Respiration Lecture 16: Pulmonary Defensive Reflexes Flashcards
4 pulmonary defensive reflexes
1) cough
2) sneeze
3) diving response (prevents H2O from entering airway)
4) laryngeal chemoreflex
dysphagia
disordered swallow
dystussia
disordered cough
cause and result of impaired airway defense
most neurological disorders. Result = dysphagia and/or dystussia
T or F: no therapy exists for impaired cough
T
Causes of enhanced airway defense
upper airway cough syndrome, asthma, gastroesophageal reflex disease, bronchitis, bronchiectasis, ACE inhibitor therapy side effect
Manifestation of enhanced airway defense
cough
One of the most common reasons why sick patients visit physicians in US
coughing. (Manifestation of many disorders)
Fx of cough/sneeze
removal of mucus or foreign matter from the nasal or pulmonary systems via generation of large expiratory airflows. Large inspiration followed by large expiration.
Sneeze vs. cough
soft palate lowers in sneeze to divert airflow out the nose
3 stages of typical cough
1) inspiratory phase (negative airflow)
2) Compression phase (0 airflow, intrathoracic P increasing behind closed airway)
3) Expiratory phase (positive airflow)
which muscles are active during inspiratory phase of cough?
diaphragm, chest wall, laryngeal dilators
Which muscles are active during compression phase of cough?
laryngeal constrictors, expiratory muscles
Which muscles are active during expiratory phase of cough?
expiratory abdominal and chest wall muscles
General reflex pathway for cough
Receptors in Larynx/lungs/airways stimulate brainstem cough generator —> respiratory muscles
C fibers and their effect on generating cough
pain/sensory receptors in lungs, esp. for chemical stimuli. Controversial influence on cough
Slowly adapting receptors and effect on generating cough
stretch receptors that monitor lung volume. Contribute to but are NOT sufficient to stimulate cough alone (passive role)
Rapidly adapting receptors and effect on generating cough
have strong influence via vagus nerve to generate cough
laryngeal receptors relay through which nerve to cause cough?
superior laryngeal n.
How is diving response stimulated?
Via nasal/facial receptors that communicate to brain through trigeminal n.
Effects of diving response
vasoconstriction, bradycardia, lung apnea via sympathetic nerves
advantage of diving response
Allows for reduction of metabolic rate/consumption of oxygen so you can stay submerged for longer periods of time. More pronounced in aquatic animals
laryngeal chemoreflex induced by:
larynx –> superior laryngeal n. –> brain
effects of laryngeal chemoreflex
laryngospasm, bradycardia, lung apnea
laryngeal chemoreflex
prevents aspiration of foreign matter. Common in neonates. Can be elicited via mechanical or electrical stimuli
Fx and distribution of smooth muscle in airway
Fx: controls diameter of airways. Present from trachea down to alveolar ducts
bronchospasm/bronchoconstriction
increased contractile activity of airway smooth muscle
bronchodilator
drug that relaxes airway smooth muscle
bronchomotor tone
baseline contractility of airway smooth muscle under normal conditions
local control of airway smooth muscle
relaxation or contraction of airways by release of various chemicals. Pro-inflammatory chemicals (serotonin, histamine, prostaglandin, leukotrienes) are released from mast cells eosinophils, and neutrophils in the airways. Norepinephrine causes relaxation
Where is norepinephrine released?
adrenal gland, sympathetic innervation
What do steroidal asthma meds inhibit?
Parasympathetic innervation to airway so they remain open
Parasympathetic control of airway
leads to bronchoconstriction via release of Acetylcholine
What do sensory C fibers release in response to chemical irritants or inflammatory mediators from mast cells, eosinophils, or neutrophils?
pro-inflammatory tachykinins
What is mucus composed of?
Glycoproteins (aka mucins)
Where is mucus formed/secreted?
Epithelial goblet and serous cells (small airways) and submucosal glands (large airways)
Where are submucosal glands found?
large airways
3 main functions of mucus
1) insulates airway from irritants
2) antibacterial
3) entrapment of particles
Factors that determine amount of mucus present in airways (4)
1) rate of secretion
2) rate of absorption by epithelium
3) ciliary transport
4) cough transport
Negative consequences of mucus accumulation
1) airflow obstruction
2) enhanced deposition of inhaled particulates
3) dilutes surfactant
Cystic fibrosis etiology
thickened mucus layer, thinned/dehydrated serous layer due to hyperactive Na channels and transfer of Na and H2O from serous to epithelial layer. Cilia therefore less able to clear pathogens.
parasympathetic control of mucus secretion
Brainstem preganglionics stimulate airway ganglia to release Acetylcholine, which stimulates mucus secretion
C fiber control of mucus secretion
C fibers directly innervate goblet cells and mucus secreting glands. They release tachykinins/mediators from inflammatory cells, which induces release of mucus.
Where are cilia found?
trachea to respiratory bronchioles. NOT in alveoli
Where do cilia “beat” to?
towards oropharynx
Where is cilia movement the greatest?
large airways
Fx of cilia
move mucus from distal airways to larger airways and ultimately out of resp. system
2 strokes of cilia
Effective stroke (actively pushes mucus layer towards oropharynx; requires more energy) and Recovery stroke (bends and moves away from oropharynx in serous layer in preparation for next stroke upward; requires less energy)
epiphase =
mucus layer
hypophase =
serous layer
Which layer is more viscous, epiphase or hypophase?
Epiphase. Floats on top of hypophase in “mucus flakes” and reduces forces needed to cough and move mucus up and out airway
