Resp 5 Flashcards by sophie rosen

The ultimate goal of

respiration is to

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

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

increase

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

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

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There are two basic controls of breathing:

Voluntary: Corticospinal tract
Automatic: Ventrolateral tract

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

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

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

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

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Respiration is Primarily Controlled by Two

Areas within the Brainstem:

Medullary Respiratory
Centers:
Pontine Respiratory
Group

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Medullary Respiratory

Centers: (2)

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

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Pontine Respiratory

Group (2)

– Pneumotaxic Center

– Apneustic Center

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Dorsal Respiratory Group: DRG—

Nucleus of the Tractus

Solitarius (NTS)

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Dorsal Respiratory Group: DRG—Nucleus of the Tractus

Solitarius (NTS) (3)

– 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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Provides excitatory inspiratory stimuli to phrenic motor

neurons (3)

• 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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DRG contains opiate receptors ( receptors) that, when

activated, (2)

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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Ventral Respiratory Group: VRG –

Nucleus Ambiguus and

Nucleus Retroambiguus

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

expiration

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Expiration is normally a passive process, so these

neurons are — during normal breathing

quiescent

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neurons are activated when

forceful expiration is required

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Control motor neurons for (3)

• 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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Pneumotaxic Center
• When activated,
• Might inhibit the

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

Apneustic
Center.

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Apneustic Center
• Its activation causes
• Antagonist to

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

Pneumotaxic
Center

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

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

A Number of Respiratory Reflexes are

Sensitive to Mechanical Stimuli (4)

Hering-Breuer Reflex (achieve optimal rate and depth)
Irritant Receptors (protective)
J Receptors (function unclear)
Joint & Muscle Proprioceptors

Hering-Breuer Reflex (achieve optimal rate and depth) (2)

• 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.

Irritant Receptors (protective) (3)

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

3. J Receptors (function unclear) (2)

• 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.

4. Joint & Muscle Proprioceptors (3)

• 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

skipped Joint & Muscle Proprioceptors purpose

“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.”

MOST important for minute-to- | minute control of breathing

Central Chemoreceptors:

Central Chemoreceptors: | located on

ventral surface of medulla

Central Chemoreceptors: | activation stimulates

the DRG

Central Chemoreceptors are | VERY sensitive to changes in

pH of CSF

``` Central Chemoreceptors are VERY sensitive to changes in pH of CSF (3) ```

``` • 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 ```

Activation of Central Chemoreceptors | by PaCO2, but not arterial [H+] (3)

``` 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. ```

``` The effect of a change in CO2 is potent acutely, but diminished chronically!! WHY??? ```

Central Chemoreceptors are most effective within --- | days after a change in central CO2

1-2

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

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

A danger for patients with chronic respiratory problems is | that the

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

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

peripheral

Peripheral Chemoreceptors | • Receptors are located in the (2)

aortic bodies and carotid | bodies

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

``` – Glossopharyngeal nerves (CN IX) from the carotid bodies – Vagus nerves (CN X) from the aortic bodies ```

Peripheral Chemoreceptors: | Sample arterial blood (2)

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

At PaO2 <60mmHg, there is a LARGE --- in | alveolar ventilation.

increase

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

increase | increase

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

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

Decreases in arterial pH --- the rate of carotid bodies

increase – Independent of CO2 control mechanisms

Hypoxemia enhances the response to

PaCO2

PaCO2 greater than --- stimulates an increase in alveolar respiration

35mmHg

Most inhaled anesthetics cause respiratory depression | by

inhibiting the DRG and abolish/attenuate the | response to hypoxemia (deceasing O2) and hypercarbia (increasing CO2).

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.

increases | decreases

Hypoxic drive is --- by nitrous oxide

decreased

Nitrous oxide -- pulmonary vascular resistance | decreases perfusion

increases

Nitrous oxide is a mild ---

sympathomimetic