66

MECHANICAL VENTILATION FOR ACUTERESPIRATORY FAILURE IN DIFFUSE

CHRONIC LUNG DISEASE

OLE MUNCKM.D. Copenhagen

ASSISTANT PHYSICIAN,DEPARTMENT B, BISPEBJERG HOSPITAL, COPENHAGEN

H. SUND KRISTENSENM.D. Copenhagen

ASSISTANT PHYSICIAN,DEPARTMENT OF EPIDEMIOLOGY, BLEGDAMSHOSPITALET, COPENHAGEN

H. C. A. LASSENM.D. Copenhagen

PROFESSOR OF EPIDEMIOLOGY, UNIVERSITY OF COPENHAGEN

From the Departments of Epidemiology and Clinical Chemistry,Blegdamshospitalet, Copenhagen

IN advanced diffuse chronic lung diseases acute

respiratory infection, overdose of morphine, operations,&c., may cause dangerous episodes of acute respiratoryfailure. The clinical picture is one of severe dyspnoea,cyanosis, confusion, drowsiness or coma, and a varyingdegree of airway obstruction due to accumulation ofsecretions. There may be congestive heart-failure andirregular muscle-twitching. Blood-pressute is often high,but severe hypotension may supervene.

In these acute respiratory crises the oxygen supply ofthe organism must be improved. This is often done byadministration of oxygen and antibiotics, removal ofsecretions by nasopharyngeal or tracheal suction after

massage of the chest, and treatment of cardiac failure.Sometimes this conservative regime fails, because hypoxiacannot be corrected without depressing ventilation dan-gerously, or because a free airway cannot be maintained.Several recent reports show that tracheotomy followed byartificial ventilation-or ventilation alone-may be life-

saving in this situation. A total of 42 cases have beenpublished; and 31 of these patients survived (Bourtourline-Young and Whittenberger 1951, Stone et al. 1953,

Data on artificial ventilation, arterial pCO2, pH, and oxygen saturation before, during,and after artificial ventilation in pulmonary fibrosis following tuberculosis.Severe purulent bronchitis of a few days duration caused the acute respiratory failure.The samples for analysis of arterial blood on Nov. 5 and 11 were taken while the

patient was breathing spontaneously with extra oxygen. The patient was breathingroom air without extra oxygen on Nov. 17.

Chermiak 1953, Lovejoy et al. 1954, Bjorneboe et al. 1955,Austen et al. 1957, Mollaret et al. 1958a, 1958b, Davidson1959, Mortensen 1959).We discuss here the selection of cases for tracheotomy

and artificial ventilation, based on experience with 23consecutive cases from 1955 to 1960.

TechniqueAfter tracheotomy at 2nd or 3rd ring-often without

anaesthetics—a rubber cuff-tube (Rusch) was inserted, andventilation with 6-10 litres per minute of a high-oxygenmixture was administered using a Lundia intermittent-positivenegative-pressure respirator giving a constant minute ventila-tion at a constant rate. Usually the arterial oxygen saturationbecame normal, and the patients regained consciousness aftera few hours. During the first one or two days ventilation wasgradually increased, and arterial carbon-dioxide tension (pCO,)often became normal. Full return to spontaneous respirationtook one to two weeks, starting with ten to fifteen minutes perhour out of the respirator. The accompanying figure illustratesthe course in a typical case.

Blood for gas analysis was obtained by puncture of the femoralartery. Oxygen saturation was measured by means of Brinkman’shaemorenector (Zijlstra 1953). Total carbon-dioxide content wasdetermined manometrically (Van Slyke and Neill 1924). Arterial pHwas measured with glass electrode and potentiometer. pCO2 wascalculated from the arterial pH and the total carbon-dioxide content(Astrup 1954).

Material

4 women and 19 men, with an average age of 56 (44-69),were ventilated with the Lundia respirator for an averageof twenty-four days (range, twelve hours to one hundredand twenty-six days).

17 patients had chronic bronchitis. In 3 the chronic ventila-

tory disability was due to pulmonary fibrosis after tuberculosis;3 had kyphoscoliosis. The duration of chronic lung diseasecannot be stated precisely-the duration of the pulmonarysymptoms had been anything from " a few years " toapproximately thirty-five.The commonest causes of the respiratory crisis were

pneumonia, influenza, and acute bronchitis. In other

patients, the precipitating factor was anoverdose of morphine, abdominal surgery,acute pancreatitis, or diabetic precoma.

16 were in coma immediately before tracheo-tomy ; the remaining 7 were semicomatose. In14 patients large amounts of secretions hadaccumulated in the airway, 10 had congestiveheart-failure, and, in 11, electrocardiographyshowed right ventricular strain. The averagearterial pCO2 was 89 mm. Hg just before

tracheotomy (range, 67-114 mm.); pH aver-aged 7-22 (7-03-7-37). In the 5 patients whowere without extra supply of oxygen duringsampling the arterial oxygen saturation aver-aged 54% (range 43-64%).

5 patients were ventilated in a tank respirator(Draeger) for some days before tracheotomy,but this treatment proved inefficient because ofairway obstruction.

Results

15 patients survived the crisis and 8 died.In those who survived, the mechanicalventilation lasted thirteen days on the

average (range, twelve hours to thirty-twodays). In those who died, the correspond-ing figures were forty-four days (twelvehours to one hundred and twenty-sixdays). 1 patient died twelve hours afteradmission from lobar pneumonia with

67

hyperthermia and shock. Another patient died fromshock following acute pancreatitis. The other 6 diedfrom irreversible cardiopulmonary failure sixteen to

one hundred and forty-seven days after admission.

On discharge from hospital analyses of arterial bloodshowed: oxygen saturation 82% (range, 71-96%), pCO244 mm. Hg (range, 30-56 mm.), and pH 7.41 (range,7.31-7.49).At a follow-up examination two to thirty months

(average nine months) after discharge from hospital,

TABLE I-MEAN VALUES FOR ARTERIAL pCO2 AND pH IMMEDIATELYBEFORE TRACHEOTOMY IN SURVIVING PATIENTS AND IN PATIENTS

WHO DIED

5 patients were back at work; 7 were out of work, butcapable of looking after themselves; and 1 was still in

hospital on spontaneous respiration without extra oxygen.Finally, 2 had died owing to relapses, four and eightmonths after discharge.

Complications were few. As could be expected therewas nearly always a minor fall in blood-pressure at thebeginning of mechanical ventilation; in only 1 patient didshock develop. This disappeared after reduction of

ventilation, and a transfusion of blood.

In 1 patient, a man aged 67 with chronic bronchitis of fifteento twenty years’ duration, congestive heart-failure, influenza,bronchopneumonix, and liver cirrhosis, a tracheo-oesophagealfistula developed owing to pressure from the cuff-tube afterfifty-five days’ ventilation. He died fifteen days later fromprogressive pulmonary infection and circulatory collapse.

Discussion

It is highly probable-though difficult to prove-thatmost of the 15 who survived would have died in the acute

TABLE II-ANAMNESTIC AND CLINICAL DATA CORRELATED TO MORTALITY

phase had tracheotomy and artificial ventilation not beenundertaken. On the other hand, several patients dieddespite the intensive treatment. Therefore criteria to

determine which patients could be expected to benefitfrom the treatment would be valuable. We have analysedthe series by correlating the results with some biochemical,anamnestic, and clinical characteristics.

Table I shows that knowledge of the pretreatmentvalues for arterial pCO2 and pH is no help in assess-ing the outcome, there being no significant differencein these parameters between the group of patientswho survived and the group of patients who died

(" t "-test).Table 11 gives the frequency of some other data relevant

to the outcome. As would be expected, the prognosis wasmuch better in patients who had been able to work (A)all the time up to the crisis than in those whose respiratoryreserve was very slight (C). Nothing can be concludedfrom the results in the intermediate group (B). Theclinical data show that there was no significant differencein mortality whether coma, congestive heart-failure, rightventricular strain, or large amounts of secretions werepresent or not. Evidently these symptoms are of no

prognostic value.

This implies that the chance of tiding patients withdiffuse chronic lung disease over an episode of life-threatening respiratory failure-and of obtaining a reason-able recovery-with the treatment described is fair, whenthe case-history is indicative of a pulmonary reserve.Such treatment, therefore, is clearly indicated for thesecases. In patients without pulmonary reserve, the resultof the active treatment is hardly better than that of anordinary conservative regime. The very alarming acuteclinical picture and the severe biochemical changes,demanding tracheotomy and artificial ventilation, are thesame in patients with pulmonary reserve as in thosewithout.

Summary23 consecutive cases of diffuse chronic lung disease with

lifethreatening respiratory failure were treated bytracheotomy and mechanical ventilation.

Analysis of the cases shows that the outcome is goodwhen the case-history indicates the presence of a pul-monary reserve, even if the clinical condition and bio-chemical changes are alarming when treatment is started.When no pulmonary reserve is present, the results arehardly better than those of ordinary conservativetreatment.

REFERENCES

Astrup, P. (1954) Ugeskr. Lœg. 116, 758.Austen, F. K., Carmichael, M. W., Adams, R. D. (1957) New Engl. J. Med.

257, 579.Bjørneboe, M., Ibsen, B., Astrup, P., Everberg, G., Harvald, B., Søttrup, T.,

Thaysen, E. H., Thorshauge, C. (1955) Lancet, ii, 901.Bourtourline-Young, H. J., Whittenberger, J. L. (1951) J. clin. Invest. 30, 838.Chermiak, R. M. (1953) ibid. 32, 1192.Davidson, L. A. G. (1959) Lancet, i, 597.Hald, A. (1957) Statistical Theory with Engineering Applications. New

York.

Lovejoy, F. W., Yu, P. N. G., Nye, R. E., Joos, H. A., Simpson, J. H. (1954)Amer. J. Med. 16, 4.

Mollaret, P., Bastin, R., Rapin, M., Pocidalo, J. J., Goulon, M., Lissac, J.,Liot, F. (1958a) Pr. med. 66, 1271.

— — — — — — — — (1958b) ibid. 66, 1326.Mortensen, E. (1959) Ugeskr. Lœg. 121, 706.Stone, D. J., Schwartz, A., Newman, W., Feltman, J. A., Lovelock, F. J.

(1953) Amer. J. Med. 14, 14.Van Slyke, D. D., Neill, J. M. (1924) J. biol. Chem. 61, 523.Zijlstra, W. G. (1953) Fundamentals and Applications of Clinical Oximetry.

Assen, Netherlands.