SECTION IV THE RESPIRATORY SYSTEM Obstructive Airway Disease A 50-year-old man comes to the pulnonary laboratory for evaluation of chronic shortness of breath.He has snoked one pack of cigarettes a day for 30 years.His arterial blood is analyzed for pa,partial pressure of oxygen (Pa0),partial pressure of carbon dioxide(PacQ),percentage saturation of heroglobin with oxygen (Sa0),and hemoglobin content:the results are shown below.The patient is at sea level and breathing ambient air (21%oxygen).His respiratory rate is 25 respirations per ninute.and tidal volune is 400 nl. 7.47 Pa0,60 mm Hg S090m Pa0030国Hw Bmoglobin 14 g/dl blood 1.What do Pa0 and SAO.signify,and how are they related? 2.What is the total oxygen content in the patient's arterial blood?Do you peed to use a hemoglobin-oxygen equilibrium curve to answer this question? 3.Is there sufficient information to calculate minute ventilation,dead space ventilation,and alveolar ventilation?If so,mke the calculation:if not,state why not.Can you discern fron the respiratory rate and/or tidal volune if he is hyperventilating? 4.From the alveolar ventilation equation below,state what determines the alveolar PC0 and under what circumstances it might change. Pa00=1C0.x0.863》/Vh
SECTION IV THE RESPIRATORY SYSTEM Obstructive Airway Disease A 50-year-old man comes to the pulmonary laboratory for evaluation of chronic shortness of breath. He has smoked one pack of cigarettes a day for 30 years. His arterial blood is analyzed for pH, partial pressure of oxygen (PaO2), partial pressure of carbon dioxide (PaCO2), percentage saturation of hemoglobin with oxygen (SaO2), and hemoglobin content; the results are shown below. The patient is at sea level and breathing ambient air (21% oxygen). His respiratory rate is 25 respirations per minute, and tidal volume is 400 ml. pH 7.47 PaO2 60 mm Hg SaO2 90% PaCO2 30 mm Hg Hemoglobin 14 g/dl blood 1. What do PaO2 and SAO2 signify, and how are they related? 2. What is the total oxygen content in the patient's arterial blood? Do you need to use a hemoglobin-oxygen equilibrium curve to answer this question? 3. Is there sufficient information to calculate minute ventilation, dead space ventilation, and alveolar ventilation? If so, make the calculation; if not, state why not. Can you discern from the respiratory rate and/or tidal volume if he is hyperventilating? 4. From the alveolar ventilation equation below, state what determines the alveolar PCO2 and under what circumstances it might change. PaCO2 = (VCO2 x 0.863)/VA
5.Is this patient's alveolar ventilation.relative to CD,production.pore or less than normal?How is the answer to this question used to deternine if a patient is hyperventilating or hypoventilating?what is the clinical significance of this information？ 6.What is his calculated PACO.?(Use the alvolar gas equation below.As is custonary.assune that PCO:reasured in arterial blood [Paco]equals nean alveolar PCO,[PACO].Also,assume his respiratory quotient is 0.8.) P0·PI0,-Pa00,FI0,+(1-F10)/R] Where PIO FIO:(harometric pressure -47 mm Hg) 7.Subtract Pa0 from the calculated PM.Is the value for (PAO-Pad)abnormally increased?What is the significance of an increased (PAO,Pad)? 8 What is your overall interpretation of the blood gas data,in terms of the patient's oxygenation and ventilation? The patient next undergoes tests of nechanical lung function.The following lung volumes and capacities are measured.(Percentages of predicted values are shown: any lung volume or capacity between 80%to 120%of predicted is considered in the nor国】range.） Forced vital capacity (FVC)3 L 75%of predicted Forced expiratory volume in one second (FEV-1)"1.6 L"55%of predicted Total lung capacity 7.8 L 1306 of predicted Residual volune 2.8 L 140%of predicted 9.What is the difference between a lung volume and a lung capacity? 10.How do you interpret the lung volune and capacity information?What do you think is the nature of his clinical problem?
5. Is this patient's alveolar ventilation, relative to CO2 production, more or less than normal? How is the answer to this question used to determine if a patient is hyperventilating or hypoventilating? What is the clinical significance of this information? 6. What is his calculated PACO2? (Use the alvolar gas equation below. As is customary, assume that PCO2 measured in arterial blood [PaCO2] equals mean alveolar PCO2 [PACO2]. Also, assume his respiratory quotient is 0.8.) PAO2 = PIO2 - PaCO2 [FIO2 + (1-FIO2)/R] Where PIO2 = FIO2 (barometric pressure - 47 mm Hg) 7. Subtract PaO2 from the calculated PAO2. Is the value for (PAO2 - PaO2) abnormally increased? What is the significance of an increased (PAO2 – PaO2)? 8. What is your overall interpretation of the blood gas data, in terms of the patient's oxygenation and ventilation? The patient next undergoes tests of mechanical lung function. The following lung volumes and capacities are measured. (Percentages of predicted values are shown; any lung volume or capacity between 80% to 120% of predicted is considered in the normal range.) Forced vital capacity (FVC) = 3 L = 75% of predicted Forced expiratory volume in one second (FEV-l) = 1.6 L = 55% of predicted Total lung capacity = 7.8 L = 130% of predicted Residual volume = 2.8 L = 140% of predicted 9. What is the difference between a lung volume and a lung capacity? 10. How do you interpret the lung volume and capacity information? What do you think is the nature of his clinical problem?
11.Which of the lung volume and lung capacity measurements cannot be deternined by spirometry alone,but requires an additional technique (such as inert gas dilution)? ANSVER 1.Pad is the partial pressure of oxygen in arterial blood and is expressed in mn Ig.This pressure is exerted by oxygen molecules in their gas phase (dissolved in the plasma component of blood,as opposed to chemically combined with hemoglobin). Note that oece oxygen is chemically bound with hemoglobin,it no longer exerts a pressure.Note also that PO:(without the a/is the generic term for partial pressure of oxygem in any gas or liquid,and it should not be used without reference to the site (e.g.,inspired air.alveolar air,pulmonary veins,etc.). Sa0,is the saturation of heroglobin with oxygen in arterial blood.and it is expressed as a percemtage of total binding sites that are combined with oxygen.Thus if 95 of every 100 hemoglobin binding sites are combined with oxygen.the blood has an Sa0 of 95%.A major,but not the only,determinant of Sal is the Pa0. The relation between Pa0,and SaD is illustrated by the oxygen-heroglobin equilibrium (dissociation)curve,the exact shape and position of which depend on several factors (pl:2.3-diphosphoglycerate:PaCD,:and body temperature). 2.Oxygen content is a reasurement of quantity.Unlike PAO and Sa0.oxygen content directly reflects the mumber of oxygen molecules in the blood:the units are al per 100 ml,or per liter,of blood (both per d/and per L will be found in various texts and also in hospital laboratories).Neither PAO,nor Sad,gives information on the coetent of oxygen in the blood;they only provide a pressure and percentage of saturation,respectively.PAO:and the shape and position of the oxygen equilibrium curve determine the Sa0.The Sa0.and the hemoglobin (Hb)content deternine the oxygen content (along with a smll contribution fron dissolved PaD ) Clearly,without knowledge of the hemoglobin content there is no way to know Aow c oxygen is in the blood.Anemia does not affect Pal or 5a0h.Hence a severely
11. Which of the lung volume and lung capacity measurements cannot be determined by spirometry alone, but requires an additional technique (such as inert gas dilution)? ANSWER 1. PaO2 is the partial pressure of oxygen in arterial blood and is expressed in mm Hg. This pressure is exerted by oxygen molecules in their gas phase (dissolved in the plasma component of blood, as opposed to chemically combined with hemoglobin). Note that once oxygen is chemically bound with hemoglobin, it no longer exerts a pressure. Note also that PO2 (without the a) is the generic term for partial pressure of oxygen in any gas or liquid, and it should not be used without reference to the site (e.g., inspired air, alveolar air, pulmonary veins, etc.). SaO2 is the saturation of hemoglobin with oxygen in arterial blood, and it is expressed as a percentage of total binding sites that are combined with oxygen. Thus if 95 of every 100 hemoglobin binding sites are combined with oxygen, the blood has an SaO2 of 95%. A major, but not the only, determinant of SaO2 is the PaO2. The relation between PaO2 and SaO2 is illustrated by the oxygen-hemoglobin equilibrium (dissociation) curve, the exact shape and position of which depend on several factors (pH; 2,3-diphosphoglycerate; PaCO2; and body temperature). 2. Oxygen content is a measurement of quantity. Unlike PAO2 and SaO2, oxygen content directly reflects the number of oxygen molecules in the blood; the units are ml O2 per 100 ml, or per liter, of blood (both per dl and per L will be found in various texts and also in hospital laboratories). Neither PAO2 nor SaO2 gives information on the content of oxygen in the blood; they only provide a pressure and percentage of saturation, respectively. PAO2 and the shape and position of the oxygen equilibrium curve determine the SaO2. The SaO2 and the hemoglobin (Hb) content determine the oxygen content (along with a small contribution from dissolved PaO2). Clearly, without knowledge of the hemoglobin content there is no way to know how much oxygen is in the blood. Anemia does not affect PaO2 or SaO2. Hence a severely
anemic patient could have a low oxygen content and a normal PaD,and Sad-Arterial oxygen content is provided hy the following formula: (Amount 0 bound to hemoglobin)(Amount 0:dissolved in blood) Sa0,x Hb (g/dl)x 1.34 ml 0:/g lb 0.003 ml 0/mm Eg Pa0y/dl Because Sad is provided in the data given,there is no need to use the henoglobin-oxygen equilibriun curve to answer this question.Based on these data. the patient's arterial O:coatent is 0.90x14gl/d1x1.34nl0/gh+0.00310.(60mle》/dl =16,9l0/d1+018nl0=17.1ml0/dlb1o0dw Or 171 ml 0/L blood 3.Minute ventilation respiratory rate x tidal volume 25 breaths/min x 400 ml=10 L/min:this value is higher than the typical resting minute ventilation of 6 L/nin.Because neither dead space volune nor alveolar volume is given,we cannot calculate dead space ventilation or alveolar ventilation.Even though his respiratory rate and minute ventilation are increased.we should not state that he is hyperventilating (for the reasons explained in the next question).However,we can answer this question and assess overall adequacy of alveolar ventilation from the measured Pal (see the next two questions). 4.The alveolar ventilation equation is called "the central equation of pulnonary physiology."In fact,this equation is crucial to understanding many physiologic derangements in patients with respiratory tract problems.Rearranging the equation we obtain P00=(WCm.x0.863)/WA Thus alveolar PCO:is directly proportional to the CO,production (VCO)and inversely proportional to alveolar ventilation (VA).Any proyportfomate changes in the VCO:and VA will not change PACO:any disproportjanate changes will affect PACO:
anemic patient could have a low oxygen content and a normal PaO2 and SaO2. Arterial oxygen content is provided by the following formula: (Amount O2 bound to hemoglobin) (Amount O2 dissolved in blood) SaO2 x Hb (g/dl) x 1.34 ml O2/g Hb + 0.003 ml O2/mm Hg PaO2/dl Because SaO2 is provided in the data given, there is no need to use the hemoglobin-oxygen equilibrium curve to answer this question. Based on these data, the patient's arterial O2 content is 0.90 x 14 g Hb/dl x 1.34 ml O2/g Hb + 0.003 ml O2 (60 mm Hg)/dl = 16.9 ml O2/dl + 0.18 ml O2 = 17.1 ml O2/dl blood* *Or 171 ml O2/L blood 3. Minute ventilation = respiratory rate x tidal volume = 25 breaths/min x 400 ml = 10 L/min; this value is higher than the typical resting minute ventilation of 6 L/min. Because neither dead space volume nor alveolar volume is given, we cannot calculate dead space ventilation or alveolar ventilation. Even though his respiratory rate and minute ventilation are increased, we should not state that he is hyperventilating (for the reasons explained in the next question). However, we can answer this question and assess overall adequacy of alveolar ventilation from the measured PaO2 (see the next two questions). 4. The alveolar ventilation equation is called "the central equation of pulmonary physiology." In fact, this equation is crucial to understanding many physiologic derangements in patients with respiratory tract problems. Rearranging the equation we obtain PACO2 = (VCO2 x 0.863)/VA Thus alveolar PCO2 is directly proportional to the CO2 production (VCO2) and inversely proportional to alveolar ventilation (VA). Any proportionate changes in the VCO2 and VA will not change PACO2; any disproportionate changes will affect PACO2
predictably.depending on whether the greater change is in the numerator or denominator.For example,a 40%rise in VA and a 10%rise in YCO will lower Pac0. 5.Alveolar PO0,in the alveolar ventilation and alveolar gas equations can be replaced by the measured arterial PCD,:this is true because there is no "gradient" between the two values,as there is between alveolar and arterial POa.Substituting PaCD:in the alveolar ventilation equation,we see that Paco,is determined by the ratio of CO:production to alveolar ventilation: P00=(N00310.563》/WA Normally.the anount of VA is sufficient to excrete the produced CO:and thereby keep PaCO:in the normal range (36 to 44 m Hg).Nith increases in CO production (as during modest exercise),VA will normally rise a proportionate anount and thereby maintain a normal PaCD.If VA does not rise along with VCO.or if VA falls while VCO.does not or if VA falls pore than VCO.VA will be reduced out of proportion for the VC0:this situation represents hypoventilation.which raises Pac0. Conversely.when VA is elevated out of proportion to the YC0,there is Byperventilation,which reduces PaCD:.By definition,then,hyperventilation and hypoventilation refer only to a specific PaCo value,which in turn reflects the state of alveolar vemtilation relative to CO production.Note that hyperventilation and hypoventilation do not refer to rate or depth of breathing.or a patient's respiratory effort.This is why you cannot say.from observation alone,that a patient is "hyperventilating."Irrespective of rate or depth of breathing,a patient with lung disease may in fact be hyper-,hypo-,or normally ventilating relative to CD production. 6.From the alveolar gas equation.PAD.114 mm Hg.This patient is hyperventilating.Bence alveolar P0.is increased.(The alveolar gas equation shows that PAD,always increases if Paco decreases,other factors remaining unchanged. 7.PAO:Pao "114 60 54 mn Hg and is definitely ahnormal:pormal (PAO Pa0)for a man this age,breathing ambient air,is about 10 to 15 m Hg.For someone who is breathing room air at sea level and who has a Pacoa of 40 mm Hg.PAO 102 m Hg.Under the same conditions,the normal Paoe for a mn this age should
predictably, depending on whether the greater change is in the numerator or denominator. For example, a 40% rise in VA and a 10% rise in VCO2 will lower PaCO2. 5. Alveolar PCO2 in the alveolar ventilation and alveolar gas equations can be replaced by the measured arterial PCO2; this is true because there is no "gradient" between the two values, as there is between alveolar and arterial PO2. Substituting PaCO2 in the alveolar ventilation equation, we see that PaCO2 is determined by the ratio of CO2 production to alveolar ventilation: PACO2 = (VCO2 x 0.863)/VA Normally, the amount of VA is sufficient to excrete the produced CO2 and thereby keep PaCO2 in the normal range (36 to 44 mm Hg). With increases in CO2 production (as during modest exercise), VA will normally rise a proportionate amount and thereby maintain a normal PaCO2. If VA does not rise along with VCO2, or if VA falls while VCO2 does not or if VA falls more than VCO2, VA will be reduced out of proportion for the VCO2; this situation represents hypoventilation, which raises PaCO2. Conversely, when VA is elevated out of proportion to the VCO2 there is hyperventilation, which reduces PaCO2. By definition, then, hyperventilation and hypoventilation refer only to a specific PaCO2 value, which in turn reflects the state of alveolar ventilation relative to CO2 production. Note that hyperventilation and hypoventilation do not refer to rate or depth of breathing, or a patient's respiratory effort. This is why you cannot say, from observation alone, that a patient is "hyperventilating." Irrespective of rate or depth of breathing, a patient with lung disease may in fact be hyper-, hypo-, or normally ventilating relative to CO2 production. 6. From the alveolar gas equation, PAO2 = 114 mm Hg. This patient is hyperventilating. Hence alveolar PO2 is increased. (The alveolar gas equation shows that PAO2 always increases if PaCO2 decreases, other factors remaining unchanged.) 7. PAO2 – PaO2 = 114 - 60 = 54 mm Hg and is definitely abnormal; normal (PAO2 – PaO2) for a man this age, breathing ambient air, is about 10 to 15 mm Hg. For someone who is breathing room air at sea level and who has a PaCO2 of 40 mm Hg, PAO2 = 102 mm Hg. Under the same conditions, the normal PaO2 for a man this age should
be about 90 m Hg:(PAO:PaD.)would then be 102-90 12 mm Hg.Although this patient's Pa0:is slightly elevated hecause of hyperventilation.his Pa0:is reduced (their difference is 54 m Hg).This large difference between PAO and Pa0 indicates a significant defect in getting oxygen from the alveoli into the pulmonary circulation. 8 Ventilation:The patient is hyperventilating:in other words,his level of alveolar veatilation is nore than needed to excrete his metabolic production C0 and to keep PaCD:in the normal range.Oxygenation:First.the transfer of oxygen from alveoli into the pulmonary capillaries is impaired:this is evident because (PAD Pa0h)is greater than normal.Second.hemoglobin content is normal,but oxygen saturation is reduced slightly at 9%;therefore his oxygen comtent is also reduced. 9.A lung volune is a quantity of air not subdivided further (e.g..tidal volume, residual volune).A lung capacity is a quantity that includes two or more lung volunes (e.g.,total lung capacity,funetional residual capacity). 10.The forced vital capacity (FVC)is slightly reduced below the lower normal limit of 80%,and the FEV-I is reduced even more.When the FEV-I is reduced more than FYC,there is some air flow obstruction (the patient cannot exhale forcefully at a normal rate).At the same time,the total lung capacity and residual volume are above normal:this finding suggests some air trapping.Overall,these changes are typical of obstructive airway disease commonly seen in long-term smokers.If air flow remains obstructed despite treatment,the patient is said to have chronic obstructive pulmonary disease (COPD). 11.Total lung capacity and residual volure cannot he deternined by spirometry alone
be about 90 mm Hg; (PAO2 – PaO2) would then be 102 - 90 = 12 mm Hg. Although this patient's PaO2 is slightly elevated because of hyperventilation, his PaO2 is reduced (their difference is 54 mm Hg). This large difference between PAO2 and PaO2 indicates a significant defect in getting oxygen from the alveoli into the pulmonary circulation. 8. Ventilation: The patient is hyperventilating; in other words, his level of alveolar ventilation is more than needed to excrete his metabolic production CO2 and to keep PaCO2 in the normal range. Oxygenation: First, the transfer of oxygen from alveoli into the pulmonary capillaries is impaired; this is evident because (PAO2 – PaO2) is greater than normal. Second, hemoglobin content is normal, but oxygen saturation is reduced slightly at 90%; therefore his oxygen content is also reduced. 9. A lung volume is a quantity of air not subdivided further (e.g., tidal volume, residual volume). A lung capacity is a quantity that includes two or more lung volumes (e.g., total lung capacity, functional residual capacity). 10. The forced vital capacity (FVC) is slightly reduced below the lower normal limit of 80%, and the FEV-1 is reduced even more. When the FEV-1 is reduced more than FVC, there is some air flow obstruction (the patient cannot exhale forcefully at a normal rate). At the same time, the total lung capacity and residual volume are above normal; this finding suggests some air trapping. Overall, these changes are typical of obstructive airway disease commonly seen in long-term smokers. If air flow remains obstructed despite treatment, the patient is said to have chronic obstructive pulmonary disease (COPD). 11. Total lung capacity and residual volume cannot be determined by spirometry alone