Respiratory Chemoreceptors

CCHS patients are characterized by (5) (what do they lack)

-Central sleep apnea -Absent CO2/H+ chemoreceptor sensitivity -Absent carotid hypoxic chemoreceptor sensitivity -Normal exercise hyperpnea -Normal airway reflexes and respiratory mechanics lack chemosensitivty

Inhibitory Respiratory neurons in the VRC (3)

1. GABA 2. Glycine 3. Opioids

Excitatory Respiratory neurons in the VRC (4)

1. Serotonin (5HT) 2. Ach 3. Substance P 4. Norepinephrine- NE

3 major excitatory inputs into respiratory control neurons

1. State dependent neuromodulation 2. Carotid Chemoreceptor activity 3. RTN

Chemoreceptor signals in the carotid body are controversial/unknown: they are likely due to a change in what (environment and ion)

1. changes in conductance in potassium 2. changes in conductance in calcium which release serotonin or Ach low PO2, high PCO2

Carotid body has what type of cells (2)

1. chemoreceptors 2. sustentacular

When is cheyne-stokes breathing induced (3)

1. high altitudes 2. heart failure patients 3. unstable sleep states

Carotid artery branches (2)

1. internal 2. external

What receptors/neurons account for the apnea in CCHS patients (2)

1. reduced excitatory neurons during sled 2. lack of chemoreceptor excitatory input (no chemoactivity)

Which passes the membrane more easily: CO2 or H+

CO2

Intracranial chemoreceptors use what kind of chemoreceptors and where are they located

CO2-H+ chemoreceptors; brainstem

Neuromodulators or Neurotransmitters: which is the precursor

Neuromods are the precursor and they can affect whether NT get released

Ach is increased during which sleep cycle

REM

The absence of chemosensitivity in CCHS patients is due to an abnormal development of what (and what is it crucial for)

RTN (retrotrapezoid nucleus)- area in rostroventrolateral nucleus crucial for chemosensitivity

Cheyne-Stokes breathing causes (describe what happens)

apnea; due to increased/deeper breathing (longer than the apnea states)

Ventilation: higher during awake or REM sleep

awake; breathing slows during REM

What vessels surround the nucleus in the carotid body

capillaries

chemoreceptor neurons location

carotid body and brainstem

What cells mediates high altitude ventilator acclimatization

carotid chemoreceptor

Most SIDS die of which apnea

central sleep apnea

Central sleep apnea (is there a change in Pes)

cessation of air flow due to lack of chemoreceptor activity (so necessary signals aren't sent to muscles) -no change in Pes

Obstructive Sleep Apnea

cessation of breathing despite Pes changes and muscle activity

What type of relationship occurs between carotid chemoreceptor activity and PO2?

curvilinear; low PO2 means high chemoreceptor activity

Activity of 5HT and NE during wakefulness and slow wave sleep and REM sleep

decreased activity and an even high decrease during REM

The carotid chemoreceptors provide what type of input to the respiratory network of neurons: excitatory/inhibitory

excitatory

Glutamate

fast acting NT

Carotid chemoreceptor activity at high altitudes: low or high

high

What type of receptor activity is involved in Cheyne-Stokes breathing

high carotid chemoreceptor sensitivity

Carotid chemoreceptor denervation causes: hyperventilation, hypoventilation

hypoventilation

Hypercapnia and Hypoxia cause what to chemoreceptor impulse frequency

increase

GAB

inhibitory NT

What type of relation occurs between carotid chemoreceptor activity and PCO2?

linear; increased PCO2 means high impulse frequency of chemoreceptor activity

Carotid body location and innervation

located at the carotid artery bifurcation carotid sinus nerve

Cause of obstructive sleep apnea (and who is it more prevalent in)

loss of rhythmic and tonic muscle activity 1. alcohol consumption 2. men 3. increases with aging

Neurotransmitter mechanism:

neurochemicals released from presynaptic membrane and go through

Respiratory neurons in the VRC (ventral respiratory column) are stimulated by

neuromodulators

chemoreceptor neurons definition

neurons who's discharge rate is altered by PCO2 or PO2 in their environment

When there is no airflow in central sleep apnea, is there motion of the abdomen/chest wall

no

Is respiratory drive solely from chemoreceptors? (and what is this answer suggested by)

no; patients with CCHS (congenital central hypoventilation system)

Decrease in Hb SaO2 happens in which apnea

obstructive sleep apnea

Which apnea is caused by changes in the upper airway

obstructive sleep apnea

Central sleep apnea is highly prevalent in the consumption of what drug

opioids

Neuromodulators mechanism:

released from presynpatic membrane and bind to GPCR on postsynaptic which causes K+ and/or Ca2+ conductance which affects excitability of the cell

Is ventilatory response greater to respiratory acidosis or metabolic acidosis and why (hypothesized why, not definite) (and are k+ channels used)

respiratory acidosis; b/c sensing mechanisms are intracellular k+ channels can change

Synaptic vesicles located in the cytoplasm of the carotid body are in contact with which nerves

sensory nerve endings branching from the carotid sinus nerve

Inputs other than chemoreceptors: in what state will they not be present (and what are they called)

sleep; neuromodulators

What accounts for the reduction in ventilation during sleep in normal humans

state dependent neuromodulation

When there is no airflow in obstructive sleep apnea, is there motion of the abdomen/chest wall

yes, no airflow despite increased effort