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PREGNANCY AND RHEUMATICHEART DISEASEBy SAMUEL ORAM, M.D., F.R.C.P.

Physician, King's College Hospital; Cardiologist, Croydon Group of Hospitals

There is no doubt that of all branches ofcardiology the effect of pregnancy upon rheumaticheart disease is the one concerning which thereis most discrepancy in the literature. There areseveral reasons for this difference of opinionamong cardiologists, the chief of which are ourincomplete knowledge of the effect of pregnancyon the normal heart, the difficulty in distinguishingcardiovascular signs resulting from normal preg-nancy from those due to early cardiac disease, andthe fact that abnormal physical signs are prone tobecome either more or less obvious as pregnancyprogresses. In addition, other inherent difficultiesare encountered as soon as one attempts to studythe effect of pregnancy on the diseased heart. Themost serious source of error is the tendency forauthors to deduce too. much from too few cases,and the number of clinics in this country devotedmainly to the study of the pregnant woman withheart disease can be counted on the fingers of onehand. Too rarely is the aid of the statisticiansought. Even where large series of cases aresummated (Julius Jensen, I938), too often thecriteria used by various authors in their diagnosesare slightly different, and for this reason theirresults are not strictly comparable. Anotherdifficulty arises from the different way in which thecardiologist and the obstetrician regard theproblem. The cardiologist considers the preg-nancy as complicating the pre-existing heartdisease, but the obstetrician considers that hispatient's pregnancy is complicated by her cardiaclesion. Another cause for ignorance is that theobstetrician rarely studies his patients once thepuerperium has been successfully passed, and iffurther pregnancies do not ensue he may neversee the patient again. On the other hand, thecardiologist rarely follows the same patient throughseveral pregnancies unless he is particularlyinterested in the subject, and his opportunities forobserving closely the heart in normal pregnancyare few. When one tries to assemble a comparableseries so many variables are discovered that theeffect of any single one acting alone is virtually

imponderable-for example, the increasing age ofthe mother with successive pregnancies, the timeinterval between pregnancies and the medical anddomestic facilities available before, during andafter delivery. Even religious principles are apt toinfluence treatment.

However, in spite of the extent of the problem,of recent years ideas are gradually becomingcrystallized particularly as a result of increasingknowledge of the physiology of the circulationduring normal and abnormal pregnancy.Circulatory Effects of Pregnancy

All investigators agree that the work of theheart is increased during pregnancy and there isalso agreement that this is never so great as tocause failure in the healthy heart. Only thepreviously diseased heart fails in pregnancy. Infact, it is unlikely that pregnancy by itself caninduce failure in a patient with heart disease whensigns of failure are absent at the commencement ofcyesis and when the severity of the heart lesion isnot such as to give rise to failure in a short timein the absence of pregnancy (Evans, 1948).

Provided the cardiac output is moderate thework performed by the heart may, for clinicalpurposes, be taken as roughly proportional to thecardiac output multiplied by the blood pressure.In normal pregnancy the blood pressure changesare slight, but the cardiac output rises considerablyuntil round about the 34th to 36th week, afterwhich time it falls. Cohen and Thomson (1936,I939) were the first to show this and until theirwork it was believed that the cardiac burdenbecame maximal only at term. This increase incardiac output is due to increased volume ofcirculating blood and both plasma and total bloodvolume are increased. Thomson et al. (1938)have shown that the plasma volume increasesprogressively until the ninth lunar month. Theyfound an average increase of 65 per cent. over theaverage normal non-pregnant value. During thetenth lunar month there is a definite decrease, theplasma volume falling by this time to some 50

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February 1956 ORAM: Pregnancy and Rheumatic Heart Disease 77

per cent. above normal. The same workers showedthat the total blood volume shows similar changes,increasing by the ninth lunar month to an averageof 45.5 per cent. above normal and falling by thetenth month to 32.4 per cent. above normal. Thetotal blood cell volume shows slighter changes butthey are of a similar trend. This water retentionin both blood and tissues during pregnancy couldbe accounted for by the considerable salt retentionwhich Chesley (I944) has found to occur duringgestation. From about the 34th to 36th weekonwards the cardiac output decreases and rapidlyfalls after delivery to reach the normal after thefirst week or two of the puerperium. The averageincrease in cardiac output is, according to Standerand Cadden (1932), 40 to' 50 per cent. of the non-pregnant output. This increase in cardiac outputcan be achieved by either an increase in strokevolume or in heart rate or both. As the increase instroke volume is less than the increase in minutevolume there must also be an increase in heart ratein pregnancy. Although the increase in cardiacoutput enables augmentation in blood flow throughthe uterus without depletion of the other organs,the exact mechanism responsible for the increasein output is still not clear. Burwell (1938) hasfound that the increase is greater than can beaccounted for by the augmented oxygen con-sumption, for the arteriovenous oxygen differenceis decreased. He has advanced the ingenioustheory that in pregnancy the placenta, with itswide shunts connecting the arterial and venoussides of the circulation, acts like an arteriovenousfistula, and in support of this is the so-called' hyperkinetic syndrome' (Harrison, 1935) whichis commonly shown during normal pregnancy,namely the vigorous apex beat, loud first sound atthe apex, with or without a systolic murmur,flushed skin, collapsing pulse, capillary pulsation,tachycardia, distended cervical and superficialchest and abdominal veins, loud pulmonary secondsound and third heart sound. It will be obviousfrom the above that from the 34th to 36th weekonwards the cardiac status of the pregnant womanis likely to improve. There are, however, otherfactors which lead either directly or indirectly toan increase in cardiac work, the most important ofwhich is a general increase in body weight. How-ever, this is not such an important factor as hasbeen claimed and even from the I2th week onwardsit can be shown that the cardiac output is beginningto increase. Clinically, too, it is well recognizedthat death of the foetus may greatly relieve themother's heart failure although the foetus remainsin utero.The dyspnoea of pregnancy is not, as was

previously thought, due to a decrease in vitalcapacity. In fact, Thomson and Cohen (1938)

have shown that the vital capacity increasesslightly, and this increase may reach some 12 percent. Although the mechanical effect of theenlarging uterus is to cause a 'splinting' effecton the lower ribs by pressure forwards against thesubcostal angle, the actual intrathoracic volumemay increase during pregnancy-the subcostalangle progressively increases, the chest circum-ference increases, the transverse and antero-posterior chest diameters increase and although thelong diameter of the chest during quiet respirationis decreased the diaphragm can be seen under thescreen to be quite capable of normal exertion.There is no evidence that the diaphragm is pushedupwards by the fundus of the uterus. Dyspnoeadepends largely on the ratio between the vitalcapacity and the pulmonary ventilation. A largeincrease in pulmonary ventilation with only arelatively slight increase in vital capacity wouldlead to dyspnoea, and this is precisely what occursin pregnancy. According to Anthony and Hansen(I933) the pulmonary ventilation in pregnancyincreases on the average by 57 per cent. Of coursein pregnant patients with heart failure the respira-tory reserve is reduced in two ways-by an increasein the resting ventilation due to the pregnancy anda decrease in the vital capacity due to the heartdisease.

Assessing the PatientAs seen by the author the assessment of a

pregnant woman suspected of heart disease resolvesitself into four separate problems. The first is toestablish as early as possible whether heart diseaseis, in fact, present. If this is confirmed then thesecond problem is to consider the risks to thepatient during pregnancy and soon after. If theserisks warrant continuation of the pregnancy, thethird question to be decided is the management ofthe case during pregnancy, labour and puerperium.Finally, after the child has been born, the remoteoutlook for the mother must be considered beforefurther pregnancies are undertaken.

The Diagnosis of Heart Disease DuringPregnancy

So closely may the signs and symptoms referableto the cardiovascular system during normal preg-nancy simulate those arising as a result of cardiacdisease that Hamilton and Thomson (I94i) havesuggested the category of' possible heart disease 'for patients in whom doubt still exists aftercareful examination. These should be observedclosely during pregnancy in exactly the same wayas are patients known to have heart disease andthey should be delivered in hospital. Fortunatelythe majority of pregnant women referred to the

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78 POSTGRADUATE MEDICAL JOURNAL February 1956

cardiologist for opinion concerning the possibilityof heart disease have healthy hearts.

Marshall (x949) has shown that only some 40per cent. of pregnant women with heart diseasehave symptoms before pregnancy and some mayhave up to five children before any symptoms oftheir heart disease appear.Of 485 pregnant women with heart disease

studied by Morgan Jones (I95I) 90 per cent. hadrheumatic heart disease.

Dyspnoea. Normal pregnancy can give rise toincreasing dyspnoea on effort and later even toorthopnoea because of the increase in pulmonaryventilation. Towards the sixth month of preg-nancy slight exertional dyspnoea is the rule, butit never becomes such that the woman is unableto attend to her housework. On the other handsome patients with damaged hearts can walk longdistances without respiratory distress. Dyspnoeaof any extent appearing before the sixth monthshould raise a suspicion that a pathological lesionis responsible for it although not necessasilycardiac. In a multipara the story that the breath-lessness is much worse than in previous pregnanciesis ominous if other causes of dyspnoea which canalso be effective in the non-pregnant are excluded,and mechanical causes associated with the preg-nancy, such as hydramnios or twins, can be ruledout. A syndrome that is little known and wasfirst described by Hamilton and Thomson(1941) is that of 'pseudo-paroxysmal nocturnaldyspnoea.' These patients are awakened byattacks of choking with respiratory distress andpalpitation, and the picture can closely simulatethat of failure of the left ventricle, although theprognosis is excellent.

According to Thomson and Cohen (I938) adecrease of vital capacity of 15 per cent. or more,or a continued decrease from month to month ofIo per cent. or more, is a sign of impending heartfailure in the pregnant patient with a cardiaclesion.

Oedema. Swelling of the ankles is so commonin pregnancy, particularly towards the end, that itis only of value as evidence of heart disease if othersigns are present. If the oedema is more than atrace then, if it is due to heart failure, obviouslyabnormal physical signs will be found in the heart.Slight oedema of the ankles in early pregnancy isprobably due to the fluid retention which takesplace, perhaps combined with excessive standing,and this is usually most noticeable in hot weather.The oedema may be contributed to in pregnancyby varicose veins, anaemia or flat feet. A trace ofoedema of the hands and face can occur in normalpregnancy.

Basal crepitations. The presence of moistsounds at the lung bases is of extreme importance.

They should be diligently searched for at everyvisit. They are not uncommon in normal preg-nancy especially at the right base, but if they donot disappear after a few deep breaths, or a coughor two, they must be regarded as a sign of pul-monary congestion from heart failure. All suchpatients are immediately fluoroscoped, when thetypical hilar congestion or, sometimes 'ground-glass' appearance of pulmonary oedema will beseen.

Distension of the cervical veins. Mackenziehimself (I92I) first drew attention to the frequencyofjugular vein pulsation during healthy pregnancy.Causation still remains obscure.

Cyanosis. This never occurs during normalpregnancy, although many subjects do developduskiness of the face and dark red lips during thesecond stage of labour.

Hepatic engorgement. Unfortunately, the en-larged uterus during the later months is apt torender palpation of the liver difficult, but the liveris never enlarged or tender as a result of normalpregnancy, and when present is a valuable sign ofearly failure of the right side of the heart.

Haemoptysis. The respiratory embarrassmentof normal pregnancy never gives rise to bloodspitting. All 2I examples of haemoptysis duringpregnancy were found by Bramwell and Longson(1938) to be due to mitral stenosis, although threehad also aortic valve disease and two had auricularfibrillation.

The pulse. Provided other causes of tachycardiahave been eliminated, it can be taken as a clinicalrule that a pulse rate of Ioo or more, persisting inspite of rest, is suggestive of cardiac embarrass-ment although not necessarily of organic heartdisease. The pulse during normal pregnancy isoften somewhat collapsing in character owing to aslight fall in the diastolic pressure rather than anincrease in the systolic, and similarly, in theso-called hyperkinetic patient, capillary pulsationmay be present. Extrasystoles may make them-selves unpleasantly obvious for the first timeduring pregnancy and, in fact, were present inone-half of Mackenzie's series of healthy preg-nancies. On the other hand, extrasystoles whichhave been conspicuous previously may disappearduring pregnancy. Paroxysmal tachycardia, ofsupraventricular type, is commonly found inpregnancy and does not increase the risk. Itshould not be treated by quinidine because of itsoxytocic effect. Pregnancy itself does not giverise to auricular fibrillation or flutter.

Fainting attacks. Transient giddiness duringpregnancy is not uncommon and brief loss ofconsciousness may be associated. Some of thesecases are hypotensive. Advanced aortic incom-petence may lead to fainting, and Naish (I937) is

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February I956 ORAM: Pregnancy and Rheumatic Heart Disease 79

TABLE ICOMPARISON OF THE PHYSICAL SIGNS OF THE NORMAL HEART IN PREGNANCY WITH THOSE OF MITRAL VALVE DISEASE

Normal heart in pregnancy Mitral valve disease

SimilaritiesApex beat .. .. .. .. Sudden; displaced to left Sudden in M.S.; displaced to leftFirst sound at apex .. .. Loud Loud in M.S.Third sound .. .. .. Present commonly Present commonly in M.I.Pulmonary second sound .. Loud and split often Loud and split oftenApical murmur .. .. .. Pansystolic or late Pansystolic or late in M.I.Extrasystoles .... .. Frequent Frequent; may presage auricular

fibrillationDistension of cervical veins .. Commonly present Present if failureOedema of ankles .. Commonly present Present if failureRadiology:

(i) Left auricular curve .. Exaggerated Exaggerated but comma shaped(ii) Pulmonary artery .. Straight or convex Straight or convex(iii) Hilar shadows .. .. Exaggerated Exaggerated if failure

DifferencesApex beat .. .. .. .. Never left ventricular type Left ventricular type in M.I.Presystolic murmur .. .. Absent; but loud, split first sound may M.S. only

closely simulateSystolic apical murmur .. Never accompanied by a thrill Thrill may be present in M.I.Middiastolic murmur .. .. Absent; but third sound may simulate M.S. loud and long. M.I. shorter and

softerOpening snap of mitral valve .. Absent; but loud, split pulmonary Present often in M.S.

second sound may simulateBasal lung crepitations .. Never persistent Present if failureAuricular fibrillation .. Absent May be presentSystolic expansion of left auricle Absent Present in M.I.

of the opinion that the fainting in these casesheralds failure.

Auscultatory cardiac signs. The physiologicalalteration of the auscultatory signs as a result ofpregnancy often produces great difficulty indistinguishing the normal heart in pregnancy fromthat of mitral stenosis. This difficulty is so greatthat at times one cannot confidently exclude mitralstenosis during the tenure of the pregnancy (seeTable i). In both conditions the first sound isloud and in pregnancy splitting of the first soundis common and may be mistaken for a shortpresystolic murmur. The physiological third soundis so common in pregnancy and, particularly if it israther blurred, may closely resemble the mid-diastolic murmur of mitral valve disease. Thepulmonary second sound is commonly accentuatedand split in both pregnancy and mitral stenosis.The accentuation of it is said to be greatest duringthe third trimester. The systolic apical murmurwhich appears during pregnancy can be sufficientlylong and loud to simulate mitral incompetence.

Gammeltoft (1928) originally described amurmur at the pulmonary area which has becometo be considered so characteristic of pregnancy byJensen (1938) that he refers to it as the gestatorymurmur. It is best heard in the second and thirdintercostal spaces close to the left of the sternumand may be so loud that pericardial friction issuggested. It is louder with the patient supine and

tends to become softer on deep inspiration. It iscommon between the fourth and fifth months andmay vary strikingly from week to week. AlthoughLandt and Benjamin (1936) are of the opinion thatits presence is due to kinking of the pulmonaryartery, there does not seem any convincing radio-logical or other evidence that this is the cause. Tothe author's ear the murmur sounds very like, ifnot identical with, that found in some cases ofthyrotoxicosis. Jensen (1938) has described athrill accompanying it but I have never en-countered one.

Fluoroscopy. Whether the heart hypertrophiesduring pregnancy is still unknown. There isdisappointingly little careful evidence based onactual ventricular weights during and afterpregnancy. Such specimens are, of course, veryhard to obtain. Radiological evidence is equivocalbut there is no doubt that the heart does appear tobecome a little larger radiologically duringpregnancy and can closely simulate the silhouettefound in mitral stenosis. Gammeltoft (1928)showed that the heart increased in both thelongitudinal and transverse diameters even as earlyas the fourth month before pressure by thediaphragm on the heart could play a part. Laterin pregnancy the displaced heart may be sufficientto move the apex beat an inch beyond the mid-clavicular line and up into the fourth intercostalspace. Sometimes the pulmonary arc becomes

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80 POSTGRADUATE MEDICAL JOURNAL February 1956

prominent giving rise to straightening of the leftborder of the heart and this, coupled with theexaggerated oesophageal curve due to pressure bythe left auricle which is commonly seen in preg-nancy, caused Gerhardt to coin the term'mitralshape without mitral lesion.' This exaggeration ofthe normal slight curve in the oesophagram due tothe impression of the left auricle occurred in Io ofi8 cases of Hollander and Crawford (1943). Theyattributed it to an increase in the size of the heartas a result of the increased blood it contains, butin my experience no diagnostic difficulty arisesuntil the heart is being pressed on from below andthe exaggeration of the curve can be reduced bygetting the patient to breathe in. Towards the endof normal pregnancy the hilar markings may be soextensive as to be mistaken for abnormal pul-monary congestion-a trap emphasized byHamilton and Thomson (I941).

The electrocardiogram. Pardee (1922) was thefirst to point out that pregnancy sometimes givesrise to a deep Q wave and inversion of the T wavein stanlard lead III. This appearance may resembleposterior cardiac infarction but in pregnancythe P wave in lead III is often inverted too,unlike in infarction. If any doubt exists unipolarlead VF taken from the left leg will settle thematter. Fortunately the problem rarely arises-Campbell (1947) cannot remember having seen apatient with angina become pregnant and Bram-well (1938) is of similar opinion concerning itsrarity. This so-called ' Q3 T3' appearance isprobably due to cardiac displacement.The Risks During and Shortly AfterPregnancy

Limitation of activity. Of recent years emphasishas shifted more and more away from the actuallesion present and towards the recognition of thegreat importance of judging the likely outcomeduring pregnancy from a simple knowledge of thedegree of activity which the patient can achieve.It is one of the first duties of the cardiologist toplace his patient in one of the four categoriessuggested by the New York Heart Association(I939). Class I consists of patients who have nolimitation of activity on considerable exertion;Class II (a) have their activity slightly limited andClass II (b) greatly so; Class III patients arelargely or entirely bed-ridden. The value of thisclassification was strikingly brought out by Jensen(1938). He collated the figures from nine differentcardiac centres and found that the mortality inClasses I and II (a) was less than i per cent., butin Class II (b) it rose to over 5 per cent. and inClass III it shot up to 23 per cent. Haig andGilchrist (1949), as a result of 20 years' experienceof the application of this method of classification,are enthusiastic about its great value.

However, notwithstanding the undisputed valueof this simple classification there is a type ofpatient, usually young, who although classifiablein Class I when first seen may for the first timeever have a sudden attack of acute pulmonaryoedema which appears to come out of the blue andunfortunately the first attack may prove fatal. Sheis almost always in normal rhythm and the overallsize of the heart is little, if at all, enlarged, althoughat autopsy the left auricle is usually found to beseverely hypertrophied (Bramwell and Jones,I944). However, the right ventricular hyper-trophy, which is invariably present, may beconfirmed by the electrocardiogram. It is in thisgroup of patients especially that routine fluoro-scopy may forewarn the cardiologist of impendingdisaster. This acute pulmonary oedema is theand in Morgan Jones' (1951) series was themost important cardiac cause of death. Its treat-ment is described below. According to Bramwelland Jones (i944) a history of haemoptysis,especially if associated with paroxysmal dypsnoea,implies a liability to acute pulmonary oedema.These attacks are apt to appear at about the middlestage of pregnancy and have been attributed toacute left auricular failure by Bramwell and Jones(1944).

Presence offailure. A history of heart failure atany time prior to pregnancy is considered bymany to be a contraindication to further preg-nancies and sufficient justification for interruptingan existing one as soon as the failure has beentreated adequately. Twenty-six of Bramwell's(1938) patients had congestive heart failure whenfirst seen and of these ten died prior to or soonafter confinement and four others died within thenext six years. The French in particular are of theopinion that congestive failure in pregnancyadvances much faster than otherwise (ils bralentles itapes) but there is no convincing evidence tosupport this idea.

Congestive failure is a factor in about three-quarters of deaths of patients with heart disease.A large proportion of the remainder die frompulmonary causes, including pulmonary oedemaand infarction, themselves a result of failure.Sometimes ' cardiac exhaustion' is the only labelthat one can apply-the patient becomes weak,apathetic, pale and shocked. McKeown (1945,1948) has produced convincing autopsy evidencethat at least some of these ' acute obstetric shock'cases die as a result of unsuspected rheumaticcarditis even in a heart which is not the site of amechanical lesion.

The 'urgency admission.' It is perhaps notsurprising that it is among the urgency admissionsto hospital that the highest mortality is found;14 out of 25 deaths in Bramwell's (1938) series

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February 1956 ORAM: Pregnancy and Rheumatic Heart Disease

were urgency admissions whereas only 1i of 325cases who had been under observation in theantenatal clinic succumbed, a striking testimonyto the value of such supervision. Of Marshall's(1949) fatal cases in Belfast 46.5 per cent. occurredamong the 43 emergency admissions.

The cardiac rhythm. The only common seriousabnormality of rhythm is auricular fibrillation. OfBramwell and Longson's (1938) 24 cases sevendied. After carefully following up their cases theyconcluded that the presence of fibrillation,although undoubtedly adding considerably to therisk, did not constitute the absolute bar to preg-nancy that Mackenzie (1921) considered it to be.In fact, as Mackenzie himself said, no single signshown by the heart itself, however abnormal itmay seem, should be a bar to pregnancy.Age and social class of mother and number and

spacing of pregnancies. An important cause ofbreakdown is inadequate rest which accompaniespregnancy and the puerperium. Hamilton andThomson (i941) state that after the age of 35 therisk of pregnancy rises steeply. Labour is apt tobe prolonged and the lesions are usually becomingmore severe. There is no doubt, too, that after thefirst pregnancy the risk rises steeply. It is usuallyaccepted that an interval of at least two years isdesirable between pregnancies but Hamilton andThomson (I94i) think that a year is adequate. Inso far as a child of one year needs closer attentionfrom the mother than a child of two or more, itseems to the author that much is to be gained bywaiting the longer period. Haig and Gilchrist(1949) have recently published their follow-upresults of two consecutive pregnancies in 169women. Their figures show that a woman whoattains Class II (b) or III in one pregnancy willdo so again in the next. Even in Classes I andII (a) there is a definite downward tendency; forexample, 50 per cent. of those women who wereClass I in the preceding pregnancy were ClassII (a) in the next. Ten per cent. advanced fromClass I to Class III but in each of these 12 yearsor more had elapsed between the two consecutivepregnancies.

The cardiac lesion and size. The commonestdisease is mitral stenosis which accounts for aboutthree-quarters of all cases. The addition of anaortic lesion to the mitral does not, in itself,influence the outlook (Harris, 1937). Although ingeneral it is true that the larger the heart the greaterthe risk (Hunt, 1926), it will be remembered that inmitral stenosis fatal acute pulmonary oedema canoccur associated with a heart which is little, if atall, enlarged.

Subacute bacterial endocarditis is a small butdefinite risk during pregnancy occurring in I percent. of cases.

Antenatal Management and Conduct ofLabour and PuerperiumThe frequency with which the patient is seen

antenatally will naturally vary according to theseverity of her lesion and her progress, but as arule she will be seen each month for the first sixmonths, fortnightly for the next two months andthen weekly until two weeks before the expecteddate of delivery, at which time she should beadmitted to hospital. The strain of travelling forso many attendances is considerable, especially inwinter months, and exposure to respiratory andother infections attendant upon a prolonged waitin a crowded out-patient department should bereduced to an absolute minimum. The days ofattendance of the cardiologist and obstetricianshould be made to coincide. At her first visit sheis introduced to the almoner and the most im-portant function of the latter is to see that sufficienthelp in the house is provided. She is instructed toretire to bed should a cold develop. In any but themost trivial respiratory or other infection thepatient should be admitted to hospital for rest andtreatment as even comparatively slight infectionscan precipitate failure during pregnancy (Oppel,1940).

It is difficult to lay down hard and fast rulesconcerning rest but at least ten hours in bed atnight and a rest of two hours in the afternoonis advised. The patient is admitted to hospital forrest in bed two weeks before her expected date ofdelivery.

. The usual dental care, including attention to thegums, is especially important during pregnancy inview of the slight risk of subacute bacterial endo-carditis. Of the usual vitamin requirements duringpregnancy the vitamin B complex is particularlyimportant in heart-failure patients. It is alsoimportant to watch for anaemia in heart patientsand, if treatment is urgent, parenteral iron ispreferable.

In addition to the usual routine clinical examina-tion cardioscopy is performed at every visit. Ifthis is omitted hilar congestion due to early heartfailure will be missed.

If, in spite of these measures, heart failuresupervenes, the patient should be admitted tohospital and the subsequent management thendepends upon whether the failure has come onearly or late in pregnancy.There are no absolute indications to terminate

pregnancy although one or two are so strong that ifthey are present there must be considerablejustification before continuation of pregnancy iscondoned. The indications are based on what hasalready been said above concerning the assessmentof the risks involved, but for convenience they canbe reconsidered as conditions which almost always

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TABLE 2

SUMMARY OF PRACTICAL MANAGEMENT OF PREGNANT PATIENTS IN HEART FAILURE

Degree orStage of progress of Primipara Multipara

pregnancy failure

Procedure Method Procedure Method

Proceed to term Natural labour Terminate (with VaginalSlight few exceptions)

Up to 14th week Considervalvotomy

Severe Terminate Vaginal Terminate VaginalProceed to term Natural labour Proceed to term Natural labour

Improvement Consider Consider ConsiderFrom 14th to 36th valvotomy valvotomy inductionweek

Deterioration Terminate as Abdominal Terminate as last Abdominallast resort hysterotomy resort hysterotomy

Improvement Proceed to term Natural labour Proceed to term Natural labourConsider induction

From 36th weekonwards Deterioration Terminate .Caesarian Terminate Caesarian

(rarely section (rarely sectionrequired) required)

indicate interruption of pregnancy and those whichdo so less commonly.Of recent years it has been shown that in some

patients mitral valvotomy can be offered as analternative to therapeutic abortion. Valvotomy istolerated surprisingly well during pregnancy byboth mother and foetus. In the author's view theoperation is practically only indicated in thosepatients prone to attacks of acute pulmonaryoedema. If this is the patient's first pregnancyvalvotomy may be indicated at any stage exceptduring the last few weeks, when her conditionalmost certainly will improve, but if the patientalready has children and is in failure when firstseen early in pregnancy it is probably better toterminate her as soon as the failure has beencleared up. If a multipara is so late in pregnancythat vaginal termination is not then feasible shecan be considered for valvotomy (see Table 2).The treatment of a case of acute pulmonary

oedema consists of attempting to lower the pul-monary hypertension by diminishing the venousreturn to the heart and of improving the diastolicfilling of the left ventricle by reducing the tachy-cardia which is usually, in part at least, of nervousorigin. A clear airway must also be maintained.These objects are achieved by allaying the patient'sanxiety with morphine, propping her upright in asitting position preferably with her legs dependentover the edge of the bed (ideally in a cardiac bed),venesecting a pint rapidly or placing cuffs roundthe thighs and maintaining them at a pressure of

50 mm. Hg, giving intravenously i mg. of ouabaineand 0.48 g. of theophylline ethylene-diamine. Therespiratory passages are kept clear of frothymucousby means of a mechanical aspirator and oxygen isadministered by a light plastic mask (BritishOxygen Company). A regime of fluid and sodiumrestriction and a mercurial diuretic is then started.

Conditions in which Therapeutic Abortion isStrongly Indicated

i. Those patients with a history of paroxysmalnocturnal dyspnoea due to acute pulmonaryoedema. The alternative, however, for somepatients is valvotomy. These patients often seemdeceptively well between attacks and the decisionbetween valvotomy and termination of the preg-nancy is a most difficult one and is discussed above.

2. Patients largely or entirely bedridden as aresult of heart failure (Class III of the New YorkHeart Association, I939). In addition to the riskto the mother there is a strong possibility that she.will not have a live baby. It is essential to treat theheart failure before the pregnancy is terminated,but unfortunately in this type of patient often thefailure only partly responds to treatment and thedecision as to the optimum moment to interruptpregnancy is difficult and is made in close consulta-tion with the obstetrician. If this patient isallowed to continue pregnancy it must be realizedthat the mortality is nearly one in four.

3. In patients greatly limited by heart diseasethe mortality is about 5 per cent. (Class II (b) of

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February 1956 ORAM: Pregnancy and Rheumatic Heart Disease 83the New York Heart Association). If pregnancy isfar advanced when the patient is first seen it issometimes possible to coax these patients throughthe remainder of their pregnancy and this may bejustified when both parents are very anxious thatit should be attempted.

4. However slight the heart failure is to beginwith if it progresses in spite of treatment in bedtermination is indicated.

Conditions Calling for Serious Considerationof Termination of Pregnancy

I. The ' urgency admission.' These patientsaccount for one-half of the total deaths of cardiacpatients during pregnancy (Bramwell, 1938). Thefailure must, of course, be treated prior totermination.

2. A past history of failure is unfavourable butnot, in the author's opinion, an absolute indicationto terminate pregnancy.

3. Auricular fibrillation in itself does not con-stitute an absolute bar but certainly warrantsserious consideration.

4. If the patient is over 35 when she first be-comes pregnant she is a poor risk and after thethird pregnancy in a cardiac patient the risk risessteeply whatever the age. It is especially in suchpatients that the availability of domestic help is ofsuch vital importance.Failure in Early Pregnancy up to the I4thWeek

If the failure is slight and the patient is a primi-para the failure should be treated in the usualmanner, including the use of mercurial diureticsintramuscularly if required, and the patient allowedto proceed with the pregnancy, but if the failure ismore than slight termination is the better course.If it is a multipara who is in failure then termina-tion is best advised but an exception might beconsidered when the failure is slight and bothparents are very anxious to have a child.The methods of interrupting pregnancy at this

stage are vaginal termination followed by contra-ceptive instruction or abdominal hysterotomy andsterilization at the same time.

It is essential to realize that termination must becarried out only after first treating the heart failureintensively.Failure Between the x4th and 35th to 36thWeek ofPregnancyWhether primiparae or multiparae the decision

to interfere surgically is deferred until the failureis treated. If the failure improves the patient isallowed to proceed to term and valvotomy may beconsidered. She should be sterilized at the endof the third week of puerperium. If the failure

increases in spite of treatment abdominal hyster-otomy will be required but the patient is by then avery poor risk indeed. If the failure responds totreatment Caesarean section is unnecessary and, asthere is a minimal mortality from this operation ofi per cent., it is never justified to carry it outmerely to permit sterilization at the same time.

Induction of labour has no place in the treat-Inent of primiparas with heart disease and verylittle, if any, place in the treatment of multiparae.Failure from the 35th to 36th Week OnwardsAs it is known that from about the 36th week

her condition is very likely to improve and thereis a possibility of labour being premature, theobject at this stage is to try and coax the patient toterm. At term, analgesia, episiotomy and, ifnecessary, low forceps should be employed readily.However if failure increases in spite of treatmentand therefore natural labour cannot be awaited,there are only two alternatives, either induction oflabour by rupture of the membranes or Caesareansection. It is the author's view that induction oflabour is never preferable to Caesarean section ifthe patient's condition is deteriorating.Even when Caesarean section is carried out it

must be realized that the mortality rate after thisoperation is at least twice as high as after pelvicdelivery (Gorenberg and McGleary, I941; Hamil-ton and Thomas, 1941; Mendelson, 1944; Haigand Gilchrist, 1949), and there is no doubt that apolicy of' non-intervention' is being employedwith increasing success and the justification forCaesarean section grows less and less. It is bestreserved for those cases who are deterioratingrapidly in spite of careful treatment and who areshowing no signs of going into labour (see Table 2).Conduct of labour. If the patient reaches termin good condition she may be expected to gothrough labour safely. Although it is commonlybelieved that labour is usually short and easy inpatients with heart disease this was not confirmedby Nelson and Eades (1935) nor by Mendelson(1944).During the first stage the patient should con-

serve her strength by resting as much as possibleand if the first stage is prolonged rest betweenpains should be ensured by sedatives such aschloral or pethidine. Sedation is especiallyimportant in mitral stenotics prone to attacks ofpulmonary oedema.

In the second stage there is evidence that theuse of the semi-recumbent position is of valueprophylactically and it should certainly be usedif the patient is dyspnoeic. Strong expulsiveefforts should be reduced as far as possible andmust be prevented by nitrous oxide and oxygen orcyclopropane and oxygen. Caudal anaesthesia has

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84 POSTGRADUATE MEDICAL JOURNAL February 1956

its advocates and episiotomy should be donewithout hesitation. As soon as full dilatation ofthe cervix has occurred forceps can be appliedbut their routine use is unnecessary.The development of pulmonary oedema during

delivery or a few hours post-partum is a dramaticcomplication, especially in mitral stenosis. It isdue to over-filling of the lesser circulation withblood returning in great quantities from theplacental sinuses and from the uterine sinusesafter the placenta has been removed and theuterus has retracted. Treatment has been des-cribed previously. The use of a sandbag acrossthe abdomen or application of a thick pad andbinder after delivery can fulfil little useful purpose.

The puerperium and subsequently. The patient iskept in bed for at least three weeks and until allsigns of failure have gone. Nearly a quarter of allfatalities occur during labour and the 24 hoursfollowing it. Lactation should be avoided onlywhere the mother is so ill that all means must beemployed to conserve her strength.. As Ward(1923) has pointed out, the disturbances entailed inmaking up artificial feeds at night and dealing witha child made more fretful by artificial feeding may'prove more exhausting than lactation.

The Remote OutlookOn first consideration it might be expected that

the strain of repeated pregnancies in a woman withheart disease would ultimately decrease theefficiency of the heart. But the cardiac reserve isnot a fixed quantity, amounts of which are used upuntil it is exhausted. Gilchrist and Murray-Lyon(1933) tried to assess the rate of progression offatal cases of rheumatic heart disease in parouswomen compared with nulliparous females andmales. Allowing for deaths occurring beforemarriageable age the average age at death was:Males, 39.3 years; nulliparae, 42.1; parouswomen, 42.0. Reid's (1934) figures support thiscontention and so do those of Jensen (1949) whostates that the death rate is not increased amongstthose with high parity nor by the occurrence oftwin pregnancy.

BIBLIOGRAPHYANTHONY, A. J., and HANSEN, R. (I933), Ztschr. f. Geburtsch.

v. Gynak, o05, 183.BRAMWELL, C., and JONES, A. M. (I944), Brit. HeartJ., 6, 129.BRAMWELL, C., and LONGSON, E. A. (1938), 'Heart Disease

and Pregnancy,' London, Oxford Medical Publications.BURWELL, C. S., and STRAYHORN, D. (1938), Arch. intern.

Med., 62, 979.CAMPBELL, M. (1947), Guy's Hosp. Gazette, 6i, 169.CHESLEY, L. C. (I944), Amer. J. Obs. Gyn., 48, 565.COHEN, M. E., and THOMSON, K. L. (I936), New Eng. J. Med.,

214, 905.COHEN, M. E., and THOMSON, K. J. (I939), J. Amer. med. Ass.,

112, I556.EVANS, W. (I948), ' Cardiology,' London, Butterworth & Co., Ltd.GAMMELTOFT, S. A. (1928), Surg., Gyn. and Obst., 46, 382.GILCHRIST, A. R., and MURRAY-LYON, R. M. (X933), Edin.

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Soc., p. 55.HAMILTON, B. E., and THOMSON, K. J. (I94I), ' The Heart

in Pregnancy and the Childbearing Age.' Boston, Little, Brown& Co.

HARRIS, K. (i937), Lancet, i, 677.HARRISON, T. R. (I935), ' Failure of the Circulation,' Baltimore,

Williams & Wilkins Co.HOLLANDER, A. G., and CRAWFORD, J. H. (I943), Amer.

Heart Y., 26, 364.HUNT, G. H. (I926), Guy's Hosp. Rep., 6, 135.JENSEN, J. (1938), "The Heart in Pregnancy,' London, H.

Kimpton.JENSEN, J. (I949), Mod. Concepts of Cardiovasc. Dis., 18, 29.LANDT, H., and BENJAMIN, J. E. (1936), Amer. Heart J., I2,

592.MACKENZIE, J. (I92I), ' Heart Disease and Pregnancy,' London,Henry Frowde and Hodder & Stoughton.MARSHALL, R. (1949), 'Heart Disease and Pregnancy: the

Clinical Aspect,' paper read before British Cardiac Society,June.McKEOWN, F. (I945), Ulster med. J., 14, 97.McKEOWN, F. (1948), J. Obst. Gyn. Brit. Emp., 55, 50.MENDELSON, C. L. (1944), Amer. J. Obst. Gyn., 48, 329.MORGAN JONES, A. (I951), 'Heart Disease in Pregnancy,'London, Harvey & Blythe, Ltd.NAISH, F. C. (I937), J. Obst. Gyn. Brit. Emp., 44, 659.NELSON, H. B., and EADES, F. S. (I935), New Eng. J. Med.,

213, 1057.NEW YORK HEART ASSOCIATION (1939), 'Diagnosis of

Diseases of the Heart,' fourth edition, New York.OPPEL, T. W. (1940), Amer. J. Obst. Gyn., 39, 24.PARDEE, H. E. B. (1922), Ibid., 3, 620.REID, W. D. (1934), J. Amer. med. Ass., 103, 889.STANDER, H. J., and CADDEN, J. F. (1932), Amer. J. Obst.

Gyn., 24, 13.THOMSON, K. J., and COHEN, M. E. (I938), Surg. Gyn. and

Obst., 66, 50oi.THOMSON, K. J., HIRSHEIMER, A., GIBSON, J. G., 2nd,and EVANS, W. A. (I938), Amer. J. Obst. Gyn., 36, 48.WARD, E. (1923), Lancet, ii, 557.

BACK NUMBERS OF THE POSTGRADUATE MEDICAL JOURNAL

If any subscribers have copies, in good condition, of JANUARY, FEBRUARY andMARCH 1953, the Fellowship of Postgraduate Medicine, 60 Portland Place, London,

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