Regulation of Breathing: Medullary Respiratory Center | Mosby PDF

Chapter 15 Regulation of Breathing Medullary Respiratory Center The rhythmic cycle of breathing originates in the medulla. Higher brain centers, systemic receptors, and reflexes modify the medulla’s output. No truly separate inspiratory and expiratory centers The medulla doe...

Chapter 15 Regulation of Breathing Medullary Respiratory Center The rhythmic cycle of breathing originates in the medulla. Higher brain centers, systemic receptors, and reflexes modify the medulla’s output. No truly separate inspiratory and expiratory centers The medulla does contain several widely dispersed groups of respiratory- related neurons. – These form dorsal and ventral respiratory groups. Mosby items and derived items © 2009 by 2 Mosby, Inc., an affiliate of Elsevier Inc. Medullary Respiratory Center (cont.) Dorsal respiratory groups (DRG) Composed mainly of inspiratory neurons located bilaterally in the medulla These neurons send impulses to the motor nerves of diaphragm and external intercostal muscles. DRG nerves extend into the Ventral respiratory groups not the reverse and they contain both inspiratory and expiratory neurons Vagus and glossopharyngeal nerves bring sensory impulses to the DRG from the lungs, airways, peripheral chemoreceptors, and joint proprioceptors. – Input modifies the breathing pattern. Mosby items and derived items © 2009 by 3 Mosby, Inc., an affiliate of Elsevier Inc. Medullary Respiratory Center (cont.) Ventral respiratory groups (VRG) Contain both inspiratory and expiratory neurons located bilaterally in the medulla VRG sends inspiratory impulses through the vagal nerve to – Laryngeal and pharyngeal muscles – Diaphragm and external intercostals Other VRG neurons send expiratory signals to abdominal muscles and internal intercostals. Inspiratory ramp signal Signal starts low and gradually increases to produce a smooth inspiratory effort instead of a gasp. Mosby items and derived items © 2009 by 4 Mosby, Inc., an affiliate of Elsevier Inc.  Pontine Respiratory Centers The pons modifies the output of medullary centers. – Two pontine centers are apneustic and pneumotaxic. Apneustic center – Its function only identified by cutting connection to medullary centers – Apneustic breathing is characterized by long gasping inspirations interrupted by occasional expirations. Pneumotaxic center – Controls “switch-off,” so controls IT (inspiratory time) – Increased signals increase RR, while weak signals prolong IT and large VT. Mosby items and derived items © 2009 by 5 Mosby, Inc., an affiliate of Elsevier Inc. Reflex Control of Breathing The Hering-Breuer inflation reflex – Receptors are located in the smooth muscle of both large and small airways – Lung distention causes stretch receptors to send inhibitory signals to DRG, stopping further inspiration. In adults active only on large VT (>800 ml) Regulates rate and depth of breathing during moderate to strenuous exercise Deflation reflex – Sudden lung collapse stimulates a strong inspiratory effort which results in hyperpnea as seen with pneumothorax. Mosby items and derived items © 2009 by 6 Mosby, Inc., an affiliate of Elsevier Inc.  Reflex Control of Breathing (cont.) Head’s paradoxic reflex – May maintain large VT during exercise and deep sighs – Periodic sighs help prevent alveolar collapse, or atelectasis. – May be responsible for babies first breaths at birth Irritant receptors – Stimulated by inhaled irritants or mechanical factors – Cause bronchospasm, cough, sneeze, tachypnea, and narrowing of glottis These are vagovagal reflexes. – In hospital triggered by Suctioning, bronchoscopy, endotracheal intubation Mosby items and derived items © 2009 by 7 Mosby, Inc., an affiliate of Elsevier Inc. Reflex Control of Breathing (cont.) J-receptors (juxtacapillary) – Located in lung parenchyma – Stimulated by pneumonia, CHF, pulmonary edema – Cause rapid, shallow breathing and dyspnea and expiratory narrowing of the glottis Peripheral proprioceptors – Found in muscles, tendons, joints, and pain receptors – Movement stimulates hyperpnea. – Moving limbs, pain, cold water all stimulate breathing in patients with respiratory depression Mosby items and derived items © 2009 by 8 Mosby, Inc., an affiliate of Elsevier Inc. True or False: The apneustic and pneumotaxic center are located in the pons of the brain? What reflex is initiated when lung volumes are high? True or False: Tachycardia, coughing, bronchospasms can occur during endotracheal suctioning? What receptors can stimulate rapid shallow breathing when stimulated by chronic disease? Mosby items and derived items © 2009 by 9 Mosby, Inc., an affiliate of Elsevier Inc.  Chemical Control of Breathing Body works to maintain proper levels. of O2, CO2, and pH through mediation of chemoreceptors as it affects VE Central chemoreceptors Located bilaterally in the medulla Stimulated directly by H+ ions, indirectly by CO 2 – The blood brain barrier is almost impermeable to H+ and HCO2– but CO2 freely crosses. – In CSF, CO2 is hydrolized, releasing H+. – An increased CO2 increases H+ in CSF, causing. increased ventilation to restore normal levels pH and CO2. Mosby items and derived items © 2009 by 10 V increased 2–3 L/min for 1–mm Hg rise in Mosby, Inc., an affiliate of Elsevier Inc. Mosby items and derived items © 2009 by 11 Mosby, Inc., an affiliate of Elsevier Inc. Chemical Control of Breathing (cont.) Peripheral chemoreceptors Located in the aortic arch and bifurcations of common carotid arteries Oxygen sensitive cells that react to reductions of oxygen levels in the arterial blood. Peripheral chemoreceptors’ response to ⇓ PaO2 Hypoxemia increases receptors sensitivity. for H+. – ⇓PaO2 causes ⇑VE for any pH, and vice versa. – In severe alkalosis, Mosby items and derivedhypoxemia items © 2009 by has little 12 Mosby, Inc., an affiliate of Elsevier Inc. Chemical Control of Breathing (cont.) Peripheral chemoreceptors’ response to ⇓PaO2 (cont.) Not a significant response until PaO2 falls to ~60 mm Hg – A further fall results in sharp increase.in VE. – This means the under normal circumstances, oxygen plays no role in drive to breathe. Hypoxemia the most common cause of hyperventilation Mosby items and derived items © 2009 by 13 Mosby, Inc., an affiliate of Elsevier Inc. Chemical Control of Breathing (cont.) Peripheral chemoreceptors’ response to ⇑PaCO2 and [H+] Less responsive than central chemoreceptors (CCRs) – One-third of hypercapnic response, but a more rapid response to changes in [H+] – Carotid bodies are directly exposed to arterial blood which is why the ventilatory system responds so quickly to a metabolic acidosis even though the H+ ions cross the BBB with difficulty. In hyperoxia, PCRs are almost totally insensitive to changes in PaCO2, so any response is due to CCRs. Mosby items and derived items © 2009 by 14 Mosby, Inc., an affiliate of Elsevier Inc.  Chemical Control of Breathing (cont.) Coexisting acidosis, hypercapnia, and hypoxemia maximally stimulate peripheral chemoreceptors Hypercapnic COPD patients depressed respiratory response to ⇑CaO2 Mosby items and derived items © 2009 by 15 Mosby, Inc., an affiliate of Elsevier Inc. Chemical Control of Breathing (cont.) Control of breathing in chronic hypercapnia Sudden rise in PaCO2 causes immediate. rise in VE In slow-rising PaCO2 (severe COPD), kidneys retain HCO3–, which maintains CSF pH, so no increased ventilation response Hypoxemia seen with hypercapnia becomes the minute-to-minute breathing stimulus via altered response to [H+]. – Hypoxemia is always present in severe COPD due to severe mismatches. in V/Q. An increased FIO2 raises the PaO2 making the PCR less sensitive to [H+] resulting in a higher PaCO2Mosby items and derived items © 2009 by 16 Mosby, Inc., an affiliate of Elsevier Inc. Chemical Control of Breathing (cont.) Oxygen-induced hypercapnia O2 therapy may cause a sudden rise in PaCO2 in severe COPD with chronic hypercapnic. Possible explanations include – Hypoxic drive is removed (traditional view). – ⇑FIO2 may worsen V/Q mismatch Hypoxic pulmonary vascoconstriction is reversed to poorly ventilated alveoli – ⇑FIO2 may make patient susceptible to absorption atelectasis. Mosby items and derived items © 2009 by 17 Mosby, Inc., an affiliate of Elsevier Inc. Chemical Control of Breathing Mosby items and derived items © 2009 by 18 Mosby, Inc., an affiliate of Elsevier Inc. Chemical Control of Breathing (cont.) Oxygen-induced Hypercapnia: KEY POINTS “COPD” does NOT signify chronic hypercapnia or that O2 therapy will induce hypoventilation. – These characteristics are only in end-stage disease. – Present in small percent of COPD patients Concern about O2-induced hypercapnia and acidemia is not warranted in most COPD patients. O2 should NEVER be withheld in hypoxemic COPD patients as tissue oxygenation is an overriding priority. Be prepared to provide mechanical ventilation MV to the rare COPD patient who does have severe hypoventilation due to oxygen therapy. Mosby items and derived items © 2009 by 19 Mosby, Inc., an affiliate of Elsevier Inc.  Abnormal Breathing Patterns Cheyne-Stokes respirations (CSR) – Characterized by cyclic waxing and waning ventilation with apnea gradually giving way to hyperpneic. – Seen with low cardiac output states (CHF) Creates lag of CSF CO2 behind arterial PaCO2 and results in characteristic cycle Biot’s respiration – Similar to Cheyne-Stokes but VT is constant except during apneic periods – Seen with patients with elevated ICP Mosby items and derived items © 2009 by 20 Mosby, Inc., an affiliate of Elsevier Inc. Abnormal Breathing Patterns (cont.) Apneustic breathing (previously described) – Indicates damage to pons Central neurogenic hyperventilation – May be caused by head trauma, severe brain hypoxia, or lack of cerebral perfusion Central neurogenic hypoventilation – Medulla respiratory centers are not responding to appropriate stimuli. – Associated with head trauma, cerebral hypoxia, and narcotic suppression Mosby items and derived items © 2009 by 21 Mosby, Inc., an affiliate of Elsevier Inc. CO2 and Cerebral Blood Flow (CBF) CO2 plays an important role in autoregulation of CBF mediated through its formation of H+. Increased CO2 dilates cerebral vessels and vice versa. In traumatic brain injury (TBI), the brain swells acutely, raising ICPs > cerebral arterial pressure (perfusion stops). – Cerebral hypoxia/ischemia Mechanical hyperventilation lowers PaCO2 and ICP. – Controversial as reduces O2 and CBF to injured brain All agree must avoid hypoventilation in TBI patients Mosby items and derived items © 2009 by 22 Mosby, Inc., an affiliate of Elsevier Inc. What is indirectly responsible for minute to minute controls of breathing? A. PaO2 levels B. HCO3 levels C. PcO2 levels D. Lactate levels At what level does the PaO2 begin to initiate a stimulation in breathing? Mosby items and derived items © 2009 by 23 Mosby, Inc., an affiliate of Elsevier Inc. Mosby items and derived items © 2009 by 24 Mosby, Inc., an affiliate of Elsevier Inc. Mosby items and derived items © 2009 by 25 Mosby, Inc., an affiliate of Elsevier Inc. Mosby items and derived items © 2009 by 26 Mosby, Inc., an affiliate of Elsevier Inc.