ELECTROCARDIOGRAPHIC CHANGES DURING ANÆSTHESIA

ELECTROCARDIOGRAPHIC CHANGES DURING ANÆSTHESIA

551 treatment" and " order " gave us some difficulty in intersince the. experimental design confounds " order " pretation with " children ". However, ...

201KB Sizes 0 Downloads 26 Views

551 treatment" and " order " gave us some difficulty in intersince the. experimental design confounds " order " pretation with " children ". However, we felt that we could safely say that the benefit attributable to the drug, if it existed at all, was only of the order of 3% of normal and not more than.7-5% of normal and that there was no real evidence that different children reacted very differently to its administration. We regard this last aspect as important in any drug trial, because a marked variation in response of individuals to a drug will not be apparent from a consideration of the mean results alone. These findings in a different age-group confirm those of Dr. Langlands and Dr. McNeill and draw attention again to the need for objective measurement in assessing the results of treatment in asthma. We are grateful to Messrs. Riker, Loughborough, for the supply of "

medihalers containing hydrocortisone medihalers. Department of Child Health, Kings College, University of Durham

acetate

and for the

placebo

L. B. STRANG* E. G. KNOX.

and

A.v. nodes,5 others consider it to be a nodal with variations in the rate of conduction of imrhythm to back the atria.The effect is the production of a pulses constant RR interval with variable PR, RP, and PP fairly intervals and these changes may be seen in all three S.A.

tracings. Ryde,

SIR,-The basic mechanism involved in the disturbance of cardiac rhythm during anaesthesia with trichlorethylene, noted by Dr. Zuck, seems to depend on the existence of a homogenetic idioventricular ectopic pacemaker situated above the bifurcation of the main bundle of His, and probably below the atrioventricular node. Retrograde conduction from this centre is blocked, so that the atria continue to be activated by the sinus node. It may be that the sinus impulse passes theough the atrioventricular

ELECTROCARDIOGRAPHIC CHANGES DURING ANÆSTHESIA was most interested in Dr. Zuck’s letter of SIR,-I 20 about his two cases with abnormal electrocardioAug. grams, because I have seen a similar case myself. This arose in a man of 55, in the course of a recent investigation into the action of thiobarbiturates on the electrocardio-

gram’! There was no history or clinical signs of cardiac disease and the pre-anaesthetic control electrocardiogram of the standard and augmented limb leads showed no abnormality. The patient had undergone cystoscopy under buthalitone/ nitrous-oxide/oxygen anaesthesia and the accompanying record was taken five minutes after the anaesthesia had been discontinued. The tracing (lead 11) shows the p wave becoming fused with and distorting the QRS, reverting to its original position and then returning to the QRS. As in Dr. Zuck’s two tracings, the RR intervals are constant while the PR, RP, and pp intervals are variable. Almost every known form of cardiac arrhythmia has been reported during trichlorethylene anaesthesia,22 and nodal rhythm often arises under any type of anxsthesia and is considered to be of little clinical significance.3 Dr. Zuck has suggested that the effect may be due to the almost synchronous discharge of impulses arising in the sinoauricular and atrioventricular nodes with the former suppressing the latter. Such a mechanism has been described and a very similar picture is produced. This type of arrhythmia, however, is associated with sinus bradycardia and the Pp intervals are constant. Neither of these features are present in Dr. Zuck’s or my

J. MACKETT.

Isle of Wight.

conducting tissues for

some

way before it is

blocked, thus rendering them refractory for the retrograde impulse from the ectopic centre-i.e., the retrograde ventriculoatrial block has a physiological and not a pathological explanation, and does not depend upon organic disease in the main bundle of His. Hence two pacemakers exist in the heart side by side competing for the conducting pathways in the presence of normal atrioventricular conduction-i.e., a pararrhythmia is present, with sometimes nodal and sometimes sinus rhythm. As the two centres have almost identical have a close relationfrequencies the P waves and QRS complexes " " ship in time. This explains the emerging p waves, and a type of reversed Wenckebach phenomenon. Vagal hypertonia may be an important factor in this disturbance of rhythm. Belfast

City Hospital.

E. FLETCHER.

BACK PAIN AND HYPERÆSTHESIA

SIR,—To sum up the letters you have published on this subject, their authors fall into two groups as might have been expected: on the one hand the qualified men who practise unashamedly osteopathic techniques, and, on the other, qualified men whose manipulation is justified in terms of classical anatomy of the intervertebral disc and its effects on the nerve-roots of the central nervous system. The fact that both groups feel that my paper is an important contribution demonstrates that although manipulation is successful, we are still very ignorant, in my opinion, as to why it is. We must clear our minds completely of previous electrocardiograms. It seems most likely that these three cases are examples theory and investigate this commonplace condition with every modern technique that is available. Ordinary still of a relatively uncommon but recognised type of phenoX-ray films have shown nothing; perhaps high-speed menon known as a wandering pacemaker or shifting or sliding nodal rhythm. While some cardiologists consider slow-motion X-ray studies of the spine during manipulathat this condition is due to the site of stimulus formation tion would be fruitful, or perhaps electrophonographic continually moving across the atrial muscle between the studies of the " click ", or finally the detailed postmortem dissection of the segment of the spine at fault in patients * Now at Hammersmith Hospital, Ducane Road, London, W.12. known to have had a recurrent syndrome or an acute 1. Henderson, A. G., Mackett, J., Masheter, H. C. Brit. J. Anœsth. 1958, 30, 302. attack immediately before death. 2. Wylie, W. D., Churchill-Davidson, H. C. A Practice of Anæsthesia; In all these investigations each patient must satisfy all p. 197. London, 1960. 3. ibid. p. 351. four P. Diseases of the points of the syndrome, namely: (1) dull ache, (2) 4. Wood Heart and Circulation; p. 219. London, 1959. limitation of a spinal movement by pain, (3) paravertebral tender spot, and (4) its overlying area of hyperaesthesia. This syndrome will not only be useful in ensuring that all investigators are studying the same condition, but will also ensure Electrocardiogram five minutes after end of buthalitone/aitrous-oxide/oxyge ansesthesia. There is lower tracings.

an

interval of

approximately 2·1

sec.

between the upper

anc

Goldberger, E. Unipoplar Lead Electrocardiography and Vectorcardiography; p. 375. London, 1954. 6. Evans, W. Cardiology; p. 112. London, 1956. 5.