Lecture 24: Regulation Of Respiration Flashcards Preview

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Flashcards in Lecture 24: Regulation Of Respiration Deck (16):

5 Respiratory Centers

* Dorsal respiratory group: DRG
* Ventral respiratory group: VRG
* Pontine respiratory group: PRG
* Botzinger complex: BotC
* Pre-Botzinger complex


Generation of Normal Breathing Pattern

* 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
* Pontine respiratory centers:
- The pontine respiratory centers include two areas located in the pons:
-- The PNEUMOTAXIC CENTER (= Pontine Respiratory Group (PRG)

- See Slide 6-9


Dorsal Respiratory Group

* 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


Ramp Signal

* 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


Pontine Respiratory Group

* 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


Ventral Respiratory Group

* 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.


Pre-Botzinger Complex

* 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


Hearing Breuer Inflation Reflex

* 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



* 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.


2 Types of Chemoreceptors

* 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


Central Chemoreceptors

* 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.


Peripheral Chemoreceptors

* 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


Slow-adapting pulmonary stretch receptors:

* 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)


Rapidly-adapting pulmonary stretch receptors

* 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


J Receptors

* 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


Cheyne Stokes Breathing

* 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