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CHEMICAL REGULATION OF RESPIRATION.pptx4-12-2015.pptx
- 2. CHEMORECEPTORS peripheral central pulmonary &myocardial Effect of Po2,Pco2,&H+ Concentrations on respiration Interaction of Po2,Pco2,&H+ in regulating respiration Other aspects related to chemical regulation
- 3. •Pco2 •Po2 • PH OFBLOOD •These factors influence the respiration in such a why that their own blood levels are maintained constant
- 4. •Have sensory nerveendings •Highly sensitive to changes inPco2 ,Po2,&PH of blood TYPES OF CHEMORECEPTORS PERIPHERAL CENTRAL PULMONARY& MYOCARDIAL
- 5. carotid bodies& Aortic bodies
- 6. This is specialnervous chemical receptors, called chemoreceptors mainly located outside brain They are important in detecting change in O2 in the blood rather than CO2 They are called “carotid bodies” located in the bifurcation of the common carotid arteries and in arch of aorta
- 8. Consists of CAPSULE SINUSOIDAL LARGE CAPILLARIES EPITHELIAL CELLS TYPE-1 TYPE -2 NERVE FIBRES
- 9. Capsule-surround eachcarotid & Aortic body Sinusoidal large capillaries-present below the capsule, surround main mass of each body EPITHELIAL CELLS- Type- 1-Glomus cells -similar to chromaffin cells of A. Gland -Have dense core granules -contain NT(NE&DOPAMINE) -Surrounded by unmyelinated N endings having D2 receptors
- 10. TYPE 2CELLS-Glial cells - surround Type 1 cells NERVE FIBRES -OUT Side the capsule they acquire myeline sheath -join with sinus nerve (9th) which ascend to Medulla -join with aortic nerve(10th) which ascend to Medulla Conduction velocity is slow- 7-12m/s BLOOD FLOW- HAVE rich blood flow- 2000ml/100gms/min FUNCTIONS-Respond to-LOW Po2 ,high PCO2 &High H+ Concentration Stimulate DRG of Neurons
- 11. DETECT CHANGESIN Po2 CAROTID BODIES-Increase both rate & depth of respiration Aortic body increases only the frequency of respiration with small increase in ventilation
- 12. 1. HYPOXIA Decreasein activity of o2 sensitive k+ channels in glomus cell membrane Depolarisation of glomus cells Opening of ca++ channels Increase in ca++ influx Release of NT NT stimulates the afferent nerve endings
- 13. 1 .O2tension Vs O2 content A.HYPOXIC HYPOXIA B.HISTOTOXIC C.ANAEMIC HYPOXIA,METHEMOGLOBINEM IA,CARBON MONOXIDE POISONING D.VASCULAR STASIS DRUGS
- 14. 2.ELEVATED PCO2 3.H+ CONCENTRATION 4 .INCREASE IN PLASMA K+ CONCENTRATION
- 15. REGULATE RESPIRATION INCREASE THE RATE & DEPTH OF RESPIRATION INCREASE B.P, TACHYCARDIA 15% OF RESPIRATORY DRIVE
- 17. Location: brainstem, ventral surface of medulla They are located near I neurons They project to respiratory neurons Central chemoreceptors and respiratory neurons are distinct They are mainly sensitive to changes in PaCO2 A rise in PaCO2 effectively stimulates central chemoreceptors
- 18. The levelsof what chemicals are going to control respiration? CO2, H+ ions and O2. In the CNS, CO2 and H+ are particularly important. O2 has a greater effect in the PNS.
- 19. In thechemosensitive areas of the respiratory center, increased H+ is the main stimulus. Activation of the central chemoreceptors by H+ excites the dorsal respiratory group of neurons (inspiratory area) and thus increase the respiration rate. Why then, does activation of central chemoreceptors occur mainly after a rise in peripheral CO2, but not so much with peripheral H+?
- 20. The blood-brainbarrier is not very permeable to H+; however, CO2 easily diffuses across the BBB (as usual). As we have discussed, increases in CO2 cause increases in H+. So, once CO2 diffuses into the chemosensitive regions of the CNS, H+ is formed and stimulates the dorsal group.
- 21. CO2 crosses theblood brain barrier (BBB) CO2 brain ISF CO2 + H2O H2CO3 Carbonic anhydrase blood H+ + HCO3 Drop in CSF pH
- 22. Central chemoreceptorneurons monitor the H+ ion concentration of brain ISF; Greater the PaCO2, > the minute ventilation; If you lower PaCO2, minute ventilation is lowered
- 23. More CO2 inblood as a result of ↑metabolism Transient rise in PaCO2 Fall in CSF pH Respiration is stimulated effectively Steady state PaCO2 is normal
- 24. Alveolar PCO2 (mmHg) Minute ventilatio n (l/min) 0 10 0 200 0 40 50 75 100
- 25. Location Pulmonary-inpulmonary blood vessels Myocardial-in coronary blood vessels INNERVATION-By vagus nerve STIMULATION- by inj. Of Veratridin or Nicotin into pulmonary&Coronary circulation produse PULMONARY CHEMORECEPTORE REFLEX & CORONARY CHEMORECEPTORE REFLEX-BEZOLD – JARISH REFLEX.
- 26. PERIPHERAL ANDCENTRA CHEMORECEPTORS WORK IN COMBINATION TO BRING ABOUT INCREASED VENTILATION AMONG THEASE THREE CHEMICALS , INCREASE IN Pco2 produse strong RESPIRATORY DRIVE
- 27. Arterial Blood Gases& pH Normal range Arterial pH 7.35 – 7.45 Arterial PO2 81 – 100 mm Hg Arterial PCO2 35 – 45 mm Hg
- 29. ARTERIAL Po2=100mmHg ARTERIAL Po2=100-60 MM OF Hg produce less effect on ventilation ARTERIAL Po2 –Below 60 mm of Hg produce marked increase in pul. Ventilation =peripheral chemoreceptores are strong
- 30. PO2 (mm Hg) Minute ventilatio n(l/min) 0 25 50 75 100 0 10 0 200
- 31. Normal Pco2=40mm of Hg IT is kept constant by chemical regulation HYPERCAPNIA=Increase in PCO2 - It occurs in restrictive lung disease - it mainly stimulates central chemoreceptors - it stimulates peripheral chemoreceptores when central chemoreceptores are depressed byAnaesthesia. - has strong breaking effect on the action of either decreased po2 or pH
- 32. Alveolar PO2 orPCO2 (mm Hg) Minute ventilatio n (l/min) 0 100 20 0 0 50 100 MVV: 125-175 l/min Max. ventilation during exercise Response to hypercapnia Response to hypoxia
- 33. Occurs whenarterial Pco2 is above 50 mm of Hg It depresses CNS, Respiratory centres. produce HEADAGHE, CONFUTION,CONVULTIONS, COMA& DEATH CAUSE –Prolonged emphysema - ACCIDENTAL INHALATION OF CO2. - EXPERIMENTALLY PRODUCED BY MAKING THE PT TO INHALE AIR PCO2 WHICH APROCHES CLOSE TO ALVIOLAR PCO2.
- 34. In comatosept with resp. depression estimation of arterial blood pco2 avoids death from co2 NARCOSIS
- 35. 1. METABOLICACIDOSIS (INCEASE IN H+ ION CONCENTRATION CAUSES- DIABETIC KETOACIDOSIS- KUSSMAULS BREATHING - RENAL FAILURE - SEVER MUSCULAR EXERCISE - KETOACIDOSIS IN STARVATION - INFANTILE DIARRHOEA
- 36. DICREASED H+CONCENTRATION (METABOLIC ALKALOSIS –Causes DEPRESSION of respiratory centre via peripheral chemoreceptors. Causes-excesive vomitings with loss of Hcl from the body
- 37. This leadsto elivated arterial Pco2 It produces resp.acidosis Causes for this- Resp. depression -neuromusculare disorders -emphysema. Compensatory mechanism-chemoreceptors produce hyper ventilation Wash out Co2 Tries to restore arterial PCO2
- 38. This causesdecrease in arterial pco2 Produce Resp alkalosis Causes- voluntary hyperventilation - Excessive artificial respiration -compulsive hyperventilation in hysteric pts. -ch, hypoxia Signs & symptoms-faintness, parasthesia due to reduction of cerebral blood flow Resp alkalosis-lowering of ca++ in plasma- tetony, corpopedal spasm -
- 39. COMPENSATORY MECHANISMS; THROUGH CHEMORECEPTORS SLOWDOWN RESPIRATION THIS LEADS TO RETENTION OF CO2 THIS INTURN RESTORES H+ CONCENTRATIONOF BLOOD TOWARDS NORMAL
- 40. In physiologicalconditions or invarious clinical situvations-more than one factor is responsible for regulation of respiration
- 41. 40 50 PACO2 Ventilatio n (l/min) PAO2= 40 PAO2 = 55 PAO2 = 100 0 25 5 0 7 5 10 0
- 42. The stimulatoryeffect of H+ concentration & pco2 are additive Fall in PH shifts the co2 response curve to left without change in slope.
- 43. The effectof co2 on respiration increases with incease in body temperature
- 44. EFFECT OFHYPER VENTILATION A.Effect of short losting sever hyperventilation----- -1 Effect on respiration Hyperventilation apnea ----periodic breathing. For prolonged period---for 1-2 mts-----for some time
- 45. EFFECT ONPO2& PCO2 During hyperventilation Arterial po2- as high as 150 mm Hg Arterial pco2-as low as 15 mmHg During apnea- Arterial po2- decreased Arterial pco2 increased During periodic breathing-APNEA FOLLOWED BY NORMAL BREATHING
- 46. During apnea—PO2Falls pco2 increases During normal breathing-po2 rises -pco2 falls During restoration of normal breathing- -po2 reaches 100 -pco2 reaches 40mmHg
- 47. Hyperventilate toexhaustion Then, note your pattern of breathing Explain your observations Periodic breathing norma l hyperventilatio n Following hyperventilatio n
- 48. Int hiscondition 2-5 fold increase in ventilation Occurs in residents of high altitude In pts with pul. Diseases This condition leads to complications like -resp. alkalosis-tetony -renal changes-defective H+ secretory mechanism -neurological changes-dizziness ,dull conciousness, loss of contiousness.
- 49. Apnea isthe temporary suspension of breathing. Normally, some episodes of apea occur. In people with sleep apnea, the episodes are longer and more frequent. 2 types of sleep apnea are: Obstructive sleep apnea Central sleep apnea
- 50. This occurswhen the pharynx collapses during sleep. The pharynx is normally held open by muscles, which at night, relax. In patients with sleep apnea, the pharynx is collapsed while the muscles relax. Some of the factors that cause this collapse include: ◦ Excess fat deposits in the soft tissues of the pharynx or fat masses in the neck. ◦ Nasal obstruction ◦ Enlarged tonsils ◦ Very large tongue ◦ Certain shapes of the palate
- 51. Loud snoringand labored breathing that often progressively worsens. Long silent periods (apnea) that cause increases in PCO2 and decreases in PO2. This stimulates respiration, which results in loud snore and gasps. This repeats.
- 52. Less commonthan obstructive sleep apnea. The CNS signal to the respiratory muscles stops. Can be caused by damage to the central respiratory center or respiratory neuromuscular junction.