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VALVULAR DEFECT IN PRIMARY VARICOSE VEINS
491
ally of girls’ schools) should positively welcome such
a
child back to school. I do not think this is enough. Because of possible confusion with morbilli, some parents and teachers (and doctors) might be reluctant to take this advice. We must ignore the infectivity of measles too. Not for an instant do I think this would harm the community. In our present urban society, isolation and quarantine of measles do not prevent a single child from catching it-they merely postpone the date. In the end, everybody catches measles. Postponement is of no advantage in measles; in german measles it is a terrible menace. Let us expunge isolation and quarantine of measles-of all sorts-from our textbooks and our minds. Whipps Cross Hospital, London, E.11.
E. HINDEN.
VALVULAR DEFECT IN PRIMARY VARICOSE VEINS
SIR,-Mr. Ludbrook’s work supports the view that the valves of the long saphenous vein fail progressively from the saphenofemoral junction, and my experience leads me to agree with him. Ligation of the long saphenous vein flush with the common femoral vein will relieve the condition, with a few exceptions, such as an isolated small varicose vein or a cluster which are not kept empty by a tourniquet at the groin, lower Hunter’s canal, or at the knee-joint. These clusters are usually cured by a sclerosing injection, followed by sustained pressure for six weeks as described by Fegan.1 Mr. Hobbs (Feb. 15) does not agree with this view, but, when there is a leak from the saphenofemoral junction only, I have found a true saphenofemoral tie effective. I have been doing this since 1926 and have seen patients subsequently for many years. Naturally, for a cure, other leaks must be located and stopped. Hobbs cites Fegan’s work. I have seen this and respect it. I have visited his hospitals twice, and, by his courtesy, have examined some of his patients. The injections had clinically relieved and cleared the varices from the lower
thigh downwards, although some saphenofemoral junctions still had a palpable saphenous varix and an impulse on coughing. I don’t think that this work invalidates Ludbrook’s premise of sequential failure of the valves of a superficial vein from above downwards, starting at its union with a deep vein. It takes time after varices have appeared for sufficient symptoms to arise that require patients to seek surgical care. We have all seen men and women with gross symptomless varices. Women whose varices began in pregnancy sometimes do not come for treatment until after the menopause. During these apparently silent years, the venous hypertension has made the long saphenous trunk hypertrophied and the subcuticular veins dilated, elongated, tortuous, pouched, and inelastic, and has stimulated degenerative changes in the skin and fat. Persistence of varicose veins after a saphenofemoral ligation is regrettably seen occasionally, especially in those done before 1950. Either the operation was inefficient or the diagnosis was wrong or incomplete-e.g., in missing concomitant leaks from Hunter’s canal, the popliteal space, the ankle perforators, and (uncommonly) other communicating veins. Dr. Rivlin (Jan.
25) digresses to ulceration-" gravitational ", deep-thrombotic ". I prefer the term venous hypertensive ulceration. Superficial hypertension is common to primary varicose veins and those associated with deep thrombosis. Ulcers arising from these comprise over 900 of leg ulcers occasionally complicated by arteriosclerosis, The superficial venous diabetes, rheumatoid arthritis, &c. hypertension is the destructive agent causing pigmentation, induration, swelling, eczema, and ulceration. This tension stems from the deep venous system through incompetent connecting veins, especially the ankle perforators. The long " varicose ", and
"
1. Fegan,
W. G.
Lancet, 1963, ii,
109.
and short
veins are connecting veins. Besides the and ankle veins, those from the superficial femoral saphenous vein in Hunter’s canal contribute to the destructive complications at the lower leg. Division of these defective veins precisely at their ending in the deep vein is curative in a large proportion of patients. Rivlin deplores the results of varicose vein operations. The anatomy, physiology, and pathology are described better now and are more widely understood, and the diagnosis and treatment are improving. Already the results are better than they were ten years ago.
saphenous
It
perhaps merits mention that the four common sites of venous leaks can give fifteen clinical presentations per limb. People’s legs are seldom alike, so each needs an accurate and complete diagnosis. A leak (a) in the groin may be caused by two to three possible faulty veins; (b) in Hunter’s canal, two; (c) from the popliteal vein, four. These yield seven combinations. A leak (d) from the ankle perforating veins yields seven or eight. These variations need knowledge and training, time, skill, and judgment to define. There are no short cuts. Stripping was an
irrational hone!
London, W.I.
.
H. DODD.
SiR,-We have been following the correspondence arising from Mr. Ludbrook’s article on valvular defect in primary varicose veins.1 " Varicose veins" is an unfortunate description, since it calls attention to one of the least important aspects of this disease. Often patients with the most severe symptoms and signs have in fact no dilated, elongated, tortuous veins. A more appropriate name is chronic venous insufficiency. Mr. Ludbrook, in our opinion, is correct in stating that valvular incompetence is the cause of chronic venous insufficiency, whether the incompetence is due to injury to the valves, a defect in the vein wall, hormone imbalance, an increased bloodvolume, or some other disorder. He is, we think, incorrect in stating that this incompetence is primarily at the saphenofemoral junction. In over 15,000 patients treated by us in the past twelve years, many of whom had large saphenovarices, not one has required flush ligation of the saphenofemoral junction.23 The disappearance of saphenovarices after blockage of an incompetant hunterian perforator leads us to believe that the emphasis on the saphenofemoral junction in the treatment of varicose veins is misplaced. It is gratifying to learn that Mr. Hobbs (Feb. 15), too, has found that saphenovarices and vulval varices, disappear after blockage of an incompetent hunterian perforator. We believe that the primary lesion in patients with chronic venous insufficiency is incompetence of a valve in one or more perforating veins. In this way the superficial veins are subjected to abnormal pressure, and consequently the portion of the vein above the incompetent perforator will, in time, dilate. The dilatation spreads upwards, causing secondary incompetence of the valves in the superficial veins. Only when the dilatation reaches the saphenofemoral junction do the valves at this site become incompetent. And when the perforator(s), transmitting blood at high pressure, are blocked, the superficial veins recover their tone; and their valves, including those at the saphenofemoral junction, regain their competence. It is in these cases of secondary saphenofemoral incompetence that the Trendelenburg test or a mid-thigh tourniquet test is misleading. Ludbrook states that a near-normal fall in pressure (45 mm. Hg) occurs in patients with varicose veins who exercise the leg after a mid-thigh tourniquet has been applied. Certainly there is some drop in pressure, but if there is an incompetent valve in a perforating vein below the tourniquet, then the fall will be slight. The pressure exerted by a midthigh tourniquet (really a modification of the Trendelenburg test) is sufficient to occlude both the deep and superficial 1. Ludbrook, J. Lancet, 1963, ii, 1289. Fegan, W. G. ibid. p. 109. Fegan, W. G. Minerva cardioangiol. europ. 1961, p. 481.
2. 3.
492 test is an inadequate diagnostic procedure, and is for many misdiagnoses and consequent failures of treatment. The pressure needed to block an incompetent saphenofemoral junction must of necessity also block the common femoral vein, since the pressure in the deep veins here is the same as in the superficial veins. But if the test is performed with a finger exerting just sufficient pressure to occlude the long saphenous vein in the upper thigh, the superficial veins will nearly always be seen to fill from incompetent perforating veins. This resembles our diagnostic test previously described.2 In our opinion, Ludbrook’s investigations of the intravenous pressures are inadequate and consequently misleading. He recorded pressure in the superficial veins only and then refers to " mean " pressure values. The results give a false picture of the functions and faults of the complex pumping mechanisms responsible for returning blood from the lower limbs. Pressures in the superficial and deep veins must be recorded simultaneously by an electronic manometer which gives a permanent record of the very rapid pressure changes in the leg during movement. We have so far made 83 intravenous pressure recordings, and have many tracings obtained simultaneously in deep and superficial veins. From these it can be shown that the pressures vary with great rapidity; the rapidity can, in fact, be compared to that of the P.Q.R.s. complex on the cardiograph. Plainly, to take a " mean " pressure in a vein is as inaccurate as taking a mean potential for the P.Q.R.S. complex. The pressure in the long saphenous vein, as Ludbrook says, does fall with exercise in the erect posture in patients with chronic venous insufficiency, and often it falls in a normal pattern. In this way many patients, because they have many normally functioning pump units, can compensate for a faulty valve in one of their perforating veins, and hence have no serious symptoms. The fallacy of obtaining mean records of the intravenous pressure is shown by Ludbrook’s statement that on exercise the superficial pressure at the ankle dropped in control patients from 95 to 45 mm. Hg. In fact, our tracings show that a healthy person can reduce the pressure in the superficial vein at the ankle to within 5 mm. of zero during exercise. Only by recording both deep and superficial pressures can one understand the mechanisms whereby the normally high-pressure system (deep) can receive blood from the low-pressure system (superficial). It is during the fraction of a second (when the muscle-pumps are in their early diastolic phase) that the pressure in the superficial veins exceeds that in the deep veins and creates a favourable gradient. Ludbrook states that in what he calls primary varicose veins the calf-pump is functioning normally. This may or may not be the case, depending upon the condition of the valves in the perforating veins connected to this pump; but even if the calf-pump does function normally, the plantar, anterior and posterior tibial, peroneal, quadriceps, adductor and hamstring pumps must also be taken into consideration, since an incompetent valve in a perforating vein connected to any of these may lead to chronic venous insufficiency. In similar cases we have always found a leaking perforator in one or more of the remaining pumps, commonly the adductor or quadriceps pumps. The success of his mid-thigh tourniquet test may lie in his occlusion of an incompetent upper hunterian perforating vein, together with a secondarily incompetent saphenofemoral junction, and compression of the deep veins. Ludbrook describes primary varicose veins as occurring in patients who have not had deep-vein thrombosis. Varicose veins are seldom primary, but usually follow some other condition, whether it be hormonal, lacerations, polycythxmia, trauma, &c. Perforating veins can thrombose without manifesting as deep-vein thrombosis; and probably quite small injuries often cause subclinical thrombosis confined to a perforating vein and a short segment of the superficial veins. After recanalisation, the valve in the perforating vein will be
veins. The
responsible
incompetent.
reply to Mr. Ludbrook’s suggestion that our technique of course be successful if most of the varices are sclerosed (Feb. 1), nothing could be further from our object. We aim to produce, as we have shown a short segment of sclerosis in the superficial vein overlying the incompetent perforating vein, and including it. We have established that the perforator is, in fact, blocked by many biopsies at varying intervals after injection, at which time the perforating vein is cut across with a knife and no bleeding has taken place. Microscopic examination proves that these veins are totally occluded. In
must
The good results using our injection technique do, in fact, remain constant with time. In a survey conducted recently on 1172 patients treated between 1956 and 1960, the results were satisfactory in 81%, and in the patients who carried out our instructions conscientiously, the results were satisfactory in 86%. The best results were in patients who were treated in 1956; this means they have stood the test of time for eight years. The average number of attendances per patient at our clinic is 5, and in 15,000 cases treated there has been no mortality. Had these all been treated by surgery there would, according to published figures, have been upwards of 40 deaths. We shall be pleased to hear Mr. Ludbrook’s views, and would like to know to what operation he refers when he talks about " before operation and " after operation"? Was it solely saphenofemoral ligation or some more elaborate procedure ? GEORGE FEGAN Research Department, DERMOT FITZGERALD Sir Patrick Dun’s Hospital, BILL BEESLEY. Dublin 2. "
.
--
MANAGEMENT OF CARDIAC ARREST
SIR,-Mr. Stewart (Jan. 11) makes two statements which we feel are questionable. First, No time should be wasted in the first instance with adrenaline, calcium salts, hypertonic glucose, and other drugs." Second, There is now ample evidence for the efficiency of bicarbonate therapy in the management of cardiac arrest, and it should come into routine use forthwith." Going back to 1896/ adrenaline has been recommended in the "
"
of cardiac arrest : thus contrary recommendations should be made with careful documentation. In most instances, cardiac arrest is associated with asphyxia during general anxsthesia; with airway obstruction in cases of coma due to head injury or barbiturate poisoning; and in drowning. In such cases it has hypoxia and respiratory acidosis as primary factors, and metabolic acidosis as a treatment
secondary feature. We are aware of theoretical reasons why bicarbonate therapy in cardiac arrest might be beneficial. Realising the difficulty of obtaining controlled observations in humans, we devised animal experiments to reproduce clinical conditions as closely as possible. We have shown the importance of the early use of adrenaline, calcium chloride, or vasoconstrictor, as an immediate accompaniment to artificial respiration and artificial circulation.23More recently we have attempted to assess the role of sodium bicarbonate in similar circumstances.4 Dogs, lightly anaesthetised with pentobarbitone, were asphyxiated by complete airway obstruction to the point of circulatory arrest. Resuscitation was started after a further interval of five minutes (not uncommon in clinical situations outside the operating theatre). The standard procedure was to apply intermittent positive-pressure breathing and closedchest cardiac massage. Any drugs were administered by needle into a heart chamber. With no drug, or with sodium bicarbonate (2 mEq. per kg.) we could restore circulation in only 10-20% of cases. With adrenaline we could restore circulation in 95-100%. 1. 2. 3. 4.
Gottlieb, R. Archiv. exp. Path. Pharm. 1896, 38, 99. Redding, J. S., Pearson, J. W. Anesthesiology, 1963, 24, 203. Pearson, J. W., Redding, J. S. Anesth. & Analg. 1963, 42, 599. Pearson, J. W., Redding, J. S. Anesthesiology (in the press).
ally of girls’ schools) should positively welcome such
a
child back to school. I do not think this is enough. Because of possible confusion with morbilli, some parents and teachers (and doctors) might be reluctant to take this advice. We must ignore the infectivity of measles too. Not for an instant do I think this would harm the community. In our present urban society, isolation and quarantine of measles do not prevent a single child from catching it-they merely postpone the date. In the end, everybody catches measles. Postponement is of no advantage in measles; in german measles it is a terrible menace. Let us expunge isolation and quarantine of measles-of all sorts-from our textbooks and our minds. Whipps Cross Hospital, London, E.11.
E. HINDEN.
VALVULAR DEFECT IN PRIMARY VARICOSE VEINS
SIR,-Mr. Ludbrook’s work supports the view that the valves of the long saphenous vein fail progressively from the saphenofemoral junction, and my experience leads me to agree with him. Ligation of the long saphenous vein flush with the common femoral vein will relieve the condition, with a few exceptions, such as an isolated small varicose vein or a cluster which are not kept empty by a tourniquet at the groin, lower Hunter’s canal, or at the knee-joint. These clusters are usually cured by a sclerosing injection, followed by sustained pressure for six weeks as described by Fegan.1 Mr. Hobbs (Feb. 15) does not agree with this view, but, when there is a leak from the saphenofemoral junction only, I have found a true saphenofemoral tie effective. I have been doing this since 1926 and have seen patients subsequently for many years. Naturally, for a cure, other leaks must be located and stopped. Hobbs cites Fegan’s work. I have seen this and respect it. I have visited his hospitals twice, and, by his courtesy, have examined some of his patients. The injections had clinically relieved and cleared the varices from the lower
thigh downwards, although some saphenofemoral junctions still had a palpable saphenous varix and an impulse on coughing. I don’t think that this work invalidates Ludbrook’s premise of sequential failure of the valves of a superficial vein from above downwards, starting at its union with a deep vein. It takes time after varices have appeared for sufficient symptoms to arise that require patients to seek surgical care. We have all seen men and women with gross symptomless varices. Women whose varices began in pregnancy sometimes do not come for treatment until after the menopause. During these apparently silent years, the venous hypertension has made the long saphenous trunk hypertrophied and the subcuticular veins dilated, elongated, tortuous, pouched, and inelastic, and has stimulated degenerative changes in the skin and fat. Persistence of varicose veins after a saphenofemoral ligation is regrettably seen occasionally, especially in those done before 1950. Either the operation was inefficient or the diagnosis was wrong or incomplete-e.g., in missing concomitant leaks from Hunter’s canal, the popliteal space, the ankle perforators, and (uncommonly) other communicating veins. Dr. Rivlin (Jan.
25) digresses to ulceration-" gravitational ", deep-thrombotic ". I prefer the term venous hypertensive ulceration. Superficial hypertension is common to primary varicose veins and those associated with deep thrombosis. Ulcers arising from these comprise over 900 of leg ulcers occasionally complicated by arteriosclerosis, The superficial venous diabetes, rheumatoid arthritis, &c. hypertension is the destructive agent causing pigmentation, induration, swelling, eczema, and ulceration. This tension stems from the deep venous system through incompetent connecting veins, especially the ankle perforators. The long " varicose ", and
"
1. Fegan,
W. G.
Lancet, 1963, ii,
109.
and short
veins are connecting veins. Besides the and ankle veins, those from the superficial femoral saphenous vein in Hunter’s canal contribute to the destructive complications at the lower leg. Division of these defective veins precisely at their ending in the deep vein is curative in a large proportion of patients. Rivlin deplores the results of varicose vein operations. The anatomy, physiology, and pathology are described better now and are more widely understood, and the diagnosis and treatment are improving. Already the results are better than they were ten years ago.
saphenous
It
perhaps merits mention that the four common sites of venous leaks can give fifteen clinical presentations per limb. People’s legs are seldom alike, so each needs an accurate and complete diagnosis. A leak (a) in the groin may be caused by two to three possible faulty veins; (b) in Hunter’s canal, two; (c) from the popliteal vein, four. These yield seven combinations. A leak (d) from the ankle perforating veins yields seven or eight. These variations need knowledge and training, time, skill, and judgment to define. There are no short cuts. Stripping was an
irrational hone!
London, W.I.
.
H. DODD.
SiR,-We have been following the correspondence arising from Mr. Ludbrook’s article on valvular defect in primary varicose veins.1 " Varicose veins" is an unfortunate description, since it calls attention to one of the least important aspects of this disease. Often patients with the most severe symptoms and signs have in fact no dilated, elongated, tortuous veins. A more appropriate name is chronic venous insufficiency. Mr. Ludbrook, in our opinion, is correct in stating that valvular incompetence is the cause of chronic venous insufficiency, whether the incompetence is due to injury to the valves, a defect in the vein wall, hormone imbalance, an increased bloodvolume, or some other disorder. He is, we think, incorrect in stating that this incompetence is primarily at the saphenofemoral junction. In over 15,000 patients treated by us in the past twelve years, many of whom had large saphenovarices, not one has required flush ligation of the saphenofemoral junction.23 The disappearance of saphenovarices after blockage of an incompetant hunterian perforator leads us to believe that the emphasis on the saphenofemoral junction in the treatment of varicose veins is misplaced. It is gratifying to learn that Mr. Hobbs (Feb. 15), too, has found that saphenovarices and vulval varices, disappear after blockage of an incompetent hunterian perforator. We believe that the primary lesion in patients with chronic venous insufficiency is incompetence of a valve in one or more perforating veins. In this way the superficial veins are subjected to abnormal pressure, and consequently the portion of the vein above the incompetent perforator will, in time, dilate. The dilatation spreads upwards, causing secondary incompetence of the valves in the superficial veins. Only when the dilatation reaches the saphenofemoral junction do the valves at this site become incompetent. And when the perforator(s), transmitting blood at high pressure, are blocked, the superficial veins recover their tone; and their valves, including those at the saphenofemoral junction, regain their competence. It is in these cases of secondary saphenofemoral incompetence that the Trendelenburg test or a mid-thigh tourniquet test is misleading. Ludbrook states that a near-normal fall in pressure (45 mm. Hg) occurs in patients with varicose veins who exercise the leg after a mid-thigh tourniquet has been applied. Certainly there is some drop in pressure, but if there is an incompetent valve in a perforating vein below the tourniquet, then the fall will be slight. The pressure exerted by a midthigh tourniquet (really a modification of the Trendelenburg test) is sufficient to occlude both the deep and superficial 1. Ludbrook, J. Lancet, 1963, ii, 1289. Fegan, W. G. ibid. p. 109. Fegan, W. G. Minerva cardioangiol. europ. 1961, p. 481.
2. 3.
492 test is an inadequate diagnostic procedure, and is for many misdiagnoses and consequent failures of treatment. The pressure needed to block an incompetent saphenofemoral junction must of necessity also block the common femoral vein, since the pressure in the deep veins here is the same as in the superficial veins. But if the test is performed with a finger exerting just sufficient pressure to occlude the long saphenous vein in the upper thigh, the superficial veins will nearly always be seen to fill from incompetent perforating veins. This resembles our diagnostic test previously described.2 In our opinion, Ludbrook’s investigations of the intravenous pressures are inadequate and consequently misleading. He recorded pressure in the superficial veins only and then refers to " mean " pressure values. The results give a false picture of the functions and faults of the complex pumping mechanisms responsible for returning blood from the lower limbs. Pressures in the superficial and deep veins must be recorded simultaneously by an electronic manometer which gives a permanent record of the very rapid pressure changes in the leg during movement. We have so far made 83 intravenous pressure recordings, and have many tracings obtained simultaneously in deep and superficial veins. From these it can be shown that the pressures vary with great rapidity; the rapidity can, in fact, be compared to that of the P.Q.R.s. complex on the cardiograph. Plainly, to take a " mean " pressure in a vein is as inaccurate as taking a mean potential for the P.Q.R.S. complex. The pressure in the long saphenous vein, as Ludbrook says, does fall with exercise in the erect posture in patients with chronic venous insufficiency, and often it falls in a normal pattern. In this way many patients, because they have many normally functioning pump units, can compensate for a faulty valve in one of their perforating veins, and hence have no serious symptoms. The fallacy of obtaining mean records of the intravenous pressure is shown by Ludbrook’s statement that on exercise the superficial pressure at the ankle dropped in control patients from 95 to 45 mm. Hg. In fact, our tracings show that a healthy person can reduce the pressure in the superficial vein at the ankle to within 5 mm. of zero during exercise. Only by recording both deep and superficial pressures can one understand the mechanisms whereby the normally high-pressure system (deep) can receive blood from the low-pressure system (superficial). It is during the fraction of a second (when the muscle-pumps are in their early diastolic phase) that the pressure in the superficial veins exceeds that in the deep veins and creates a favourable gradient. Ludbrook states that in what he calls primary varicose veins the calf-pump is functioning normally. This may or may not be the case, depending upon the condition of the valves in the perforating veins connected to this pump; but even if the calf-pump does function normally, the plantar, anterior and posterior tibial, peroneal, quadriceps, adductor and hamstring pumps must also be taken into consideration, since an incompetent valve in a perforating vein connected to any of these may lead to chronic venous insufficiency. In similar cases we have always found a leaking perforator in one or more of the remaining pumps, commonly the adductor or quadriceps pumps. The success of his mid-thigh tourniquet test may lie in his occlusion of an incompetent upper hunterian perforating vein, together with a secondarily incompetent saphenofemoral junction, and compression of the deep veins. Ludbrook describes primary varicose veins as occurring in patients who have not had deep-vein thrombosis. Varicose veins are seldom primary, but usually follow some other condition, whether it be hormonal, lacerations, polycythxmia, trauma, &c. Perforating veins can thrombose without manifesting as deep-vein thrombosis; and probably quite small injuries often cause subclinical thrombosis confined to a perforating vein and a short segment of the superficial veins. After recanalisation, the valve in the perforating vein will be
veins. The
responsible
incompetent.
reply to Mr. Ludbrook’s suggestion that our technique of course be successful if most of the varices are sclerosed (Feb. 1), nothing could be further from our object. We aim to produce, as we have shown a short segment of sclerosis in the superficial vein overlying the incompetent perforating vein, and including it. We have established that the perforator is, in fact, blocked by many biopsies at varying intervals after injection, at which time the perforating vein is cut across with a knife and no bleeding has taken place. Microscopic examination proves that these veins are totally occluded. In
must
The good results using our injection technique do, in fact, remain constant with time. In a survey conducted recently on 1172 patients treated between 1956 and 1960, the results were satisfactory in 81%, and in the patients who carried out our instructions conscientiously, the results were satisfactory in 86%. The best results were in patients who were treated in 1956; this means they have stood the test of time for eight years. The average number of attendances per patient at our clinic is 5, and in 15,000 cases treated there has been no mortality. Had these all been treated by surgery there would, according to published figures, have been upwards of 40 deaths. We shall be pleased to hear Mr. Ludbrook’s views, and would like to know to what operation he refers when he talks about " before operation and " after operation"? Was it solely saphenofemoral ligation or some more elaborate procedure ? GEORGE FEGAN Research Department, DERMOT FITZGERALD Sir Patrick Dun’s Hospital, BILL BEESLEY. Dublin 2. "
.
--
MANAGEMENT OF CARDIAC ARREST
SIR,-Mr. Stewart (Jan. 11) makes two statements which we feel are questionable. First, No time should be wasted in the first instance with adrenaline, calcium salts, hypertonic glucose, and other drugs." Second, There is now ample evidence for the efficiency of bicarbonate therapy in the management of cardiac arrest, and it should come into routine use forthwith." Going back to 1896/ adrenaline has been recommended in the "
"
of cardiac arrest : thus contrary recommendations should be made with careful documentation. In most instances, cardiac arrest is associated with asphyxia during general anxsthesia; with airway obstruction in cases of coma due to head injury or barbiturate poisoning; and in drowning. In such cases it has hypoxia and respiratory acidosis as primary factors, and metabolic acidosis as a treatment
secondary feature. We are aware of theoretical reasons why bicarbonate therapy in cardiac arrest might be beneficial. Realising the difficulty of obtaining controlled observations in humans, we devised animal experiments to reproduce clinical conditions as closely as possible. We have shown the importance of the early use of adrenaline, calcium chloride, or vasoconstrictor, as an immediate accompaniment to artificial respiration and artificial circulation.23More recently we have attempted to assess the role of sodium bicarbonate in similar circumstances.4 Dogs, lightly anaesthetised with pentobarbitone, were asphyxiated by complete airway obstruction to the point of circulatory arrest. Resuscitation was started after a further interval of five minutes (not uncommon in clinical situations outside the operating theatre). The standard procedure was to apply intermittent positive-pressure breathing and closedchest cardiac massage. Any drugs were administered by needle into a heart chamber. With no drug, or with sodium bicarbonate (2 mEq. per kg.) we could restore circulation in only 10-20% of cases. With adrenaline we could restore circulation in 95-100%. 1. 2. 3. 4.
Gottlieb, R. Archiv. exp. Path. Pharm. 1896, 38, 99. Redding, J. S., Pearson, J. W. Anesthesiology, 1963, 24, 203. Pearson, J. W., Redding, J. S. Anesth. & Analg. 1963, 42, 599. Pearson, J. W., Redding, J. S. Anesthesiology (in the press).