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PHYSIOLOGY > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

what happens to barometric pressure as altitude increases

A

it decreases

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2
Q

why is surfactant needed for lungs to inflate

A

b/c the fluid that coats the lungs has a higher surface tension and makes it harder for them to inflate

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3
Q

what things can cause a LOW V/Q ratio

A

lung disease, airway obstruction or lung stiffening

ventilation gets reduced

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4
Q

what happens to alveoli in low V/Q ratios

A

they are over-perfused and underventilated

getting blood but not enough air

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5
Q

what things can cause a HIGH V/Q ratio

A

vascular obstruction
pulmonary hypotension

pulmonary blood flow is reduced

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6
Q

what happens to alveoli in high V/Q ratios

A

ventilation is higher than blood flow

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7
Q

what things can result in hyperventilation?

A
  • hypoxia
  • increased temp
  • acidosis
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8
Q

what things can result in hypoventilation?

A
  • CNS depressed by injury or drugs
  • injured phrenic nerve
  • damaged thorax or resp. muscles
  • severe airway obstruction
  • lung disease that decreases compliance
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9
Q

what happens to PaCO2 in alveolar hypoventilation

A

it is elevated due to insufficient alveolar ventilation

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10
Q

what happens to PaCO2 in alveolar hyperventilation

A

it decreases due to an increase in ventilation

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11
Q

what factors affect the rate of gas movement between alveolus and blood (VO2)

A

surface area
the thickness of blood air barrier
driving pressure gradient

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12
Q

in diseased lungs where there is edema or inflammation, what factors of gas movement are affected

A

thickness of blood-air barrier (thickened)
reduced SA available for lung exchange

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13
Q

how does a Right to left vascular shunt result in a lower PaO2?

A

R ventricle blood bypasses the ventilated lung and the deoxygenated blood mixed w/ the oxygenated blood of the left atrium,

dilutes the [O2] in the blood going into systemic circulation = decreased PaO2

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14
Q

what are the steps of exhilation

A
  • phrenic nerve stops firing
  • inspiratory muscles relax = passive recoil of the chest wall and diaphragm
  • elasticity of the thorax and lung decreases, alveoli size decreases and Palv increases
  • when Palv > Patm, air leaves lungs
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15
Q

what are the steps of inhalation

A
  • motor neurons fire in phrenic nerve
  • stimulates diaphragm to contract
  • increases thoracic cavity
  • pressure inside pleural cavity becomes more (-) and alveoli expand
  • P atm > Palv so air enters lungs
  • air moves down pressure gradient from atmosphere to alveoli passively by bulk flow
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16
Q

what is functional residual capacity

A

the volume of gas remaining in lungs when the chest wall is relaxed

(‘left over’ air in lung)

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17
Q

what is tidal ventilation

A

the movement of air bidirectionally into and out of the lung via the same pathway

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18
Q

what are the elastic forces for lung resistance during expiration

A
  • elastin fibers in lungs
  • surface tension
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19
Q

what things cause a left shift in the O2-Hb curve

A

decreased PCO2
increased pH
decreased temp
decreased 2,3 DPG

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20
Q

what things cause a right shift in the O2-Hb curve

A

increased PCO2
decreased pH
increased temp
increased 2,3 DPG
hypoxia
high altitude

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21
Q

why is the O2-Hb curve sigmoidal?

A

positive co-operativity

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22
Q

what form of O2 can exert partial pressure

A

only dissolved O2

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23
Q

what is p50

A

the partial pressure at which Hb is 50% saturated

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24
Q

what causes an increase in 2,3 DPG

A

hypoxia

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25
Q

what are the 3 major types of respiratory surfaces

A

invaginated - lungs
evaginated - gills
trachea - insect air-filled tubes

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26
Q

is ventilation active or passvie

A

active!

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27
Q

what is the importance of the pleural cavity?

A

pleural cavity = thin, fluid filled space

the fluid it contains reduces the friction, allowing pleurae to slide against each other

fluid also acts to glue lungs to the chest wall

the pressure in the pleural cavity is negative compared to atm pressure, this keeps the lungs slightly expanded

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28
Q

slight changes in what are responsible for the movement of air into/out of lungs

A

Alveolar pressure (Palv)

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29
Q

under what pressure conditions does air enter the lung? when does it exit?

A

enters lungs when Palv < Patm
exits lungs when Palv > Patm

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30
Q

Amount of air that can be exhaled after a normal
exhalation

A

expiratory reserve volume (ERV)

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31
Q

Amount of air that can be further inhaled after a
normal inhalation

A

inspiratory reserve volume (IRV)

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32
Q

Air left in the lungs after a forced exhalation

A

residual volume (RV)

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33
Q

Maximum amount of air that can be moved in or
out of the lungs in a single respiratory cycle

A

vital capacity (VC)

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34
Q

Total volume of air in the lungs after a maximal
inspiration

A

total lung capacity (TLC)

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35
Q

is surface tension higher during expiration or inspiration

A

higher during inspiration (inflation)

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36
Q

affect of activation of parasympathetic system on ventialtion

A

parasympathetic system releases ACh on muscarinic receptors —> bronchoconstriction

*protective mechanisms that is activated by irritant materials or inflammatory mediators like histamines / cytokines

*activated in heaves and asthma

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37
Q

affect of activation of sympathetic system on ventialtion

A

sympathetic system releases Epinephrine from adrenal medulla, activating B2 adrenergic receptors
—> relaxation of smooth muscle + dilation

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38
Q

Some species utilize nitric oxide as
a _________ via a
nonadrenergic noncholinergic
inhibitory nervous system

A

bronchodilator

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39
Q

term for volume of gas contained in conducting airways

A

anatomical dead space

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40
Q

equation for Tidal Volume

A

VT = VA + VD

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41
Q

what is VA (Alveolar ventilation volume)

A

the amount of tidal volume available for gas exchange

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42
Q

what is VD

A

dead space volume (amount of VT NOT available for gas exchange)

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43
Q

what is ‘alveolar ventilation’

A

the amount of ‘fresh’ air reaching lungs per minute

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44
Q

what is minute volume (VE)

A

the total volume of air moved into and out of the lungs per minute

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45
Q

equation for minute volume (VE)
*includes ventilation of dead space)

A

VE = VT x f

f : respiratory frequency (breaths/min)

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46
Q

Functional (alveolar) minute ventilation (dot on V) (VA)
*better than VE b/c excludes ventilation of dead space

A

dot VA = VA x (breaths/min)

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47
Q

alveolar ventilation equation

A
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48
Q

alveolar gas PO2 (PAO2)

A

100mmHg

49
Q

alveolar gas PCO2 (PACO2)

A

40mmHg

50
Q

PO2 of cells, interstitial fluid

A

<40 mmHg

51
Q

PCO2 of cells, interstitial fluid

A

> 46 mmHg

52
Q

Pressure gradient for O2 is 10x that of CO2, yet CO2 diffuses 2x as fast as O2, how?

A

Diffusivity (D) for CO2 is 20 times that of O2 at any
given partial pressure gradient

CO2 is much more soluble than O2 in water and lipid
membranes

53
Q

how to calculate gas partial pressure (Pgas)

A

Pgas = barometric pressure x fractional concentration of gas

54
Q

What causes PO2 to drop during inspiration?

A

air gets saturated w/ water
water reduces the partial pressure of gas in air

55
Q

PIO2 (partial pressure of O2 in HUMIDIFIED air)

A

subtract H2O vapor pressure, 47 mmHg, from the barometric pressure

56
Q

what is FIO2

A

fraction of oxygen in inspired air

57
Q

what is PAO2 and how do we estimate it

A

Partial pressure of O2 in alveoli
estimated using alveolar gas equation

58
Q

what is R, or RQ

A

respiratory quotient = the ratio of carbon dioxide production to oxygen consumption

R = 0.8

59
Q

what factors contribute to the normal PAO2 - PaO2 gradient (PAO2 > PaO2) alveolar O2 > arterial

A

– diffusivity of O2 across alveolar membranes
– shunting of blood to non-respiratory areas of the lung
– venous admixture of blood from bronchial and coronary circulation

60
Q

what things could increase the PAO2 - PaO2 gradient?

A

diseases that cause edema/inflammation, V/Q mismatch, or increased shunts

61
Q

Extra alveolar vessels dilate in response
to ???

A

expansion of the pleural cavity —> increased negative pleural pressures —-> increase transmural
pressure

62
Q

what happens to capillary resistance if the lungs expand to max volume

A

it begins to deform the capillaries making them more
elliptical, increasing resistance

63
Q

why does hypoxia cause vasoconstriction of pulmonary arteries

A

hypoxia is the result of poorly ventilated alveoli w/ low pO2s.

no point in sending blood to areas that are not receiving oxygen so vasoconstriction redistributes the blood to areas of the lung that are ventilated

64
Q

how could vasoconstriction during hypoxia cause right-sided heart failure?

A

Resistance increases during vasoconstriction and thus pulmonary arterial pressure increases causing the right ventricle to work harder

65
Q

explain the relationship b/w the thickness of vascular smooth muscle (VSM) in pulmonary arteries and hypoxic vasoconstriction (HV)

A

VSM is species-dependent (thick in cows and pigs, intermediate in horses, thin in dogs and sheep)

the thickness of VSM layers affects resposde to HV

the thicker the VSM, the stronger the response to HV

66
Q

role of nitric oxide in hypoxia

A

Some animals like sheep and llama release NO in
response to change in altitude and this acts as a
vasodilator to counteract the constriction due to
hypoxia

67
Q

how can exercise cause an INCREASE in diffusion capacity (DL)?

A

exercise can cause a 3 fold increase in diffusion capacity by….

surface area (A) increases
* more pulmonary capillaries open to ventilated areas
* deeper breathing stretches alveoli

thickness (L) decreases
* deeper breathing stretches alveoli, thinning membrane

68
Q

what is the primary determinant of the rate of gas exchange?

A

pressure gradient

(since diffusion capacity is typically unchanged)

69
Q

what things could cause an impaired diffusion capacity (DL)?

A
  • Pulmonary Fibrosis:
    – interstitial fibrous tissue increases diffusion distance
  • Pneumonia:
    – fluid or pus in alveoli increases diffusion distance (L)
  • Congestive heart failure:
    – edema in lung increases diffusion distance (L)
70
Q

What ultimately limits the amount of O2 that can be taken up by the lungs

A

cardiac output
—-> the maximum rate at which blood can be
delivered to the lungs by the heart

called the perfusion limitation hypothesis

71
Q

under what conditions can oxygen uptake be diffusion limited?

A

if there is insufficient time for equilibration to occur between the blood and the alveolar gas (rare in
healthy animals), and/or if the diffusion capacity (DL) is abnormally low

72
Q

why is it impossible for the V/Q (ventilation:perfusion) ratio to be = 1

A

due to branching patterns in the respiratory system and gravity.

73
Q

Dissolved oxygen is directly proportional to what

A

partial pressure of O2 (PO2)

74
Q

The degree of saturation of Hb is proportional to

A

partial pressure of O2 (PO2)

75
Q

What does a higher P50 mean in regards to Hb affinity for O2

A

higher P50 = lower affinity of Hb for O2

and a lower P50 = higher affinity of Hb for O2

76
Q

Oxygen carriage directly dependent on…

A

hemoglobin content

77
Q

erythropoietin stimulates _______ in the _______

A

red blood cell production (erythropoiesis) in bone marrow

78
Q

what is erythropoietin produced by and what stimulates its synthesis?

A

produced by interstitial cells in the peritubular capillary bed of the renal cortex

synthesis is stimulated by : hypoxia and androgens

79
Q

how does erythropoietin work

A

It increases the number of erythropoietin-
sensitive stem cells in the bone marrow that are converted into red blood cell precursors.

80
Q

Factors that lower the affinity of Hb for O2 and promote the unloading of O2 at tissues (Bohr
effect)

A
  • increased temp
  • increased CO2
  • increased [H+] (decreased pH)

**all can be a result of metabolism

81
Q

what is the effect of increased nitrite levels in the blood

A

increased nitrite levels can trigger the oxidation of Hb, leading to methemoglobinemia

82
Q

what is methemoglobinemia

A

oxidized Hb, cannot bind oxygen =functional anemia

83
Q

what is the role of methemoglobin reductase?

A

converts methemoglobin back to hemoglobin

84
Q

what is the initial response of the respiratory system at high altitude?

A

increased ventilation to increase tissue PO2
this decreases PCO2 and increases pH
increased 2,3 DPG shifts curve to the Right, enhancing O2 unloading at tissues

85
Q

what is the long-term effect / response of the respiratory system at high altitude?

A

increased hematocrit which increases O2 carrying capacity of blood

increased capillary density which enhances tissue O2 delivery

86
Q

what is 2,3 DPG a product of

A

glycolysis

87
Q

what can cause an increase in 2,3 DPG

A

hypoxia

88
Q

what is the effect of 2,3 DPG on Hb

A

it binds to Hb, causing a conformational change that reduces its affinity for O2

this shifts the curve to the right
increasing O2 unloading at tissues

89
Q

why does PO2 remain high in carbon monoxide poisoning

A

b/c tissues are unable to take up O2

90
Q

why are ruminants susceptible to methemoglobinemia?

A

because the gut flora reduces nitrate to ammonia, with nitrite as an intermediate product.

91
Q

clinical signs of methemoglobinemia?

A

Rapid, weak heartbeat with subnormal body temperature, muscular tremors, weakness, and ataxia are early signs of toxicosis when methemoglobinemia reaches 30%–40%.

Brown, cyanotic mucous membranes develop rapidly as methemoglobinemia exceeds 50%.

92
Q

what makes carbon monoxide so toxic

A

it has 240 x greater affinity for
Hb than O2.
– binds to Hb in same location as O2, reducing ability of Hb to carry O2
– also increases affinity of Hb for O2
– shifts dissociation curve to the left & Ihinders O2 unloading at tissues

93
Q

In what two scenarios is CaO2 (arterial oxygen) decreased

A

in anemia and carbon monoxide poisoning

94
Q

Most CO2 that diffuses into RBC reacts with H2O to
form

A

carbonic acid

95
Q

what is the Haldane effect

A

the removal of O2 from Hb at tissue allows more CO2 and H+ to be removed from tissues at any given PO2

96
Q

what are the respiratory control centers in the brainstem

A

Medullary
- rostral ventromedial neurons (pre-Botzinger)
-dorsal respiratory group
- ventral respiratory group

Pons
- pneumotaxic center
- apneustic center

97
Q

what are the higher centers of resp control

A

cortical control
limbic system
hypothalamic center

98
Q

what is the role of the rostral ventromedial neurons (pre-Botzinger) in respiration

A

rhythm generators

99
Q

what is the role of the dorsal respiratory group in respiration? when is it active

A

inspiration

active during eupnea & innervates the diaphragm via phrenic nerve

100
Q

what is the role of the ventral respiratory group in respiration?

A

has both inspiratory and expiratory neurons

active during forced expiration (coughing)

101
Q

role of pneumatic center in respiration ?

A

turns off inspiration at the dorsal respiratory group

102
Q

role of apneustic center in respiration?

A

prolongs inspiration, shortened expiration

103
Q

role of cortical control in respiration

A

voluntary control of vocalization, sighs, breath-holding

104
Q

role of lymbic system in respiration

A

emotionally induced changes in ventilation

105
Q

hypothalamic control of respiration

A

temperature control
like fever

106
Q

what are the sensors of the respiratory system

A

central and peripheral

central = chemoreceptors
peripheral = both chemo and mechanoreceptors

107
Q

where are the central and peripheral resp. sensors located

A

central : ventral surface of medulla
peripheral : carotid and aortic bodies

108
Q

what are the glomus cells related to and what do they respond to

A

peripheral respiratory sensors
glomus cells respond to hypoxia (likely hypercapnia and low pH too)

109
Q

what do peripheral sensors detect changes in

A

changes in PaO2 (if drop below 60-70 mmHg)

110
Q

what do central sensors detect changes in

A

increased H+ in CSF (as a result of CO2 diffusing across BBB)

sensitive to CO2 levels

111
Q

what is the Hering-Breuer reflex

A

has to do with pulmonary stretch receptors, which respond to stretch (inflation of lungs)

Hering-Breuer reflex inhibits further inspiration

typically only active at large tidal volumes >1

112
Q

mechanoreceptors that increase ventilation w/ limb movement

A

chest wall and proprioceptive receptors
(muscle spindles, tendon organs, joint receptors)

113
Q

what is the response of irritant receptors?

A

bronchoconstriction

114
Q

what are J receptors? what causes them to be active?

A

they stimulate respiration in response to the engorgement of pulmonary capillaries (ex: left heart failure “backs up” pulmonary circulation)

located in alveolar walls near capillaries

115
Q

what is the likely reason for the ventilatory response to exercise?

A

impulses from the motor cortex (hypothesis)

116
Q

what things depress the activity of macrophages in the respiratory fluid lining

A

Glucocorticoids, corticosteroids, hypoxia and viral activity

117
Q

Endotherms can respond to changes in temperature by changing their…..

A

metabolic rate - rate at which they consume O2 and produce CO2

118
Q

what mechanisms do animals use within the thermoneutral zone

A

pilomotor responses (hair and feathers)
vasomotor responses change the rate of blood flow to skin
postural responses alter the amount of SA exposed to the environment

119
Q

methods of evaporative cooling

A

sweating
panting
gular fluttering
**all require Energy

PHYSIOLOGY (25 decks)

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