Pulmonary Physiology: Regulation of Respiration Flashcards
Activates muscles of breathing via spinal and cranial motor neurons innervating thoracic/abdominal and laryngeal/pharyngeal muscles
Central respiratory controller
Feedback from peripheral and central chemoreceptors assess changes in blood and CSF levels of
O2, CO2, and pH
Higher brain centers such as those responsible for sleep, wake, exercise, and emotion also regulate
Respiratory drive
Terminates inspiration (lung inflation)
Peripheral vagal feedback
Located in the rostral third of the pons
-The location of the pneumotaxic center
Pontine respiratory neurons (PRG)
Mediates smooth transition from inspiration to expiration by inhibiting inspiratory activity
-Located in PRG
Pneumotaxic center
The caudal 2/3 of the pons contains the
Apneustic center
In the absence of vagal feedback and the pneumotaxic center inspiratory terminating influences, we see the emergence of an
Apneustic breathing pattern (prolonged inspiration)
Contains the neurons responsible for spontaneous rythm generation
Medulla
Contains both inspiratory and expiratory neurons
PRG (n. parabrachialis and kolliker-fuse n.)
Activation of PRG leads to
Rapid, shallow breathing
Contians only inspiratory neurons
DRG (in nucleus tractus solitarius)
Contains both inspiratory and expiratory neurons
VRG (n. ambiguous, retrofacial n. and n. retroambigualis)
The respiratory “pacemaker” that can initiate rhythm generation
-part of VRG
Pre-Bötzinger complex
Respiratory rhythm is generated through a process of reciprocal inhibition between the
Inspiratory and expiratory neurons
Peripheral (carotid & aortic bodies) and central (rostroventral medulla) sites that make adjustments in breathing depth and rate based on changes in arterial blood gas tensions and pH
Chemoreceptors
Make adjustments in breathing depth and rate based on expansion of the lung and chest as well as irritation of the airways
Mechanoreceptors
The carotid body changes its level of activity in response to changes in
PaO2, PaCO2, and pH
Carotid body activity increases when PaO2 drops below
60 mmHg
Carotid body activity increases when
PCO2 increases (pH decreases)
Carotid body activity decreases when
PCO2 decreases (pH increases)
The central chemoreceptors change their activity in response to changes in
PCO2 and pH
Increases in PaCO2 normally increase
Ventilation
Respiratory diseases which severely impair the ability to excrete CO2 (e.g., severe COPD) result in chronic CO2 retention causing a desensitization of this center and these patients rely on their
Hypoxic drive ventilation
Ventilation during the awake state is regulated by
Chemical and mechanical drives and arousal
During sleep we lose the “wakefullness stimulus” this results in
Hypoventilation
During sleep, respiratory drive is controlled
Chemically
Can also result with narcotics, COPD, or deep anesthesia
Hypoventilation
Hypoventilation can be caused by
Sleep, narcotics, COPD, and deep anesthesia
Occurs with metabolic acidosis due to either peripheral or central chemosensory stimulation
Hyperventilation
Chemical drive alters ventilation due to a combination of both
CO2 drive and hypoxic drive
When PaO2 is 100 mm Hg, ventilation is regulated by the level of PCO2 primarily due to stimulation of
Central chemoreceptors (some contribution from carotid body)
When PaO2 levels decline below 60 mmHg, ventilation is regulated by both
PCO2 and PO2
Sensed by peripheral (primarily carotid body) chemoreceptors as O2 tension (PaO2) only and not O2 content (CaO2) or saturation (SaO2) (i.e., no response to breathing carbon monoxide)
Hypoxia
Hypoxic drive is a result of stimulation of the
Carotid body chemoreceptors
Hypoxia alone will have what affect?
Increased ventilation and decreased PCO2
Simultaneous increases in PaCO2 potentiates the increase in 𝑉ventilation at any given PaO2 enhancing the
Hypoxic drive
H+ does not cross the blood-brain-barrier so metabolic acidosis results in hyperpnea due to stimulation of the
Peripheral chemoreceptors
Hyperpnea (Ventilatory compensation) decreases PaCO2 and causes a rise in pH and a reduction in
Peripheral chemoreceptor drive
The reduction in arterial blood PCO2 creates a downhill CO2 gradient from the CSF to the arterial blood which results in an increase in CSF pH and a reduction in the
Central chemoreceptor drive
The ventilatory response to exercise can be broken down into
Three phases
Characterized by an abrupt increase in ventilation, which reflects the anticipatory response
Phase I
Gradual increase in ventilation involving a variety of afferents
Phase II
Steady state of ventilation that reflects a precise matching of ventilation to metabolism
Phase III
During slow wave sleep, we have
Hypoventilation
Repetitive episodes of upper airway collapse during sleep, resulting in partial or complete cessation of airflow despite persisting respiratory effort
Obstructive sleep apnea
The respiratory control centers are located in the
Medulla and Pons
The brain centers responsible for respiratory rhythm generation and patterning (amplitude and frequency) of the integrated neural output consist of the
Pneumotaxic center, apneustic center and the medullary dorsal and ventral respiratory groups
There are three major classes of vagal mechanoreceptors. What are they?
Slowly-adapting (stretch receptors), rapidly adapting (irritant receptors), and non-myelinated nerve endings (J receptors)
