Neural control of respiration

Card Set Information

Author:
marshenski
ID:
205361
Filename:
Neural control of respiration
Updated:
2013-03-12 19:38:31
Tags:
Boston College resp
Folders:

Description:
Flash cards for neuro unit
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user marshenski on FreezingBlue Flashcards. What would you like to do?


  1. What are the three main neuronal control centers involved in normal respiration?
    • Dorsal
    • Ventral
    • Pneumotaxic
  2. What is the most funamental group in control of respiration?
    Dorsal
  3. What aspects of respiration do the dorsal control neurons effect?
    Inspiration and the respiratory rhythm
  4. What aspects of respiration does the ventral group of neurons control?
    Inspiration and expiration.
  5. What is the end organ that the dorsal groups' rhythmic signaling goes to?
    The diaphragm
  6. In which specific area of the brain stem is the dorsal group located?
    The tractus solarius
  7. What are the three places that transmit signals to the dorsal group?
    • Peripheral Chemoreceptors
    • Barrorecptors
    • Lung receptors
  8. Through what two nervous pathways does the dorsal respiratory group receive feedback from the receptors?
    • Glosopharyngeal nerve
    • Vagus nerve
  9. Complete the sentence.
    In normal respiration a nervous signal is transmitted to the diaphragm that  begins ______ and increases _______ in a ramp like manner.
    Weakly, Steadily
  10. Typically, how long does the ramp like signal last?
    2 seconds.
  11. How long does the ramp signal cease allowing for passive exhalation?
    3 Seconds
  12. By what two means can the inspiration ramp be controlled?
    Increasing or decreasing the rate of increase in the ramp.

    Change of the limiting point.
  13. If the ramp signal ceases earlier than normal, how does that effect the inspiration?
    It would cause the inspiration to stop earlier.
  14. Name two neural centers that decrease the duration of inspiration.
    • Pneumotaxic center
    • Dorsal group
  15. How does the pnemotaxic center act to increase the number of breaths?
    It inhibits the dorsal group
  16. How will a strong pneumotaxic signal effect respitory rate? And a weak signal?
    • strong: increase
    • weak: decrease
  17. T or F:
    The ventral group has a strong effect on inspirations?
    false
  18. When is the ventral group active?
    When respritory drive become greater than normal (exercise)
  19. Does the ventral group control both expiration an inspiration?
    Yes
  20. What types of respiration is the apneustic center involved in?
    Abnormal resp (chene stokes)
  21. What effect does signaling of the apneustic center have on respiration?
    prolongs inspiration (gasps)

    "Apnesustic center is poorly understood" (repeated 3 times)
  22. How do lung stretch receptors effect respiration?
    When the lung is overinflated they inhibit the ramp signal ("switch off the inspiratory ramp") and stop further inspiration.
  23. What is the Hering-Breuer reflex?
    When stretch receptors in the lung switch off the inspiratory ramp to stop further inspiration in response to abnormally high tidal volume.
  24. The respiratory control center is extremely sensitive to changes in what three substances?
    oxygen, Co2 and H+ ions
  25. What is the site that oxygen acts on to produce changes in respiration?
    Peripheral chemoreceptors
  26. Where are the perpheral chemoreceptors located that respond to oxygen?
    Carotid and aortic bodies
  27. What specific area is sensitive to changes in H+?
    chemosensitive area, or the central chemoreceptors
  28. Of CO2 and H+ ions, which effects the chemosensitive area directly?
    H+ ions
  29. H+ cannot cross the blood brain barrier. How is it that H+ can  effect the chemosensitive area then?
    CO2 Crosses the BBB freely and is hydrated in the CSF to becomes carbonic acid  (H2CO3) and dissociates into H+ and bicarbonate (HCO3-)
  30. What effect does H+ stimulation have on respiration?
    H+ causes an increase in respiration
  31. Which of the following has a profound effect on inspiratory drive? H+ or CO2
    CO2 has a profound effect and H+ has a direct effect.
  32. How does an increased CO2 in the blood change respiratory drive?
    High CO2 can "drive" the effects of increasing H+ ions in the CSF thereby increasing respiratory drive
  33. What is the main controller of ventiltion under normal conditions?
    CO2
  34. Under normal breathing conditions which central neural group is in control of respiration?
    Dorsal group
  35. where are the central chemoreceptors found?
    Brain stem
  36. Where are the peripheral chemoreceptors located?
    In the aortic and carotid bodies.
  37. When is the excitation effect of CO2 greatest?
    The first few hours
  38. After the first few hours of CO2 excitation, what mechanism reduces the total H+ ion concentration in the CSF?
    Bicarbonate (HCO3-) is actively pumped through the BBB and combines with H+ to form carbonic acid. (H2CO3)
  39. As CO2 levels increase we would expect to see a profound increase in ________?
    alvelolar ventilation
  40. Which change in blood levels causes a greater change in respiration, low pH or increased CO2?
    CO2
  41. In abnormal conditions what is a back up mechanism for control of ventilation?
    Oxygen chemoreceptors.
  42. Where are the oxygen chemoreceptors located?
    In the carotid and aortic bodies.
  43. At what level of hypoxia do the oxygen receptors transmit signal to increase respiration?
    70 mmHg oxygen
  44. What is important to consider in a patient with a history of bilateral carotid endartectomies?
    Possible loss of hypoxic drive.
  45. At what of the two sites of peripheral chemoreceptors is the greatest number of receptors found?
    Carotid body vs the aortic body
  46. What would the composite effects of hypoxia and hypercarbia be?
    even greater increase in alveolar ventilation than either of hypoxia or hypercarbia individually.
  47. Voluntary control of respiration is controlled through what area?
    The cortex
  48. Where are the irritant receptors of the respiratory system found?
    • Epithelium of the:
    • trachea
    • bronchi
    • bronchioles
  49. When the irritant receptors are activated what is the bodies response?
    Coughing and bronchoconstriction
  50. When the pulmonary cappillaries are engorged they stimulate the "J Receptors" which can cause a person to experience what sensation?
    dyspnea
  51. What can happen to the respiratory central control if the pressure in the brain is increased too much?
    Depression of respiratory drive or cessation thereof.
  52. Why is art oxygenation impaired in pt's under general anesthesia?
    • decrease in FRC because of supination thus leading to collapsed airways.
    • General anesthesia decreases FRC though relaxation of the diaphragm
    • There is a higher % of shunt under anesthesia
    • Repiratory pattern is effected by anesthesia
    • "pt is breathing at a lower volume so their airways have a tendency to collapse."
  53. What can effect the respiratory pattern in anesthesia?
    The type of anesthesia and the depth of anesthesia.
  54. What is the respiratory pattern going to be like using a N2O/narcotic combination?
    RR will be slower and Tv will be larger
  55. What respiratory pattern will be manifested using volitile anesthetics?
    All volatile anesthetics cause an increase in RR and shallow breathing occurs.
  56. Why is it that under very deep anesthesia patients are noted to have jerky and irregular respirations?
    Lack of intercostal muscle contribution.
  57. What is paradoxical respiration?
    When the diaphragm descends but the chest does not expand.

    Aside from anesthesia, paradoxical respirations can be noted by airway obstruction.
  58. What effect does anesthesia (volitile anesthetic) have on spontaneous minute ventilation(SMV)?
    As volitile anesthetic increased in %concentration sensitivity to CO2 is decreased.
  59. What is the proposed reasoning behind chene stokes breathing?
    Heart failure.  The hypothesis is that in heart failure the blood slows to the point that CO2 builds up causing a temporary hypercarbia.  In response to the hypercarbia respiration increases and the pt hyperventilates and blows off enough CO2 to make the chemoreceptors shut off thereby allowing the CO2 to build back up again and the cycle repeats itself. (this is my understanding and may be flawed. I did not get this from any text or from Denise)

What would you like to do?

Home > Flashcards > Print Preview