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61 Cards in this Set

  • Front
  • Back
What are the central controllers of respiration?
Brainstem, cortex, and limbic system (fear and rage)
Where are the respiratory centers in the brainstem?
Pons/Medulla. Scattered group of neurons
What are the three main groups of neurons in the brainstem? Which is the main headquarters?
Medullary respiratory center (main), apneustic (fine control), and pneumotaxic (fine control)
Where is the medullary respiratory center?
reticular formation under the 4th ventricle.
What is the pre-Botzinger complex similar to?
SA NODE! Sets rhythm.
What are the overlapping regions in the MRC?
Dorsal respiratory group and ventral respiratory group.
What does DIVE refer to?
Dorsal = inspiration Ventral= expiration
Where is the pre-botzinger complex located anatomically?
Superior to the other respiratory groups and caudal to the botzinger complex
Pre botzinger is ... to the ventral respiratory group
Rostral (located in the rostral ventrolateral medulla) RVLM
In the PBC what is the order of events for an inspiration to occur?
latent period, crescendo of action potentials, stronger inspiratory muscles activity, AP decreases, inspiratory muscle tone falls to pre-inspiratory levels.
What happens if the nucleus ambiguus in the medullary respiratory center is damaged?
Respiratory failure (bulbar poliomyelitis)
How can the inspiratory "ramp" be turned off?
pneumotaxic center. inspiration becomes shorter and breathing rate INCREASES
vagal and glossopharyngeal nerves usually have what affect on respiration?
Shorter breaths. just like pneumotaxic center
Where do the afferent signals terminate for the dorsal respiratory group?
CN IX and X which then go into the tractus solitarus
Where is the expiratory area?
medulla. usually expiration is quiet. Passive.
Where is the apneustic center and what does that thing do?
Lower pons. prolonged inspiratory gasps interupted by transient expiratory efforts. EXCITATORY effect on the inspiration center of medulla.
What do we see in severe brain injury?
apneuses. NO one knows why but we need to know it.
What other stuff does the pneumotaxic center do?
INHIBITS inspiration and controls inspiratory volume. Fine tuning of respiratory rhythm.
So if we had apnea (transient) this would be due to a legion in the
What about permanent apnea?
And what about Cheyne-Stokes?
Temporal lobe
lower pons and medulla (around nucleus ambiguss)
Diffuses cerebral cortex, diencephalon (pyramidal tracts) ARENT YOU GLAD WE HAD NEURO ALREADY?
What causes central neurogenic hyperventilation?
Ondine's Curse (loss of automaticity) is due to what?
medial reticular formation
medial reticular formation or anterolateral C2
Explain what happens in Cheyne-Stokes?
10-20 second periods of apnea followed by equal periods of hyperpnea. High altitude, severe heart disease, severe neurological injury. Unstable feedback in respiratory control system (cycle of breathing)
Main issue with Cheyne-Stokes?
We are trying to control CO2 but once it gets too low the person stops breathing to let it build then begins again once it is too high
What's going on in the Cortex?
it can override the function of the brainstem within limits. Voluntary hyperventilation can halve the PCO2 to the point of muscular tetany. Voluntary hypoventilation is more difficult.
Is the breathing reflex regulated by CO2 or O2 more?
CO2
What are the 4 sensors for drive of breathing?
Central chemo
peripheral chemo
lung receptors
others (??)
Where are the central chemoreceptors and what do they contain?
Rostral zone (lateral to pyramids OF EGYPT) and medial to CN VII to X rootlets

Also the Caudal Zone (lateral to pyramids and medial to CN XII rootlet)
What is the most important receptor?
What does it respond to mainly?
The central chemoreceptors! 80% control of respiration here.
[H+] increase causes ventilation and vice versa.
What is the most important region for central chemoreceptors?
CSF! Impermeable to H+ and HCO3- but permeable to CO2 from cerebral BVs. Will liberate H+ from the CSF and stimulate chemoreceptors.
How do CO2 levels in blood regulate ventilation?
Because CO2 causes a pH change in CSF that gets relayed to the respiratory centers.
What happens in the brain as arterial PCO2 rises?
cerebral vasodilation. results in an increase CO2 washout in the brain and results in reduced brain acidification. Causes a reduction in the increased ventilatory drive from central chemoreceptors.
What causes hyperventilation?
What is the apneustic threshold?
decrease in PCO2= increase pH in CSF.
point at which rhythmic ventilation ceases at a given PCO2
Is changes in CSF pH for a given PCO2 higher or lower than in blood?
HIGHER. Really sensitive stuff.
Is the CSF ph higher or lower?
Lower. dues to reduced protein in fluid and less buffering capacity.
What happens if CSF pH is displaced for a long period of time? how quickly can it return to 7.32?
HCO3- can diffuse and compensate for the pH. pH does NOT return all the way to 7.32 but it occurs more rapidly than blood
The rapid compensation in the CSF suggests..?
CSF is more important in effect on changes in arterial PCO2 and level of ventilation!
In chronic lung disease, what is the CSF pH like? Ventilation?
Normal CSF pH but abnormally low ventilation for their given PCO2.
Where are those peripheral chemoreceptors?
bifurcation of the common carotid arteries (carotid bodies and above/below the arch of the aorta (aortic bodies) <20% of ventilatory response due to these.
What are the cells of the carotid receptors called?
Glomus cells.
Type I has alot of dopamine
Type II (sustentacular) has rich capillary supplies. Modulation of NT release by physiologic and chemical stimuli affects discharge rate of carotid afferent fibers
What is the chief stimulant that peripheral receptors respond to?
At what mmHg are the peripheral receptors sensitive to?
Arterial PO2 also pH and PCO2 increase to a lesser degree.
75. much more when less than 50. Carotid bodies have a high flow rate for their size.
What is the main role peripheral receptors play in hypoxemia?
they causes the increase in ventilation when they sense low PO2. W/o these, sever hypoxemia depresses ventilation.
SO, with hypotension what happens?
The carotid bodies sense there is decreased blood flow (PO2 and ventilation increases). Sepsis/shock
Are the peripheral receptors more sensitive to changes in CO2 or O2?
O2!
What are the 3 lung receptors?
Pulmonary stretch receptors ( in airway smooth muscle and dischage in response to distention of the lung and activity is sustained with lung inflation),
Irritant receptors (lie between airway epithelial cells and stimulated by noxious gases, smoke, dust, cold air)
and J receptors (alveolar walls near capillaries, respond quickly to chemicals injected into the pulmonary circuit!)
What does stimulation of the pulmonary stretch receptors cause?
increase expiratory time and reduce respiratory rate (Hering-Breuer inflation reflex)
Inflation of the lungs further inhibits inspiratory muscle activity
deflation will initiate inspiratory activity (neg feedback loop)
Are the pulmonary stretch receptors active in adults?
NO unless large tidal volumes are encountered (exercise). Bilateral blockade of vagus nerve does not affect respiratory rate or volume (reflex important in babies)
Where do the irritant receptors run near?
Vagus. Reflex effects include bronchoconstriction and hyperpnea. MAY play a role in bronchoconstriction of asthma due to histamine
What is the net effect of the J receptors and where are they?
travel up vagus slowly in non-myelinated fibers and produce rapid, shallow breathing (intense stimulation causes apnea)
What is the primary disease that J receptors play a role in?
Left heart failure. Engorgement of the pulmonary capillaries and increases in the interstitial fluid volume of alveolar wall activates them. Play a role in dyspnea.
What do the nasal and upper airway receptors respond to?
mechanical and chemical stimulation (extension of irritant receptors). Reflex responses include sneeze, cough, bronchoconstriction, laryngeal spasm.
What do the joint and muscle receptors do?
impulses from moving limbs in early stage exercise will stimulate ventilation
What is the gamma system? where is it?
in intercostal muscles and diaphragm. Sense elongation and involved in the sensation of dyspnea (large respiratory efforts that are required to move lung and chest wall)
What do the arterial baroreceptors respond to?
increased BP (hypoventilation or apnea)
decreased BP (hyperventialtion (shock/sepsis)
What do pain and temperature receptors stimulation cause?
Pain = apnea followed by hyperventilation
Heating of skin= hyperventilation
what is THE MOST IMPORTANT FACTOR IN CONTROL OF VENTILATION UNDER NORMAL CONDITIONS?
ARTERIAL PCO2!!!!!! DO NOT FORGET THIS!
How much variation is usually seen throughout the day in mmHg?
3 (tight control)
Responses to PCO2 are decreased by multiple factors like what?
age, sleep, genetics, race, narcotics, etc
So does PO2 have any effect in day to day management of minute ventilation?
Not really. Not as much as CO2. EXCEPT HIGH ALTITUDE ASCENT! (large increase in Ve)
What happens w/ chronic lung disease?
hypoxic ventilatory drive is very important for these people. CO2 retention is chronic and brain ECF pH near normal + renal compensation. If given HIGH FIO2, Ve may become very depressed. ?
Does hypoxemia have an effect on central chemoreceptors?
No. In absence of the peripheral chemoreceptors, hypoxemia produces respiratory depression. Can cause cerebral acidosis, which in turn leads to increase in Ve
What happens when pH is decreased w/o increased PCO2?
Increased minute ventilation. Chief site of action is the peripheral chemoreceptors. Centrals can be involved in the change if serum pH is large enough? The BBB will become partially permeable to H+
What happens to minute ventilation during exercise?
mechanism for increased Ve is unknown during maximal exercise. Fit young people at maximum O2 consumption can increase Ve by 15x. Arterial PCO2 falls slightly. Arterial PO2 stays constant. Arterial pH falls w/ heavy exercise due to lactic acidosis.