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THE MANAGEMENT OF COR PULMONALEBy J. F. GOODWIN, M.D., M.R.C.P.

Physician and Lecturer in Mcdicine, Postgraduate Medical Sch9ol of London

Pulmonary heart disease (cor pulmonale) maybe divided into acute, subacute, and chronic types(Wood, I950; McMichael, 1948). The acutetype is typified by massive pulmonary embolism,and will be considered first.

Massive Pulmonary EmbolismMany pulmonary emboli cause little or no

circulatory disturbance, but when a large embolusobstructs the bifurcation of the main pulmonaryartery, or multiple emboli obstruct more than twothirds of the peripheral branches, acute pulmonaryheart disease results. Acute right ventricularfailure ensues, and left ventricular filling isimpaired, which results in arterial hypotension,and a fall in cardiac output. The objects oftreatment are to encourage the embolus to moveon, to prevent additive thrombosis, and to supportthe failing right ventricle and systemic circulation.Since the systemic blood pressure is usually low,the patient should be nursed flat. Oxygen shouldbe administered and, in very severe cases, respira-tion may require stimulation by Nikethamide(2.5 to 5 ml. intravenously) or Aminophylline(0.24 to o.48 g. intravenously). Persistent arterialhypotension, with systolic levels below 70 to80 mm.Hg may require treatment with pressoramines. A successful outcome has been reportedfollowing the use of a slow intravenous infusionof 1-nor-adrenalin (laevophed) (4 mg. dissolved ini litre of dextrose) (Wolff, I954), but the use ofsympatheticomimetic drugs is open to the objec-tion that they may cause pulmonary, as well asperipheral, vasoconstriction (Besterman, 1951),and so further embarrass the right ventricle. It iswise, therefore, to withhold 1-nor-adrenalin, orsimilar drugs, unless all other measures fail toproduce clinical improvement. The failing rightventricle, meanwhile, can be supported by digitalis,and a full dose of digoxin (i to 1.5 mg.) or ofstrophanthus (0.5 to i mg.) should be givenintravenously, provided the patient has notpreviously been taking digitalis. Thereafter,digitalis should be continued in maintenancedosage until all signs of right ventricular failurehave disappeared. The suggestion has been made

that the raised venous pressure may be compensa-tory in pulmonary embolism, assisting auricularfilling and thus maintaining cardiac output, so thatagents which lower venous pressure might, there-fore, not be of value (Wood, I947). It is verydoubtful if this is a practical consideration,however, since digitalis primarily acts by increasingthe strength of ventricular contraction, and thebenefit of this action would outweigh any possibledisadvantage resulting from direct lowering ofvenous pressure. Additive thrombosis, or furtheremboli, must be discouraged by anticoagulants.Heparin, which acts rapidly, should be given in theearly stages of the illness (50 mg. 4 to 6 hourlyintravenously) as single injections or via a Gordhneedle and adaptor. This should be continueduntil the effect of an oral anticoagulant of theCoumarin series becomes manifest. Ethyl bis-coumacetate (Tromexan) in an initial dose of900 to 1,200 mg. and a maintenance dose of 300 to600 mg. daily, or Phenylindanedione (Dindevan)in an initial dose of I50 to 200 mg. and a dailymaintenance dose of 25 to Ioo mg. should be givenat the same time as the first dose of heparin, or assoon as the patient can take it by mouth. Suchanticoagulant therapy must be controlled byfrequent prothrombin times, and should becontinued for at least three weeks.When severe pain or restlessness are important

features, sedatives may be necessary, but morphineshould not be given if respiratory failure threatens,and under no circumstances administered topatients with chronic pulmonary disease, asthma,or severe thoracic deformities. Pethedine (50 toioo mg.) causes less respiratory depression, but isless effective than morphine in relieving anxietyand restlessness. The use of atropin, to preventdangerous vagal reactions, and of papaverine, todilate the pulmonary vasculature, has been recom-mended (Wolff, I952), but in the author's opinionthey are not of striking value. Pulmonary embo-lectomy (Trendelenberg operation) is a desperatemeasure which is seldom now practised.The prophylaxis of acute pulmonary embolism

and of its recurrence lies principally in the pre-vention of peripheral venous thrombosis, since

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approximately 80 per cent. of emboli arise fromthis source (Belt, I939). Elderly patients confinedto bed may develop a deep calf vein thrombosisinsidiously, the first indication being a pulmonaryembolism. This is especially true of patients withcongestive cardiac failure, or with a fixed lowcardiac output. The pelvic veins may also be asource of embolism. Daily leg exercises help toprevent local thrombosis and the routine use ofelastic stockings has been advised (Wilkins et al.,1952). Daily examination of the calves should bemade. The presence of tenderness, swelling, ora positive Homan's sign, indicate the need foranticoagulants, which reduce the tendency tofurther thrombosis and to embolisation (Allenet al., I946). Repeated pulmonary emboli despiteadequate anticoagulant therapy may requireligation of the inferior vena cava, but this shouldonly be considered as a last resort.

Subacute Cor PulmonaleSubacute cor pulmonale is a form of rapidly

progressive pulmonary heart disease due to block-ing of the pulmonary circulation by small vascularor tumour emboli, or by miliary lymphatic carcino-matosis (McMichael, 1948; Wood, 1950).Chronic Cor Pulmonale

Chronic cor pulmonale may be classified in thefollowing way: (Modified from McMichael, 1948,and Wood, I950).I. Obstructive

Specific forms of pulmonary arteritisIdiopathic pulmonary hypertensionRecurrent pulmonary emboli

In this group a progressive reduction in thepulmonary vascular bed and an increase inpulmonary vascular resistance, due to obstructivelesions in the small vessels, produce failure of theright ventricle.2. Anoxic

Chronic bronchitisEmphysemaPulmonary fibrosisBronchietasisCystic diseaseTuberculosisPheumoconiosis(Kyphoscoliosis).

The diseases in this group (when severe enoughto cause pulmonary heart disease) all have thecommon features of impaired pulmonary function,anoxia, and carbon dioxide retention.Pulmonary hypertension (of varying degree) is a

constant finding in both groups, resulting in thefirst from obstruction to the pulmonary circulation,and in the second from anoxia, obliteration of thepulmonary vascular bed by pulmonary fibrosis or

emphysema and from other factors not yet fullyunderstood.The commonest cause of chronic cor pulmonale is

severe emphysema and bronchitis, and the manage-ment of this condition will be considered in detail.Treatment both of the acute phase of cor pulmonalesupervening on chronic lung disease, and of thesubsequent management and prevention of furtherexacerbations, must be considered.The development of a pulmonary infection in a

subject with chronic lung disease sets in motion atrain of events which may result in respiratory andcardiac failure. The effect of emphysema andchronic bronchitis is to produce impedance to theflow of air in and out of the lungs, uneven ventila-tion of the alveoli, and uneven distribution of theblood through the lungs. An attack of acutebronchitis intensifies these abnormalities andresults in further anoxia and carbon-dioxideretention. This results in pulmonary hyier-tension, hypervolaemia, polycythaemia, and anincrease in cardiac output (Harvey et al., 195 ).Such patients have a relatively high cardiac output(McMichael, I948) with central cyanosis, raisedjugular venous pressure, warm extremities, anda bounding arterial pulse. Further anoxia andright ventricular insufficiency will then lead to aprogressive fall in cardiac output in the terminalphase of the disease.

Treatment should be directed towards combat-ting the pulmonary infection, reducing the anoxia,and supporting the right ventricle.

Treatment of the Pulmonary InfectionAdequate chemotherapy at the earliest possible

moment is of the greatest importance (Simpson,I954). At least 2 mega units per day of crystallinepenicillin should be given in divided doses4-hourly, after a sample of sputum has beenobtained for bacteriological examination. If animmediate response is not obtained, alternativeantibiotics should be used and, if time permits, thesensitivity of the organisms in the sputum shouldbe determined. May (I953) has shown that themost important organisms in chronic bronchitisare Haemophilus influenzae and the pneu-mococcus. These bacteria are also likely to bepresent in acute exacerbations (Flint, 1954).Chloramphenicol may be effective against Haemo-philus influenzae, but the danger of toxic effectson the bone marrow, especially after repeatedcourses, should discourage its use. Streptomycinis effective but its use as the sole antibiotic en-courages the emergence of resistant organisms,and may also make subsequent diagnosis difficultif there is a tuberculous lung infection. If em-ployed, streptomycin should be given in highdosage for a short period (2 to 3 g./day for 4 to 5

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100 POSTGRADUATE MEDICAL JOURNAL February 1956

days). In the seriously ill patient, the combina-tion of penicillin and streptomycin is probably themost satisfactory, but in less severe cases, tetra-cycline, chlortetracyclin (aureomycin), or oxytetra-cycline (terramycin), in a dosage of 250 mg.6-hourly, can also be effective. They should notbe given for long periods because of the risk ofgastro-intestinal disturbance and fungus infectionsof the lung. Whenever possible, however, thesensitivity of the organisms in the sputum shoulddictate the choice of antibiotic. While early andadequate chemotherapy may do much to alleviateanoxia, other factors tend to perpetuate it. Thereis often swelling of the bronchial mucosa withblocking of the swollen air passages with tenacioussputum, and sometimes bronchospasm. Broncho-dilators such as ephedrine or isopropylnoradre-nalin (isoprenalin) should be used, an effectivesolution for use in a nebuliser or Collison inhalerbeing Neb. Isoprenaline Co. (N.F.). Attemptshave been made (mainly in children with acutebronchitis) to liquefy tenacious sputum by the useof aerosol detergents, such as ' Alevaire' (Gans,1954). Such aerosols must be administered by anebuliser (such as the Oxygenaire Vaporiser)capable of producing particles no larger than 3p indiameter. Further work is necessary to determinethe value of aerosols in the treatment of acuterespiratory infections, but the old fashionedinhalations of friar's balsam may sometimes beeffective in loosening tenacious sputum. Coughingand breathing exercises, and vigorous chestpercussion are also of value (Westlake, 1954).Bronchoscopic aspiration of tenacious bronchialsecretions has been recommended by Westlake etal. (I955), if simpler methods fail to dislodge them,but many patients are not fit for bronchoscopy,which in any event will not drain the smaller airpassages.

Treatment of Respiratory FailureOne of the most important complications of

acute or chronic cor pulmonale is respiratoryfailure. Patients with severe lung disease have areduced maximum ventilatory capacity, whichleads to carbon dioxide retention and anoxaemia.Scott (I920) has shown that in emphysema thenormal respiratory response to carbon dioxide isreduced, and that hypercapnoea depresses therespiratory centre, the normal stimulus to respira-tion being provided by the low arterial oxygensaturation. Such severely anoxic patients have arespiratory acidosis, with shallow ineffectiverespirations. The failing respiratory centre shouldbe stimulated by large doses of nikethamide (io toI5 ml.) intravenously (Westlake et al., I955).Mechanical stimulation of respiration has notproved of great value (Westlake, 1954), although

Boutourline-Young and Whittenberger (I95I) andStone et al. (1953) have had some success with aDrinker type of respirator. Nevertheless, ifrespiration fails, manual artificial respirationshould be performed until respiratory stimulantsand oxygen can produce an effect.The use of morphine is absolutely contra-

indicated in cor pulmonale, its depressant effectupon the respiratory centre being lethal. This isalso true in kyphoscoliotic heart disease (Daley,1945). Should morphine have been given, how-ever, its effects can be reversed by the use of themorphine antagonist, N-allyl-nor-morphine(Nalorphine. Lethedrone) (Io mg. intravenously)(Eckenhoff et al., I952), although it must beadministered quickly (Westlake, 1954).The Place of Oxygen Therapy

Patients with severe anoxic cor pulmonale arefrequently drowsy and irrational and may exhibitmuscular twitchings. A raised cerebrospinalfluid pressure is not uncommon, and papilloedemamay occur (Simpson, I954). Westlake and Kaye(I954) have shown that the increase in intra-cranial pressure is the result of anoxia and hyper-capnoea which produces cerebral vasodilatation.The neurological manifestations are the direct

result of acidaemia and hypercapnoea on thecerebrum (Westlake et al., 1955). Oxygen therapyin such patients may exacerbate these symptoms,and even produce coma (Davies and MacKinnon,1949), and respiratory failure, since the responseof the respiratory centre to carbon dioxide isdiminished, and anoxia is the main stimulus torespiration (Harvey et al., I95I).Oxygen must, therefore, be administered with

great caution, careful observation being necessaryto detect impending respiratory failure, and thedevelopment of neurological signs, or of coma.Harvey et al. (1953) recommended that the carbondioxide content of the arterial blood should alwaysbe estimated before starting oxygen therapy, butwhile highly desirable, this is not always practi-cable, and lack of suitable facilities for thisinvestigation should not prohibit the use of oxygen.Oxygen should be given initially by nasal

catheters, B.L.B. mask, or lightweight B.O.C.' polymask,' at a rate of I to 3 litres/min. Thisslow rate of flow produces only partial relief ofanoxaemia, but avoids a rapid and considerablerise of arterial carbon-dioxide tension (Simpson,I954; Westlake, 1954; Westlake et al., 1955).Oxygen may also be administered in a tent, thepatient being allowed to breathe room air for tenminutes in every hour (Donald, 1953). Simpson(1954) considers the threat of coma to be ofgreater importance than the relief of cyanosis, andany impending signs of the former should indicate

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February 1956 GOODWIN: The Management of Cor Pulmonale i

C

"r

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·irr.r, I .c. ..:i3..U'"·LII. :I *i';

·:::.:·

.:iHi,:

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FIG. i.-Postero anterior chest radiograph of a patientwith congestive cardiac failure due to chronicbronchitis and emphysema. There is considerablecardiac enlargement involving mainly the rightauricle, right ventricle, and pulmonary arteries.

ilXI··I:i····

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FIG. 2.-Postero anterior chest radiograph of the samepatient after relief of acute respiratory infection andcardiac failure. There is a considerable reductionin heart size, although the pulmonary arteriesremain enlarged.

a reduction in the flow rate of oxygen, even thoughthe latter is severe.

It should be stressed that although the dangersof oxygen are appreciable in cor pulmonale, theycan be overcome by meticulous observation andmanagement, and that the benefits of oxygentherapy when properly used are so great that nopatient should be denied it.

The Treatment of Congestive Heart Failurein Cor PulmonaleAs has been stated, the initial stages of acute

pulmonary heart failure are associated with ahyperdynamic circulation: rapid, bounding pulse,warm extremities and raised venous pressure,with hepatic enlargement and often peripheraloedma (McMichael, 1948). The treatment of thisstage is still somewhat controversial. It ispossible that the raised venous pressure is com-pensatory, and helps to keep the cardiac output ata level necessary to keep the tissues supplied withoxygen. Howarth et al. (I947) found thatdigitalis and venesection produced a decrease incardiac output in these circumstances, andMcMichael (1948) advised against the use ofdigitalis or venesection.

Furthermore, the action of digitalis uponventricular function in these patients is not alwayspredictable. Gray et al. (I952) gave intravenousdigitalis to nine patients with cor pulmonale andfound that in two the work of the heart increased,while in only three was any clinical benefit noted.Ferrer et al. (I950) found an increase in rightventricular pulse pressure, and a slight rise inoutput in similar patients, while Mounsey et al.(1952) obtained the same results, but without anyrise in output. Both groups of workers found thatthe pulmonary artery pressure rose slightly afterdigitalis. Although the effect of digitalis is un-likely to be as dramatic as in left ventricularfailure, its use may do good and is unlikely to doharm. It should be remembered, however, thatthe most important aspect of therapy is the relief ofanoxia. Mounsey et al. (1952) have shownthat the pulmonary artery pressure rises during anattack of failure, and falls when the failure is undercontrol. High pulmonary artery pressures areassociated with low arterial oxygen saturations,and when anoxia has been relieved the pulmonaryarterial pressure falls, the work of the rightventricle is lessened, and the failureresolves.The relief of cardiac failure is well illustrated in

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102 POSTGRADUATE MEDICAL JOURNAL February 1956

Figs. i and 2, which show a remarkable reductionin heart size after recovery from an attack ofpulmonary heart failure. The reduction in rightventricular stress is also well shown cardio-graphically (Figs. 3 and 4) (Mounsey et al., I952a;Camerini et al., 1955).

Venesection is not now frequently practised,but its value has been stressed in patients withmarked polycythaemia and vascular engorgement(Donald, I953). Aminophyllin 0.24 to 0.48 g. in ioc.c. sterile water as an intravenous injection may beof great help in reducing bronchospasm, stimulatingventricular contraction and the respiratory centre,and acting as a mild diuretic. In patients withmarked oedema, mercurial diuretics are needed,and in any event, the patient should be placed on alow salt diet. The use of acetazoleamide (Diamox)in the treatment of acute respiratory acidosis hasbeen reported by various workers (Nadell, I953;Wishart and Isaacs, 1955). Acetazoleamide in-hibits the enzyme carbonic anhydrase, the mainaction being upon the renal tubules, producingincreased excretion of sodium, potassium, andbicarbonate, reduced ammonia excretion, a re-duction in serum bicarbonate level and blood pH,and a rise in urinary pH (Nadell, 1953; Counihanet al., 1954). Both the fall in blood bicarbonateand the increased sodium excretion and diuresismight be expected to be beneficial in acute corpulmonale. Nadell (I953) reported encouragingresults in six cases, and thought that carbondioxide removal by the lungs seemed to be moreeffective after acetazoleamide, while Bell et al.(I955) also comment favourably on the use of thisdrug in respiratory disorders. Wishart andIsaacs (1955) point out, however, that increasedremoval of carbon dioxide by the lungs is unlikelyto occur in a subject with grossly impaired ventila-tory function and a respiratory centre alreadyinsensitive to the stimulus of hypercapnoea, andthat the urinary loss of bicarbonate would tend tolower further the blood pH, which would beharmful in an acidotic state. They treated threepatients with acute respiratory acidosis withacetozoleamide; all three cases deteriorated, twodied and one recovered after the drug waswithdrawn.

It is doubtful, therefore, whether acetozoleamideshould be given to patients with severe respiratoryacidosis.

In severe cases in which signs of cadiac failurepersist despite energetic therapy, some benefit maybe obtained from reducing metabolism andoxygen requirements, by depression of the thyroidgland (Sharpey-Schafer, I946). Ablation withradio-active iodine may be attempted, or anti-thyroid drugs, such as neomercazole, admin-istered. The latter must be given in full dosage

Or.K&....

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FIG. 3.-Cardiogram of a patient taken during anexacerbation of pulmonary heart failure. There isevidence of right ventricular hypertrophy, shownby the dominant Rwave in leads V4R and VR, the rSpattern in V5, and the augmented P waves of rightauricular enlargement.

...

ft. ftCii~fllritt

ILL

FIG. 4.-Cardiogram of the same patient six monthslater, after recovering from cardiac failure. Theonly evidence of right ventricular enlargementwhich remains is the r S complex in lead V5.Leads V4R and VR are normal and the R wave inV1 has greatly decreased in size.

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February 1956 GOODWIN: The Management of Cor Pulmonale I03

over long periods to achieve any result, which isoften not dramatic.

The Treatment ofPulmonary HypertensionIn many patients, as has been said, the pulmon-

ary artery pressure returns to normal after recoveryfrom an acute attack of respiratory infection andanoxia. In some, however, pulmonary hyper-tension persists, either because of obstruction tothe small lung vessels (obstructive cor pulmonale)or because of persistent anoxia and destruction oflung substance by severe pulmonary disease.Progressive failure of the right ventricle is likely tofollow, unless the pulmonary vascular resistancecan be reduced. Fowler et al. (1950) haveshown that ganglion blocking agents may producepulmonary arteriolar dilatation and reduction inpulmonary artery pressure. Davies et al. (I954)showed that hexamethonium bromide produced afall in pulmonary artery pressure in patients withsevere pulmonary hypertension due to mitralstenosis, and considered that the drug probablyproduced its effect by blocking vasoconstrictorimpulses to the pulmonary vasculature. Whitesideand Coigley (I952) reported favourably on the use ofhexamethonium in patients with cor pulmonale, andpersonal experience has shown that this drug canreduce the pulmonary vascular resistance in thiscondition. Ganglion blocking agents are worthyof trial in patients with persistent pulmonaryhypertension, and may also be of value in relievingbronchospasm although it should be rememberedthat they block sympathetic as well as parasympa-thetic impulses, and might therefore actuallyincrease spasm.

Imidazoline (Tolazoline) (Priscol), which hasbeen of value in idiopathic pulmonary hyper-tension (Dresdale et al., 1951), may also be tried.

Steroid Hormones in Chronic PulmonaryDisease

Cortisone or ACTH have been used in patientswith chronic pulmonary fibrosis but the results arevariable (West et al., 1951; Galdston et al., I951).If there is persistent and severe bronchospasmwhich does not respond to the usual methods oftreatment, ACTH may be lifesaving (Bordleyet al., I949). ACTH may be administered slowlyby intravenous drip, or ACTHAR gel may begiven intramuscularly (20 to 80 units b.d.).Unfortunately, withdrawal of the drug may befollowed by relapse. Patients with any evidence ofheart failure who are receiving ACTH should beon a low sodium diet with potassium supplements,and mercurial diuretics may be required. Adequateantibiotic cover is essential.The long term treatment of severe asthma has

been reported by Ball (x954), and by Savidge and

Brockbank (I954), with variable results, but thelatter authors point out that cortisone is not with-out risk in these patients, two of whom diedunexpectedly (Savidge and Brockbank, 1954).Very recently, Davies and Williams (I955)have reported somewhat more encouraging longterm results with hormone therapy.After-care and the Prevention of AcuteRespiratory InfectionsThe importance of prevention of further attacks

of respiratory infection, with their attendant risksto the chronic bronchitic cannot be stressed toostrongly. Simpson (I954) recommends the use ofbreathing exercises, and most patients can betaught to do them. The onset of even an ap-parently trivial 'cold' or upper respiratoryinfection should be treated seriously. The patientshould remain in a warm, humid atmosphere.The effect of cold and fog is particularly to befeared (Brit. med. J., I954), (Elmes et al., 1953),(Lancet, 1953), and a satisfactory ' smog' mask isurgently required. The early administration ofchemotherapy may prevent a serious respiratoryinfection, although the choice of drug is difficult.Kilpatrick and Oldham (I954) conducted a clinicaltrial of continuous sulphonamide therapy duringthe winter in patients with chronic bronchitis, butfailed to produce any evidence that these drugsprevented acute exacerbations. Elmes et al.(I953) observed the effects of penicillin, sul-phadimidine, aureomycin, and chloramphenicolon the sputum in a group of chronic bronchitics.Each drug, except sulphadimidine, reduced thebacterial counts, and the purulence of the sputum,but the clinical effects were slight. The mostsatisfactory antibiotic may prove to be Tetracycline(Fletcher, 1955). In practice, however, the earlyuse of adequate doses of penicillin, combined withthe general measures outlined above, and withexpectorants or inhalation of friar's balsam toencourage expectoration, may do much to avert aserious attack. Bronchodilators should be used ifthere is any evidence ofspasm. Smoking should bereduced or discontinued, as the incidence ofbronchitis is higher in smokers than non-smokers(Palmer, I954).The importance of infection in the production

of heart failure in chronic respiratory disease hasbeen stressed by Flint (954), and the magnitudeof the problem is such that the energetic investi-gation and treatment of chronic bronchitis is ofthe greatest urgency.

BIBLIOGRAPHYALLEN, E. V., BARKER, N. W. and HINES, E. A. (1946),

'Peripheral Vascular Diseases,' Philadelphia and London,W. B. Saunders, p.639.Bibliography continued on page I o.

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because the book is directed towards an extramedicalreadership, but many doctors will feel a sense of lossin the absence of a critical evaluation of availabletherapeutic methods which Dr. Hamilton isobviously well fitted to provide. Despite thisomission, there can be little doubt that this workrepresents the most useful contribution to psychoso-matic medicine which the past year has offered.The references are relevant yet wide in scope, the

style is authoritative yet eminently readable, and theauthor has put considerable work into the task ofassessing statistically the often vague and highlygeneralized results so common in the earlier papers.'Psychosomatics' will be appreciated as muchwithin the medical profession as in the scientificcircles for whom it has been written, not only forthe information it contains, but also for the highstandard of medical authorship which it reflects.

0/ /lantacitvCet Ilote'DRINAMYL SPANSULE' CAPSULES

Smith Kline & French International Co.,represented by Menley & James, Limited,Coldharbour Lane, London, S.E.5, announce theintroduction of 'Drinamyl Spansule' capsules.Taken on rising one capsule affords day-longcontrol of worry and harassment. By presenting'Drinamyl,' already widely used and recom-

mended for this purpose, in' Spansule ' form, thepatient's mood is kept stable throughout the day.When prescribing it is important to specify the

strength required: Strength No. i contains io mg.' Dexedrine ' and 65 mg. amylobarbitone; StrengthNo. 2 contains 15 mg. 'Dexedrine' and 97 mg.amylobarbitone. Both strengths are available incontainers of 30 capsules.

Bibliorrabhv continued from tpae Io0-7. F. Goodwin, M.D., M.R.C.P.BALL, K. (x9S4), Lancet, i, Ix62.BELL, A. L. L., Jr., SMITH, C. N. and ANDREAE, E. (x955),

Amer. 7. Med., 18, 536.BELT, T. H. (I939), Brit. Heart J., I, 283.BESTERMAN, E. M. M. (i9Si), Brit. med. Y., ii, 205.BORDLEY, J. E., CAREY, R. A., HARVEY, A. M., HOWARD,

J. E., KATTUS, A. A., NEWMAN, E. V. and WINKEN-WERDER, W. L. (1949), Bull. Johns Hopk. Hosp., 85, 396.

BOUTOURLINE-YOUNG, H. J. and WHITTENBERGER,J. L. (19s), J. clin. Invest., 30, 838. Brit. med. 7., (x954),ii, 457.

CAMERINI, F., GOODWIN, J. F. and ZOOB, M. (1955), Brit.Heart J., in presq.

COUNIHAN, T. B., EVANS, B. M. and MILNE, M. D. (1954),Clin. Sci., 13, 583.

DALEY, R. (I945), Brit. Heart J., 7, loI.DAVIES, C. E. and McKINNON, J. (I949), Lancet, ii, 883.DAVIES, L. G., GOODWIN, J. F. and VAN LEUVEN, B. D.

(I954), Brit. Heart Y., x6, 440.DONALD, K. W. (I953), Lancet, i, 495.DRESDALE, D. SCHULTZ, M. and MICHTOM, R. J. (X95I),

Amer. J. Mej., Ix, 686.ECKENHOFF, J. E., ELDER, J. D., Jr. and KING, B. D. (1952),

Amer. J. med. Sci., 223, 19I.ELMES, P. C., KNOX, K. and FLETCHER, C. M. (I953),Lancet, ii, 903.FERRER, M. I., HARVEY, R. M., CATHCART, R. T.

WEBSTER, C. A., RICHARDS, D. W., Jr. and COURNAND,A. (x950), Circulation, x, 161.FLETCHER, C. M. (955s), Personal communication.FLINT, F. J. (1954), Lancet, ii, Si.FOWLER, N. O., WESTCOTT, R. N., HAUENSTEIN, V. D.,SCOTT, R. C. and McGUIRE, J. (95so), 7. din. Invest, 29,

1387.GALDSTON, M., WEISENFELD, S., BENJAMIN, B. and

ROSENBLUTH, M. B. (x95x), Amer. .. Med., xo, i66.GANS, B. (x954), Lancet, i, IoIx.GRAY, F. D., Jr., WILLIAMS, M. H., Jr. and GRAY, F. G. (1952),Amer. Heart Y., 44, 57.

HARVEY, R. M., FERRER, M. I. and COURNAND, A. (1953),Circulation, 7, 932.

HARVEY, R. M., FERRER, M. I., RICHARDS, D. W., Jr. andCOURNAND, A. (i951), Amer. J. Med., 10, 719.

HOWARTH, S., McMICHAEL, J. and SHARPEY-SCHAFERE. P. (1947), Clin. Sci., 6, 187.

KILPATRICK, G. S. and OLDHAM, P. D. (1954), Brit. med. J.,ii, 385. Lancet (I953), 1i, 976.

McMICHAEL, J. (I948), Edinb. med. J., 55, 65.MAY, J. R. (i953), Lancet, ii, 899.MOUNSEY, J. P. D., RITZMANN, L. W. and SELVERSTONE,

N. J. (1952), Brit. Heart 7., 14, 442.MOUNSEY, J. P. D., RITZMANN, L. W., SELVERSTONE,

N. J., BRISCOE, W. A. and McLEMORE, G. A. (1952),Ibid., 14, I53.

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WESTLAKE, E. K. (1954), Brit. med. J., ii, 1012.WESTLAKE, E. K. and KAYE, M. (I954), Ibid., 1, 302.WESTLAKE, E. K., SIMPSON, T. and KAYE, M. (x955), Quart.

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