Control of Breathing (B2: W7) Flashcards Preview

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Flashcards in Control of Breathing (B2: W7) Deck (57)

Where is the "central controller" for respiration?

  • Brainstem
  • Cortex - voluntary control
  • Limbic system, hypothalamus
    • Lesser degree
    • E.g. fear and rage


Where are the respiratory centers in the breainstem?

In the pons and medulla

  • Poorly defined collection of neurons rather than discrete nuclei 
  • 3 main groups of neurons
    • Medullary respiration center (main headquarters)
    • Apneustic center
    • Pneumotaxic center


What two regions of the medullary response center are overlapping, and what is each responsible for?

Dorsal respiratory group = inspiration

Ventral respiratory group = expiration



What is the organization of the medullary respiratory center?

Reticular formation below the 4th ventricle


Where is the pre-Botzinger complex, and what is it responsible for?

Medullary respiratory center

  • Intrinsic respiratory rhythm generator (liken to SA node)
    • Mechanism unknown
  • Caudal to Botzinger complex
  • Rostral to the ventral respiratory group 
    • Located in the reostral ventrolateral medulla (RVLM)


How do pre-Botzinger complex nuclei affect inspiration?

  • Starts with a latent period
  • Crecendo of action potentials
    • Causes stronger inspiratory muscle activity (ramp-type pattern)
  • Action potentials then cease
    • Inspiratory muscle tone falls to pre-inspiratory level 


What is the motor nucleus of CN IX and CN X, and what are the implications if it is destroyed?

Nucleus ambiguus

  • If destroyed, there is complete respiratory failure


How does the pneumotaxic center (dorsal) affect inspiration?

Input from the pneumotaxic center shortens breathing

  • Breathing rate increases
  • Breathing rate is also modulated by glossopharyngeal and vagal nerves 
    • Terminate in the tractus solitarus, close to the inspiratory center


Where do afferent signals from airways, lungs, heart, and peripheral chemoreceptors terminate?

CN IX and CN X

  • Glossopharyngeal and vagal
  • These nerves go into tractus solitarus
    • Part of the medulla


Describe the expiratory area during normal breathing

  • Quiescent during normal quiet breathing
    • Ventilation in this state is achieved by active contraction of inspiratory muscles (mainly diaphragm)
    • Followed by passive relaxation of the chest wall
  • More forceful breathing: increased activity of expiratory cells


What happens in animals if there is a transection above the apneustic center (lower pons)?

Affects breathing patterns

  • Expiramental sectioning leads to prolonged inspiratory gasps (apneuses)
    • Interrupted by transient expiratory efforts 
  • Apneuses are seen in severe breain injury 


What effect do impulses from the apneustic center have on inspiration?

Excitatory effect on the inspiratory center of the medulla


What is the role of the pneumotaxic center (upper pons) on inspiration?

  • Inhibits inspiration and controls inspiratory volume
  • Involved in fine tuning of respiratory rhythm
    • If ablated, normal respiratory rhythm intact  


What effect does a transection of the pneumotaxic center have on breathing?

Irregular rate or depth of breathing

  • Gasping, ataxic, or both


What areas are damaged, causing transient vs. permanent apnea?

  • Transient apnea: lesion in the temporal lobe
  • Permament apnea: lower pons and medulla (around nucleus ambiguus)


What causes central neurogenic hyperventilation?

Medial reticular formation


What is Ondine's curse and what causes it?

Loss of automaticity

  • When you fall asleep, you lose the ability to breathe on your own
  • Medial reticular formation or anterolateral C2 (reticulospinal pathway from cordotomy)


Describe Cheyne-Stokes respirations

  • 10-20 second periods of apnea followed by equal periods of hyperpnea
    • Seen with high altitude, severe heart disease, or sever neurological injury
  • Unstable feedback in respiratory control system
    • Overblow the PCO2 so that it is too low, then breathing has to stop (apnea) to bring it back up
    • Then PCO2 will be too high, and rapid breathing returns


How does the cortex influence breathing?

Cortex can override the function of the breainstem within limits

  • Voluntary hyperventilation can halve the PCO2 to the point of muscular tetany 
    • Will increase pH by 0.2
  • Voluntary hypoventilation is more difficult
    • Influenced by PCO2 and PO2


What sensors in the body affect drive of breathing?

  • Central chemorecptors
  • Peripheral chemoreceptors
  • Lung receptors 
  • Other receptors 


Where are the central chemoreceptors located?

  • Rostral zone
    • Lateral to pyramids
    • Medial to CN VII to X rootlets 
  • Caudal zone
    • Lateral to pyramids
    • Medial to CN XII rootlet


What changes are central chemoreceptors responsive to?

  • Respond to change in H+ concentration
    • Increase in [H+] stimulates ventilation, and vice versa
  • Composition of the extracellular fluid is managed by CSF, local blood flow, and local metabolism


How do CO2 levels in the blood regulate ventilation?

CSF = most important region

  • CO2 levels in blood regulate ventilation by its effect on pH in the CSF
  • CSF is impermeable to H+ and HCO3- ions
  • Permeable to CO2 from cerebral blood vessels
    • Will liberate H+ from the CSF
    • Stimulates chemoreceptors
    • Hyperventilation


WHat happens in the brain as arterial PCO2 rises?

Cerebral vasodilatation

  • Results in increase CO2 washout in brain PCO2 levels
    • Leads to reduced brain acidification
    • Causes a reduction in the increased ventilatory drive from central chemoreceptors 
  • This is the reason for morning headaches in people who have sleep apnea
    • Apnea → increased PCO2
    • Vasodilation in the brain


How does hyperventilation affect pH in CSF?

Decrease in PCO2 → increase in pH in CSF

  • Less acidic



What is the apneic threshold?

The point at which rhythmic ventilation ceases at a given PCO2

  • PCO2 is so low that breathing stops


What is the normal pH of the CSF?


  • Due to reduced protein in fluid and less buffering capacity
  • Change in CSF pH for a given PCO2 is much greater than with blood



What happens if CSF pH is displaced for a prolonged period of time?

  • A compensatory change in [HCO3-] occurs as a result of transport across the blood-brain barrier
  • CSF pH does not return all the way to 7.32, but occurs more rapidly than blood
    • Renal compensation takes 2-3 days
  • More rapid compensation means CSF is more important in effect on changes in arterial PCO2 and level of ventilation 


What happens to the CSF of patients with chronic lung disease and chronic CO2 retention (i.e. advanced COPD or idiopathic pulmonary fibrosis)?

These patients have normal CSF pH

  • Have abnormally low ventilation for their given PCO2
  • They breathe normally, but the PCO2 is elevated
    • Compensation
    • Do not hyperventilate to blow off CO2


Where are peripheral chemoreceptors located?

Carotid bodies: In the bifurcation of the common carotid arteries

Aortic bodies: Above and below the arch of the aorta 


What are the two cell types in the carotid body peripheral chemoreceptors?

  1. Type I: glomus cells
    1. Large amounts of dopamine
  2. Type II: sustentacular cells
    1. Rich capillary supply
    2. Modulation of neurotransmitter release by physiologic and chemical stimuli affects discharge rate of carotid afferent fibers 


What changes do peripheral chemoreceptors respond to?

  • Arterial PO2 (chief stimulant)
    • Sensitivity to changes areound 75 mm Hg
    • Increases markedly PO2 < 50 mm Hg
  • pH
  • Arterial PCO2 increases


What happens in the absence of peripheral chemoreceptors?

Severe hypoxemia depresses ventilation

  • Presumed through a direct effect on respiratory centers
  • These receptors are responsible for all of the increase in ventilation in response to arterial hypoxemia 


How does hypotension affect the peripheral chemoreceptors and subsequently ventilation?

  • With hypotension, there is decreased blood flow to the carotid bodies
    • Decreased O2 delivery
  • Increase in ventilation


What are the different lung receptors that have an effect on breathing?

  • Pulmonary stretch receptors
  • Irritant receptors
  • J receptors 



Where are pulmonary stretch receptors and when are tehy activated?

  • Lie within the airway smooth muscle
  • Discharge in response to distention of the lung
  • Activity is sustained with lung inflation


What happens upon stimulation of pulmonary stretch receptors?

Increase expiratory time

  • Reduced respiratory rate (Hering-Breuer inflation reflex)
  • Inflation of the lungs further inhibits inspiratory muscle activity
  • Deflation will initiate inspiratory activity (deflation reflex)
    • Negative feedback loop


Why are plumonary stretch receptors more important in infants?

  • In infants: as the lung is stretched, there is a reflexive decrease in respiration
    • Can reduce minute volume
  • These reflexes are inactive in adults unless large tidal volumes are encouraged
    • E.g. exercise with > 1L tidal volumes



How does a transient bilateral blockade of the vagus nerve affect respiration?

Bilateral blockade of vagus does not affect respiratory rate or volume


Where are the irritant receptors of the lung and how are they activated?

  • Lie between airway epithelial cells
    • Travel via the vagus nerve
  • Stimulated by nocious gases, smoke, dust, and cold air
    • All of these are important stimulators of COPD and asthma exacerbations


How do the irritant receptors of the lung respond to stimulation?

Reflex effects include bronchoconstriction and hyperpnea

  • May play a role in bronchoconstriction of asthma attacks in response to released histamine


Where are the J (juxta-capillary) receptors of the lung and how are they activated?

  • Located in the alveolar walls near the capillaries
    • Travel up vagus nerve slowly in non-myelinated fibters
  • Respond quickly to chemicals injected into the pulmonary circuit
  • Net effect: rapid, shallow breathing
    • Intense stimulation = apnea 


What is the significance of the nasal and upper airway receptors?

  • Respond to mechanical and chemical stimulation
    • An extension of teh irritant receptors
  • Reflex responses include sneeze, cough, bronchoconstriction, and laryngeal spasm


What is the significance of the joint and muscle receptors?

  • Impulses from moving limbs in early stage exercise will stimulate ventilation
    • Increase in minute volume


What is the significance of the gamma system?

  • Located in intercostal muscles and diaphragm
  • Sense elongation
  • Involved in the sensation of dyspnea
    • Dyspnea = shortness of breath
    • Large respiratory efforts that are required to move lung and chest wall


How are arterial baroreceptors involved with ventilation?

  • Increase in blood pressure - hypoventilation or apnea
    • Not very common
  • Decrease in blood pressure - hyperventilation
    • Common
    • E.g. sepsis with shock


How do pain and temperature play a role in ventilation?

  • Pain - apnea followed by hyperventilation
  • Heating of skin - hyperventilation 


What is the most important factor in the control of ventilation under normal conditions?

Arterial PCO2

  • Variation of PCO2 curing the day is about 3 mm Hg
    • Tight control


How does PCO2 affect minute ventilation?

For every 1 mm Hg rise in PCO2, there is a 2-3 L/min increase in minute ventilation (Ve)

  • Large effect
  • Higher Ve for given PCO2 - the synergistic response
  • Lowering PO2


What are the various factors that decrease PCO2?

  • Sleep
  • Increased age
  • Genetics 
  • Race
  • Personality factors
  • Trained athletes 
  • Divers 
  • Narcotics
  • Increased work of breathing


A small change in PCO2 has a large effect on minute ventilation; how much of a change in PO2 is necessary to affect Ve?

Arterial PO2 has to be reduced to <50 mm Hg in order to produce an increase in Ve

  • Versus slight increase in PCO2 that produces the same effect
  • Increased PCO2 will increase Ve at PO2 < 100 mm Hg
    • Hypoxia and hypercarbia synergistic
  • PO2 has little effect on day-to-day management of minute ventilation
    • Except at high altitudes
    • Leads to a large increase in Ve


Why is hypoxic ventilatory drive extremely important in patients with chronic lung disease?

  • These patients have chronic retention of CO2
    • High PCO2 is normal for them
    • The body doesn't try to change it
    • Brain ECF pH near normal - little pH stimulation in peripheral chemoreceptors
  • Their breathing is driven by hypoxia
    • Hypoxia increases breathing rate
    • These patients need to be kept on reduced oxygen percentages
      • If O2 saturation is too high, they hypoventilate


What effect does hypoxemia have on central chemoreceptors?



What happens when there is hypoxemia in the absence of peripheral chemoreceptors?

Hypoxemia produces respiratory despression

  • When hypoexemia is prolonged, it can cause mild cerebral acidosis
    • Leads to increase in minute ventilation (Ve)


Does reduced pH without increased PCO2 have an effect on minute ventilation?


  • E.g. diabetic ketoacidosis
    • PCO2/bicarbonate is very low
    • Minute volume/ventilation (Ve) is very high
    • Blowing off a lot of CO2
      • Bicarbonate in blood is down less than a 5
    • pH can get to 6.6
  • Peripheral chemoreceptors - chief site of action
    • Need ventilation to get the minute volume back up


Can central chemoreceptors be involved in minute ventilation in response to pH?

Can be involved if the change in serum pH is large enough

  • The blood-brain barrier will become partially permeable to H+ ions


How does minute ventilation increase during exercise?

  • Mechanism unknown
  • Can increase Ve 15-fold
  • PCO2 falls slightly
  • PO2 remains nearly constant
  • Arterial pH falls with heavy exercise due to lactic acidosis