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FHB II Pulmonary/Renal > Pulmonary 8: Control of Respiration > Flashcards

Pulmonary 8: Control of Respiration Flashcards

1
Q

Describe the phases of breathing.

What happens during exercise?

A

3 phases: inspiratory air flow, expiratory airflow, expiratory apnea

during exercise the frequency of breathing accelerates primarily by decreasing the pause time, and tidal volume increases by using the inspiratory reserve and expiratory reserve capacities

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2
Q

What does the neural respiratory controller do?

A

matches act of breathing with metabolic demands of the body

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3
Q

Describe the control of respiration in regards to sensors/effectors/central controller.

A

Slide 4

central controller (pons, medulla, other parts of brain) send output to effectors (respiratory muscles) which activate sensors (chemoreceptors, lung and other receptors) which send input to the central controller

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4
Q

What are the major sites of respiratory control in automatic respiration and voluntary respiration.

A

Automatic respiration:

  1. respiratory control center
  2. central chemoreceptors
  3. peripheral chemoreceptors
  4. pulmonary mechanoreceptors/sensory nerves

Voluntary respiration:
motor cortex–> corticospinal tracts

Peripheral chemoreceptors:
Small highly vascular bodies located in the region of the aortic arch and just medial to the carotid sinus at the bifurcation of the internal and external carotid arteries (near the baroreceptors).

Primarily activated by low arterial PO2 (like severe hypoxia) but also is affected by high arterial PCO2 and low arterial pH (high H+).

Afferent nerve activity from the carotid and aortic bodies is carried through the IX and X nerve, respectively, to the medulla (similar to the baroreceptors).

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5
Q

Draw a flow chart of starting with cerebral cortex showing how respiratory center/medulla activates mechano and chemoreceptors.

A

Slide 5

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6
Q

Describe the control of respiration as it pertains to medulla and pons in more detail. What are the main components?

For the pontine respiratory group (PRG) what effect does the apneustic center and pneumotaxic center have on DRG?

Draw/ refer to diagram

A 
medulla (generates breathing pattern) 
-dorsal respiratory grouup (DRG)
(nucleus tractus solitarius)
-ventral respiratory group (VRG)
(nucleus retrofacilias, nucleus retroambiguus, nucleus paraambiguus)
pontine respiratory group (PRG- controls breathing pattern)
apneustic center (excitatory effect on DRG)
pneumotaxic center (inhibits DRG)

Slide 6

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7
Q

What controls inspiratory and expiratory neurons?

A

DRG of medulla - inspiratory neurons

VRG of medulla - inspiratory and expiratory neurons

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8
Q

Describe the PRG components: apneustic center and pneumotaxic center

A

PRG controls breathing pattern

apneustic center: excitatory effect on DRG
(DRG=inspiratory neurons)

pneumotaxic center: inhibits DRG (inhibits inspiratory neurons)

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9
Q

Where are central chemoreceptors? What are they sensitive to?

Describe blood brain barrier (its permeability to H+ and HCO3- and CO2)

How do chemoreceptors respond to changes in PCO2 and PO2?

How do change sin PaCO2 affect PCO2 in CSF?

A

Slide 9
-located on ventrolateral surface of the medulla oblongata

  • sensitive to changes in pH in CSF
  • Blood brain barrier is relatively impermeable to H+ and HCO3- but is permeable to CO2

Respond to changes in PCO2 but not to changes in PO2

PCO2 in CSF changes with changes in PaCO2 within minutes

slide 9

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10
Q

Describe peripheral receptors. Where are they?

What do they respond to?

What are they responsible for?

A

carotid bodies, aortic bodies

Respond to decreases in PO2, decreases in pH (carotid bodies only), increases in PCO2

Responsible for 20-40% of the ventilatory response to CO2

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11
Q

What are the only chemoreceptors that respond to changes in PO2?

A

peripheral chemoreceptors

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12
Q

Draw a graph of robust firing activity of peripheral chemoreceptors when PaO2 is less than 70-80mmHg.

(arterial PO2 mmHg on horizontal axis and %maximal response on vertical axis)

A

Slide 11

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13
Q

Draw a diagram of how central, peripheral chemoreceptors and pulmonary mechanoreceptors and sensory receptors all send inhibitory or excitatory input to respiratory centers.

A

Slide 12

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14
Q

Describe pulmonary stretch receptors.

Where are they?

What is the Hering-Breuer inflation Reflex?

What is the Herine-Breuer deflation Reflex?

When are they active in adults/when may they be important?

A
  • within the smooth muscle cells of airways
  • inflation of lung inhibits inspiratory muscle activity (via vagus nerve)=Hering-Breuer reflex
  • deflation of the lung initiates inspiratory activity= Hering-Breuer deflation reflex

Hering-Breuer reflexes are largely inactive in adults, unless tidal volumes are very high
-may be important in newborns

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15
Q 
Describe irritant receptors. 
Where are they?
What stimulates them?
Where do impulses travel through?
What clinical role may they play?
A
  • thought to lie between airway epithelial cells
  • stimulated by noxious gases, cigarette smoke, dust, cold air
  • impulses travel through vagus nerve
  • may play a role in asthma
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16
Q

What do the J (juxtacapillary) receptors and bronchial C fibers respond to?

A

respond to chemicals injected into the pulmonary (J receptors) and bronchial (C fibers) circulation

17
Q

What are some other receptors involved in breathing control?

A

nose/airway receptors (irritant receptors)
-diving, aspiration, sneeze reflex

joint/muscle receptors

pain/temperature receptors

arterial baroreceptors

18
Q

Draw a response to CO2 graph in which alveolar PCO2 is on the horizontal axis and ventilation on the vertical axis.

What does slope resent?

At a normal PaO2 how much does ventilation increase for each mmHg rise in PaCO2?

What does reduction of PaCO2 result in?

At a lower PaO2 how will ventilation at a given PaCO2 change?/What happens to slope?

A

slope of curve= ventilatory response to CO2, test of CO2 sensitivity

At a normal PaO2, ventilation increases by 2-3L/min for each mmHg rise in PaCO2

Reduction of PaCO2 reduces the stimulus to ventilation (hyperventilation)

At lower PaO2:
ventilation at a given PaCo2 is higher
ventilation response to CO2 (slope) becomes steeper

19
Q

Evaluating the ventilatory response to CO2 graph how does it change in the following situations? Draw the lines on the graph (alveolar PCO2 is on the horizontal axis and ventilation on the vertical axis)

sleep, aging, trained athletes, divers, metabolic acidosis, drugs (morphine, anesthetics), if work of breathing is increased (COPD)

A

Slide 19

Both the slopes of response (sensitivity) and the position of the response curves (threshold, the point at which curve crosses the x axis) are changes, thus indicating differences in ventilatory responses and response thresholds

20
Q

When looking at a response to O2 graph (alveolar PO2 on the horizontal axis and ventilation on the vertical axis) how will ventilation at high PaCO2 change?

When will ventilation change at low and normal PaCO2?

Describe role of hypoxic stimulation in regulation of ventilation in healthy individuals.

A

At high PaCO2, ventilation increases when PaO2 is below 100mmHg

At low and normal PaCO2, PaO2 can be decreased to 50-70mmHg before ventilation increases

Hypoxic stimulation (response to O2) plays only a small role in the regulation of ventilation in healthy individuals

21
Q

Describe the stimulus for ventilation in patients with severe lung disease and chronic CO2 retention. (cave)

A

hypoxic stimulus becomes the main stimulus for ventilation

22
Q

Describe the response to pH:

How will metabolic acidosis affect ventilation? (What can be causes of metabolic acidosis?)

What regulates the ventilatory response to low arterial pH?

What happens in regards to the BBB at very low arterial pH?

A

Response to changes in arterial pH are often difficult to differentiate from the response to CO2

Metabolic acidosis (uncontrolled diabetes mellitus, kidney failure) increases ventilation despite low PaCO2

Ventilatory response to low arterial pH is regulated by peripheral chemoreceptors

At very low arterial pH, the blood brain barrier becomes partly permeable to H+

Graph explanation:
The ventilatory response to PCO2 is affected by the [H+] of CSF and brainstem interstitial fluid. During chronic metabolic acidosis (e.g., diabetic ketoacidosis), the [H+] of CSF is
increased and the ventilatory response to inspired PCO2 is
increased (steeper slope). Conversely, during chronic metabolic alkalosis (a relatively uncommon condition), the [H+] of CSF is decreased and the ventilatory response to inspired PCO2 is decreased (reduced slope). The positions of the response lines are also shifted, thus indicating altered thresholds

23
Q

Describe how exercise changes ventilation. By how much might ventilation change from resting levels?

Moderate exercise?
Severe exercise?

Between the following factors, which rise and which fall during exercise after the threshold for anaerobic threshold has been reached?

lactate, ventilation, pH, VCO2 (oxygen consumption), PaO2, PaCO2

A

ventilation increases promptly
-may reach 15x resting levels

O2 consumption of 4L/min
ventilation of 120L/min

(PaO2, PCO2 and pH do not change significantly during moderate exercise and the reason for increased ventilation is largely unknown)

Severe exercise: pH decreases as lactic acid is released,
anaerobic threshold is the point where the variables below change and is due to lactic acidosis

VCO2, lactate, PaO2 and ventilation increase
PaCO2 and pH decrease

24
Q

Describe obstructive sleep apnea syndromes by drawing how airflow and pleural pressure change.

A

Slide 23

in obstructive sleep apnea the pleural pressure oscillations increase as CO2 rises, this indicates that resistance to airflow is very high as a result of upper airway obstruction

(about 30% of normal individuals have brief episodes of apnea or hypoventilation during sleep which have no effects on blood gases

25
Q

Show how airflow and pleural pressure change in central sleep apnea. What is the most severe form?

A

Slide 24

central sleep apnea- no attempt to breathe (no oscillations in pleural pressure)

Most severe form: central alveolar hypoventilation (CAH, Ondine’s curse)
(CAH), also known
as Ondine’s curse, is a rare disease in which voluntary
breathing is intact but abnormalities in automaticity
exist. It is the most severe of the central sleep apnea
syndromes. As a result, people with CAH can breathe
as long as they do not fall asleep. For these individuals,
mechanical ventilation or, more recently, bilateral diaphragmatic
pacing (similar to a cardiac pacemaker) can
be lifesaving.

26
Q

Show by drawing how Kussmaul breathing is different than normal breathing pattern.

A

Slide 25

  • deep breathing with normal or reduced frequency
  • typical in severe acidosis (diabetic ketoacidosis)
27
Q

Show by drawing how apneustic respiration (apneusis) is different than normal breathing pattern.

Explain what apneustic respiration is and what it results from, what can result?

A

Slide 26.

Sustained periods of inspiration, followed by brief periods of exhalation

loss of input from vagal nerve and pneumotaxic center

brain damage, intoxication

28
Q

Show by drawing how Cheyne-Stokes ventilation is different than normal breathing pattern.

What can result?

A

Slide 27

  • varying tidal volume and ventilatory frequency
  • after a period of apnea, tidal volume and respiratory frequency increase progressively over several breaths, and then they progressively decrease until apnea occurs

brain injury, increased intracranial pressure, brain tumors, encephalopathy (can also be present during sleep at high altitude)

29
Q

Show by drawing how Biot’s respiration is different than normal breathing pattern.

What can result?

A

neuronal damage, poor prognosis

FHB II Pulmonary/Renal (20 decks)

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