Lecture 24: Regulation Of Respiration Flashcards

1
Q

5 Respiratory Centers

A
  • Dorsal respiratory group: DRG
  • Ventral respiratory group: VRG
  • Pontine respiratory group: PRG
  • Botzinger complex: BotC
  • Pre-Botzinger complex
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2
Q

Generation of Normal Breathing Pattern

A
  • Medullary respiratory centers:
  • These centers that initiate breathing are located in the reticular formation of the medulla. These centers include:
    • The DORSAL RESPIRATORY GROUP (DRG): Located in the nucleus of the tractus solitarius
    • The VENTRAL RESPIRATORY GROUP (VRG)
  • Pontine respiratory centers:
  • The pontine respiratory centers include two areas located in the pons:
    • The APNEUSTIC CENTER
    • The PNEUMOTAXIC CENTER (= Pontine Respiratory Group (PRG)
  • See Slide 6-9
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3
Q

Dorsal Respiratory Group

A
  • Located in the dorsal portion of the medulla
  • Sets basic rhythm of respiration
  • Most of the neurons are in the nucleus of the tractus solitarius (NTS) and medulla reticular substance.
  • NTS is the sensory termination of both the Vagal and Glossopharyngeal nerves.
  • Receives information from:
    • Peripheral chemoreceptors
    • Baroreceptors
    • Several types of receptors in the lungs
  • Principal initiators of phrenic nerve activity
  • Receive many fibers from the ventral respiratory group
  • Receives lots of sensory information via the nucleus tractus solitarius
  • Mainly associated with inspiration:
  • Establishes ramp signal
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4
Q

Ramp Signal

A
  • The nervous signals transmitted to the inspiratory muscles (mainly diaphragm) during normal respiration:
  • Begin weakly
  • Increase steadily for about 2 seconds
  • Cease abruptly for about 3 seconds:
    • Allows for elastic recoil of lungs and chest wall to cause expiration
  • During heavy respiration:
  • Rate of increase of ramp signal increases rapidly.
  • Usual method for controlling rate of respiration:
  • Control limiting point at which ramp suddenly ceases
  • The earlier the ramp ceases, the shorter the duration of inspiration and expiration.
  • Thus, the primary function of the PRG (Pneumotaxic center) is to control the “switch-off” point of the inspiratory ramp.
  • A strong PRG signal results in 30-40 breaths per minute.
  • A weak PRG signal results in 3-5 breaths per minute.
  • See Slide 13
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5
Q

Pontine Respiratory Group

A
  • Pneumotaxiccenter
  • Located in the superior pons
  • In the 1920’s, lesions of the PRG were found to also influence respiratory timing.
  • Specifically, lesions of the PRG result in the loss of the ability to turn off inspiration.
  • Without additional input from vagus nerves
  • Mainly controls rate and depth of breathing
  • Transmits signals to the inspiratory center (DRG)
  • Apneustic center:
  • Located in the inferior pons
  • Loss of function causes prolonged inspiratory gasping (apneuses).
  • Normal function may be to limit lung expansion.
  • See Slide 16
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6
Q

Ventral Respiratory Group

A
  • Located in the ventrolateral portion of the medulla
  • Neurons of this group are found in the retrofacial nucleus, nucleus ambiguous and nucleus retroambiguous.
  • The rostral part of the VRG is the Botzinger complex and may be associated with coordinating VRG output.
  • The intermediate part of the VRG is associated with the dilation of the upper airway during inspiration.
  • Neurons of the caudal region synapse with motor neurons to the internal intercostals and other muscles used for forced expiration.
  • The neurons of this group are almost totally inactive during normal quiet respiration.
  • These neurons do not participate in the basic rhythmical oscillation that controls respiration.
  • During increased pulmonary ventilation, respiratory signals spill over from the DRG into the VRG, which then contributes to the increased respiratory drive.
  • The retrofacial nucleus contains expiratory neurons which form the Botzinger complex.
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7
Q

Pre-Botzinger Complex

A
  • This is a small area in the rostral part of the VRG.
  • Believed to be the site which generates the timing (frequency) of the respiratory rhythm (Central pattern generator).
  • Deciding the length of inspiration and expiration is also important in determining the frequency.
  • See Slide 20
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8
Q

Hearing Breuer Inflation Reflex

A
  • This reflex is a protective mechanism to prevent excess inflation of the lungs.
  • It begins with stretch receptors in the muscular portions of the walls of the bronchi and bronchioles.
  • See Slide 22
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9
Q

Chemoreceptors

A
  • An increase in carbon dioxide levels (hypercapnia) or a decrease in oxygen levels (hypoxia) result in decreased activity in most neurons.
  • This would be counterproductive for chemoreceptors, because it would result in a decrease in gas exchange.
  • Chemoreceptors INCREASE their rate of activity when hypoxia or hypercapnia occur.
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10
Q

2 Types of Chemoreceptors

A
  • Central:
  • Located on ventral surface of medulla
  • Indirectly sensitive to carbon dioxide levels in blood (based on pH)
  • Peripheral:
  • Sensitive to concentrations of oxygen (especially), carbon dioxide, and hydrogen ions
  • Include:
    • Receptors in aortic arch
    • Carotid body receptors
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11
Q

Central Chemoreceptors

A
  • The central chemosensitive area is located bilaterally 0.2 mm beneath the ventral surface of the medulla.
  • These receptors are especially sensitive to [H+].
  • H+does not easily cross the blood-brain barrier.
  • CO2 easily crosses the blood brain barrier.
  • CO2 + H2O –> HCO3 + H+
  • Heightened sensitivity to increased levels of carbon dioxide lasts for several hours but then begins to decline due to renal adjustments to the plasma pH.
  • Kidneys increase blood bicarbonate levels:
    • Reduces plasma and CSF [H+]
    • Bicarbonate ions diffuse through the blood-brain barrier.
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12
Q

Peripheral Chemoreceptors

A
  • Peripheral receptors are more sensitive to changes in oxygen levels in the blood and less sensitive to changes in plasma concentrations of carbon dioxide and hydrogen ions.
  • Some peripheral chemoreceptors are located in the aortic arch (aortic bodies).
  • Most peripheral chemoreceptors are located in the carotid bodies at the bifurcation of the common carotids.
    • (Note that these are not the same as the carotid baroreceptors, which are more important in regulating blood pressure.)
  • Carotid body cells:
  • Type I (glomus) cells:
    • Chemosensors
    • PO2-dependent K+channels result in K+ efflux when PO2 is high, leading to hyperpolarization of the cells.
    • ↓PO2closes channels and results in a depolarization that opens calcium channels, leading to neurotransmitter release.
    • Located close to fenestrated capillaries
  • Type II (sustentacular cells).
    • Play a support role similar to glial cells
  • Note that:
  • Chemoreceptors are exposed to PO2 of arterial blood not venous blood.
  • PCO2and H+are mainly responsible for regulating ventilation (at sea level) for PO2 between 60 and 80 mm Hg
  • See Slide 30-31
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13
Q

Slow-adapting pulmonary stretch receptors:

A
  • These receptors are located within the airways of the lungs.
  • These are slowly adapting receptors that are sensitive to stretch of airways.
  • Signals from these receptors travel in the vagus nerves to the medulla.
  • Signals from these receptors:
  • Terminate inspiration
  • Prolong expiration
  • Are probably not important in controlling tidal volume in adults at rest.
  • Are important in controlling respiration in:
  • Infants and Adults during exercise (Not sure if this is a mechanoreceptor)
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14
Q

Rapidly-adapting pulmonary stretch receptors

A
  • Appears to officially be a mechanoreceptor
  • These receptors are located within the airways of the lungs.
  • Sensitive to irritation, foreign bodies in airway, and stretch
  • Signals from these receptors travel in the vagus nerves to the brain.
  • Signals from these receptors elicit cough
  • These receptors override the normal respiratory control mechanisms
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15
Q

J Receptors

A
  • These are sensory endings (C fibers) in the alveolar wall in juxtaposition to pulmonary capillaries.
  • They are sensitive to:
  • Pulmonary edema (i.e., congestive heart failure)
  • Signals travel from these receptors to the brain via the vagus nerves.
  • Stimulation of these receptors elicits:
  • Cough
  • Tachypnea
  • These reflexes override the normal respiratory control mechanisms
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16
Q

Cheyne Stokes Breathing

A
  • Abnormal pattern of breathing characterized by a repeating pattern of:
  • Increasingly deeper and rapid breathing (HYPERPNEA)
  • Followed by gradual decrease
  • Resulting in temporary stop = (APNEA)
  • Repeat of pattern
  • Each cycle = 30 seconds to 2 minutes
  • If the apnea segment of the cycle is replaced with hypopnea (abnormally small breaths), the phenomenon may be called PERIODIC BREATHING.
  • The small breaths characteristic of hypopnea are not enough to ventilate the lungs, so, physiologically, it is similar to apnea.
  • If this phenomenon occurs during sleep, it is referred to as:
    • CENTRAL SLEEP APNEA SYNDROME: Caused by damage to the central respiratory centers or Abnormalities of the respiratory neuromuscular apparatus
  • Normally the lungs cannot build up enough carbon dioxide or depress the oxygen sufficiently in a few seconds to cause the next cycle to begin, so Cheyne-Stokes does not occur.
  • So what conditions can override the damping factors leading to Cheyne-Stokes breathing?
  • A long delay in the transport of blood from the lungs to the brain such as might occur in cardiac failure.
  • Increased negative feedback such as might occur in brain damage.
  • See Slides 39-40