250 H. Sund Kristensen, Ove Jessen and Knud Rasmussen

CASTAING, R., CHEVAIS, R., GILLARDAEU, G., FAVAREL-GARRIQUES, J.-C., COURTY, G. & FERRUS, L. (1965)Bilan therapeutique de 168 cas d'insuffisance respiratoireaigue survenus chez des defaillants respiratoires chroniques.Bull. physio-pathol. Resp. 1, 463.

ENGBERG, E. (1961) Family flats with a nursing annexe. ADanish experiment for the disabled. Lancet, i, 1106.

GAY, R. & GROSS, A. (1965) Les modificateurs de l'equilibreacido-basique dans le traitement de l'hypercapnie. Bull.physio-pathol. Resp. 1, 358.

GOTSMAN, M.S. & WHITBY, J.L. (1964) Respiratory infectionfollowing tracheostomy. Thorax, 19, 89.

GRENDAHL, H. & REFSUM, H.E. (1965) Artificial ventilationwith tank respirators in the routine treatment of severepulmonary failure due to chronic pulmonary disease.Acta med. scand. 177, 539.

HERZOG, H. & ENGELHART, G. (1964) Ventilation artificielle(IPPB) dans l'insuffisance respiratoire du syndromeobstructif. Rev. Tuberc. (Paris), 28, 1289.

LASSEN, H.C.A. (1956) Management of life-threateningPoliomyelitis. Livingstone, Edinburgh.

LASSEN, H.C.A. (1962) Problemes de Reanimation, 2 Serie(Ed. by A. Larcan), p. 511. Doin, Nancy.

LISSAC, J. & POCIDALO, J.-J. (1963) La tracheotomie aucours de l'emphyseme pulmonaire chronique. Etude de 80cas personnels. Rev. Tuberc. (Paris), 27, 808.

MOLLARET, P., BASTIN, R., RAPIN, M., POCIDALO, J.-J.,GOULON, M., LISSAC, J. & LIOT, F. (1958) La respirationartificielle dans les insuffisances respiratoires aigu&s,au cours des bronchopneumopathies avec coeur pulmonairechronique. Presse med. 66, 1271.

MUNCK, O., KRISTENSEN, H.S. & LASSEN, H.C.A. (1961)Mechanical ventilation for acute respiratory failure indiffuse chronic lung disease. Lancet, i, 66.

ROCKEY, E.E., BLASZIK, C.F., THOMPSON, S.A. & VIRABUTR,S. (1961) Four and one half years' experience in the treat-ment of emphysema and other respiratory insufficienciesby tracheal fenestration. Dis. Chest, 39, 117.

SADOUL, P. (1965) Use of sedatives, relaxants and respiratorystimulants in respiratory failure. Ann. N. Y. Acad. Sci.121, 836.

SADOUL, P., AUG., M.-C. & GAY, R. (1965) Traitement parventilation instrumentale de 100 cas d'insuffisance res-piratoire aigue severe (pA CO2 > 70) chez des pulmonaireschroniques. Bull. physio-pathol. Resp. 1, 489.

SADOUL, P., LACOSTE, J. & SAUNIER, C. (1961) Les gestesessentiels de la reanimation respiratoire chez pulmonaireschroniques. J. frac. Med. Chir. thor. 15, 747.

SLUITER, H.J., BLOKZIJL, E. & VAN DIJL, W. (1963) Treatmentof severe respiratory insufficiency in primary lung disease.Actes du Symposium sur le Traitement de l'InsuffisanceRespiratoire (Ed. by A. Vanotti). Minerva Medica, Torino.

Discussion to the paper by H. Sund Kristensen, O. Jessen and K. RasmussenFINNEGAN. I would like to illustrate the respirator

treatment of acute or chronic lung disease at WhistonHospital in the period from May 1962 to January 1966.Twenty-two men and three women developed acute

cardiorespiratory illnesses and became moribund despite

TABLE A1Respirator treatment of acute-on-chronic lung disease (May 1962 to

January 1966)

Age (years) No. of patients

40-50 650-60 1160-70 8Total 25 (22 men +3 women)

TABLE A2Deaths during respirator treatment

Causes No. of Days ofpatients treatment

Failure of resuscitation 2 1Massive pulmonary infarcts 1 3Undiagnosed carcinoma of bronchus 1 6Perforated duodenal ulcer 1 24Renal failure 1 11Cross-infection 2 10 and 11Bronchopneumonia 1 13Total 9

antibiotics, controlled oxygen and chest physiotherapy.All the patients had acute-on-chronic cor pulmonale dueto chronic bronchitis, bronchiectasis or pulmonarythrombo-embolism (Table A1). The treatment of the

acute illness consisted of mechanical ventilation through atracheostomy, antibiotics and metabolic care.The mean duration of ventilation was 10-6 days and

the range was 12 hr to 35 days. Nine patients died duringthe period of respirator treatment; the causes of deathare listed in Table A2.Four patients died within 1 year and three patients

within 2 years of treatment. Nine of the original groupare still alive, six with moderate disability and three withsevere disability (Table A3).

TABLE A3Follow-up of nine patients surviving for

6 months to 3 years

Disability Grade of No. ofdyspnoea patients

Moderate 1-2 6Severe 3 3

The criteria for selection, the management and thecomplications are similar to those reported by DrKristensen.

ROBERTSON. I note that Dr Kristensen has had somecomplications with tracheal stenosis after IPPV, andwonder whether this was because the cuff of the rubbertube was blown up too tight, perhaps by the nursing staff,since this has been the experience of Mr Peter Gibson ofPerth, Australia.

Finally, may I ask whether anyone in the audience hasany properly controlled evidence that either methyl-or acetyl-cysteine is effective? I have heard many speakerspraise its usefulness, but I am more impressed by theabsence of any properly controlled trial.SCARROW. Pulmonary angiography was employed to

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Treatment of severe respiratory insufficiency 251

help in the interpretation of tomograms and plain chestfilms in chronic bronchitis and emphysema. A pressurerecord was taken before and after the investigation andduring and after exercise of the legs with the patient in arecumbent position. Multiple exposures made followingthe injection of Urografin into the main pulmonaryartery enable one to determine the sizes of the pulmonaryarteries and veins and their rates of filling. A study ofeighteen patients with chronic bronchitis and emphysema(Scarrow, 1966), suggested that the angiograms couldbe classified into three types. Type III correspondedclinically to the 'blue-bloater' picture. To illustrate theseresults I would like to show pictures taken during con-valescence, of two patients treated at Whiston by pro-longed IPPV. Clinically both men were blue-bloaters andthe initial chest film showed opacities in the lung fieldswhich cleared after treatment.

First case. A bronchitic man aged 42 rapidly deterior-ated into respiratory failure and the ECG suggestedpulmonary infarction. During treatment, bronchoscopyand a left bronchogram showed that the airways wereclear. The patient responded well to intensive therapy.The angiogram made 3 months later (Fig. A1) showed

02...,,,0.,e . . . ....................

:,~~~~~~~~~~~~~~~

FIG. Al. Case No. 1.

only moderate dilation of the main pulmonary arteries,poor flow to the left lower lobe and occlusion of theperipheral vessels. The appearances of the arteries tothe left lower lobe suggested old thrombosis which hadpartially recanalized.

Second case. A chronic blue-bloater aged 62 had asimilar illness. The angiogram taken 5 months aftertreatment (Fig. A2), however, was strikingly different.The main pulmonary arteries were large, the arteries ofthe right upper lobe and left lower lobe were also largeand these lobes were hyperaemic. The right lower lobeand left upper lobe do not fill as well as the other areasand occluded vessels can be identified at the level of thesecond or third generation of branches.

E

: ; i - ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~.............#e:e~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ c,.......l ...

.:X

*:. ~ ~~~~~~~~~~~~~~~~..........

:.: ::. ... ..

.. .. . .'

.. .......

.............

FIG. A2. Case No. 2.

ReferenceSCARROW, G.D. (1966) The pulmonary angiogram in chronic

bronchitis and emphysema. Clin. Radiol. 17, 54.

SHERWOOD JONES. I was privileged to read the paperby Dr Kristensen and his colleagues before the Sym-posium. For years we had regarded their earlier paper(Munck, Kristensen & Lassen, 1961) as one of the half-dozen classics on intensive therapy. The selection ofpatients for IPPV, the methods, the results and follow-up are crystallized in just two pages of the Lancet!The results given today support the earlier work. I wassurprised to see how many references he was able tofind which were quite unknown to us. This emphasizesthe difficulties of collecting together all the relevantliterature on intensive therapeutics. For example, DrAmbiavagar and myself spent many hours of our sparetime over a period of 6 months before we were satisfiedthat we had consulted most of the literature on statusasthmaticus. Indeed, one of the aims of our Symposiumis to remedy this state of affairs.

I would like to build up my own picture of respiratoryfailure due to chronic bronchitis and emphysema byreferring to the studies made here since 1958. I wish tostress the importance of abnormalities in the pulmonarycirculation and right-heart and their relation to treatment.During the winter of 1958-59 a study was made on

ninety men admitted with exacerbations of chronicbronchitis, bronchopneumonia and cor pulmonale.Two findings emerged which are relevant to my presenttheme. The first concerned the chest radiograph insevere acute chest illnesses. Dr Scarrow concluded thatthe changes in the chest film associated with the acuteillness could only be interpreted when this film wascompared to one taken before or some weeks later. Inthose men who survived the winter illness we waiteduntil the summer of 1959 to get a basic film. A carefulcomparison of the films revealed (Scarrow, 1964) that

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252 Discussion

only one third had opacities in the lung fields or radio-logical pneumonia, but that in 40% of the X-rays oneor more areas in the lung fields were abnormal in that thevascular pattern was obscured or there was an apparentincrease in the number and size of the vessels. Oswald,Simon & Shooter (1961) reported a similar sign whichthey described as 'very fine, ill defined areas of clouding'.In about 40% of the Whiston films, a hilum or the hilaenlarged during the acute illness. To me, these X-rayfindings focused attention on the pulmonary circulation inthe acute chest illnesses of chronic bronchitis. The secondfact relates to the ECG in such illnesses. Cor pulmonalemay be overt-cyanosis, oedema, triple rhythm-orsuspect and yet there is no evidence of right ventricularhypertrophy (RVH) or strain in the ECG. This is awell-recognized shortcoming of the ECG (Caird &Wilcken, 1962; Harvey & Ferrer, 1960; McMichael,1960; Mounsey, 1954) and led us to explore the use ofthe vectorcardiogram (VCG). The use of the VCG inthe recognition of RVH or strain in pulmonary heartdisease certainly paid off. Since vectorcardiographyhas not really caught on in this country as it has done inthe U.S. a few words of explanation would not be amiss.Scalar and vectorcardiography are based on the dipolehypothesis and assume that there is a point of origin ofthe electrical potentials of the heart situated in the middleof the chest in a plane corresponding to the V2 electrodeposition. When we take a strip of V2 we are recording thechanges in potential as projected on to this point of thechest. The term 'vector' is a mathematical one used by allsixth-formers upwards, and means a force which isconstantly changing in size, direction and polarity.There are P, QRS and T vectors and each describes athree-dimensional loop. Since one cannot display anelectrical signal in three dimensions, the loops arerecorded photographically in horizontal, sagittal andfrontal planes. Fig. A3 shows a normal QRS loop looked

V5

FIG. A3. Showing the relation of the normal horizontalQRS vector loop to the unipolar chest leads V1 and V1.

at in the horizontal plane and its relation to chest leadsV1 and V_. When the VCG was recorded in chronicbronchitis and emphysema, it was frequently found tobe abnormal in this disease. Brown (1963) working inmy laboratory analysed the ECGs and VCGs of fiftymen with chronic bronchitis, some with clinicallyrecognizable cor pulmonale. In ten men both testswere normal; in sixteen, both results showed RVH.Twenty-four patients, however, had RVH on the VCGbut only nine of these showed RVH on the ECG.Similar findings were published in the U.S.A. by Coelho

et al. (1962) and by Walsh, Roman & Massie (1960).We were naturally pleased to have found a simple methodfor detecting RVH due to lung disease (Jones et al.,1964). To return to the principal theme. The VCG wastaken on some of the patients treated by IPPV at Whiston,and briefly referred to by Finnegan. Clinically thesepatients had chronic bronchitis and emphysema and mosthad oedema and enlargement of the abdomen and liver;thus cor pulmonale was clinically overt or highly suspect.Despite this, not all had RVH on the ECG. VCGs takenon seven patients showed RVH. The VCGs of Fig. A4

A

B ,'I

C I.

D

%I I

I I

E I

F

G

FIG. A4. Horizontal QRS vector loops showing rightventricular hvpertrophy.

are all abnormal and are examples of the varied typesseen in chronic bronchitis. Vector D of Fig. A4 is atype also seen in severe RVH due to congenital heartdisease; the pulmonary angiogram of this man wasshown by Scarrow (Case 2). The ECGs of patients A,D, F and G showed RVH but B, C and E did not.Finally, on this topic, the VCG showed striking changesduring and after treatment (running and broken linesin Fig. A4). The small number of VCGs taken on menwith chronic bronchitis treated by IPPV emphasizedagain the importance of stress in the pulmonary cir-culation.

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Treatment of severe respiratory insufficiency

The last evidence I would like to describe concernsright heart pressures. Since we had no apparatus withwhich to measure the cardiac output the pulmonaryvascular resistance could not be calculated. To get togrips with the problem I repeated the experiments of the1950s on the effects of leg exercise in the supine positionon the right ventricular pressures in chronic bronchitisand emphysema. These results (Jones et al., 1964)confirm that in severe chronic bronchitis and emphysema,moderate exercise promptly produced dyspnoea andrapidly elevated the right ventricular pressures whichremained high for some time after exertion stopped.What is the relevance of this to the chronic bronchiticforced to bed rest by an acute illness? The likely answeris that the increased airways obstruction and lung stiff-ness means that the patient is exercising hard to breathe.With this information in mind isolated catheter studieswere made during IPPV treatment of respiratory failurein the chronic bronchitic. The following case historiesmay illustrate my hypothesis.

First case. A man of 53 years had worked at the coalface for 34 years and gave a 20-year history of cough.The patient was investigated for recent breathlessness,9 months before his admission, requiring intensive care.Clinically the diagnosis was chronic bronchitis withmoderate obesity and spirometry showed airwaysobstruction (vital capacity 2-3 litres, FEV 1-2 litres, peakflow 260 l/min). A chest radiograph showed changes inthe lung fields of chronic bronchitis and emphysema andtomograms revealed pulmonary arterial hypertension.At this time the ECG was normal but the VCG showedRVH (loop C of Fig. A4). Cardiac catheterization showedpulmonary arterial hypertension in response to lightexercise.The patient remained at work until a week prior to his

emergency admission. The illness presented the classicalfeatures of the 'blue-bloater' with copious purulentsputum, cyanosis, orthopnoea, abdominal distension,triple cardiac rhythm and confusion. The ECG hadchanged from the previous trace in that the T waves werenow negative in V3 and V4. For 2 days the patient receivedintensive chest physiotherapy, oxygen by Venturi mask,ampicillin and methyl cysteine from a Bird ventilator.Despite these measures, which were supervised by themedical-anaesthetic team, deterioration occurred and thepatient was accordingly transferred to the I.C.U.Tracheostomy with frequent tracheal suction and con-trolled ventilation with O2 enriched air from an East-Radcliffe ventilator was carried out. Neither tubocurarine

nor sedatives were needed to control ventilation and air-way pressures of 20/0 cmH2O gave minute volumes of 16-20 1. Controlled ventilation was continued for 10 days.On days 11 and 12 a Cyclator was used intermittently.The excellent progress enabled the cuffed tracheostomytube to be removed on day 16. During treatment therewas intermittent fever associated with copious purulentsecretions. Three pathogens were isolated and the in-fection was finally overcome with the aid of chloram-phenicol. The fever was attributed directly to infectionsof the bronchial tree since no opacities appeared in thelung fields. Following a brief period of convalescence thepatient returned to work. The right heart pressures weremeasured on day 7 when the patient could breathespontaneously for 1 hr without distress. Four sets ofobservations were made over 41 min (Table A4). Whenbreathing air spontaneously, the right ventricular pressurewas raised above normal. The pressure was reducedeither by allowing the patient to breathe oxygen-enriched air or during controlled ventilation (East-Rad-cliffe pressures 25/0, minute volume 18 litres). Themaximum reduction in the systolic right ventricularpressure was obtained during controlled ventilation withoxygen-enriched air. It will be seen from Fig. A5 that

FIG. A5. Right ventricular pressure trace from first case.(a) When breathing air spontaneously; (b) duringIPPV with oxygen enriched air.

during spontaneous breathing (a) the right ventricularpressures show a respiratory variation which was abolishedby controlled ventilation (b). Observations made on asimilar case ofrespiratory failure due to chronic bronchitis

TABLE A4Pressures in the right ventricle and blood gases during spontaneous and controlled ventilation

Time Ventilatory Minute Arterial Paco2 Pao2 Right ventricular pressures (mmHg)(min) conditions volume pH (mmHg) (mmHg)

(1.) Systolic Diastolic

0 Respirator/02 18 7-40 31 110 38 -220 Respirator/air 14 7'42 38 49 45 -833 Spontaneous/O02 7-38 45 72 50 -941 Spontaneous/air 7-22 64 63 57 -8

In the traces which showed marked respiratory variation the values shown below were obtained asfollows; the maximum systolic pressures were measured and the diastolic pressures of the same waveforms were then read.

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Discussion

also suggested that IPPV relieved pulmonary arterialhypertension in addition to improving the oxygenationof the blood (cf. Ambiavagar, p. 232).

Second case. The next set of observations are moreimpressive in terms of the height of the pulmonaryhypertension and illustrate rather well the relief of thisby IPPV. A woman of 61 years was crippled by asthma,bronchitis and emphysema. There was hypercarbia andpolycythaemia. The chest film showed enlargement ofthe heart and pulmonary hypertension (Fig. A6). The

+

FIG. A7. Pressure-volume loops from the second casewhen breathing spontaneously (A1) and during control-led IPPV (A). A normal loop (B) is shown for comparison.

PA tUAV#VAkE

FIG. A6. Radiograph of the chest from the second case.

VCG (loop G, Fig. A4) showed RVH. We first saw thepatient in respiratory failure and after 2 weeks IPPV itwas evident that the patient was respirator dependentand that the treatment was doomed to fail. The clinicalimpression of severe irreversible airways obstructionwas confirmed by the pressure-volume loops shown inFig. A7. On day 18 the pulmonary arterial pressures wererecorded, first on controlled IPPV from a Bird machineusing 100% oxygen and later breathing air spontaneously.The two traces are shown in Fig. A8. The systolic,

diastolic and electronic mean pressures were as follows;during IPPV-39/21, 31 mmHg, and when breathingspontaneously-68/22, 43 mmHg. The brachial arterypressure recorded by cuff did not change significantly.Deductions are hampered by lack of the cardiac outputbut my conclusion seemed inescapable; this woman waskept alive for a month by IPPV and this treatment partlyrelieved serious pulmonary hypertension.The last example chosen to support my thesis is a

cases of thromboembolic pulmonary disease.

ECG

IPPV SpontoneousFIG. A8. Pulmonary artery pressure trace from thesecond case during controlled IPPV with oxygen andwhen breathing spontaneously.

Third case. A 51-year-old housewife was transferredto the Intensive Care Unit in extreme respiratory distressand hypoxaemia. The hospital notes gave a history of anacute chest illness 14 months previously with cyanosis,chest pain, confusion, hypotension, pulmonary cre-pitations and ECG signs of right ventricular hypertrophy.There was no overt respiratory tract infection. Thesesigns improved over a month. Five and 3 months beforethe present illness transient cerebral episodes occurredthought to be epileptic or anoxic in origin; at thesetimes no RVH was seen on the ECGs. The progressivedeterioration of the patient indicated the need forcontrolled ventilation to take over the work of breathing,relieve hypoxia and pulmonary hypertension. The latter

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Treatment of severe respiratory insufficiency 255

was seen on X-ray together with enlargement of the heartbut clear lung fields. RVH was seen on the ECG. Ven-tilation was controlled for 6 days with the aid oftubocurarine for the first 2 days. Ventilation was againemployed during sleep on days 7-14. In addition totracheostomy, humidification and mechanical ventilationthe patient was given digoxin, antibiotics and anticoagu-lants. Phenindione was given initially but on day 5jaundice developed and heparin was substituted. Theheparin was changed to marevan on day 13. Theclinical response to treatment was continuous improve-ment and the patient was partially ambulant by day10 and fully ambulant by day 20. On X-ray, theheart decreased in size during treatment and remainedso when controlled ventilation was stopped. Duringtreatment respiratory tract infection was not seenclinically or radiologically. Staph. aureus was isolatedon day 2 but did not produce clinical effects. Theantibiotics given were tetracycline and fucidin. Theclinical improvement has been maintained for somemonths and the patient was able to do her own shoppingand housework. An ECG was normal but a VCG (loopA of Fig. A4) showed RVH. The chest radiograph showedpulmonary arterial hypertension only.

Although no pressure measurements were made, theclinical, X-ray and electrocardiographic signs all suggestedpulmonary arterial hypertension and right heart strainwhich was relieved only by prolonged IPPV. In the futureI hope we will be enabled to measure pulmonary vascularresistance and record simultaneously the right heart,aortic and oesophageal pressures during IPPV forrespiratory failure.

ReferencesBROWN, I.K. (1963) M.D. thesis, University of Liverpool.COELHO, E., AMRAM, S.S., ESA, A.B., MENDEC, J.C.F. &

TAVARES, V. (1962) Electrocardiographic and vector-cardiographic alterations in chronic cor pulmonale.Amer. J. Cardiol. 10, 20.

HARVEY, R.M. & FERRER, M.I. (1960) A clinical considera-tion of cor pulmonale. Circulation, 21, 236.

JONES, E.S., SCARROW, G.D., SECHIARI, G. & ROBERTS, D.V.(1964) Methods for the early recognition of cor pulmonale.Lancet, i, 146.

McMICHAEL, J. (1960) Clinical Disorders of the PulmonaryCirculation (Ed. by R. Daley, J. F. Goodwin and R. E.Steiner), p. 304. London.

MOUNSEY, J.P.D. (1954) Emphysema heart disease. Brit. J.Tuberc. 48, 63.

MUNCK, O., KRISTENSEN, H.S. & LASSEN, H.C.A. (1961)Mechanical ventilation for acute respiratory failure indiffuse chronic lung disease. Lancet, i, 66.

OSWALD, N.C., SIMON, G. & SHOOTER, R.A. (1961) Pneu-monia in hospital practice. Brit. J. Dis. Chest, 55, 109.

SCARROW, G.D. (1964) The radiology of chronic bronchitis.Brit. J. Radiol. 37, 344.

WALSH, T.J., ROMAN, G.T. & MASSIE, E. (1960) The vector-cardiographic QRS's E-Loop findings in chronic corpulmonale. Amer. Heart J. 60, 592.

SMITH. I wonder if I might be allowed a moment toemphasize a point which seems to me to be in danger ofbeing lost. In the last 18 months to 2 years we have treatedtwenty-one patients with obstructive lung disease withIPPV. Eleven of these patients were artificially ventilatedfor 24 hr with endotracheal tubes. These tubes wereremoved at the end of the 24-hr period and no furtherIPPV was necessary. These eleven patients included allfive cases of status asthmaticus treated in this way andI would re-state the fact that every case of status asth-maticus which we ventilated artificially could be weanedfrom IPPV at the end of a 24-hr period. Six patientswith acute-on-chronic bronchitis could also be weanedin this way. Three other patients with acute-on-chronicbronchitis could not be weaned and required tracheotomyand IPPV for varying periods, but were subsequentlydischarged. Eight patients died, but these were allrespiratory cripples before treatment.

I think it is important to realize that the patient is notnecessarily committed to tracheotomy when IPPV isundertaken in a patient with obstructive lung disease.Patients with asthma who may present in status asth-maticus on more than one occasion may, we believe, haveconservative measures persisted with too long in anunderstandable effort to avoid tracheotomy. In ourexperience, all our patients in status asthmaticus havebeen weaned after 24 hr and our physicians are nowmuch more willing to submit a patient with asthma totreatment in this way.BROOM. It is perhaps a pity that the follow-up in Dr

Rees' excellent paper did not quite match up to thatlater seen in Dr Kristensen's beautiful results. DrKristensen tells me that follow-up in Denmark is greatlyfacilitated by a Central Health Registry, but we mustremember, I think, that our Social Class V patients, i.e.most of our chest patients, have a very low geographicalmobility.Dr Kristensen's paper gets my Mersey Festival Award

for the Paper of the Year. What a comfort to realizethat if you try like hell for a decade or more, you cannot only do good, but ultimately get enough evidence tobe seen to be doing good. His results, as far as I know,have yet to be equalled, let alone bettered.Another small point. I believe that some of Dr Kris-

tensen's patients who showed increased neuromuscularexcitability were suffering from acute relative hypocapniaimmediately after their tracheostomy, and that closerattention to a more gradual decline of Paco2 afteroperation might lead to somewhat smoother post-operative management.

I was particularly intrigued by the prominent partplayed by early ambulation in the management of thesepatients, resembling that, I think, of other Scandinavianworkers in their attack on the problem of acute myo-cardial infarction. Perhaps we might say that, 'earlyfrom bed, early to rise will help to make us healthy andwise'.

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Postgrad. med. J. (July 1967) 43, 512.

Errata

Postgraduate Medical Journal (1967) Vol. 43, No. 498,'Intensive Therapy.'

PLEASE NOTE THE FOLLOWING:

Page 222. The last sentence of the first paragraph should read:'During hypotension a metabolic acidosis was found inall patients but the base deficit showed no correlation withthe concentrations of lactate. There was statisticalcorrelation with AL/P %.'

Page 223. The last sentence of paragraph (b) should read:'Hypotension responded . . . '

Page 254. The legend to Fig. A7 should read:'Pressure - volume loops from the second case whenbreathing spontaneously (A1) and during controlledIPPV (B). A normal loop (A) is shown for comparison.

Page 268. The formula in the second column should read:

Q 1

Qs (A-V diff) x 3301 ---

PAo2 - Pao2

Postgrad. med. J. (July 1967) 43, 512.

Errata

Postgraduate Medical Journal (1967) Vol. 43, No. 498,'Intensive Therapy.'

PLEASE NOTE THE FOLLOWING:

Page 222. The last sentence of the first paragraph should read:'During hypotension a metabolic acidosis was found inall patients but the base deficit showed no correlation withthe concentrations of lactate. There was statisticalcorrelation with AL/P %.'

Page 223. The last sentence of paragraph (b) should read:'Hypotension responded . . . '

Page 254. The legend to Fig. A7 should read:'Pressure - volume loops from the second case whenbreathing spontaneously (A l) and during controlledIPPV (B). A normal loop (A) is shown for comparison.

Page 268. The formula in the second column should read:

Q 1

Qs (A-V diff) x 3301 +

PAo2 - Pao2