Control Of Respiration Flashcards
Medullary respiratory center
. Generate basic rhythmic pattern of breathing
. Both inspiratory and expiratory neurons
. Dorsal respiratory group (inspiratory) synapse on motor neurons that supply mm. Of inspiration
. Ventral respiratory group (inspiratory and expiratory) only active during forced inspiration/expiration
. Pre-Botzinger complex: contain network of neurons that is involved in respiratory rhythm-generating process
Nucleus tractus solitarius
Important autonomic integrative center w/in brainstem
. DRG neurons located w/in ventrolateral portion of NTS
. Cardio-respiratory afferent project to NTS subdivisions
. Peripheral chemoreceptors and pulmonary stretch receptors project onto lat. regions
. Arterial baroreceptors project to dorsolat. And med. portions
Pontine respiratory center
. Apneustic center: prolongs inspiratory effort by providing excitatory input to inspiratory neurons in pre-botzinger complex
. Pneumatic center: switch off further inspiration
. Influence output from medullary respiratory centers
. Provide fine-tuning of the activity of medullary respiratory centers
Cortex control of respiration
Modifies activity of brainstem neurons bc breathing can be voluntarily altered
. Alllows speaking, yawning, coughing
T/F limbic system and hypothalamus are involved in control of emotional responses and can alter breathing pattern
T
Neural control of ventilation
. Main inspiratory mm. Are innervated by phrenic n. And intercostal n.
. Cell bodies of nn. In spinal cord
. Neural impulses from inspiratory neurons
. When inspiratory neurons w/in brainstem are activated and motor neurons connected to inspiratory mm. Activate
. Produces contraction of mm. Producing inspiratory effort
. When inspiratory neuron stop firing, the inspiratory mm. Relax producing passive expiration
. Expiratory neurons will fire during forced expiration
Chemoreceptors
. Responds to change in chemical composition of blood or fluid
Arterial chemoreceptors
. Located in carotid bodies at bifurcation of common carotids
. Respond to changes in blood, specifically PaO2
. Send afferent impulses to the lat. NTS w/in medulla
. Carotid body chemoreceptor afferents travel via CN IX
. Aortic body chemoreceptor afferents travel via CN X
What happens when PaO2 falls below 60 mmHg?
Respiratory centers w/in the brainstem are stimulated by signals from peripheral chemoreceptors to inc. ventilation
. Shows that peripheral chemoreceptors only function when PaO2 is dangerously low level
Carotid body structure
. Contains 2 types globus cells
. Type I cells: large vesicles containing dopamine
. Cells in close opposition to the endings of carotid sinus n. (Branch of CN IX)
. Type II cells: no dopamine vesicles
Carotid body function
. When PaO2 dec. there is inc. in dopamine release by type I cells inc. in firing rate along carotid sinus n.
. Partial pressure of O2 (not O2 content) of arterial blood is stimulus for inc. discharge rate
. Type I cell is site of chemoreception
. Carotid body excitation may depends upon ratio of ATP to ADP w/in Type I cell mitochondria
. Modulation of neurotransmitter release from these cells by physiological and chemical stimuli may affect discharge rate of carotid soy afferent fibers
Central chemoreceptors
. Important in minute-by-minute control of ventilation
. Situated along ventrolat. Surface of the medulla
. Located near the VRG
. Applying H or dissolved CO2 to the brain ECF that babes the central chemoreceptors stimulates breathing
.
Function of central chemoreceptors
. Inc. in PaCO2 causes rise in PCO2 of cerebrospinal fluid
. BBB is impermeable to to HCO3 and H but is permeable to CO2
. When CO2 diffuses into brain, it dissociates and causes corresponding inc. in H conc. In CSF
. The H ions diffuse from CSF into the ECF
. Dec. ECF pH stimulates central chemoreceptors which stimulates medullary respiratory centers to inc. ventilation to blow off excess CO2
. Opposite occurs for higher pH from dec. PaCO2
Dec. in PaCO2 effect of peripheral and central chemoreceptors
. P: stimulates when PaO2 falls under 60 mmHg
. C: no direct effect, severe hypoxia depresses neuronal activity of all brain tissue, including respiratory centers
Effect of inc. arterial PCO2 on peripheral and central chemoreceptors
. P: weakly stimulates
. C: strongly stimulates (primary respiratory signal)
Inc. arterial H effect on peripheral and central chemoreceptor
. P: stimulates
. C: does not effect (can’t penetrate BBB)
Types of pulmonary receptors
. Pulmonary stretch receptors
. Irritant receptors
. J receptors
Pulmonary stretch receptors
. Located w/in smooth m. Layer of lung airways
. Stretching of the lungs during inspiration activates receptors
. Towards end of inspiration APs from these travel to medullary respiratory centers to inhibit further activity from inspiratory neurons
. Neg. feedback called Breuer-Hering reflex
. Most important when tidal volume is over 1000 ml (during exercise)
Irritant receptors
. Lie btw airway epithelial cells
. Noxious stimulus stimulates these which reflexively produce bronchoconstriction and rapid shallowing breathing
. Can limit penetration of dangerous agents
.. May play role in asthma attacks
. Can also initiate cough or sneeze
Pulmonary C fibers/J receptors
. Located in interstitium near alveolar capillaries
. Stimulated by interstitial edema
. Activates J reflex causing laryngeal closure and apnea followed by rapid and shallow breathing
. Responsible for rapid breathing seen in patients w/ pulmonary embolus, edema, or pneumonia
. May be responsible for feeling of dyspnea encountered during pulmonary vascular congestion from LV failure
Joint and muscle receptors
. Found in skeletal joints and muscles
. Innervated by spinal nn.
. Limb movement stimulates it
. Causes inc. ventilation during exercise
Nasal receptors
. W/in mucosa of nose and nasal passages
. Innervated by CN V
. Mechanical and chemical irritants stimulate it
. Causes sneeze or apnea
Laryngeal receptors
. W/in laryngeal mucosa
. Innervated by CN X
. Stimulated by mechanical and chemical irritants
. Causes sniff, aspiration, or swallowing movement
Most important factor in control of ventilation
PCO2 of arterial blood
. Usually varies less than 3 mmHg
. Inc. produces inc. ventilation
What occurs at any level of PO2 when PCO2 inc.?
Inc. ventilation
What occurs when PCO2 is constant and PO2 dec.?
Inc. ventilation
. If PCO2 is normal at 40 mmHg, the PO2 can be reduced to 60 mmHg before you really see the inc. in ventilation
. Overall role of hypoxia in minute-by-minute ventilation is small
. At low PO2 there is a greater inc. in ventilation for every mmHg inc. in PCO2
Hypocapnia
CO2 below 40 mmHg
. Hypercapnia is over normal level
Alveolar PO2 and PCO2 when breathing air w/ low PO2
. PO2 dec.
. PCO2 no change
Alveolar PO2 and PCO2 when there is inc. ventilation and unchanged metabolism
. PO2 inc.
. PCO2 dec.
Alveolar PO2 and PCO2 when there is dec. in alveolar ventilation and unchanged metabolism
. PO2 dec.
. PCO2 in.
alveolar PO2 and PCO2 when there is inc. in metabolism and unchanged alveolar ventilation
. PO2 dec.
. PCO2 inc.
Alveolar PO2 and PCO2 when there is proportional inc. in metabolism and alveolar ventilation
No change in either
Cheyne-stokes breathing
. Periodic breathing patterncharacterized by period of apnea 10-20s in duration
. Separated by periods of hyperventilation when tidal volume gradually and cyclically inc. and dec.
. Alternating periods of apnea and hyperventilation caused by time delay in ECF pH changes
. Manifestation of instability in central respiratory control system
. Often seen at high altitude and at night during sleep
. Also seen in patients w/ severe hypoxemia from CHF
Regulation of breathing during sleep
. During slow wave sleep, there is withdrawal of cerebral influences and dec. ventilation which inc. PaCO2 and CO2 response curve is shifted right
. Tonic REM: sleep breathing maintains regularity but tidal volume may inc.
. Phasic REM: irregular breathing due to intrinsic activity of higher brain centers dominates respiratory neuron activity
. Activity of upper airway muscles is reduced causing dec. of caliber of upper airways that inc.r existence to flow
. Brief periods of obstruction can be normal during sleep (snoring)
Sleep apnea
. Apneic periods that can last for over 10s and assoc. w/ drop in PaO2 as low as 75%
. Occur at all sleep stages but more common during REM and lighter stages of slow wave
Central sleep apnea
. Cessation of respiratory effort (absence of changes in pleural pressure
Obstructive sleep apnea
. Air flow ceases bc of total obstruction of upper airways despite persistent respiratory efforts
. Common sites: larynx, pharynx, and oropharynx
. Arousal from apnea results from chemoreceptors activation due to developing hypoxia and hypercapnia
. May lead to right-sided heart failure and pulmonary hypertension
Respiration in fetus
. Gas exchange through placenta
. Maternal blood enters placenta from uterine aa.
. Gas exchange occurs across barrier that separates mother and fetal blood w/in intervillous sinusoids
. PO2 of fetal blood is about 30 mmHg bc placental blood mixes w/ mixed venous blood
. PO2 in fetal descending aorta is only 22 mmmHg
. After 24 weeks the respiratory epithelium begins to thin out and become closer to pulmonary capillaries and surfactant synthesis and storage begins
first breath in newborn
. High distending forces needed in first few breaths to move liquid out of lung and to overcome surface forces that oppose movement or air
. Intrapleural pressure can fall to -40 cmH2O before air enters lungs
. Pulmonary surfactant stabilizes open alveoli
Respiratory distress syndrome (RDS)
. Surfactant deficiency in newborns
. Affects 10-15% of premature infants
Transitions from fetal and newborn respiration systems
. Fetus has high pulmonary vascular resistance, low blood flow, and high arterial pressure
. At birth: dec. in vascular resistance that occurs during 1st breaths from abrupt inc. in PO2 that abolishes hypoxic pulmonary vasoconstriction
. Pulmonary circulation now receives entire CO not just 7%
. Placental circulation closes
. All open valves only foe fetus close
Apnea in newborns
. Predominantly central because central respiratory control is still immature
. Occurs mostly in preemies
Sudden infant death syndrome (SIDS)
. Pure obstructive apnea
. Lack of chemoreceptors responsiveness esp. to CO2 bc it is less well-developed
Diffusing capacity as infants transition to children
. Diffusing capacity inc. as alveolar surface area enlarges
. By 6 y/o the capacity is about the same as adult
. New alveoli are added until child is about 8 y/o
Respiration in. Older adults
. Elastic recoil dec. and compliance inc. causes inc. FRC
. Inc. RV and closing capacity
. FEV1 and FEF are dec.
. Chest wall stiffens and becomes less compliant from structural changes
. Respiratory mm. Strength dec. which dec. vital capacity and forced expiration flow rate
. Total lung capacity stays constant w/ age if adjusted for dec. in height seen
. Internal lung SA dec., alveoli become wider and shallower causing dec. diffusing capacity and dec. exchange rate
. Inc. in difference of PaO2 and PAO2
. Ventilator responses reduced but PCO2 unchanged
Asphyxia
. O2 starvation of tissues
. Caused by lack of O2 in air, Respiratory impairment , or Inability of tissues to utilize O2
Eupnea
Normal breathing
Respiratory arrest
. Permanent cessation of breathing unless clinically corrected
Suffocation
. O2 deprivation as result of inability to breath oxygenated air
