Resp 5 Flashcards
The ultimate goal of
respiration is to
maintain
proper concentrations of O2,
CO2 and H+ in the tissues.
Excess CO2 or H+ activates
respiratory centers to —
alveolar ventilation.
increase
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.
There are two basic controls of breathing:
Voluntary: Corticospinal tract
Automatic: Ventrolateral tract
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.
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)
Respiration is Primarily Controlled by Two
Areas within the Brainstem:
Medullary Respiratory
Centers:
Pontine Respiratory
Group
Medullary Respiratory
Centers: (2)
– Dorsal Respiratory
Group (DRG)
– Ventral Respiratory
Group (VRG)
Pontine Respiratory
Group (2)
– Pneumotaxic Center
– Apneustic Center
Dorsal Respiratory Group: DRG—
Nucleus of the Tractus
Solitarius (NTS)
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
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
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.
Ventral Respiratory Group: VRG –
Nucleus Ambiguus and
Nucleus Retroambiguus
Ventral Respiratory Group: VRG – Nucleus Ambiguus and
Nucleus Retroambiguus
– Mostly involved in
– Primarily responsible for
expiration
expiration
Expiration is normally a passive process, so these
neurons are — during normal breathing
quiescent
neurons are activated when
forceful expiration is required
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.
Pneumotaxic Center
• When activated,
• Might inhibit the
shortens the
time of inspiration (possibly by
inhibiting the Apneustic Center).
Apneustic
Center.
Apneustic Center
• Its activation causes
• Antagonist to
excitation
of the DRG which results in
prolonged inspiration with brief
periods of expiration.
Pneumotaxic
Center
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.
- 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.
- 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
