regulation of ventilation Flashcards

1
Q

why is the buffer system so effective?

A

when acid is added to the body fluids, concentration of HCO3- decreases by conversion to H2CO3 (made from water and CO2), CO2 is eliminated by respiration, minimizing the effect of change in numerator of fraction in equation, and also pH.

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2
Q

COPD is?

A

elasticity of the lung is lost-> incomplete exhalation and therefore retention of CO2. CO2 increases, pH decreases-> respiratory acidosis
increase CO2 also causes shift in O2 dissociation curve-> less O2 bound to Hb.

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3
Q

hyperventilation causes respiratory…?

A

alkalosis. CO2 is blown off and pH increases. when CO2 decreases, respirations slow and may even temporarily stop-> hypoxia

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4
Q

what is primary factor in respiratory control?

A

CO2

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5
Q

What does the voluntary control of ventilation?

A

neurons in cerebral cortex. Impulses sent to respiratory motoneurons via corticospinal tracts-> function in speech, voluntary breath holding, fear and pain

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6
Q

what do the centers in the medulla and pons do?

A

generate rhythmic, patterned excitatory output to muscle groups or either inspiration or expiratory muscles. Lower motor neurons located in phrenic nucleus (C3-C5)

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7
Q

what does transection of the brainstem below medulla do the respiration?

A

stops it completely

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8
Q

If transecting above medulla does not stop breathing completely, what does this mean?

A

indicates that medulla contains neurons sufficient for rhythmic breathing-> constitute central pattern generator (CPG)

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9
Q

what group of neurons are apart of the CPG?

A

neurons capable of rhythmic patterned output in absence of outside influence or sensory feedback. If cut the sensory neurons in vagus nerve, does not block patterned breathing

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10
Q

what is the primary stimulus for inspiration?

A

Dorsal respiratory group (DRG).

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11
Q

Where does DRG get stimulus inputs from?

A

central and peripheral chemoreceptors, pulmonary stretch receptors, somatic pain receptors and mechanoreceptors.

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12
Q

how does inspiration increase tidal volume?

A

during inspiration, phrenic nucleus activity increases in terms of rate and number of units discharged-> increase causes more and more muscle fibers to be recruited-> increase in number of motor units increases tidal volume

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13
Q

how is inspiration terminated?

A

by natural CPG rhythm modulated by sensory feedback

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14
Q

how is expiration termed?

A

primarily passive, although always tonic expiratory output and this may increase and become important in forced exhalation

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15
Q

what does the ventral respiratory group neurons control?

A

contain both inspiratory and expiratory neurons, inspiratory neurons go to accessory muscles

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16
Q

transection of pons causes?

A

no effect on breathing

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17
Q

why does a transcetion of the inferior pons cause sustained gasping?

A

due to unregulated output by inspiratory neurons by apneustic center which is regulated by pneumotaxic center in superior pons. cutting of inferior pons causes prolonged inspiration

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18
Q

how can inspiration be stopped with a cut inferior pons?

A

is vagus is cut and proximal stump is stimulated then inspiration can be stopped.

19
Q

Hering-breuer reflex?

A

vagal feedback is from stretch receptors in the lungs which when activated send efferent impulses via vagus to inhibit inspiration

20
Q

what is the main conclusion about breathing control?

A

medulla is capable of sustaining patterned breathing but pattern can be fine tuned by neurons in pons and by feedback via vagus

21
Q

what are the chemical controls of ventilation?

A

CO2 and H+ in CSF acting on central chemreceptors and by carotid and aortic body receptors responsive to pH, CO2 and O2.

22
Q

what is the principal chemical control of ventilation?

A

arterial CO2 acting at central chemoreceptors

23
Q

why CO2 an effective means of control?

A

CO2 production is directly related to rate of oxidative metabolism and to pH via the bicarbonate system

24
Q

what nerves are associated with carotid and aortic bodies?

A

afferents from the carotid are carried to medulla by CN IX and aortic bodies by X.

25
Q

what does each peripheral chemoreceptor contain?

A

island of 2 cell types (I and II) surrounded by sinusoidal capillaries. Sensory nerve fibers make ending among two cell types. These endings are probably the sensory structures for gas and or H+. Type I cell makes synapses with nerve endings

26
Q

when do neurons in the carotid and aortic bodies increase firing?

A

increase their discharge when pH decreases. Effect is to increase ventilation by increasing both rate and tidal volume.

27
Q

what does ablation of the carotid bodies result in?

A

loss of compensatory ventilatory response to hypoxia and about 30% reduction in ventilatory response to high CO2. (same effect if both carotid and aortic body are cut).

28
Q

maximal receptor activity is at?

A

very low PO2 values, but hypercapnea and acidosis augment the response to lowered PO2.

29
Q

where does CSF PCO2 and arterial PCO2 equilibrate rapidly?

A

ventral surface of medulla (near CN 6-10 and 11) cell have no direct contain with arterial blood but are bathed in CSF. CSF in close proximity to choroid plexus Blood flow high

30
Q

What is the blood brain barrier is poorly permeable to?

A

H+

31
Q

Can CO2 cross BBB?

A

Yes. hydrated to H2CO3, which dissociates to CO2 and H+

32
Q

what does acidosis in medullary CSF case?

A

enhances tidal volume

33
Q

central chemoreceptors respond..?

A

directly to H+ and indirectly to CO2.

34
Q

why does ventilatory response to high PCO2 wane after a couple hours?

A

compensatory transport of HCO3- across BBB via anion exchanger (HCO3- for CL-)

35
Q

Metabolic acidosis produces what?

A

respiratory stimulation.

36
Q

hyperventilation causes?

A

Metabolic alkalosis because fall in blood H+ by blowing off CO2. this depresses ventilation causing a rise in arterial CO2 and H+ eventually restoring normal pH.

37
Q

what happens to ventilation when metabolism increases?

A

PCO2 rises and ventilation increases to lower PCO2.

38
Q

the relationship between alveolar PCO2 and ventilation rate is?

A

nearly linear, but when PCO2 of inspired air comes near to alveolar PCO2-> CO2 elimination becomes difficult.

39
Q

what happens when inhaled CO2 levels are above 7%?

A

arterial PCO2 rises rapidly resulting in CNS depression, including the respiratory centers, and eventually CO2 narcosis and coma

40
Q

decrease in PO2 below 60 mmHg increases what?

A

discharge from peripheral chemoreceptors (carotid and aortic bodies)

41
Q

Why is carbon monoxide poisonous?

A

CO binds to Hb forming carboxyhemoglobin-> affinity between Hb and CO is 230 times stronger than affinity to O2. Binding of CO causes retention of O2 and failure of O2 to be released to tissues, shift of curve to LEFT.

42
Q

what are some non-chemical influences on ventilation?

A

proprioceptors and stretch receptors-> located in muscles and joints-> can stimulate ventilation
irritant receptors-> stimulated by chemical or mechanical irritants (histamine) and bradykinin during allergic reactions-> receptors in trachea and extrapulonary bronchi cause coughing and receptors in lungs cause rapid shallow breathing and bronchoconstriction

43
Q

when does the hering-breuer reflex function in adults?

A

at tidal volumes of 1 liter, during strenuous exercise. important in normal breathing in human and infants and other mammals.

44
Q

what may contribute to ventilatory response during pulmonary congestion or edema?

A

deflation receptors that stimulate rapid shallow breathing