Control of Respiration
Respiration vs. Cardiac Autorhythmicity:
Cardiac muscle:
¾
1. Pacemaker cells
2. Contractile cells
3. Neural input controls rate of contraction, not
action potentials
Respiratory muscle:
¾
1. Skeletal
2. NEEDS NEURAL INPUT
Message Input:
(excitatory or inhibitory)
Medulla
Spinal cord
Phrenic nerve
Diaphragm
Figure 13.34 Page 498
1
2 Neural Components:
Figure
13.33
Page 497
Rhythmic inspiration/expiration
1.
Respiratory control center
Pons
Pons
respiratory
centers
Respiratory
control
centers in
brain stem
Pre-Bötzinger
complex
Medullary
respiratory
center
Medullary
respiratory
center
Pneumotaxic center
Apneustic center
Dorsal respiratory
group
Ventral respiratory
group
Medulla
Dorsal respiratory
group
Ventral respiratory
group
Dorsal Respiratory Group (DRG)
1.
•
Inspiratory neurons
9 Firing causes inspiration (diaphragm & external
intercostals)
9 Cease firing causes expiration
Ventral Respiratory Group (VRG)
2.
•
Inspiratory & expiratory neurons
9 Inactive during normal quiet breathing
9 Work as “overdrive” for active breathing (muscles of
expiration & inspiration)
Pre-Bötzinger
complex
Pre-Botzinger complex
3.
•
•
•
Rhythm of ventilation
Neuronal configuration similar to SA node
Believed to control rate of DRG inspiratory
neurons
2
Pons
respiratory
centers
Pneumotaxic center
Apneustic center
“Fine-tuning” center
Pneumotaxic center
1.
•
Neuronal input aiding in “turning off” inspiration
Apneustic center
2.
•
Prevents inspiratory neurons from being “turned
off”
Hering-Breuer reflex & pulmonary stretch
receptors
3.
•
Prevents overinflation (exercise)
2 Neural Components:
Magnitude of ventilation
2.
Sensory
nerve fibers
Three chemical factors:
i.
Carotid bodies
PO2
•
Monitored by peripheral
chemoreceptors
ii. PCO2
iii. H+
Aortic bodies
PO2 fluctuation does NOT generally cause
increased respiration
i.
•
Hb-O2 saturation curves
3
Only if PO2 is dangerously LOW will
it cause ventilation stimulation!
Relieves
Arterial PO2 <60 mm Hg
Emergency
life-saving
mechanism
Medullary
respiratory
center
Peripheral
chemoreceptors
No
effect
on
Central
chemoreceptors
Ventilation
Arterial PO2
Figure 13.36 Page 498
PCO2
ii.
•
Major role in magnitude of ventilation
Central chemoreceptors:
1. Sensitive to changes in CO2 induced H+
concentrations in the brain ECF
2. Increased brain H+ directly stimulates central
chemoreceptors
Arterial PCO2
Relieves
Brain ECF PCO2
(when arterial PCO2
>70-80 mm Hg)
Brain ECF H+
Weakly
Peripheral
chemoreceptors
Medullary
respiratory
center
Ventilation
Arterial PCO2
Central
chemoreceptors
Figure
13.37
Page 501
4
¾
Arterial H+
• Aortic and carotid bodies highly sensitive to
changes in H+
Arterial H+
Acidosis
Cannot penetrate
blood-brain barrier
Relieves
Peripheral
chemoreceptors
Medullary
respiratory
center
No
effect
on
Central
chemoreceptors
Ventilation
Arterial PCO2
Arterial -CO2
-H+
Figure
13.38
Page 502
Questions?
5