Mashour: Control of Breathing Flashcards
Reticular formation below the fourth ventricle
Medullary respiratory center
Intrinsic respiratory rhythm generator, likened to the SA node
Pre-Botzinger complex
2 regions of the medullary respiratory center
- dorsal respiratory group = inspiration
2. ventral respiratory group = expiration
Where is the pre-Botzinger complex located?
Caudal to the Botzinger complex
Rostral to the ventral respiratory group
Located in the Rostral ventrolateral medulla
Discuss how the Pre-Botzinger Complex works?
starts with a latent period
crescendo of action potentials
stronger inspiratory muscle activity (ramp-type pattern)
action potentials then cease
inspiratory muscle tone falls to pre-inspiratory level
Motor nucleus of CN IX and CN X
Nucleus ambiguus
If this is destroyed, may cause respiratory failure
Nucleus ambiguus (seen in polio)
Fasciculus solitarious
Smaller collection of neurons similar to nucleus ambiguus
Inspiratory ramp can be turned off by this center. It can cause shortened inspiration and an increased breathing rate.
Pneumotaxic center
Inspiration can also be modulated by these two nerves
Glossopharyngeal and vagal nerves
The medulla is the (blank) area
Expiratory
During quiescent breathing, ventilation is achieved by (blank) contraction of inspiratory muscles, followed by (blank) relaxation of chest wall
Active; passive
This is found in the lower pons
Apneustic center
Impulses from this center have an excitatory effect on the inspiratory center of the medulla
Apneustic center (sectioning in experiments above this area leads to prolonged inspiratory gasps interrupted by transient expiratory efforts
This is found in the upper pons
Pneumotaxic center
This inhibits inspiration and controls inspiratory volume. Involved in fine tuning of respiratory rhythm
Pneumotaxic center
10-20 second periods of apnea followed by equal periods of hyperpnea. Seen with high altitude, severe heart disease, or neurological injury
Cheyne-Stokes respirations
Describe apneustic breathing
Deep breath in, hold it, then exhale
This structure can override the function of the brainstem within limits
Cortex
Which is easier, voluntary hyperventilation or voluntary hypoventilation?
Voluntary hyperventilation, because when you hold your breath, it becomes very uncomfortable, and your midbrain will override your cortex and cause you to start breathing
Involved in affective states such as fear and rage
Limbic system and hypothalamus
Sensors for drive of breathing
Central chemoreceptors
Peripheral chemoreceptors
Lung receptors
These receptors respond to changes in H+ concentration. Increase in [H+] stimulates ventilation
Central chemoreceptors
How does CO2 levels in the blood regulate ventilation?
By its effect on pH in the CSF
As arterial PCO2 rises, what occurs to ensure that the brain does not become too acidified?
Cerebral vasodilatation → increases CO2 washout in brain → results in reduced brain acidification → reduces increased ventilatory drive from central chemoreceptors
The point at which rhythmic ventilation ceases at a given pCO2
Apneic threshold
What is the normal pH of CSF?
7.32
For a given increase in PCO2, is there a greater change in pH in the CSF or blood?
CSF
If CSF pH is displaced for a prolonged period of time, there will be a compensatory change in (blank)
[HCO3-]
With the high levels of CO2, does the CSF pH return all the way to 7.32?
No, but the response occurs more rapidly than in blood.
Renal compensation for high pCO2 takes 2-3 days, while CSF pH is mitigated much more rapidly. What does the more rapid compensation for rising CO2 in the CSF mean?
The CSF is more important in its effect on changes in arterial pCO2 and level of ventilation
Located in the bifurcation of the common carotid arteries (carotid bodies) and above and below the arch of the aorta (aortic bodies)
Peripheral chemoreceptors
2 cell types in the carotid bodies that work hand in hand to modulate our response to pO2
Type I (large amount of dopamine) Type II (rich capillary supply)
Three things peripheral chemoreceptors respond to
- arterial pO2 (chief stimulant)
- pH
- arterial pCO2 increases
When does sensitivity to changes in arterial pO2 begin? What level in mmHg?
Less than 50mmHg
Responsible for all of the increase in ventilation in response to arterial hypoxemia
peripheral chemoreceptors
Hypotension provides a clinical example of how the peripheral chemoreceptors work. Discuss.
With hypotension, there is decreased blood flow or O2 delivery to the carotid bodies, and this leads to an increase in ventilation.
3 types of lung receptors
- pulmonary stretch receptors
- irritant receptors
- J receptors
lie within the airway smooth muscle
discharge in response to distention of the lung
activity is sustained with lung inflation
Pulmonary stretch receptors
Stimulating these receptors will increase expiratory time and therefore reduce the respiratory rate
Pulmonary stretch receptors
Important reflex in newborns, in which inflation of the lungs further prohibits inspiratory activity, while deflation initiates inspiratory activity.
Hering-Breuer inflation reflex
lie between airway epithelial cells
stimulated by noxious gases, smoke, dust, and cold air
Irritant receptors
When you have a stimulus like smoke, it may cause broncoconstriction, which can be especially problematic for what type of patients?
Patients with COPD
Pulmonary edema is a classic example of activation of these receptors.
J receptors
These are located in the alveolar walls near the capillaries
J receptors
What’s the net effect of activation of the J-receptors?
Rapid, shallow breathing. When a patient comes in with pneumonia, this can be relevant.
engorgement of the pulmonary capillaries and increases in the interstitial fluid volume of alveolar wall activates what type of receptors?
J receptors
This system is located in the intercostal muscles and the diaphragm. Senses elongation and dyspnea (inability to breathe). Think of COPD, flattened diaphragm, so more work involved.
Gamma system
Concerning the arterial baroreceptors, a decrease in BP causes
hyperventilation
The most important factor in the control of ventilation under normal conditions is
Arterial pCO2
You only need a slight change in (blank) to cause a response in ventilation rate, but a larger change in (blank) to cause a response in minute ventilation rate.
CO2, O2
(blank) has little effect in day-to-day management of minute ventilation.
O2
Does hypoxemia have an effect on central chemoreceptors?
No
If no peripheral chemoreceptors, what would occur in the case of hypoxemia?
Respiratory depression
If you reduce pH without an increase in pCO2, this can produce an increase in (blank)
Ve (minute volume)
Minute volume (Ve)
Minute volume= tidal volume * respiratory rate
