neural control of respiration - abnormal breathing patterns - sanjoy sanyal

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Neural Control of Respiration -Abnormal Breathing Patterns Dr Sanjoy Sanyal, MBBS, MS (Surgery), MSc (Royal College of Surgeons of Edinburgh), ADPHA Professor and Course Director of Neuroscience and FCM-III Neurology It’s as natural as breathing. Well, maybe not!

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Neural control of respiration (like neural control of many other physiological functions, micturition, for example) is highly complex and not fully elucidated. Research is still going on to determine the centers in the brain and their complex interactions. There may be variations of opinion between different researchers depending on newer findings. Every effort has been made to keep this information as current and authoritative as possible, yet in a simple enough form for the student to understand and digest the information. Dr Sanjoy Sanyal, Professor and Course Director of Neuroscience and FCM-III Neurology in Caribbean created this PPTX after studying this complex topic for a very long time. Tags: Respiration, Breathing, Respiratory Centers, Brainstem, Apneustic Breathing, Biots Breathing, Cheyne-Stokes, Ataxic, Agonal, Kussmaul, Brainstem Reticular Nuclei, NTS, Locus Ceruleus, Fastigial, Raphe nucleus, Vagus, RTN nucleus, pFRG nucleus, Kolliker-Fuse, PBC nucleus, RVL nucleus "Copyright Disclaimer Under Section 107 of the Copyright Act 1976, allowance is made for "fair use" for purposes such as criticism, comment, news reporting, teaching, scholarship, and research. Fair use is a use permitted by copyright statute that might otherwise be infringing. Non-profit, educational or personal use tips the balance in favor of fair use." Educational Value: A very complex and poorly understood topic has been rendered in as simple a format and style as possible, so as to make it easily digestible to any Basic Science medical student and Medical Resident

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  • 1. Dr Sanjoy Sanyal, MBBS, MS (Surgery), MSc (Royal College of Surgeons of Edinburgh), ADPHA Professor and Course Director of Neuroscience and FCM- III Neurology Its as natural as breathing. Well, maybe not!

2. Chemoreceptors (CR) Chemoreceptors (CRs) monitor Body Fluid chemistry and respond to their H+ (pH), PCO2, PO2 concentrations Input from CRs to CNS and Output from CNS to Lungs drive Alveolar Ventilation Types of CR: Central CR (CCR) Peripheral CR (PCR) 3. Central Chemoreceptors (CCRs) 1. Pre-Btzinger Complex (PBC) in Rats 2. Retrotrapezoid Nucleus (RTN) in Pons 3. Parafacial Respiratory Group (pFRG) in Medulla 4. Raphe Nuclei in Brainstem Reticular Formation 5. Locus Ceruleus in Pons 6. Nucleus Tractus Solitarius (NTS) in Medulla 7. Fastigial Nucleus in Cerebellum (PBC, RTN, pFRG, Locus Ceruleus are also Respiratory Rhythm centers) Location: Close to CSF surfaces of Medulla, Pons, Cerebellum; Bathed in CSF; Monitors CSF H+ and PCO2 directly 4. Central Chemoreceptors (CCRs) Receptor Type: H+ / PCO2 Receptor; NO PaO2 receptors in CCR Stimulus: CSF H+ (Most Sensitive), CSF PCO2, Arterial PCO2 (Indirectly); NOT Arterial PO2 Less Sensitive To: Systemic Arterial pH (Because H+ passes very slowly across Blood-CSF Barrier) Adaptation: within 12-24 hrs; Due to pumping of HCO3 - in/out of CSF There are NO PO2 Receptors in the CCR 5. CCR Bottom Line CCRs are very sensitive Provide main drive to ventilation under normal conditions at Sea Level Atmospheric Pressure Ventilation responds much more to moderate Arterial PCO2 (Hypercapnia) than to large in Arterial PO2 (Hypoxia), because of lack of central PO2 Receptors in CCR 6. CCR Respiratory Stimulants Progesterone acts on CCR via Steroid Receptor- Mediated Mechanism to help Respiration Naloxone is -Opiate Receptor Antagonist, Used in Opioid-induced Central Respiratory Depression Doxapram is PCR and CCR Stimulant; Overcomes Opioid-induced Central Respiratory Depression Acetazolamide (Carbonic Anhydrase Inhibitor) causes Acidification of CSF, acting as CCR Respiratory Stimulant, especially at High Altitude 7. Peripheral Chemoreceptors (PCR) Locations: Aortic and Carotid Bodies; Bathed in Arterial Blood; Monitor Arterial Blood PO2 directly 1. Aortic Bodies: Near Aortic Arch; CN10 Afferent 2. Carotid Bodies (Most important): Near Carotid Sinus at Carotid Bifurcation; CN9 Afferent [Very small structure; Receives maximum Blood per Gm of tissue; Meets metabolic requirements by utilizing O2 dissolved in Blood; Type 1 Glomus Cells are main sensors of Hypoxia] 8. Peripheral Chemoreceptor (PCR) Receptor Types: PO2 Receptor (Mainly); Also H+ / PCO2 Receptor Stimulus: Arterial PO2 (Most sensitive); Monitor PO2 (Partial Pressure of O2 in Blood, which is O2 Dissolved in blood), NOT O2 Content (O2 in Hb) Less Sensitive To: Systemic Arterial pH / PCO2; Very small contribution to normal drive for ventilation Adaptation: Nil (Receptor keeps firing so long as Arterial Hypoxic Stimulus exists) 9. PCR Bottom Line When Systemic Arterial PaO2 >100 mmHg: There is NO Stimulus to PO2 receptors PCRs do NOT contribute to drive for Normal Ventilation When Systemic Arterial PaO2