03a: Regulation Flashcards
Rhythmic firing of neurons controlling respiration can generally modified by:
- Chemoreceptors, stretch receptors
- Immediate chemical environment
- Other control centers
- Voluntary control
Typical neuron associated with (inspiration/expiration) will show augmenting behavior, aka (X).
Inspiration;
X = High AP firing frequency to inspiratory muscles at onset of inspiration, then quickly decreases near end of inspiration
T/F: the phrenic nerve is one that shows augmenting behavior.
True
An increase in depth of inspiration can be brought about with which changes in nerve AP?
- Increase in frequency (steep uprise in slope)
- Recruit more fibers/motor units
- Longer “burst” duration
Increasing AP “burst” frequency will (increase/decrease) tidal volume, (increase/decrease) respiratory frequency, and (increase/decrease) minute ventilation.
Increase, decrease;
Thus, no overall effect on minute ventilation
Transaction of (X) part of brain stem results in respiratory arrest.
X = below medulla
List the three major groups of respiratory control center in brain stem.
- Dorsal resp group (DRG) in solitary tract nucleus
- VRG in medulla
- Pneumotaxic (PRG) in upper pons
(X) group in respiratory control center acts to produce early cutoff for inspiration.
X = pneumotaxic center (pons)
Removing input from pneumotaxic center is similar to removing input from (X). How is respiratory depth and frequency affected?
X = vagus
Increase depth, decrease frequency
Apneustic breathing is a result of loss of (X) input. Describe this respiratory pattern.
X = both vagal and pontine
Prolonged inspiratory period, interrupted by brief expiratory gasps
Hering-Breuer reflex: (X) receptors, activated by (Y), travel in (Z) to (directly/indirectly) stimulate respiratory (on/off) switch.
X = pulmonary stretch Y = lung inflation Z = vagus
Indirectly; off
T/F: there’s a lack of firing of inspiratory neurons during expiration.
True and vice versa
The thoughts are that respiratory pacemaker may be located in:
Pre-Botzinger complex (rostral portion of VRG)
Respiration: central chemoreceptors detect (X) and peripheral detect (Y) changes in arterial blood.
X = PCO2 Y = PO2, pH
Central chemoreceptors located in (X). And peripheral located in (Y).
X = medulla Y = carotid and aortic bodies
Effects of gas partial pressures on ventilation are most pronounced when PCO2 (changes/constant) and PO2 (changes/constant).
When they both change reciprocally (I.e. One increases while the other decreases)
Plot of Pa(CO2/O2) and ventilation is linear.
PaCO2; PO2 less effective at affecting ventilation
As PaCO2 increases, ventilation continues to (increase/decrease) until (X).
Increase;
PCO2 around 70-80 mmHg (toxic) decrease ventilation
T/F: inactivating peripheral chemoreceptors has an effect on ventilatory response to PCO2 levels.
False - essentially no effect at all!
Chronic elevation of PCO2, and thus (X) in immediate chem environment of central chemoreceptors, results in compensatory (increase/decrease) (Y).
X = H+
Increase
Y = HCO3-
T/F: central chemoreceptors are immune to sensitivity shifts in chronically high PCO2 levels.
False
T/F: arterial pH changes are not directly capable of affecting central chemoreceptors.
True
(X) peripheral receptors, in (Y) landmark, are more important than (Z) peripheral receptors as respiratory regulators
X = carotid bodies Y = bifurcation (common to internal/external carotid) Z = aortic bodies (on aortic arch)
Peripheral chemoreceptors are relatively insensitive to changes in O2 level unless there’s (increase/decrease) more than (X)%.
Decrease;
X = 10