PRESENT fclLf "iO THE ARft-'iY MEDICAL LIBRARY SURGEONS ivr BY THE ASS'H.OF MILITARY March, 1939] NOTES ON CLINICAL HEART DISEASE : KELLY 129

When we speak of left-sided failure, e.g., hyper- tensive or failure of the left ven- Original Articles tricle behind high systemic blood pressure, we / visualize adequate filling but inadequate empty- ing of the left side of the heart with correspond- SOME NOTES ON CLINICAL HEART ing increase in its size. Our conception of right- DISEASE* sided heart failure, e.g., failure of the right ventricle behind mitral stenosis or behind chronic By GERARD KELLY, f.r.c.p. (I.) bronchitis and emphysema is precisely similar. MAJOR, I.M.S. Just over a century ago an English physician, Professor of Clinical Medicine; Medical College James Hope, inspired by the work of Corvoisart, Hospitals, Calcutta evolved the ' of cardiac ' back-pressure theory' HAVE these few notes in order to failure. As an obstacle to the circulation', he in c]' compiled ' Jcate to the general practitioner something of said, operates on the heart in a retrograde substance of heart disease: there is direction, the cavity situated immediately hing in them for the specialist. behind is the first to suffer from its influence Otherwise back of the ^y choice and I have stated, congestion failing in c i a?ly partly by request chamber is the cardinal feature of uded a few remarks on the following :? congestive failure rather than inadequate of the The or output v problem of the cardio- C problems failing chamber. This rediscovery of Hope's $cular dysfunction case. Heart failure? Heart failure. Left-sided heart failure. Right-sided heart failure. Mixed failure. ? Symptomatology? Dyspnoea. Pain. Palpitation. ? asthenia. ? Neurocirculatory Auscultation. of blood pressure. 7 ? estimation Radiography of the heart and aorta.

problem or problems of the cardio- vascular DYSFUNCTION CASE Diagram illustrating the back pressure theory of Patient (left-sided and right-sided) heart failure. v complaining of symptoms of cardio- congestive (left-sided right-sided) ^ ar dysfunction presents for your apprecia- tirf^ one or more of the following problems :? vital observation is a recent landmark in the ? Is he a neuropath or a cardiopath ? study of heart failure. ? If a is there evidence of failure cardiopath, Left-sided (congestive) heart failure or impending failure, and to what ex- tent is the heart incapacitated ? This is the commonest of all forms of heart ? If failure. Its causes are left ventricular defeat a patient is a it does not by cardiopath, and of the left follow that all the are due overstrain disease ventricle, symptoms disease to the heart. There may be a neurotic namely, hypertension, coronary (arterio- sclerotic or and valvular disease element. That is to say?a patient syphilitic) or stenosis and mitral may be both a cardiopath and a neuro- (aortic regurgitation disease with Pul- path : if so, what is the responsibility preponderant regurgitation). or a rise of in the of each factor in the case ? monary hypertension pressure pulmonary circuit behind the failing left ven- tends to become a neuro- tricle constitutes the first of left ventri- p cardiopath stage ^'?Mackenzie. Actually, many cardiopaths cular failure. This is manifested clinically bi ,Gra^G their disablement with great fortitude, by an accentuated pulmonic second sound, often those with but little dilatation of the vessels ca v ProPortion only, by pulmonary <:Celiac damage, suffer more from psycho- seen in the lung roots of the radiogram and ^an heark- A very occasional cardio- by mitralization of the heart radiologically, Path0^8 his to the of the conus add .ay proclaim psycho-neuropathy by owing enlargement pulmonary v^^sing his doctor as if the doctor had given of the right ventricle behind the pulmonary hs disease. hypertension. In the next stage there is trans- shall refer to the commoner udation from the vessels with the inn / very briefly engorged danisms, left-sided and right-sided failure. production of pulmonary cedema, often later Hence the classical * g . paroxysmal persistent. reac* at Calcutta Medical symptoms of left-sided failure are effort dyspnoea 1 paPpr College ^eUniorfJ aJOQ, and cardiac both of which own the same 130 THE INDIAN MEDICAL GAZETTE [March, 1939

fundamental mechanism, i.e., pulmonary con- the heart-rate. A regular rhythm failure may gestion and cedema. The most ominous signs of occur with a normal or moderate ventricular left-sided failure are gallop rhythm and pulsus rate, or a high rate \ Failure with normal alternans which may be combined with cardiac rhythm may be more serious than when auri- asthma to form the gravest triology in the cular consorts with failure. Gavey domain of heart disease. Negativity of T in and John Parkinson's recent investigation lead I of the electro-cardiogram is of correspond- regarding the clinical value of digitalis in heart ingly evil prognosis. A widened low voltage and failure with normal sinus rhythm reveals the ' usually a bifid or flat-topped P-wave have following pertinent facts : In heart failure with recently been described by Wood and Selzer as normal rhythm digitalis is helpful in rather more an early sign of left ventricular failure. than half the cases. In heart failure with auri- Left ventricular failure is usually a passing cular fibrillation, digitalis is more often helpful phase, for the increased resistance in the lungs than it is in normal rhythm, for it benefits more soon stresses the right ventricle which fails in than two-thirds. The real difference in the res- turn thereby relieving somewhat the symptoms ponse of heart failure to digitalis lies not between of left ventricular failure. While the phase of auricular fibrillation and normal rhythm, but left ventricular failure lasts there is no oedema rather between rheumatic auricular fibrillation nor venous congestion, although pulmonary and all other kinds of heart failure irrespective hypertension and even pulmonary cedema are of rhythm. The course of the disease after the present and periodic attacks, of nocturnal onset of failure in normal rhythm is short?18 dyspnoea occur. Even hydrothorax may occur of 29 patients died within a year Failure with at this stage before the right ventricle fails. normal rhythm is relatively more common in Much less commonly the ventricular imbalance India in that for one thing cardiac rheumatism of a forceful right ventricle and av failing left which accounts for about half the cases of auri- ventricle may be long maintained to the greater cular fibrillation in Great Britain and Ireland respiratory distress of the patient; this form of is correspondingly less prevalent in India. left ventricular failure is sometimes improperly ' failure called dry failure a term that more correctly Right-sided (congestive) heart describes a right-sided congestive failure dehy- This is most frequently a proclamation of drated by salyrgan. previous left-sided failure due to hypertension, is a combination of left coronary disease or aortic valvular disease. But heart failure and of peripheral circulatory the causal example par excellence of right ven- failure. When the usual clinical sequence tricular strain and failure is the correspondingly obtains in a case hitherto free from congestive infrequent congenital condition, namely pul- failure, the first phase of coronary thrombosis is monary stenosis, which incidentally produces marked by pain or. dyspnoea and by shock, pulmonary ischsemia and a proclivity to pul- of whereas the second phase, denoted by the offset monary tuberculosis?the converse effects of shock, is characterized by the appearance of mitral stenosis. congestive failure. In any case, the greater the The middle share of responsibility for right- shock the less apparent is cardiac failure and sided heart failure is claimed, firstly, by the pul- vice versa. In shock the heart's income is monary hypertension that is most emphatically reduced to an extent which is unembarrassing produced by mitral stenosis, and, secondly, by even to the grossly infarcted heart. With the pulmonary disease, notably emphysema, both of passage of shock, however, the venous income which quite obviously obstruct the blood flow increases and the failure of the left heart to rise through the lesser circulation. The ultimate to the occasion is soon translated to the right determinant, however, of right-sided failure is heart in terms of congestive failure. coincident right ventricular disease, e.g., arterio- the In pure left ventricular failure the rhythm is sclerosis, which so conspicuously involves regular. The inquiry of Parkinson and Clark- left ventricle, and expectedly implicates the right- Kennedy in 1926 regarding failure with normal ventricle as well. 1 rhythm established that there is an important A most exceptional cause of right heart failure, relation between the pathological basis for a i.e., primary endarteritis of the pulmonary cardiac disease and failure and the absence of arteries, is nevertheless worthy of recall on this fibrillation. In general, auricular fibrillation occasion because Sir Leonard Rogers of this was the rule in rheumatic heart disease arid College described some cases in Bengal soon goitre, while failure with normal rhythm was the after its original description by Ayerza of rule in hypertension, coronary disease and Buenos Ayres. emphysema \ It is also the rule in cardiovas- The clinical picture of right-sided heart failure cular syphilis. In the latter setiological groups, is reflected in the venous reservoir formed by the ventricular strain and disease cause the ventricles systemic and portal venous systems behind the to give way before the auricles have reached failing^ right ventricle. Its main features are, the stage of fibrillation. and John cervical veins ' Gavey accordingly, engorged (Lancisi's Parkinson remind us that apart from the factor sign), engorgement of the liver, and systemic of rhythm and the factor of specific pathology cedema. Dyspnoea is an almost invariable conditioning rhythm, there is a third factor of symptom in right-sided failure owing to the fact Ji March, 1939] NOTES ON CLINICAL HEART DISEASE : KELLY 131

in heart disease and in that the causes of failure essentially Excepting pulmonary right-sided manner heart the rate the circuit in the hypertensive failure, respiratory implicate pulmonary in exceeds 30 minute. same reason cardiac dyspnoea rarely per indicated above. For the cyanosis ' in left- As Christian said is poorly, sometimes is rather more here than dyspnoea conspicuous not at the charted rate of res- sided failure. all, depicted by to \ When encounter shallow In the ventricle has piration you rapid pneumonia right should look for evidence of operate the pulmonary lesion, neverthe- respiration, you against heart acute or or the clinical of pulmonary pleural disease, interpret picture right-sided such is less evident because failure is pre- neurocirculatory asthenia; polypncea failure is rarely when We have already usually absent in cardiac disease excepting dominately peripheral. between the is involved. referred to the antagonism existing coronary shock and congestive cardiac failure in Another remarkable respiratory symptom of thrombosis, evidently peripheral failure nearly neurocirculatory asthenia is sighing or suspirous always prevails in pneumonia. respiration. Now sighing respiration is a sub- jective feeling of difficulty in taking a full breath. Mixed failure This is eventually overcome and a deep breath auricular Mixed failure is usually seen in is taken, followed by a long sighing expiration or less fibrillation. Both ventricles fail more and relief. Sighing respiration often masquerades in- ' from stress of excessive and as shortness of breath1 breathlessness simultaneously ' ' effective beating. difficult breathing at times ', or a feeling of suffocation'. Gallavardin's le trepid, palpi- Symptomatology tation, left inframammary pain and sighing res- ' worth many In diagnosis one physical sign is piration is diagnostic of neurocirculatory that this symptoms.'?Horder. I am not sure asthenia. This triad of symptoms is a pleasing holds for heart disease, in that, contrast to the evil triology of left ventricular generalization or of a ! ?r example, a history of effort failure. previous thrombosis without abnormal coronary Cardiac asthma is a severe grade of paroxys- or a of nocturnal cardiac asthma slSns, history mal due to sudden or acute failure of are all value. dyspnoea of the highest diagnostic the left ventricle. Its basis is most of clinically frequently . The best method, to my mind, and arteriosclerotic heart heart case is hypertensive disease, investigating the ordinary probably the leisured classes as commonplaces amongst follows :? of Indians. The of life and the diet of what are tempo The first is to have in mind the Indian on the other are point decide if ryot, hand, certainly he symptoms of cardiac damage and less conducive to such developments. Bronchial tle unessential patient has them, ignoring asthma and cardiac asthma are con- of effort, frequently symptoms, e.g., has the patient angina fused and so I have tabulated their differential ? Incidentally uyspncea of effort, cardiac asthma diagnosis. 'he of cardio- three most outstanding symptoms to standard vascular dysfunction, according Bronchial asthma Cardiac asthma are and palpitation, authors, dyspnoea, pain, and indents call them the 3 Ps?panting, pain 1. The majority of cases Cardiac asthma is very Palpitation. of true rare before the age of 2. What are the spasmodic . The next consideration is, asthma begin before 40. the got ^?ns of heart disease and has patient the age of 25. the*n? e.g.? valvular 2. There is a history of 2. The history of attacks disease, of cardiac asthma cardiac years of sensitiveness rarely enlargement, to foreign proteins exceeds 2 years: I am hypertension, and of respiratory constantly having patients dilatation of the aorta, infections, e.g., winter sent up as cardiac asthma when congestive cough. they have failure, had attacks for 5 to 10 auricular fibrillation or flutter, and years, which, of course, abnormal electrocardiograms. excludes it. Duration is therefore an important differential Dyspnea point. term means laboured breathing dyspnoea 3. is invari- 3. There be no reg- le the Wheezing may 0n consci?usness difficulty experi- able. encerl their wheezing, simply dysp- heart and lungs in meeting noea and oedema of the liabTr be ^arc^ac dysPnoea may clinically lung bases. Often this divide^-' t oedema affects the small tubes thereby producing o' on exertion. some spasm. ^yspncea?dyspnoea at rest? (1) Orthopncea, 4. The dyspnoea of 4. The dyspnoea of cardiac (2) Cardiac asthma and acute pul- bronchial asthma is asthma is both inspira- tory and expiratory. monary cedema. mainly expiratory. 132 THE INDIAN MEDICAL GAZETTE [March, 1939

Cardiac asthma Bronchial asthma The causal factors, therefore, of cardiac pain are . Rhonchi are mainly 5. Rales moist inspira- are coronary arterio-sclerosis which narrows, and tory and basal. lumen expiratory, widespread Quite coronary thrombosis which occludes the and well frequently they are the especially of the and aortitis which heard over squeaky rales of the coronaries, syphilitic bilaterally dias- the front of the emphysematous asthma- obstructs the coronary orifices. The low or low chest. No moist rales tic subject. In fact the tolic pressure of aortic regurgitation the in cardiac can be detected at lung signs cardiac in may likewise the bases behind. asthma may be indis- output as a result of the of Bronchial asthma is tinguishable from those cause cardiac pain delivery characterized by bron- of bronchial asthma. In an inadequate volume of blood to the coronary chial spasm without cardiac asthma there is circulation and myocardial fibres. oedema of the lungs. oedema with or without in- spasm: if with spasm Marked left ventricular enlargement by the smaller tubes are creasing the territory of the coronary circuit, involved. imposes a further liability resulting in the easier Signs of heart disease G. Signs of heart disease provocation of pain in the subjects of hyperten- are absent in uncom- are invariably present in sive heart disease or aortic regurgitation. cardiac asthma? plicated bronchial Cardiac is elicited on exertion or excite- asthma. (1) Hypertension. pain (2) Cardiac enlargement. ment because the total coronary diastole per (3) Markedly accen- minute is thereby shortened and because coro- tuated pulmonic nary sclerosis the extent of coronary second sound. by limiting dilatation the coronaries from rising to (4) Gallop rhythm. prevents (5) Pulsus alternans. the occasion. (6) Abnormal electro- It is rather interesting to recall that, although cardiograms espec- Heberden a classical of angina ially Ti negativity. gave description Confusing factors are? pectoris (paroxysmal substernal oppression) (1) The heart rate may about 1768, it was his friend William Jenner be only slightly who evolved the essential lesion, accelerated. pathologic sclerosis. As Jenner's master, (2) The heart rhythm namely, coronary remains normal. however, the great John Hunter, was at the time (3) Heart murmurs are a victim of angina, his faithful pupil did not usually absent, disclose his discovery until after though sometimes pathologic some lest the aortic valvular mur- Hunter's death twenty years later, murs or the mur- announcement might prejudice Hunter's career. mur" of mjtral Jenner predicted and found extensive coronary stenosis is heard. sclerosis in his of John Hunter. There- The may necropsy (4) lung signs a almost mask after coronary disease was regarded as pathol- entirely to the heart sounds ogical curiosity and occlusion was considered and any existing be quite incompatible with life, until Herrick's murmurs. clinical description of coronary thrombosis (pro- 7. Bronchial asthma is 7. Cardiac asthma is likely longed substernal oppression) in 1912. unlikely to lead to to lead to congestive ventricular) failure right-sided failure. (right Palpitation before long. ' the to 8. Cardiac implies Palpitation (from Latin, pcilpitare 8. Bronchial asthma asthma_ action, a bad such throb) is the consciousness of the heart's implies a good prog- prognosis: _ live 2 or or It is nosis and very many patients rarely whether fast slow, regular irregular. years of useful life. years. generally a disagreeable sensation and sometimes 9. Rapid and favourable 9. Responds to morphine in a sensitive person it is very distressing.'? to adrenalin. and atropine. White. was described and attributed to Pain Palpitation cardiac dysfunction by Galen, centuries before The coronary, or third circulation, may be cardiac pain or cardiac dyspnoea were recognized. conveniently studied by the Harvey film which It is, however, the least important of the three shows the exposed heart beating. In ventricular main symptoms of cardio-vascular dysfunction. systole the musculature and subsequently the The majority of people who complain of palpi- coronary arteries are tightly contracted pro- tation alone have no organic heart disease. ducing thereby a notable pallor of the ventri- When palpitation is associated with heart disease, cular walls in testimony to their relatively carSiac dyspnoea and pain are present as well- bloodless state. In ventricular diastole the When palpitation is symptomatic of neuro- musculature and subsequently the coronaries circulatory asthenia it is the leading component relax and the walls become flushed with blood, of Gallavardin's le trepid. The child very clearly indicating that the rate of the coronary rarely complains of palpitation, but the nervous circulation is optimal in those whose coronary adult may complain of a variety of sensations, trunks are most highly elastic. Coronary in- often of wide reference, to be interpreted as pal- sufficiency productive of myocardial ischsemia pitation. Associated [erophagy often confirms results in cardiac pain. the suspicion of a neurogenic origin. 133 March, 1939] NOTES ON CLINICAL HEART DISEASE : KELLY

3. Symptoms expressive of physical and be a sy P Palpitation may primary ^ weak- > mental exhaustion and anxiety states, e.g., neurocirculatory asthenia, thyrotoxic and nervous- : a ness, fatigue, irritability of more or of lassitude, hypertension, commonly, ness. flutter, or , fibrillation, r;uec\ , 4. of note the sensations describe Symptoms suggestive hyperthroidism; monly. Carefully observe the tremor of the outstretched and, if occurs in bouts, fingers palpitation en^J" of the cold hands. This tremor and the onset and offset of such attacks. T y clammy o of the feet and axillse may be may obtain a clue as to the nature sweating hands, tie indicative of and the 'Feeling _ . potential hyperthyroidism underlying . be found a trifle hard or - thyroid may a jump', u occasionally turning over', 'giving sJeml"? on Palpitation _ palpation. stop' \ suggests extrasystoles. o is felt at times' should arouse a suspicion Physical type.?The individual endowed with paroxysmal , fibrillation, or a hyposthenic constitution is the physical type most likely to exhibit neurocirculatory asthenia. Neurocirculatory asthenia The physique of the hyposthenic individual is outstan When a neurasthenic subject's most poor, the chest long and narrow or flat. The mg is instability and an easy & heart is central, vertical and pear-shaped with inferiority co ' ability of his neurocirculatory apparatus, a low-lying diaphragm. The term drop heart' tions of strain are likely to elicit expresses the classical configuration of the ne^irocl[*j- - so nervous heart which is likened unto that of a tory asthenia, variously designated ' or cardiac heart, D. A. H., effort syndrome hanging drop '. The nervous make-up is cor- : the individual to neurosis. , respondingly poor belongs deline Neurocirculatory asthenia may_ be the anxious, worrying, highly-strung, jumpy type neurasthenia itself with circu a y with exaggerated deep reflexes. presenting ov symptoms and with signs usually of an Physical signs.? (1) Peripheral. (2) Central norm active circulation, such as might occur m or cardiac. if fatigue o Persons on severe physical exertion Peripheral signs.?The rapid Corrigan-like the or of the central nervou skeletal muscles pulse with widened pulse pressure is suggestive system to such exer- did not intervene prevent of aortic regurgitation. The systolic pressure is tion. young It is most commonly displayed by moderately elevated from the increased vis a more females. It may adults, especially tergo, but the diastolic pressure is normal or plicate other chronic.cof^ 1 infection, heart disease, even subnormal?thereby distinguishing this nesses and trauma. central hypertension from essential hypertension. Its importance is twofold Central or cardiac signs.? (1) Precordial. car These re- .1. It is frequently mistaken for (2) Ausculatory. signs superficially stressed jac semble the of mitral disease. over 200 years ago Senac signs disease; disease difficult distinction between organic heart Precordial signs.?The cardiac impulse is and nervous disorders. ,. forcible and (forcible impulse implies cardiac jerky 2. It is often superimposed upon increased force plus quick out-thrust, whereas Pathology?rheumatic, coronary, hypertensive, a heaving impulse implies increased force plus 0r consequent, syphilitic heart disease?with a slow deliberate out-thrust). Its wide diffusion ot enhancement of strain and worsening due to cardiac overaction on perhaps a thin m sue Prognosis : the assessment of each factor chest wall further simulates cardiac enlargement. a uiicom- case is often not a little difficult. Not Palpation, however, reveals the maximal impulse change nionly in the presence of mild organic within the mid-clavicular line. In the absence the of the symptoms is quite dispropor- of radiology, palpation of the maximal impulse severity mam tionate to the available signs, and so the is the only fairly reliable guide as to the posi- burden of them is rightly attributed to attendant tion of the left heart border, provided the heart neurocirculatory asthenia. is not displaced. Precordial or substernal tenderness is not uncommonly noted and is to Symptomatology be regarded as a sign of a sensitive chest wall on the . The general impression left physicianfurther sensitized by cardiac overaction. is the of the manifestations . extreme diffuseness Auscidtatory signs.?The first sound is accen- there are that there are so many things tuated or Accentuation and slur- of excite- reduplicated. many?Gallavardin. The combination of the first sound a maxi-ring apical may produce ment, exertion and the ' ' fatigue precipitate bogus slight presystolic murmur just as accen- mum of , degree symptoms. tuation of the second sound may sometimes in The cardinal are four, namely. ' }? symptoms these cases produce a bogus aortic dias- or mframammary slight Palpitation, left mammary tolic whiff' at the left lower end of the sternum. Pain, dyspnoea, and exhaustion. . is 2. Temporary gallop rhythm occasionally Yaso-vagal and vaso-motor symptoms murmur and basal cmde and col n present. Cardio-respiratory faintness, dizziness, flushing, and murmurs are find- of be somewhat apical systolic expected bands and feet, which may ings in a markedly overacting heart and further cyanotic.

w 134 THE INDIAN MEDICAL GAZETTE [March, 1939 contribute to the not infrequent misdiagnosis of Angina pectoris Left injramammary pain heart disease. 1. Commoner in men. 1. Far commoner in women. Diagnosis 2. Occurs during effort 2. Occurs any time associated with or excitement; effort especially during fatigue; Palpitation.?Palpitation effort heart action is limited by pain. is limited by rapid regular suggests neuro- exhaustion rather than circulatory asthenia. Gallavardin's triad is pain. diagnostic of it as we have already pointed out in connection with sighing respiration which is 3. Pain in brief 3. Pain generally continu- paroxysms, onset and ous, lasting weeks or never a feature of heart disease. Pre- " organic offset abrupt; the months with intermis- mature beats and paroxysms of tachycardia paramount symptom. sions, onset and offset cause the most prominent palpitation in the sub- gradual, duration indefi- jects of neuro-circulatory asthenia. nite: one of many Incidentally symptoms. overdosage with insulin may also cause tachy- cardia, palpitation and cardiac overaction. Site of pain sternal, 4. Site of pain left infra- Pain.?The heartache of or across the chest, mammary extension to neurocirculatory or left less often asthenia the headache of supramammary scapula, replaces ordinary brachial; spinal distri- supramammary, rarely neurasthenia or the abdominal discomfort of bution C8, Dl, 2, 3, and slightly left nervous dyspepsia. It is a dull and heavy left also 4. brachial; spinal distri- bution and 6. breast ache or soreness or gnawing pain due to D5, the of an heart a sensi- impact overacting upon 5. Aspect expresses great 5. No outward aspect of tive chest wall. It may be punctuated by pain. pain. characteristic, transient, short, stabbing pains 6. Hyperesthesia none 6. common like pin-pricks or like sword thrusts in severe Hyperesthesia or only following a and persistent, especially cases. The is not patient's aspect, however, paroxysm. in long-standing cases. that of one suffering pain. The heartache or left of neuro- of neurocirculatory mammary pain Dyspnoea.?The dyspnoea It circulatory asthenia has been inaccurately des- asthenia is subjective rather than objective. cribed as the fact the rather more of a respiratory precordial notwithstanding gives impression is that it extends far outside the precordium. Left dysrhythmia than of laboured breathing. It but rather to inframammary pain, for instance, may be not remarkably related to exertion referred to the left scapula and the extension of emotional upsets. It is unattended by evident document a left supramammary pain into the left arm often distress or cyanosis such as may the or her friends to a severe of cardiac dyspnoea. misleads patient mis- correspondingly grade and diagnosis of angina pectoris. Left supramam- We have already referred to tachypncea of neuro- may also extend to the left side of the sighing so characteristic mary pain respiration, and neck. is common and persistent circulatory asthenia. Cardiac enlargement Hyperesthesia by cases of left of heart failure are conspicuous in established mammary pain. the^ signs in Chest-wall tenderness is, as a rule, remarkable their absence. Dyspnoea in a young person heart by its absence in cases of pain of coronary origin, association with an overacting normal-sized including that of coronary thrombosis. is commonly symptomatic of neurocirculatory in at The onset and offset of heartache are usually asthenia. Exertional dyspnoea persons and above middle life should be thoroughly It may occur at any time gradual. especially : it is> during fatigue. Effort on the part of the neuro- investigated from the cardiac standpoint as we have the symp" circulatory asthenic subject is limited by exhaus- already said, paramount torn of tion and not If an left-sided failure. by pain. anginal subject's of asthenia is elicited by emotion or eating, it will Weakness.?Patients complaining pain that it must somehow always be induced by exertion as well. Finally often subconsciously feel be due to heart disease still undiscovered and the heartache of neurocirculatory asthenia may not this subtle sugges- last for weeks or months with intermissions. they infrequently convey tion to their In actual fact when Clifford Allbutt has outlined for us physician. vividly general weakness is attributable to heart disease the dissimilar clinical pictures of left infra- ' the signs of cardiac disease are obvious inasmuch mammary and of angina pectoris. These are pain as the cardiac causes of general weakness faintnesses, palpitation, gasping, stiflings, bodily heart failure and active . agitations, hyperesthesias and psychical com- asthenia ' In pronounced neurocirculatory motions he are so unlike the now ', said, wholly general weakness is more prominent being of as these frantic ruthless grip angina pectoris translated into exhaustion. But the most pr?" alarms are unlike its silent passion.' minent causes of general weakness, exhaustion A differential diagnostic table of left infra- and prostration are infectious diseases, nutri- nervous mammary pain and angina pectoris by Doris tional disturbances, malignant disease, Baker is given below. Her investigation of disorders, etc., and to these the physician shouW left inframammary pain under the direction primarily address himself. of John Parkinson is a model of clinical research and severe Thyrotoxicosis.?Thyrotoxicosis of an in heart disease. anaemias are also common causes March, 1939] NOTES ON CLINICAL HEART DISEASE : KELLY 135

an ox rhythm commonly signifies heart Exclude thyro ? overacting overactive heart. or a severe anaemia or acute ? in diph- the of a staring expression, y absence 0| or elevated B.M.R. an theria, scarlatina, typhoid thyroidal signs, ns fever. Persistent cases yr gi gallop rhythm usually pro- In latent _ weight. thyrotoxic en_ claims failure of the hypertensive or arterio- may be absent and the thyroid is not notab y t sclerotic heart, or it may be a sign of coronary In heart disease, larged. thyrotoxic thrombosis or of a bundle branch etc. are not cold an block, warm and moist and With the i abolition of failure the gallop dis- in asthenia, the hair neurocirculatory appears for the time being. The prognostic grey and frequently prematurely 1 significance of is . persistent gallop rhythm sounds are loud and angry very obviously bad. The advent of gallop rhythm sometimes be foretold at an earlier Auscultation may phase by impurity of the first The of successful cardiac sound, i.e., prolongation secret an(j with a tendency to splitting. is the positive identification of theallsP^a fi o ^ > second heart sounds by a technique The estimation op blood pressure ear and thumb well trained in the syn This is one of the commonest and for all that tion of and touch. Apply_y? hearing imaj one of the most of all clinical piece to the mitral area the important proce- oyer 1 terv> dures. Nevertheless many doctors are rather and thumb to the caro impulse your y_ nebulous about its most vital ,. , determination, Shut your eyes as an aid to dissociating namely, the diastolic pressure. the else from mind and feel the Obviously thing your first essential in the estimation of blood thumb coincident Witt. pressure impact against your is an accurate of the whereabouts of 1 , conception single intense demarcated auditory F' 1 the standard systolic and diastolic pressure of the first heart sound. this , Employ levels. These are as follows : The in the auscultation of every > systolic deliberately in* pressure is the point where the first distinct rather than spasmodically invoke it in a sound is heard during decompression and the auscultatory stress. Thus only can be a xue diastolic pressure is the point where the loud calm sure in disentangling and efficiency clear sounds in and more and murmurs. abruptly drop intensity sounds _ complex suddenly become dull and muffled, or abruptly Bedford and Parkinson invariably emp oy advantag disappear. The upper normal blood pressure technique and so we might with the nr limits are 160 systolic and 100 diastolic. The likewise. Remember that systole equals diastole blood pressure rises only \ mm. for each year of sound plus the short pause and that ? life : otherwise age has by no means the equals the second sound plus the long p stated, c that was attached to it. Observe that the first sound is lower-pi , importance formerly tna The standard levels are of such primary im- !?nger and louder than the second^sound, tnan it portance that I do not propose to say much more is preceded the long pause and by ?it about the estimation of blood pressure beyond followed the short pause which separates by a a few cardinal in from the second sound. Trace the fiis indicating points technique:? the cuff on the inside of the arm second sounds down from the pulmonary area (1) Apply to in order to compress the artery against the the . cardiac impulse. A facile ana bone : its application on the outside of the arm . Gallop rhvthm is such a striking, re- is an abortive attempt to bend the bone towards important auscultatory sign that I cannot m the frain some reference to it. artery. from making lower end is intro- (2) So apply the cuff that its lies gallop a third or extra sound rhythm above the bend of the elbow, thus duced into the cardiac cycle. Gallop rhy ini,immediately the Korotkow sounds are best heard. consists of the usual first and seco therefore, im inflate the armlet to obviate con- sounds an extra sound which is some (3) Quickly plus of the arm : slow inflation occludes the 5?t only audible but palpable as well. 1 maygestion a a veins before the arteries, hence blood continues discuss the origins of this extra sound in ^to enter the limb but is unable to escape with Paper. However it may gallop rhyt be, resultant of the arm. must be distinguished from congestion of clearly reduplication (4) Inflate the armlet to a pressure of 200 the heart sounds which is a partial idea. mm. lest you miss the silent gap. three sounds of a gallop are fairly equidistant. In souna (5) Decompress gradually and at a presystolic rhythm the extra uniform gallop tnerate. ?ccurs somewhat before the first sound and n Take at least three to four or more read- spacing of the sounds is more even than (6) extraings until you obtain two concordant readings : Protodiastolic gallop rhythm where the the initial reading in nervous is unduly ^ound occurs after the sec?7* subjects immediately as of the arm is liable to lead sound. The maximum of gallophigh compression punctum ito reflex vaso-motor of the brachial rhythm is about the impulse, though spasm 18 usually area, audible over a much wider artery. frequently In exclude resemblance to the foot-falls of a galloping (7) young hypertensives especially, jts coarctation of the aorta bv of the horse is best when the heart rate palpation appreciated femoral arteries. surpasses 80 per minute. Temporary gallop 136 THE INDIAN MEDICAL GAZETTE [March, 1939

At this year's session of the American Heart Stroud advised the routine Association, 1 taking of blood pressure in both arms. For the ' past eight yearshe said, I have been taking the blood pressure in both arms of all patients that have come to me, and I can confirm the impres- sion that has been given by this last paper, namely, that there is quite a marked difference in the blood pressure in the two arms in a vast majority of cases. The main reason I have taken the blood pres- sure in both arms is that eight years ago, before the insurance companies had stopped granting total disability insurance, one of Walter " " Cramp's all American football players took out a life insurance containing a total disability clause. His blood pressure was taken by the doctors in the left arm only. His was a $250,000 policy taken up by three or four companies. This in- dividual had a blood pressure of 120/80 in the left arm. Three weeks after he took out this policy, a cardiac infarct developed while he was playing golf. I saw him six weeks after this infarct occurred, and at that time he had a blood pressure of 120/80 in the left arm, but a pressure of 200/110 in the right arm. Presum- ably then, if these companies doctors had taken the pressure in both arms, this gentleman would not have been living in Santa Barbara for the last eight years on his income from his total dis- ability insurance Dr. Stroud's advice is a counsel of perfection to the busy general practitioner who may be not content with an accurate unjustifiably reading in (Continued jrom previous column) one arm. method which is packed with fallacies and im- there have been to Radiography of the heart and aorta perfections, attempts square the results of percussion with those of radiology, The modern routine examination of a heart but they have led to nothing. The best proof case includes clinical, electrocardiographic and that it (cardiac percussion) is to be extruded radiological investigations. In Indian medical from our important and growing number of centres electrocardiography is. a rightly estab- clinical and laboratory methods is the fact that lished Cardiovascular procedure. radiology, it is sterile. The tokens of sterility are upon it- however, has not yet come into its own, probably Nothing has been added to medical knowledge or because the profession is not quite aware of progress through cardiac percussion since the the fact that precordial percussion has been beginning of this century, and in the light of almost entirely abandoned at home on the a>rays it will shrink into obsolescenceIt has, that it is a unreliable 1 ' grounds demonstrably rc-rays ', he continues, tells us literally every- in procedure excepting that it may reveal pul- thing that percussion can tell us and tell it more monary emphysema or . The amply and precisely \ 1 More faithful witnesses traditional clinical methods of estimating cardiac are eyes than ears' of the heart fell into enlargement by percussion I acknowledge my great indebtedness to the disuse complete about 1936 when John Parkin- writings of Continental and son's studies disclosed the British, American, radio-cardiological other cardiologists past and present. inaccuracies inherent in this time-honoured My grati- gross tude to my more to Dr. Evan In the first Lumleian for teachers, especially procedure. lecture Bedford, is certainly not less. In conclusion 1 1936 John Parkinson made some trenchant would strongly advise those who wish to keep remarks on the method of of percussion1 studying abreast the times in the matter of clinical cardiac enlargement. The inaccuracy of per- heart disease to to new ' add their library the cussion ', he said, is inseparable from a method official mouthpiece of the Cardiac Society of which is indirect and inferential : and this is Great Britain and the British Heart ' Ireland, now generally admitted. No longer shall we tell Journal. As the calorimeter tells the activity of the who at the front professor by knocking of the patient's metabolism, so you may deter- out who was in door could find the drawing- mine the plus or minus activity of the local pro- a final to a room. As effort resuscitate dying fession in any district by the condition of its (Continued at foot of next column) library \?Harvey Cushing.