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Pulmonary Embolism A-Nd Thrombosis R Postgrad Med J: first published as 10.1136/pgmj.38.435.13 on 1 January 1962. Downloaded from POSTGRAD MED. J. (I962), 38, 13 PULMONARY EMBOLISM A-ND THROMBOSIS R. MARSHALL, M.D., M.R.C.P. Nuffield Department of Surgery, Radcliffe Infirmary, Oxford SUDDEN death following a call for a bedpan is a chest pain and ECG changes when the balloon classical mode of presentation of pulmonary em- was inflated in a smaller artery (Brofman, Charms, bolism, but it is probable that cases of this severity Kohn, Elder, Newman and Rizika, I957). On the form only a small proportion of the total. Pul- other hand, it is a common practice to impact the monary embolism may be caused by blood clot, tip of a cardiac catheter in branches of the pul- fat, cells or foreign bodies, but most commonly by monary artery of about 2 mm. diameter with no blood clot. ill effects. In spite of the undoubted ability of emboli to produce reflex effects under certain cir- cumstances, there is a growing body of evidence The Physiological Effects that the effects of pulmonary embolism by inert The physiological effects ofpulmonary embolism particles are produced by the magnitude of the depend upon the size and number of the emboli mechanical blockage of the pulmonary vessels and and they may produce these effects either by are not dependent upon the size of the emboli or mechanical blockage of the circulation when they reflex vasoconstriction (Daley, I957; McEvoy, are of sufficient size or number, or by the initiation Harder and Dale, 1958; Williams, 1956). Comroe, of reflex broncho- or vasoconstriction. This point van Lingen, Stroud and Roncoroni (I953) have by copyright. is of considerable clinical importance because of suggested that some of the effects of pulmonary the possibility that reflex effects may be reduced embolization may be caused by serotonin liberated by drug treatment, whereas mechanical blockage is from the platelets in a thrombus. Serotonin is less likely to be affected by drugs. There has been one of the few substances with a strong vaso- much controversy over the part played by reflex constrictor action on the pulmonary arteries. action in causing the symptoms and disability of Following pulmonary embolization of dogs with pulmonary embolism. Removal of one lung in autologous blood-clot the level of serotonin in the man has no effect on the pulmonary arterial arterial blood has not been found to be raised pressure and causes very little respiratory dis- (Sanders, Waalkes, Gilbert and Terry, I959), but http://pmj.bmj.com/ ability. Dogs are able to live with less than 25% this is probably an insensitive way of detecting the of their pulmonary vascular bed remaining. These liberation of serotonin in the lungs. Work in observations have led people to suppose that in progress suggests that the cardiovascular effect of clinically severe pulmonary embolism the throm- embolization by platelet agglutinates is greater bus itself is unlikely to block so much of the than that of an equivalent mass of blood clot and pulmonary vascular tree that it can cause right this difference may be due to the serotonin heart failure. It has been supposed that reflexes, liberated. initiated by impaction of emboli in the smaller With this physiological evidence in mind it is on September 24, 2021 by guest. Protected arteries, cause reflex vasoconstriction of the whole useful to consider the clinical picture. Small of the pulmonary vessels. Much experimental emboli, if they do not produce reflex vasoconstric- work has been done to try to determine the role tion, will cause no symptoms and give rise to no played by reflex action in pulmonary embolism. signs; they will therefore pass unnoticed. A Reflex vasoconstriction has been demonstrated in single large embolus will have to obstruct more the contralateral lung of dogs when small glass than one main pulmonary artery if it is to cause beads are injected into the other lung, care being symptoms in a subject with normal Lings. This taken that none of the beads escaped from the raises the problem of the importance and the embolized lung (Niden and Aviado, I956). Most incidence of repeated small pulmona-ry e-nboli of the investigators attribute reflex activity to which could in time obstruct so much of the emboli which lodge in vessels of ioo t or less in pulmonary vascular tree that heart failure r sulted, diameter, i.e. in the arterioles. In man a balloon or could quietly reduce the size of the pulmonary inflated in the main pulmonary artery produces no vascular bed so that when a massive pulmonary reflex effects, but an instance has been reported of embolism did occur it could bie fatal. &l Postgrad Med J: first published as 10.1136/pgmj.38.435.13 on 1 January 1962. Downloaded from 14 POSTGRADUATE MEDICAL JOURNAL _7anuary I962 Detection of Emboli large embolus and the blood flow to an embolized Because of the clinical importance of silent, region may start to increase only a few minutes repeated pulmonary embolism it would be of value after the embolus impacts. to know when and under what circumstances silent Measurement of the diffusing capacity of the pulmonary embolism occurs and to what extent lungs may provide another method for the detec- the body's defence mechanisms are able to deal tion of pulmonary embolism. The diffusing with the emboli. Pulmonary emboli may not be capacity ofthe lungs is most conveniently measured detectable clinically or by X-ray or ECG examina- as the diffusing capacity for carbon monoxide and tion and other methods of investigation may have it is a measure both of the permeability of the to be used. A method which promised to be of alveolar membrane to carbon monoxide and of the some use was the measurement of the dif- surface area of the alveolar membrane in contact ference in carbon dioxide tension (Pco2) between with blood in the capillaries. If the blood supply the end tidal gas and the arterial blood. In a to some of the alveoli is cut off the diffusing subject with uniform distribution of gas in his capacity will be reduced and the reduction in dif- lungs the air sampled at the end of a normal fusing capacity, in the absence of other lung breath is representative of the gas from the alveoli disease, nm,ay give an indication of silent pulmonary and this should have the same Pco2 as the embolism. The single breath method of measure- arterial blood, since the alveolar wall presents no ment of the diffusing capacity for carbon monoxide diffusion barrier to carbon dioxide. If some of the is probably particularly useful for this purpose alveoli have no blood supply, because the arteries because the full inspiration which is necessary for have been blocked by emboli, then these alveoli this test probably minimizes any inequality of will contain no carbon dioxide and the gas from ventilation which might be caused by the emboliza- these alveoli will dilute the carbon dioxide in the tion. The usefulness of the method would depend gas coming from alveoli perfused with blood and on the detection of a fall in diffusing capacity on so the end tidal (alveolar) Pco2 will be less than repeated measurements; the normal range is too that measured simultaneously in the artery. wide for a single measurement to be of value. by copyright. This method, suggested by Severinghaus (Sever- inghaus and Stupfel, 1957), could, in theory, give Clinical Features a measure of the proportion of alveoli from which Small or medium-sized pulmonary emboli may the blood supply has been cut off. Experimenta be completely 'silent'. Larger emboli, which work on dogs (Julian, Travis, Robin and Crump, cause gross obstruction of the pulmonary circula- I960) and observations in man (Robin, Forkner, tion, cause the sudden onset of symptoms. Dys- Bromberg, Croteau and Travis, I960) have sug- pncea is often the main symptom and may be the gested that the method may indicate the extent of only one. A history of sudden attacks of dyspncea pulmonary artery obstruction following embolism. is often obtained from patients who have had More recently Severinghaus, Swenson, Finley, recurrent emboli. The cause of the dyspncea, http://pmj.bmj.com/ Lategola and Williams (i96i) have found that the as of the dyspnea secondary to pulmonary hyper- difference between end tidal and arterial Pco2 is tension, is not known. It may be reflex from dis- much less than would be expected from the tension of the right side of the heart or it may amount of pulmonary circulation obstructed. The result from inadequate blood supply to the respira- reason for this is a compensatory mechanism by tory muscles. Pain in the chest may be of two which abolition of the blood supply to a part of types. First, massive embolism may cause sub- the lung causes a reflex bronchoconstriction which sternal pain or discomfort similar to that of myo- on September 24, 2021 by guest. Protected reduces the ventilation to that part. Measurements cardial infarction. This may arise from distension of the end tidal, arterial Pco2 difference before of the pulmonary artery or may be of myocardial and after experimental pulmonary embolism of origin due to reduction in coronary blood flow. dogs with blood thrombi (Marshall, Allison, Bos- Substernal pain is not necessarily of cardiac origin; man, Sabiston and Dunnill, in preparation) have cesophageal pain may be indistinguishable from also shown only small and variable values for the that of myocardial infarction. The second type of Pco2 difference, but in these dogs the ventilation pain is pleural pain, which is usually only present in the embolized lung was reduced by only a if subpleural infarction occurs.
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