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Theafferent signals from these receptors in the smoothmuscle of airway walls are transmitted through the vagusnerve to the medulla, where they inhibit the apneusticcenter, thereby terminating inspiration. This response tolung inflation is known as the Hering-Breuer reflex(specifically, the Hering-Breuer inspiratory-inhibitoryreflex).Irritant receptors in the large airways respond to noxiousgases and particulate matter, for example, in cigarettesmoke. Activation of these receptors results in afferentcentral sleep apnea, brain centers are dysregulated, resulting in alack of effort to breathe; in obstructive sleep apnea, althoughrespiratory effort is normal, obstruction prevents airflow. Disrupted sleep and fatigue are common symptoms.
Chronic sleepapnea is associated with increased incidence of heart disease andstroke.Obstructive apneaNormal breathingin sleep188Respiratory PhysiologyCLINICAL CORRELATERespiratory Control in Chronic ObstructivePulmonary DiseaseChronic obstructive pulmonary disease (COPD) is most oftenassociated with tobacco smoking and may be exacerbated by occupational exposure to certain pollutants. It is characterized bychronic bronchitis (coughing with sputum production) andemphysema (destruction of alveolar walls resulting in fewer,enlarged “alveoli” with reduction in total surface area for gas diffusion). As a result, patients with this disease become hypoxic andhypercapnic (PaO2 is below normal and PaCO2 is elevated); pH issomewhat lower than normal, although significant compensationoccurs by elevation of HCO3− through renal mechanisms.
In otherwords, the patients suffer from chronic respiratory acidosis, withmetabolic compensation. In this state of chronic hypercapnea,normal CSF pH is maintained by elevation of HCO3− in the CSF.The CNS is chronically exposed to high PCO2, and the centralchemoreceptors become unresponsive to CO2. Thus, patients withCOPD develop “hypoxic respiratory drive,” in which respiratorydrive is mainly mediated by peripheral chemoreceptor responsesto low PaO2. When an acute exacerbation arises in such a patient,if supplemental O2 is administered carelessly, results can be catastrophic and even fatal: PaO2 will rise, but respiratory drive mayfail as a result, causing a fall in minute ventilation and a furtherrise in PaCO2.
Ventilatory support with some supplemental oxygenmay be beneficial, but suppression of ventilatory drive must beavoided.Interrelationship of Chronic Bronchitis and EmphysemaNormalBlue bloaterChronicbronchitisEmphysemaPink pufferMixed(in variabledegree)COPD is characterized by chronic bronchitis and emphysema. COPD patients usually suffer to some extent from both and areclassified based on the dominant symptomatology. “Pink puffers” suffer mainly from emphysema and have ruddy complexionsand elevated respiratory rate; “blue bloaters” suffer mainly from chronic bronchitis, resulting in hypoxema, cyanosis (bluish lipsand skin), and often, symptoms of right heart failure, including swelling of feet and ankles (“bloating”).Oxygen and Carbon Dioxide Transport and Control of RespirationChemical Control of Respiration (Feedback Mechanism)Glossopharyngeal (IX) nerveVagus (X) nerve3.
Elevated PCO2of blood and ofcerebrospinalfluid affectscentralchemoreceptors2. Lowered PO2of blood affectschemoreceptors ofcarotid and aorticbodies (which arealso responsive tolowered pH)1. Inadequateventilation forbodily needs maydepress PO2 and/orelevate PCO2 ofblood (elevatedPCO2 tends tolower pH)24. Impulses fromcarotid and aorticbodies reachrespiratory centervia glossopharyngeal andvagus nerves4Medulla35Blood PCO2 (pH)Cerebrospinal3fluid PCO2 (pH)625. Impulses fromcentral chemoreceptors reachrespiratory center6. Phrenic nerve61O2 7CO26.
Impulses fromrespiratory centersdescend in spinalcord to reachdiaphragm viaphrenic nerves andintercostal musclesvia intercostalnerves to increaserate and amplitudeof respiration6. Intercostal nervesIntercostal musclesAlveolar capillaryDiaphragmAlveolus7. Accelerated respiration improves ventilation andthus tends to normalize PO2, PCO2, and pH of bloodVentilation (L/min)4030O2CO220100203040506070Partial Pressure (mm Hg)8090100Figure 15.5 Control of Respiration Central and peripheral chemoreceptors regulate respiration byresponding to arterial blood gas levels.
Central chemoreceptors respond primarily to changes in arterialPCO2, which diffuses into the CSF and alters pH of the CSF (the blood-brain barrier is largely impermeableto HCO3− and H+), while peripheral chemoreceptors in the carotid bodies and aortic bodies respond tochanges in PaO2, and also PaCO2 and pH. Brainstem respiratory centers adjust the rate and depth of respiration, producing changes in PaO2 and PaCO2 (and thus pH). In the bottom graph, the effects of PaCO2 and PaO2on minute ventilation are illustrated.189190Respiratory PhysiologyAVenExerciseRecoveryona titilHeart ratePO2PCO2Arterial pHratureBody tempe012Factors that may accountfor initial abrupt rise andsharp terminal drop inventilation4 5 60Time (minutes)123Factors that may play apart in continued elevationof ventilation duringcontinuing exerciseRise in body temperature accounts for asmall part of elevationCollaterals torespiratory centerfrom motor pathwaysfor muscle activationProprioceptiveafferents fromjoint receptors torespiratory centers3HⴙLactateOther unknownfactorsRespiratory neuronsseem to be moreresponsive to changein chemoreceptoractivity.
Centers maybe more sensitive tofluctuation than toabsolute values ofPO2, PCO2, or pHLactic acid productiondue to anaerobicmetabolism in musclemay increase H+concentratin of blood,thus affecting chemoreceptorsPossible metabolicreceptors inexercising muscleBOther unknown factorsFigure 15.6 Respiratory Response to Exercise Increased oxygen consumption and carbondioxide production during exercise requires adjustments of cardiac output and respiration (A). Factorsaccounting for the rapid adjustments in respiration at the onset and termination of exercise, as well asfeedback mechanisms during continued exercise, are illustrated (B).■■signals to the CNS mainly through the vagus nerve andcauses reflexive bronchoconstriction and coughing.Juxtacapillary receptors (J receptors) in the alveoli arestimulated by hyperinflation of the lungs and variouschemical stimuli; reflexive rapid, shallow breathingoccurs as a result.Joint and muscle mechanoreceptors are stimulatedduring movement of joints and muscles, producing anincrease in respiratory rate.Respiratory Control in ExerciseControl of respiration is a critical component of the integrated response to exercise (Fig.
15.6). During dynamic(aerobic) exercise, oxygen consumption rises from the averageresting rate of 250 mL O2/min to as high as 4 L O2/min,without substantial change in either PaO2 or PaCO2. At the onsetof dynamic exercise, there is a rapid increase in respirationthrough neural and reflexive mechanisms, although the controlOxygen and Carbon Dioxide Transport and Control of Respirationmechanisms are not fully understood. Activation of motorpathways results in collateral activation of the respiratorycenter, and respiration is further stimulated by afferent signalsfrom muscle and joint mechanoreceptors and other, unknownfactors.
With continuing exercise, feedback mechanismsbecome important. The rise in core body temperature andelevation of lactic acid production (and plasma H+ concentration) contribute to the further, more gradual rise in ventilation. Although PaO2 and PaCO2 change only modestly (exceptat high levels of exercise), respiratory control systems may bemore sensitive to such changes during exercise. When exerciseis terminated, ventilation diminishes rapidly at first butrequires some time to fall to the resting level, due to the continued activation of feedback mechanisms until the metabolicalterations associated with exercise (including the elevation oflactic acid) are reversed.Adaptation to High AltitudeThe control of respiration is also important in adaptationto high altitude. At the lower atmospheric pressures associated with high altitudes, the PO2 of inspired air is reduced,resulting in hypoxemia.
The fall in PaO2 stimulates ventilationthrough peripheral chemoreceptors, but this effect is tempered by the resulting fall in PaCO2 and the accompanyingalkalosis, which inhibit ventilation through central andperipheral chemoreceptor mechanisms. Over a period of time,renal compensatory mechanisms result in elevation of plasmaHCO3−, and as pH returns to normal, ventilation againincreases.
In addition to increased ventilation, other factorsthat contribute to the adaptation to high altitude include thefollowing:■■Hypoxemia stimulates red blood cell production; theresulting polycythemia (and higher plasma hemoglobin) increases the oxygen-carrying capacity of blood.Elevation of 2,3-DPG causes a rightward shift of theoxyhemoglobin dissociation curve, and thus, oxygenmore readily dissociates from hemoglobin at the tissuelevel.191CLINICAL CORRELATEAcute Altitude SicknessAcute altitude sickness is a relatively common response to highaltitude (greater than 8000 feet above sea level) in people whoare accustomed to living at low altitudes, especially when theascent is rapid. Symptoms include headache, tachycardia, shortness of breath, nausea and vomiting, loss of appetite, lightheadedness, and fatigue.
In most cases, symptoms are mild andresolve in a matter of days as acclimation takes place. In rare,extreme cases, life-threatening pulmonary edema or cerebraledema may develop. Pulmonary edema occurs as a result ofpulmonary vasoconstriction and an increase in pulmonary vascular permeability. As discussed earlier, pulmonary vasoconstriction is a normal response to alveolar hypoxia, but it isexaggerated in high-altitude pulmonary edema.
The cause ofhigh-altitude cerebral edema has not been established but likelyinvolves cerebral vasodilation in response to hypoxemia, resulting in high capillary hydrostatic pressure. Descent to loweraltitude is a critical component of treatment in these severecases.Effects of High Altitude on Respiratory MechanismResponse to hypercapnia persists,thus maintaining normal blood gastensions; but CO2 response maybe lost under anesthesia, resultingin dangerous hypoxemiaCO2O2Respiratory responseto hypoxemia isblunted or lost192Respiratory PhysiologyReview QuestionsCHAPTER 13: PULMONARY VENTILATION ANDPERFUSION AND DIFFUSION OF GASESD.
the ventilation-to-perfusion ratio approaches zero.E. the ventilation-to-perfusion ratio approaches infinity.1. The reduction in pulmonary vascular resistance that occurswhen pulmonary artery pressure is increased is mainly aresult of:CHAPTER 14: THE MECHANICS OF BREATHINGA.B.C.D.E.recruitment and distension of pulmonary capillaries.autoregulation by myogenic mechanisms.redistribution of pulmonary blood flow.metabolic vasodilation.active vasodilation of pulmonary arterioles.2. Which of the following lung volumes or capacities canNOT be measured by spirometry alone?A.B.C.D.E.Tidal volumeExpiratory reserve volumeInspiratory reserve volumeTotal lung capacityVital capacity3.
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