Lecture 15- Respiratory 3 Flashcards

1
Q

How is CO2 transported in the body?

A

-Dissolved in blood 10% -Bound to globin portion of Hb 30% - Forms carbamino Hb (HbCO2) =Reduced Hb > affinity for CO2 than HbO2 - Transported as bicarbonate (HCO3- )=combines with water 60% -Carbonic anhydrase catalyses the reaction in red blood cell CO2 + H2O=H2CO3 (carbonic acid)=H+ HCO3-

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2
Q

Describe the picture of how is CO2 transported:

A

-to prevent the bicarbonate built up it is dissociated and pushed into the plasma shunted out in swap for Cl- ions
1 to 1 swap
chloride shift

-O2 is dropping as it goes out to the tissue cell while the CO2 goes in from the tissue cell and is taken up by the Hb

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3
Q

What happens to CO2 in the lungs (pic)?

A

most CO2 in bicarb will be shunted in for Cl- that will drive the the reaction to go to H2CO3 and wtare and CO2 which can then leave

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4
Q

What are the respiratory centers in the brain?

A

brain stem
medullary respiratory center= controls inspiration and expiration (dorsal does only the inspiration) so control of the process of breathing in and out, how long for so determining the Tidal volume
- how to get it right? feeding in from a few areas= pre-botzinger area=time keeper the rthytmicity = vital in normal breathing

-pons respiratory centers:apnestic cntr-increasing and decreasing inspiratory neurons= overriding effect when imalance in gas to emergency button sort of

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5
Q

How is respiration controlled?

A

Your respiratory rate changes. When active, for example, your respiratory rate goes up; when less active, or sleeping, the rate goes down. Also, even though the respiratory muscles are voluntary, you can’t consciously control them when you’re sleeping. So, how is respiratory rate altered & how is respiration controlled when you’re not consciously thinking about respiration?

The rhythmicity center of the medulla:

controls automatic breathing
 consists of interacting neurons that fire either during inspiration (I neurons) or expiration (E neurons)
 I neurons - stimulate neurons that innervate respiratory muscles (to bring about inspiration)
 E neurons - inhibit I neurons (to 'shut down' the I neurons & bring about expiration)
 Apneustic center (located in the pons) - stimulate I neurons (to promote inspiration)
 Pneumotaxic center (also located in the pons) - inhibits apneustic center & inhibits inspiration

Factors involved in increasing respiratory rate

Chemoreceptors - located in aorta & carotid arteries (peripheral chemoreceptors) & in the medulla (central chemoreceptors)
Chemoreceptors (stimulated more by increased CO2 levels than by decreased O2 levels) > stimulate Rhythmicity Area > Result = increased rate of respiration

-Heavy exercise ==> greatly increases respiratory rate

Mechanism?

NOT increased CO2
Possible factors:
reflexes originating from body movements (proprioceptors)
increase in body temperature
epinephrine release (during exercise)
impulses from the cerebral cortex (may simultaneously stimulate rhythmicity area & motor neurons)

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6
Q

How are higher brain centers connected to respiration control?

A

feeding in to the area in the brain stem

  • Emotions & pain sympathetic nerves in hypothalamus E.g. rise in temperature, anger
  • links to the autonomic nervous system though it’s not part of it

holding breath= even in animals but not as much control

race horses= when really excited in races and stop breathing (only small percentage) = they stop and start breathing once they relax

-in giving birth= can stop breathing etc

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7
Q

What is Hering-Breuer reflex?

A

Respiratory system mechano/stretch receptors monitor degree of inflation ␣ Over-inflation of lungs results in inhibition of breathing (Hering-Breuer reflex)

-also feedback from lungs= then inhibition of lungs if breathing too much= hering-breuer reflex

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8
Q

Where do the respiratory centers in the brain get their feedback from?

A
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9
Q

What is the chemical control of respiration?

A
  • Changes in arterial PO2 =Only important during an emergency(will have effect on tidal volume, but only works when in very low O2 conditions= only emergencies)
  • Changes in arterial PCO2= Most dominant mechanism for regulating ventilation on a minute-to- minute basis(CO2 is the important regulator

can assume that rise in CO2 means drop in O2 so we breathe in more so it’s leveled out= works most of the time
but shortfalls if CO2 rich environment)

  • Changes in arterial H+ unrelated to CO2 =Special circumstances & metabolic conditions =Important in regulating acid-base balance in the body
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10
Q

What are the effects of hyperventilation & hypoventilation on arterial PO2 and PCO2?

A
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11
Q

What are the Peripheral chemoreceptors?

A

aortic arch= nerve endisng that attach to aortic bodies and carotid bodies(carotid artery goes to the brain)
brain is the most sensitive to the change in oxygen

-detect changes in arterial PO2, H+, and PCO2 levels

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12
Q

What are the Central chemoreceptors?

A
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13
Q

What happens when PO2 decreases?

What is the Role of decreased arterial PO2?

A
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14
Q

What is the role if increased PCO2?

A
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15
Q

What is the Role of increased H+ (non-CO2 induced)?

A
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16
Q

How are diving animals adapted to not breathing under water?

A
  • normally when under water for us the CO2 builds up and then we need to breathe
  • their their brain is less responsive to the small changes
  • Nitrogen narcosis=due to changing pressure, they can control the nitrogen levels so they don’t come out of the solution
  • Dive refle:- decrease blood flow except to brain, heart and adrenal gland
  • decrease heart rate
  • decrease body temp
  • also decrease dtrenous movement
  • increase in haemoglobin (higher than most animals)
  • increased splenic contraction (more red blood cells in circulation need for oxygen and CO2)
  • decreased blood flow to skeletal muscle /high buffering (histidine dipeptides)=pH drop modified by the histidine dipeptides
  • have L and R breathing centers (left and right breathing center, so they can turn off half of the brain so less O2 is needed, so sleep om one side of the brain and then switch)
17
Q

What are the aseous euthanasia techniques?

A
  • CO2=pigs, dropped into a pit where there is CO2, high conc of CO2 damage to tissues especially brain= depression, dopey-sudden= they fall unconcious, however CO2 level makes O2 more needed= so high brathing, stressed= can there be high enough level of CO2 so it’s fast enough and no stress?
  • Carbon monoxide-irreversibly binding to Hb so death, so sheep put into a truck, the exhaust pipe in= death as the CO binds and no O2 can be bound, also change in pH, depends when unconcioussness occurs no CO2 build up so no reflex for stressed breathing do we get fast enough to unconsciousness without respiratory distress
  • nitrogen
  • Anaesthetic agents: sevoflurane, isoflurane
  • decompression=decrease the pressure of all the gases: decrease in all the gases so no build up= not the fast breathing, leads to difficulty in breathing