pulmonaryfunction in status asthmaticus: effect of therapy · thorax(1970), 25, 581....

Thorax (1970), 25, 581.

Pulmonary function in status asthmaticus:effect of therapy

DAN C. STANESCU and DAN B. TECULESCU

Pulmonary Laboratory, Department of Occupational Diseases, Hospital Colentina, and Institute of Hygiene,Bucharest 10, Romania

In 11 patients with bronchial asthma, lung volumes, FEV1.0, PaO2, and lung diffusing capacity(single breath CO method) were measured in status asthmaticus and after recovery.

Ventilatory capacity improved following therapy. The improvement was associated with a rise invital capacity and a fall in residual volume, but the total lung capacity might either decrease,increase or remain unchanged.A decreased value of PaO2 was found in all patients in status asthmaticus. After treatment PaO2

increased in all patients. In two of them PaO2 increased despite the unchanged values of the otherparameters of pulmonary function. The improvement of PaO2 after treatment is considered to bethe result of adjustment of perfusion to ventilation.The lung diffusing capacity was below normal values in three patients before treatment. After

treatment the diffusing capacity increased in six patients. The diffusion constant, although withinthe normal range in status asthmaticus, increased after treatment in one and decreased in threeother patients. The decreased diffusing capacity in status asthmaticus is the consequence of areduced effective alveolar volume due to uneven distribution of ventilation. The changes observedin the diffusion constant following corticotherapy are ascribed to a dependence of this constant onthe different level of the alveolar volume at which the single breath test is performed.

In recent years much information has beenpublished about the impairment of lung functionin bronchial asthma. However, most of it wasobtained at one stage in the evolution of thedisease only, i.e., at a symptom-free period orduring exacerbation of bronchial asthma. Weconsider that a better insight into pulmonaryfunction impairment in bronchial asthma can beobtained by following the same patient fromstatus asthmaticus to a symptom-free interval.Although serial changes of lung volume in

bronchial asthma have been reported already, lessattention has been paid to serial changes ofoxygen arterial tension (PaO2) and lung diffusingcapacity.The purpose of this study was to assess the

changes of lung volumes, ventilatory capacity,PaO2, and lung diffusing capacity in patients withbronchial asthma in status asthmaticus and afterrecovery.

MATERIAL AND METHODS

Eleven patients (six females) with bronchial asthmain status asthmaticus were studied after admission to

the Department of Allergy of the Institute of InternalMedicine in Bucharest. All had been previously fol-lowed in this department for several years. The diag-nosis of bronchial asthma was based on clinicalcriteria (Ciba Guest Symposium, 1959). They had ahistory of paroxysmal dyspnoea and wheezing inter-spaced with symptom-free intervals. As some of themwere corticodependent, free intervals occurred duringthe last years only following treatment. Blood orsputum eosinophilia was found in all but one patient.In order to exclude coexisting chronic bronchitis and/or pulmonary emphysema patients with chronic puru-lent sputum and attenuation of peripheral vessels onthe chest radiograph (Laws and Heard, 1962) werenot included.

Vital capacity (VC), forced expiratory volume at1 second (FEVI.o), and minute ventilation weremeasured on a ventilated spirograph (Pulmotest,Godart). Residual volume (RV) was measured usingthe closed circuit helium dilution method. In order tomaintain a constant volume of the spirograph, oxygenwas continuously added during the test through asemi-automatic device. Rebreathing was continueduntil equilibration of the helium in the system wasachieved, less than 0-002-0003% decrease per minute(initial helium concentration 2%) for at least 20minutes in all patients. Residual volume determina-

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tions were carried out in each patient in duplicate,with a pause of about 40 minutes between the tests.Measurements were discarded whenever a differencegreater than 1000 in functional residual capacity(FRC) between two successive tests was found. Nor-mal values for static lung volumes and FEVj.o inmales were those of Jouasset (1960). For VC andFEV1.o in females we used the prediction equationsof Berglund, Birath, Bjure. Grimby, Kjellmer, Sand-quist, and Soderholm (1963). Normal values for resi-dual volume and total lung capacity (TLC) in femaleswere computed from the RV/TLC ratio of Jouasset(1960) and normal values for VC in females.The oxygen tension in the arterialized blood

(PaO2) was measured with the Radiometer electrode(E 5046) calibrated with an oxygen free solution andambient air. Arterialized capillary blood was obtainedfrom the pulp of the finger after at least 10 minutes'warming in a water-bath at 45° C. Three to fourblood samples were obtained and measured withinfive minutes. The results retained represented themeans of measurements differing by less than 2 mmHg.Pulmonary diffusing capacity (DL') and 'diffusion

constant' (DL'/VA') were measured by the singlebreath method, using the 'effective' alveolar volume(VA/) obtained from helium dilution in the testbreath (McGrath and Thomson, 1959) and breath-holding time according to Jones and Meade (1961).Pulmonary diffusing capacity (DL) was also com-puted as recommended by Ogilvie, Forster, Blakemore,and Morton (1957) using the sum of RV (heliumclosed circuit) and inspired vital capacity. Wheneverthe alveolar sample after anatomical and instrumentaldead space washout (minimum 700 ml.) was too re-duced (less than 600 ml.) to permit analysis, thealveolar sample was diluted with air in a tonometer.Details of the method have been given elsewhere(Teculescu and Stinescu, in press). Normal valuesfor DL' and DL'/VA' ratio for males were obtainedin this laboratory (Teculescu and StAnescu, in press).For females we used the prediction values of Billiet(1966) verified in our laboratory.

PROCEDURE Patients were investigated, while in statusasthmaticus (American Thoracic Society, 1968), assoon as they were able to reach the laboratory andperform the tests. At this time they had corticotherapyfor one to three days but were still severely short ofbreath. Bronchodilator drugs were withdrawn eighthours before testing. The sequence of pulmonaryinvestigation was as follows: duplicate measurementsof residual volume, determination of oxygen tensionin arterialized blood and then duplicate measurementsof diffusing capacity. Patients were retested in theirbest clinical condition 7 to 26 days after the initialinvestigation. Treatment consisted of corticotherapy.bronchodilators. adrenaline and theophylline deri-vates.The significance of differences in various functional

parameters before and after corticotherapy was ascer-tained with Fisher's t test for paired variates.

RESULTS

After treatment all patients claimed that cortico-therapy had improved their clinical condition.Some of them, however, were not symptom-freebut a better result had not previously beenachieved.

Physical data, lung volumes, and ventilatorycapacities in all patients before and after treat-ment are shown in Table I. Vital capacity wasreduced in all patients and rose significantly aftertreatment (P

Pulmonary function in status asthmaticus: effect of therapy 583

TABLE IPHYSICAL DATA, LUNG VOLUMES AND VENTILATORY CAPACITIES BEFORE AND AFTER CORTICOTHERAFY IN

ASTHMATIC PATIENTS

Patient Sex Age Height (vC VC TLC TLC VA' RARV RV/TLC FEV .° FEV,.o/VC(mlght(' of (%/ of VA'TLC ml. /TL mlPatietSexAge (m.) (). prdic- (ml. pei- (ml. m. % (l(cm.) BTPS) prtedi)c- BTPS) pred)c BTPS) BTPS) BTPS) /°I M 43 168 2,700 57 4,600 73-6 4,250 0-92 1,900 41-5 1,180 43-8

4,470 95 6,130 98-0 5,530 0 90 1,660 27-0 3,240 72-5

2 M 45 164 3,020 69 6,830 118 3,820 0 56 3,780 55-5 790 26-44,350 99 6,900 119 6,120 0-88 2,550 37 0 1,910 44-0

3 F 31 155 1,380 43 3,900 93 2,990 0 77 2,530 65-0 410 3002,920 91 5,290 126 5,250 0-99 2,370 45-0 1,070 36-6

4 M 53 159 2,880 74 5,180 97-7 4,100 0 79 2,300 44-5 1,470 51-02,850 74 4,430 83-5 4,500 1-00 1,580 36-0 1,680 59-0

5 F 29 153 3,160 99 5,320 131 4,300 0 81 2,160 40 0 1,610 63-24,250 133 5,340 132 5,350 1-00 1,090 20-5 2,750 64-8

6 F 54 155 2,070 76 5,470 147 3,510 0-64 3,400 62-0 650 31-33,110 114 5,380 144 4,790 0-89 2,270 42-0 1,550 49-8

7 F 40 168 3,200 90 6,200 132 5,1j0 0-83 3,000 48 5 1,280 40 54,230 119 6,100 130 5,340 0-89 1'870 31 0 2,360 56-0

8 F 34 160 1,750 52 4,600 106 3,980 0-86 2,850 62-0 560 27-83,950 118 6,000 139 5,390 0 90 2,040 34-0 2,350 59 5

9 M 52 168 1,750 38 4,620 74 3,100 0-82 2,870 62-0 780 41-81,750 38 4,530 725 3,820 0-82 2,780 61 5 680 39-0

10 M 47 165 3,150 71 6,130 103 5,320 0-85 2,970 48 5 1,200 36-43,300 74 6,240 105 5,450 0-87 2'840 47 0 1,470 44-5

11 F 30 155 2,240 69 4,000 96 3,330 0-83 1,760 440 1,280 4853,450 106 4,190 100 3,900 0-93 740 17-5 2,540 74-0

TABLE IILUNG DIFFUSING CAPACITY, DIFFUSION CONSTANT ANDARTERIALIZED OXYGEN TENSION BEFORE AND AFTER

CORTICOTHERAPY IN ASTHMATIC PATIENTS

DL' DL"I DL DLVA(mi. CO (' of (ml. CO (lCoD'/VA" PaO,Patient min.-' pred min-' fli.n (/ of (mm.mm. Hg-1) dicted) Hg-)M. predicted) Hg)

1 25-0 81 25 3 6-64 104 58349 114 36 1 7 12 112 93

2 18-7 64-5 318 5.35 85-5 6632-9 113 39-1 6 56 105 85

3 17-3 68 22-7 7 05 114 5921 8 85-5 22-0 5 04 81-5 74-5

4 22-5 90 29-3 6-87 118 7125-7 103 25-3 6-92 119 87-5

5 25-5 J00 31-6 7 21 100 70 524-9 98 25-8 5 85 80 6 81-5

6 17-6 80 27-4 6-07 95 6718-0 82 20-3 4 58 71-5 78

7 25 5 95 30 5 5 95 86 5 66 524-7 93 28-7 5-71 83 88

8 20-9 80 24-0 6-32 89 6424-7 94 5 27-2 5.49 77.5 79

9 18-0 64 22-0 5-77 98 66-518-0 64 21-4 5'72 98 78 5

10 26-3 90 31-4 6-20 101 6128-1 96 32-8 6-35 103 86

11 22-1 865 253 765 106 6823-8 93 23-4 6-74 93-5 91 5

1ormai rangeA 0/ or_ maies ancs I i 2z0r_r _eas_I Normal range 74-126 /% for males and 72-1255/ for females.2 Normal range 73-127% for males and 75-125S% for females.

more than 15% in the DL was taken into account.Previous investigations had shown a coefficientof variation of DLCO measurements on separatedays of between 4 0 and 7-8% (Smith and Hamil-ton, 1962; Englert, 1967; Billiet, 1966). Aftertreatment DL' remained below normal in onepatient; in another patient, DL'/VA' becamenormal.

DISCUSSION

LUNG VOLUMES A few studies have dealt with theserial changes of lung volumes in asthmaticpatients (Engstr6m, 1964; Woolcock and Read,1966; Gold, Kaufman, and Nadel, 1967;Meisner and Hugh-Jones, 1968; Weng and Levi-son, 1969).Lung volume in the above-mentioned studies

was measured either as thoracic gas volume(TGV) by body plethysmograph or using dilutionmethods (helium closed circuit, TLCxe; or N2washout procedure, TLCN2). As is known, whenthere is no communication between ambient air andsome pulmonary regions, dilution methods under-estimate the measurement of FRC compared withthe plethysmographic method. No comparativedeterminations of TGV and TLCHe or TLCN2from status asthmaticus to the symptom-freeinterval have been done, except by Meisner and



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Hugh-Jones (1968). However, these authors madea further sub-estimation of the TLCHe, limiting thehelium equilibration time to 7 minutes.Our results are similar to those of other studies

using the helium dilution method. After treatmentTLCHe deCreased, increased or remained un-changed. In all these circumstances FRC and RVeither decreased or remained unchanged and VCincreased or remained unchanged. The increasedFRC and RV after treatment in some of thepatients reported by Woolcock and Read (1966)is a surprising result, not confirmed by the presentdata or by other studies.Any attempt to explain the mechanisms govern-

ing lung volume changes in bronchial asthma musttake into account that only FRC is determined'objectively', while RV and inspiratory capacitycan be influenced by the fatigue and/or lack ofco-operation of the subjects. RV is related in someway to airway obstruction and FRC is determinedby the equilibrium between the opposite forcesof the lung and thorax, but we know very littleabout the factors limiting maximal inspiratoryvolume in health and disease.The results reported by Gold et al. (1967) with

the plethysmographic method showed that TGVin status asthmaticus is increased or has the samevalue comparatively as after treatment. No de-crease of TGV in status asthmaticus was reported.One can conclude that the decrease of TLC, asmeasured with the dilution methods, observed inexacerbations of asthma is probably due, as hasbeen previously pointed out, to an underestimationof FRC due to closure and /or plugging withmucus of some airways resulting in regions inwhich helium does not dilute. The increase ofTLC (observed with both dilution and plethysmo-graphic methods) during symptomatic asthma hasnot as yet received a satisfactory explanation.Recently, Finucane and Colebatch (1969) sug-gested a reduction of tissue forces in overinflationof the lung in asthma. Their explanation is, how-ever, not compatible with the rapid deflation ofthe lung following the use of bronchodilator drugs.It is puzzling that some patients 'respond' to air-ways obstruction with closure of airways, leadingto a decrease of TLCHe, while in others there isapparently no airways closure but hyperinflation(an increase of both TLCHe and TGV). There isstill another category in which both TLCHe andTGV remain unchanged and there is only a rela-tive hyperinflation, i.e., the increase in RV iscounterbalanced by an equal decrease of VC. Thedifferent behaviour of the TLC bears no relationto the degree of airway obstruction as measured

by FEVy.o It is of interest to point out that inboth studies of lung volumes in asthmatic chil-dren no increase of TLCHe during asthmaticattacks was reported (Engstrom, 1964; Weng andLevison, 1969). The lack of increase in TLC inasthmatic exacerbations in children may be due toplugging of airways with mucus (smaller airwaysdiameter) and/or an underestimation of inspira-tory capacity due to exhaustion of respiratorymuscles.Comparative determinations of the multibreath

(TLCHe) and single breath helium technique (VA')showed a lower than unity (VA'/TLCHe) ratio in allour patients during status asth.maticus, confirmingprevious experience that the helium single breathmethod underestimates TLC compared with theclosed circuit method in patients with obstructiveairways (Morton and Ostensoe, 1965; Teculescuand Stanescu, 1969). Improvement in the clinicalcondition resulted in a marked increase of VA'irrespective of the divergent changes of TLCHe,leading to a rise in the VW'/TLCHe ratio, whichreached unity in most of the subjects. We agreethat this phenomenon occurred although theFEV1.0 and RV/TLC ratio did not reach normalvalues. We might think that below a certain levelof obstruction an apnoea of 10 seconds allowshelium to reach by diffusion the terminal airspaces, i.e., the series component -of the distribu-tion impairment is cancelled. If this is the correctexplanation, we can assume that no major paralleldistribution component is present at this time.

ARTERIAL OXYGEN TENSION A decreased value ofPaO2 was found in all patients in status asthmati-cus. PaO2 increased significantly (P

Pulmonary function in status asthmaticus: effect of therapy

suggest the intervention of a protective homeo-static mechanism matching the perfusion to venti-lation, as an uneven distribution of ventilation waspreviously found in asymptomatic patients(Stanescu, Teculescu, Pacuraru, and Popa, 1968).In patients 9 and 10, PaO2 values increased signifi-

cantly after corticotherapy although the airway ob-struction remained unchanged. Recently, Fuleihan,Feisal, and Malouf (1967) also reported a signi-ficant increase of PaO2 after corticotherapy inpatients with chronic bronchitis, without anychange in the clinical condition or spirographicperformance. They thought that a more uniformdistribution of ventilation in relation to perfusionwas responsible for this improvement in PaO2values, and probably the same mechanismoperated in our two patients.

LUNG DIFFUSING CAPACITY Previous studies haveshown that the diffusing capacity of the lung isnormal in bronchial asthma (Burrows, Kasik,Niden, and Barclay, 1961; Kanagami, Katsura,Shiroishi, Baba, and Ebina, 1961; Bedell andOstiguy, 1967; Pecora, Bernstein, and Feldman,1966), and so this test has been considered usefulto differentiate bronchial asthma from pulmonaryemphysema. However, the clinical condition of thepatients investigated in these studies has not beenmentioned. A significant fall of DL was reportedby Palmer and Di-ament (1969) in a group ofasthmatic patients with severe obstructive ventila-tory impairment compared with a group withmild obstruction. No influence of the ventilatoryobstruction on DL was found by McFaddenand Lyons (1968) when comparing asthmaticswith severe and mild to moderate obstruction. Theabove-mentioned studies presented the results ofDL as mean values, so that individual trends couldbe overlooked: these investigations were carriedout only at one moment in time. In our presentsurvey only the studies dealing with the singlebreath method were mentioned. The othermethods for measuring DLCO are too sensitive tothe distribution of ventilation and perfusion to beuseful in patients with bronchial asthma.Our results show that in status asthmaticus the

DL'/VA' ratio was normal in all patients and DL'was below normal in 3 out of 11 patients. Aftertreatment the DL'/ VA' ratio became abnormal inone patient while DL' reached normal levels in all.DL' increased in five patients and the DL/VA'ratio increased in one and decreased in threeothers. This variable pattern of response of theDL' and DL'/VA' ratio was present despite adefinite increase of FEV1 0 in 10 and PaO2 in all

patients. An increase of DL and a decrease ofthe DL/VA ratio was reported in three asthmaticpatients when the ventilatory obstruction im-proved (Meisner and Hugh-Jones, 1968).The decrease of DL' observed in our patients in

status asthmaticus is due to the reduced value ofthe effective alveolar volume. Although the DLsingle breath method is reputed to be less sensitiveto functional unevenness than other methods, inextreme cases an impaired distribution of inspiredair, regional variations of V/Q and the DL/Qratio can decrease DL'WO (Piiper and Sikand, 1966).A decrease of DL' was previously found by us inasthmatic patients following an induced attack ofasthma (Stiinescu and Teculescu, 1969). Whenevera ventilation unevenness is present Piiper andSikand (1966) proposed to calculate the true DLby multiplying DL' by the VA/VA' ratio, i.e., usingDL instead of DL'. It is evident that as TLC isgreater than VA', DL would be greater than DL'(see Table II). At present there is no agreementconcerning the use of VA' or TLC to compute DL'.In recent years, however, several investigationshave used VA' as this is the actual volume involvedin the uptake of CO during the single breath test.To use DL instead of DL' is merely to ascribe tothe total lung capacity the diffusion characteristicsmeasured in a smaller lung volume.

In normal subjects it has been shown that DLincreases and the DL/VA ratio decreases with theincrease of alveolar volume (McGrath and Thom-son, 1959; Cadigan, Marks, Ellicott, Jones, andGaensler, 1961). The rate of change of DLCO andDL/VA with the alveolar volume is variable fromone subject to another. This relationship is notlinear over the whole alveolar volume. One canobserve an increase in DL with a concomitantdecrease or little change in DL/VA, or a decreasein DL/VA with little change in DL (Billiet, 1965).It may be questioned whether this relationship isvalid in the nonhomogeneous lung. Apart from thesix patients with chronic bronchitis and emphy-sema of McGrath and Thomson (1961) studiedover a limited range of alveolar volume, there areno other studies in patients with obstructed air-ways. We believe that in our patients one canascribe the changes of DL' and DL'/VA' ratioto the increase in effective alveolar volume. Thisexplanation is compatible with the results of allbut one patient, in whom an increase of VA' wasaccompanied by an increase in both DL' and DL'/VA' ratio. We think that in status asthmaticus thelow VA' is well ventilated and perfused. As theclinical condition improved new lung territorieswere included with a smaller blood to gas ratio,

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leading to a reduced uptake of CO.We believe that the decrease of DL' in status

asthmaticus is 'apparent', i.e., does not representa true impairment of diffusing capacity of thelung. The decrease of Pa02 in status asthmaticusis not considered to be the result of diffusionlimitation, as an uneven ventilation-perfusionratio and an increased venous admixture, bothdocumented findings, fully explain hypoxaemia.Moreover, if DL' bears any relationship to PaO2,it is difficult to explain the increase of PaO2 ob-served in several of our patients without anincrease in DL' and in the DL'/VA' ratio.

Irrespective of the hypothesis advanced for thealterations of DLCO, the abnormal values of thisparameter in some of our patients in statusasthmaticus may limit the value of the DLCOmethod to differentiate asthmatics from emphy-sematous patients, though the return to normalvalues of DLCO after treatment may help in thisseparation.

The authors are indebted to Dr. I. Gr. Popescu,Institute of Internal Medicine, Bucharest, for referringthe patients in this study.

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