of opacity all over the right and left lung fields. The astic attack was relieved only after giving 100 mg of hydroordsone sodium succinate intravenously. - A 62-year-old man with grade III chronic coronary insufficiency was to be treated with propranolol in an initial daily dose of 120 mg. On compression of the right carotid sinus he was found to develop a brief syncope and marked bradycardia resulting from sinus arrest followed by junctil escapes (see fig., A). Thus a hyperactive carotid sinus refex syndrome was d. A test dose of 2 mg of propranolol was administered intravenously as a bolus injion and 10 minutes later hyperextension of the head provxed a more prologed syncope and a more marked bradycardia than previously. Thus the hyperactive carotid sinus reflex syndroe had been transformed into a carotid sinus syndrome after propralol.Digital compression of the carotid sinus for a shorter period than previously provoked a much more lasting sinus arrest 15 minutes after propranolol (see fig., B).Twenty minutes after prIpranolol 1 of atropine was ineted intravenously; five minutes later th right carotid sinus was mssaged for several seconds. No effect was observed either on the electrical activity of the heart (see fig., C) or on the clinical condition of the patient. This last procedure and the corresponding result show the innocuity of our methods. It is imperative to search for a hyperactive carotid sinus reflex syndrome in every patient who is to be treated with beta-adrenergic bloking drugs and this therapy avoided if the syndrome is diagnosed and the participation of a central cardiac mechanism in it demonstrated.-I am, etc., ARIEL J. REYES Fundacion Procardias,
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