Neural Control of Respiration - Abnormal Breathing Patterns - Sanjoy Sanyal
 

Neural Control of Respiration - Abnormal Breathing Patterns - Sanjoy Sanyal

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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 ...

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

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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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Neural Control of Respiration - Abnormal Breathing Patterns - Sanjoy Sanyal Neural Control of Respiration - Abnormal Breathing Patterns - Sanjoy Sanyal Presentation Transcript

  • 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!
  • 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)
  • Central Chemoreceptors (CCRs) 1. Pre-Bötzinger 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
  • 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
  • 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
  • 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
  • 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]
  • 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)
  • 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 <100 mmHg:  Strong Stimulus to PO2 receptors, ↑Drive for Alveolar Ventilation  Main Drive for ventilation in Hypoxemic Hypoxia  This drive increases with CO2 Retention (Hypercapnia)
  • PCR Respiratory Stimulants  Almitrine Bismesylate is Carotid Body (PCR) stimulant  Doxapram is PCR and CCR Stimulant; Overcomes Opioid-induced Central Respiratory Depression General Information:  Partial Pressure of Gases in Blood / CSF is measured in Pascals (Pa) / kiloPascals (kPa).  1 kPa = 7.5 mm Hg; 133 Pa = 1 mm Hg
  • Summary of CCRs and PCRs CCR PCR Location Medulla, Pons, Cerebellum Aortic / Carotid Bodies Samples What CSF Arterial Blood Receptor Type H+ / PCO2 PaO2 Stimulus CSF H+ (Main); CSF PCO2; Arterial PCO2 (Indirectly) Arterial PO2 (Main); Arterial pH, PCO2 (Less) Less Sensitive To Systemic Arterial pH Systemic Arterial pH / PCO2 Adaptation 12 – 24 hours Nil
  • Respiratory Rhythm / Control Afferents: From Mechano- receptors in:  Lungs: Via Thoracic Cardiopulmonary Splanchnic Nerves (T2-5)  Intercostal Muscles: Via Intercostal Nerves  Diaphragm: Via Phrenic Nerve (C3-5)  Overview: Input from CRs to CNS and Output from CNS to Lungs drive Alveolar Ventilation
  • Respiratory Rhythm / Control Afferents: From Peripheral and Central Chemo-receptors:  Carotid Body  Aortic Body  CCRs: 7 (Slide #3)
  • Respiratory Rhythm / Control Rhythm Centers:  Rostroventrolateral (RVL) Nucleus in Medulla  Kölliker-Fuse Nucleus  Para-brachial Complex  Locus Ceruleus in Pons (This is also a CCR) Inspiratory Centers:  Pre-Bötzinger Complex (PBC) in rats only (This is also a CCR) Expiratory Centers: (These are also CCRs)  RTN  pFRG
  • Respiratory Rhythm / Control Pathway 1:  Carotid Body (CN9) / Aortic Body (CN10)  → NTS (CCR)  → RTN (CCR / Expiratory Center)  → Respiratory Rhythm
  • Respiratory Rhythm / Control Pathway 2:  RVL (Lateral Medulla) → Lateral Medullary RST  Rhythmic discharge to Phrenic Nucleus (C3-5)  Phrenic Nerve → Diaphragm  Spontaneous Respiratory Rhythm
  • Respiratory Rhythm / Control Central Respiratory Integration  Above-mentioned centers in Brainstem Reticular Formation Generate central Respiratory Drive  Govern inherent Respiratory Rhythm  Transmit to Upper Airway and to Main and Accessory Respiratory Muscles Bottomline:  Input from CRs to CNS and Output from CNS to Lungs drive Alveolar Ventilation
  • Respiratory Rhythm / Control Autonomic Control:  SNS: Thoracic CP Splanchnic Nerve (Sympathetic from T2-5 Ganglia) relaxes Bronchi  PSNS: Dorsal Nucleus of Vagus (Parasympathetic) constricts Bronchi Supramedullary Areas: Cortex / Sub- cortex Initiate or Modulate breathing with Volition, Emotion, Exercise etc
  • Summary CCR Respiratory Rhythm Centers CCR Inspiratory Centers Expiratory Centers Other Rhythm Centers Pre-Botzinger Complex (PBC) (Rats) PBC (Rats) Rostroventrolateral (RVL) Nucleus in Medulla Retrotrapezoid Nucleus (RTN) in Pons RTN Kolliker-Fuse Nucleus Parafacial Respiratory Group (pFRG) pFRG Parabrachial Complex Raphe Nuclei in Brainstem Reticular Formation Locus Ceruleus (Pons) Locus Ceruleus (Pons) Nucleus Tractus Solitarius (NTS) in Medulla Fastigial Nucleus in Cerebellum
  • Respiratory Control – Clinical Aspects Spinal Cord Lesions:  Complete lesion at or above C3 Spinal Segment interrupt Diaphragmatic Respiration  Complete lesion at or below C6 Spinal Segment will not Respiratory Depressants:  Opioids act on -Opiate Receptors in Brainstem Reticular Formation and Inhibit Brainstem Respiratory Rhythm (See Naloxone in Slide 24)
  • Respiratory Control – Clinical Aspects Brainstem Pathology:  Breathing control can be disturbed by many Brainstem Pathology.  Previously undiagnosed such pathology may be revealed by Abnormal Breathing during Sleep Sleep-Awake States:  Important in regulating breathing  Thus, respiratory control abnormalities are most often evident during Sleep, or during transition from Sleep to Wakefulness (Next 2 slides)
  • Respiratory Control – Clinical Aspects Central (Diaphragmatic) Sleep Apnea:  Inhibition of ‘Respiratory Center’ (RVL in Caudal Brainstem Reticular Formation)  → Intermittent Diaphragmatic Arrest, causing (a)Cheyne-Stokes Respiration (60-second Hyperventilation → Apnea) in (b)Elderly
  • Respiratory Control – Clinical Aspects Ondine's Curse vs. Locked-in Syndrome: Distinguish Brainstem (Volitional) from Supramedullary (Autonomic) regulatory failure  Former loses Autonomic Respiratory control and requires Volitional Breathing for survival. So patient has Hypoventilation during Sleep  Latter loses CST / CBT in Pons that is required for Volitional Breathing, but retains Autonomic Control
  • Respiratory Stimulants  Progesterone acts on CCR via Steroid Receptor- Mediated Mechanism to help Respiration  Almitrine Bismesylate is Carotid Body (PCR) Stimulant  Naloxone is -Opiate Receptor Antagonist, Used in Opioid-induced Central Respiratory Depression  Doxapram is PCR / CCR Stimulant; Overcomes Opioid-induced Central Respiratory Depression  Acetazolamide (Carbonic Anhydrase Inhibitor) causes Acidification of CSF, acting as CCR Respiratory Stimulant, especially in High Altitude
  • Abnormal Breathing – Apneustic Description  Prolonged Inspiration  Alternating with short Expiration  (No equivalent Expiration attempt) Causes  Loss of normal balance between Vagal Input and the Pons-Medullary Interactions  Lesion usually in Caudal Pons
  • Abnormal Breathing – Biot’s (Cluster) Description  Several Breaths of identical Rate and Depth  Alternating with irregular periods of Apnea Causes  Increased ICP  Midbrain Lesions  Serious Head Trauma with Medullary Injury  Brainstem Strokes
  • Abnormal Breathing – Cheyne-Stokes Description  A type of Periodic Breathing: 60-Second Hyperventilation followed by Apnea  Cycles of gradually increasing Depth and Frequency  Followed by gradual decrease in Depth and Frequency  Between periods of Apnea Causes  Midbrain Lesions  Head Trauma  Stroke  Infants and During Sleep, especially High Altitudes  Central (Diaphragmatic) Sleep Apnea in Elderly  With Type-B ICP Waves in Normal Pressure Hydrocephal
  • Abnormal Breathing – Ataxic / Agonal Description  Ataxic Breathing: Irregular breathing intermixed with irregular periods of Apnea  As breathing continues to deteriorate it becomes Agonal Respirations, and finally Apnea Causes  Head Trauma  Medullary Stroke
  • Abnormal Breathing – Kussmaul Description  Deep, Rapid Breathing to expels excess CO2 in Metabolic Acidosis Causes  Diabetic Ketoacidosis (DKA)  CNS Disorders
  • Reference  Pattinson KTS. Opioids and the Control of Respiration. Posted: 10/03/2008; Br J Anaesth. 2008; 100(6):747-758. © 2008 Oxford University Press URL: www.medscape.com  Asher R, Knight A et al. EMT Basic - Airway Management Module 2.1 URL: http://www.ceu- emt.com/airway-ceu.php (Accessed 16 Mar 2014)
  • Disclaimer  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.