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Physiology > Resp 5 > Flashcards

Resp 5 Flashcards

1
Q

The ultimate goal of

respiration is to

A

maintain
proper concentrations of O2,
CO2 and H+ in the tissues.

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2
Q

Excess CO2 or H+ activates
respiratory centers to —
alveolar ventilation.

A

increase

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3
Q

Decreased O2 increases alveolar
ventilation. However, it does not
directly impact

A

central respiratory
centers but instead acts on peripheral
chemoreceptors that relay the signal
to the central respiratory center.

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4
Q

There are two basic controls of breathing:

A

Voluntary: Corticospinal tract
Automatic: Ventrolateral tract

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5
Q

Voluntary: Corticospinal tract
– Involves
– Activated during (8)

A

descending input from the thalamus and
cerebral cortex, can bypass the respiratory control
centers in pons & medulla

talking, sneezing, singing,
swallowing, coughing, defecation, anxiety, fear, etc.

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6
Q

Automatic: Ventrolateral tract
– Primarily controlled by changes in
– Activated by

A

PCO2
• Less sensitive to PO2 and H+
• Pulmonary mechanical receptors

Respiratory Centers in the pons &
medulla (ex. DRG and VRG)

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7
Q

Respiration is Primarily Controlled by Two

Areas within the Brainstem:

A

Medullary Respiratory
Centers:
Pontine Respiratory
Group

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8
Q

Medullary Respiratory

Centers: (2)

A

– Dorsal Respiratory
Group (DRG)
– Ventral Respiratory
Group (VRG)

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9
Q

Pontine Respiratory

Group (2)

A

– Pneumotaxic Center

– Apneustic Center

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10
Q

Dorsal Respiratory Group: DRG—

A

Nucleus of the Tractus

Solitarius (NTS)

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11
Q

Dorsal Respiratory Group: DRG—Nucleus of the Tractus

Solitarius (NTS) (3)

A

– Inspiratory Center
– Receives afferent input from Cranial Nerves IX
(chemoreceptor) and X (chemoreceptor & mechanoreceptor)
– Provides excitatory inspiratory stimuli to phrenic motor
neurons

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12
Q

Provides excitatory inspiratory stimuli to phrenic motor

neurons (3)

A

• Sets the basic rhythm for breathing by setting the frequency of
inspiration—Central Pattern Generator
• Signal begins weakly, increases steadily for 2 seconds, then will
abruptly cease for ~3 seconds before resuming the cycle (12-20
breaths per minute)
• This mirrors the activity of the diaphragm

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13
Q

DRG contains opiate receptors ( receptors) that, when

activated, (2)

A

inhibit respiration and decrease sensitivity to
changes in PCO2. Opiate induced respiratory depression is
a challenge in pain treatment with opioids.

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14
Q

Ventral Respiratory Group: VRG –

A

Nucleus Ambiguus and

Nucleus Retroambiguus

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15
Q

Ventral Respiratory Group: VRG – Nucleus Ambiguus and
Nucleus Retroambiguus
– Mostly involved in
– Primarily responsible for

A

expiration

expiration

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16
Q

Expiration is normally a passive process, so these

neurons are — during normal breathing

A

quiescent

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17
Q

neurons are activated when

A

forceful expiration is required

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18
Q

Control motor neurons for (3)

A

• Expiratory muscles (abdominals, internal intercostals)
• Accessory inspiratory muscles
• There are a group of neurons in the pre-Bötzinger
complex that have respiratory pacemaker control.

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19
Q

Pneumotaxic Center
• When activated,
• Might inhibit the

A

shortens the
time of inspiration (possibly by
inhibiting the Apneustic Center).

Apneustic
Center.

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20
Q

Apneustic Center
• Its activation causes
• Antagonist to

A

excitation
of the DRG which results in
prolonged inspiration with brief
periods of expiration.

Pneumotaxic
Center

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21
Q

Afferent (sensory) information regulates the activity of the
medullary inspiratory center (DRG) via

A

central and peripheral
chemoreceptors and also mechanoreceptors (lung stretch and
muscle/joint receptors).

22
Q

A Number of Respiratory Reflexes are

Sensitive to Mechanical Stimuli (4)

A
  1. Hering-Breuer Reflex (achieve optimal rate and depth)
  2. Irritant Receptors (protective)
  3. J Receptors (function unclear)
  4. Joint & Muscle Proprioceptors
23
Q
  1. Hering-Breuer Reflex (achieve optimal rate and depth) (2)
A

• Stretch receptors in bronchi and bronchioles are activated when
the lungs over-stretch. To activate this reflex, tidal volume must
increase > 3 times (~1.5L/breath)
• Result: Stops further inspiration and decreases rate.

24
Q
  1. Irritant Receptors (protective) (3)
A

• Located between epithelial cells in conducting zone
• Stimulated by noxious exogenous substances, endogenous
agents, and mechanical stimulation
• Promotes rapid, shallow breathing, coughing, sneezing, etc.

25
Q
  1. J Receptors (function unclear) (2)
A

• In alveolar walls, “Juxtacapillary” and stimulated by alveolar
inflammatory processes (pneumonia), pulmonary vascular
congestion (congestive heart failure), and edema.
• Causes rapid, shallow breathing and a sensation of dyspnea.

26
Q
  1. Joint & Muscle Proprioceptors (3)
A

• Receptors are sensitive to change in position and muscle
movements—not metabolism
• Increase activity of DRG to increase rate of breathing
• Both active and passive movements stimulate respiration

27
Q

skipped
Joint & Muscle Proprioceptors
purpose

A

“Proprioceptors (positional sensors) in muscles, tendons, and joints,
and pain receptors in muscles and skin send stimulatory impulses to
the medullary centers, increasing inspiratory activity and hyperpnea.
For this reason, moving the limbs, slapping the skin, and other painful
stimuli stimulate ventilation in patients who have respiratory
depression. Splashing cold water on the skin has a similar
effect……Proprioceptors in joints and tendons may be important in
initiating and maintaining increased ventilation at the beginning of
exercise.”
“The diaphragm and intercostal muscles have muscle spindles that
adjust muscle tension to an increased load. “In this way, inspiratory
muscle force automatically adjusts to the load imposed by decreased
lung compliance or increased airway resistance.”

28
Q

MOST important for minute-to-

minute control of breathing

A

Central Chemoreceptors:

29
Q

Central Chemoreceptors:

located on

A

ventral surface of medulla

30
Q

Central Chemoreceptors:

activation stimulates

A

the DRG

31
Q

Central Chemoreceptors are

VERY sensitive to changes in

A

pH of CSF

32
Q 
Central Chemoreceptors are 
VERY sensitive to changes in pH 
of CSF (3)
A 
• A drop in CSF pH is reflective of 
(only) a higher-than-normal 
amount of PCO2
• Chemoreceptors in the CSF are 
only sensitive to changes in H+ 
concentration. 
• When CSF [H+] increases, , increase in respiratory volume and rate
33
Q

Activation of Central Chemoreceptors

by PaCO2, but not arterial [H+] (3)

A 
1. CO2 is permeable to the Blood Brain 
Barrier
2. In the CSF, CO2 is converted to H+ and 
HCO3- via Carbonic Anhydrase
3. The H+ produced in the CSF activates 
the Central Chemoreceptors which 
stimulates the DRG.
34
Q 
The effect of a change 
in CO2 is potent acutely, 
but diminished 
chronically!!  
WHY???
A
35
Q

Central Chemoreceptors are most effective within —

days after a change in central CO2

A

1-2

36
Q

Central Chemoreceptors are most effective within 1-2
days after a change in central CO2.
• This is because during (& after) that time period (2)

A

– the kidneys will have begun to compensate, reabsorbing
HCO3-
– HCO3- has slowly diffused through the BBB and CSF
barriers to buffer H+

37
Q

A danger for patients with chronic respiratory problems is

that the

A 
kidney and buffer mechanisms compensate for the 
elevated PaCO2 (and H+) so that they no longer stimulate 
the medullary respiratory centers.
38
Q

Then the — chemoreceptors-the only receptors
that sample oxygen content—become critical for
respiratory control.

A

peripheral

39
Q

Peripheral Chemoreceptors

• Receptors are located in the (2)

A

aortic bodies and carotid

bodies

40
Q

Receptors are located in the
aortic bodies and carotid
bodies (2)

A 
– Glossopharyngeal nerves 
(CN IX) from the carotid 
bodies
– Vagus nerves (CN X) from 
the aortic bodies
41
Q

Peripheral Chemoreceptors:

Sample arterial blood (2)

A 
– Sensitive to (activated by) 
Low PaO2, High PaCO2, and 
Low pH
– Only sensitive to dissolved 
gases
42
Q

At PaO2 <60mmHg, there is a LARGE — in

alveolar ventilation.

A

increase

43
Q

Increases in PaCO2 —
the rate of firing of both aortic
and carotid bodies to —
respiration.

A

increase

increase

44
Q

increases in PaCO2 increase
the rate of firing of both aortic
and carotid bodies to increase
respiration. (2)

A 
– Not as powerful as 
responses to central 
changes in PaCO2
– BUT respond 5 times 
more quickly than central 
chemoreceptors
45
Q

Decreases in arterial pH
— the rate of carotid
bodies

A

increase
– Independent of CO2
control mechanisms

46
Q

Hypoxemia
enhances the
response to

A

PaCO2

47
Q

PaCO2 greater than
— stimulates
an increase in
alveolar respiration

A

35mmHg

48
Q

Most inhaled anesthetics cause respiratory depression

by

A

inhibiting the DRG and abolish/attenuate the

response to hypoxemia (deceasing O2) and hypercarbia (increasing CO2).

49
Q

Not a problem seen with nitrous oxide (N2O). Nitrous oxide
actually — respiratory rate (tachypnea) and — tidal
volume (via central stimulation) so there is minimal change in minute
ventilation and PaCO2 levels.

A

increases

decreases

50
Q

Hypoxic drive is — by nitrous oxide

A

decreased

51
Q

Nitrous oxide – pulmonary vascular resistance

decreases perfusion

A

increases

52
Q

Nitrous oxide is a mild —

A

sympathomimetic

Physiology (53 decks)

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