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Ch 14 Egans
Regulation of Breathing
| Question | Answer |
|---|---|
| Dorsal respiratory groups | contain mainly inspiratory neurons that are located bilaterally in the medulla. |
| ventral respiratory groups | contain both inspiratory and expiratory neurons that are located bilaterally in the medulla in 2 different nulclei. |
| Where do DRG neurons send impulses to? | motor neves of the diaphragm and external intercostal muscles providing main inspiratory stimulus |
| Where do VRG send impulses to? | Some send motor impulses through the vagus nerve to laryngeal and pharyngeal muscles increasing the diameter of the glottis/others to diaphragm and external intercostal muscles/other internal intercostal and abd ex muscles |
| What are the 2 predominate thories of rythum generation? | pacemaker hypothesis, network hypothesis |
| Pacemaker hypothesis? | certain medullary cells have intrinsic pacemater properties. These cells drive other medullary neurons |
| Network hypothesis? | rythmic breathing is the result of a particular pattern of interconnections between neurons dispersed throughout the rostral VRG, pre Botzinger complex, and Botzinger complex. Inspiratory and expiratory neruons inhibit one another |
| Firing rate of DRG and VRG inspiratory neurons increases gradually at the end of what phase? Creating what? | expiratory. Ramp signal |
| During quiet breathing inspiratory neurons fire with increasing frequencyfor approximately how many seconds? | 2 |
| After the 2 second firing then an abrupt switch off occurs allowing expiration to proceed for how many seconds? | 3 |
| The inhibitory neurons that switch off the inspiratory ramp signal are comtrolled by? | pneumotaxic center and pulmonary stretch receptors |
| The pons does not promote rythmic breathing but rather? | modifies the output of the medullary centers |
| What are the 2 groups of neurons in the pons? | apneustic center, pneumotaxic center |
| Apneustic Center | collection of neurons in the pons located at the level of the area vestibularis that moderates the rythmic activity of medullary resp centers |
| Pnumotaxic center | bilater group of neurons in upper pons that control swith off point of inspiratory ramp controlling inspiratory time |
| Strong pneumotaxic siganal increase what? | RR |
| Weak pneumotaxic signal prolong inspiration and increase what? | tidal volumes |
| Hering-Bruer inflation reflex | parasympathetic inflation reflex mediated via lungs stretch receptors that appears to influence the durationof the expiratory pause occuring between breaths |
| In adults the Hering-Bruer reflex is activated only at? | large tidal volumes |
| What reflex is important in regulating respiratory rate and depth during moderate to strenuous exercise? | Hering-Breuer Inflation Reflex |
| What reflex is probably responsible for the hyperpnea observed with pneumothorax? | deflation reflex |
| What reflex may help maintain large tidal volumes during exercise and may be involved in periodic deep sighs during quiet breathing | Head's Paradoxic Reflex |
| Rapidly adapting receptors in the epithelium of the larger conducting airways have vagal sensory nerve fibers | Irritant receptors |
| Reflexes that have both sensory and motor vagal components? | vagovagal reflexes |
| Reflexes that are responsible for laryngospasm, coughing, and slowing of the heartbeat | vagovagal reflexes |
| Endotracheal intubation, airway suctioning, and bronchoscopy readily elicit what reflex? | vagovagal reflexes |
| C fibers in the lung parenchyma near the pulmonary capillaries are called? | juxtacapillary receptors, or J-receptors |
| Alveolar inflammatory processes (pneumonia), pulmonary vascular congestion (congestive heart failure), and pulmonary edema stimulate what receptors? | J receptors |
| This stimulation causes rapid, shallow breathing; a sensation of dyspnea; and expiratory narrowing of the glottis? | J receptor stimulation |
| Proprioceptors | send stimulatory signals to the medullary respiratory center. increase medullary inspiratory activity and cause hyperpnea |
| Muscle spindles | in the diaphragm and intercostal muscles are part of a reflex arc that helps the muscles adjust to an increased load |
| The extrafusal fibers that elevate the ribs are innervated by? | alpha fibers |
| Those that innervate the intrafusal spindle fibers are called? | gamma fibers |
| The body maintains the proper amounts of oxygen (O2), carbon dioxide (CO2), and hydrogen ions (H+) in the blood mainly by regulating | ventilation |
| Hypercapnia, acidemia, and hypoxemia stimulate specialized nerve structures called | Hypercapnia, acidemia, and hypoxemia stimulate specialized nerve structures called |
| chemoreceptors transmit impulses to the medulla, increasing | ventilation |
| Centrally located chemoreceptors are located in the? They respond to what? | medulla. Hydrogen |
| The stimulatory effect of chronically high CO2 on the central chemoreceptors gradually declines over 1 or 2 days, because? | the kidneys retain bicarbonate ions in response to respiratory acidosis, bringing the blood pH level back toward normal |
| The peripheral chemoreceptors are? | small, highly vascular structures known as the carotid and aortic bodies |
| The carotid bodies are located where? | bilaterally in the bifurcations of the common carotid arteries |
| The carotid bodies send their impulses to the respiratory centers in the medulla via? | glossopharyngeal nerve |
| aortic bodies send their impulses via? | vagus nerve |
| Which peripheral chemoreceptors exert much more influence over the respiratory centers? And especially with respect to what 2 things? | carotid bodies. hypoxemia and acedemia |
| venous blood leaving the carotid bodies has how much O2 content as the arterial blood entering them | Same amount. Because the carotid bodies are exposed at all times to arterial blood |
| peripheral chemoreceptors fire more frequently in the presence of? Why? | arterial hypoxemia. because hypoxemia makes them more sensitive to hydrogen |
| the ultimate effect of hypoxemia is to increase the neural firing rate of the? Which causes? | peripheral chemoreceptors. Increased ventilation |
| why don't conditions associated with low arterial O2 content but normal Pao2 (e.g., anemia and carbon monoxide poisoning) do not stimulate ventilation? | carotid bodies' extraction of O2 from each unit of rapidly flowing blood is so small that their O2 needs are met entirely by dissolved O2 in the plasma |
| When pH and Paco2 are normal (pH = 7.40 and Paco2 = 40 mm Hg), the carotid bodies' nerve-impulse transmission rate does not increase significantly until the Pao2 decreases to | about 60 mm Hg |
| arterial hypoxemia does not stimulate ventilation greatly until the Pao2 decreases below? | 60 mm Hg |
| The peripheral chemoreceptors account for how much of the ventilatory response to hypercapnia? | 20-30% |
| high Po2 renders the peripheral chemoreceptors almost unresponsive to? | PCO2 |
| low Paco2 renders the peripheral chemoreceptors almost unresponsive to? | hypoxemia |
| Co-existing arterial hypoxemia, acidemia, and high Paco2 (i.e., asphyxia) maximally stimulate? | peripheral chemoreceptors |
| Hypoxia-induced hyperventilation lowers the? and creates? | PaCO2. alkalemia |
| People with chronic hypercapnia secondary to advanced COPD have depressed ventilatory responses to acute rises in? WHY? | arterial CO2. because of their altered acid-base status and partly because their deranged lung mechanics prevents them from increasing their ventilation adequately |
| The ventilatory response to hypoxemia is greatly enhanced by? | hypercapnia and acidemia |
| A sudden rise in arterial Pco2 causes an immediate increase in? why? | ventilation. because CO2 rapidly diffuses from the blood into the CSF, increasing the [H+] surrounding the central chemoreceptors |
| O2 breathing causes more blood flow to be directed to? Which does what to well ventilated alveoli? | poorly ventilated alveoli. takes blood flow away from well ventilated alveoli |
| kidneys compensate for the acidic effects of chronic hypercapnia by raising the? This does what to the pH | plasma bicarbonate level. Keeps it within normal range |
| what are the 2 theories that describe how ventilation increases during exercising? | 1.cerebral motor cortex sends impulses to exercising muscles and sends collateral excitatory impulses to the medullary respiratory center 2. exercising limbs moving around their joints stimulate proprioceptors, which transmit excitatory impulses to the me |
| Cheyne-Stokes respiration | respiratory rate and tidal volume gradually increase and then gradually decrease to complete apnea |
| When does the cheyne stokes respiration pattern occur? | This pattern occurs when cardiac output is low, as in congestive heart failure, delaying the blood transit time between the lungs and the brain. brain injuries in which the respiratory centers overrespond to changes in the Pco2 level |
| Biot's respiration | similar to Cheyne-Stokes respiration, except that tidal volumes are of identical depth |
| When does biots respiratory pattern occur? | patients with increased intracranial pressure |
| Apneustic breathing indicates damage to? | pons |
| Central neurogenic hyperventilation is characterized by? | persistent hyperventilation driven by abnormal neural stimuli |
| neurogenic hyperventilation occurs when? | midbrain and upper pons damage associated with head trauma, severe brain hypoxia, or lack of blood flow to the brain |
| central neurogenic hypoventilation? | respiratory centers do not respond appropriately to ventilatory stimuli |
| central neurogenic hypoventilation ocuurs when? | associated with head trauma and brain hypoxia, as well as narcotic suppression of the respiratory center |
| CO2 plays an important role in regulating? | cerebral blood flow |
| Increased Pco2 on cerebral blood flow causes? | dilates cerebral vessels, raising cerebral blood flow |
| Decreased PCO2 on cerebral blood flow causes? | constricts cerebral vessels and reduces cerebral blood flow |
Created by:
blh