ACUTE MYOCARDIAL INFARCTION · TURNER: Acute Myocardial Infarction the picture of shock or pulmonaryoedemadoes not develop noris there subsequent pericarditis, leucocytosis, fever,

POSTGRAD. MED. J. (1964), 40, 393

ACUTE MYOCARDIAL INFARCTIONR. W. D. TURNER, O.B.E., M.A., M.D., F.R.C.P., F.R.C.P.E.

Senior Lecturer in Medicine, University of Edinburgh.Physician, Physician-in-Charge of the Cardiac Department,

Western General Hospital, Edinburgh.

Clinical Features and DiagnosisThe usual history and clinical picture of

acute myoracardial infarction is familiar anddoes not warrant detailed description here.Most often cardiac pain is retrosternal in situ-ation and constricting in character with orwithout radiation to shoulders, arms, throator jaws but there are many variations. Thepain usually comes on suddenly and thenincreases. It may be very severe indeed andas bad as any known to man. Occasionally,despite unequivocal evidence of infarction,there may be no complaint of pain at all. Inthe latter instance pain may be overshadowedby some more impressive manifestation sucha pulmonary cedema or syncope or there maybe retrograde amnesia, but painless infarctionis an established entity. Even when pain is notsevere it is usually described as being veryunpleasant. In some cases there is only a senseof oppression in the chest but whilst describingthe symptoms, the patient may place his handover the upper thorax and perhaps close thefist, thus depicting the diagnosis better thanwords. Rarely pain is felt only over the leftpazecordial region or at the apex of the heartor only peripherally in jaws or wrists.

Occasionally the attack precipitates anarrhythmia which may be the dominant clini-cal finding. Sometimes infarction is heraldedby the sudden onset or excerbation of anginaof effort and the physician is surprised to findelectrocardiographic evidence of old or recentinfarction.

In a severe attack the principle feature maybe shock or, if left ventricular failure hasoccurred, pulmonary cedema.Sometimes at the bedside, objective confirm-

atory evidence that the patient has hadLa heartattack may be found by noting that the jugularvenous pressure is raised or the systemic press-ure is low or that a triple rhythm can be heard.

In most cases an electrocardiogram (ECG),when first recorded, will show the pattern ofinfarction or of acute ischemia, but in some

cases changes will only be evident in serialrecords and occasionally only if special leadsare taken, such as those high up on the leftside of the chest. A full series of precordialleads may be persistently negative in casesof infarction but this is uncommon and in aclinically doubtful case, calls for considerationof other possible causes for pain.

It is, however, important to remember thatcardiac pain may actually be due to a dis-secting aneurysm of the aorta obstructing thecoronary arteries, in which case anticoagulantswill be contraindicated, or to massive pulmo-iiary embolism causing a fall in cardiac outputand acute coronary insufficiency, in which caseanticoagulants may be given or, under parti-cularly favourable circumstances, surgicaltreatment should be considered. Accuracy indiagnosis is therefore important.

rhe following day there may be fever, peri-cardial friction, leucocytosis, a raised sedimen-tation rate or an increase in the serum glutamictransaminase level and urobilinogen mayappear in the urine, any of which help inconfirming a suspected diagnosis.

Breathlessness, sweating or vomiting mayoccur and anxiety is usual.Vomiting on the way to hospital or shortly

after admission is frequently due to a previousinjection of morphine but, as discussed below,this could usually be prevented.Fever

Fever occurs in most cases of severe in-farction and probably arises from the absorptionof necrotic tissue. The temperature usuallyrises within 24 hours of the onset, rarely exceeds1020F., is at its height for 48-72 hours and thensubsides. Persistent fever suggests some com-plication or an error in diagnosis. There is noindication for special treatment. It has beenclaimed that the prognosis is worse in thosewith high fever but undoubtedly exceptionsoccur and there is no close correlation betweenfever and prognosis. The temperature may be

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POSTGRADUATE MEDICAL JOURNAL

subnormal if shock is present despite severeinfarction.LeucocytosisA mild leucocytosis with increase in the

proportion of polymorphs, occurs in manycases of infarction. Usually it develops within48 hours, is maximal about the third day andsubsides by the end of the first week. Thetotal count is not often above 15,000 but maybe very high and in general this reflects theseverity of infarction.Sedimentation Rate

In general the sedimentation rate reflects thedegree of myocardial necrosis and a subsequentfall runs parallel with healing.ElectrocardiographyWhenever possible, electrocardiography

should form part of the routine assessment.This is not of course because an accuratediagnosis is not often possible without it butbecause in its absence the examination is in-complete. The physician may remain inignorance of useful information and some avoid-able errors in diagnosis will be made.

In the differentiation of equivocal cases,positive ECG changes may clinch the diagnosisand negative findings may give added supportin reassuring the patient as to the absence ofevidence for heart disease. It must beemphasized that errors in diagnosis are frequent-ly made.As always ECG changes must be interpreted

in the light of the clinical information. Inparticular it is very helpful to know if therehas been a history of previous infarction, ifsevere hypertension is present or if the patientis on digitalis. Difficulties in interpretation mayarise owing to previous infarction, multipleareas of infarction, bundle branch block,ventricular hypertrophy or ventricular tachy-cardia and changes may be confused with thosedue to pulmonary embolism or pericarditis.

In the majority of patients with acute mvo-cardial infarction there will be unequivocalevidence of necrosis or ischaemia in the firstECG to be recorded after the onset. In someinstances there may be no abnormality althoughdiagnostic changes appear if serial records aretaken. However infarction may undoubtedlyoccur without significant ECG changes even inserial records and it is particularly in this groupthat the estimation of transaminase is of value.

In the days following acute infarction manypatients experience pain arising in the chestwall which may be difficult to distinguish from

further ischaemia and in such instances alsoelectrocardiography is of value.

Serum TransaminaseThe enzyme glutamic oxalo-acetic trans-

aminase (GOT) is widely distributed in manytissues including the heart and is liberatedinto the blood stream as the result of injuryor death of metabolically active cells. Par-ticularly high titres are found after myocardialinfarction and this test is therefore of valuewhen other causes may reasonably be excluded.The normal level of GOT in the serum

(SGOT) ranges from 5 to 40 units. Readingsof 40-50 are borderline and those above 50definitely abnormal. Fortunately the level isnot influenced by meals, anticoagulants orsteroids.

Following acute myocardial infarction thelevel rises after about 6 hours, usually reaches apeak between 24 and 36 hours and graduallyreturns to normal after 3 to 7 days, althoughoccasionally longer. It is therefore importantthat timing should be taken into considerationwhen deciding on the significance of thelaboratory report. Serial readings are oftenrequired. The enzyme is stable up to 4 days,or ,longer if kept cool. Haemolysis must beavoided in collecting the specimen.The estimation of SGOT is also useful when

a patient already under treatment for myo-cardial infarction develops a fresh attack ofpain or some other manifestation compatiblewith extension of the infarct. It is of coursein such cases as this that serial estimationsare of greatest value since there will be a baseline to which changes can be referred. Thetest is also of value when the ECG is equivocalor obscured by previous infarction, ventricularhypertrophy or bundle block and in distinguish-ing between acute coronary insufficiency andactual myocardial infarction.Very high levels (> 500 units) probably

signify associated hepatic necrosis secondaryto the fall in blood pressure. It is noteworthythat shock from any cause may be accompan-ied by high levels .

Acute Coronary InsufficiencyIn some cases cardiac pain is prolonged but

yet there is no evidence of myocardial infarc-tion. This condition is sometimes referred toas "Acute Coronary Insufficiency" on the as-sumption that there is a disparity betweenblood supply and myocardial needs withoutactual necrosis. In such cases the venouspressure is not raised, there is no triple rhythm,

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TURNER: Acute Myocardial Infarction

the picture of shock or pulmonary oedema doesnot develop nor is there subsequent pericarditis,leucocytosis, fever, a raised sedimentation rateor increase in serum transaminase.Sometimes there is a spontaneous onset of

angina without obvious precipitating cause andthis has been referred to as "impending infarc-tion".Although occasional instances of coronary

disease localised to one small vessel occur, itis best to assume that the condition is usuallywidespread, that there is progressive coronaryarterial disease and that the sudden onset ofsymptoms is due to thrombosis, subintimalhemorrhage or protrusion of atheromatousmaterial, with or without actual occlusion of thelumen.

In my experience there are some patientswith clinical features very similar to thosedescribed above as "acute coronary insuffi-ciency" but with minor evidence of myo-cardial necrosis in the form of slight fever orleucocytosis, a mildly raised sedimentation rateor SGOT level and electrocardiographicallythere may be minor abnormalities barely dis-tinguishable from normal but definite changesin serial records.

Clinically and pathologically there is a con-tinuous spectrum and in the early stages atleast, it is unwise to modify treatment on theassumption that there is a different underlyingbasis between cases. In fact, usually there isalmost certainly pathological evidence of myo-cardial necrosis in some degree, either local-ised or focal and diffuse.

Certainly in the individual patient it is adangerous assumption to conclude that acutecoronary insufficiency is a relatively benigndisorder. It is impossible to forecast the out-come and sudden death may occur, so thatin the early days rest in bed with anticoagulanttreatment is the wisest course. However, inview of increasing evidence as to the lack)f value of anticoagulants in the relativelygood risk cases, this initial programme of treat-ment may be modified and it is my ownpractice, having started anticoagulants in allpatients, to reconsider the likely clinical courseafter a few days.

Differential Diagnosis of Myocardial InfarctionThere are a large number of causes for pain

in the chest but few which should give anyreal difficulty in differentiation if sufficient careis taken over the history and physical examin-

ation. The most important are pericarditis,pulmonary embolism, dissecting aneurysm ofthe aorta and upper abdominal disorders.Acute Pericarditis.

Pericarditis, and in particular idiopathic"benign serous" pericarditis, may be respons-ible for severe pain in the chest and has oftenbeen mistaken for myocardial infarction. Radia-tion may occur to the neck, shoulder, left armand back but rarely to the right arm or jaws.A number of points are of assistance in

differential diagnosis. In pericarditis the rubusually appears at the onset whereas it com-monly appears on the second or third day fol-lowing myocardial infarction. In pericarditispain is more influenced by respiration andposture. Shock is more likely to indicate myo-cardial infarction but occasionally a profoundfall in pressure may occur with pericarditis.Arrhythmias or defects of conduction suggestinfarction.

Unfortunately ECG changes are non-specific and variable. Characteristically, inacute pericarditis the ST segments are elevatedwith upward concavity in limb and precordialleads and there is subsequent inversion of theT waves. There is no change in the QRScomplex. In myocardial infarction there isoften reciprocal ST displacement in standardleads 1-3 and in leads recorded over the rightand ileft ventricles, with an upward convexityin the elevated segments, and often also changssin QRS. When pericarditis complicates myo-cardial infarction Q waves are almost alwayspresent. Sometimes, however, there may be nochange and similar patterns may occur in eithercondition. Even serial records do not alwayshelp.

Radiographically there may be no changeor there may be apparent enlargement of thecardiac outline in either condition. There maybe general impairment of pulsation in peri-carditis and local impairment in infarction,local pulmonary infiltrations in acute pericard-itis and pulmonary cedema in infarction.

Myocardial infarction may of course beassociated with pericardial friction. It mustalso be remembered that bouts of pericarditisand pleurisy occasionalily occur during conva-lescence from myocardial infarction as des-cribed below.Pulmonary Embolism.The distinction between myocardial infarc-

tion and massive pulmonary embolism is not

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always easy and the two conditions may bealmost identical. Pulmonary embolism is mostlikely to occur after surgical operations, frac-tures, parturition, thrombophlebitis or the onsetof atrial fibrillation. It may follow enforcedrest in bed in the elderly and sometimes appears"6out of the blue" even in an ambulant patient.It is a frequent complication of cardiac failure.

In pulmonary embolism, breathlessness isusually more prominent than pain, and even ifpain is severe it is unlikely to radiate as inmyocardial infarction. The venous pressure isoften elevated at the onset and peripheralcyanosis may be intense. Shock or triplerhythm may occur in either condition. In pul-monary embolism dilatation of the pulmonaryartery may be visible and palpable to the leftof the sternum and the pulmonary second soundmay be accentuated.

Electrocardiography may be of value in dif-ferentiation. In massive pulmonary embolismthe signs are those of clockwise rotation andright ventricular dilatation, that is, right axisdeviation, a shift of the transitional zone to theleft in precordial leads, inverted T waves overthe right ventricle and incomplete right bundlebranch block. ECG changes are usually moretransient with pulmonary embolism than withmyocardial ischaemia but may persist for aweek or two. In less severe cases the ECGwill be unaffected. Sometimes ECG changesdevelop from secondary myocardial ischamiadue to coronary insufficiency and in the earlydays only be evident in left ventricular leads.

Estimation of serum transaminase may beof assistance.Pulmonary embolism may be followed by

hemoptysis, pleural pain or pleural effusion.Myocardial infarction, of course, is itself notinfrequently complicated by pulmonary embo-lism and infarction.Dissecting Aneurysm of the Aorta.

Dissecting aneurysm of the aorta may alsobe difficult to distinguish from myocardial in-farction. Pain in the chest may be similarbut tends to be more sudden in onset with animmediate, devastating, tearing quality andmore widespread radiation to the back, neck,epigastrium or lower limbs. Bizarre manifesta-tions may appear, such as parnsthesix, paralysisof a limb, loss of vision, dysphagia, abdominalpain, changes in the pulses or a difference inblood pressure in the two arms.The development of an early diastolic mur-

mur from aortic incompetence secondary todilatation of the valve ring is a very character-

istic sign. Jaundice may follow from absorp-tion of blood.

Radiography is not always practical butmay show progressive dilatation of the aorta.Electrocardiography may be helpful in notshowing signs of myocardial infarction butsometimes there are non-specific ischeemicchanges and occasionally the pattern of myo-cardial infarction is present from compressionof the coronary arteries by downward dissectionof the aneurysm.Acute Abdominal Emergencies

Perforation of a peptic ulcer, acute chole-cystitis and pancreatitis may all give rise tohigh epigastric or low retrosternal pain andhave been mistaken for myocardial infarctionbut careful attention to the history and physicalexamination, together with electrocardiography,should serve to differentiate these conditionswhich will not therefore be described here.

TREATMENT OF MYOCARDIALINFARCTION

The immediate treatment of myocardialinfarction consists in the alleviation of pain,restlessness and anxiety and the provision ofadequate nursing care. Later, treatment maybe required for shock, cardiac failure or othercomplications. Subsequent arrangements mustbe made for convalescence and, in most cases,a gradual return to normal activity.

Pain, restlessness and anxiety are all bestrelieved by an injection of morphine. If symp-toms are severe this drug should be given intra-venously. In any case, absorption is morerapid after intramuscular than subcutaneousinjection. 15-30 mg. (i to j grain) shouild begiven and can be repeated, if necessary, withinhalf an hour.

If symptoms are mild there is no indicationfor morphine and it is better withheld. A seda-tive, such as amytal, or a milder analgesic suchas tab. codeine co., will suffice in such cases.

In view of the strong tendency for vomitingto be induced by morphine, especially inpatients with myocardial infarction, and theobvious undesirability of this complication,morphine should never be given alone. It maybe combined with an injection of atropine, orhyoscine or an anti-histamine such as cyclizine.

In many cases vomiting can be avoided bygiving a tablet of cyclizine 15 minutes beforethe injection.Removal to HospitalTreatment at home is difficult unless ade-

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quate nursing facilities are available. Relativeswill naturally be concerned over many detailsand much is left to chance. It is a compro-mise on which patient, doctor and family mustdecide together, but I have no doubt that, onbalance, after the first few hours, and exceptfor those too ill to move, the acute stage is bestmanaged in hospital.

In any case no patient should be "rushedto hospital" within the first twenty-four hoursfor the sake of anticoagulant treatment. Thisis the period of greatest danger to life andan uncomfortable ambulance journey with thepsychological upset of sudden, and perhapscold, nocturnal change to a strange environ-ment can only be detrimental. If desired, itis perfectly safe to initiate anticoagulant treat-ment without laboratory control, as discussedbelow.

Treatment in hospital is relatively easy.There will be a standard regime modified toindividual needs, but one with which the staffare famiiliar and into which most patientsreadily fit. Standard observations can be madeat regular intervals and emergency measures areready to hand by day and night.Rest in BedMany physicians still adhere to the traditional

six weeks' rule. In my opinion, this is unneces-sarily long for most patients and a fixed periodfor cases of varying severity is illogical. Bycontrast, some physicians now get theirpatients up into a chair within a day or twoof the onset. However, a period of three weeksin bed is probably advisable for most casesof average severity. In mild cases and forthose who feel really well, sitting in a chairby the hospital bedside or in the same room,may soon be permitted for part of the day.

Initial rest, with resultant decrease in cardiacwork, seems logical in order to allow time fora damaged myocardium to commence healingand to cover the period during which compli-cations are most frequent.For severely ill patients a longer period will,

of course,- be required. Too early ambulationmay encourage the patient to take liberties.Too long in bed will engender anxiety andintrospection.

Three weeks not only gives initial rest butimpresses on the patient that there has beenan illness of moderate but obviously not ofgreat severity. He will appreciate that a returnto work within a reasonable period is likelyto be the reward of taking advice but thatthere may have to be some reduction in overall

activities. He will realise that there may besome price to pay for health but this is notexcessive and clearly his doctor is taking areasonably optimistic view.

There can be no question that in the pastrestrictions were too great. There would seemnow to be a danger of moving to the oppositeextreme.

OxygenIt is customary to give oxygen in all severe

cases but the benefit derived is questionable.Certainly it is required if there is dyspnoea orpulmonary aedema and possibly it is of value forshock. I have not been impressed by the allegedproperty of alleviating severe pain. Theadministration of oxygen is usually uncomfort-able and often engenders anxiety.Digitalis

Digitalis should not be administered as aroutine but only for the treatment of cardiacfailure which does not respond to diuretics orto control the ventricular rate if there is atrialfibrillation.Some physicians consider that digitalis is of

value in the treatment of shock but there islittle actual evidence for this opinion. In generalit is best not to give a potentiailly toxic drugunless there is some special indication.

DiureticsDiuretics are extremely valuable for the

treatment of pulmonary cedema from left ven-tricular failure. They should also be given forsevere or persistent congestive failure. Mildperipheral cedema will usually clear of itselfas the patient improves and it is best not toinduce a diuresis which contributes to exhaus-tion and possibly to venous thrombosis.Quinidine

Quinidine should not be given as a routinemeasure for the prevention of arrhythmias butonly for the treatment of ventricular tachy-cardia, persistent flutter or atrial fibrillation orfor multiple extrasystoles which may preceedventricular tachycardia or fibrillation.Anticoagulants

After twenty years the place of anticoagulantsin the treatment of coronary artery diseaseremains unsettled, and except for those whohave themselves carried out clinical trials,physicians can but read the same evidence anddraw their own conclusions. With so muchdoubt and conflicting evidence, it would seem

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that at best there cannot be very much in it,either as regards the efficacy of short-termtreatment in reducing the mortality, or oflong-term treatment in influencing the ultimateprognosis. There is general agreement thatanticoagulants are of some value in diminishingthe incidence of thrombo-embolic compli-cations. These may include extension ofcoronary thrombosis or fresh thrombosis, thelaying down of clot on the endocardial surfaceof the heart, venous thrombosis and pulmonaryembolism.Some are of the opinion that the small gain

from the prevention of venous thrombosis andpulmonary embolism is balanced by the risksof hemorrhage. This, however, should notapply where good laboratory control is avail-able. Despite criticism, the balance of opinionis in favour of anticoagulants, at least in theacute stage, for the relatively severe risk groupand for impending myocardial infarction asjudged by the sudden onset of angina or thesyndrome of acute coronary insufficiency. Longterm treatment and the treatment of the goodrisk group is more debatable. The generaltrend is to restrict their use to shorter periodsin fewer patients.

All willl agree that the prognosis of myo-cardial infarction is very different in the goodand poor risk groups but it is impossible totell in the first few days after the onset whethera patient will change from a good to a poorrisk group. Consequently, our practice is togive anticoagulants to all patients at the onsetof myocardial infarction but after a few daysor weeks gradually to tail them off in thosewho are clearly in the good or fairly goodrisk group.As regards long-term treatment, from the

statistical point of view, it seems that youngmales are most likely to derive benefit, par-ticularly during the first 6 to 12 months, butthere is little evidence in favour of continuingtreatment for a longer period than this.

AdministrationHeparin interferes with the blood clotting

sequence at several stages and has a rapid andtransitory action because it acts solely on clot-ting substances already present in the circu-lating blood. It must be given by injection.A suitable dose is 100 to 150 mg. (10,000 to15,000 international units) preferably by intra-venous injection but if necessary intramuscu-larly. This should be followed by 7,500 unitsevery six hours for 24-36 hours, by which time

the oral anticoagulant, given simultaneously,will be effective.

Phenylindanedione (Dindevan) is the oralanticoagulant in most frequent use in thiscountry. The initial dose is 150 to 300 mg.,and the average daily maintenance dose usually50-125 mg., to keep the prothrombin activityof the patient as near as possible to 15 to 20per cent of a normal individual tested eachday by the same method.

Hamorrhage from Over-dosageHeparin. An antidote exists in the form of

protamine sulphate, which should be givenintravenously in the form of 1 ml. of a 1 percent solution to each 1,000 international unitsof heparin given in the last dose. A transfusionof fresh blood may also be required.Phenylindanedione. Vitamin Kl by mouth

in adequate doses will usually restore the pro-thrombin time to normal within eight hoursbut, with severe haemorrhage, it can be givenby injection. It is a powerful drug and shouldonly be used with caution and only whenspecifically indicated. It may be used in smalldoses to reduce an unduly prolonged pro-thrombin time or when more than slighthkmorrhage has occurred. In the first instance2.5 to 5 mg. may be sufficient, but 10 to 20mg. may be given of hkmorrhage is moresevere.

It should be emphasised that 10 mg. is alarge dose and unless the situation is seriousand it is not intended to continue with anti-coagulants, it is better to give small repeateddoses controlled by the prothrombin time orthere may be undue delay in regaining anti-coagulant control with, of course, risk of freshcomplications of the type for which prophy-lactic treatment was instigated.A transfusion of fresh blood will also be

necessary in severe cases.Contra-indications to treatment are recent

bleeding from the gastro-intestinal tract, blooddyscrasias, and severe hepatic or renal insuffi-ciency and, as regards long-term therapy,inabillity of the patient to co-operate or lackof adequate laboratory control.

Risks of anticoagulant treatment. HWmorr-hagic complications occur in about 2 to 3 percent of patients and it is for this reason thattreatment requires co-operation by the patientand adequate laboratory control. HWmatemesis,melena, haematuria or uterine bleeding may bethe first indication of unsuspected underlyingdisease.

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Abrupt withdrawal of anticoagulants may bedangerous and the rebound phenomenon withthrombosis is a real risk, although in some casesit may be due to the restoration of the normalpattern of the natural history of the patient'sdisease.Care of the BowelsOnly those who are severely ill need the

imposition of the bed-pan. Apart from psycho-logical effects it is undesirable from the physicalpoint of view. The use of a bed-pan is oftendifficult and the effort required is greater thanthe use of a bed-side commode. Better stillis the modern wheeled chair, with hollow seatwhich fits over the ordinary lavatory pan.If necessary, the patient can be lifted or helpedon and off the chair. There is no hurry toencourage bowel movement for the first fewdays; thereafter light purgatives or an enemacan be given as required.Subsequent Management

Following acute myocardial infarction mostpatients settle down rapidly within a few daysand thereafter make an uncomplicated recovery.Our practice in those of this group who areadmitted to hospital, is to advise three weeksin bed, one week getting up and about the wardand four weeks at home gradually increasingactivity under the supervision of the familydoctor and then reporting for review beforereturning to work. This means no more thantwo months off work which minimises anypotential economic handicap and the develop-ment of a cardiac neurosis, and gives ampletime for readjustment.

During the second month, walking shouldbe encouraged and gradually increased, shortof pain, dyspncea or undue fatigue, and initiallywalking upstairs can be limited and takenslowly. Exercise is not only of value in pro-moting a coronary collateral circulation but inimproving effort tolerance. It should beexplained that normal individuals who are outof training and take little exercise experiencea striking increase in effort tolerance after afew days of walking or climbing during a holi-day. Unquestionably, walking is the best formof exercise for the coronary patient. Competi-tive games should be abandoned.

Early to bed and early to rise means lesshurry in the morning and more time for gettingto work. The majority of patients can expectto return to their previous occupation or tomodified work if this is unduily heavy. Theprincipal problem is to obtain more suitableemployment for the unskilled labourer but it

is most important not to change a man'socupation unless it is really unsuitable. Forthose with responsibility delegation of dutiesmay be important but only in the severely dis-abled need premature retirement be con-sidered. Social and civic responsibilities canfrequently be curtailed without hardship andin fact many are glad of such a reasonableexcuse. Emotional stress is unquestionablyadverse and an understanding wife or husbandcan do much to prevent tension and otheradverse factors.Whether or not to advise giving up smoking

is controversial but there can be no questionthat in some patients smoking aggravatesangina and can produce quite striking changesin the electrocardiogram or ballistocardiogramwhich may be of clinical significance. Smokinghas no beneficial effects other than satisfyinga craving for this drug and has other dis-advantages which are well known, in additionto ill effects on the cardiovascular system.

Alcohol may have a beneficial sedative effectbut is not a coronary vasodilator. When takenin moderation it is probably the best of tran-quillisers.

Over-eating should be avoided and also exer-cise after a meal. Reduction of weight in theobese is clearly an advantage. There is, asyet, no conclusive evidence that alterations inthe quality or quantity of ingested fat effecthuman atherosclerosis but there is considerablepresumptive evidence in its favour. If diet-ing is necessary for reduction of weight andin those with a high blood cholesterol it wouldbe sensible to cut down the intake of animalfat and cook in vegetable oil. This can readilybe done, without materially spoiling the pleas-ures of the table, if the habit of mind is formedof avoiding obviously fatty food, cutting visiblefat off all meat, only taking lean bacon, pouringthe top off the milk and getting accustomed tobread and scrape rather than thickly spreadbread and butter. Such rules can be ignoredon special occasions.

COMPLICATIONSShock

Varying statistics on the incidence and sig-nificance of cardiogenic shock following myo-cardial infarction, are ilargely explained bydifferences in the criteria used for diagnosis.Shock is not synonymous with hypotension butis a readily recognisable clinical state, of whicha fall in blood pressure is but one manifestation.The other principle features are pallor, weak-

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ness, sweating, a rapid thready pulse andoliguria. Without these the diagnosis shouldnot be made.The previous blood pressure will influence

the level at which shock appears.Shock usually appears at the onset of myo-

cardial infarction and in about 50 per centof patients the episode is transient and not ofserious significance although hypotension mayreappear a few hours later in some cases.

Left ventricular failure may appear with theonset of shock and the simultaneous develop-ment of an arrhythmia may intensify hypo-tension.The disturbed physiological mechanisms

present have not been completely clarified. Theblood volume is not significantly decreasedand there is no close relationship with a lowcardiac output.

Myocardial failure and peripheral circu-latory collapse are the two factors which maypresumably be responsible but the precisepathogenesis is obscure. Experimentally it hasbeen shown that shock is not solely due tothe amount of myocardial damage, nor can itbe accounted for by tachycardia.Simulation of coronary shock

Errors in diagnosis are sometimes madebecause the clinicail picture assumed to be dueto myocardial infarction with shock may bevery similar to that occurring from other causes.These include: (1) cardiac tamponade; (2)rupture of a dissecting aneurysm of the aorta;(3) rapid ventricular tachycardia; (4) massivepulmonary embolism; (5) acute pulmonarycedema; (6) acute myocarditis; (7) fulminatingbacterial infection; (8) cerebral hemorrhage;(9) internal hemorrhage; (10) anaphylaxis.These conditions should therefore be kept

in mind in any patient with atypical featuresfor myocardial infarction.Treatment

If initial treatment has been ineffective, painand anxiety should be relieved by a furtherinjection of morphine together with atropine,hyoscine or an anti-histamine as explainedabove.Oxygen by mask or tent has been shown

to raise the arterial oxygen tension and mayhelp in such cases. The use of positive pres-sure apparatus is still controversial.PostureRecumbency or semi-recumbency is best

unless there is pulmonary cedema, when thepatient may have to be propped up. In general,

the position of maximum comfort should beused.

100 to 200 mg. hydrocortisone intra-venously should be given first. If the bloodpressure does not respond a vasoconstrictordrug should be administered. Metaraminol isprobably the best available preparation andhas the advantage that it can be given intra-venously, intramuscularly or subcutaneously.5-10 mg. can be given by I.V. injection or 10-25mg. by intramuscular or subcutaneous injec-tion, repeated as required, or 200 mg. canbe dissolved in 250 ml. 5 per cent glucosein water and given by intravenous drip at arate required to control the blood pressure.The vasoconstrictor drug formerly most fre-

quently used is noradrenaline. This has to begiven by constant intravenous drip, one infusioncontaining 4 mg. noradrenaline dissolved in500 ml. of glucose. It is given at a rate suffi-cient to maintain the systolic blood pressureat about 100 mm. Hg. A dose of 1 mg.of noradrenaline is equivalent therapeuticallyto 20 mg. of metaraminol.An important point to stress is that if treat-

ment has any chance of success it must bestarted !as soon as possible. There is far fromuniversal agreement as to the value of differentmethods of treatment and, as already indicated,the prognosis of severely shocked patients isbad.Pericarditis

Pericarditis occurs in about 20 per cent ofpatients with acute myocardial infarction andis usually recognised by the detection of peri-cardial friction between the second and fourthdays of the illness. Pain may be mistaken fora recurrence of myocardial ischaemia but tendsto be aggravated by respiration, coughing orposture. No special treatment is required andthe prognosis is not adversely affected.Post Myocardial Infarction Febrile SyndromeA much rarer type of pericarditis has come

to be known as the "post myocardial infarctionfebrile syndrome". In these cases, friction isheard between the second and tenth weeks ofillness and persists for days or weeks. Thecondition has a characteristic tendency torelapse. Pericardial effusion develops in morethan half the cases and there may be associ-ated pleuritis or pneumonitis.

Steroids frequently relieve pain and feverdramatically but there is a tendency to recur-rence of symptoms when the dosage is reducedand because of this such treatment should notbe given unless symptoms are severe.

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Pleural or pericardial effusion may be extens-ive and require paracentesis for the relief ofsymptoms. The exudates are often hemorr-hagic.

Anticoagulants should be avoided or cardiactamponade may result.Post Myocardial Infarction Pain

Following myocardiall infarction, referredsomatic pain in the chest wall is of frequentoccurrence and not always easy to distinguishfrom a recurrence of true cardiac pain. Itmay develop within a few days or later andpersist or recur for days, weeks or occasionallylonger. Tender areas in the chest wall areoften present and in such cases, pain may berelieved by the local injection of 1 per centprocaine or superficial "freezing" with an ethylchloride spray.

Pain may be felt near the sternum or in theleft pectoral region. It often comes at restand may be aggravated by movement, postureor respiration, but the patient may be unableto distinguish its quality from the originalcardiac pain so that there will be undesirableanxiety on this account.The mechanism is presumably that of

visceromotor reflex muscle spasm similar tothat which occurs elsewhere, e.g., in the abdom-inal muscles with appendicitis. In the case ofreferred pain from the heart this peripheralsomatic effect sometimes persists and becomesa very important secondary factor which isoften perpetuated not so much by the under-lying disease as by anxiety and unwarrantedrestriction on movement.

It is worth keeping in mind that once thepain of acute myocardial infarction has sub-sidised spontaneously or with treatment, per-sistent or recurrent pain in the chest wall ismore likely to be of somatic than cardiacorigin.Due caution is of course required but if

in doubtful cases there is no supporting evi-dence for further myocardial infarction byelectrocardiography or the estimation of trans-aminase, strong reassurance is indicated andthe general management of myocardial infarc-tion and subsequent rehabilitation continued.Although thoroughly established, this syndromeis not sufficiently recognised, with consequentmisinterpretation and mismanagement.Arrhythmias

Cardiac arrhythmias following myocardial in-farction are of serious prognostic importanceand sometimes associated with sudden death.The incidence is higher in the older age groups.

ExtrasystolesExtrasystoles often develop. Supraventricu-

lar extrasystoles are less frequent andless important than ventricular extrasystoles.The physiological importance depends on thefrequency with which they occur and the conse-quent effect on coronary blood flow and sys-temic blood pressure. More important is thefact that they may precede atrial fibrillationor ventricular tachycardia. Consequently, ifthey occur frequently quinidine should be given.If this fails, oral pronethalol 100 mg. 4-6times a day cay be tried but watch kept fora fall in blood pressure. This drug is best forventricular arrhythmias.Supraventricular tachycardia

Supraventricular tachycardia is not a fre-quent occurrence but of serious significance.If the attack cannot be terminated by vagalstimulation, the patient should be digitalised.If necessary, vagal stimulation can then be triedagain and is more likely to be effective. Ifthe blood pressure is low, pressor aminesshould be given and may themselves convertthe arrhythmias to sinus rhythm.A trial fibrillation

Mortality is little influenced by transientfibrillation but the persistent arrhythmia isof more serious prognostic importance. Theventricular rate should be controlled with digi-talis and, if necesary, pressor agents should alsobe given. Anticoagulants should be continuedin all such cases. It is best to delay the restor-ation of sinus rhythm with quinidine until afterthe acute phase of infarction is over unlessthe ventricular rate cannot be controlled.A trial flutterThe significance and management of atrial

flutter is similar to that of atrial fibrillation.Ventricular tachycardia

Ventricular tachycardia is responsible formany sudden deaths following myocardialinfarction. Frequent ventricular extrasystolesshould be taken as a warning sign of impendingventricular tachycardia and quinidine should begiven prophylactically as mentioned above.

In urgent cases procainamide is superior toquinidine for treatment because it has a similaraction, but can be used intravenously withmore safety (100 mg. a minute up to IG).When ventricular tachycardia is due to digitalisintoxication potassium salts should be given.

If quinidine or procainamide fail pronethalolshould be given in a dose of 100 mg. intra-venously which can be repeated if necessary.

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This drug is often effective and can be con-tinued by mouth until the danger period isover.

Decreased coronary flow may be responsiblefor the arrhythmia and increasing the systemicpressure with pressor amines may be successfulin restoring sinus rhythm or in potentiatingthe effect of other drugs.Defects of Conduction

Severe dearees of atrioventricular block areof serious prognostic significance. First andsecond degree blocks are usually asymptomaticbut may procede to third degree block.Complete A-V association carries a 50 per

cent mortality and may be complicated byAdams-Stokes attacks.

Hydrocortisone (200 mg.) should be givenintravenously in the first place and 100 mg.may be repeated every 4 to 6 hours as required.Sublingual or, if necessary, intravenous iso-propylnoradrenaline (isoprenaline) may abolishthe block. If these measures fail, adrenalineshould be tried and, if the blood pressure islow, pressor amines should be given as supple-mentary treatment.Another drug which has been used with

success is molar sodium lactate.Cardiac Failure

Cardiac failure after myocardial infarctionmay be in the form of pulmonary oedema fromleft ventricular failure, or of the peripheralsigns of increased venous pressure, cedema andcongestion in the liver. Treatment should beon the usual lines with digitalis and diuretics.EmbolismPulmonary or systemic embolism is an

important complication occurring usually insevere cases of myocardial infarction but hasbecome less frequent following the introductionof anticoagulant drugs. Statistics compiledprior to 1948 suggest that thromboembolic com-plications occurred in at least 10 per cent ofcases of myocardial infarction, accounted forabout 10 per cent of deaths and contributedto more.Pulmonary EmbolismPulmonary embolism is frequently mistaken

for further myocardial infarction. It may resuiltfrom thrombosis in peripheral veins or occa-sionally, and especially if there is right-sidedfailure or atrial fibrillation, in the right atriumand less frequently from trans-septal infarctioninvolving the right ventricular wall. It mayoccur in the first few days but more oftenafter the first week and sometimes unexpectedly

when the patient gets out of bed. It is for thisreason that anticoagulants should be continuedover this period.Systemic Embolism

Cerebral embolism with the resultant infarc-tion or softening of the brain and the develop-ment of hemiplegia, aphasia or mental changesis a not infrequent complication of myocardialinfarction. These effects may be difficult orimpossible to distinguish from similar mani-festations due to a fall in cardiac output withdecreased blood flow in atheromatous cerebralor extracranial vessels. Emboli may lodge inkidneys, spleen, mesenteric vessels or the limbs.Rupture of the lInterventriculr Septum

Involvement of the septum by myocardiailinfarction is a frequent occurrence but per-foration is rare. This is a serious complica-tion and most patients die within a week or twoalthough occasional long survival has beenreported. The physical signs are those of asystolic murmur and thrill maximal atthe left sternal border. Successful surgicalrepair has been reported in a few cases and thisform of treatment may therefore reasonably beconsidered in patients who are deteriorating,if adequate facilities are available.Cardiac Aneurysm

Cardiac aneurysm is an infrequent compli-cation of myocardial infarction due to replace-ment fibrosis usually involving the anterior wallof the left ventricle. Although sometimes sus-pected by the palpation of a double cardiacimpulse or an outward thrust during systole,the diagnosis is usually made by radiography.There is an abrupt change of contour on theleft heart border producing a shelf with reducedor paradoxical pulsation on radioscopy.

Electrocardiographic changes are not diag-nostic but there is usually evidence of extensiveinfarction and in some cases persistent eleva-tion of the ST segment in precordial leads.Cardiac rupture is rare but incapacitating

symptoms may result from impairment of func-tion produced by the expansile but non-contractile aneurysm. Sometimes embolismresults from mural thrombosis.The importance of recognising this condi-

tion lies in the fact that in such cases refractorycardiac failure may respond dramatically tosurgical excision of the aneurysm.

Frozen ShoulderPain, stiffness and limitation of movement

at the shoulder joint is a well recognised

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complication of myocardial infarction butshould be an infrequent one. In some casesswelling, stiffness and discolouration of thehands and fingers has followed.The remarkable variation in the reported

incidence of this syndrome is probably a reflec-tion on the degree to which patients areimmobitlised in bed following myocardial infarc-tion. In our Unit they have always beenallowed to move about as freely as inclinedand "frozen" shoulder has been a rare occur-rence. The patient in pain or with shockwill naturally lie still but we have always feltthat immobility enforced by medical and nurs-ing staff is liable to lead to complications anda degree of anxiety more adverse than anypotential benefit. In uncomplicated cases, asreferred to above, no patient has been kept inbed for more than three weeks, and is alwaysencouraged to move about and be wheeled outto the lavatory in a special chair, on theassumption that the physical exertion andmental anguish of using a bedpan were adverse.Although the condition may take months to

improve, the syndrome, which is similar to thatwhich may follow trauma, hemiplegia or cervi-cal arthritis, is self-limiting and the long-termprognosis is good. Numerous forms of treat-ment have been recommended but the com-bination of analgesics and physiotherapy isusually sufficient. The local injection of hydro-cortisone is probably of no benefit.

DeathThe principle causes of death from myo-

cardial infarction are:

1. Shock;2. Cardiac failure;3. Cardiac arrest;4. Acute arrhythmias;5. Thromboembolic complications;6. Cardiac rupture.

Treatment may be effective in all except thelast of these.

PrognosisCoronary artery disease can rarely be diag-

nosed before symptoms are present and usuallythe onset of symptoms gives no indication ofthe extent of underlying disease. In fact, thereis no medical condition in which the futureis more uncertain and unpredictable. Analysesof large series do not help in the individualcase but statistics, of course, do give overallguidance which is of value. The practitionermust instill confidence and optimism into thepatient but cover all eventualities with therelatives. To the lay mind angina is associatedwith sudden death and this does in fact occurin some 10 per cent of cases. Sometimes, theincreased frequency and severity of attackshave brought realisation of progression to allconcerned but more often, when myocardialinfarction occurs, although the practitioner willhave had such eventualities in mind, it comesunexpectedly to the family.

Following myocardial infarction the prog-nosis is influenced adversely by a history ofprevious infarction or systemic hypertension;by the presence of cardiac enlargement; byevidence of extensive infarction as judged byprolonged pain, triple rhythm, shock, cardiacfailure, extensive ECG changes or a highlevel of SGOT; or by recurrence of painor by pulmonary or systemic embolism, anarrhythmia or defects of conduction.Although the influence of long-term anti-

coagulant therapy in affecting life expectancyis uncertain, as discussed above, few woulddoubt the value of anticoagulants in severecases, at least as regards their 'limiting effecton venous thrombosis and pulmonary embolism.Many patients, of course, die before admis-

sion to hospital or before treatment can beinstituted. Probably some 20 per cent who areadmitted to ;hospital die within a month, butin the remainder the outlook is much betterthan used to be thought, especially -in thosewho make a good recovery without compli-cations or after effects. At least 75 per centof those who leave hospital well will survivefor five years and probably thereafter the mor-tality rate is not more than 5-10 per centper annum.

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Documents

ACUTE MYOCARDIAL INFARCTION · TURNER: Acute Myocardial Infarction the picture of shock or pulmonaryoedemadoes not develop noris there subsequent pericarditis, leucocytosis, fever,