Regulation of Respiration PDF

REGULATION OF RESPIRATION (Dr. Hızır Kurtel)  This lecture examines control systems in general and presents the respiratory control system as two interrelated components; the neural and chemical control systems.  Additionally, regulation of respiration during exersize as well as d...

REGULATION OF RESPIRATION (Dr. Hızır Kurtel)  This lecture examines control systems in general and presents the respiratory control system as two interrelated components; the neural and chemical control systems.  Additionally, regulation of respiration during exersize as well as dysfunction of respiratory control will be discussed. After completing this lecture, students should be able to 1- Describe and localize the brain stem integrating centers responsible for producing the spontaneous rhytmicity of breathing, 2- Identify and describe how sensors detect and send information into the brain stem centers to alter breathing rate, 3- Identify and locate chemoreceptors that monitor extracellular fluid pH, carbon dioxide and oxygen tension, 4- Describe how alterations in pH, carbon dioxide and oxygen interact to influence or alter ventilation 5- Describe how respiratory control is done during exersize, 6- Identify the major respiratory rhythm abnormalities. respiratory muscles do not have auromaticity Like cardiac muscles, the inspiratory muscles normally contract rhythmically. However the origins of these contractions are quite different. Certain of the cardiac muscle cells have automaticity, they are capable of self- excitation. internal intercosatl mucles help exhalaltion while external intercostals help inhalation On the other hand, the diaphragm and intercostal muscles are skeletal muscles, which can not contract unless stimulated by nerves. Thus, breathing depends entirely upon cyclical respiratory muscle contraction by the nerves to the diaphragmn and the intercostal muscles.  Destruction of these nerves or the areas from which they originate (as in poliomyelitis) results in paralysis of the respiratory muscles and death unless some form of artificial respiration can be rapidly instituted.  where can you find the respiratory centers ? 1- The Respiratory Center:  The respiratory center is composed of several widely dispersed groups of neurons located bilaterally in the medulla oblongata and pons. a- Dorsal respiratory group. Located in the dorsal portion of the medulla, which mainly causes inspiration. The dorsal respiratory group of neurons plays the fundamental role in the control of respiration. b- Ventral respiratory group. Located in the ventrolateral part of the medulla, which can cause either respiration or inspiration, depending upon which neurons in the group are stimulated.  The basic rhythm of respiration is generated mainly in the dorsal respiratory group of neurons.  Even when all the peripheral nerves entering the medulla are sectioned and the brain stem is transected both above and below the medulla, Medullary neurons still emits repetitive bursts of respiratory action potentials. Unfortunately though, the basic cause of these repetitive discharges is still unknown.  P: Fine tuning of respiratory P & A (Pontine respiratory rate and depth group) both receive peripheral Inhibit inspiration/transition stimulus from exp to insp (Pneumotaxic) P (Apneustic) A A: Prolong inspiratrion, send signals to cause inspiration VRG: contains 4 main nuclei Bötzinger complex (Exp) Prebötzinger complex (Ins) - Pacemakers/Special cation channels Trigger insp. constantly leaking) spontaneously - N. Ambiguous (Laringeal, faringeal muscles) - N. Retroambiguous (insp & exsp) C3 to C5 to diaphgram (phrenic nerve) T1 to T11 (intercostal nerves) Gray matter 2- The Inspiratory Ramp Signal: The nervous signal that is transmitted to the inspiratory muscles is not an instantaneous burst of action potentials. Instead, in normal respiration, it begins very weakly at first and increases steadily in a ramp fashion for about 2 seconds. It rapidly ceases for approximately the next 3 seconds, then begins again for still another cycle, and again and again.  Thus the inspiratory signal is said to be a ramp signal. The obvious advantage of this is that it causes a steady increase in the volume of the lungs during inspiration, rather than inspiration gasps. in a patient with tachophynea with increase respirtatory rate of 40 a drug is givwn to dercease the rate this drug inhabits which center? paitents with tavhopnea have weak pneumotaix center signalse false 3- The Pneumotaxic Center: Transmits impulses continuously to the inspiratory area. The primary effect of these is to control the switch-off point of the inspiratory ramp, thus controlling the duration of the filling phase of the lung cycle. eg: When the pneumotaxic signals are strong, inspiration might last for as little as 0.5 second, but when weak, as long as 5 or more seconds, thus filling the lungs with a great excess of air. Thus a strong pneumotaxic signal can increase the rate of breathing up to 30 to 40 breaths per minute. 4- The Ventral Respiratopy Group of Neurons: true or false Activity is low during normal quite respiration. Therefore normal quite breathing is caused mainly by repetitive inspiratory signals from the dorsal respiratory group transmitted mainly to the diaphragm, and expiration results from elastic recoil of the lungs and thoracic cage.  When the respiratory drive for the increased pulmonary ventilation becomes greater than normal respiratory signals then spill over into the ventral respiratory neurons from the basic oscillating mechanism of the dorsal respiratory area then does contribute its share to the respiratory drive as well. we only see dorsal activity in excersise false 5- Reflexes a) Stretch receptors (Hering Breuer Reflex):  Located in the walls of small airways and visceral pleura are stimulated by increases in lung volume.  Afferent vagal impulses from these receptors inhibit medullary and pontine centers and function to terminate inspiration (prevent over ventilation).  P A OVERALL effect is the inhibition of DRG (CNX-Vagus) Decreased depth and RR C3 to C5 to diaphgram (phrenic nerve) T1 to T11 (intercostal nerves) Stretch Receptors Gray matter (>800 ml) Bronchi,& Visceral Pleura in a patient with asthma problems which recepter activity is suspected ? b) Irritant Receptors:  Located between epithelial cells in the large airways, are stimulated by smoke, noxious vapors, cough.  Afferent signals from irritant receptors are transmitted via the vagus, trigeminal, or olfactory nerve to the integrator to initiate couging, bronchoconstriction, and breath-holding. a pateint with plumonary emoli fells dysonea which recepter is resposible ? j receptersz are seen in very blood vessel false c) J-Receptors:  Juxtacapillary receptors, stimulated by distension and distortion of the pulmonary microvasculature. Information from the J-receptors is also delivered via vagal afferents to brain stem. When stimulated by emboli or vasocongestion (pulmonary edema) they cause reflex tachypnea, rapid shallow breathing.  These receptors are thought to be responsible for the physiological sensation of “air hunger” also known as dyspnea. d) Chest Wall Receptors:  Located in the chest wall muscles and their tendons, transit afferent information on chest wall position and respiratory effort to the CNS. Input from these stretch receptors may give rise to the sensation of dyspnea when the respiratory effort is excessive for the volume change produced.  P A Fasiculus gracilis, Muscle Spindle Golgi Tendon Organs Fasiculus cuneatus Dorsal Column – Medial Lemniscus Pathway D.M.N C3 to C5 to diaphgram (phrenic nerve) T1 to T11 (intercostal nerves) Gray matter 6- Central Chemoreceptors:  An additional neuronal area, a very sensitive chemosensitive area is located bilaterally and lies less than 1 millimeter beneath the ventral surface of the medulla.  This area is highly sensitive to changes in either blood CO2 or hydrogen ion concentration, and in turn excites the other portions of the respiratory center.  When increased, H+ stimulates respiration through an effect on the central chemoreceptors; when decreased, H+ depresses respiration.  Although H+ is the stimulus that activates the central chemoreceprors H+ does not readily cross blood-brain barrier (BBB). b) C02 Readily crosses blood brain barrier and affects respiration primarily by acidifying the cerebrospinal and interstitial fluids surrounding the central chemoreceptors. Though carbon dioxide has very little direct effect in stimulating the neurons in the chemosensitive area, it does have an indirect effect. It does this by reacting with the water of tissues to form carbonic acid. This in turn dissociates into hydrogen and bicarbonate ions; the hydrogen ions then have a potent direct stimulatory effect. c) Cerebrospinal Fluid (CSF) Buffering:  Carbondioxide present in blood can readily diffuse into the CSF where, in the presence of carbonic anhydrase, it can undergo hydration to form H+ and HCO3-.  It appears the central chemoreceptors are propably more sensitive to changes in the H+ than the CO2 of CSF. H+ +HCO3 H2CO3   Thus, chemoreceptor stimulation depends largely on the free entry of CO2 into CSF and subsequent hydration to H+. The central chemoreceptors are not sensitive to changes in blood PO2 and H+ because entry of H+ into the CSF is limited by the BBB. H+ +HCO3 H2CO3   Normally, CSF has only small amounts of protein, thus the bicarbonate-carbonic acid system provides important buffers. Loss of HCO3 from CSF decreases the buffer capacity, so that H+ formation from CO2 becomes an even stronger respiratory stimulus H+ +HCO3 H2CO3  in respiratoery acidosis centeral chemorecpters are un respunsive due to increaed buffer capaity Conversely, the increased HCO3 concentration that occurs in chronic respiratory acidosis can reduce the responsiveness of the central chemoreceptors by increasing buffer capacity  P H+ +HCO3 H2CO3  pCO2 Increased depth and RR C3 to C5 to diaphgram (phrenic nerve) T1 to T11 (intercostal nerves) Gray matter 7- Peripheral Chemoreceptors  Located in the carotid and aortic bodies, respond to changes in the O2 CO2 and H + concentrations of the arterial blood. a) O2  The blood flow to carotid bodies is 2000 ml/min/100 g tissue, which results in a very small arteriovenous difference. Dissolved O2 (PaO2) can stimulate these not the bound O2(HbO2).  Because of this, carotid bodies essentially monitor the PO2 of the plasma and changes in the Hb levels do not alter the response of these organs  The peripheral chemoreceptors are only receptors that monitor O2 levels in the body. When a person breathes air that has too little oxygen (