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BIOL 364 > Respiration: Regulation of Respiratory Systems > Flashcards

Respiration: Regulation of Respiratory Systems Flashcards

1
Q

how do RBCs modify their micro-environment to make O2 uptake/delivery more efficient (3)

A
  • regulation of organic phosphates
  • regulation of pH values
  • goal is to optimize blood P50
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2
Q

O2, CO2, and Hb transport interaction (3)

A
  • strong interactions within RBC due to Bohr and Haldane effects
  • O2 uptake facilitates CO2 removal at gas exchanger
  • CO2 removal from tissues enhances O2 unloading from blood
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3
Q

how does increased PCO2 affect the body (3)

A
  • increases [HCO3-]
  • decreases pH (increase in [H+])
  • reaction shifts to produce bicarbonate
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4
Q

how does decreased PCO2 affect the body (3)

A
  • decreased [HCO3-]
  • increased pH (decrease in [H+])
  • reaction shifts to produce CO2
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5
Q

how does hyperventilation affect PCO2

A
  • decreases PCO2
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6
Q

how does hypoventilation affect PCO2

A
  • increases PCO2
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7
Q

what is the predominant regulator of acid-base balance in air breathers (2)

A
  • respiration for modulation blood CO2 levels
  • kidneys/gills for regulation HCO3- levels
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8
Q

respiratory alkalosis (2)

A
  • caused by hyperventilation and blowing off of CO2
  • increases pH
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9
Q

respiratory acidosis (2)

A
  • caused by hypoventilation, which permits CO2 to accumulate
  • decreases pH
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10
Q

metabolic acidosis (2)

A
  • acidosis during anaerobic respiration
  • due to elevated lactate levels
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11
Q

regulation of respiratory systems
- regulation
- responds to…
- requirements (2)

A
  • respiratory systems are tightly regulated
  • respond to changes in external and internal environments
  • must be able to supply sufficient O2 to meet metabolic demands
  • must be able to remove CO2 to prevent pH disturbance
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12
Q

how do vertebrates regulate respiratory systems (3)

A
  • regulating ventilation (frequency & depth)
  • regulating oxygen carrying capacity and affinity
  • regulating tissue perfusion
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13
Q

what kind of process is ventilation (2)

A
  • an automatic process
  • continues when we are unconscious
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14
Q

what regulates ventilation and where is it located (2)

A
  • central pattern generator (groups of neurons) in medulla
  • Pre-Botzinger complex
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15
Q

Pre-Botzinger complex

A
  • important respiratory rhythm generator in mammals
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16
Q

how are rhythm generators further modulated (5)

A
  • other receptors and emotional stimuli act through hypothalamus
  • peripheral and central chemoreceptors
  • receptors in muscles and joints
  • stretching receptors in lungs
  • irritant receptors in lungs/trachea
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17
Q

basic ventilation function (3)

A
  1. rhythmic firing of central pattern generators initiate ventilatory movements via interneurons
  2. send nerve signal to somatic motor neurons
  3. activates skeletal muscles for breathing (intercostal and diaphragm muscles)
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18
Q

ventilation modulation via feedback (3)

A
  • chemosensory input modulates output of central pattern generators
  • most animals have central and peripheral sensors
  • chemoreceptors detect changes in CO2, H+ and O2
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19
Q

central sensor location

A
  • brain
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20
Q

peripheral sensor location

A
  • outside of the brain
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21
Q

what determines what chemoreceptors mainly sense for

A
  • depends in the medium that the animal respires
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22
Q

water breathers: primary sensing mode

A
  • O2
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23
Q

air breathers: sensing mode (2)

A
  • primary: CO2
  • secondary: O2
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24
Q

air breathers: central sensors

A
  • detect pH (related to CO2) of cerebrospinal fluid, fluid surrounding brain and spinal cord
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25
Q

air breathers: peripheral sensors (2)

A
  • have 2 peripheral sensors that primarily sense low PO2
  • aortic body and carotid body
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26
Q

air breathers: aortic body sensor

A
  • blood going to body
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27
Q

air breathers: carotid body sensor

A
  • blood going to brain
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28
Q

water breathers: sensors (2)

A
  • internal PO2 sensors within gills, gill cavity, and on gill surface
  • PCO2/pH sensors in gills for environmental levels
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29
Q

other ventilation control mechanisms (3)

A
  • mechanoreceptors
  • secondary chemoreceptors
  • conscious control
30
Q

ventilation control mechanism: mechanoreceptors location (2)

A
  • lungs
  • bronchi
31
Q

ventilation control mechanism: secondary chemoreceptors exmaples

A
  • eg. CO2 sensors in lungs or pulmonary circulation
32
Q

ventilation control mechanism: conscious control location (2)

A
  • hypothalamus
  • cerebrum
33
Q

hyperoxia (2)

A
  • higher than normal PO2 in environment, blood, or organ system
  • rare terrestrial environmental condition, mostly aquatic
34
Q

hypoxia

A
  • lower than normal PO2 in environment, blood, or organ system
35
Q

hypoxemia

A
  • lower than normal arterial blood O2 content
36
Q

hypoxia causes (3)

A
  • environmental hypoxia (high altitude, burrows, etc)
  • inadequate ventilation (hypoventilation)
  • reduced blood Hb content (anemia)
37
Q

hypercapnia

A
  • higher than normal PCO2 in environment or blood
38
Q

hypocapnia

A
  • lower than normal PCO2 in environment or blood
39
Q

high altitude conditions (3)

A
  • barometric pressure drops, so PO2 drops as well
  • low temperature
  • low relative humidity
40
Q

mount everest elevation

A
  • highest altitude where people can survive a few hours breathing air
41
Q

how can the blood adjust to high altitude (2)

A
  • increase hematocrit/RBCs
  • polycythemia
42
Q

what are the negative implications of increasing hematocrit in high altitude (3)

A
  • increases pulmonary arterial pressure due to high viscosity of blood
  • causes right ventricular hypertrophy (thicker muscle) and congestive heart failure over time
  • causes chronic mountain sickness
43
Q

acute mountain sickness (3)

A
  • 4-8 hours after ascent to 3300m or higher
  • results in nausea, headache, insomnia, and possibly death
  • 3 phases: acute response, acclimatization, and long term acclimatization
44
Q

acute mountain sickness: acute response (3)

A
  • increased ventilation
  • decreased PCO2
  • increased pH
45
Q

acute mountain sickness: acclimatization (3)

A
  • decreased ventilation
  • PCO2 and pH recover
  • hypoxemic
46
Q

acute mountain sickness: long term acclimatization

A
  • pH in cerebral spinal fluid slowly adjusted so ventilation can be elevated without disturbing CSF pH
47
Q

how can mountain sickness be alleviated (a drug)

A
  • a carbonic anhydrase inhibitor
48
Q

how can a carbonic anhydrase inhibitor (acetazolamide) alleviate mountain sickness (3)

A
  • bicarbonate cannot be converted to CO2 as easily
  • ensures that CSF pH does not raise too high so that ventilation can stay elevated to avoid hypoxia
  • excess bicarbonate will be released in urine through kidneys
49
Q

how can organic phosphate levels change in high altitude

A
  • increase concentration to increase tissue O2 delivery
50
Q

is a higher or lower P50 more beneficial during exposure to environmental hypoxia? (3)

A
  • lower P50 is more beneficial in OEC
  • higher affinity for O2, aiding in O2 loading at the lungs
  • P50 cannot be too left shifted or O2 will not deliver to tissues
51
Q

adaptations to altitude: examples (2)

A
  • high altitude llama has lower P50 than the P50 range of lowland animals
  • deer mouse native to high altitudes have lower P50 levels than low altitude deer mice due to changes in organic phosphate levels
52
Q

what adaptation must high altitude animals have to accommodate for their low P50 (2)

A
  • must have tissue-level mechanisms to aid in O2 delivery
  • eg. increased capillary density or myoglobin
53
Q

P50 difference in Andean Goose and Greylag loose (2)

A
  • P50 of Andean Goose (can fly over Everest) is much lower than P50 of Greylag goose (cannot fly over Everest)
  • difference from single aa substitution on Hb function
54
Q

how can human P50 be genetically lowered

A
  • site directed mutagenesis altering 1 aa in human Hb converts Hb functionally to that of the Andean goose
55
Q

at what levels can enhancement to O2 flux occur at on the O2 transport cascade

A
  • can occur at every level: ventilation, pulmonary diffusion, circulatory diffusion, muscle diffusion, muscle utilization, muscle ATP turnover
56
Q

O2 transport cascade: important avian characteristics in ventilation

A
  • tolerance of the hypocapnia caused by respiratory CO2 loss
57
Q

O2 transport cascade: unique features of high fliers in ventilation (2)

A
  • enhanced hypoxic ventilatory response
  • more effective breathing pattern
58
Q

O2 transport cascade: important avian characteristics in pulmonary O2 diffusion (2)

A
  • crosscurrent gas exchange
  • extremely thin and mechanically strong gas exchange barrier
59
Q

O2 transport cascade: unique features of high fliers in pulmonary O2 diffusion

A
  • larger lungs increase surface area for diffusion
60
Q

O2 transport cascade: important avian characteristics in circulatory O2 diffusion (2)

A
  • relatively large hearts
  • cerebral perfusion is insensitive to hypocapnia
61
Q

O2 transport cascade: unique features of high fliers in circulatory O2 diffusion (2)

A
  • hemoglobin with higher O2 affinity
  • multiple cardiac specializations
62
Q

O2 transport cascade: important avian characteristics in muscle O2 diffusion (2)

A
  • high capillary density/SA
  • small muscle fibers
63
Q

O2 transport cascade: unique features of high fliers in muscle O2 diffusion (2)

A
  • even higher capillary density/SA
  • mitochondria are redistributed closer to capillaries, reducing diffusion difference
64
Q

O2 transport cascade: important avian characteristics in muscle O2 utilization (2)

A
  • high aerobic capacity
  • high capacity for fat oxidization
65
Q

O2 transport cascade: unique features of high fliers in muscle O2 utilization

A
  • sometimes greater aerobic capacity in flight muscles
66
Q

O2 transport cascade: important avian characteristics in muscle ATP turnover

A
  • fast-contracting aerobic fibers in flight muscle
67
Q

O2 transport cascade: unique features of high fliers in muscle ATP turnover

A
  • greater respiratory control by mitochondrial creatine kinase
68
Q

adaptations to aquatic hypoxia (2)

A
  • left shift of OEC due to reduction in ATP/GTP:Hb ratio
  • hypoxia tolerant fish generally have low P50s
69
Q

how might gills change in response to hypoxia (2)

A
  • increased SA
  • decreased thickness
70
Q

adaptations to aquatic hypoxia: carp (2)

A
  • experiences large increase in gill surface area during hypoxia
  • cells packed between lamellae disappear in hypoxic and reappear again when conditions stabilize
71
Q

if lamellae surface area increases by 2x ad thickness decreases by 2x, how would O2 uptake be affected

A
  • 4x more O2 uptake
72
Q

how do Lake Qinghai scale-less carp adapt to hypoxia (2)

A
  • increase in total SA of gills during exposure to hypoxia
  • reduction in blood water diffusion distance

BIOL 364 (44 decks)

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