Pulmonary Exam: Physiology Flashcards

(132 cards)

1
Q

physiologic dead space =

A

anatomic dead space + alveolar dead space

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2
Q

alveolar dead space in a healthy person

A

should be minimal

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3
Q

circumstances in which alveolar dead space increases

A

low cardiac output, high alveolar pressure, pulmonary embolism

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4
Q

Partial pressure of oxygen depends on

A

barometric pressure (decreases with altitude)

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5
Q

most oxygen travels in the bloodstream how

A

bound to hemoglobin

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6
Q

Movement of O2 between alveoli and pulmonary capillary blood is determined by

A

Fick’s principle

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7
Q

what can impair diffusion

A

thickened barrier (pulmonary fibrosis) or reduced driving pressure (altitude or COPD)

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8
Q

O2 content equals

A

total amount of O2 carried in blood (dissolved plus bound to hemoglobin)

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9
Q

total oxygen delivery equals

A

cardiac output times oxygen content

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10
Q

rightward shift in HbO2 diss curve results in

A

increased P50, increases O2 deliver to tissues

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11
Q

rightward shift in HbO2 diss curve results from

A

increased PCO2, decreased pH, increased temp, increased 2-3 BPG

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12
Q

leftward shift in HbO2 diss curve results in

A

decreased P50, decreased O2 deliver to tissues

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13
Q

leftward shift in HbO2 diss curve results from

A

decreased temp, decreased PCO2, decreased 2,3-DPG, increased pH

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14
Q

critical blood component in determining O2 content

A

hemoglobin

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15
Q

3 forms of transport of CO2

A

Bicarbonate ion, carbaminohemoglobin, dissolved

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16
Q

predominant form of transport of CO2

A

Bicarbonate ion

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17
Q

Haldane effect

A

as blood becomes deoxygenated in the tissues, it can care more CO2, facilitating CO2 transport. As blood becomes oxygenated in the lungs, the blood can carry less CO2, allowing additional CO2 to be released and expired

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18
Q

what is true of pulmonary arteries

A

they are not highly muscular

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19
Q

what is true of pulmonary capillaries

A

they are arranged in dense networks to facilitated gas exchange

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20
Q

what is true of pulmonary veins

A

they transport oxygenated blood and larger veins have a layer of cardiac muscle

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21
Q

passive factors affecting PVR

A

recruitment and distention (decrease), lung volume (PVR is lowest at FRC and increases with either inspiration or forced expiration), hematocrit (increases PVR)

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22
Q

what is responsible for locally matching ventilation and perfusion

A

hypoxic pulmonary vasoconstriction

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23
Q

mechanism of hypoxic pulmonary vasoconstriction

A

hypoxic inhibition of K channels and calcium influx through calcium channels resulting a direct contractile effect on pulmonary arterial smooth muscle

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24
Q

drugs for pulmonary HTN

A

endothelin receptor antagonists, PDE-5 inhibitors, prostacyclin analogs

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25
mechanism of pulmonary HTN
chronic hypoxia leads to vascular remodeling, polycythemia, and vasoconstriction, which causes increased vascular resistance, HTN, and RV hypertrophy
26
endothelin receptor antagonist mechanism
competitively antagonizes endothelin-1 receptors to decrease pulmonary vascular resistance
27
example of endothelin receptor antagonist
bosentan
28
PDE-5 inhibitors mechanism
prolonged vasodilatory effect of NO
29
example of PDE-5 inhibitor
sildenafil
30
prostacyclin analog mechanism
direct vasodilatory effects on pulm/systemic arteries. Also inhibits platelet aggregation.
31
prostacyclin analog example
epoprostenol
32
types of hypoxia
arterial hypoxemia, ischemic hypoxia, anemic hypoxia, histotoxic hypoxia
33
cause of histotoxic hypoxia
decreased cellular metabolism
34
cause of anemic hypoxia
insufficient hemoglobin
35
cause of ischemic hypoxia
hypoperfusion
36
characteristics of hypoxemia
decreased PaO2, responds to 100%FiO2 unless it's due to a large shunt
37
causes of hypoxemia
VQ mismatch, diffusion impairment, decreased FiO2, hypoventilation
38
characteristics of ischemic hypoxia
Normal PaO2, decreased SvO2 and PvO2. No response to 100% FiO2
39
causes of ischemic hypoxia
shock, LV failure, hypovolemia, hypothermia
40
characteristics of anemic hypoxia
no response to FiO2 unless it's due to CO poisoning
41
causes of anemic hypoxia
CO poisoning, anemia, methemoglobinemia
42
cause of histotoxic hypoxia
cyanide poisoning
43
characteristics of histotoxic hypoxia
poisoning of cellular machinery that uses O2, so no response to 100% FiO2
44
what is the A-a gradient
reflects efficiency of oxygen exchange and is used to identify etiology of hypoxemia
45
A-a gradient formula
PAO2 - PaO2
46
what does a normal A-a gradient indicate
extra-pulmonary cause of hypoxemia (high altitude, hypoventilation)
47
causes of increased A-a gradient
pulmonary cause of hypoxemia (diffusion impairment, VQ mismatch, shunt)
48
where are ventilation and perfusion increased
base of the lungs due to gravity
49
what is true of ventilation and perfusion at the bases
both increase but perfusion increases more leading to a decreased V/Q ratio
50
compensatory mechanism for hypoxic vasoconstriction
bronchiolar constriction and decreasing alveolar surfactant production leading to decreased compliance and ventilation
51
characteristics of hypoventilation
normal A-a gradient, associated with increased PCO2
52
causes of hypoventilation
CNS depression, obesity hypoventilation, muscular weakness
53
5 causes of hypoxemia
decreased FiO2, hypoventilation, V/Q mismatch, diffusion impairment, shunt
54
most common cause of hypoxemia
V/Q mismatch
55
causes of V/Q mismatch
obstructive lung disease, PE, mild alveolar filling disease
56
causes of diffusion impairment
interstitial lung disease, emphysema, pulmonary vascular disease, increased cardiac output states (increased transit time through alveolar-capillary membrane)
57
causes of shunts
full alveoli (blood, water, pus, protein), alveolar collapse, pulmonary AVM, intracardiac shunts
58
what connects the central/peripheral chemoreceptors to the brainstem
vagus and glossopharyngeal nerves
59
where is the basic respiratory rhythm generator
the medulla
60
how is arterial pH sensed
peripheral chemoreceptors
61
mechanism of chronic CO2 retention and hypoxemia in COPD
V/Q mismatch
62
initial effect of CO2 retention on arterial/CSF pH
decreased pH. CSF has its own buffering system.
63
renal compensation for CO2 retention
kidneys produce bicarbonate in response to lowered pH, this raises blood pH back to near normal levels
64
which chemoreceptors mediate hypoxic drive
peripheral
65
effects of 100% O2 therapy on a chronically hypercapneic person
can lead to increased hypercapnea and acidemia due to elimination of hypoxic drive (hypoventilation) and worsening of VQ mismatch
66
what to do about the hypoxic drive issue in COPD patients
start O2 low and titrate slow
67
effect of acute hypoxia on ventilation
increased ventilation due to hypoxic stimulation of peripheral chemoreceptors
68
hyperventilation
ventilation in excess of that required to match VCO2
69
effect of acute hypoxia on PaCO2
increased alveolar ventilation leads to decreased PaCO2
70
effect of decreased PaCO2 on ventilation
CO2 ventilatory drive is suppressed
71
ventilation response to high altitude (chronic hypoxia)
respiratory alkalosis from hyperventilation
72
renal response to respiratory alkalosis at altitude
increased pH stimulates kidneys to eliminate HCO3- which lowers arterial pH (this can be augmented by acetazolamide)
73
effect of lowered pH on ventilation at altitude
allows the hyperventilation due to hypoxia to continue
74
effects of lowered blood HCO3- on CSF buffering at altitude
central chemoreceptors become more sensitive to CO2 and ventilatory drive is increased
75
response to exercise
increased CO2 production and O2 consumption making a right shift of ODC. Increased ventilation rate to meet O2 demand. VQ ratio from apex to base becomes more uniform. Increased CO and increased pulmonary blood flow. Decreased pH during strenuous exercise due to lactic acidosis.
76
Blood gas response to exercise
PaO2 and PaCO2 are unchanged, increased venous CO2 and decreased venous O2
77
transmural pressure =
alveolar pressure minus intrapleural pressure
78
what does transmural pressure determine
lung volume
79
resting intrapleural pressure
-5 cm H20
80
intrapleural pressure during inspiration
-8 (more negative than at rest)
81
alveolar pressure during inspiration
(-)
82
alveolar pressure at rest
0
83
transmural pressure during inspiration
+7 (more positive than at rest)
84
alveolar pressure at maximal inspiration
0
85
alveolar pressure during expiration
(+)
86
intrapleural pressure during expiration
less negative (approaching -5)
87
transmural pressure during expiration
less positive
88
cause of airway collapse in obstructive disease
migration of equal pressure point towards the alveoli
89
why don't airways collapse during forceful expiration
the equal pressure point occurs in the cartilaginous airways
90
forceful expiration intrapleural pressure
very positive
91
alveolar pressure during forceful expiration
very positive
92
why does pressure drop moving proximally along airways
resistance
93
equal pressure point
point along airway at which pressure inside airway is equal to intrapleural pressure
94
minute ventilation is comprised of
dead space ventilation and alveolar ventilation
95
anatomic dead space consists of
conducting airways
96
alveolar dead space consists of
alveoli that do not participate in gas exchange
97
surface tension contributes to
the recoil properties of the lung
98
Law of LaPlace
Pressure in alveoli = (2*surface tension)/radius
99
implications of law of LaPlace
smaller alveoli have higher pressures, so surfactant must be present in order to keep smaller alveoli open (decrease surface tension)
100
what is true of surface tension in alveoli
it is surface-area dependent due to surfactant (surface tension has a greater impact on smaller alveoli)
101
obstructive diseases destroy
elastic tissue
102
pressure-volume curve for restrictive lung disease
smaller (less volume at any given pressure due to decreased compliance)
103
pressure-volume curve for obstructive lung disease
taller (greater volume at any given pressure due to decreased elasticity)
104
functional residual capacity in restrictive lung disease
decreases
105
functional residual capacity in obstructive lung disease
increases
106
effects of increase in pCO2 on airway diameter
bronchodilation (to facilitate CO2 removal)
107
effects of decrease in pCO2 on airway diameter
bronchoconstriction
108
basal tone in airways results from
basal vagal cholinergic activity
109
is there endogenous activation of B2 adrenergic receptors in airway smooth muscle
no
110
why does airflow velocity decrease in the respiratory zone of the lungs
large cross-sectional area of respiratory zone (velocity = flow/area)
111
standard respiratory quotient
0.8
112
alveolar gas equation PAO2 =
O2 in minus O2 out
113
causes of physiologic A-a gradient
1. deoxygenated blood from coronary circulation bypasses pulmonary circulation and is returned to left atrium via thebesian vein 2. Bronchial vein supplies blood to distal lungs and does not participate in gas exchange 3. Intrapulmonary shunts
114
normal A-a gradient formula
(Age +10)/4
115
Zone 1 (apex)
PA>Pa>Pv. No bloodflow. Only used on PPV or during hemorrhage
116
Zone 2
Pa>PA>Pv moderate bloodflow and is pulsatile based on alveolar pressure
117
Zone 3
Pa>Pv>PA greatest blood flow with most gas exchance
118
Compensatory response to pulmonary embolism
bronchiolar constriction
119
central chemoreceptors
sense increase in CO2 and H+
120
peripheral chemoreceptors
sense decrease in O2, increase in CO2, increase H+
121
peripheral chemoreceptors location and innervation
carotid sinus and aortic arch, cranial nerves IX and X
122
central chemoreceptors location
ventral surface of medulla
123
pontine receptor group
fine-tunes breathing based on info received from stretch receptors in lung
124
basic respiratory rhythm generator
medulla (DRG/VRG)
125
dorsal respiratory group
receives info from peripheral chemoreceptors and forwards it to VRG and inspiratory motor neurons
126
ventral respiratory group
contains inspiratory and expiratory neurons and forwards motor neurons involved in both inspiration and expiration
127
locations of peripheral chemoreceptors
carotid bodies (IX), aortic bodies (X)
128
primary stimulus for ventilation
PaCO2
129
central chemoreceptors responsible for how much control of ventilation
80%
130
central chemoreceptors are insensitive to
acidemia
131
arterial pH is sensed only by
peripheral chemoreceptors
132
PAO2= (simplified alveolar gas equation)
PIO2-PCO2