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25 Cards in this Set
- Front
- Back
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CNS control of respiratory function
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- Medulla oblongata (brainstem)
- Control of respiratory via chemoreceptors - aortic arch and carotid - Monitor PO2, PCO2, and pH - Other inputs to Medulla oblongata = receptors in skeletal mm (exercise) -> initiate more breathing - Also stretch receptors in lungs -> keep from blowing up too fast and causing damage - Irritant receptors -> make you cough -> keep from inhaling things... - Spontaneous breathing - cycles initiated from CNS (don't have to consciously think about it) - Cycles can be modified by higher controls (conscious thought) |
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Medullary repiratory centers
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- Dorsal respiratory group (DRG) = Primarily activates inspiration
- Inhibitory afferents from glossopharyngeal (XI) and Vagus (X) slow, fine tune actions - Ventral respiratory group (VRG) = contains both inspiratory and expiratory neurons |
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Pontine centers
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- Apneustic center - just above DRG and VRG in lower 2/3 of pons
- Reinforces inspiratory drive - Inhibitory afferents from Vagus (X) check action here - Pontine respiratory group (pneumotaxic center) - upper 1/3 of pons - Inhibits apneustic center - regulates breathing pattern |
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Regulation of respiratory rhythm
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- Based on transection of spinal cord - different results
- Level I - cut above pontine respiratory group = normal breathing pattern - no more conscious override from cortex, however - Level II - cut between PRG and apneustic centers - Normal if vagus (X) is intact - Apneustic (crazy long breaths) if vagus cut - Level III - cut below apneustic center, above DRG and VRG - Breathing maintained, but irregular intervals - Level Iv - cut below DRG/VRG - complete apnea! |
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Higher brain influences
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- Hypothalamus = changes breathing per emotional state
- Cerebral cortex - profound modification abilities - Talking, singing, instrument playing, breath-holding, etc. |
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Motor control of breathing muscles
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- Diphragm - C3,4,5
- Intercostals = thoracic innervation - Abdominal muscles = lower thoracic and lumbar supply |
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Respiratory motor neuron tracts in cord
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- Corticospinal = just lateral of dorsal horn = voluntary breathing
- Autonomic tracts are just ventral of ventral horn |
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Slowly adapting receptors in lungs
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- Myelinated afferents in vagal nerves - Stretch receptors in large/small airways
- Monitor stretch of airways - keep you from popping lungs - As lungs expand, smooth mm sustained firing - increased tone keeps from further stretching |
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Hering-Breuer inflation reflex
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- Stretch of lungs prompts expiration
- Inspiration cut short, expiration prolonged - Keeps from over-inflating lungs! - Largely inactive in adults unless TV exceeds ~1L (exercise) |
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Rapidly adapting receptors
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- Myelinated afferents in vagal nerves - irritant receptors in large/small airways
- Irritant receptors, mechanical/chemical receptors for sudden stimulation - Collapse of lungs prompts inspiration, increased resp. frequency |
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Hering-Breuer deflation reflex
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- Prompts inspiration when lungs are collapsing
- Try to keep airways, alveoli open |
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C-fiber endings in lungs
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- UNmyelinated afferents in vagal nerves - irritant receptors in pulmonary capillaries/interstium
- Also sensitive to irritants AND stretch - Has repiratory and cardiovascular effects - Bradycardia, hypotension - Bronchoconstriction - Apnea followed by rapid shallow breathing |
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Mechano- and Chemo receptors in upper airway
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- In nose, pharynx, larynx, uppermost trachea
- Similar to C-fiber endings in lower resp. tree - Sneeze reflex - receptors in vagal mucosa - Trigeminal (V) and olfactory (I) afferents - Cough reflex - upper airway afferents from vagus (X) - Diving reflex - Afferent fibers of trigeminal (V) - Via immersion of face in water - Apnea, profound bradycardia, increased systemic vascular resistance |
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Other reflex mechanisms
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- Pain fibers = somatic pain -> hyperventilation
- Visceral pain -> hypoventilation - Temperature fibers = Heat, fever -> increased ventilation - Cold shower, etc. -> deep inspiration - Skeletal mm. fibers = increase inspiration - Baroreceptors = decreased pressures -> increased respiration |
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Peripheral chemoreceptors
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- In carotid and aortic bodies (carotid response > aortic)
- Monitor PO2, PCO2, and pH - Does NOT respond to O2 content! - Anemic hypoxia, CO poisoning = DON'T stimulate breathing! - Carotid afferents - glossopharyngeal (XI) - Aortic = Vagus (X) |
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Carotid body cell mechanism
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- Type I Glomus cells
- If passing PO2 is low -> K+ channels shut - K+ shutting -> action potential -> Ca2+ channels open -> NT's released -> signal sent to breathe! |
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Ventilation changes due to various stresses
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- Highest affector = voluntary hyperventilation!
- Next is PACO2 level! - Finally, acidosis, PO2 |
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Ventilatory response to PAO2
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- The lower the PAO2, higher the drive to breathe
- Minute ventilation increases - Resulting hyperventilation -> lowers PACO2 *** If PCO2 kept constant during hypoxia -> profound increase in minute ventilation - Body really wants to get rid of excess CO2, even if O2 levels rise! |
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Overall low PO2 mech
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Low inspired PO2 -> low PAO2 -> low PaO2 -> chemoreceptors -> increased (hyper) ventilation -> PA and Pa O2 go towards normal...
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Ventilatory response to PACO2
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- Most important factor under normal conditions!
- Normally held within 3-4mmHg window! - Increase from 40 -> 45mm Hg = double VA! - When holding breath -> burning, need to breathe -> SpO2 really 98%... - Effect from PCO2! - Low PCO2 inhibits ventilation - Narcotics depress normal response to PCO2! |
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Hypercapnia
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High PCO2
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Factors affecting response to PACO2
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Sleep, narcotics, anesthesia
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Central chemoreceptors
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- Respond primarily to H+ changes based on PCO2
- CO2 readily diffuses across blood-brain barrier - Higher levels -> increased H+ - Lower pH stimulates signal to breathe - Breathing reduces PACO2, PaCO2 -> CO2 diffusion levels normalize -> pH normalizes |
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Integrated response to high PCO2 (hypercapnia)
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- Peripheral (carotid, aortic) chemoreceptors respond first to high PaCO2 - contribute ~50%
- Primarily for short-term responses though - Central chemoreceptors (in brain, CNS) - manage normal, resting PaCO2 - Take over, manage long-term responses if PaCO2 stays high - Physcally takes longer for CO2 to diffuse across barrier, dissociate, make H+ and be sensed... |
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Ventilatory response to H+ (plasma [H+])
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As plasma [H+] increases -> stimulates increased ventilation
- Can be response to lactic acid as well! - Overall H+ response is weaker than PCO2 response! |
