Case reports 423 Delayed papillary muscle rupture is well documented.' The forces exerted on the heart from dynamic chest trauma are variable and depend on the elasticity of the thorax and the intra-abdominal pressure. A further variation depends on the points in the respiratory and cardiac cycles at which the insult occurs. The most vulnerable points are at maximal inspiration, and during isovolumic systole when all the valves are closed and the cavities hold the maximum amount of blood. The pathophysiology of the muscle rupture is not clear but it has been suggested that the intramural blood flow redistribution caused by local oedema, fibre rupture, and haematoma produces sufficient endocardial ischaemia to cause papillary muscle necrosis. Papillary muscles, being projections from the ventricular wall, are particularly prone to ischaemia in this way as they cannot benefit from a collateral supply. The subsequent proteolytic process reaches a maximum over 24 hours that accounts for the delayed presentation.In conclusion this case illustrates the need for the possibility of cardiac trauma to be considered in patients who sustain a blunt chest injury. This consideration should be a dynamic one, and the diagnosis should be reconsidered after any change in the patient's condition even where cardiac trauma was previously excluded. Although TTE may be useful in some cases, it has limited sensitivity compared with TOE and consideration should be given to more widespread application of the latter in ICUs. Fatal flecainide intoxicationFlecainide acetate is a potent class IC antiarrhythmic agent used mainly for the treatment of supraventricular arrhythmias. Acute overdose of this drug is rare but frequently fatal. The clinical course of a patient that ingested a large quantity of flecainide as a suicide attempt is described and current therapeutic strategies discussed. (JAccid Emerg Med 1998;15:423-425)