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What is spontaneous respiration totally dependent upon?
- rhythmic discharge of nerve impulses originating in the brain that ultimately stimulates respiratory muscles to contract
- transection of the spinal cord above the origin of the phrenic nerves (at C1) stops breathing
What regulates these rhythmic discharges from the brain?
- changes in arterial pH, PO2, & PCO2 & several non-chemical influences
- respiration is under AUTOMATIC control via centers in the medulla & under VOLUNTARY control via the cerebral cortex
normal, quiet breathing
increased respiratory rate
increased rate & depth
sensation of breathlessness, labored breathing
dyspnea at rest while recumbent
cessation of breathing
- an abnormal pattern w/ waxing & waning tidal volume & periodic apnea
- it usually indicates severe CNS disorder
a regular rapid rate w/ large tidal volume usually caused by metabolic acidosis
- highly irregular inspirations usually separated by long periods of apnea
- usually seen with lesions to the medulla
- larger than normal breaths that occur automatically at regular intervals in normal subjects
- a yawn is an exaggerated sigh
prolonged inspirations separated by brief expirations
What part of the brain is responsible for automatic control of respiration?
- medullary centers: they generate respiratory rhythm
- medulla is made up of the bilateral dorsal respiratory group (DRG) & ventral respiratory group (VRG)
Dorsal & Ventral Respiratory Group (DRG & VRG)
- these fire in phase w/ the respiratory cycle
- regular breathing continues even after transection of the brain to separate medulla from pons
- this indicates that a Central Pattern Generator exists in the medulla
What type of neurons are mainly contained in the Dorsal Respiratory Group (DRG)?
- INSPIRATORY neurons
- they initiate inspiration w/ a weak burst of action potentials that gradually increase in amplitude over the next few seconds (Ramp Signal)
- connect to inspiratory muscles
- specifically they synapse w/ either Phrenic or Thoracic Spinal nerves
- the phrenic nerve connects to the diaphragm
- the thoracic spinal nerves connect to the external intercostals
- ceases for ~3 seconds to allow expiration, then the cycle begins again
- these signals correspond to the normal pattern of breathing
- the gradually rising ramp signal provides for a gradual increase in lung volume during normal inspiration
- RAMP PICTURE
- every time activity increases → air inspiration
- every time activity decreases → expiration
- originate in the DRG then go on to innervates the diaphragm to stimulate diaphragmatic contraction (pulled taught → more room as lungs expand during inhalation)
- can see from above diagram that as DRG neuron signals increase, the Phrenic n. signal gets larger as well
- the medullary center is probably stimulating the Phrenic n.
What part of the medulla is thought to act as a respiratory rhythm generator?
- the Botzinger Complex in the the VRG (Bot.C)
- it appears to contain pacemaker cells that spontaneously generate the respiratory rhythm & may excite or inhibit inspiratory cells in the DRG
Lower Part of the VRG
- contains both inspiratory & expiratory neurons
- inspiratory neurons receive input from the DRG neurons
- expiratory neurons in the VRG connect to outputs of expiratory muscles (are ONLY active during FORCED expiration)
- may be active in breathing during exercise but DO NOT fire during resting breathing
- the axons of motor neurons in the VRG leave the medulla via cranial nerves V, VII, IX, X, & XI to supply the larynx, pharynx, & other structures that INCREASE the diameter of the upper airways during Inspiration
- it also sends signals down the spinal cord to the inspiratory muscles
- caudal region of the VRG sends fibers down the spinal cord to the expiratory muscles
- respiratory pattern generator (Pre-Botzinger Complex?) activates inspiratory neurons in the VRG that stimulates the DRG ramp signal
- both the VRG & DRG stimulate inspiratory motor neurons in the spinal cord
- when inspiratory neurons STOP firing, the inspiratory muscles relax & allow passive expiration
- expiratory neurons in the VRG are important when large increases in ventilation are required to stimulate expiratory muscles (eg. during exercise)
- inspiratory & expiratory neurons in the medulla exhibit Reciprocal Inhibition: when inspiration is occurring, expiratory neurons are INHIBITED & vice versa
What might be the function of the apneustic & pneumotaxic centers in the Pons?
- may modulate medullary respiratory output
- are centers that exist above the DRG/VRG of the medulla in the PONS
- located in the lower pons just above the medullary centers
- electrically stimulating neurons in the apneustic center stimulate the DRG/VRG to cause more deep & rapid breathing (‘to breathe harder’)
- has a general excitatory effect on these medullary structures
- when stimulated it SHUTS OFF inspiratory activity
- is thought to ↓ inspiratory activity & ↑ expiratory activity
- (probably inhibits apneustic center, DRG, & VRG, or perhaps stimulating the VRG → forced expiration)
What part of the nervous system can OVERRIDE the functions of the brainstem?
- Cortical Centers
- they can override the functions of the brainstem to exert VOLUNTARY control of breathing
How do we regulate respiration?
the DRG RECEIVES input signals from peripheral cardiopulmonary sensors (peripheral CHEMOreceptors) that regulate respiratory rhythm
What are the 2 key places where Peripheral Chemoreceptors are located?
- 1. Arch of the Aorta, called the Aortic Bodies (entrance to the systemic circulation)
- 2. Carotid Bifurcation, called the Carotid Bodies (at the entrance to the brain)
- signals from these receptors reach the DRG via the afferent fibers of cranial nerves IX (glossopharyngeal) & X (vagus)
- specialized cells that are chemosensitive
- they respond to changes in PaO2, PaCO2, & pH in arterial blood passing through the aortic arch
- we expect the PO2 =100, PCO2 = 40, & the pH = 7.4
Afferent Fibers to the DRG
- from the picture it looks like Aortic Bodies project to the Vagus (Cranial X) n. → DRG
- while Carotid Bodies project to the Glossopharyngeal (Cranial IX) → DRG
- these cranial nerves might also project to the apneustic
What are the chemosensing cells of the Aortic & Carotid bodies called?
- Glomus cells
- Type I Glomus cells are depolarized by low PaO2, high PaCO2, & low pH → they release a neurotransmitter (NT)
- the NT stimulates afferent nerve fibers of cranial nerves IX & X that signal the DRG to increase ventilation
- these cells are essentially part of the nervous system
Which are more sensitive to hypoxia, the cells of the Aortic or Carotid bodies?
those of the CAROTID bodies are more sensitive than aortic bodies to hypoxia (low PaO2)
What is the response brought about by peripheral chemoreceptors to Hypercapnia (↑ PaCO2)?
• at normal Pa
(40 mmHg) we have normal alveolar ventilation (1)
• as the Pa
goes up there’s a STEEP rise in alveolar ventilation; this is brought about by ↑ firing of chemoreceptors
- • reaches a peak at ~100 mmHg PaCO2; any higher than that & a person’s in CO2 narcosis → ventilation is depressed, receptors become poisoned by the CO2
- • y-axis = rate & depth of breathing (how much air is being brought INTO the alveoli) as a function of PaCO2 (x-axis, amount of CO2 is in arterial blood)
How the Response to ↑ PaCO2 is Different When in Different States
- when the patient is asleep, the curve shifts to the right
- when under anesthesia or narcotics, both of which INHIBIT the response of the DGR, the curves are shifted right & their slopes diminished
- overall, the response is linear in the physiological range of PaCO2 values
- normally there is a 2-5 L/min increase in ventilation for each 1 mmHg increase in PaCO2
Why when under deep anesthesia does a person need to be ventilated?
- because the chemoreceptors that signal to the DRG via afferent cranial nerves are essentially non-functional
- a person’s own ventilation will be suppressed b/c the response of the chemoreceptors is suppressed under these circumstances
How do O2 levels affect ventilation in conjunction with different Pa or PA CO2 levels?
- chemosensors are more sensitive to PaCO2 when there is simultaneously decreased PaO2 or PAO2
- a rise in PaCO2 coupled to a drop in PaO2 would produce a GREATER stimulation of ventilation than either change alone
- (opposite way to say that is high PaO2 DECREASES the CO2 effect)
- O2 is often low when CO2 is high b/c that often happens when you’re under-ventilating
Why is it that arterial PO2 can decrease to ~75 mmHg before ventilation starts to increase?
- b/c between a PO2 of 100 & 75 mmHg, even though diffused O2 has decreased, oxygen from Hemoglobin hasn’t been unloaded/used up yet
- (O2 content hasn’t really changed EVEN THOUGH the PO2 has dropped)
- a PaO2 between 75-60 mmHg is when Hb begins to fail at adequately oxygenating peripheral tissues
At what point must PO2 drop to for chemoreceptors to stimulate an increase in ventilation?
- when PaO2 is below ~60 mmHg, the activity of receptors in Aortic & Carotid Bodies increases rapidly to increase ventilation
- this response to a drop in PO2 is INCREASED when there is simultaneously high PaCO2
Why do people often say that the chemoreceptor system is more sensitive to changes in CO2?
- b/c CO2 isn’t buffered by binding to hemoglobin - there’s less wiggle-room for changes
- linear changes in PCO2 manifest as changes in bicarbonate & carbamino hemoglobin as well
- there’s a buffer effect you see w/ O2 that isn’t seen with CO2
What is the ventilatory response to Hypoxemia?
- hypoxemia + hypercapnia → marked increases in ventilation
- changes in PCO2 also have an effect on ventilation response to hypoxemia
- as PCO2 increases, there’s an increase in ventilation as a function of arterial O2
- a rise in CO2 amplifies the O2 effects on ventilation
What happens to ventilation if you keep PO2 & PCO2 constant & JUST change the pH?
- it will all by itself produce an INCREASE in ventilation
- addition of a non-CO2 acid (eg. lactic) to the blood while keeping PaCO2 constant induces hyper-ventilation
- the response of chemo-receptors to both increased PaCO2 & decreased PaO2 is enhanced at lower pH
- same as peripheral but located within the CNS, specifically the medulla
- they provide sensory input to the DRG
- are stimulated by changes in the pH of the cerebrospinal fluid (CSF)
- a ↓ in pH → ↑ in ventilation
If H+ ions don’t readily diffuse through the blood-brain barrier, what is the only way the pH of cerebrospinal fluid changes?
- when ↑ CO2 crosses into the brain from the bloodstream (CO2 can pass through the BBB)
- ↑CO2 → ↑[H+]
- occurs when overinflation of the lung sends signals via the Vagus n. → Pneumotaxic Center to TERMINATE inspiration
- slowly adapting pulmonary stretch (mechano-) receptors located in the tracheobronchial tree or the lungs themselves fire & initiate this reflex when lung volume INCREASES
What would lack of input from these receptors lead to?
an Apneustic breathing pattern, aka one that consists of deep & prolonged inspirations + short expirations
Other Rapidly Adapting Mechano(stretch)receptors in the Upper Airway
can be found in lung parenchymal tissue + extrapulmonary airways that respond to tissue distention & irritation
Where are receptors for the sneeze reflex located? Coughing?
- in the nasal mucosa & pharynx
- those for coughing are located in the larynx, trachea, & bronchi
- stimulation of these centers cause a deep inspiration (rapid ↑ pressure in thoracic cavity) followed by a violent expulsion of gas
- for a cough, pressure first builds against a closed glottis, which then opens suddenly to allow forceful expiration of high pressure air
- are mechanoreceptors located among airway epithelial cells & respond to chemical irritants such as SO2, NH3, NO2, & inhaled particles such as dust, smoke, or cold air
- they also respond to histamine & leukotrienes
How do irritant receptors function?
- when stimulated they stimulate respiratory centers to augment respiratory activity & to CONSTRICT airways
- this promotes rapid, shallow breathing in an attempt to limit penetration of the noxious agents
- very small UNmyelinated nerve endings located right around the alveoli & alveolar capillaries
- [a rich network of small axons that innervate receptors (juxtacapillary or J receptors) within the alveoli & small conducting airways]
What do J receptors respond to?
- interstitial edema & engorgement of pulmonary capillaries
- they cause RAPID shallow breathing (& mediate the closure of the larynx → apnea)
- they also mediate tachypnea in response to pulmonary embolism
Mechanoreceptors in the Chest Wall
- they detect impediments to breathing in the chest wall & stimulate increased inspiratory activity
- include proprioceptive (positional) input from joints, tendons, & muscle spindles in the ribs + inspiratory muscles
- some spindle fibers project to the brain cortex to provide conscious sensation of respiratory movements
- eg. if someone sits on your chest THESE receptors detect that impediment & would subsequently ↑ the force of breathing
What do higher brain centers have the power to do?
- besides coordinate breathing w/ other behaviors, input from the cortex can temporarily OVERRIDE automatic control of breathing
- the CNS balances ventilation from automatic centers w/ the need to carry out non-respiratory activities such as talking, eating, sniffing, vomiting, breath holding, singing, playing a wind instrument, etc.
- these actions involve voluntary control over respiration but it is not absolute (eg. voluntary breath holding will be overcome by the ventilatory drive from chemoreceptors - their increased firing will overcome voluntary centers & the functions of automatic centers will kick in)