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duce a definite but acceptably low frequency of minor intra-operative and postoperative bleeding". This seems to me to bea fair assessment of the evidence, and it is now up to those whodisagree to show that another prophylactic regimen associatedwith a lower incidence of unwanted side-effects gives equallybeneficial results.

National Institute for

Biological Standards and Control,London NW3 6RB DUNCAN P. THOMAS

HYPERKALÆMIA AND OVERDOSE OFANTIHYPERTENSIVE AGENTS

SIR,-We have seen a patient who had severe hyperkataemiaas a result of an overdose of ’Trasicor’ (oxprenolol) and’Navidrex-K’ (cyclopenthiazide and potassium chloride).A 67-year-old man was admitted as an emergency having

collapsed at home. He was confused and dysarthric but wasnot shocked. He had generalised hyporeflexia and reducedmuscle tone. He was in sinus rhythm at a rate of 70/min, andhis blood-pressure was 110/60 mm Hg. The heart sounds werenormal but bilateral basal crepitations were audible in thechest. Abdominal examination was negative. His plasma ureawas 14.8 mmol/1 (87 mg/dl), sodium 135 mmol/l, potassium9-1 mmol/1 and bicarbonate 21 mmol/1. Electrocardiographyshowed the characteristic changes of hyperkalsemia with broa-dened QRS complexes and tall, peaked T waves (figure, March12) and chest X-ray showed pulmonary oedema. He was treatedwith intravenous dextrose, insulin, and frusemide. His plasma-potassium fell to 5.4 mmol/1 within an hour and returned tonormal thereafter. By the following day he was much

improved and gave a history of ingestion of approximatelytwenty-five navidrex-K tablets, thirty oxprenolol 80 mgtablets, and forty nitrazepam 5 mg tablets 2-4 h before admis-sion. These had been prescribed for hypertension 6 monthspreviously. Blood-pressure increased slowly over 3 days to sta-bilise around 150/90 mm Hg on no treatment. E.C.G. (figure,March 14) showed resolution of the changes of hyperkalxmia,and the chest X-ray rapidly returned to normal. Further inves-tigation showed no evidence of myocardial infarction: renalfunction was normal (plasma-urea 5-4 mmol/1, creatinineclearance 95 ml/min); plasma-cortisol during the period ofhypotension was 2044 nmol/1 (75 µg/d1) indicating adequateadrenocortical function.

E.C.G.s (V4,5,6) on (a) March 12 and (b) March 14, 1977.

This patient had ingested approximately 15 g potassium inthe form of navidrex-K (which contains 600 mg potassiumchloride per tablet) 2-4 h before presenting with severe hyper-kala:mia. Severe hyperkalæmia rarely follows an overdose oforal potassium of this magnitude in patients with normal renalfunction’ because of increased renal excretion of potassium.2Furthermore, the diuretic component of navidrex-K wouldhave been expected to accelerate potassium excretion.3 Webelieve that the concomitant overdose of oxprenolol contri-buted significantly to the hyperkalxmia by lowering cardiacoutput and blood-pressure and, therefore, renal blood-flow andglomerular filtration-rate. In this situation renal potassiumexcretion declines sharply,4 and the effect of diuretics in

enhancing the urinary excretion of sodium and potassium ismuch reduced. 1

Preparations of a diuretic combined with potassium arewidely used in conjunction with more potent hypotensiveagents in the treatment of hypertension. Severe hyperkalxmiais a risk after concurrent overdoses of potassium and beta-adrenergic-blocking drugs.

Royal Infirmary,Edinburgh, EH3 9YW

L. HUME

J. C. FORFAR

POSTOPERATIVE ATELECTASIS

SIR,—Can we reasonably assume, as you suggest (Nov. 5,p. 965), that from four hours after operation a decline in P.o2is caused by a pulmonary complication of the usual atelectatictype? Every medical student knows that Pao2 may fall due todiminished alveolar ventilation (from postoperative narcoticsperhaps), from ventilation-perfusion abnormalities (related tofunctional residual capacity and closing capacity probably),and from a reduced cardiac output (with reduced venous

oxygen saturation), as well as from frank alveolar collapse, areduction in inspired oxygen concentration, and diffusiondefects in certain circumstances.

Is it also sound to focus, as you do, on Pao2 in the postopera-tive period when the oxygen available to the tissues, the

oxygen flux, is of paramount importance? A mention of theneed for an adequate amount of well-saturated hxmoglobinand optimum conditions for a suitable cardiac output wouldhave been fitting, and these were noted en passant by P. S.Parfrey to whose work you refer. 5Your mention that the lung-closing volume is inevitably

altered when the vital capacity is reduced is too vague to beuseful. Surely the conventional explanation would have beenappropriate-namely, that breathing at low lung volumescauses the tidal volume to take place within the closing capa-city so that some alveoli, not ventilated throughout the respira-tory cycle, are relatively overperfused and therefore give riseto a venous admixture effect.Few would deny that oxygen administration usually has a

place postoperatively when Peo2 falls below 8 kPa (60 mm Hg)during air breathing, but it would be dangerous to assume thatthis is always attributable to "atelectasis" and the treatmentshould therefore be directed towards each factor producingarterial hypoxaemia and a diminished oxygen flux.Wessex Cardiac and Thoracic Centre,Southampton Western Hospital,Southampton S09 4WQ J. M. MANNERS

***We see nothing strange in the idea that atelectasis shoulddevelop as early as four hours after operation. After all, Nunn

1. Black, D. A K. Essential of Fluid Balance; p. 74. Oxford, 1967.2. Keith, N. M., Osterberg, A. E., Burchell, H. B. Ann. intern Med. 1942, 16,

879.3. Dybkaer, R., Frantzen, A. Acta med. scand. 1964, 175, 135.4. Dirks, J. H., Seely, J. F. Modern Trends in Physiology; p 205. London,

1972.5. Parfrey, P. S., Harte, P. J., Quinlan, J. P., Brady, M. P. Br. J. Surg. 1977,

64, 390.