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ACUTE PHASE OF MYOCARDIAL INFARCTION
Saturday
September
J. D. ALLEN R. G. G. JAMES S. A. ZAIDI
J. F. PANTRIDGE
Patients and
Royal Victoria Hospital and Queen’s University, Belfast Summary Summary
one
Introduction
IT has been shown that 40% or more of all deaths from the coronary attack occur within an hour of the onset of symptoms,1-5 and that, among middle-aged and younger males, 63% of the deaths occur within one hour. Yet the median delay in admission to a hospital ward may be more than eight hours. 3,7 Hospital coronary-care units affect the outcome in only 10% of the patients admitted to such units. 8,9 Thus most patients when they reach a hospital coronary-care unit are either convalescent or moribund and the acute phase of the illness is infrequently seen. It has been said that " it is difficult to conceive that under any system much can be done about patients dying within one hour of the onset of symptoms 11.4 This view may be unduly pessimistic. The operation of a prehospital coronary-care scheme reduces the interval MANAGED
WITHIN
SYMPTOMS
AN
HOUR
four-year period 1966-69, 1150 patients with myocardial infarction were managed by a mobile coronary-care unit. The criteria for the diagnosis of acute myocardial infarction were (a) indubitable electrocardiographic evidence of recent infarction (272), or (b) sequential ST and T wave changes accompanied by significant and transient rise in s.G.o.T. (7), or (c) left-bundle-branch block with similar enzyme changes (5). 284 (25%) of the
acute
Dysrhythmias occurring within
I-PATIENTS
Management
In the
hour of the onset of symptoms of acute myocardial infarction have been documented in 284 patients. A high incidence of bradyarrhythmia was noted. Ventricular dysrhythmias were also and a disappointing response to showed frequent lignocaine therapy. Early initiation of intensive care not only prevents deaths from ventricular fibrillation but also diminishes the incidence of shock and pump failure by preventing or immediately correcting dysrhythmias and limiting the size of the myocardial infarct. The resources for coronary care should be directed towards the pre-hospital phase of the coronary attack.
TABLE
I97I
between the onset of symptoms and the initiation of intensive care and permits the observation of many patients soon after the onset of the coronary attack. 10- 13 We report here certain clinical features among 284 patients seen within one hour of the onset of symptoms who were alive when seen or who were resuscitated.
ACUTE PHASE OF MYOCARDIAL INFARCTION A. A. J. ADGEY J. S. GEDDES S. W. WEBB
4
OF
ONSET
OF
1150 patients were under intensive care within one hour of the onset of symptoms (table i). A clearcut history of the time of onset of chest pain or collapse was obtained for each patient. 224 patients were male and 60 were female; the age of the two groups ranged from 24 to 79 years and 46 to 79 (mean 62) years, respectively. Sites of infarction were anterior (135), posterior (133), combined anterior and posterior (4), and acute subendocardial (7). 5 patients had left-bundle-branch block. 79 (28%) of the 284 patients were seen within thirty minutes of the onset of symptoms. 91 patients had had a previous myocardial infarction and 108 patients had had angina without previous infarction. 85 patients had had no previous symptoms of ischxmic heart-disease. 203 patients (72%) were considered to have had a mild coronary attack in that when they were first seen clinical hsemodynamic disturbance was absent or was corrected immediately by suppression of the primary dysrhythmia. 46 patients (16%) were considered to have had a moderately severe attack in that there was mild hypotension-i.e., systolic blood pressure 90-95 mm. Hg or clinical evidence of pulmonary congestion. The attack was considered severe in 35 patients (12%) in that there was evidence of gross cardiac failure or cardiogenic shock. 19 patients (7%) had cardiogenic shock. 10 of these had had one or more previous episodes of myocardial infarction. 16 of the 19 patients had cardiogenic shock when first seen; the other 3 developed shock in the hospital coronary-care unit. The patients were in the cardiac unit throughout their hospital stay. The average stay in hospital was three weeks, and the average duration of monitoring was forty-eight hours. Terminal arrhythmias in patients dying of shock or cardiac failure have not been analysed.
(mean 56)
Results
(65%) of the 284 patients required therapy the site of the attack before they were considered fit for transport. 170 patients (60%) required therapy for either bradyarrhythmia, ventricular dysrhythmia, or supraventricular tachyarrhythmia, and, of these 170, 12 had dysrhythmia associated with acute left 185
at
7723
502 TABLE II-INCIDENCE OF DYSRHYTHMIAS AMONG
ventricular failure. 15 patients required therapy at the site of attack because of left ventricular failure unrelated to rhythm disturbance. The incidence of dysrhythmias among the 284 patients related to the time after the onset of symptoms when the dysrhythmia first appeared is shown in table II. Among patients seen within the first hour, bradyarrhythmia, either within that hour or later, 125 (44%) of the 284 patients had was common. bradyarrhythmia-i.e., sinus or nodal bradycardia (ventricular rate 60 per minute or less) or atrioventricular block (second-degree or complete). 88 patients (31 %) had bradyarrhythmia within the first hour. 37 patients (13%) developed bradyarrhythmia later. The incidence of sinus and nodal bradycardia and atrioventricular block, second-degree or complete, in relation to the site of infarction and to the time after the onset of symptoms is shown in table ill. 75 patients (26%) had sinus or nodal bradycardia in the first hour; 33 patients (12%) had sinus or nodal bradycardia later. 17 patients (6%) had heart-block, second-degree or complete, in the first hour, whereas 11
(4%) developed heart-block, second-degree or Bradyarrhythmia occurred more complete, later. frequently in patients with posterior infarction than in 60 patients (45%) those with anterior infarction. with posterior infarction had bradyarrhythmia within the first hour and a further 25 developed bradyarrhythmia later. Thus 85 (64%) of patients with posterior infarction had bradyarrhythmia at some time. 92 patients (32%) had ventricular dysrhythmias within the first hour. 70 patients (25%) (table 11) had ventricular ectopics either of the R-on-T variety, multifocal, bigeminal, or more frequently than 5 per minute. 28 patients had ventricular fibrillation within the first hour and were successfully resuscitated; 27 of these 28 had ventricular fibrillation outside hospital. Ventricular tachycardia was present in 10 patients (3-5%) in the first hour, whereas 55 patients (19%) developed ventricular tachycardia after four Atrial fibrillation or flutter occurred in 11 hours. TABLE III-INCIDENCE OF BRADYARRHYTHMIA AMONG
284
PATIENTS SEEN WITHIN FIRST
HOUR, 1966-69
the first hour and in 15 (5%) further 9 patients with ventricular fibrillation occurring within the first hour atrial fibrillation was apparent after resuscitation. In 7 of these 9 the atrial fibrillation cleared spontaneously. In 5 of the 7 spontaneous reversion to normal rhythm occurred within an hour. Only 1 of the 284 patients had supraventricular tachycardia within the first hour. 10 patients developed this dysrhythmia later-all more than four hours after the onset of symptoms. Only 51 patients (18%) of the 284 patients were free from rhythm disturbance during the period of hospital stay. 42 (15%) of the 284 patients died in hospital. The concept of pre-hospital coronary care required time to be accepted by the general practitioners and by the public. Over the four-year period increasing numbers of patients came under intensive care within one hour of the onset of symptoms (table i). In the of its the mobile early years operation coronary-care unit was activated predominantly for patients considered to have had a severe myocardial infarction. That the patient thought to have had a mild infarction is at risk and is the most rewarding patient if ventricular fibrillation is corrected or prevented has taken some time to be accepted, and indeed may not yet be completely accepted.144 Thus the data in the early years were weighted by the inclusion of a relatively large number of gravely ill patients. It was thought that a more accurate spectrum of the clinical features of the acute phase of the coronary attack might be obtained from the records of patients seen within the first hour in 1969. Since the management of the early dysrhythmias had progressively improved it was also thought that an evaluation of the therapeutic measures employed in that year would be of interest. In 1969 among the 447 patients with acute infarction managed by the mobile coronary-care unit, 123 were seen within one hour. Bradyarrhythmia occurred in 42 patients (34%) and ventricular ectopics occurred in 37 patients (30%) within the first hour. The effect of lignocaine on ventricular ectopics occurring within
patients (4%) within later. In
284 PATIENTS RELATED INFARCTION, 1966-69
a
TO TIME AFTER ONSET OF SYMPTOMS AND SITE OF
503
the first hour
was
studied. 37 patients had ventricular
either of the
variety, multifocal,
ectopics bigeminal, or more frequently than 5 per minute. In 11 patients the ventricular ectopics were abolished or reduced by raising the heart-rate by intravenous atropine. In the remaining 26 patients lignocaine was considered to be indicated. A bolus of lignocaine 100 mg. intravenously was administered and its effect studied over the subsequent ten minutes. In only 7 patients (27%) were the ectopics abolished and in 10 patients (38%) lignocaine had no effect. The data concerning the patients managed in 1969 show a significantly lower incidence of shock and a lower hospital mortality among those seen early than among those seen after three hours, although all were managed in the same way (table iv). The age-range was R-on-T
been shown that elevation of the arterial pressure increases coronary flow proportionately more than myocardial oxygen consumption. 25 Conversely, a fall in arterial blood-pressure and coronary perfusion pressure might be expected to result in a reduction of coronary flow disproportionate to the reduction of myocardial oxygen consumption and thus lead to extension of the area of ischaemic injury.
Tachyarrhythmia
or
frequent ventricular ectopics
may also reduce the blood-pressure. 26, 27 The high incidence of ventricular fibrillation among those seen early was predictable, since the community mortality is around 42 %,a high proportion of deaths occur within the first hour, and the mechanism of early death is usually ventricular fibrillation. ’12,2The high incidence of ventricular fibrillation among those seen early may be connected with the high incidence of TABLE IV-DATA ON PATIENTS MANAGED IN 1969 early bradyarrhythmia, since the ventricular fibrillation threshold falls at slow heart-rates. 29 Lignocaine is considered effective in correcting ventricular dysrhythmias complicating acute myocardial infarction.18, 3 0, 31 It has been reported that lignocaine suppressed ventricular ectopics in 88-95% of patients studied in hospital coronary-care units.32,33 Routine administration of lignocaine prior to transport * Groups (a) and (b) combined differ significantly from (c) (p =< O’OOl)." of patients to hospital has, therefore, been suggest Groups (a) and (b) combined differ significantly from (c) (0-01 > P > 0.001). H 32,31-37 However, in this study in more than a third of the patients lignocaine was completely in30-86 years. There was no significant difference in effective in abolishing ventricular irritability. This age, sex, or number of patients with previous infarction finding is supported by the experimental evidence that among the groups indicated (table iv). 116 of the 123 lignocaine is less effective in the control of ventricular patients seen within the first hour were aged 70 or less. ectopics occurring immediately after coronary ligaThe incidence of shock among these patients was 3-5% tion. 3 8 The limitations of lignocaine in the control of and the hospital mortality 9 %. 111 of the 123 patients the early ventricular dysrhythmias may be related to seen within the first hour survived to leave hospital high blood or tissue levels of catecholamines.39 The and 99 (89%) of these patients were alive at the one&bgr;-blocking agent, practolol, may be effective in year follow-up. lignocaine-resistant ventricular dysrhythmias occurring soon after the onset of myocardial infarct. 40 Discussion Lignocaine may be hazardous in the presence of The incidence of dysrhythmias among patients with bradyarrhythmia.41If this is so, the high incidence of acute myocardial infarction in hospital coronary-care bradyarrhythmia soon after the onset of the coronary attack indicates that the drug should be used with some units has been well documented. 15- 20 However, since caution. Lignocaine would appear to be particularly the majority of patients are admitted to hospital hazardous in the presence of uncorrected metabolic than units more four after the hours onset coronary-care acidosis.41 of symptoms, the incidence of dysrhythmias-particularly the incidence of bradyarrhythmias-has been Hospital coronary-care units appear to lower the underestimated. mortality of patients in hospital from 30% to 20%.9 The data from this study indicate the high inciHowever, conventional coronary care has had no dence of rhythm disturbance among patients seen impact on the incidence of shock and pump failure and within one hour of the onset of symptoms. 233 (82%) is unlikely to result in further reduction of the inof the 284 patients seen within one hour had rhythm hospital mortality. It is therefore of interest that disturbance, and in 170 (73%) dysrhythmia appeared among patients seen early, in the majority of whom within the first hour and required therapy before the dysrhythmias were either prevented or quickly corpatient was considered fit for transport to hospital. rected, the incidence of shock and pump failure was The present data confirm our previous findings low and the in-hospital mortality low. This finding differs from experience elsewhere. Thus it has been regarding the high incidence of bradyarrhythmia within the first hour.21 In the absence of previous infarction, stated that a high proportion of patients admitted during first few hours will increase the overall mortality the was bradyarrhythmia invariably present among patients with posterior infarction seen within half an hour of whereas admitting patients several hours after infarcthe onset of symptoms. 222 tion produces a lower mortality during the period in Doubt has been cast on the importance of sinus or hospital. 20,42The Birmingham group reported a nodal bradycardia. 23, 24 However, a fall in heart-rate in mortality of 23 % among patients admitted to a coronarycare unit within three hours of the onset of symptoms. 422 association with acute myocardial infarction is usually The lower hospital mortality among those seen early in in It has a reduction blood-pressure. accompanied by
504
this study is likely to be related to the different method of management and indicates the need for pre-hospital therapy, including the relief of pain and stabilisation of the rhythm before transport to the hospital coronarycare unit. It seems likely that cardiogenic shock is related to the magnitude of the area of myocardial damage. It has been suggested that the prevention or immediate correction of the early dysrhythmias and associated reduction in coronary perfusion may limit the size of the area of infarction. 27 This view is supported by recent experimental evidence. It has been noted that, following coronary ligation, reduction of the blood-pressure and heart-rate resulted in an increased area of myocardial injury and that elevation of the blood-pressure following coronary ligation limited the area of myocardial injury. 43 Braunwald’s group concludes that " the hxmodynamic status and neurohumoral background at the time of occlusion and for up to 3 hours thereafter can alter the extent and severity of myocardial ischxmic injury and myocardial necrosis".3 This is of interest in view of the significantly greater mortality among patients seen after three hours than in those seen earlier. Since the current therapeutic measures directed towards reducing the appallingly high mortality from cardiogenic shock are singularly unrewarding, the effort should be directed towards preventing shock and thus towards the early initiation of intensive care. In view of the limitations of antiarrhythmic drugs in the management of the early dysrhythmias which so commonly complicate acute myocardial infarction, it seems that if the early high mortality from primary ventricular fibrillation and the hospital mortality from shock and pump failure are to be reduced, there can be no alternative to pre-hospital coronary care. This means that individuals trained in coronary care and conversant with the use and limitations of antiarrhythmic agents should reach the patient as soon as possible after the onset of symptoms, relieve pain, stabilise the rhythm, and monitor the patient continuously during his transport to the coronary-care unit. It also means that the patient must be admitted directly to the hospital coronary-care unit, since delay and disturbance in the casualty department may aggravate the early dysrhythmias and lead to extension of the area of infarction. Requests for reprints should be addressed to J. F. P., Royal Hospital, Grosvenor Road, Belfast BT12 6BA.
Victoria
REFERENCES 1. 2. 3. 4. 5. 6. 7.
8. 9. 10. 11. 12. 13. 14.
Yater, W. M., Traum, A. H., Brown, W. G., Fitzgerald, R. P., Geisler, M. A., Wilcox, B. B. Am. Heart J. 1948, 36, 334, 481, 683. Kannel, W. B., Barry, P., Dawber, T. R. Proceedings of the 4th World Congress of Cardiology, 1963, vol. III, p. 176. McNeilly, R. H., Pemberton, J. Br. med. J. 1968, iii, 139. Fulton, M., Julian, D. G., Oliver, M. F. Circulation, 1969, 40, suppl. 4, 182. Gordon, T., Kannel, W. B. J. Am. med. Ass. 1971, 215, 1617. Bainton, C. R., Peterson, D. R. New Engl. J. Med. 1963, 268, 569. McDonald, E. L. in Acute Myocardial Infarction: Proceedings of a Symposium (edited by D. G. Julian and M. F. Oliver); p. 29. Edinburgh, 1968. Julian, D. G. Ann. intern. Med. 1968, 69, 3, 607. Lown, B. Arch. klin. Med. 1969, 216, 201. Pantridge, J. F., Geddes, J. S. Lancet, 1966, i, 807. Pantridge, J. F., Geddes, J. S. ibid. 1967, ii, 271. Pantridge, J. F., Adgey, A. A. J. Am. J. Cardiol. 1969, 24, 666. Pantridge, J. F. Chest, 1970, 58, 229. McNamee, B. T., Robinson, T. J., Adgey, A. A. J., Scott, M. E., Geddes, J. S., Pantridge, J. F. Br. med. J. 1970, iv, 204.
Julian, D. G., Valentine, P. A., Miller, G. C. Am. J. Med. 1964 37, 915. 16. Day, H. W., Averill, K. Dis. Chest, 1966, 49, 113. 17. Meltzer, L. E., Kitchell, J. B. Prog. cardiovasc. Dis. 1966, 9, 50. 18. Lown, B., Fakhro, A. M., Hood, W. B., Thorn, G. W. J. Am. med. Ass. 1967, 199, 188. 19. Restieaux, N., Bray, C., Bullard, H., Murray, M., Robinson, J., Brigden, W., McDonald, L. Lancet, 1967, i, 1285. 20. Lawrie, D. M., Greenwood, T. W., Goddard, M., Harvey, A. C., Donald, K. W., Julian, D. G., Oliver, M. F. ibid. 1967, ii, 109. 21. Adgey, A. A. J., Geddes, J. S., Mulholland, H. C., Keegan, D. A. J., Pantridge, J. F. ibid. 1968, ii, 1097. 22. Webb, S. W. Unpublished. 23. Norris, R. M. Lancet, 1969, i, 313. 24. Norris, R. M. in Lidocaine in the Treatment of Ventricular Arrhythmias: Proceedings of a Symposium (edited by D. B. Scott and D. G. Julian); p. 99. Edinburgh, 1971. 25. Braunwald, E., Sarnoff, S. J., Case, R. B., Stainsby, W. N., Welch, G. H., Jr. Am. J. Physiol, 1958, 192, 157. 26. Corday, E., Gold, H., De Vera, L. B., Williams, J. H., Fields, J. Ann. intern. Med. 1959, 50, 535. 27. Pantridge, J. F. Q. Jl Med. 1970, 39, 156, 621. 28. Adgey, A. A. J., Nelson, P. G., Scott, M. E., Geddes, J. S., Allen, J. D., Zaidi, S. A., Pantridge, J. F. Lancet, 1969, i, 1169. 29. Han, J., Millet, D., Chizzonitti, B., Moe, G. K. Am. Heart J. 1966, 71, 481. 30. Gianelly, R., Van der Groeben, J. O., Spivack, A. P., Harrison, D. C. New Engl. J. Med. 1967, 277, 1215. 31. Jewitt, D. E., Kishon, Y., Thomas, M. Lancet, 1968, i, 266. 32. Lown, B., Vassaux, C. Am. Heart J. 1968, 76, 586. 33. Killip, T. in Acute Myocardial Infarction: Proceedings of a Symposium (edited by D. G. Julian and M. F. Oliver); p. 110. Edinburgh, 1968. 34. Shillingford, J. P. ibid. p. 323. 35. Killip, T. Med. Clins N. Am. 1968, 52, 1061. 36. Scott, D. B., Jebson, P. J., Vellani, C. W., Julian, D. G. Lancet, 1968, ii, 1209. 37. McDonald, E. L., Gent, G., McDonald, A. Practitioner, 1969, 202, 238. 38. Lown, B. in Acute Myocardial Infarction: Proceedings of a Symposium (edited by D. G. Julian and M. F. Oliver); p. 323. Edinburgh, 1968. 39. Pantridge, J. F. in Lidocaine in the Treatment of Ventricular Arrhythmias: proceedings of a symposium (edited by D. B. Scott and D. G. Julian); p. 202. Edinburgh, 1971. 40. Allen, J. D., Pantridge, J. F., Shanks, R. G. Postgrad. med. J. 1971, 47, suppl. p. 29. 41. Astrom, A. in Lidocaine in the Treatment of Ventricular Arrhythmias: Proceedings of a Symposium (edited by D. B. Scott and D. G. Julian); p. 135. Edinburgh, 1971. 42. Pentecost, B. L., Mayne, N. M. C. Br. med. J. 1968, i, 830. 43. Maroko, P. R., Kjekshus, J. K., Sobel, B. E., Watanabe, T. Covell, J. W., Ross, I., Jr., Braunwald, E. Circulation, 1971, 43, 67. 44. Maxwell, A. E. Analysing Qualitative Data; p. 57. London, 1961 15.
RENAL AND INTRARENAL BLOOD-FLOW IN CIRRHOSIS OF THE LIVER M. C. KEW R. R. VARMA H. S. WILLIAMS
P. W. BRUNT K. J. HOURIGAN S. SHERLOCK
Departments of Medicine and Medical Physics, Royal Free
Hospital, London WC1X 8LF
Renal hæmodynamics were studied with the 133Xe washout technique in thirty-three cirrhotic patients with normal blood-urea levels. Mean renal blood-flow was often reduced, and this was usually associated with a redistribution of intrarenal blood-flow, the distribution to and flowrate through the outer cortex being reduced while juxtamedullary and medullary flow was maintained. This pattern of intrarenal blood-flow was confirmed with the gamma-camera nephrogram. With slight or moderate decreases in cortical blood-flow creatinine clearance was maintained, but poor cortical perfusion was associated with low glomerular filtration-rates. Renal hæmodynamic changes were found in patients with well-compensated cirrhosis, and no correlation Summary
September
J. D. ALLEN R. G. G. JAMES S. A. ZAIDI
J. F. PANTRIDGE
Patients and
Royal Victoria Hospital and Queen’s University, Belfast Summary Summary
one
Introduction
IT has been shown that 40% or more of all deaths from the coronary attack occur within an hour of the onset of symptoms,1-5 and that, among middle-aged and younger males, 63% of the deaths occur within one hour. Yet the median delay in admission to a hospital ward may be more than eight hours. 3,7 Hospital coronary-care units affect the outcome in only 10% of the patients admitted to such units. 8,9 Thus most patients when they reach a hospital coronary-care unit are either convalescent or moribund and the acute phase of the illness is infrequently seen. It has been said that " it is difficult to conceive that under any system much can be done about patients dying within one hour of the onset of symptoms 11.4 This view may be unduly pessimistic. The operation of a prehospital coronary-care scheme reduces the interval MANAGED
WITHIN
SYMPTOMS
AN
HOUR
four-year period 1966-69, 1150 patients with myocardial infarction were managed by a mobile coronary-care unit. The criteria for the diagnosis of acute myocardial infarction were (a) indubitable electrocardiographic evidence of recent infarction (272), or (b) sequential ST and T wave changes accompanied by significant and transient rise in s.G.o.T. (7), or (c) left-bundle-branch block with similar enzyme changes (5). 284 (25%) of the
acute
Dysrhythmias occurring within
I-PATIENTS
Management
In the
hour of the onset of symptoms of acute myocardial infarction have been documented in 284 patients. A high incidence of bradyarrhythmia was noted. Ventricular dysrhythmias were also and a disappointing response to showed frequent lignocaine therapy. Early initiation of intensive care not only prevents deaths from ventricular fibrillation but also diminishes the incidence of shock and pump failure by preventing or immediately correcting dysrhythmias and limiting the size of the myocardial infarct. The resources for coronary care should be directed towards the pre-hospital phase of the coronary attack.
TABLE
I97I
between the onset of symptoms and the initiation of intensive care and permits the observation of many patients soon after the onset of the coronary attack. 10- 13 We report here certain clinical features among 284 patients seen within one hour of the onset of symptoms who were alive when seen or who were resuscitated.
ACUTE PHASE OF MYOCARDIAL INFARCTION A. A. J. ADGEY J. S. GEDDES S. W. WEBB
4
OF
ONSET
OF
1150 patients were under intensive care within one hour of the onset of symptoms (table i). A clearcut history of the time of onset of chest pain or collapse was obtained for each patient. 224 patients were male and 60 were female; the age of the two groups ranged from 24 to 79 years and 46 to 79 (mean 62) years, respectively. Sites of infarction were anterior (135), posterior (133), combined anterior and posterior (4), and acute subendocardial (7). 5 patients had left-bundle-branch block. 79 (28%) of the 284 patients were seen within thirty minutes of the onset of symptoms. 91 patients had had a previous myocardial infarction and 108 patients had had angina without previous infarction. 85 patients had had no previous symptoms of ischxmic heart-disease. 203 patients (72%) were considered to have had a mild coronary attack in that when they were first seen clinical hsemodynamic disturbance was absent or was corrected immediately by suppression of the primary dysrhythmia. 46 patients (16%) were considered to have had a moderately severe attack in that there was mild hypotension-i.e., systolic blood pressure 90-95 mm. Hg or clinical evidence of pulmonary congestion. The attack was considered severe in 35 patients (12%) in that there was evidence of gross cardiac failure or cardiogenic shock. 19 patients (7%) had cardiogenic shock. 10 of these had had one or more previous episodes of myocardial infarction. 16 of the 19 patients had cardiogenic shock when first seen; the other 3 developed shock in the hospital coronary-care unit. The patients were in the cardiac unit throughout their hospital stay. The average stay in hospital was three weeks, and the average duration of monitoring was forty-eight hours. Terminal arrhythmias in patients dying of shock or cardiac failure have not been analysed.
(mean 56)
Results
(65%) of the 284 patients required therapy the site of the attack before they were considered fit for transport. 170 patients (60%) required therapy for either bradyarrhythmia, ventricular dysrhythmia, or supraventricular tachyarrhythmia, and, of these 170, 12 had dysrhythmia associated with acute left 185
at
7723
502 TABLE II-INCIDENCE OF DYSRHYTHMIAS AMONG
ventricular failure. 15 patients required therapy at the site of attack because of left ventricular failure unrelated to rhythm disturbance. The incidence of dysrhythmias among the 284 patients related to the time after the onset of symptoms when the dysrhythmia first appeared is shown in table II. Among patients seen within the first hour, bradyarrhythmia, either within that hour or later, 125 (44%) of the 284 patients had was common. bradyarrhythmia-i.e., sinus or nodal bradycardia (ventricular rate 60 per minute or less) or atrioventricular block (second-degree or complete). 88 patients (31 %) had bradyarrhythmia within the first hour. 37 patients (13%) developed bradyarrhythmia later. The incidence of sinus and nodal bradycardia and atrioventricular block, second-degree or complete, in relation to the site of infarction and to the time after the onset of symptoms is shown in table ill. 75 patients (26%) had sinus or nodal bradycardia in the first hour; 33 patients (12%) had sinus or nodal bradycardia later. 17 patients (6%) had heart-block, second-degree or complete, in the first hour, whereas 11
(4%) developed heart-block, second-degree or Bradyarrhythmia occurred more complete, later. frequently in patients with posterior infarction than in 60 patients (45%) those with anterior infarction. with posterior infarction had bradyarrhythmia within the first hour and a further 25 developed bradyarrhythmia later. Thus 85 (64%) of patients with posterior infarction had bradyarrhythmia at some time. 92 patients (32%) had ventricular dysrhythmias within the first hour. 70 patients (25%) (table 11) had ventricular ectopics either of the R-on-T variety, multifocal, bigeminal, or more frequently than 5 per minute. 28 patients had ventricular fibrillation within the first hour and were successfully resuscitated; 27 of these 28 had ventricular fibrillation outside hospital. Ventricular tachycardia was present in 10 patients (3-5%) in the first hour, whereas 55 patients (19%) developed ventricular tachycardia after four Atrial fibrillation or flutter occurred in 11 hours. TABLE III-INCIDENCE OF BRADYARRHYTHMIA AMONG
284
PATIENTS SEEN WITHIN FIRST
HOUR, 1966-69
the first hour and in 15 (5%) further 9 patients with ventricular fibrillation occurring within the first hour atrial fibrillation was apparent after resuscitation. In 7 of these 9 the atrial fibrillation cleared spontaneously. In 5 of the 7 spontaneous reversion to normal rhythm occurred within an hour. Only 1 of the 284 patients had supraventricular tachycardia within the first hour. 10 patients developed this dysrhythmia later-all more than four hours after the onset of symptoms. Only 51 patients (18%) of the 284 patients were free from rhythm disturbance during the period of hospital stay. 42 (15%) of the 284 patients died in hospital. The concept of pre-hospital coronary care required time to be accepted by the general practitioners and by the public. Over the four-year period increasing numbers of patients came under intensive care within one hour of the onset of symptoms (table i). In the of its the mobile early years operation coronary-care unit was activated predominantly for patients considered to have had a severe myocardial infarction. That the patient thought to have had a mild infarction is at risk and is the most rewarding patient if ventricular fibrillation is corrected or prevented has taken some time to be accepted, and indeed may not yet be completely accepted.144 Thus the data in the early years were weighted by the inclusion of a relatively large number of gravely ill patients. It was thought that a more accurate spectrum of the clinical features of the acute phase of the coronary attack might be obtained from the records of patients seen within the first hour in 1969. Since the management of the early dysrhythmias had progressively improved it was also thought that an evaluation of the therapeutic measures employed in that year would be of interest. In 1969 among the 447 patients with acute infarction managed by the mobile coronary-care unit, 123 were seen within one hour. Bradyarrhythmia occurred in 42 patients (34%) and ventricular ectopics occurred in 37 patients (30%) within the first hour. The effect of lignocaine on ventricular ectopics occurring within
patients (4%) within later. In
284 PATIENTS RELATED INFARCTION, 1966-69
a
TO TIME AFTER ONSET OF SYMPTOMS AND SITE OF
503
the first hour
was
studied. 37 patients had ventricular
either of the
variety, multifocal,
ectopics bigeminal, or more frequently than 5 per minute. In 11 patients the ventricular ectopics were abolished or reduced by raising the heart-rate by intravenous atropine. In the remaining 26 patients lignocaine was considered to be indicated. A bolus of lignocaine 100 mg. intravenously was administered and its effect studied over the subsequent ten minutes. In only 7 patients (27%) were the ectopics abolished and in 10 patients (38%) lignocaine had no effect. The data concerning the patients managed in 1969 show a significantly lower incidence of shock and a lower hospital mortality among those seen early than among those seen after three hours, although all were managed in the same way (table iv). The age-range was R-on-T
been shown that elevation of the arterial pressure increases coronary flow proportionately more than myocardial oxygen consumption. 25 Conversely, a fall in arterial blood-pressure and coronary perfusion pressure might be expected to result in a reduction of coronary flow disproportionate to the reduction of myocardial oxygen consumption and thus lead to extension of the area of ischaemic injury.
Tachyarrhythmia
or
frequent ventricular ectopics
may also reduce the blood-pressure. 26, 27 The high incidence of ventricular fibrillation among those seen early was predictable, since the community mortality is around 42 %,a high proportion of deaths occur within the first hour, and the mechanism of early death is usually ventricular fibrillation. ’12,2The high incidence of ventricular fibrillation among those seen early may be connected with the high incidence of TABLE IV-DATA ON PATIENTS MANAGED IN 1969 early bradyarrhythmia, since the ventricular fibrillation threshold falls at slow heart-rates. 29 Lignocaine is considered effective in correcting ventricular dysrhythmias complicating acute myocardial infarction.18, 3 0, 31 It has been reported that lignocaine suppressed ventricular ectopics in 88-95% of patients studied in hospital coronary-care units.32,33 Routine administration of lignocaine prior to transport * Groups (a) and (b) combined differ significantly from (c) (p =< O’OOl)." of patients to hospital has, therefore, been suggest Groups (a) and (b) combined differ significantly from (c) (0-01 > P > 0.001). H 32,31-37 However, in this study in more than a third of the patients lignocaine was completely in30-86 years. There was no significant difference in effective in abolishing ventricular irritability. This age, sex, or number of patients with previous infarction finding is supported by the experimental evidence that among the groups indicated (table iv). 116 of the 123 lignocaine is less effective in the control of ventricular patients seen within the first hour were aged 70 or less. ectopics occurring immediately after coronary ligaThe incidence of shock among these patients was 3-5% tion. 3 8 The limitations of lignocaine in the control of and the hospital mortality 9 %. 111 of the 123 patients the early ventricular dysrhythmias may be related to seen within the first hour survived to leave hospital high blood or tissue levels of catecholamines.39 The and 99 (89%) of these patients were alive at the one&bgr;-blocking agent, practolol, may be effective in year follow-up. lignocaine-resistant ventricular dysrhythmias occurring soon after the onset of myocardial infarct. 40 Discussion Lignocaine may be hazardous in the presence of The incidence of dysrhythmias among patients with bradyarrhythmia.41If this is so, the high incidence of acute myocardial infarction in hospital coronary-care bradyarrhythmia soon after the onset of the coronary attack indicates that the drug should be used with some units has been well documented. 15- 20 However, since caution. Lignocaine would appear to be particularly the majority of patients are admitted to hospital hazardous in the presence of uncorrected metabolic than units more four after the hours onset coronary-care acidosis.41 of symptoms, the incidence of dysrhythmias-particularly the incidence of bradyarrhythmias-has been Hospital coronary-care units appear to lower the underestimated. mortality of patients in hospital from 30% to 20%.9 The data from this study indicate the high inciHowever, conventional coronary care has had no dence of rhythm disturbance among patients seen impact on the incidence of shock and pump failure and within one hour of the onset of symptoms. 233 (82%) is unlikely to result in further reduction of the inof the 284 patients seen within one hour had rhythm hospital mortality. It is therefore of interest that disturbance, and in 170 (73%) dysrhythmia appeared among patients seen early, in the majority of whom within the first hour and required therapy before the dysrhythmias were either prevented or quickly corpatient was considered fit for transport to hospital. rected, the incidence of shock and pump failure was The present data confirm our previous findings low and the in-hospital mortality low. This finding differs from experience elsewhere. Thus it has been regarding the high incidence of bradyarrhythmia within the first hour.21 In the absence of previous infarction, stated that a high proportion of patients admitted during first few hours will increase the overall mortality the was bradyarrhythmia invariably present among patients with posterior infarction seen within half an hour of whereas admitting patients several hours after infarcthe onset of symptoms. 222 tion produces a lower mortality during the period in Doubt has been cast on the importance of sinus or hospital. 20,42The Birmingham group reported a nodal bradycardia. 23, 24 However, a fall in heart-rate in mortality of 23 % among patients admitted to a coronarycare unit within three hours of the onset of symptoms. 422 association with acute myocardial infarction is usually The lower hospital mortality among those seen early in in It has a reduction blood-pressure. accompanied by
504
this study is likely to be related to the different method of management and indicates the need for pre-hospital therapy, including the relief of pain and stabilisation of the rhythm before transport to the hospital coronarycare unit. It seems likely that cardiogenic shock is related to the magnitude of the area of myocardial damage. It has been suggested that the prevention or immediate correction of the early dysrhythmias and associated reduction in coronary perfusion may limit the size of the area of infarction. 27 This view is supported by recent experimental evidence. It has been noted that, following coronary ligation, reduction of the blood-pressure and heart-rate resulted in an increased area of myocardial injury and that elevation of the blood-pressure following coronary ligation limited the area of myocardial injury. 43 Braunwald’s group concludes that " the hxmodynamic status and neurohumoral background at the time of occlusion and for up to 3 hours thereafter can alter the extent and severity of myocardial ischxmic injury and myocardial necrosis".3 This is of interest in view of the significantly greater mortality among patients seen after three hours than in those seen earlier. Since the current therapeutic measures directed towards reducing the appallingly high mortality from cardiogenic shock are singularly unrewarding, the effort should be directed towards preventing shock and thus towards the early initiation of intensive care. In view of the limitations of antiarrhythmic drugs in the management of the early dysrhythmias which so commonly complicate acute myocardial infarction, it seems that if the early high mortality from primary ventricular fibrillation and the hospital mortality from shock and pump failure are to be reduced, there can be no alternative to pre-hospital coronary care. This means that individuals trained in coronary care and conversant with the use and limitations of antiarrhythmic agents should reach the patient as soon as possible after the onset of symptoms, relieve pain, stabilise the rhythm, and monitor the patient continuously during his transport to the coronary-care unit. It also means that the patient must be admitted directly to the hospital coronary-care unit, since delay and disturbance in the casualty department may aggravate the early dysrhythmias and lead to extension of the area of infarction. Requests for reprints should be addressed to J. F. P., Royal Hospital, Grosvenor Road, Belfast BT12 6BA.
Victoria
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RENAL AND INTRARENAL BLOOD-FLOW IN CIRRHOSIS OF THE LIVER M. C. KEW R. R. VARMA H. S. WILLIAMS
P. W. BRUNT K. J. HOURIGAN S. SHERLOCK
Departments of Medicine and Medical Physics, Royal Free
Hospital, London WC1X 8LF
Renal hæmodynamics were studied with the 133Xe washout technique in thirty-three cirrhotic patients with normal blood-urea levels. Mean renal blood-flow was often reduced, and this was usually associated with a redistribution of intrarenal blood-flow, the distribution to and flowrate through the outer cortex being reduced while juxtamedullary and medullary flow was maintained. This pattern of intrarenal blood-flow was confirmed with the gamma-camera nephrogram. With slight or moderate decreases in cortical blood-flow creatinine clearance was maintained, but poor cortical perfusion was associated with low glomerular filtration-rates. Renal hæmodynamic changes were found in patients with well-compensated cirrhosis, and no correlation Summary