxation)

239
Q

in inspiration pleural pressure is __________ and electrical activity is ________

A

decreased
increased

240
Q

in expiration pleural pressure is __________ and electrical activity is ________

A

increased (to baseline)
decreased (to baseline)

241
Q

Where does the DRG receive input from?

A

chemo and mechanoreceptors
pneumotactic center

242
Q

what is the inspiratory ramp signal

A

-signal transmitted to inspiratory muscle increases steadily for 2-3 second during quiet respiration

-ramp allows for a steady increase in volume rather than short gasps

243
Q

inspiratory phase is (shorter/longer) than expiratory phase

A

Shorter

244
Q

what makes the ramp effect

A

transmission of impulse
length of time of muscle activation

245
Q

what is the role of the pneumotactic center

A

regulates DRG
controls rate and duration of inspiration
depth and speed or breathing

246
Q

when is VRG activated

A

during times of increased respiratory need (exercise)
when forced expiration needed

247
Q

when is VRG inactive

A

quiet respiration

248
Q

what respiratory control center stimulates forced expiration

A

VRG

249
Q

why is CO2 the trigger for respiration

A

has a smaller range of intravascular levels (40 arterial, 46 tissues)

250
Q

increased CO2 (increases/decreases) respiratory depth and rate

A

increases

251
Q

what is feedforward control

A

proprioceptors in joints/muscles can trigger increased respiration in response to increased movement

252
Q

is feedforward control CO2 controlled

A

no

253
Q

what fine-tunes the feed forward control

A

negative feedback

254
Q

what nerve primarily carries mechanoreceptor impulses

A

vagus nerve

255
Q

Where are pulmonary stretch receptors located?

A

airway smooth muscle in bronchi and bronchioles

256
Q

what stimulates the pulmonary stretch receptors to fire

A

increased pressure in lungs (stretch)

257
Q

What is the Hering-Breuer reflex?

A

reflex triggered to prevent over-inflation of the lungs.

Pulmonary stretch receptors present in the smooth muscle of the airways respond to excessive stretching of the lung during large inspirations.

258
Q

what prevents overstretch of lungs during inspiration

A

Hering Breuer reflex of pulmonary stretch receptors

259
Q

When is the Hering-Breuer reflex activated?

A

3x tidal volume (1500 ccs)

260
Q

where are irritant mechanoreceptors found

A

epithelium of larger conducing airway

261
Q

what triggers irritant receptors

A

particulate matter causing inflammation mediators (histamine, serotonin, prostaglandins)

262
Q

what are the conducting airways

A

trachea, bronchi, bronchioles, terminal bronchioles

263
Q

do conducting airways have air exchange

A

NO

264
Q

what is response of irritant receptor activation

A

cough/sneeze
bronchoconstriction

265
Q

what illnesses can irritant receptor activation cause issues in

A

asthma, emphysema

266
Q

what cells does asthma cause issues with

A

goblet cells

267
Q

where are the J receptors located

A

in/near alveoli- juxtapulmonary receptors

268
Q

What do J receptors respond to?

A

acute congestion/edema
damage

269
Q

what is response of J receptors

A

stimulates increased ventilation

270
Q

what do the peripheral chemosensors respond to

A

CO2, H+, O2 (in that order)

271
Q

What do the central chemoreceptors respond to?

A

primarily
CO2
secondarily
H

272
Q

what is goal of all mechanoreceptors

A

increase ventilation
get O2 to body

273
Q

when do chemo receptors respond to PO2

A

<60mmHg

274
Q

T/F the blood brain barrier is highly permeable to H and HCO3

A

False

its poorly permeable

275
Q

T/F metabolic acidosis significantly lower CSF pH

A

False

276
Q

T/F respiratory acidosis significantly lower CSF pH

A

true

277
Q

T/F the blood brain barrier is permeable to CO2

A

True
its a gas passes freely

278
Q

what happens after CO2 crosses BBB

A

combines with water and becomes H and HCO3 in CSF

279
Q

how long does it take the kidney respond to acid/base imbalances

A

2-3 days

280
Q

how long does it take the lungs to respond to acid/base imbalances

A

immediate

281
Q

what triggers the respiratory centers in the medulla

A

H+ in CSF

282
Q

where does H+ in CSF come from

A

CO2 crossing BBB

283
Q

where do peripheral chemoreceptors send their signals

A

DRG

284
Q

what kind of oxygen do peripheral chemoreceptors read

A

PaO2,
not total oxygen content

285
Q

what else are peripheral chemoreceptors sensitive to

A

cyanide
arterial pressure <60

286
Q

what chemo receptors sense hypoxia

A

only peripheral

287
Q

hyperventilation leads to (hypo/hyper) capnia

A

hypo
resp alk

288
Q

T/F hyperpnea during exercise causes abnormal blood CO2

A

False
increased metabolism creates CO2, no no hypocapnia

289
Q

hypoventilation leads to (hypo/hyper) capnia

A

hyper
resp acidosis

290
Q

what can trigger hyperventilatoin

A

hypoxia

291
Q

when is hyperventilation triggered by hypoxia

A

PaO2 < 60 mmHg,
causes decreased PaCO2 and high pH in short term

292
Q

how does body respond to high altitude

A

hypocapnia initially increases CSF pH
overtime bicarb is excreted by the kidneys, allowing an increase in ventilation

293
Q

do arterial O2, CO2 and pH change during exercise

A

NO

294
Q

what are bodies fluid chemical buffers for hydrogen ions

A

Rapid but temporary

Bicarbonate
proteins
ammonia
phosphate

295
Q

how do the lungs regulate hydrogen ions

A

rapid

respond to acidosis by increasing ventilation, thus eliminating CO2 and decreasing pH

296
Q

how do the kidneys regulate hydrogen ions

A

slow, powerful

eliminate non-volitile acids
secretes H+
reabsorbs HCO3-
generates new HCO3

297
Q

what is the most important ECF buffer?
formula?

A

bicarb
H2O+ + CO2 <-> H2CO3 <-> H+ + HCO3

298
Q

what is the phosphate renal buffer
formula

A

phosphate
HPO4- + H+ <-> H2PO4- (phosphoric acid)

299
Q

what is the ammonia renal buffer formula

A

ammonia
NH3 + H+ <-> NH4+ (ammonium)

300
Q

what is an important intracellular buffer

A

proteins
H+ + Hb <-> HHb (hemoglobin)

301
Q

where does 60-70% of buffering occur

A

cells

302
Q

what determines the effectiveness of a buffer system

A

-concentration of reactants
-pK of system and pH of body fluids

303
Q

what is pK

A

concentration of H+ per pH reading. balanced is pK=6.1

304
Q

know the bicarb buffer equation

A

H2O+ + CO2 <-> H2CO3 <-> H+ + HCO3

305
Q

what enzyme has to be present to convert H2O and CO2 to carbonic acid and vise versa

A

carbonic anhydrase

306
Q

what is the most important buffer in ECF

A

bicarbonate buffer system

307
Q

what organs closely regulate the bicarb formula

A

lungs- CO2
kidney- HCO3-

308
Q

How do the lungs regulate pH?

A

increased H+ -> increased alveolar ventilation -> decreased pCO2

309
Q

How do kidney regulate pH?

A

eliminate non-volatile acids (sulfuric acid, phosphoric acid)
filter bicarb (HCO3)
secretion of H+
reabsorption of bicarb
production of new bicarb
excretion of bicarb

310
Q

for every HCO3 reabsorbed, the must be a __________ secreted

A

H+

311
Q

where is most bicarb reabsorbed in the kidney

A

proximal tubule- 85%
thick ascending loop of henle- 10%
late distal tubule - 4.9%
collecting duct- .1%

312
Q

how is sodium bicarb reabsorbed/excreted in proximal tubule and thick loop of henle

A

1) Na+ H+ pump exchange takes Na from tubule, puts H into tubule
2) carbonic acid formed
3) carbonic acid broken into CO2 and H2O
4)H2O excreted
5) CO2 reabsorbed into cell
6) CO2 combines with H2O in cell with carbonic anhydrase to form H2CO3 (carbonic acid)
7) H+ breaks off from carbonic acid
8) HCO3 (bicarb) reabsorbed into blood
9) H+ is available to exchange for another Na (step one)

313
Q

how does aldosterone affect renal pH control

A

causes sodium uptake and H+ secretion (Na/H pump)

314
Q

how is bicarb reabsorbed and H secreted in intercalated cells of late distal and collecting tubules

A

1) CO2 absorbed from blood
2) CO2 combines with water in intercalated cell to form carbonic acid
3) carbonic acid dissociates into HCO3 and H+
4) HCO3 is reabsorbed
5) H is secreted (into urine) by use of ATP or with a K exchange

315
Q

increase CO2 = ___________ H+ secretion

A

increased

316
Q

what is increased CO2 in body leading to acidotic state

A

resp acidosis

317
Q

increased extracellular H = _____________ H+ secretion

A

increased

318
Q

what causes an increase in tubular fluid buffers to increase H+ secretion

A

respiratory or metabolic acidosis

319
Q

what conditions cause you to increase H+ secretion and HCO3 reabsorption

A

increased PCO2 (resp acidosis)
increased H+ and decreased HCO3 (metabolic acidosis)

increase in aldosterone
increased angiotensin 2 (increases aldosterone)

decreased ECF volume
hypokalemia

320
Q

what conditions cause a decrease in H secretion and HCO3 reabsorption

A

decreased PCO2
decreased H+ and decreased HCO3 (metabolic alkalosis)

decrease in aldosterone
decreased angiotensin 2 (decreases aldosterone)

increased ECF volume
hyperkalemia

321
Q

what is renal compensation for acidosis

A

increased H secretion
increased HCO3 reabsorb
produce new HCO3

322
Q

what is kidneys response to alkalosis

A

decreased H secretion
decreased HCO3 reabsorb
loss of HCO3 in urine

323
Q

in acidosis when H+ is being in secreted what must be present in urine

A

buffers, limited to the amount of free H kidneys can excrete

324
Q

what is the minimum pH of urine before damage occur

A

4.5, this is why we need buffers for H excretion

325
Q

what occurs when NaHPO4- acts as a buffer in urine

A

one Na used to exchange for H for excretion, forms with NaHPO4- as a buffer
Turns NaHPO4 to H2PO4, phosphoric acid

new HCO3 formed in cell to be reabsorbed into blood

326
Q

what is NH3

A

ammonia

327
Q

what is NH4

A

ammonium

328
Q

where is NH4 secreted in nephron

A

proximal,
thick loop of henle,
distal tubules

329
Q

where does glutamine come from

A

amino acid metabolism from liver

330
Q

what does glutamine break down into

A

2 bicarbs
2 ammonium

331
Q

how does ammonium get removed from tubular cell

A

Na+ /NH4+ exchange pump (NH4 excreted)

332
Q

how is H+ and NH3 buffered in collecting tubules

A

NH3 is permeable, freely passes through tubular cell wall into tubular lumen

CO2 froms with H2O to form bicarb in cell, with H+ as byproduct

H+ excreted with ATP from tubular cell

NH3 and H form NH4, excreted with Cl- to form ammonium chloride

333
Q

what causes acidosis (pH <7.4)

A

metabolic: decreased HCO3
respiratory: increased pCO2

334
Q

what causes alkalosis (pH>7.4)

A

metabolic: increased HCO3
respiratory: decreased pCO2

335
Q

what is normal body pH

A

7.35-7.45

336
Q

what is normal ratio of HCO3 to CO2

A

20:1

337
Q

what is the pH range that is compatible with life

A

6.8-7.8

338
Q

acid base imbalance chart

A
339
Q

what is Respiratory acidosis:
pH:
Primary disturbance:
Compensation:

A

pH: low
PD: increased CO2
Comp: renal acid excretion, bicarb reabsorption

340
Q

what is metabolic acidosis:
pH:
Primary disturbance:
Compensation:

A

pH: low
PD: decreased HCO3
Comp: hyperventilation to cause low CO2

341
Q

what is Respiratory alkalosis:
pH:
Primary disturbance:
Compensation:

A

pH: high
PD: decreased CO2
Comp: decreased renal acid excretion (retain more H) increased bicarb excretion (B intercalated cells)

342
Q

what is metabolic alkalosis:
pH:
Primary disturbance:
Compensation:

A

pH: high
PD: increased HCO3
Comp: hypoventilation with increased CO2

343
Q

what is normal ABG HCO3

A

22-26 mEq/L

344
Q

what is BG interpretation for
pH: 7.12
PCO2: 50
HCO3: 18

A

mixed acidosis

345
Q

what is BG interpretation for
pH: 7.6
PCO2: 30
HCO3: 29

A

mixed alkalosis

346
Q

what is measured in anion gap

A

Cation
Na +

Anion
Cl-
HCO3-

347
Q

in body fluids anions should be ___________ cations

A

equal to

348
Q

what is a normal anion gap

A

8-16

349
Q

how do you calculate anion gap

A

Na-(Cl+HCO3)

350
Q

when do we use anion Gap

A

metabolic acidosis

351
Q

what are the unmeasured anions

A

proteins
sulfates,
ketones,
phosphates,
lactate,

352
Q

what does an increased anion gap tell us

A

an increase in the unmeasured anions

353
Q

what is a metabolic acidosis with a normal anion gap

A

hyperchloremic metabolic acidosis
(increased Cl, decreased HCO3)

354
Q

what is metabolic acidosis with an increased anion gap

A

(so Cl normal, HCO3 low)

normochloremic metabolic acidosis
-diabetic ketoacidosis
-lactic acidosis
-salicylic acid

355
Q

what is BG interpretation for
pH: 7.2
PCO2: 55
HCO3: 26

A

resp acidosis

356
Q

what are causes of respiratory acidosis

A

brain damage
pneumonia
emphysema
lung disorders

357
Q

what is BG interpretation for
pH: 7.5
PCO2: 40
HCO3: 30

A

metabolic alkalosis

358
Q

What are the causes of metabolic alkalosis?

A

increased base intake (NaHCO3)
vomiting gastric acid
mineralcorticoid excess (aldosterone)
overuse of diuretics (except carbonic anhydrase inhibitors)

359
Q

what is BG interpretation for
pH: 7.34
PCO2: 29
HCO3: 15

A

metabolic acidosis (resp compensation)

360
Q

what is BG interpretation for
pH: 7.49
PCO2: 48
HCO3: 35

A

metabolic alkalosis (resp compensation)

361
Q

what is BG interpretation for
pH: 7.34
PCO2: 60
HCO3: 31

A

respiratory acidosis (metabolic compensation)

362
Q

what is BG interpretation for
pH: 7.62
PCO2: 20
HCO3: 20

A

respiratory alkalosis (metabolic comp)

363
Q

what is BG interpretation for
pH: 7.09
PCO2: 50
HCO3: 15

A

mixed acidosis

364
Q

how does the kidney regulate the body fluid acidity

A

bicarbonate

365
Q

what is carbonic acid

A

H2CO3

366
Q

what actually drives respiration

A

H+ ions around pons in CSF

367
Q

where do loop diuretics work

A

thick ascending loop of henle

368
Q

what are the loop diuretic examples

A

furosemide
bumetanide
ethacrynic acid

369
Q

which transporter does the loop diuretic work on

A

1 na, 2 cl and 1 K transporter
“triple transporter”

370
Q

what do loop diuretics bind up to have effect

A

2 chloride on triple transporter

371
Q

what does loop diuretic cause excretion of from triple transporter

A

Na
K
Cl

372
Q

where do thiazide diuretics work

A

early distal tubule- on sodium chloride transporter

373
Q

what does thiazide diuretic inhibit

A

sodium chloride transporter- so sodium stays in lumen and draws water into lumen for excretion

374
Q

what are some aldosterone antagonists

A

spironolactone, eplerenone

375
Q

what are some sodium channel blockers

A

amiloride, triamterene

376
Q

how do osmotic diuretics work and where?

A

proximal convoluted tubule

pull water in to dilute the extra concentrates in the lumen

377
Q

where do loop diuretics work

A

thick ascending loop of henle

block Cl on triple symporter, so K and Na stay in the lumen to be excreted along with Mg and Ca

378
Q

where do thiazide diuretics work

A

distal convoluted tubule

blocks the Na Cl sympoter

379
Q

where do K sparing diuretics work

A

collecting duct

block aldosterone and Na channels on Na K antiporter

379
Q

what are types of K sparing diuretics

A

Na channel blockers ( amiloride)

Aldosterone antagonist (spironolactone)

380
Q

define pulmonary ventilation

A

inflow and outflow of air between the atmosphere and lung alveoli

381
Q

how can lungs be contracted

A
  • downward and upward movement of the diaphragm to lengthen or shorter the chest cavity

-elevation and depression of the ribs to increase or decrease AP diameter

382
Q

what is considered quiet breathing

A

the movement of diaphragm to expand lungs

383
Q

What is minute respiratory volume

A

Total amount of new air moved into the respiratory passages each minute

Min resp vol= tidal vol + resp rate per min

384
Q

What is a normal min resp vol

A

6L/min

385
Q

What are the lung volumes

A

Tidal volume
Inspiratory residual volume
Expiratory reserve volume
residual volume

386
Q

What are the four lung capacities

A

Vital lung capacity (tv+ irv+ erv)
Inspiratory capacity (tv+irv)
Functional residual capacity
Total lung capacity

387
Q

When bicarb is being brought into the RBC through a transporter what is being pushed out

A

Chloride molecule

388
Q

How much non-volatile acid produced a day

A

~60-80 mmol/day

389
Q

What are the important renal tubular buffers

A

Phosphate
Ammonia

390
Q

Renal regulation of acid base

A

Eliminate non volatile acids

Filter bicarb
Reabsorb bicarb
Produce new bicarb
Excrete bicarb

Secrete H ions

391
Q

How is glutamine formed

A

From metabolism of amino acids

392
Q

What is the systolic and diastolic for systemic circ

A

93/2

393
Q

What’s the average MAP for pulmonary capillaries

A

10

394
Q

What happens to pulmonary resistance as CO increases? Why?

A

Decreases

Recruitment and distention

395
Q

Reduced airflow to a particular region of the lung leads to:

A

Reduced blood flow to that area

Blood shunts to alveoli that has airflow

396
Q

Generalized hypoxemia=

A

Generalized vasoconstriction

Leads to high pressures backing up in the heart

397
Q

What’s the interstitial osmotic pressure

A

14 mmHg

398
Q

Colloid osmotic pressure ____ and hydrostatic pressure _____

A

Pulls

Pushes

399
Q

How does smooth muscle tone affect flow

A

PNS causes constriction and increased mucous production

SNS causes dilation and increased fluid secretion

Environmental insults can cause vasoconstriction

High CO2 causes dilation of resp tract

400
Q

How does turbulence influence resistance

A

Increases resistance

Branching airways decreases resistance

401
Q

Define Bohr effect

A

CO2 and H are affecting the affinity of Hb for oxygen

402
Q

Define Haldane effect

A

Oxygen is affecting the affinity of Hb for CO2 and H

403
Q

What airway generations are the conducting zone

A

0 trachea

1-2/3 bronchi

4-7 bronchioles

8-16 terminal bronchioles

404
Q

What airway generations are the respiratory zones

A

17-18 respiratory bronchi

19-21 alveoli duct

22-23 alveoli sac

405
Q

Physiological dead space is about ____ of ____ _____ in healthy people

A

1/3

Tidal volume

406
Q

How can you determine alveolar ventilation

A

Measure CO2 output

407
Q

Equal pressure point

A

The pressure inside the alveolar duct/respiratory bronchi is = the pressure in the pleural cavity

408
Q

What factors affect the rate of diffusion in a fluid

A

Solubility of gas in the fluid

Cross sectional area of the fluid

Distance through which the gas must diffuse

Molecular weight of the gas

Temp of the fluid

409
Q

The O2 conc/ partial pressure is controlled by

A

Rate of absorption of O2 into the blood

Rate of entry of new O2 into the lungs

410
Q

What does the pneumotaxic center do

A

Controls the “switch off” point in the inspiratory ramp

Controls the filling phase of the lung cycle

411
Q

When does dead space occur

A

When there is ventilation but no perfusion

412
Q

When does a shunt occur

A

When there is perfusion but no ventilation

413
Q

What is a normal FEV1/FVC%

A

80%

Airway obstruction is 47%

414
Q

What causes chronic pulmonary emphysema

A

Infection
Obstruction
Loss of parenchyma

415
Q

What are consequences of COPD

A

High airway resistance
Decrease diffusing capacity
Pulm hypertension

416
Q

Consequences of pna

A

Significant decrease in arterial hgb saturation

417
Q

Hypoxia is sensed by

A

Peripheral chemoreceptors

418
Q

Define hypoxia

A

Low O2 supply at lungs and tissue

419
Q

Define hypoxemia

A

Low PaO2
Low blood O2

420
Q

Control of ramp signal

A

Rate of increase

Control of limiting point (drop off point)