Showing papers in "Heart in 1944"

CARDIAC OUTPUT IN MAN BY A DIRECT FICK METHOD Effects of Posture, Venous Pressure Change, Atropine, And Adrenaline

Abstract: In the Fick method of estimating cardiac output (C.O.), where C.O. (litres/min.)=oxygen consumption (c.c./min.) divided by arterio-venous oxygen difference (c.c./litre), the measurement of the numerator can easily be made by spirometric methods. Hitherto the measurement of the arterio-venous oxygen difference in man by respiratory techniques has proved difficult and laborious, and it has not been possible to make frequent serial observations. The difficulties seem to be largely overcome by the method of cardiac catheterization first introduced by Forsmann (1929) and developed by Cournand and Ranges (1941). Over 394 catheterizations can now be recorded without any accidents (Forsmann (1), de Carvolho and Moniz (48), Ameuille et al. (60+), Cournand et al. (150) and the present authors (135)). The catheter has been left in situ as long as 24 hours (Cournand et al.), but the present authors have limited the period to one hour in normal subjects. Clotting does not occur on the unwettable surface of the catheter, and a slow drip of 3-8 per cent sodium citrate through the catheter prevents any thrombus formation round the hole at the tip.

Complete heart block

Abstract: This paper discusses 64 cases of heart block, mostly complete, seen during the same period as 29 cases with dropped beats and 140 cases with latent heart block (Campbell, 1943, b and c). Of the patients attending the Cardiographic Dept., Guy's Hospital, during 12 years, 0-6 per cent had complete, 0*5 per cent partial, and 2-2 per cent latent heart block. Comeau (1937) found 0 55 per cent of cardiovascular cases had complete block; and Paul White (1937) found 0O8 per cent had complete, 2-6 per cent partial, and 3-0 per cent latent. It is curious that with such close agreement between the other figures he should have found so many more with partial block. An analysis of the age and sex of the cases and of their actiology was similar to that found in other series, so this and the' clinical features will be dealt with shortly. Three aspects will be dealt with rather more fully-the prognosis, the incidence and significance of StokesAdams attacks, and the extent to which complete block remains persistent or varies to lower grades of partial or latent block. This leads to a more complete classification of the subdivisions of heart block. I had the impression that, apart from the cases in hospital with frequent changes of rhythm. and Stokes-Adams attacks, complete heart block was as a rule persistent once it had been found. But half my cases had more than one grade of heart block graphically recorded; and more than 60 per cent were observed clinically to have such changes. Sometimes these were frequent and one did not know with what rhythm the patient would be seen next: sometimes, after a long period of complete block, partial or latent block was seen for no apparent reason.

Congenital pericardial defects.

Abstract: Congenital pericardial defects are among the most uncommon of reported cardiac anomalies. In 1925 Moore was able to find 64 references to pericardial defects, but a detailed re-examination of the records by Southworth and Stevenson in 1938 reduced the number of confirmed cases in man to 52 and 7 of these occurred in monsters. They added another case to this series, and in a footnote to their paper referred to the case described by Dahl (1937) in which, however, a traumatic or pathological basis for the defect could not be definitely excluded: their review did not include Ladd's (1936) case. The purpose of this paper is to record the findings in two additional specimens. One is of especial interest in that the defect was directly responsible for the death of the patient Such a result has been recorded on one previous occasion only. It is not proposed to review the literature in any detail since this has already been comprehensively covered in excellent papers by Moore (1925), de Garis (1934), and Southworth and Stevenson (1938).

Adrenal-sympathetic syndrome: chromaffin tissue tumour with paroxysmal hypertension

Abstract: The chromaffin cells of the adrenal medulla are a part of the scattered \" chromaffin tissue system.\" The tumours of these cells, the pheochromocytomata or adrenal paragangliomata are nearly always benign, but usually produce paroxysmal hypertension ending fatally if the tumour is not removed. There are reports of 152 cases of pheochromocytoma. The only extra-adrenal paragangliomata that have produced the hypertensive picture are those arising in the retroperitoneal tissues between the kidneys: of 13 such cases, 9 had the cardiovascular syndrome typical of the adrenal cases, and they form part of one clinical problem and are considered with the adrenal cases here. Of these 165 cases, 90 have been described since 1929, and 36 operations have been reported.

Casual and basal blood pressures iv. their relationship to the supplemental pressure with a note on statistical implications

Abstract: In an article entitled Casual and Basal Blood Pressures in Essential Hypertension (Alam and Smirk, 1943, b), two statements were made in the discussion upon which it is desired to offer further evidence. 1. \" It seems desirable to regard the casual blood pressure as made up of two parts, namely, the relatively stable basal blood pressure and a variable supplemental pressure. The supplemental pressure is the part of the casual blood pressure that is elevated as the result of the patient's physical, mental, and emotional activity, chiefly the latter; the elevation of the basal blood pressure in essential hypertension requires some other explanation.\" This statement that the supplemental pressure varies and the basal pressure is relatively constant refers, as is indicated in the last sentence, to the individual and not to comparisons between different individuals. Measurements of the basal pressure, whatever technique be adopted to obtain it, aim at removing these known causes of variation and at measuring a pressure that has been obtained under standard conditions of mental and physical rest. There is a high probability, therefore, that basal readings obtained under standard conditions will be more constant for the individual than casual readings taken under a variety of conditions. This has now been shown, experimentally, by Kilpatrick. 2. \" The lability of the blood pressure in a case of essential hypertension may be judged by the degree of difference between the casual and basal pressures.\" In Fig. 4 of the paper referred to above the relationship of this difference, which we call the supplemental pressure, to the casual and basal pressures is set out graphically. It was suggested by the authors that the patients with the higher supplemental pressures are in general those with higher casual blood pressures, but their basal pressures are no higher than those of essential hypertension patients with lower supplemental pressures. The object of the present paper is to describe some further observations that confirm the views previously expressed as to the relationship of the basal and supplemental pressures in essential hypertension, to study this relationship in health, to rediscuss the conditions under which the basal blood pressure should be measured, and to make reference to the significance which this conception has in relation to the statistical analysis of the ordinary casual (clinical) readings of the blood pressure. The opportunity is taken of referring to a comment by the editor of the British Heart Journal upon a statement in a previous paper (Alam and Smirk, 1943, b), which was to the effect that our results shown in Fig. 4 did not seem to support one of our conclusions. The basal and supplemental pressures have a practical importance which should make their separate determinations a matter of clinical routine in certain classes of patient.

Heart block with aneurysm of the aortic sinus.

Abstract: Disturbances of conduction in the heart may be purely functional, when for example demands are made on the conduction path very early in diastole as seen in blocked and aberrantly conducted auricular extrasystoles (Scherf and Boyd, 1940), or when too many stimuli are presented for conduction within a short time as with the incomplete A-V block that always exists in auricular fibrillation. Conduction disturbances may also be due to vagal inhibition. They may occur transiently after pneumonia and influenza, and are well known in diphtheria; recently Neubauer (1942) found many examples of partial and complete block in 100 cases of diphtheria. Over-digitalization may through poisoning of the A-V node lead to prolongation of conduction time, partial, or complete block. A permanent block can be established through coronary sclerosis, coronary thrombosis, rheumatic heart disease, syphilitic gumma, and more rarely through diphtheria, tuberculosis, and carcinoma affecting the A-V node or bundle directly. Congenital complete heart block is also known, and a few cases were found by Yater (1929), Aitken (1932), Campbell and Suzman (1934), and Currie (1940). The exceptional event of heart block as a result of direct trauma to the chest wall is described by Coffen (1930), Walker (1933), and White (1937). The following is the report of a case in which complete heart block was associated with an intracardiac aneurysm and aortic stenosis.

Auriculo-ventricular rhythm.

Abstract: assumes control over the ventricles. When this happens, two types of auriculo-ventricular rhythm may arise. One is called A-V nodal rhythm and is recognized by the inverted P waves, which are as a rule either abnormally close to the QRS complex or may follow it. The second type of auriculo-ventricular rhythm is known as A-V dissociation, characterized by the rate of the ventricular contractions being slightly faster than those of the auricles so that there is no constant P-R or R-P interval. Theoretically, the difference between the two rhythms is due to retrograde conduction being present in A-V nodal rhythm in order to allow the auricles as well as the ventricles to respond to the new pace-maker in the A-V node, while in A-V dissociation retrograde conduction from A-V node is blocked so that the auricular contractions must arise above the A-V node, probably in the sino-auricular node (Cutts, 1937; Richardson, 1922). When ventricular bigeminy complicates A-V rhythm it is described

Acute left auricular failure.

Abstract: Case 1, M. H. H. A primigravida, aged 37, was admitted to hospital, in the fifth month of pregnancy, on account of recurrent attacks of acute dyspncea with hemoptysis. She gave a history of rheumatic fever at the age of seven but, apart from slight shortness of breath on exertion, had been free from symptoms until the third month of pregnancy when she became increasingly dyspnceic and developed a persistent cough with blood-streaked sputum. Two months later she had a sudden acute attack of dyspnoea at rest and coughed up a moderate amount of bright red blood. Three further attacks occurred during the next three days and she was admitted to St. Mary's Hospital, Manchester, under the care of Dr. J. W. A. Hunter, very collapsed, extremely dyspnceic, and coughing up considerable quantities of pink frothy sputum. The radial pulse was only just palpable and there was a trace of cedema at the ankles. Moist sounds were present all over the chest. The blood pressure was 100/70. The clinical picture was that of acute left-sided heart failure. Under treatment her condition improved rapidly and next morning there were only scattered moist sounds in the chest with slight hzemoptysis; the cedema had disappeared and there was no systemic venous engorgement. The heart was grossly enlarged, but its rhythm was regular, and there was a loud apical presystolic but no other diastolic murmur. With rest in bed her condition steadily improved, the dyspncea subsided, and the hzemoptysis ceased in a few days. She remained well for two weeks, but then, without apparent cause, became acutely dyspnceic and coughed up a considerable quantity of blood. The suddenness of this relapse suggested the possibility of a pulmonary embolus. She failed to respond to treatment, developed severe pulmonary cedema, and died in a few hours. Autopsy was performed by Dr. F. A. Langley.The lungs were grossly cedematous, but there was no sign of recent pulmonary embolism, nor of old infarction. The heart weighed 400 g. There was a button-hole stenosis of the mitral valve, measuring 15 x 3 mm. The aortic valve was slightly scarred and the cusps were adherent for a short distance from their bases. The pulmonary and tricuspid valves were healthy. The left auricle was considerably dilated and hypertrophied, its wall being 4 mm. thick. The right ventricle also was considerably hypertrophied, the wall being 9 mm. thick. The pulmonary arteries were moderately atheromatous. Apart from some cortical congestion the kidneys were normal. The estimated age of the foetus was 6k months.

The unity of paroxysmal tachycardia and auricular flutter.

Abstract: OF CASE NOTES Case 1. A man, aged 47, with mitral stenosis. Complained of shortness of breath and attacks of palpitation. Systolic and mid-diastolic murmurs in mitral area. No clinical evidence of heart failure. Cardioscopy showed moderate enlargement of heart from mitral stenosis, and slight pulmonary congestion. Electrocardiogram (EC.) shown in Fig. 3. Quinidine failed to prevent or abort attacks. Digitalis converted arrhythmia into auricular fibrillation. 234 WILLIAM EVANS PAROXYSMAL TACHYCARDIA AND AURICULAR FLUTTER Case 2. A woman, aged 60, with mitral stenosis. Complained of shortness of breath and palpitation. Clinical evidence of mitral stenosis with much cardiac enlargement, and failure. Cardioscopy showed aneurysmal dilatation of left auricle and pulmonary congestion. When attack of tachycardia persisted (Fig. 4), digitalis converted it into auricular fibrillation. Quinidine was never tried. Case 3. An otherwise healthy man, aged 21. Complained of palpitation for over three years. Latterly attacks had lasted for some months. No abnormal signs on clinical or cardioscopic examination. EC. shown in Fig. 5. Digitalis restored normal rhythm in four days. Quinidine was not tried. Case 4. A man, aged 69, with hypertensive heart failure. Admitted to hospital because of nocturnal breathlessness. Blood pressure 170/110. Triple rhythm from addition of fourth heart sound, and other signs of left ventricular failure. Diffuse chronic bronchiectasis. Developed bronchopneumonia and tachycardia. EC. showed auricular tachycardia with 2: 1 A-V dissociation; A.R., 254; both auricular waves outside ventricular waves. Quinidine changed rhythm to auricular fibrillation and to normal rhythm. Further attacks of tachycardia uninfluenced by quinidine or digitalis, and patient died. Case 5. A woman, aged 28. Attacks of tachycardia and symptoms of heart failure over some years. Presystolic murmur of mitral stenosis. Cardioscopy showed moderate cardiac enlargement, and pulmonary congestion. EC. shown in Fig. 6. On one occasion arrhythmia converted into auricular fibrillation by digitalis therapy, but later neither digitalis nor quinidine prevented or relieved attacks. Death took place from heart failure and pulmonary infarction. Case 6. A man, aged 68, with hypertensive heart failure. Increasing breathlessness for five months. Severe nocturnal dyspncea for three months. Four attacks of palpitation in last ten days; last attack had been persisting for four days. Great cardiac enlargement and pulmonary congestion from hypertension. EC. shown in Fig. 7. Quinidine for ten days had no effect on abnormal rhythm, but digitalis over same period slowed ventricular rate and established normal rhythm seven days later. Case 7. A woman, aged 58, with mitral stenosis and hypertension. Dyspncea for a year and attacks of tachycardia for a month. Blood pressure 220/115. Clinical signs of mitral stenosis. Cardioscopy showed moderate cardiac enlargement, and pulmonary congestion. EC. shown in Fig. 8. Digitalis on one occasion changed rhythm to auricular fibrillation. Quinidine was never prescribed. Death came suddenly from pulmonary infarction. Case 8. A woman, aged 65. Attacks of palpitation for 3 years. Systolic and mid-diastolic murmurs of mitral stenosis. Cardioscopy showed moderate enlargement of heart. EC. shown in Fig. 10. Quinidine restored normal rhythm on one occasion, and digitalis converted it into auricular fibrillation another time. Case 9. A woman, aged 53. Sudden onset of tachycardia eight days before. Clinical diagnosis obscured by tachycardia, but cardioscopy showed great enlargement of heart from mitral stenosis. EC. shown in Fig. 11. Quinidine for 7 days had no effect, but digitalis converted it into auricular fibrillation. Case 10. A man, aged 52. Frequent attacks of palpitation lasting an hour or a day at a time for eight years. Presystolic murmur of mitral stenosis. Cardioscopy showed moderate enlargement of heart, and slight pulmonary congestion. EC. shown in Fig. 12. Neither quinidine nor digitalis prevented or aborted attacks. Case 11. A woman, aged 63, with hypertensive heart failure. Symptoms and signs of left ventricular failure for some months with recent onset of attacks of paroxysmal tachycardia. Cardioscopy showed enlargement of left ventricle, and pulmonary congestion. EC. showed auricular tachycardia with 2:1 A-V dissociation; A.R., 292; alternate auricular waves within S wave. Digitalis and quinidine had no effect on attacks. Case 12. A man, aged 58, with mitral stenosis. Frequent short attacks of palpitation over many months. EC. shown in Fig. 9. Quinidine was never given. Digitalis on one occasion changed rhythm to auricular fibrillation and thence to normal rhythm. Case 13. An otherwise healthy woman, aged 38. Brief attacks of palpitation. No abnormal clinical findings in between attacks. EC. shown in Fig. 13. Neither quinidine nor digitalis prevented or relieved attacks. Case 14. An otherwise healthy woman, aged 34. Complained of attacks of palpitation, lasting -a few minutes or hours, for 18 months. No abnormal signs on clinical examination which included tcardioscopy. EC. shown in Fig. 14. Neither quinidine nor digitalis was tested for relief or prevention of attacks. 235

Perforation of the interventricular septum due to cardiac infarction.

Abstract: Until December 1943 thirty-eight cases of rupture of the interventricular septum have been reported; of these eight were diagnosed ante-mortem. Rupture of the septum usually occurs in the seventh and eighth decades in patients who have had long-standing high blood pressure. It is more common in first infarctions, where the infarct is small and the blood pressure remains above 160/100 after infarction. The average time of rupture is between the third and twelfth days (Edmunson and Hoxie, 1942). Stanley (1937) reported that, at the time of rupture of the septum, his patient complained of sudden substernal pain and became shocked. After rupture a systolic murmur, which may be rough or blowing, has been noticed over the sternum in the fourth and fifth interspaces in all reported cases, generally accompanied by a systolic thrill (Sagar, 1934). In all cases observed within two or three hours of rupture there has been cyanosis and dyspncea and usually there has been some degree of congestive failure throughout the illness; death usually being due to right ventricle failure (Bayley and Fader, 1941). Although most reported cases have died during the first week after perforation of the septum, diminution of the congestive failure has followed prolonged use of mercurial diuretics (Wood and Livezey, 1942) and digitalis therapy (Leonard and Daniels, 1938). Seven cases have been reported that lived for more than four weeks, of which Moulton (1942) mentions four. The longest recorded duration of life after perforation is four years and ten months (Wood and Livezey, 1942). Gross and Schwartz (1936) record a case which survived two months and Stanley (1937) one which lived five months.

Circulatory failure due to vitamin b deficiency.

Abstract: Cases of cardiac failure due to deficiency in vitamin BI have been recognized in this country, and although the number of reported cases is small, their recognition is important since treatment by adequate doses of vitamin Bl is rapidly effective, whereas the usual methods of treatment fail. Most cases so far reported occurred in patients drinking too much alcohol and living on an inadequate diet, but a few were caused by deficient diet alone. Observations on thiee cases of \" avitaminosis-Bl heart \" showed some unusual features which seem to justify a communication. Two of the three drank too much alcohol, but in the remaining one the condition was caused solely by deficient diet.

A case of tuberculous pericarditis.

Abstract: A man, aged 22, who worked as a shop assistant, was admitted to Addenbrooke's Hospital on March 11, 1943, with the following history. About mid-February he first began to feel generally out of sorts and over the space of a few days developed a dry, irritating cough which kept him awake at night, a dull pain over the pracordium, nausea, weakness, and slight breathlessness on exertion. These symptoms persisted until his admission. His previous health had been good and the only illness he remembered was an attack of\" pleurodynia \" at the age of 18. His family history was healthy with no tuberculosis. On admission the heart was greatly enlarged both to left and right, the apex beat could not be seen or felt, the sounds were faint and tic-tac in quality, the pulse small, regular, and rapid (110), the respiratory rate 22, the temperature intermittent and rising to 100 or 101, and the blood pressure 110/80. The m6st arresting physical sign was a loud rub audible over the ' . rnd whole pericardium but most marked at the base. The cardiogram showed low voltage curves with inversion of T in leads I, II, IVR, and IVF (Fig. 1) and X-ray showed the typical shadow -=of a large pericardial effusion (m.t.d. 17 cm.; see Fig. 2). The sedimentation rate (Westergren) was 60 mm. in one hour. Progress. Except for a period of two months in September and October when he rested at home, he remained under observation in hospital until his death on December 9. The progress of the disease appeared to fall into three clinical phases. (1) The phase of increasing effusion leading to congestive failure * _ (4 months). .. ...... ...

Stokes-adams attacks in a child

Abstract: It is recognized that heart block may occur in several acute infections, but apart from diphtheria and acute rheumatism it is rare and even in the latter it is uncommon. Often the outcome of this complication in children is fatal, but in the following case, a boy aged 12, with heart block and pericarditis, recovery took place. For three months before admission to hospital he had felt tired and had to rest on returning from school. He had been restless for the past few nights and eventually had to remain in bed for three days. During this time he had throbbing of his heart and headache. For two days he had a troublesome unproductive cough, and on the day before admission he had two attacks of unconsciousness. On coming round he perspired and vomited. He had one attack of unconsciousness the day before coming to hospital and on admission he complained of giddiness, shortness of breath, and persistent coughing. Apart from measles there was no history of any previous illness. On admission the patient was very ill. He presented grey cyanosis and was distressed by severe dyspncea. The temperature was normal and the pulse was small and 160 a minute. The blood pressure was 80/40. The respiration rate was 44. There was prominent pulsation and distension of the cervical veins. The apex beat was diffuse and was just outside the midclavicular line. The heart sounds were distant and the second sound was split and accentuated in the pulmonary area. There were no murmurs. Numerous rales were heard over the chest. No other abnormal sign presented on further examination; there was no distension of

A case of myxoma of the left auricle.

Abstract: In their paper on this subject Fawcett and Ward (1939) remark that only rarely do descriptions of this interesting lesion appear in British publications, there being only one report in the nine years preceding their article. The condition is well reviewed in their paper and in that of Gilchrist and Millar. (1936). It is the purpose of this article to describe a further case with an autopsy report.

Nicotinic acid in the treatment of angina pectoris.

Abstract: Glyceryl trinitrate has had no equal in the relief and prevention of the anginal attack. The claims of new drugs must, however, be tested if their pharmacological action includes dilatation of the coronary artery and if clinical benefit has been observed. Since improvement in patients with angina pectoris has been reported recently by Moncrieff (1942) and Neuwahl (1942) from treatment with nicotinic acid, it became necessary to test the drug in a series of cases under controlled conditions. Moncrieff recorded benefit in three patients with doses varying from 10 to 50 mg. by mouth. Neuwahl claimed prolonged improvement in six patients after intravenous administration: one of these had received antisyphilitic treatment for aortitis, another showed aortic incompetence and great dilatation of the aorta, and a third with mitral stenosis was subject to paroxysmal auricular fibrillation ; electrocardiography was not a part of the examination, and no mention was made of the period of rest associated with the nicotinic acid infusions of which six were given within three weeks. Transient benefit was also claimed from oral administration of the drug, but no dosage was mentioned. Masek (1940) watched temporary improvement in four cases of old cardiac infarction, and in three with coronary sclerosis and angina pectoris, after the intravenous injection of the chloride of nicotinic acid in doses up to 0416 g. He suggested that this effect might not only be due to coronary dilatation but also to an improvement in the metabolism of the myocardium by saturation with coenzymes.

Incomplete bundle branch block.

Abstract: Lewis (1925) stated that delay in the passage of the impulse down a bundle branch could alter materially the form of the electrocardiogram. Wilson (1940) defined incomplete bundle branch block as due to a conduction defect that merely retards the passage of the impulse through one of the main bundle branches, and stated that it gives rise to electrocardiograms which are \" transitional, both as regards the length of the QRS interval and the form of the ventricular deflections between those that represent complete bundle branch block and those of normal outline.\" Partial bundle branch block is used to describe curves that contain both bundle branch block and normal complexes. There may be a rhythmic sequence, as in 2: 1 bundle branch block, or occasional normal QRS deflections may occur in a record predominantly composed of bundle branch block complexes. In common with the New York Heart Association's nomenclature, Wilson (1944) regards 0-12 sec. as the minimum QRS duration ordinarily compatible with the diagnosis of conmplete bundle branch block. In this country, however, a QRS that exceeds 0-10 sec. has generally been considered as indicating complete bundle branch block providing other criteria are present (Lewis, 1925; and Hunter, Papp, and Parkinson, 1940). This small divergence may be due to a different technique in measurement. In the cases to be described the QRS has been measured straight across at the widest point in any lead. In no case has it measured more than 0 10 sec., when incomplete bundle branch block has been judged to be present.

Clinical evaluation of the pressor activity of methedrine, neo-synephrine, paredrine, and pholedrine.

Abstract: Recently a number of pressor drugs of the adrenaline type have come into clinical use for the treatment of low blood pressure following surgical procedures, spinal anxsthesia, circulatory collapse, and surgical and traumatic shock. For therapeutic purposes the ideal pressor drug should be effective by the intramuscular or intravenous route; it should act rapidly; it should produce a sustained elevation of blood pressure, so that frequent injections of the drug are not necessary; and it should have no undesirable effects on the cardiovascular system and no untoward side effects. Adrenaline and ephedrine were the first drugs to be used clinically to raise the blood pressure in cases of operative shock. Their limitations, however, are nowv well known. Adrenaline may do more harm than good beca4se in therapeutic doses intrayenously it causes a considerable rise of blood pressure, e.g. 200 mm. to 300 mm. of mercury, with a precipitous fall after a few minutes to a level lower than before. Similarly ephedrine, which for dependable results must be given intravenously, produces a sharp rise of blood pressure that lasts only for ten to twenty minutes. Other pressor drugs have been introduced with a more sustained action. In most of the studies reported on these, however, no definite criteria seem to have been employed in their evaluation, nor have the conditions of administration been standardized. In general the drugs have been, given to patients showing a fall of blood pressure after spinal anaesthesia or during surgical operations, but few comparative studies have been made on them. In this investigation an attempt has been made to evaluate in similar conditions the pressor activity of the sympatho-mimetic drugs methedrine (d-desoxyephedrine, pervitin), neosynephrine, paredrine, and pholedrine (paredrinol, veritol). Their chemical relationship ta adrenaline and ephedrine is shown in the following formulk:

Pulmonary embolism: the clinical and cardiographic progress of a case

Abstract: Although severe pulmonary embolism is not an uncommon complication of abdominal operations, the opportunities for a close clinical study of the condition are few. Too often the medical officer arrives at the bedside when it is too late. Even those patients who do not succumb at once rarely survive a few hours. In such circumstances, emergency measures connected with treatment take the place of clinical observations, which might include cardiographic records. The account that follows is about a patient who developed severe pulmonary embolism, eight days after abdominal hysterectomy, and was observed continuously from the onset of the embolism until recovery took place.

Unusual electrocardiogram in dextrocardia

Abstract: The case here described was found in the course of a mass radiographic survey. Case History.-The patient was a well-grown man aged 35 years. He was free from symptoms. He had no significant past medical history. He had always lived a normal life and had been moderately athletic in his school days. On clinical examination it was found that cardiac pulsation was palpable in the right fourth intercostal space just internal to the mid-clavicular line. Normal heart sounds were heard in this area and between it and the sternum. At the left border of the sternum sounds were faint and further to the left were inaudible. No bruits were heard. There was no dyspncea, cyanosis, clubbing of the fingers, or other indication of cardiac disorder. Blood pressure was 120/70. Radiography showed a heart in the position of complete dextrocardia, but otherwise of normal contour. The lung fields were clear. The left dome of the diaphragm was raised. The liver and stomach were not transposed. Electrocardiographic Findings.-A cardiogram consisting of the three standard limb leads and three chest leads is shown in Fig. 1.