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Control of breathing

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The Mechanism of Breathing

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Control of breathing

  1. 1. DR.SASWAT SUBHANKAR CONTROL OF BREATHING
  2. 2. INTRODUCTION  SPONTANEOUS RESPIRATION IS PRODUCED BY RYTHMIC DISCHARGES OF MOTOR NEURONS THAT INNERVATE RESPIRATORY MUSCLES.  2 SEPARATE NEURAL MECHANISMS REGULATE RESPIRATION: 1. VOLUNTARY: a.LOCATED IN CEREBRAL CORTEX. b.SENDS IMPULSES TO RESPIRATORY MOTOR NEURONS VIA CORTICOSPINAL TRACTS.
  3. 3. 2. AUTOMATIC: a. RUN BY PACEMAKER CELLS IN MEDULLA. b. ACTIVATES MOTOR NEURONS IN CERVICAL & THORACIC SPINAL CORD.  PHENOMENON OF RECIPROCAL INHIBITION IS SEEN IN INSPIRATORY AND EXPIRATORY MUSCLES DUE TO ACTIVITY IN DESCENDING PATHWAYS.
  4. 4. COMPONENTS OF AUTOMATIC RESPIRATION CENTRAL CONTROLLER EFFECTORSSENSORS INPUT OUTPUT
  5. 5. STIMULI AFFECTING RESPIRATORY CENTRE  CHEMICAL: 1. CO2 (VIA CSF,BRAIN INTERSTITIAL FLUID H+ CONC.) 2. O2 3.H+ VIA CAROTID AND AORTIC BODIES.
  6. 6.  NON CHEMICAL: 1. VAGAL AFFERENTS FROM RECEPTORS IN AIRWAYS AND LUNGS. 2. AFFERENTS FROM PONS,HYPOTHALAMUS,LIMBIC SYSTEM. 3. AFFERENTS FROM PROPRIOCEPTORS. 4. AFFERENTS FROM BARORECEPTORS: ARTERIAL,ATRIAL,VENTRICULAR,PULMONARY.
  7. 7. CENTRAL CONTROLLER
  8. 8. MEDULLARY SYSTEM  MAIN COMPONENT OF AUTOMATIC RESPIRATION OR RESPIRATORY CONTROL PATTERN GENERATOR IS LOCATED IN MEDULLA.  RYTHMIC RESPIRATION IS GENERATED BY A SMALL GROUP OF SYNAPTICALLY COUPLED PACEMAKER CELLS IN THE PRE-BOTZINGER COMPLEX(pre-BOTC) ON EITHER SIDE OF MEDULLA BETWEEN NUCLEUS AMBIGUUS AND LATERAL RETICULAR NUCLEUS.
  9. 9. LOCATION OF pre- BOTC.
  10. 10.  NEURONS CONTAIN NK1 AND µ-OPIOID RECEPTORS.  DORSAL AND VENTRAL RESPIRATORY GROUPS: - DORSAL RESPIRATORY GROUP(DRG) IS MAINLY A/W INSPIRATION;VENTRAL RESPIRATORY GROUP(VRG) WITH EXPIRATION. - POSSESS THE PROPERTY OF INTRINSIC PERIODIC FIRING AND ARE RESPONSIBLE FOR BASIC RYTHMS OF VENTILATIONS.
  11. 11. PONTINE INFLUENCES.  PNEUMOTAXIC CENTRE: - LOCATED IN UPPER PONS. - SWITCH OFF CENTRE OR INHIBITS INSPIRATION AND THUS REGULATES INSPIRATION VOLUME.  APNEUSTIC CENTRE: - LOCATED IN LOWER PONS. - IMPULSES FROM THIS CENTRE HAVE AN EXCITATORY EFFECT ON THE INSPIRATORY AREA .
  12. 12. CENTRAL CHEMORECEPTORS.  LOCATED ON THE VENTRAL SURFACE OF MEDULLA.  MEDIATE THE HYPERVENTILATION PRODUCED BY INCREASING ARTERIAL PCO2.  MONITOR THE H+ CONC. OF CSF,INCLUDING THE BRAIN INTERSTITIAL FLUID.  CO2 PENETRATES BBB H2CO3 H+ + HCO3-
  13. 13. LOCATION OF THE CENTRAL CHEMORECEPTORS.
  14. 14. CENTRAL NEURAL MECHANISM  A 3-PART RHYTHM IS SEEN: 1. INSPIRATION. 2. POST-INSPIRATORY ACTIVITY. 3. EXPIRATION.
  15. 15. 1.INSPIRATION: - INSPIRATORY NEURONS THAT ARE PRE-MOTOR TO THE PHRENIC AND INTERCOSTAL MOTOR NUCLEI DISPLAY AN AUGMENTING DISCHARGE. - THE NEURONS RECEIVE INCREASING EXCITATORY POST-SYNAPTIC ACTIVITY DURING INSPIRATION. - AT THE END OF INSPIRATION, DISCHARGE FROM INSPIRATORY NEURONS ARE EXTINGUISHED BY AN INHIBITORY ACTIVITY FROM OTHER NEURONS.
  16. 16. 2. POST INSPIRATORY ACTIVITY: - INSPIRATORY NEURONS RECEIVE BOTH EXCITATORY AND INHIBITORY POST-SYNAPTIC POTENTIALS. - A/W ACTIVE BRAKING OF AIRFLOW AT THE BEGINNING OF EXPIRATION. - DURATION OF THIS PHASE IS AN IMPORTANT DETERMINANT OF TOTAL DURATION OF EXPIRATION.
  17. 17. 3. EXPIRATION: - INSPIRATORY NEURONS RECEIVE INHIBITORY POST-SYNAPTIC POTENTIALS IN AN AUGMENTING MANNER. - THROUGHOUT EXPIRATION THERE IS A DECREASING INHIBITION OF THE FOLLOWING INSPIRATION-EARLY IN EXPIRATION, LARGE STIMULI ARE NEEDED TO TRIGGER THE ONSET OF INSPIRATION THAN LATE EXPIRATION.
  18. 18. PERIPHERAL CHEMORECEPTORS.
  19. 19. CAROTID AND AORTIC BODIES  CAROTID BODY IS PRESENT NEAR CAROTID BIFURCATION.  2 OR MORE AORTIC BODIES ARE PRESENT NEAR ARCH OF AORTA.  CAROTID BODY:-COMPOSED OF 2 TYPES OF CELLS. - TYPE I CELLS/GLOMUS CELLS:RESEMBLE ADRENAL CHROMAFFIN CELLS-CONTAIN DENSE CORE GRANULES CONTAINING CATECHOLAMINES THAT ARE RELEASED ON EXPOSURE TO HYPOXIA,CYANIDE.
  20. 20. O2 SENSITIVE K+ CHANNELS. DECREASED K+ EFFLUX DEPOLARISING THE CELL AND CAUSING Ca2+ INFLUX TRIGGERS AP AND NEUROTRANSMITTER RELEASE. EXCITATION OF AFFERENT NERVE FIBRE
  21. 21. -TYPE II CELLS/GLIAL CELLS: EACH CELL SURROUNDS 4-6 TYPE I CELLS. FUNCTION IS PROBABLY SUSTENTACULAR. - BLOOD FLOW IS ABOUT 2000ml/100g/min. - O2 NEEDS OF THE CELLS ARE MET BY DISSOLVED O2 ALONE-RECEPTORS ARE NOT STIMULATED BY ANEMIA/CO POISONING BUT IN CONDITIONS WHEN ARTERIAL PO2 IS LOW.
  22. 22.  AFFERENTS FROM CAROTID BODIES ASCEND TO MEDULLA VIA GLOSSOPHARYNGEAL NERVES.  FIBRES FROM AORTIC BODIES ASCEND IN THE VAGI.  THE PERIPHERAL CHEMORECEPTORS ARE RESPONSIBLE FOR ALL THE INCREASE OF VENTILATION A/W ARTERIAL HYPOXEMIA.
  23. 23.  COMPLETE LOSS OF HYPOXIC VENTILATORY DRIVE HAS BEEN SEEN IN PATIENTS OF B/L CAROTID BODY RESECTION.  RESPONSE OF PERIPHERAL CHEMORECEPTORS TO ARTERIAL PCO2 IS LESS IMPORTANT THAN THAT OF CENTRAL CHEMORECEPTORS.  IN HUMANS,THE CAROTID AND NOT THE AORTIC BODIES RESPOND TO INCREASED H+ CONCENTRATION.
  24. 24. NON-LINEAR RESPONSE OF CAROTID BODIES TO ARTERIAL PO2. •SENSITIVITY OF CAROTID BODIES TO ARTERIAL PO2 BEGINS AT AROUND 500mm Hg. •RELATIVELY LITTLE RESPONSE OCCURS UNTIL THE ARTERIAL PO2 DROPS BELOW 100mm Hg.
  25. 25. LUNG RECEPTORS.  PULMONARY STRETCH RECEPTORS: - SLOWLY ADAPTING PULMONARY STRETCH RECEPTORS. - PRESENT WITHIN AIRWAY SMOOTH MUSCLE. - DISCHARGE IN RESPONSE TO DISTENSION OF THE LUNG. - IMPULSES TRAVEL VIA LARGE MYELINATED FIBRES IN VAGUS N.
  26. 26. - HERING-BREUER REFLEX: STIMULATION OF PULMONARY STRETCH RECEPTORS INHIBITION OF APNEUSTIC CENTRE AND INSPIRATORY AREA EXPIRATION.
  27. 27. - THE OPPOSITE RESPONSE IS ALSO SEEN; i.e. DEFLATION OF THE LUNGS TENDS TO INITIATE INSPIRATORY ACTIVITY. - BILATERAL VAGOTOMY CAUSES SLOW,DEEP BREATHING IN MOST ANIMAL MODELS.
  28. 28.  IRRITANT RECEPTORS:- LIE BETWEEN AIRWAY EPITHELIAL CELLS. - RAPIDLY ADAPTING. - STIMULATED BY NOXIOUS GASES, CIGARETTE SMOKE, DUSTS AND COLD AIR. - IMPULSES TRAVEL UP THE VAGUS IN MYELINATED FIBRES. - REFLEX INCLUDES HYPERPNEA AND BRONCHOCONSTRICTION.
  29. 29.  J RECEPTORS:- ENDINGS OF UNMYELINATED C FIBRES. - IMPULSES PASS UP THE VAGUS N IN SLOWLY CONDUCTING UNMYELINATED FIBRES. - RESULTS IN RAPID,SHALLOW BREATHING. - ENGORGEMENT OF PULMONARY CAPILLARIES AND INCREASE IN INTERSTITIAL FLUID VOLUME OF ALVEOLAR WALL CAN ACTIVATE THESE RECEPTORS.
  30. 30.  BRONCHIAL C FIBRES: - RESPOND TO CHEMICALS INJECTED INTO BRONCHIAL CIRCULATION. - REFLEXES INCLUDE RAPID SHALLOW BREATHING, BRONCHOCONSTRICTION AND MUCUS SECRETION.
  31. 31. OTHER RECEPTORS  NOSE AND UPPER AIRWAY RECEPTORS: - RESPOND TO MECHANICAL AND CHEMICAL STIMULI. - REFLEXES INCLUDE SNEEZING,COUGHING AND BRONCHOCONSTRICTION.  JOINT AND MUSCLE RECEPTORS: - ACTIVE DURING EXERCISE,ESPECIALLY IN EARLY STAGES.
  32. 32.  GAMMA SYSTEM: - MOST MUSCLES CONTAIN MUSCLE SPINDLES THAT SENSE ELONGATION OF MUSCLE. - INVOLVED IN THE SENSATION OF DYSPNEA THAT OCCURS WHEN UNUSUALLY LARGE RESPIRATORY EFFORTS ARE REQUIRED TO MOVE THE LUNG AND CHEST WALL e.g. AIRWAY OBSTRUCTION.
  33. 33.  ARTERIAL BARORECEPTORS: - AN INCREASE IN ARTERIAL B.P. CAN CAUSE REFLEX HYPOVENTILATION THROUGH STIMULATION OF AORTIC AND CAROTID SINUS RECEPTORS. - A DECREASE IN B.P. CAN CAUSE HYPOVENTILATION.  PAIN AND TEMPERATURE:- PAIN OFTEN CAUSES A PERIOD OF APNEA FOLLOWED BY HYPERVENTILATION. - HEATING OF SKIN MAY CAUSE HYPERVENTILATION.
  34. 34. INTEGRATED RESPONSES.
  35. 35. RESPONSE TO CO2  ARTERIAL PCO2 IS THE MOST IMPORTANT STIMULUS TO VENTILATION UNDER MOST CONDITIONS.  ARTERIAL PCO2 IS NORMALLY MAINTAINED AT 40mm Hg. WHEN PCO2 RISES,VENTILATION IS STIMULATED AND THE RATE OF PULMONARY EXCRETION OF CO2 INCREASES.  MOST OF THE STIMULUS COMES FROM CENTRAL CHEMORECEPTORS.  RESPONSE IS MAGNIFIED IF ARTERIAL PO2 IS LOWERED.
  36. 36. RELATIVELY LINEAR RESPONSE OF VENTILATION WITH INCREASING PCO2 IS DUE TO INCREASE IN BOTH RATE AND DEPTH OF VENTILATION.
  37. 37. RESPONSE TO O2  WHEN O2 CONTENT OF INSPIRED AIR DECREASES, RMV INCREASES.  MARKED STIMULATION OCCURS WHEN PO2 FALLS <100mm Hg.  ROLE OF THIS HYPOXIC STIMULUS IN DAY-TO- DAY CONTROL OF VENTILATION IS SMALL. IT IS USEFUL DURING ASCENT TO HIGH ALTITUDES.
  38. 38. AT PCO2 35.8, ALMOST NO INCREASE OF VENTILATION OCCURS UNTIL PO2 IS REDUCED TO ABOUT 50mm Hg.
  39. 39.  PTS. WITH SEVERE LUNG DISEASE HAVE CHRONIC CO2 RETENTION AND THE pH OF BRAIN ECF HAS RETURNED TO NEAR NORMAL IN SPITE OF A RAISED PCO2.UNDER THESE CONDITIONS ARTERIAL HYPOXEMIA BECOMES THE CHIEF STIMULUS TO VENTILATION. IF SUCH A PT. IS GIVEN A HIGH O2 MIXTURE TO BREATHE, VENTILATION MAY BECOME GROSSLY DEPRESSED.
  40. 40. RESPONSE TO pH.  A REDUCTION IN ARTERIAL BLOOD pH STIMULATES VENTILATION.  CHIEF SITE OF ACTION IS THE PERIPHERAL CHEMORECEPTORS.  CENTRAL CHEMORECEPTORS OR THE RESPIRATORY CENTRE ITSELF CAN BE AFFECTED BY A CHANGE IN BLOOD pH IF IT IS LARGE ENOUGH-IN THIS CASE,BBB BECOMES PARTLY PERMEABLE TO H+ IONS.
  41. 41. RESPONSE TO EXERCISE  INITIAL RAPID RESPONSE THAT IS NEURALLY MEDIATED FOLLOWED BY A SLOWER EXPONENTIAL RESPONSE THAT PLATEAUS.  IN SEVERE EXERCISE,ACCUMULATION OF LA LEADS TO FURTHER INCREASE.  AN ADDITIONAL STIMULUS IS THOUGHT TO ACT DURING EXERCISE WHICH INCREASES VENTILATION SUFFICIENTLY SO THAT THERE IS LITTLE CHANGE IN PCO2 DESPITE THE RISE IN METABOLIC RATE.
  42. 42.  ROLE OF CAROTID BODY IS DISPUTED-ONE HYPOTHESIS SUGGESTS THAT OSCILLATIONS IN PO2 AND PCO2 MAY STIMULATE THE PERIPHERAL CHEMORECEPTORS.
  43. 43. ABNORMALITIES OF RESPIRATORY RHYTHM.
  44. 44. TRANSECTION AT VARIOUS LEVELS
  45. 45.  CHEYNE-STOKES BREATHING: - PERIODIC BREATHING CHARACTERISED BY A CYCLIC RISE AND FALL IN VENTILATION WITH PERIODS OF APNEA OR NEAR APNEA. - CAUSES: CCF,UREMIA,DRUGS(SEDATIVES, OPIATES), CNS TUMORS. - IN CARDIAC DISEASE, THERE IS PROLONGATION OF LUNG-TO-BRAIN CIRCULATION SO THAT IT TAKES LONGER FOR CHANGES IN ARTERIAL GAS TENSIONS TO AFFECT THE RESPIRATORY AREA IN MEDULLA.
  46. 46. CHEYNE- STOKES BREATHING.
  47. 47.  SLEEP APNEA: - CAUSES MAY BE CENTRAL(FAILURE OF DISCHARGE IN NEURONS) OR OBSTRUCTIVE. - DUE TO RELAXATION OF PHARYNGEAL MUSCLES OR IN SOME CASES DUE TO FAILURE OF GENIOGLOSSUS MUSCLE TO CONTRACT DURING INSPIRATION. - COMMON IN REM SLEEP. - SEEN IN PREMATURE INFANTS,ADULT MALES AND POST-MENOPAUSAL WOMEN.
  48. 48.  BIOTS BREATHING: - - PERIODS, OR "CLUSTERS", OF FAIRLY RAPID RESPIRATIONS OF CLOSE TO EQUAL DEPTH FOLLOWED BY REGULAR PERIODS OF APNEA THAT CAN LAST BETWEEN 15 SECONDS TO 120 SECONDS. - CAUSES: DAMAGE TO THE MEDULLA OBLONGATA BY STROKE (CVA) OR TRAUMA, OR PRESSURE ON THE MEDULLA DUE TO UNCAL OR TENORIAL HERNIATION, PROLONGED OPIOID ABUSE.
  49. 49. BIOTS BREATHING

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