Pulmonary oedema without critical increase in left atrial pressure in acute myocardial infarction

A D Timmis, M B Fowler, R J Burwood, P Gishen, R Vincent, D A Chamberlain
1981 BMJ (Clinical Research Edition)  
pacemaker was working satisfactorily and there had been complete resolution of the pneumopericardiurn. Three months later the patient presented with pleuritic chest pain and was admitted to hospital after a syncopal episode. She was found to be feverish and to have radiological evidence of both pericardial and pleural effusions. In addition the epicardial pacemaker was intermittently failing to capture. Postcardiotomy syndrome was diagnosed and, though aspirin resulted in rapid improvement of
more » ... mptoms and of the pericardial and pleural effusions, the pacemaker continued to show intermittent failure to capture. In view of the syncopal episode a new permanent endocardial pacing system was inserted electively through a right cephalic vein cut-down, using a wedged electrode. Thereafter she made an uncomplicated recovery and was discharged home. Discussion In most cases effective permanent cardiac pacing may be established with a low incidence of complications.'4 The common causes of early failure of endocardial pacing are poor positioning of the electrode initially and subsequent displacement.' Less common but well recognised are perforation of the myocardium, fracture of the lead, infection, and failure of the generator. Temporary endocardial pacing in our patient resulted in a pneumopericardium. Presumably the electrode had penetrated not only the right ventricle but also the pericardium into the adjacent lung. Pericarditis after epicardial pacing is a well-recognised complication.5 In our patient the early postoperative pericarditis was followed by recurrent attacks: these were thought to be due to the postcardiotomy syndrome as no infective, autoimmune, or other cause could be identified. The epicardial electrodes themselves, however, may result in focal inflammation and cause a relapsing pericarditis.5 References Parsonnet V, Bilitch M, Furman S, et al. Early malfunction of transvenous pacemaker electrodes. A three centre study. Circulation 1979;60:590-6. 2 Seremetis MG, de Guzman VC, Lyons WS, Peabody JW Jr. Cardiac pacemakers. Clinical experience with 289 patients. Am Heart J 1973; 85:739-48. 3 Davidson DM, Braak CA, Preston TA, Judge RD. Permanent ventricular pacing: effect on long term survival, congestive heart failure, and subsequent myocardial infarction and stroke. Ann Intern Med 1972; 76:345-51. 4 Gould L, Reddy CVR, Maghazeh P, et al. Three hundred and fifty-three consecutive patients with permanent transvenous pacemakers. Pace 1980;3 :452-5. 5 Peters RW, Scheinman MM, Raskin S, Thomas AN. Unusual complications of epicardial pacemakers. Recurrent pericarditis, cardiac tamponade and pericardial constriction. Abstract Twelve patients with acute myocardial infarction and radiological evidence of pulmonary oedema were observed in whom the left atrial pressure, measured indirectly as pulmonary artery end-diastolic pressure, was not critically increased (range 5-12 mm Hg with reference to sternal angle). Eight of the patients had been treated with frusemide, but only six had responded; hence in at least half of the series diuresis could not account for the anomalous finding. Six patients with low cardiac output were given infusions to expand plasma volume. Appreciable increments in mean values for cardiac index (1-6 to 2-0 1/min/ m2), stroke index (18 to 23 ml/beat/m2), mean arterial pressure (65 to 86 mm Hg), and pulmonary artery end-diastolic pressure (8 to 15 mm Hg) were recorded. This group, and the remaining six patients with higher cardiac output, survived to leave hospital. Delay in radiographic clearing after a fall of left atrial pressure was a possible explanation for the rela-Royal
doi:10.1136/bmj.283.6292.636 fatcat:dhgvmza2kzfrnbsr2gshhhtcuq