Feb 13, 1982 - FRANCO CLARA. Intensive Care Department,. Ospedale ... Drs A Burns and Tom Brown (12 December, p 1607) add two more patients with ...
BRITISH MEDICAL JOURNAL
VOLUME 284
blood pressure. This dramatic situation was reversed with heart massage and dopamine. Tachycardic rhythm disturbance in the acute phase of myocardial infarction certainly needs immediate reversion, but the hypotension or shock that may be induced by intravenous administration of amiodarone more seriously jeopardises myocardial perfusion and the patient's recovery. The authors strongly recommend that amiodarone should not be used by the intravenous route. FRANCO CLARA Intensive Care Department, Ospedale Civico, CH-6900 Lugano, Switzerland
Staubli M, Studer H. Schweiz Med Wochenschr 1981 ;111 :460-5.
SIR,-The effectiveness of intravenous amiodarone in controlling fast atrial fibrillation and restoring sinus rhythm was reported by Dr Roger L Blandford and others (2 January, p 16). We wish to support his findings and to emphasise particularly the value of intravenous amiodarone in patients with fast atrial fibrillation complicated by frequent ventricular ectopic beats or runs of ventricular tachycardia. We have recently successfully treated two such patients, both elderly males-one with hypertension who had had a stroke recently and who had atrial fibrillation complicated by frequent extrasystoles, and the other with chronic bronchitis and a segmental pneumonia who had atrial fibrillation complicated by ventricular tachycardia. Each received 300 mg of amiodarone in 250 ml of 5 0, dextrose given intravenously over 20 minutes, followed by an intravenous infusion for 24 hours in one case and 18 hours in the other at a rate of 300 mg every six hours. In both patients the ventricular arrhythmia was rapidly corrected. In the first the rate of atrial fibrillation was rapidly reduced from 160 to 120 beats/min. Restoration of sinus rhythm occurred after six hours but after a further six hours was replaced by slow atrial fibrillation. Oral amiodarone (200 mg thrice daily) was begun before the intravenous therapy was stopped. In the second patient atrial fibrillation persisted but the ventricular rate dropped rapidly from 150 to 120 beats/min. Further slowing was achieved by introducing digoxin rather than continuing with oral amiodarone, which had again been started before intravenous therapy was stopped.
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clinical problems suggested that those who did not have hypercapnia usually had other disorders that would be likely to stimulate ventilation. The reports of Drs Shahrokh Javaheri and Edward N Nardell (17 October, p 1016) and Drs A Burns and Tom Brown (12 December, p 1607) add two more patients with metabolic alkalosis to those with hypoventilation, hypercapnia, and hypoxaemia previously reported by others. The cause of the hypoventilation is uncertain. Drs Javaheri and Nardell wrote about "depression of central and peripheral chemoreceptors by the alkalaemia." Potassium depletion or hypokalaeniia or both, which are common in patients with metabolic alkalosis, could cause weakness of respiratory muscles; but in our series2 hypercapnia did not correlate with hypokalaemia. Several authors (including Drs Javaheri and Nardell) demonstrated normal pulmonary function in their patients after recovery from alkalosis. However, it would be interesting to have measurements of vital capacity and forced timed expiratory volumes in patients with hypercapnia and metabolic alkalosis when they actually have hypercapnia. The patient reported by Drs Burns and Brown, whose blood pH was 7 44, illustrates another interesting point about metabolic alkalosis and the occurrence of hypercapnia. In the past the diagnosis of metabolic alkalosis was based mainly on the finding of a high blood pH together with a high serum total carbon dioxide content. The accompanying table shows the arterial carbon dioxide tension (Paco.) and plasma bicarbonate values calculated from several sets of normal-to-high values of blood pH and CO2 content on the basis of the Henderson-Hasselbalch equation. Arterial C°2 tension and plasma bicarbonate concentration calculated from normal-to-high values of blood pH and plasma total CO2 content Plasma
CO2
Set a
b c
d e f g h i
content Blood pH (mmol/l)
7 40 ,, ,, 755 ,, ,, 770 ,,
25-2 37 8 504 25 2 37-8 504 25 2 37-8 50-4
Plasma HCO,-
Paco,
24-0 36-0 48-0 24-3 36 5 487 24-6 36-9 492
5-3 80 10-7 3-8 58 77 28 41 5-5
(mmol/l)
(kPa)
Intravenous amiodarone would thus appear using the Henderson-Hasselbalch equation. to be an effective alternative to digoxin in *Calculated Conversion: SI to traditional units-Carbon dioxide: 1 controlling the ventricular rate in fast atrial mmol/l 045 ml/100 ml. Bicarbonate: 1 mmol/l= fibrillation and sometimes in restoring sinus 1 mEq/l. Pressure: 1 kPa z 75 mm Hg. rhythm. Its particular advantage lies in its speed of action and its effectiveness in control- Arterial CO2 tension so calculated seldom exceeds 6 7 kPa (50 mm Hg) except in patients ling associated ventricular arrhythmias. with either (1) a moderately high serum CO2 P C HAYES content and a near-normal blood pH (as in G H LOVE sets b and c in the table and as in the patient of Burns and Brown) or (2) an extremely high J A TULLOCH Drs serum CO2 content and a moderately elevated Department of Medicine, blood pH (as in set f). The type (1) patient, not Stracathro Hospital, Brechin, Angus DD9 7QA having alkalaemia, may have been excluded from earlier series; the type (2) patient is uncommon. When those measurements are used for case finding, the more frequently Severe metabolic alkalosis encountered patients with metabolic alkalosis, SIR,-Until recently it was generally believed with moderate elevations of both blood pH that patients with metabolic alkalosis did not and serum CO2 content (as in set e), will not exhibit compensatory hypercapnia, presum- have a particularly high calculated Paco2. ably because the resulting hypoxaemia limited Patients with very severe alkalaemia (as in hypoventilation.' However, recent case reports, sets g, h, and i) will have a normal, or even and our own experience,' suggest that hyper- low, calculated Paco2. Arterial CO2 tension is now usually measured capnia is not unusual in patients with metabolic alkalosis. An analysis of our alkalotic patients' directly, so we are less likely to overlook
patients with metabolic alkalosis who have hypercapnia. That may explain why now we do appreciate that the combination is not rare, even in the absence of underlying chronic lung disease. MILFORD FULoP Department of Medicine, Albert Einstein College of Medicine, Yeshiva University, USA
Goldring RM, Cannon PJ, Heinemann HO, Fishman AP. J Clin Invest 1968;47:188-202. 2Fulop M. NY State Med 1976;76:19-22. _
Planovalgus feet SIR,-Mr S C Gallannaugh (9 January, p 97) rightly emphasises the futility of remedial exercises in physiotherapy departments for the treatment of postural planovalgus feet, but he might have mentioned the value of encouraging the child to skip on the toes at home. In deciding about the need for treatment of pronated feet one should look at the footwear rather than at the feet. If the shoes are trodden over then treatment is required. Alterations to shoes are tedious and often inefficient. A better way of reinforcing the shoes is by means of heel seats (manufactured by Myron Medical Products Ltd, Chester House, Windsor End, Beaconsfield, Bucks HP9 2JJ). These are highdensity plastic cups which fit into the backs of the shoes. They have the advantage of being comfortable and inconspicuous and they can be transferred from one shoe to another. A W FOWLER Bridgend General Hospital, Bridgend, Mid Glam CF31 1JP
Importation of pathogenic Entamoeba histolytica
SIR,-Entamoeba histolytica, an intestinal parasite of man found in very low incidence in the United Kingdom but in high incidence in endemic areas throughout the world, is known to invade tissue. The resulting disease may produce extraintestinal involvement,' which if allowed to progress can rapidly result in death of the host. This species, however, has been shown to contain representatives which may belong to any of numerous zymodemes2 (a zymodeme is a population of amoebas differing from similar populations in the electrophoretic mobility of specified enzymes). Only a limited number of these zymodemes are associated with disease and the remainder originate from symptomless carriers. This holds true even in endemic areas.3 With the increase in world travel it becomes exceedingly important to recognise E histolytica that can cause disease as promptly as possible after they are imported into Britain. Most dysenteric diseases result in similar clinical signs and symptoms. Only laboratory study of specimens from the patient yields the specific diagnosis, and without this study incorrect diagnosis and non-specific treatment of a pathological condition may result.4 Over the past year 39 faecal specimens from patients (residents of the United Kingdom) with dysenteric symptoms, and all containing F histolytica cysts, have been referred to the department of medical protozoology at the London School of Hygiene and Tropical Medicine. From these samples the first example of an Entamoeba histolytica belonging to a pathogenic zymodeme has now been
