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The pattern of water and solute excretion during paroxysmal tachycardia has been studied by Borst and his colleagues (Blomhert, 1951;Borst, 1941;Borst et al., 1960). They showed that with the onset of paroxysm there was a striking water diuresis which continued for the duration of the paroxysm and then stopped. An increase in sodium chloride excretion was also recorded at some time in the attack. Creatinine excretion was constant. A case studied by Wood (1963) developed a diuresis during a paroxysm which was associated with an increased output of sodium. This was not a water diuresis as the urine specific gravity was high.Wood (1963) accumulated statistics on the diuresis accompanying paroxysmal tachycardia. Diuresis occurs with all forms of paroxysmal arrhythmia when the heart rate exceeds 110 a minute; and with heart rates varying from 120 to 280 a minute. Diuresis starts after 20 to 30 minutes, but sometimes not for 60 minutes after the onset, the time interval being remarkably constant in the individual: it does not occur with a paroxysm of 5 to 20 minutes' duration.Because these changes are of interest and of possible physiological importance, the changes in urine composition were recorded during two episodes of paroxysmal tachycardia in a young woman. CASE REPORTA healthy, single girl of 23 was investigated. She had experienced bouts of palpitations lasting a few minutes from the age of 16 years. For 2 years the episodes had become more frequent and tended to last several hours, and she had noted that occasionally she passed more urine during attacks. Physical examination between attacks was normal. Pulse was regular with a rate of 68 a minute; blood pressure was 120/70 mm. Hg; electrocardiogram showed sinus rhythm with a rate of 70 a minute. During attacks, apex rate rose to 160 a minute. Venous pressure was not raised at any time. Blood pressure rose to 130/100 mm. Hg at the beginning of some attacks. Electrocardiograms during paroxysms showed a supraventricular nodal tachycardia. Carotid sinus pressure was without effect.Investigations. Plasma sodium, 137 mEq/l.; potassium, 4 mEq/l.; chlorides, 104 mEq/l.; bicarbonate, 24-8 mEq/l.; osmolality, 295 m.osm./kg.; urea, 32 mg./100 ml.; true creatinine, 0 7 mg./100 ml.; 24-hour endogenous creatinine clearance, 132 ml./min.; random 24-hour urine collection, 1870 ml., with excretion of sodium, 56 ,Eq/min., potassium, 73 ,uEq/min., and urea, 300 juM./min. Hemoglobin, 13X5 g./100 ml.Chest radiograph was normal. Urine contained no albumin and was sterile on culture.At the beginning of the paroxysm, the subject was put to bed in a recumbent position. Free collections of urine were timed. During the paroxysm, venous blood was withdrawn into heparinized tubes and centrifuged. Blood pressure was recorded every 15 minutes with a mercurial sphygmomanometer. Apex rate was recorded every 15 minutes. Only small quantities of fluid were ingested during the paroxysm. Observations were continued for several hours after the heart rate fell below 100 a minute.Biochemical measure...

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