- Email: [email protected]
PRE-HOSPITAL VENTRICULAR DEFIBRILLATION
1361
genesis of serious hypoxsemia. Cardiopulmonary investigations show that established hypoxaemia in fat-embolism cases is
or
secondary
factors in the
veno-arterial admixture corresponding to between 20% and 50% of the cardiac output as well as a considerable increase in alveolar The gross pulmonary haemordead-space. 12 found in some cases could account for rhagiooedema serious hypoxaemia, but it would not account for the common association between systemic fat embolism and respiratory insufficiency. To explain an enhanced passage of emboli from the lungs to the aorta and a simultaneous increase in pulmonary veno-arterial admixture, anatomical lung shunting must probably be invoked. SEVITT has postulated under conditions of downstream that, pulmonary blockage by many emboli and in the face of continuing embolism, the interrelationships between pulmonary hypertension, arteriolar constriction of the lung bed, and hypoxia may precipitate lung shunting and thereby promote the onset of a vicious circle which favours hypoxaemia and systemic embolism. IS Experimentally this combination is influenced by large numbers of lung emboli, limitations of the filtering
associated with
a
capacity of the lungs, a phase of shock, a rise in pulmonary-artery pressure, pulmonary vasoconstriction, hypoxia, and pre-existing pulmonary disease.H, 15 It is important that experimentally the breathing of oxygen reduces not only post-embolic pulmonaryartery pressure, hypoxaemia, and mortality, but also the quantity of emboli reaching the brain, kidney, and other organs. 14, 15 This suggests that oxygen may break the vicious circle within the lungs which promotes hypoxaemia and systemic passage of globules. Oxygen at present is the only therapeutic tool of proven worth in clinical fat embolism, and in suitable subjects it may prevent, the onset of clinical signs. In fracture subjects prophylactic oxygen therapy is worthy of further study.
PRE-HOSPITAL VENTRICULAR DEFIBRILLATION A VIGOROUS controversy over the relative merits of paramedical and medical staffed mobile coronary-care units 16-19 makes the published experience of the Miami fire-rescue teams of particular interest. 10 The paramedical staff of the Miami teams are trained in a more comprehensive range of skills than their counterparts 12. 13.
14.
Prys-Roberts, C., Greenbaum, R., Nunn, J. F., Kelman, G. R. J. clin. Path. 1970, 23, suppl. 4, p. 143. Sevitt, S. Reactions to Injury and Burns and their Clinical Importance; chap. 13. London, 1974. Molenaar, A. Post-traumatische Vetembolie: een experimenteel
onderzoek. Nijmegen, 1967. 15. Szabo, G. J. clin. Path. 1970, 23, suppl. 4, p. 123. 16. Orchard, T. J. Lancet, 1974, i, 263. 17. Webb, S. W. ibid. p. 539. 18. Crampton, R. S., Michaelson, S. P., Aldrich, R. F., Gascho, J. A. ibid. July 13, 1974, p. 101. 19. Adgey, A. A. J. ibid. Aug. 3, 1974, p. 287. 20. Lithberson, R. R., Nagel, E. L., Hirschman, J. D., Nussenfeld, S. D. New Engl. J. Med. 1974, 291, 317.
in the U.K. 21, 22
They undertake
not
only cardiac
defibrillation but also endotracheal intubation and intravenous administration of anti-arrhythmic drugs.
Drugs are given under the guidance of hospital-based physicians who, by telemetry, can observe the heart rhythm after resuscitation. Of the patients encountered over a 42-month period, 301 were found to be in ventricular fibrillation (v.F.); of these, 199 were resuscitated with initial success, and a total of 101 patients survived to reach hospital. During hospital admission a further 59 patients died, reducing the survivors to 42. Discussing the ptehospital phase, the Miami group draw attention to the poor outlook when bradycardia, junctional rhythm, or idioventricular rhythm follow resuscitation. In the patients with bradycardia the estimated mean delay between collapse and defibrillation was 16 minutes, compared with 10 minutes in those with post-resuscitation heart-rates of 100 per minute or more; the difference in prognosis presumably reflects the duration of hypoxaemia, with its ill-effects on myocardium. An important observation in the 101 survivors to reach hospital was the high incidence of myocardial ischaemia without evidence of infarctioni.e., without subsequent appearance of abnormal Q waves. Whereas infarction preceding v.F. seemed to be equally distributed between anterior and inferior aspects of the heart, ischaemia alone was almost entirely confined to the anterior aspect. Patients with anterior myocardial ischaemia who survived to leave hospital had a disturbingly high incidence of sudden death, and at least some of these were known to have been in v.F. at their final collapse. This observation may single out a group at particularly high risk, on whom antiarrhythmic-drug therapy might be concentrated, though the relative ineffectiveness of existing drug regimens is highlighted by the high rates of recurrent v.F. both within hospital and after discharge. Of the patients leaving hospital, 60 % returned to their previous way of life, but 12% (5 patients) had neurological injury bad enough to necessitate institutional care and a further 28 % had some neurological deficit. This frequency of neurological injury seems higher than is usual in hospital coronary-care units and, again, probably reflects the duration of hypoxaemia. The experience of the Miami group has shown the value of training non-medically qualified staff to a high level The long-term survival among of technical skill. v.F. will with be improved, firstly, by reducing patients the delay between collapse and attempted resuscitation
and, secondly, by devising better anti-arrhythmic drugs. TRAINING THE BASIC DOCTOR THE creation of the basic doctor, who would subsequently require postgraduate training for whatever discipline of medicine (including general practice) he chose to follow, should be the primary aim of medical education today. This was the view of the Royal Commission on Medical Education in 1968; and it was the main message in this year’s Marsden lecture by Prof. P. S. Byrne, president of the Royal 21. 22.
Gearty, G. F., Hickey, N., Bourke, G. J., Maleaby, R. Br. med. J. 1971, iii, 33. Chamberlain, D. A., White, N. M., Parker, W. S., Binning, R. A. ibid. 1973, iii, 619.
genesis of serious hypoxsemia. Cardiopulmonary investigations show that established hypoxaemia in fat-embolism cases is
or
secondary
factors in the
veno-arterial admixture corresponding to between 20% and 50% of the cardiac output as well as a considerable increase in alveolar The gross pulmonary haemordead-space. 12 found in some cases could account for rhagiooedema serious hypoxaemia, but it would not account for the common association between systemic fat embolism and respiratory insufficiency. To explain an enhanced passage of emboli from the lungs to the aorta and a simultaneous increase in pulmonary veno-arterial admixture, anatomical lung shunting must probably be invoked. SEVITT has postulated under conditions of downstream that, pulmonary blockage by many emboli and in the face of continuing embolism, the interrelationships between pulmonary hypertension, arteriolar constriction of the lung bed, and hypoxia may precipitate lung shunting and thereby promote the onset of a vicious circle which favours hypoxaemia and systemic embolism. IS Experimentally this combination is influenced by large numbers of lung emboli, limitations of the filtering
associated with
a
capacity of the lungs, a phase of shock, a rise in pulmonary-artery pressure, pulmonary vasoconstriction, hypoxia, and pre-existing pulmonary disease.H, 15 It is important that experimentally the breathing of oxygen reduces not only post-embolic pulmonaryartery pressure, hypoxaemia, and mortality, but also the quantity of emboli reaching the brain, kidney, and other organs. 14, 15 This suggests that oxygen may break the vicious circle within the lungs which promotes hypoxaemia and systemic passage of globules. Oxygen at present is the only therapeutic tool of proven worth in clinical fat embolism, and in suitable subjects it may prevent, the onset of clinical signs. In fracture subjects prophylactic oxygen therapy is worthy of further study.
PRE-HOSPITAL VENTRICULAR DEFIBRILLATION A VIGOROUS controversy over the relative merits of paramedical and medical staffed mobile coronary-care units 16-19 makes the published experience of the Miami fire-rescue teams of particular interest. 10 The paramedical staff of the Miami teams are trained in a more comprehensive range of skills than their counterparts 12. 13.
14.
Prys-Roberts, C., Greenbaum, R., Nunn, J. F., Kelman, G. R. J. clin. Path. 1970, 23, suppl. 4, p. 143. Sevitt, S. Reactions to Injury and Burns and their Clinical Importance; chap. 13. London, 1974. Molenaar, A. Post-traumatische Vetembolie: een experimenteel
onderzoek. Nijmegen, 1967. 15. Szabo, G. J. clin. Path. 1970, 23, suppl. 4, p. 123. 16. Orchard, T. J. Lancet, 1974, i, 263. 17. Webb, S. W. ibid. p. 539. 18. Crampton, R. S., Michaelson, S. P., Aldrich, R. F., Gascho, J. A. ibid. July 13, 1974, p. 101. 19. Adgey, A. A. J. ibid. Aug. 3, 1974, p. 287. 20. Lithberson, R. R., Nagel, E. L., Hirschman, J. D., Nussenfeld, S. D. New Engl. J. Med. 1974, 291, 317.
in the U.K. 21, 22
They undertake
not
only cardiac
defibrillation but also endotracheal intubation and intravenous administration of anti-arrhythmic drugs.
Drugs are given under the guidance of hospital-based physicians who, by telemetry, can observe the heart rhythm after resuscitation. Of the patients encountered over a 42-month period, 301 were found to be in ventricular fibrillation (v.F.); of these, 199 were resuscitated with initial success, and a total of 101 patients survived to reach hospital. During hospital admission a further 59 patients died, reducing the survivors to 42. Discussing the ptehospital phase, the Miami group draw attention to the poor outlook when bradycardia, junctional rhythm, or idioventricular rhythm follow resuscitation. In the patients with bradycardia the estimated mean delay between collapse and defibrillation was 16 minutes, compared with 10 minutes in those with post-resuscitation heart-rates of 100 per minute or more; the difference in prognosis presumably reflects the duration of hypoxaemia, with its ill-effects on myocardium. An important observation in the 101 survivors to reach hospital was the high incidence of myocardial ischaemia without evidence of infarctioni.e., without subsequent appearance of abnormal Q waves. Whereas infarction preceding v.F. seemed to be equally distributed between anterior and inferior aspects of the heart, ischaemia alone was almost entirely confined to the anterior aspect. Patients with anterior myocardial ischaemia who survived to leave hospital had a disturbingly high incidence of sudden death, and at least some of these were known to have been in v.F. at their final collapse. This observation may single out a group at particularly high risk, on whom antiarrhythmic-drug therapy might be concentrated, though the relative ineffectiveness of existing drug regimens is highlighted by the high rates of recurrent v.F. both within hospital and after discharge. Of the patients leaving hospital, 60 % returned to their previous way of life, but 12% (5 patients) had neurological injury bad enough to necessitate institutional care and a further 28 % had some neurological deficit. This frequency of neurological injury seems higher than is usual in hospital coronary-care units and, again, probably reflects the duration of hypoxaemia. The experience of the Miami group has shown the value of training non-medically qualified staff to a high level The long-term survival among of technical skill. v.F. will with be improved, firstly, by reducing patients the delay between collapse and attempted resuscitation
and, secondly, by devising better anti-arrhythmic drugs. TRAINING THE BASIC DOCTOR THE creation of the basic doctor, who would subsequently require postgraduate training for whatever discipline of medicine (including general practice) he chose to follow, should be the primary aim of medical education today. This was the view of the Royal Commission on Medical Education in 1968; and it was the main message in this year’s Marsden lecture by Prof. P. S. Byrne, president of the Royal 21. 22.
Gearty, G. F., Hickey, N., Bourke, G. J., Maleaby, R. Br. med. J. 1971, iii, 33. Chamberlain, D. A., White, N. M., Parker, W. S., Binning, R. A. ibid. 1973, iii, 619.