Regulation of Breathing.txt

  1. Rhythmic breathing begins in the?
  2. Rythmic breathing is mainly from neurons located in the?
  3. Contains mainly inspiratory neurons. They send impulses to the motor nerves of the diaphragm and external intercostal muscles, providing the main inspiratory stimulus.
    Dorsal Respiratory groups (DRG)
  4. The basic breathing pattern is modified by sensory impulses transmitted back to the DRG via the _______ and ______ from the lungs, airways, peripheral cheoreceptors, and joint proprioceptors,
    Vagus and glossopharyngeal nerves
  5. Contain both insiratory and expiratory neurons.
    Ventral respiratory groups (VRG)
  6. They affect abduction of the vocal cords, expiratory discharge patterns and send impulses to the internal intercostal and abdominal expiratory muscles.
  7. These neurons have mostly inspiratory discharge patterns and transmit impulses to the diaphragm and external intercostal muscles. This area may be the pacemaker of rhythmic breathing.
  8. Neurons associated with this may function as the respiratoty rhythm generator.
    Botzinger complex
  9. During quiet breathinf inspiratory neurons from the DRRG and VRG fire with increasing frequency for Approx. ______ then they switch off allowing expiration for ______.
    2 sec. and 3 sec.
  10. At the start of expiration, inspiratory neurons fire briefly, _______ the earlt phase of expiration.
  11. Inhibitory neurons are controlled by
    pneumotaxic center and pulmonary stretch receptors
  12. The Pons modify the output of the medullary centers. There are two groups of neurons:
    Apneustic and Pneumotaxic centers
  13. if isolated will cause prolonged inspiratory gasps interrupted by occasional expirations.
    Apneustic center
  14. The Vagal and pneumotaxic center impulses appear to hold the __________ in check.
    Apneustic center
  15. Controls the "switch-off" point of the inspiratory ramp, thus controlling inspiratory time.
    Pneumotaxic Center
  16. It appears that the pneumotaxic and apneustic centers work together to?
    control the depth pf inspiration.
  17. Strong pneumotaxic signals do what?
    increase the respiratory rate
  18. Weak pneumotaxic signals do what?
    prolong inspiration and increase tidal volume
  19. is generated by strech receptors located in the smooth muscle of both large and small ariways. Overstretching of the lungs sends inhibitory impulses through tthe vagus nerve to the DRG neurons to stop inspiration.
    Hering-Breuer Inflation reflex
  20. This reflex is activated by a large VT (.800ml-1.0L or greater) Not important control mechanism for quiet breathing, but is important in exercise, regulates respiratory rate and depth of breathing.
    Herin-Breuer Inflation Reflex
  21. Sudden collapse of the lung stimulates strong inspiratory efforts wia the vagus nerve. It causes hyperpnea (eg., pneumothorax)
    Deflation Relflex
  22. helps with deep brethds during exercise, periodic deep sighs during quiet breathing, and baby's first breath. The receptors for this reflex stop firing promptly after the volume change occurs so they are called " rapidly adapting receptors".
    Head's Paradoxical Reflex
  23. Are vagal sensory nerve fibers in the epithelium of the larger conduction airways. Stimulation can be by inhaled irritants or mechanical factors causing bronchoconstriction, coughing ,sneezing, tchypnea, and narrowing of the glottis.
    Irritant Receptors
  24. Irritant receptors are called ______, which are responsible for laryngospasm, coughing, and slowing of tyhe heart rate. eg. airway suctioning, ET intubation, bronchoscopy
    Vagovagal Reflexes
  25. Are juxtacapillary receptors found in the lung parenchyma near the pulmonary capillaries. When stimulated they cause rapid, shallow breathing; a sensation of dyspnea; and expiratory narrowing of the glottis.
    J Receptors
  26. J Receptors are stimulated by three things:
    Alveolar inflammation, pulmonary vascular congestion, and edema.
  27. These are in the muscles, tendond, and joints, as well as pain receptors in muscles and skin. Send impulses to the medullary resiratory center to increase inspiratory activity causing hyperpnea.
    Peripheral Proprioceptors
  28. May be important in starting and maintaining increased ventilation at the strat of exercise. Involved with moving limbs, respond to slapping or splashing cold water on the skin, and other painful stimuli increasing ventilation.
    peripheral propriocptors
  29. these are in the diaphragm and intercostal muscles. They are part of a reflex arc that helps the muscles adjust to an increased load.
    Muscle Spindles
  30. As the intrafusal muscle fiber and extrafusal muscle fibers contract ( to elevate the ribs); the intrafusal muscle sensing element (spindle) streches and sends impulses over the _________________.
    spindle affernt nerves to the spinal cord
  31. Once the impulses have moved from the spindle afferant nerves to the spinal cord, it synapses directly with the alpha motor neuron in the spinal cord, sending impulses back to the main _______.
    extrafusal muscle.
  32. The impulse in the extrafusal muscle creates a single __________ causing the extrafusal muscle fibers to contract more and thus unload.
    Synapse arc
  33. Respiratory reflexes are involuntary nervous response located in the airways, muscles and tissues that influence breathing by sending information directly to the medulla by?
    Vagus Nerve
  34. Stimulus of hering-Breuer reflex?
  35. Responce of the Hering-Breuer reflex?
    inhibit via vagus
  36. Location of hering-Breuer reflex?
    airway, muscle
  37. Stimulus of deflation reflex?
  38. responce to deflation reflex
    strong insp. effort.
  39. location of deflation reflex?
  40. Stimulus of Head's Paradoxical reflex?
  41. responce of Head's paradoxical reflex?
    increased effort
  42. Location of Head;s paradoxical reflex?
  43. Stimulus of irritant receptor reflex
    physical irritation
  44. responce of the irritant receptor.
    Cough, sneeze, tachypnea, and bronchospasm
  45. location of irritant receptor reflex?
    epithelium in airway
  46. Stimulus of J receptors?
    alveolar inflammation
  47. responce of j receptors
    rapid shallow breaths, dyspnea
  48. location of J receptors
    near capillaries
  49. Stimulus of proprioceptors
    Movement, pain
  50. responce of proprioceptors
    stimulate ventilation
  51. Location of proprioceptors
    Muscle, tendon
  52. Neural impulses from the respiratory center travel to the diaphragm by way of the right and left
    phrenic nerves
  53. The cervical, thoracic, and lumbar motor nerves stimulate the?
    external intercostal muscles (accessory muscles of inspiration)
  54. Coordinates signals from the higher brain region, great vesselsm airways, lungs and chest wall.
    respiratory center
  55. Increased ventilatory rate =
  56. Decreased ventilatory rate =
  57. Is maintained by regulation of ventilation to adjust oxygen, carbon dioxide, and hydrogen ions in the blood.
  58. Are specialized nerve structures that respond to hypercapnia, acidemia, and hypoxemia.
  59. Transmit impulses to the medulla, increasing ventilation. Are centrally located in the medulla and peripherally located in the common carotid and peripherally located in the common carotid arteries and aortic arch.
  60. Located bilaterally in the medulla. Stumulated by hydrogen ions rather than CO2. Sensitive to CO2 in an indirect fashion. They are bathed in cerebrospinal fluid (CSF), separated from arterial blood by the blood-brain barrier. It is also almost impereable to hydrogen and bicarbonate ions, but permeable to CO2.
    Central Chemoreceptors
  61. When this is high, CO2 diffuses rappidly through the BBB into the CSF, CO2 reacts w/ H@O to form HCO3-. The H+ stimulates the central chemoreceptors to increase ventilation.
    Arterial PCO2
  62. Is the primary rapid controller of ventilation. It can get a response within secods.
    arterial PCO2
  63. For every mmHg rise of PCO2 causes a?
    measureable ventilatory response.
  64. The BBB is highly permeable to CO2 but almost impermeable to?
    H+ and HCO3-
  65. The effects of CO2 on the central chemoreceptors will gradually decline over?
    1-2 days
  66. This occurs because the kidneys will retain bicarbonate ions in responce to the respiratory acidosis, bringing the blood pH level back toward normal and homeostasis.
    Gradual decline of the effect of CO2
  67. These increase in the blood from kidney retention, diffuse across the BBB into the CSF. Here they will buffer the H+ and bring the CSF pH back to normal.. It removes the stimulus to the chemoreceptors, and ventilation decreases.
    bicarbonate ions
  68. Have a powerful effect on ventilation, which is greatly weakened after a dory or two of adaptation.
    Acute increases in PaCO2
  69. Two peripheral chemorecptors
    The carotid and aortic bodies
  70. Highly vacularized structures located bilaterally in the bifurcations of the common carotid arteries.
    Carotid bodies
  71. Highly vascularized structures located bilaterally in the bifurcations in the arch of the aorta.
    The aortuc bodies
  72. Stimulated by decreased PaCO2, increased PaCO2 and decreased arterial pH.
    Peripheral Chemorecptors
  73. Impulses from the cartid bodies travel to the medulla through?
    The glossopharyngeal nerve
  74. Impulses from the aortic bodies travel to the medulla through the?
    Vagus nerve
  75. These peripheral chemorecptors exert the most influence over respiratory centers.
    The Carotid Bodies
  76. Respond to a decreased PaCO2, oxygen that is dissolved in the plasma, rather than oxygen content (CaO2), which is combined with hemoglobin pus dissolved.
    Carotid bodies
  77. Oxygen content problems such as anemia and carbon monoxide poisoning do not?
    Stimulate Ventilation
  78. The carotid bodies are not stimulated significantly until the PaO2 falls to about?
    60mm Hg
  79. A the PaO2 drops below 60 mmHg the drive to ventilate increases proportionallu until it reaches about?
    30 mmHg
  80. In healthy individuals at sea level, thsis plays no role in the drive to breathe.
  81. As Co2 diffuses out of the CFS in responce to the low arterial blood PCO2, HCO3- remains behind in the CSF. This exposes the central chemoreceptors to an?
    Alkalotic enviroment
  82. The alkalotic enviroment has what kind of effect on the central chemorecpetors?
    diminishes the effect of the hypoxic vent. stimulus.
  83. The Blood pH level falls toward normal while the hypoxic ventilatory stimulus keeps the?
    PaCO2 low
  84. It takes how long for high altitude exposure before ventilation increases to its maximum level?
  85. peripheral chemorecptors account for what poercentage of the ventilatory responcse to hypercapnia.
  86. How much faster does the peripheral respond compaired to the central chemorecptors in responce to PaCO2
  87. The peripheral chemoreceptors respond synergistically to three things:
    Incease of PaCO2, decrease in pH, and decrease in Pa)2
  88. If a high PaCOS percists for days, the kidneys will do what?
    Retain bicarbonate
  89. This will sslowly move across the BBB meutralizing the pH of the CSF and negating any need to increase ventilation even though the CO2 level is high.
  90. COPD patients are not sensitive to elevated PCO2 but breathe off their? hypoxic drive
  91. The hypoxia in a COPD PT is caused two ways:
    1. Their High aveolar PCO2 dilutes alveolar PO2, casuing it to fall. 2. Many alveoli are underventilated with respect to blood.
  92. Oxygen-induced hypercapnia is caused by a combination of factors. The most important of which are these two:
    1. removal of the hypoxic stimulus 2. redistribution of V/Q in the lungs
  93. Low V/Q unit is hypoxic and hypercapnic while breathing ambient air. The hypoxia induces?
    Pulmonary vasoconstriction
  94. Predisposes the poorly ventilated unit to absorption atelectasis, decreasing ventilation morem while increasing its blood flow by relieving vasoconstriction.
    50% O2
  95. This lowers V?Q on bad alveoli while now creating dead space ( high V/Q) in others. The end result is an increased level of arterial PCO2.
  96. Uncontrolled O2 therapy can lead to ________ and _____ in chronically hypercapnic individuals
    hypoventilation and acute acidemia
  97. It is important to give spontaneourly breathing, hypoxemic, and chronicallt hypercapnic patients _____________ and then monitor O2 therapy closely with ABG, watching for acute CO2 retention and acidemia.
    low concentrations of O2 (24-28%)
  98. Lathough uncontrolled O2 therapy may lead to hypoventilation and acute hypercapnia in the PT with chronic CO2 retention, hyoxia is?
    more life-threatening
  99. Strenuous exercise will increase carbon dioxide production and oxygen consumption by?
  100. Do not change as long as ventilation keeps up with acid-base and oxygenation
    Arterial Blood Gases
  101. When the cerebral motor cortex send impulses to exercising muscles, it hay send collateral excitatory impulses to?
    the medullary respiratory centers
  102. Exercisinf limbs stimulate ______, which transmit excitatory impulses to the meduaalry centers.
  103. The increase in ventilation at the start if exercise may be a?
    learned responce
  104. The respiratory rate and tidal volume gradually increase, then gradually decrease to complete apnea which may last several seconds. Then the cycle repeats again. Occurs when cardiac output is low as with CHF, delaying the blood transmit time between the lungs and the brain.
    Cheyne-Stokes respiration
  105. The lag time between ventilation and the medullary center Seen in cheyne-Stokes breathing is seen with CHF, but it can alos bee seen with?
    Brain Injuries
  106. Is similar to Cheyne=Stokes except that tidal columes are identical depth.
    Biot's Respiration.
  107. Biot's repiration occurs with patients with?
    increased intracranial pressure
  108. indicates damage to the pons
    apneustic breathing
  109. it is related to midbrain and upper pons damage associated with head trauma, severe brain hypoxia, or lack of blood flow to the brain. This is gasping inspirations.
    Apneustic breathing
  110. High levers of __________ dilate cerebral blood vessels, increasing the normal brain's blood flow.
    Arterial carbon dioxide
  111. Hypercapnia dilates _______, which can increase intracranial pressure.
    cerebral vessels
  112. With brain trauma, as the brain swells, intracranial pressure may increase. To reduce intracranial blood flow, __________________ may help.
    hyperventilation w/ vasoconstriction
Card Set
Regulation of Breathing.txt
regulation of breathing