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Over a longer period (hours to days), renal mechanisms compensate by adjusting acid secretion andbicarbonate regeneration. When a respiratory acid–base disturbance occurs, the compensation is primarily renal.important in this regard. Acid balance is also maintained byrenal excretion of acid (renal mechanisms are covered inChapter 20).
Normally, CO2 formed during metabolism oflipids and carbohydrates is readily eliminated by the respiratory system, but disturbances in respiration can result inacid–base imbalance, because changes in CO2 elimination willdirectly affect carbonic acid levels. In addition, by adjustingrespiration, the respiratory system can compensate for pHimbalances produced by metabolic disturbances.solved CO2, and thus, 0.03 × PCO2 (0.03 mmol/L/mm Hg isthe solubility coefficient for PCO2) can be substituted for[H2CO3] and the equation becomes:pH 6.1 logSubstituting normal values for arterial [HCO3−] and PCO2yields the normal pH of 7.4:pH 6.1 logThe Henderson-Hasselbalch EquationThe pH of buffer systems can be calculated by the HendersonHasselbalch equation:pH pK log[A][HA]where K is the acid dissociation constant. For the bicarbonatebuffer system,pH pK log[HCO3][H2CO3]The pK for this system is 6.1.
H2CO3 exists in low concentrations in extracellular fluids but is in equilibrium with dis-[HCO3]0.03 PCO2[24] 7.40.03 40Based on these equations, it should be apparent that changesin PCO2 will result in alteration of pH. If hypoventilationresults in a rise in alveolar PACO2, for example, the accompanying rise in PaCO2 will cause a fall in blood pH.ACID–BASE DISTURBANCESAcid–base disturbances are covered briefly in the followingdiscussion, and in detail in Chapter 20. Acidemia is definedas increased acidity of blood (pH below 7.35), whereas alkalemia is increased alkalinity of blood (pH above 7.45). Technically, acidosis and alkalosis are more general terms referring186Respiratory PhysiologyTable 15.1Acid–Base DisordersDisorderpH1o AlterationDefense MechanismsMetabolic acidosis↓↓ [HCO3−]Buffers, ↓PCO2, ↑NAEMetabolic alkalosis↑↑ [HCO3−]Buffers, ↑PCO2, ↓NAERespiratory acidosis↓↑ PCO2Buffers & ↑NAERespiratory alkalosis↑↓ PCO2Buffers & ↓NAENAE, net acid excretion.(Reprinted with permission from Hansen J: Netter’s Atlas of Human Physiology, Philadelphia, Elsevier, 2002.)to low pH and high pH, respectively, in body fluids and tissuesbut are usually used synonymously with acidemia and alkalemia.
Alterations in pH caused by respiratory abnormality arereferred to as respiratory acidosis or respiratory alkalosis.Respiratory alkalosis is caused by hyperventilation, whereasrespiratory acidosis is caused by hypoventilation (due to eitheran acute cause, such as airway obstruction or central nervoussystem [CNS] depression, or a chronic lung disease). In contrast, when the primary cause of the acid–base imbalance ismetabolic, for example due to a metabolic disease or abnormal renal function, it is described as metabolic acidosis ormetabolic alkalosis.
Compensation for respiratory acidosis oralkalosis occurs by renal mechanisms, whereas respiratoryadjustments compensate for metabolic acidosis or alkalosis(Table 15.1). The general role of the kidney and lungs inacid–base balance is illustrated in Figure 15.4.Differentiating between metabolic and respiratory causesof acidosis and alkalosis is usually a relatively simpleprocess. To identify the condition:Ultimately, signals involved in control of breathing are integrated in the medullary respiratory center, resulting in regulation of the activity of respiratory muscles (see Fig. 14.1) andaffecting tidal volume and respiratory rate and pattern.
Withinthe medulla, respiratory control is accomplished by the:■■■First examine the pH. Values below 7.35 are defined asacidosis; pH above 7.45 is by definition alkalosis.Second, examine the PaCO2. If the pH disturbance is respiratoryin origin, the PaCO2 level will be abnormal and predictive ofthe pH change. In other words, in respiratory acidosis, PaCO2will be elevated above 40 mm Hg, whereas in respiratoryalkalosis (caused by hyperventilation), PaCO2 will be lowerthan 40 mm Hg.
If the condition is acute, HCO3− level willbe normal; if the respiratory condition is chronic, HCO3− willbe elevated in acidosis and depressed in alkalosis, reflectingrenal compensation. Because of the compensation, pH willbe closer to normal in chronic acidosis or alkalosis thanwould be expected based on a change in PaCO2 alone.If PaCO2 level is abnormal in the opposite direction predictedfor it to be the primary alteration, the disturbance ismetabolic.
Examination of HCO3− should reveal that its levelis consistent with a primary metabolic disturbance: HCO3−will be high in metabolic alkalosis and low in metabolicacidosis. PaCO2 levels will be depressed in metabolic acidosisand elevated in metabolic alkalosis, reflecting respiratorycompensation. Because of this compensation, the pH will becloser to normal than would be predicted based on a changein HCO3− alone.CONTROL OF RESPIRATIONAlthough breathing can be controlled voluntarily (for example,during breath holding or hyperventilation), it is ultimately aninvoluntary process that closely controls PaO2 and PaCO2.Changes in both depth and rate of respiration are involved inthis process. Three essential components of the involuntarycontrol system are as follows:■■■■■brainstem respiratory centersperipheral and central chemoreceptorsmechanoreceptors in lungs and jointsVentral respiratory group, which includes the nucleusretroambiguous, nucleus ambiguous, and nucleus retrofacialis and innervates both inspiratory and expiratorymuscles.
It is involved in regulation of inspiratory forceand in voluntary expiration.Dorsal respiratory group within the nucleus tractus solitarius, which innervates inspiratory muscles.The medullary respiratory center receives input from twoimportant pontine areas:■■The pneumotactic center, which regulates rate anddepth of respiration by cyclical inhibition of inspiration.This center has input from the cerebral cortex.The apneustic center, which stimulates inspiration.
It isantagonized by the pneumotactic center.Damage to the pons or upper medulla may result in apneusis(breathing characterized by prolonged inspiratory efforts andOxygen and Carbon Dioxide Transport and Control of Respirationbrief, intermittent exhalations). Experimentally, apneusis canbe produced by ablation of the pneumotactic center and transection of the vagus nerve.Role of Central and Peripheral ChemoreceptorsSensory information from central and peripheral chemoreceptors is important in this regulation of respiration by thebrainstem.
Central chemoreceptors located at the ventrolateral surface of the medulla respond indirectly to changes inarterial Pco2 and play a critical role in acute regulation ofPaCO2. The blood-brain barrier is largely impermeable toHCO3− and H+, but CO2 readily diffuses across the barrier andinto the cerebrospinal fluid (CSF), where it affects CSF pH (bymechanisms discussed earlier). Thus, when PaCO2 is altered,respiration is affected:■■A rise in PaCO2 will cause a fall in CSF pH, which isdetected by central chemoreceptors, resulting in anincrease in respiratory rate.A fall in PaCO2 will cause a rise in CSF pH, which isdetected by central chemoreceptors, resulting indecreased ventilation.Peripheral chemoreceptors, located in the carotid bodiesand aortic bodies (see Section 3), also convey informationconcerning the quality of arterial blood to the respiratorycenter in the brainstem, thereby affecting ventilation.
Unlikethe central chemoreceptors, these receptors respond directlyto changes in PaO2 and PaCO2, as well as pH. Throughthe peripheral chemoreceptor mechanism, ventilation isstimulated by the following:CLINICAL CORRELATESleep ApneaSleep apnea is a disorder whereby normal breathing is periodicallyinterrupted during sleep; the pauses in breathing can be the lengthof two to three breaths, and thus there can be a significant reduction in gas transport during these episodes. Sleep apnea can becentral, obstructive, or complex (both central and obstructive).
InNormal breathingin sleepRecordingsfrom patientwithobstructivesleep apneaEEGNasalRespirationOralChestO2 saturationECG■■■187A fall in PaO2: The ventilatory effects of changes in PaO2are relatively small when PaO2 is above 60 mm Hg, butperipheral chemoreceptors are very responsive whenPaO2 falls below this level.A rise in PaCO2: Changes in PaCO2 affect respirationthrough both central and peripheral chemoreceptors,although the central chemoreceptor mechanism is moreresponsive to the changes.A fall in pH: Changes in H+ concentration in arterialblood affect peripheral chemoreceptors directly, independently of the effects of PaCO2.Chemical control of respiration by PaO2 and PaCO2 is illustratedin Figure 15.5.Additional Mechanisms Controlling RespirationRespiration is also controlled by a number of additionalperipheral mechanisms:■■Pulmonary mechanoreceptors respond to inflation ofthe lung and result in termination of inspiration.
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