Flashcards in Neural and Chemical Control of Respiration Deck (27)
what generates the basic breathing rhythm?
-influenced by ventilatory reflexes from central and peripheral chemoreceptors via blood gas concentrations and lung stretch receptors
what is the most important factor for control of respiratory drive at rest?
what do central VS peripheral chemoreceptors detect changes in?
CC: changes in arterial CO2 (correspond to [H+] in CSF, which is dependent on CO2 crossing BBB)
PC: chhanges in arterial PO2, PCO2, and pH
is breathing or heart beating neurogenic or myogenic?
breathing = neurogenic
heart beating = myogenic
what is the central pattern generator?
where is it located?
what does it do?
what is it made of?
what does it receive input from?
CPG is in the medullary respiratory center below the floor of the 4th brian ventricle
-made of dorsal and ventral respiratory groups (DRG and VRG)
-sends out rhythmic drive to motoneurons controlling respiratory muscles, thus respiration rate and tidal volume
-receives input from higher brain centers and peripheral and central chemoreceptors
how is inspiratory output mediated?
medullary DRG and VRG are connected via spinal respiratory motoneurons to phrenic nerve, which innervates diaphragm, and to the spinal nerves, which innervate external intercostals
how is expiratory output mediated?
medullary VRG is connected via spinal respiratory motoneurons to spinal nerves that innervate the internal intercostals and abdominal muscles
-DRG is not related
action potential frequency during eupnea
phrenic or external intercostals are constantly firing, at a max during inspiration
abdominal or internal intercostals don't fire often, but at a max during expiration
action potential frequency during hyperpnea
phrenic or external intercostals fire more frequently, at a max during inspiration
abdominal or internal intercostals fire more frequently, but still less than phrenic/externals, and at a max during expiration
Hering-Breuer inflation reflex
during deep inspirations, lung inflation activates stretch receptors that inhibit further inflation via vagal afferents and phrenic efferents
-not important during normal breathing, b/c threshold for activating stretch receptors is not typically reached during eupnea
-thus this only occurs when TV increases during deep breaths, exercise, and COPD
-done by paralyzing respiration muscles, so inspiration is set by ventilation
what are the respiratory control centers?
pneumotaxic center (AKA pontine respiratory group; in pons) and respiratory center (in medulla)
-establish and modulate neurogenic respiratory rhythm and receive input from peripheral and central chemoreceptors, and from higher centers in the brain
where is the DRG located, what is it made of, and what does it do?
bilaterally in the NTS, and made of inspiratory neurons
-initiator of activity of phrenic nerves innervating diaphragm
-sends collateral neurons the VRG
-receives vagal afferents from chemoreceptors sensing arterial PCO2, PO2, and pH
-integrates info in modulating frequency and depth of breathing
where is the VRG located, what is it made of, and what does it do?
located bilaterally in the retrofacial nucleus, nucleus ambiguous, and nucleus retroambifualis
-made of both inspiratory and expiratory neurons
-contains Botzinger complex (BOT) cluster of mostloy expiratory neurons in ventrolateral medulla for pacemaker activity associated with respiratory rhythm, and modulated by afferent input and higher brain centers
--targeted by drugs aimed at stimulating breathing when breathing is depressed
what is the pontine respiratory group, where is it located, and what does it do?
AKA pneumotaxic center in nucleus parabrachialis medialis and Kolliker-Fuse nucleus of pons
-functions to fine-tune the respiratory pattern inr esponse to vagal afferents responding to hypercapnea or hypoxia
effect of transection at or below level IV, with vagi intact or cut
either intact or cut, apnea will result
-cessation of breathing with no movement of respiratory muscles
-associated with lesion below medullary respiratory centers
-thus the CPG for breathing is located above level IV in the medulla, near the floor of the 4th ventricle
effect of transection at level III, with vagi intact or cut
either intact or cut, breathing is rhythmic but consists of series of irregularly timed gasping efforts
-thus while CPG is between III and IV, the normal breathing pattern requires input from higher levels
effect of transection at level II, with vagi intact or cut
intact: breathing rhythmic with decreased frequency and increased tidal volume
cut: apneusis occurs b/c inactivates inspiratory cutoff switch
-usually associated with head injury, with prolonged inspiratory phases lasting 30-90 seconds, followed by short passive expirations, with 1.5 breaths/minute
-thus vagal feedback is essential for establishing regular pattern of alternating inspirations and expirations of similar durations
region between II and III of lower pons is apneustic center, and is the site of "inspiratory cut-off switch"
abnormal pattern of breathing
-alternating periods of hyperpnea and apnea, each cycle taking 30 seconds to 2 minutes
-associated with altered PO2 and PCO2 due to injuries in respiratory centers, CHF, CO poisoning, strokes, brain tumors, in newborns with immature respiratory centers, individuals getting morphine, or those who sleep at high altitudes
Cluster breathing (Biot's respiration)
abnormal form of breathing
-associated with stroke, head trauma, pressure, or lesion in lower pontine region of brainstem
-characterized by closely grouped series of shallow breaths similar in size, and separated by intervals of apnea
-generally indicative of poor prognosis
abnormal form of breathing
-associated with a lesion in the medullary respiratory center
-characterized by completely irregular series of inspirations and expirations with irregular pauses and increasing periods of apnea progressing to complete apnea
abnormal form of breathing
-deep and labored, desperate and gasping breathing
-associated with severe metabolic acidosis, esp. in diabetes
-shallow rapid hyperventilation becomes Kussmaul as acidosis progresses from mild to severe
why is alveolar PCO2 a major controller of respiration rate?
after intense hyperventilation, there is a period of apnea b/c CO2 levels are below normal (to 15 mmHg)
-must reach 38 mmHg before respiratory activity begins, and PO2 can rise again
-Cheyne-Stokes rhythm is produced by the oscillations in partial pressure of blood gases
what does increasing PACO2 do to alveolar ventilation? how can this be changed?
they have a positive relationship
-sensitivity of alveolar ventilation to PACO2 is increased by hypoxia (decreasing O2 will increase slope) and metabolic acidosis
-decreased by sleep > narcotics, chronic obstruction > deep anesthesia
what is the "set point" for steady state ventilatory response?
occurs at intersection of "sensitivity curve"" (effect of PaCO2 on ventilation steady state) and "effector curve" (effect of ventilation on PaCO2 breathing air)
what is the effect of arterial pH on minute ventilation at constant PCO2 and varied PCO2?
if CO2 is constant and pH is varied, ventilation changes in a lot (decreases)
if CO2 is allowed to vary with pH, then ventilation doesn't change as much b/c PCO2 decreases as ventilation increases, thus reducing its stimulatory effect on ventilation
what is the effect of PaO2 on respiratory minute volume at constant PCO2 and varied PCO2?
if CO2 is constant and PaO2 varies, then ventilation changes a lot (decreases)
if CO2 changes with pH, then ventilation doesn't change as much