Resp 6 Flashcards
feedback control for regulation of ventilation
-control system includes centers in the cerebrum and brainstem, drives the resp muscles that bring about ventilation
-changes in ventilation cause changes in blood gas tensions and pH, which are monitored by central and peripheral chemoreceptors
neural control of ventilation; 2 principle activities
-Neural Centres in the brain that control respiration have 2 principal
activities:
1) Establish and Regulate rhythmic breathing (automatic, subconscious
control) to maintain normal blood gas levels
2) Adjust the rhythm to changes in:
* Activity level (O2 consumption rate)
* Metabolism (arterial blood gases & pH)
* Posture -> mechanical influences on respiration
* Non-respiratory behaviours (eating, sniffing, vocalizing)
Complex system
* Multiple inputs regulate the rhythm of breathing
* Multiple mechanisms of moving air (different muscles can expand
lungs)
innervation of the resp system
Motor Innervation:
* Somatic efferents to skeletal muscles controlling ventilation. Intercostal muscles innervated by thoracic spinal segments. Diaphragm innervated by phrenic nerve from
C3 - C5 segments
* ANS efferents to airway smooth muscle:
-parasymp innervation via vagus nerve. sympathetic innervation via thoracic segments
-ANS (Motor) innervation of airway smooth muscle:
* PSNS: bronchoconstriction via cholinergic stimulation – Vagus nerve
* SNS: bronchodilation via β2 adrenergic stimulation – sympathetic innervation from first few thoracic segements
sensory inputs to the respiratory centers
- Airway Receptors
1a) Slowly Adapting Stretch
receptors (SARs) (via vagus n.)
* In airway smooth muscle
* Sense increase in airway volume (stretch) -> terminate inspiration
* By speeding inspiratory termination they increase respiratory frequency
* Sustained stimulation of SARs causes activation of expiratory neurons
1b) Irritant receptors (via vagus n.)
-In airway epithelium (coryna)
-Sense irritant gases, dust, smoke,
histamine, etc. -> trigger sm. m.
contraction -> bronchoconstriction,
cough, increased mucus production
1c) J receptors (“juxtacapillary
receptors”) also known as “C-fiber
receptors”. Via vagus n.
-In pulmonary interstitium near
capillaries
-Monitor blood composition and
interstitial volume à alter RR
(e.g. ↑RR when interstitial pressure
rises during infectious, allergic, or
vascular disease)
sensory input from skeletal muscles
(2) Sensory input from skeletal muscles (via muscle spindles/spinal cord) -> monitor force of contraction of respiratory muscles (respiratory effort) -> inhibit if too great (Stretch)
chemoreceptor sensory input
(3) Chemoreceptor Sensory
input from carotid and aortic bodies -> sense abnormally high or low pH, PaO 2 , Pa CO 2
-From central chemoreceptors
in brain (medulla etc.).
-Hypoxia, acidosis, and hypercapnia are potent stimuli for increased rate and depth of breathing
peripheral chemoreceptors
-Peripheral Chemoreceptors
-Carotid bodies (plus aortic bodies in fetuses)
* Monitor PaO 2 , Pa CO 2 , arterial pH (H+ concentration)
* Located at bifurcation of carotid arteries
* Carotid bodies are the only structures monitoring Pa O 2 in adults (aortic bodies do this in utero)
carotid bodies cells
Carotid Bodies
* Type I cells (“glomus” cells – sensory); trigger APs in CNS afferents
* Type II cells (“sustentacular” cells – supportive)
* Significant increase in ventilation with tiny ↑ in Pa CO 2 or ↓ in pH
* Modest increases in ventilation in response to ↓ PaO 2, until tension falls below about 60 mm Hg after which strong stimulation occurs
central chemoreceptors
Central Chemoreceptors
* CO2 diffuses readily across BBB into brain/CSF, causing a drop in pH
* Chemoreceptors in brain (medulla, pons, ventricles) respond to very small increases in P CO 2 mainly by sensing the drop in pH in brain and
CSF -> triggers robust increase in ventilation to keep pH within a
narrow normal range
sensory input from peripheral receptors
(4) Sensory input from peripheral receptors. (Pain)
-Stimulation of pain receptors can increase RR and depth
neural control of ventilation summary
The respiratory pattern generator uses simple reflexes to create the respiratory cycle, which is then modified by numerous central and peripheral sensory inputs
pulmonary defense; 1st line
1st Line – Anatomy and Barriers at Portals of Entry
* Primarily Innate and Nonspecific
Anatomy
* Physical locations of particle deposition
Respiratory Epithelial Cells
* Physical barrier
* Mucus
* Production of antimicrobial mediators (e.g. defensins, lysozyme, lactoferrin)
Mechanical
* Sneezing, cough, mucociliary clearance
particle deposition for pulmonary defense mechanism
(A) Large particles: Deposited by impaction in the bends in the larger airways
(B) Medium Sized particles: are deposited in the smaller airways by sedimentation
(C) Small particles: contact the walls of alveoli by diffusion
sources of mucus in resp tract
- In the Larger Airways: Goblet Cells
- In the Bronchi: Submucosal Bronchial Glands
- In the Respiratory Bronchioles: Non-ciliated Clara cells are the source
resp tract mucus
- The secretion of respiratory mucus is under autonomic regulation
- Changes in amount and composition occur in response to many stimuli and can be the cause or result of respiratory disease.
- Changes in the viscosity of the
aqueous sol layer (in which the cilia
beat) impairs ciliary function. - Changes in the viscoelastic properties of the superficial gel layer
alter clearance rates
