Control of Ventilation /Lung Physiology by Nahid Sherbini

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Control of Ventilation /Lung Physiology by Nahid Sherbini

  1. 1. Dr . Nahid Sherbini Consultant IM &Pulmonary KFH ,Medina ,Saudi Arabia
  2. 2. Breathing is controlled by the central neuronal network to meet the metabolic demands of the body – Neural – Chemical
  3. 3. Keep arterial levels of O2 & CO2 constant. Match perfusion by pulmonary blood flow with ventilation of the lungs with overall metabolic demand.
  4. 4. Control of Breathing Central neurons determine minute ventilation (VE) by regulating tidal volume (VT) and breathing frequency (f). VE = VT x f
  5. 5. Definition: A collection of functionally similar neurons that help to regulate the respiratory movement.
  6. 6.  Higher respiratory center: cortex, hypothalamus & limbic system. Medulla & Pons : Basic respiratory center: produce and control the respiration.  Spinal cord: motor neurons.
  7. 7. Affect rate and depth of ventilation Influenced by: • higher brain centers • peripheral mechanoreceptors • peripheral & central chemoreceptors
  8. 8. Voluntary breathing center Cerebral cortex. Automatic (involuntary) breathing center – Medulla – Pons
  9. 9. CAN BYPASS LOWER CENTERS. SPEECH,SINGING,COUGHING, BREATH HOLDING .
  10. 10.  Voluntarily – speaking, blowing, whistling, pushing, defecation.  Voluntary control is bilateral – cannot contract half of diaphragm or larynx.  Descend via pyramidal tracts.  Destroy voluntary control without losing involuntary control can be.. i.e. stroke
  11. 11. To larynx and bronchi To respiratory muscles Nucleus parabrachialis medialis (part of PRG) Dorsal respiratory group – nucleus of the solitary tract Pons Medulla Ventral respiratory group - Nucleus ambiguus - Nucleus retroambigualis PRG = pontine respiratory group
  12. 12.  Rhythmicity center: • Controls automatic breathing. • Interacting neurons that fire either during inspiration (I neurons) or expiration (E neurons).
  13. 13.  I neurons located primarily in dorsal respiratory group (DRG): • Regulate activity of phrenic nerve.  E neurons located in ventral respiratory group (VRG): • Passive process.  Activity of E neurons inhibit I neurons. • Rhythmicity of I and E neurons may be due to pacemaker neurons
  14. 14. Inspiratory Muscles Expiratory Muscles Inspiratory Neurons Expiratory Neurons • This implies that each group exhibits “self-inhibition” – they can switch themselves off. • Stops breathing getting stuck in inspiration or expiration.
  15. 15.  Apneustic center (lower pons) – to promote Inspiration. Pneumotaxic center (upper pons) – inhibits apneustic center & inhibits inspiration -helps control the rate and pattern of breathing.
  16. 16. Pons Medulla Cuts off Produces apneustic effect – long, powerful inspirations Stops breathing since no automated output to respiratory system – cause of death
  17. 17. DRG VRG pons medulla Neural Control of Breathing – Respiratory neurons
  18. 18. Neural Control of Breathing – The efferent pathway Phrenic n. muscle supply autonomic
  19. 19. DECENDING BULBOSPINAL FIBRES ARE IN THE VENTRAL AND LATERAL COLUMNS. RESP NEURONS ARE IN VENTRAL Horn EXP NEURONS -VENTROMEDIAL INSP NEURONS- LATERAL
  20. 20. ASCENDING SPINORETICULAR FIBRES CARRY PROPRIOCEPTIVE INPUTS TO STIMULATE RESP CENTRE. BILAT CERVICAL CORDOTOMY LEADS TO RESPIRATORY DYSFUNCTION (SLEEP APNEA).
  21. 21.  Diaphragm controlled directly by  motor neurons – “C3,4 & 5 keeps the diaphragm alive”.  Motor neurons take turns to stimulate different groups of muscle fibres active to minimise fatigue.  Due to poor supply of muscle spindles , control comes from DRG &VRG. And this explains why rare to feel fatigue in diaphragm.
  22. 22.  Larynx movements are synchronized with breathing.  Superior and recurrent laryngeal nerves are branches of vagus nerve. Expiration – vocal cords together. Inspiration – vocal cords apart.  Automatic rhythm that we can override consciously.  Opera singers try and maximise control of breathing using these muscles.
  23. 23.  Control of breathing affected profoundly by vagus nerves (Cranial Nerve X).  Two of these run down either side of neck and torso, near trachea.  Regulate receptors which are most involved in respiration: • Slowly-adapting pulmonary stretch receptors (PSR’s) • Rapidly-adapting (irritant) receptors (RAR’s) • C-fibre receptors (J receptors)
  24. 24. Paintel et al (1970) : Propose J receptors function TO LIMIT EXERCISE WHEN INTERSTITIAL PRESSURE INCREASES(J REFLEX) MECHANISM: INHIBITION OF RESP MOTOR NEURONS.
  25. 25. •+ when pulmonary caps are engorged or pulmonary edema. create a feeling of dyspnea
  26. 26.  UNMYELINATED NERVE ENDINGS .  RESPONSIBLE FOR BRONCHOSPASM IN ASTHMA.  INCREASED TRACHEOBRONCHIAL SECRETIONS.  MEDIATORS: HISTAMINE, PROSTAGLANDINS , BRADYKININ.
  27. 27.  Herring-Breuer Inflation reflex • stretch receptors located in wall of airways • + when stretched at tidal volumes > 1500 ml • inhibits the DRG Inflation Apnoea Phrenic nerve activity Lung volume Safety threshold that triggers reflex
  28. 28. Airway Receptors: Slowly adapting (stretch - ends inspiration) Rapidly adapting (irritants - cough) Bronchial c-fiber (vascular congestion - bronchoconstriction) Parenchymal c-fiber (irritants - bronchoconstriction) Xth n. Reflex Control of Breathing – Neural receptors afferents
  29. 29. EXPT ANIMAL STUDIES Rapid shallow breathing pattern in response to bronchospasm is mediated through vagal afferents.
  30. 30. MECHANORECEPTORS - SENSE CHANGES IN LENGTH ,TENSION AND MOVEMENT. ASCENDING TRACTS IN ANTERIOR COLUMN OF SPINAL CORD TO RESP CENTRE IN MEDULLA.
  31. 31. SENSE CHANGES IN MSL LENGTH. INTERCOSTALS > DIAPHRAGM . REFLEX CONTRACTION OF MUSCLE IN RESPONSE TO STRETCH. INCREASE VENTILATION IN EARLY STAGES OF EXERCISE.
  32. 32. SENSE DEGREE OF CHEST WALL MOVT. INFLUENCE THE LEVEL & TIMING OF RESP ACTIVITY.
  33. 33.  Neural control  Beta receptors causing dilatation  Parasympathetic-muscarinic receptors causing constriction  NANC nerves (non-adrenergic, non-cholinergic) ○ Inhibitory release VIP and NO  bronchodilitation ○ Stimulatory  bronchoconstriction, mucous secretion, vascular hyperpermeability, cough, vasodilation “neurogenic inflammation”.
  34. 34. Local factors • histamine binds to H1 receptors-constriction • histamine binds to H2 receptors-dilation • slow reactive substance of anaphylaxsis- constriction-allergic response to pollen • Prostaglandins E series- dilation • Prostaglandins F series- constriction
  35. 35.  Monitor changes in blood PC02, P02, and pH.  Central: • Medulla.  Peripheral: • Carotid and aortic bodies.  Control breathing indirectly.
  36. 36. RESPONSE TO HYPERCAPNIA • 20-50% CAROTID BODIES • 50-80% CENTRAL CHEMORECEPTORS
  37. 37. CO2, H+ Control of Breathing by Central chemoreceptors Central chemoreceptors major regulators of breathing CO2, H+ Central chemoreceptors Resp neurons VE
  38. 38. Carotid body O2 Chemical Control of Breathing – Peripheral chemoreceptors IXth n. CO2 pH ~10% contribution to breathing
  39. 39. CO2 tension in blood (mm Hg) 35 40 45 VE 5 50 (L/min) quiet breathing hypercapnia CO2 drives ventilation
  40. 40. CO2 tension in blood (mm Hg) 35 40 45 VE 5 50 (L/min) Hypoxia is a weak ventilatory stimulus blood pO2 = 100 mmHg blood pO2 = 50 mmHg
  41. 41. Are not stimulated directly by changes in arterial PC02. H20 + C02 H2C03 H+ Stimulated by rise in [H+] of arterial blood. • Increased [H+] stimulates peripheral chemoreceptors.
  42. 42.  NO CHANGE CAROTID BODY ACTIVITY TILL PaO2 < 75mmHg.  VENTILATION MARKEDLY INCREASED When PaO2<50mmHg
  43. 43. RAPID PHASE- RAPID INCREASE IN VE WITHIN SECONDS DUE TO ACIDIFICATION OF CSF. SLOWER PHASE- DUE TO BUILDUP OF H+ IONS IN MEDULLARY INTERSTITIUM. CHRONIC HYPERCAPNIA- WEAKER EFFECT DUE TO RENAL RETENTION OF HCO3 WHICH REDUCES THE H+.
  44. 44. VENTILATORY RESPONSE TO ALV O2  CO2 POTENTIATES VENTILATORY RESPONSE TO HYPOXEMIA .  BOTH HYPOXEMIC AND HYPERCAPNIC RESPONSES DECREASE WITH AGEING AND EXERCISE TRAINING.
  45. 45. Normal level of HCO3- = 25 mEq/L Metabolic acidosis (low HCO3-) will stimulate ventilation (regardless of CO2 levels). Metabolic alkalosis (high HCO3-) will depress ventilation (regardless of CO2 levels) .
  46. 46. EFFECT OF PaCO2 & pH ON VENTILATION
  47. 47. SENSATION OF DYSPNEA WHEN INCREASED RESP EFFORT DUE TO “LENGTH- TENSION INAPPROPRTATENESS” REMOVAL OF FLUID RESTORES THE END EXP MSL FIBRE LENGTH RESTORES THE LENTH TENSION RELATIONSHIP RELIEF.
  48. 48. SV & CO decreased Coronary blood flow decreased Repolarization of heart impaired Oxyhemoglobin affinity increased Cerebral blood flow decreased Skeletal muscle spasm & tetany Serum potassium decreased • (common thread in most of above is hypocapnic alkalosis)
  49. 49. Effect of brain edema • depression or inactivation of respiratory centers Effect of Anesthesia/Narcotics • respiratory depression  sodium pentobarbital  morphine
  50. 50. BILATERAL CAROTID BODY RESECTION CAROTID ENDARTERECTOMY REDUCES VE. 30% DECREASE IN RESPONSE TO HYPERCAPNIA.
  51. 51. 59Y FEMALE COPD,CVA ( OLD) CAROTID ENDARTERECTOMY 1YR ELECTIVE CE (R) DONE PREOP ABG ON R/A- 7.43/50/48/31 DAY 3 EXTUBATED O2 3L/MIN DAY5: SOMNOLENT AND CONFUSED ABG- 7.28/62/69/31 BiPAP INITIATED IMPROVED ABG-7.38/72/54/36
  52. 52. COPD WITH HYPERCAPNIA & WORSENING RESP ACIDOSIS FULL OXYGEN THERAPY • LOSS OF HYPOXIC DRIVE • WORSENING V/Q MISMATCH PHYSIOLOGIC DEAD SPACE • CO2 CARRYING CAPACITY AS OXYGENATION OF Hb IMPROVES ( HALDANE EFFECT)
  53. 53. PERIODIC BREATHING PATTERN WITH CENTRAL APNEAS. Causes 1. BILATERAL SUPRAMEDULLARY LESION 2. CARDIAC FAILURE 3. HIGH ALTITUDE 4. SLEEP
  54. 54.  Response to hypoxia and hypercapnia.  Response to MECHANORECEPTORS Pa O2 AND PaCO2 BY 4-8 mmHg
  55. 55. HYPOTONIA OF UPPER AIRWAY- OBSTR SLEEP APNEA. HYPOTONIA OF SKELETAL& RESP MUSCLES- (Ventilation DEPENDS ON DIAPHRAGM)
  56. 56. PHASE I - IMMED VE WITHIN SECONDS,NEURAL IMPULSES MSL SPINDLES, JOINT PROPRIOCEPTORS . PHASE II- WITHIN 20-30 SEC VENOUS BLD FROM MSL,SLOW VE( VENTILATION LAGS BEHIND CO2).
  57. 57. PHASE III - PULM GAS EXCHANGE MATCHES THE METAB RATE TO MAINTAIN STABLE O2, CO2, PH. PHASE IV - BEGINS AT ANAOERBIC THRESHOLD, O2 CONSUMTION> O2 DELIVERY AND LACTIC ACID ACCUMULATES.
  58. 58. VENTILATORY RESPONSE TO EXERCISE

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