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Egan's Ch. 14

Regulation of Breathing

apnea absence of spontaneous breathing
apneustic center anatomically ill defined, localized collection of neurons in the pons located at the level of the vestibular area that moderates the rhythmic activity of the medullary respiratory centers
biots respiration breathing characterized by irregular periods of apnea alternating with periods in which 4 or 5 breaths of identical depth are taken
chemoreceptors sensory nerve cell activated by changes in the chemical environment surrounding it; the chemoreceptors in the carotid artery are sensitive to PCO2 in the blood, signaling the respiratory center in the brain to increase or decrease ventilation
cheyne-stokes respiration abnormal breathing pattern with periods of progressively deeper breaths alternating with periods of shallow breathing apnea
hering-breuer inflation reflex the parasympathetic inflation reflex mediated via the lungs stretch receptors that appears to influence the duration of the expiratory pause occurring between breaths
pneumotaxic center bilateral group of neurons in the upper part of the pons that rhythmically inhibits inspiration independently of the vagi
vagovagal reflexes reflexes caused by stimulation of parasympathetic receptors in the airways that can result in laryngospasm, bronchoconstriction, hyperpnea, and bradycardia
what stimulates vagovagal reflexes? often associated with mechanical stimulation, as during procedures such as tracheobronchial aspiration, intubation, or bronchoscopy
is breathing conscious or automatic activity? automatic
can breathing patterns be consciously changed? yes; until willful breathing stops and the neural mechanisms resume
where does the rhythmic cycle of breathing originate? the brain stem, specifically the neurons in the medulla
higher brain ___ and many systematic receptors and ___ modify the output of the medulla. centers; reflexes
the structures of the brain function an an ____ manner to precisely control ventilation rate and depth in order to accommodate the ____ needs of the body. integrated; gas exchange
do separate inspiratory and expiratory centers exist? no; the neurons are anatomically intermingled and do not inhibit one another
the ___ contains several widely dispersed respiratory related neurons. medulla
which respiratory group contains mainly inspiratory neurons? dorsal
which respiratory group contains both inspiratory and expiratory neurons? ventral
what does DRG stand for? dorsal respiratory group
what does VRG stand for? ventral respiratory group
characteristics of DRG? bilateral in the medulla, send impulses to motor nerves of diaphragm and intercostals, provides main inspiratory stimulus
the medulla generates the ___ ___ ___, but the exact origin is unknown. basic breathing pattern
what modifies the medullas basic breathing pattern? sensory impulses that the lungs, airways, peripheral chemoreceptors, and joint proprioceptors have transmitted to the DRG
do drg nerves extend into vrg nerves? yes, many of them
do vrg nerves extend into drg nerves? only a few
characteristics of the vrg. bilateral in the medulla, send motor impulses through the vagus nerve to increase the diameter of the glottis, transmitting impulses to the diaphragm and intercostals, send expiratory impulses to the internal intercostals and abdominals
what are the two predominant theories of rhythm generation? pacemaker and network
what is the principle of the pacemaker hypothesis? that medullary cells have intrinsic pacemaker properties which drive other medullary neurons
what is the principle of the network hypothesis? that rhythmic breathing is the result of a particular pattern of interconnections between neurons dispersed throughout the vrg, the pre-Botzinger complex, and the Botzinger complex; inspiratory and expiratory neurons inhibit one another
does spontaneous respiration continue if the brain stem is transected above the medulla? yes, though irregular
does the pons promote rhythmic breathing? no; it modifies the output of medullary centers
what are the two respiratory centers of the pons? apneustic and pneumotaxic
what happens when the apneustic center gets severed from the pneumotaxic center and vagus nerve? drg neurons fail to switch off, causing prolonged inspiratory gasps interrupted by occasional expirations; aka apneustic breating
what do strong pneumotaxic signals do? increase the respiratory rate
what do weak pneumotaxic impulses do? prolong inspiration and increase tidal volume
tha apneustic and pneumotaxic centers seem to work together to control ___. depth of inspiration
where are the hering-breuer inflation reflex receptors located? in the smooth muscle of both the large and small airways
which nerve carries the inhibitory impulses from the hering-breuer reflex receptors to the drg? the vagus nerve
is the hering-breuer inflation reflex an important control mechanism in quiet breathing? no, this reflex in only activated at large tidal volumes (in adults)
why is the hering-breuer inflation reflex important? it regulates rate and depth during moderate to strenuous exercise
rapidly adapting irritant receptors in the epithelium of the larger conducting airways have ____ ____ nerve fibers. vagal sensory
stimulation of irritant receptors can cause... reflex bronchoconstriction, coughing, sneezing, tachypnea, and narrowing of the glottis
what can stimulate vagovagal reflexes? endotracheal intubation, airway suctioning, and bronchoscopy
airway suctioning and bronchoscopy can cause severe ____, ____, and ____. bronchoconstriction, coughing, and laryngospasm
what is the main trigger of chemoreceptors? H+ (indirectly CO2)
where are the central chemoreceptors located? bilaterally in the medulla
are the central chemoreceptors in direct contact with arterial blood? no, they are bathed in the csf separated by the blood-brain barrier
what is the blood-brain barrier? the semipermeable membrane that separates the cerebrospinal fluid (csf) and the blood
how does CO2 effect the central chemoreceptors? arterial CO2 easily diffuses across the blood-brain barrier, once inside it reacts with H2O, carbonic anahydrse follows resulting in H+ and HCO3, and the central chemoreceptors are extremely sensitive to H+
can H+ pass through the blood-brain barrier? rarely, it is almost impermeable to H+ and HCO3 so CO2 has to pass through then react with water once its inside
CO2 diffusing from te blood into the csf increases H+ almost instantly, exciting the chemoreceptors within seconds. T or F true
how much does alveolar ventilation increase in response to and increase in PaCO2? 2-3 L/min for each 1 mm Hg increase in PaCO2
how long does central chemoreceptor stimulation usually last while in respiratory acidosis? 1-2 days, long enough for the kidneys to raise levels of HCO3 in the blood and enough can pass the blood brain barrier to buff the H+
where are the periperal chemoreceptors located? aortic arch and bilaterally in the bifurcations of the common carotid arteries
the peripheral chemoreceptors increase their firing rates in response to what? increased arterial H+ regardless of origin
which nerve carries impulses from the carotid cemoreceptors to the medulla? glossopharyngeal
which nerve carries impulses from te aortic chemoreceptors to the medulla? vagus
which peripheral chemoreceptors have more influence over the respiratory center? carotid, due to an extremely high rate of blood flow, little time to deposit O2, and exposure to arterial blood 100% of the time
how does hypoxemia effect the peripheral chemoreceptors? low O2 makes them more sensitive to H+
why does decreased PaO2 cause incresae ventilation? because it makes the carotid chemoreceptors more sensitive to H+, which causes them to fire more frequently
how does increased PaO2 effect the periperal chemoreceptors? it makes them less sensitive to H+
why does increased PaO2 cause a decrease in ventilation? the carotid chemoreceptos become less sensitive to H+, which causes them to fire less often
when does hypoxemia not have an effect on the carotid chemoreceptors? in severe alkalemia, because even though the carotid chemoreceptors are more sensitive to H+ there is a lot less in blood at that time
the carotid bodies meet their O2 needs from dissolved O2. T or F true, because the flow rate is so fast; therefore it depends less on content and more on partial pressure
when will the nerve-impulse transmissions of the carotid bodies increase when pH and PaCO2 are normal? when PaO2 decreases to approximately 60 mm Hg
what accounts for the sharpest decrease in O2 content on the O2-Hb equilibrium curve? a decrease in PaO2 from 60 mm Hg to 30 mm Hg
what percentage do the peripheral chemoreceptors account for in the ventilatory response to Hpercapnia? 20-30%
which responds more rapidly to increased H+? peripheral
when peripheral chemoreceptors become insensitive to H+ levels because of high PaO2, what does ventilatory response depend on? the central chemoreceptors, which are uneffected by hypoxemia
high PaO2 renders peripheral chemoreceptors almost unresponsive to PCO2. T or F true
low PaCO2 renders peripheral chemoreceptors almost unresponsive to Hypoxemia. T or F true
what is asphyxia? coexisting arterial hypoxemia, acidemia, and high PaCO2
does a diagnosis of COPD on a patients chart automatically mean high PaCO2 or that O2 administration may be associated with hypercapnia? no, these characteristics are only displayed in severe end-stage disease; a small percentage of patients
O2 should never be withheld from acutely hypoxemic patients with COPD. T or F true, fear of hypoventilation and/or hypercapnia does not override oxygenating the tissues
what should you be prepared to do if O2 administration is accompanied by severe hypoventilation? support ventilation mechanically
which breathing pattern occurs when cardiac output is low, as in congestive heart failure, or brain injuries? chyene-stokes
why does decreased cardiac output cause chenye-stokes? because there is a delay in blood transit time between the lungs and the brain
what causes biot respiration? increased intracranial pressure
what can apneustic breathing indicate? damage to the pons
central neurologic hyperventilation is characterized by what? persistent hyperventilation driven by abnormal neural stimuli; related to mid-brain and upper pons damage associated with head trauma, severe brain hypoxia, or lack of blood flow to the brain
what are characteristics of central neurogenic hypoventilation? unresponsive to ventilatory stimuli; associated with head trauma, brain hypoxia, and narcotic suppression of the respiratory center
CO2 plays an important role in cerebral blood flow. T or F true
how does high CO2 effect cerebral blood flow? dilates the cerebral vessels increasing blood flow
how does low CO2 efect cerebral blood flow? constricts cerebral vessels decreasing blood flow
why is high intracranial pressure (icp) bad? if it exceeds cerebral arterial pressure, blood flow to the brain will stop, leading to cerebral hypoxia (ischemia)
why does decreasing PaCO2 help relieve icp? for every 1 mm Hg reduction in PaCO2--> 3% reduction in cerebral blood flow and for every 0.5-0.7 drop in cerebral blood flow--> 1 mm Hg reduction in icp
why is mechanical hyperventilation a cause for concern for patients with traumatic brain injuries? because with the drop in icp also comes a drop in cerebral blood flow, which can end up causing ischemia as well
what is the normal icp? 10
how long does it take for the brain to reach max swelling? 3 days
what is the most common cause of hypoxemia? hyperventilation
strenuous exercise can increase O2 consumption and CO2 production by how much? 20 fold
Created by: sarah72388
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