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Flashcards in Control of Breathing Deck (24):

2 major variables that are regulated via changes in respiration?

pO2 and pCO2.


What/where are the sensors for regulation of respiration? What do they detect?

Peripheral, carotid bodies: sense pO2.
Central: sense CO2


What cell type is the chemoreceptor in the carotid body? How does it transmit signals?

Glomus cells - transmits signal via neurotransmitter releasse -> carotid sinus nerve (a branch of CN IX).


What kind of stimulus makes the carotid body fire? How is the firing rate dependent on CO2?

Hypoxia makes the carotid body fire more frequently. The impulse frequency vs. arterial PO2 has a non-linear relationship.

High pCO2 shifts this curve upward (more rapid firing), low pCO2 shifts it downward.

(One could also show it such that carotid body impulse frequency has a linear relationship with pCO2, with the slope determined by degree of hypoxia)


What do the central chemoreceptors for respiration control actually respond to?

Local pH.


Where is the central chemoreceptor anatomically? (kind of a trick question)

There are some chemoreceptors in the ventral medulla, but there are many areas of the brain that respond to pH.


What kind of sensors are there in the lungs? (3 examples)

Sensors of lung inflation. ("slowly-adapting")
Irritant/airflow receptors. ("rapidly-adapting")
Noxious agent/edema receptors. ("non-myelinated")


Respiratory muscles have sensors - those good old muscle spindles and tendon organs.

Right. The diaphragm has few muscle spindles, though.


What role does CN XII play in respiration?

Stiffens upper airway just before diaphragm contracts.


What does CN X do in respiration?

Narrows larynx during expiration as a "brake"


What's the area with pacemaker cells in the brainstem called?

The Pre-Boetzinger Area


3 accessory inspiratory muscles?
How useful are they?

Scalenes (elevated first 2 ribs)
Sternocleidomastoids (raise sternum)
Alae nai (flare nostrils)

They're not very useful - they use almost as much oxygen as is gained from extra ventilation.


What mainly controls ventilatory response to hypercapnia (hypercarbia)?

Central chemoreceptors


1 substance that increases slope of ventilatory response to hypercapnia?
2 drugs that decrease it?

Progesterone increases slope of response.
Opiates and benzos decrease the slope of response.


Ventilatory response is to low O2 is most important in what kind of situations?

In a healthy pt, high altitude.
Lung disease.
(low pO2 overrides central pCO2 sensing)


Why do blood gas levels not adequately explain ventilation changes in exercise?

After a dip in pO2 / rise in pCO2, ventilation is ramped up and blood gases returned to normal. Despite normal pO2 and pCO2, ventilation remains increased during exercise, suggesting some other mechanism driving ventilation is present.


Respiration rates in REM sleep vs. non-REM sleep?

Reduced respiration in NREM.
Irregular respiration in REM sleep.


In terms of wake stimulus and chemical stimulus (eg. pCO2) which has a greater effect on the phrenic n./diaphragm? On the upper airway?

Why is this important?

Chemical stimuli -> diaphragm.
Wake stimuli -> upper airway.

The most common type of sleep apnea is obstructive, because the muscles aren't keeping the upper airway patent.


Definition of apnea?
2 major types of apnea?
Which is more common?

Apnea = cessation of breathing for > 10s.
Obstructive: occlusion of upper airway - (drive for rhythmic diaphragm contraction continues/strengthens as pO2 drops/pCO2 rises).
Central: cessation of rhythmic motion of diaphragm / other respiratory muscles.

Obstructive apnea is way more common.


Does the brainstem seem to be more important for driving respiration when asleep or when awake?

Seems to be more important during sleep.


What's the weird thing about CO2-dependence of respiration during sleep?

During NREM, pCO2 seems to be key stimulus for breathing - ignoring pO2.
If pCO2 drops really low in NREM, people will stop breathing.
(thus hypocapnea = risk factor for central sleep apnea)


Two situations in which hypocapnia promotes central apnea?

CHF - due to high ventilation stimulated by edema (when pCO2 drops to low, apnea will occur) - explains Cheyne-Stokes respiration.

High altitude - high ventilation in response to hypoxia -> apnea when pCO2. (can cause periodic breathing)


What happens in congenital hypoventilations syndrome? (aka. Ondine's curse... but who the fuck would call it that?)
With what kinds of syndrome's is it associated?

Hypoventilation during sleep.
Associated with neural crest disorders (such as Hirschsprung's disease, neural crest tumors).
Treatment = chronic tracheostomy w/ ventilation, usually.


Gene mutated in Congenital Hypoventilation Syndrome?

PHOX2B - a transcription factor