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Respiratory Diseases

Respiratory Diseases

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Section 1 Development and FunctionChapter 370 Respiratory Pathophysiology and Regulation
The age- and growth-dependent changes in physiology and anatomy of the respiratory controlmechanism, airway dynamics, and lung parenchymal characteristics have a profound influence onthe pathophysiologic manifestations of the disease process. Smaller airways, a more compliantchest wall, and poor hypoxic drive render a younger infant more vulnerable compared to an older child with similar severity of disease. The main function of the respiratory system is to supplysufficient oxygen to meet metabolic demands and remove carbon dioxide. A variety of processesincluding ventilation, perfusion, and diffusion are involved in tissue oxygenation and carbon dioxideremoval. Abnormalities in any one of these mechanisms can lead to respiratory failure. A child maybe identified as being in respiratory distress because of the presence of signs such as cyanosis,nasal flaring, grunting, tachypnea, wheezing, chest wall retractions, and stridor. Respiratory failurecan be present without respiratory distress; a patient with abnormalities of central nervous system(CNS) or neuromuscular disease may not be able to mount sufficient effort to appear in respiratorydistress. A child who appears in respiratory distress may not have a respiratory illness; a patient withprimary metabolic acidosis (diabetic ketoacidosis) or central nervous system excitatory states(encephalitis) may present in severe respiratory distress without respiratory disease.
370.1Â Lung Volumes And Capacities In Health And Disease
Lung volumes are traditionally measured with a spirogram. Tidal volume (VT) is the amount of air moved in and out of the lungs during each breath. At rest, it is usually 6-7 mL/kg body weight.Inspiratory capacity (IC) is the amount of air inspired by maximum inspiratory effort after tidalexpiration. Expiratory reserve volume (ERV) is the amount of air exhaled by maximum expiratoryeffort after tidal expiration. The volume of gas remaining in the lungs after maximum expiration isresidual volume (RV). Vital capacity (VC) is defined as the amount of air moved in and out of thelungs with maximum inspiration and expiration. VC, IC, and ERV are decreased in lung pathologybut are also effort dependent. Total lung capacity (TLC) is the volume of gas occupying the lungsafter maximum inhalation.Functional residual capacity (FRC) is the amount of air left in the lungs after tidal expiration. FRChas important pathophysiologic implications. Alveolar gas composition changes during inspirationand expiration. Alveolar PO2 (PAO2) increases and alveolar Pco2 (PACO2) decreases duringinspiration as fresh atmospheric gas enters the lungs. During exhalation, PAO2 decreases andPACO2 increases as pulmonary capillary blood continues to remove oxygen from and add CO2 intothe alveoli. FRC acts as a buffer, minimizing the changes in PAO2 and PACO2 during inspirationand expiration. FRC represents the environment available for pulmonary capillary blood for gasexchange at all times. A decrease in FRC is often encountered in alveolar interstitial diseases andthoracic deformities. The major pathophysiologic consequence of decreased FRC is hypoxemia.Reduced FRC results in a sharp decline in PAO2 during exhalation because a limited volume isavailable for gas exchange. PO2 of pulmonary capillary blood therefore falls excessively duringexhalation, leading to a decline in arterial PO2 (Pao2). Any increase in PAO2 (and therefore Pao2)during inspiration cannot compensate for the decreased Pao2 during expiration. The explanation for this lies in the shape of O2-hemoglobin dissociation curve, which is sigmoid shaped. Since most of the oxygen in blood is combined with the hemoglobin, it is the percentage of oxyhemoglobin (SO2)that gets averaged rather than the PO2. While an increase in arterial PO2 cannot increase oxygen-hemoglobin saturation more than 100%, there is a steep desaturation of hemoglobin below a PO2 of 50 torr; thus, decreased SO2 during exhalation as a result of low FRC leads to overall arterialdesaturation and hypoxemia. The adverse pathophysiologic consequences of decreased FRC areameliorated by application of positive end expiratory pressure (PEEP) and increasing the inspiratorytime during mechanical ventilation.FRC is abnormally increased in intrathoracic airway obstruction, which results in incompleteexhalation, and abnormally decreased alveolar-interstitial diseases. At excessively low or high FRC,tidal respiration requires higher inflation pressures compared to normal FRC. Abnormalities of FRCresult in increased work of breathing with spontaneous respiration and increased barotrauma inmechanical ventilation.
370.2Â Chest Wall
One important area where an infant's respiratory system differs from that of an older child or adult isits chest wall. Although a soft, highly compliant chest wall is beneficial to a baby in its passagethrough the birth canal and allows future lung growth, it places the young infant in a vulnerablesituation under certain pathologic conditions. Chest wall compliance is a major determinant of FRC.Since the chest wall and the lungs recoil in opposite directions at rest, FRC is reached at the pointwhere the outward elastic recoil of the thoracic cage counterbalances the inward lung recoil. Thisbalance is attained at a lower lung volume in a young infant because of the extremely high thoraciccompliance compared to older children. The measured FRC in infants is higher than expectedbecause respiratory muscles of infants maintain the thoracic cage in a slight inspiratory position at alltimes. Additionally, some amount of air trapping during expiration occurs in young infants.The increased chest wall compliance is a distinct disadvantage to the young infant under severalpathologic conditions. A decrease in muscle tone, as occurs in rapid eye movement (REM) sleep or with CNS depression, allows greater chest wall retraction because of less opposition to the lungrecoil; the FRC decreases in such states. The respiratory muscles of infants are poorly equipped tosustain large workloads. They are more easily fatigued than those of older children, limiting their ability to maintain adequate ventilation in lung disease. In diseases of poor lung compliance(atelectasis, pulmonary edema), excessive lung recoil results in greater retraction of the soft chestwall and more loss of FRC than occurs in older children and adults with stiffer chest walls. Increasednegative intrathoracic pressure required to overcome airway resistance in obstructive lung diseasealso produces greater chest wall recoil and reduced FRC in young infants. Application of PEEP isbeneficial in such states for stabilization of the chest wall and restoration of FRC.Abnormalities of the chest wall are encountered in certain pathologic conditions. Chest wallinstability can result from trauma (fractured ribs, thoracotomy) and neuromuscular diseases that leadto intercostal and diaphragmatic muscle weakness. The increased chest wall compliance makessuch children more vulnerable to respiratory decompensation when faced with similar pulmonarypathology compared to older children and adults with stiffer chest walls. Children with rigid,noncompliant chest wall (asphyxiating thoracic dystrophy of Jeune [], achondroplasia [ 416.4 ]) havemarkedly diminished lung volumes and capacities.
370.3Â Pulmonary Mechanics And Work Of Breathing In Health And Disease
For air to move in and out of the lungs, a sufficient pressure gradient is needed between alveoli andatmosphere during both inspiration and expiration. Part of the pressure gradient is required toovercome the lung and chest wall elastance; another part is needed to overcome airway resistance.Elastance refers to the property of a substance to oppose deformation or stretching. It is calculatedas a change in pressure (ΔP) ÷ change in volume (ΔV). Elastic recoil is a property of a substancethat enables it to return to its original state after it is no longer subjected to pressure. Compliance(ΔV ÷ ΔP) is the reciprocal of elastance. In the context of the pulmonary parenchyma, airways, andthe chest wall, the compliance refers to their distensibilty. Resistance is calculated as the amount of pressure required to generate flow of gas across the airways. Resistance to laminar flow is governedby Poiseuille's law stated as: R = 8 lη ÷ Ï€r4 where R is resistance, l length, η viscosity, and r radius. The practical implication of pressure-flow relationship is that airway resistance is inverselyproportional to its radius raised to the 4th power. If the airway lumen is decreased in half, theresistance will increase 16-fold. Newborns and young infants with their inherently smaller airwaysare especially prone to marked increase in airway resistance from inflamed tissues and secretions.In diseases in which airway resistance is increased, flow often becomes turbulent. Turbulencedepends to a great extent on the Reynolds number (Re), a dimensionless entity, which is calculatedas Re = 2rvd ÷ η where r is radius, v velocity, d density, and η viscosity. Turbulence in gas flow ismost likely to occur when Re exceeds 2000. Resistance to turbulent flow is greatly influenced bydensity. A low-density gas such as helium-oxygen mixture decreases turbulence in obstructiveairway diseases such as viral laryngotracheobronchitis and asthma. Neonates and young infants arepredominantly nose breathers and, therefore, even a minimal amount of nasal obstruction is poorlytolerated.The diaphragm is the major muscle of respiration. When additional work of breathing (WOB) isrequired, intercostal and other accessory muscles of respirations also contribute to the increasedwork. The tidal volume and respiratory rate are adjusted, both in health and disease, to maintain the
required minute volume with the least amount of energy expenditure. The total WOB (necessary tocreate pressure gradients to move air) is divided into 2 parts. The 1st part is to overcome the lungand chest wall elastance, and is referred to as elastic work (Welast). The 2nd part is to overcomeairway and tissue resistance, and is referred to as resistive work (Wresist). Welast is directlyproportional to tidal volume, whereas Wresist is determined by the rate of airflow and, therefore, therespiratory rate. The total WOB is lowest at a rate of 35-40/min for neonates and 14-16/min for older children and adults. Welastis disproportionately increased in diseases with decreased complianceand Wresist is increased in airway obstruction. Respirations are therefore shallow (low VT) and rapidin diseases of low compliance and deep and relatively slow (low flow rate) in diseases of increasedresistance. Compared to older children, young infants have disproportionately greater Welastbecause the negative intrapleural pressure during inspiration causes the retractile (more compliant)chest wall to collapse and pose an impediment to air entry. Young infants increase their respiratoryrate with any mechanical abnormality. Other examples of compliant chest wall being a disadvantageinclude flail chest resulting from rib fractures, thoracotomy, and neuromuscular weakness. One of the salutary effects of continuous positive airway pressure in such situations is the stabilization of thechest wall.Time constant, measured in seconds, is a product of compliance and resistance. It is a reflection of the amount of time required for proximal airway pressure (and, therefore, volume) to equilibrate withalveolar pressure. It takes 3 time constants for 95%, and 5 time constants for 99% of pressureequilibration to occur. Since airways expand during inspiration and narrow during expiration,expiratory time constant is longer than inspiratory time constant. Diseases characterized bydecreased compliance (pneumonia, pulmonary edema, atelectasis) are associated with a shorter time constant and therefore require less time for alveolar inflation and deflation. Diseases associatedwith increased resistance (asthma, bronchiolitis, aspiration syndromes) have prolonged timeconstant, and therefore require more time for alveolar inflation and deflation. Pathologic alterations intime constants have practical significance during mechanical ventilation. Patients with shorter timeconstants are best ventilated with relatively smaller tidal volumes and faster rates to minimize peakinflation pressure. In patients with increased airway resistance, a fast respiratory rate (and,therefore, less time) does not allow enough pressure equilibration to occur between the proximalairway and the alveoli. Inadequate inspiratory time results in lower tidal volume, whereas insufficientexhalation time results in inadvertent PEEP, often referred to as auto-PEEP or intrinsic PEEP. Suchpatients are therefore best ventilated with relatively slower rates and larger tidal volumes.
370.4Â Airway Dynamics In Health And Disease
The trachea and airways of an infant are much more compliant than those of older children andadults, thus changes in intrapleural pressure result in much greater changes in airway diameter. Theairway can be divided into 3 anatomic parts: the extrathoracic airway extends from the nose to thethoracic inlet; the intrathoracic-extrapulmonary airway extends from the thoracic inlet to the mainstem bronchi; and the intrapulmonary airway is within the lung parenchyma. During normalrespirations, intrathoracic airways expand in inspiration as intrapleural pressure becomes morenegative and narrow in expiration as they return to their baseline at FRC. The changes in diameter are of little significance in normal respiration. In diseases characterized by airway obstruction, muchgreater changes in intrapleural pressure are required to generate adequate airflow, resulting ingreater changes in airway lumen. The changes in the size of airway during respiration areaccentuated in young infants with their softer, more compliant airways.In extrathoracic airway obstruction (choanal atresia [ 373 ], retropharyngeal abscess,laryngotracheobronchitis [ 382 ]), the high negative intrapleural pressure during inspiration istransmitted up to the site of obstruction, after which there is a rapid dissipation of pressure.Therefore, the extrathoracic airway below the site of obstruction has markedly increased negativepressure inside, resulting in its collapse, which makes the obstruction worse 6A ). This producesinspiratory difficulty, prolongation of inspiration, and inspiratory stridor. Also, the increased negativeintrapleural pressure results in chest wall retractions. During expiration, the increased positiveintrapleural pressure is again transmitted up the airways to the site of obstruction, leading to adistension of the extrathoracic airway and amelioration of obstruction 6 B).Because of the increased positive intrapleural pressure, the chest wall tends to bulge out, whichproduces the classical paradoxical respiration, in which the chest retracts during inspiration andbulges out during expiration. The younger the child, the softer is the chest wall and the more markedis the paradoxical respiration of extrathoracic airway obstruction. A pattern of seesaw respirationmay also be evident in newborns and young infants as the compliant chest wall is sucked in and theabdomen bulges out during inspiration, with the converse happening during expiration.In obstruction of intrathoracic-extrapulmonary airway (vascular ring [ 383 ], mediastinal tumors) andintrapulmonary airway (asthma, bronchiolitis), the increased negative intrapleural pressure results ina distention of intrathoracic airways during inspiration, thus providing some relief from obstruction .During expiration, the increased positive intrathoracic pressure is transmitted up to the site of obstruction, after which it dissipates rapidly. The intrathoracic airway above the site of obstruction istherefore subjected to much greater intrapleural pressure from outside, which cannot be adequatelybalanced by enough positive pressure inside, resulting in collapse above the site of obstruction.The site at which pressures inside and outside the airway during exhalation are equal is referred toas the equal pressure point (EPP). With intrathoracic airway obstruction, the EPP is shifted distallytoward the alveolus, causing airway collapse above. Marked inspiratory/expiratory changes in ayoung infant's airway lumen above the EPP is often termed collapsible trachea. Tracheal collapse isoften a sign of airway obstruction, and even contributes to its severity, but is rarely the primaryabnormality. With intrapulmonary airway obstruction, an even wider portion of intrathoracic airway issubjected to pressure swings during inspiration and expiration.Both intrathoracic-extrapulmonary and intrapulmonary airway obstruction result in increasingdifficulty during expiration, prolongation of expiration, and expiratory wheezing. Any airwayobstruction within the thorax results in expiratory wheezing.
370.5Â interpretation of clinical signs to localize the site of pathology
Appropriate interpretation of clinical findings is the 1st step in establishing the diagnosis of respiratory disease. Respiratory distress can occur without respiratory disease, and severerespiratory failure can be present without significant respiratory distress. Diseases characterized byCNS excitation, such as encephalitis, and neureoexcitatory drugs are associated with centralneurogenic hyperventilation. Similarly, diseases that produce metabolic acidosis, such as diabeticketoacidosis, salicylism, and shock, result in hyperventilation as a compensatory response. Patientsin either group could be considered clinically to have respiratory distress; they are distinguished frompatients with respiratory disease by their increased tidal volume as well as the respiratory rate. Their blood gas values reflect a low PaCO2 and a normal Pao2. Patients with neuromuscular diseases,such as Guillain-Barré syndrome or myasthenia gravis, and those with an abnormal respiratorydrive may develop severe respiratory failure but are not able to mount sufficient effort to appear inrespiratory distress. In these patients, respirations are ineffective or may even appear normal in thepresence of respiratory acidosis and hypoxemia.The rate and depth of respiration and the presence of retractions, stridor, wheezing, and grunting arevaluable signs in localizing the site of respiratory pathology. Rapid and shallow respirations(tachypnea) are characteristic of parenchymal pathology, in which the elastic work of breathing isincreased disproportionately to the resistive work of breathing. Chest wall, intercostal, andsuprasternal retractions are most striking, with increased negative intrathoracic pressure duringinspiration. This occurs in extrathoracic airway obstruction as well as diseases of decreasedcompliance. Inspiratory stridor is a hallmark of extrathoracic airway obstruction. Expiratory wheezingis characteristic of intrathoracic airway obstruction, either extrapulmonary or intrapulmonary.Grunting is produced by expiration against a partially closed glottis and is an attempt to maintainpositive airway pressure during expiration for as long as possible. Such prolongation of positivepressure is most beneficial in alveolar diseases that produce widespread loss of FRC, such as inpulmonary edema, hyaline membrane disease, and pneumonia. Grunting is also effective in smallairway obstruction (bronchiolitis) to maintain a higher positive pressure in the airway duringexpiration, decreasing the airway collapse.
370.6Â Ventilation-Perfusion (V/Q) Relationship in Health and Disease
During tidal respiration, alveoli and airways in the nondependent parts (the upper lobes in uprightposition) of the lung are subjected to greater negative intrapleural pressure, and therefore keptrelatively more inflated, compared to the dependent alveoli and airways (the lower lobes in uprightposition). This is because of the gravitational force pulling the lung away from the nondependent partof the parietal pleura. The nondependent alveoli are less compliant because they are already moreinflated. During tidal inspiration, ventilation therefore occurs preferentially in the dependent portionsof the lung that are more amenable to expansion. Although perfusion is also greater in thedependent portions of the lung because of greater pulmonary arterial hydrostatic pressure due togravity, the increase in perfusion is greater than the increase in ventilation in the dependent portionsof the lung. Thus, the V/Q ratios favor ventilation in the nondependent portions and perfusion in thedependent portions. Since the airways in the dependent portion of the lung are narrower, they closeearlier during expiration. The lung volume at which the dependent airways start to close is referred toas the closing capacity. In normal children, the FRC is greater than the closing capacity. During tidalrespiration, airways remain patent both in the dependent and the nondependent portions of the lung.In newborns, the closing capacity is greater than the FRC, resulting in perfusion of poorly ventilatedalveoli during tidal respiration; therefore, normal neonates have a lower Pao2 compared to older children.The V/Q relationship is adversely affected in a variety of pathophysiologic states 10 ). Air movementin areas that are poorly perfused is referred to as dead space ventilation. Examples of dead spaceventilation include pulmonary thromboembolism and hypovolemia. Perfusion of poorly ventilatedalveoli is referred to as intrapulmonary right-to-left shunting or venous admixture. Examples includepneumonia, asthma, and hyaline membrane disease. In intrapulmonary airway obstruction, theclosing capacity is abnormally increased and may exceed the FRC. In such situations, perfusion of poorly ventilated alveoli during tidal respiration results in venous admixture.
370.7Â Gas Exchange in Health and Disease
The main function of the respiratory system is to remove carbon dioxide from and add oxygen to thesystemic venous blood brought to the lung. The composition of the inspired gas, venti lation,perfusion, diffusion, and tissue metabolism have a significant influence on the arterial blood gases.The total pressure of the atmosphere at sea level is 760 torr. With increasing altitude, theatmospheric pressure decreases. The total atmospheric pressure is equal to the sum of partialpressures exerted by each of its component gases. Alveolar air is 100% humidified and, therefore,for alveolar gas calculations, the inspired gas is also presumed to be 100% humidified. At atemperature of 37°C and 100% humidity, water vapor exerts pressure of 47 torr, regardless of altitude. In a natural setting, the atmosphere consists of 20.93% oxygen. Partial pressure of oxygenin inspired gas (PiO2) at sea level is therefore × 20.93% = 149 torr. When breathing 40% oxygenat sea level, PiO2 is × 40% = 285 torr. At higher altitudes, breathing different concentrations of oxygen, PiO2 is less than at sea level, depending on the prevalent atmospheric pressures. InDenver (altitude of 5,000 feet and barometric pressure of 632 torr), PiO2 in room air is (632 - 47) ×20.93% = 122 torr; and in 40% oxygen, it is × 40% = 234 torr.Minute volume is a product of VT and respiratory rate. Part of the VT occupies the conductingairways (anatomic dead space), which does not contribute to gas exchange in the alveoli. Alveolar ventilation is the volume of atmospheric air entering the alveoli and is calculated as (VT - deadspace) × respiratory rate. Alveolar ventilation is inversely proportional to alveolar Pco2 (PACO2).When alveolar ventilation is halved, PACO2 is doubled. Conversely, doubling of alveolar ventilationdecreases PACO2 by 50%. Alveolar PO2 (PAO2) is calculated by the alveolar air equation asfollows: PAO2 = PiO2 - (PACO2 ÷ R); where R is the respiratory quotient. For practical purposes,PACO2 is substituted by arterial Pco2 (PaCO2) and R is assumed to be 0.8. According to thealveolar air equation, for a given PiO2, a rise in PaCO2 of 10 torr results in a decrease in PAO2 by10 ÷ 0.8 or 10 × 1.25 or 12.5 torr. Thus, proportionately inverse changes in PAO2 occur to theextent of 1.25× the changes in PACO2 (or PaCO2).After the alveolar gas composition is determined by the inspired gas conditions and process of ventilation, gas exchange occurs by the process of diffusion and equilibration of alveolar gas withpulmonary capillary blood. Diffusion depends on the alveolar capillary barrier and amount of available time for equilibration. In health, the equilibration of alveolar gas and pulmonary capillaryblood is complete for both oxygen and carbon dioxide. In diseases in which alveolar capillary barrier is abnormally increased (alveolar interstitial diseases) and/or when the time available for equilibration is decreased (increased blood flow velocity), diffusion is incomplete. Because of itsgreater solubility in liquid medium, carbon dioxide is 20 times more diffusible than oxygen.Therefore, diseases with diffusion defects are characterized by marked alveolar-arterial oxygen (A -aO2) gradient and hypoxemia. Significant elevation of CO2 does not occur as a result of a diffusiondefect unless there is coexistent hypoventilation.Venous blood brought to the lungs is “arterialized” after diffusion is complete. After completearterialization, the pulmonary capillary blood should have the same PO2 and Pco2 as in the alveoli.The arterial blood gas composition, however, is different from that in the alveoli, even in normalconditions. This is because there is a certain amount of dead space ventila tion as well as venousadmixture in a normal lung. Dead space ventilation results in a higher PaCO2 than PACO2, whereasvenous admixture or right-to-left shunting results in a lower Pao2 compared to the alveolar gascomposition (see . 370-10 ). Pao2 is a reflection of the amount of oxygen dissolved in blood, which isa relatively minor component of total blood oxygen content. For every 100 torr PO2, there is 0.3 mLof dissolved O2 in 100 mL of blood. The total blood oxygen content is composed of the dissolvedoxygen and the oxygen bound to hemoglobin. Each gram of hemoglobin carries 1.34 mL of O2 when100% saturated with oxygen. Thus, 15 g of hemoglobin carries 20.1 mL of oxygen. Arterial oxygencontent (CaO2), expressed as mL O2/dL blood, can be calculated as (Pao2 × 0.003) + (Hb ×1.34 × SO2), where Hb is grams of hemoglobin per dL blood and SO2 is percent of oxyhemoglobin saturation. The relationship of PO2and the amount of oxygen carried by thehemoglobin is the basis of the oxygen-hemoglobin (O2-Hb) dissociation curve. The PO2 at whichhemoglobin is 50% saturated is referred to as P50. At a normal pH, hemoglobin is 94% saturated atPO2of 70, and little further gain in saturation is accomplished at a higher PO2. At PO2 below 50,there is a steep decline in saturation and, therefore, the oxygen content.Oxygen delivery to the tissues is a product of oxygen content and cardiac output. When hemoglobinis near 100% saturated, the blood contains ~20 mL oxygen per 100 mL or 200 mL/L. In a healthyadult, the cardiac output is ~5 L/min, oxygen delivery 1,000 mL/min, and oxygen consumption 250mL/min. Mixed venous blood returning to the heart has PO2 of 40 torr and is 75% saturated withoxygen. Blood oxygen content, cardiac output, and oxygen consumption are important determinantsof mixed venous oxygen saturation. Given a steady state blood oxygen content and oxygenconsumption, the mixed venous saturation is an important indicator of cardiac output. A decliningmixed venous saturation in such a state indicates decreasing cardiac output.
370.8Â Interpretation of Blood Gases
Interpretation of blood gas values is important in localizing the site of the lesion and estimating itsseverity, especially when considered with clinical observations (Table 370-2 ). In airway obstructionabove the carina (subglottic stenosis, vascular ring), blood gases reflect overall alveolar hypoventilation. This is manifested by an elevated PACO2 and a proportionate decrease in PAO2 asdetermined by the alveolar air equation. A rise in PACO2 of 20 torr will decrease PAO2 by 20 ×1.25 or 25 torr. In the absence of a significant parenchymal disease and intrapulmonary shunting,such lesions respond very well to supplemental oxygen in reversing hypoxemia. Similar blood gasvalues, demonstrating alveolar hypoventilation and response to supplemental oxygen, are observedin patients with a depressed respiratory center and ineffective neuromuscular function, resulting inrespiratory insufficiency . Such patients can be easily distinguished from those with airwayobstruction by their poor respiratory effort.

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