Foetal Paroxysmal Auricular Tachycardia

Abstract

Although paroxysmal auricular tachycardia is most common in adults between the ages of 20 and 40 years, many examples of its occurrence in children have been described following Buckland's (1892) account of the condition in an eleven-year-old girl. During the past 25 years the arrhythmia has been recognized in antenatal life and the present paper reports two further examples affecting the foetus.CASE REPORTS Case 1. P.H. was the second child of healthy parents. The mother's first pregnancy in 1944 was uneventful and at term she was delivered of a normal, female child. Three years later in 1947 the mother had a miscarriage at two months. Her third pregnancy in 1949 was normal until two weeks before the expected date of delivery when there was a sudden increase in the size of her abdomen, due to the development of hydramnios, which necessitated her admission to hospital. A plain X-ray of the mother's abdomen showed the baby to be in full extension, a position considered to be the result of gross distension of the feetal abdomen. The feetal heart rate was recorded as varying between 130 and 140 beats a minute, the rhythm being regular. Two days after the mother was admitted to hospital her membranes were ruptured artificially, labour commenced within an hour and 91 hours later she was delivered of a live, female child.At birth the baby was very ill with severe dyspncea and cyanosis. There was extensive cedema affecting the skin and subcutaneous tissues of the limbs, face, chest, and abdomen. The abdomen was distended by fluid in the peritoneal cavity. The heart size and cardiac sounds were normal The heart rate was above 200 beats a minute and the rhythm appeared regular although electrocardiography (Fig. 1) revealed the rate to be 228 beats a minute with a slight irregularity of the rhythm. The tracing was consistent with a 1: 1 auricular tachycardia. A chest X-ray showed the heart to be normal in size, shape, and position; the lung fields were clear.The child was nursed in an oxygen tent and no fluids were administered during the first 48 hours of life. Ten hours after birth quinidine sulphate was administered orally in the dose of 1/6 grain, four-hourly, but as there was no slowing of the heart rate and her condition deteriorated, the quinidine was abandoned after 24 hours and digoxin substituted in a dosage of 0-125 mg. intramuscularly at two-hourly intervals for three doses. An immediate response followed (Fig. 2) with the heart rate falling to 120 beats a minute and there was an associated improvement in the baby's condition. An electrocardiogram taken at this period confirmed that the cardiac rate and rhythm were normal. Following a large diuresis the oedema subsided rapidly and by the ninth day the weight had dropped from the birth weight of 9 lb. 1 oz. to 6 lb. 5i oz. Breast feeding was satisfactorily established and the baby was discharged home on the twelfth day of life weighing 6 lb. 8i oz.At the age of six weeks, a routine visit was made to Out-Patients where it was found that her general progress had ...

Atrial tachy-arrhythmias associated with massive edema in the newborn

“…As early äs 1953, ANDERSON [1], in a review of thirteen infants with PST commented on the large weight of the patients but did not describe the presence of either edema or anasarca. In RADFORD'S [14] recent report of twelve cases of congenital PST the birthweight was generally large for gestational age. Presumably the relatively large birthweights are directly related to fluid retention from heart failure.…”

Differential diagnosis of hydrops fetalis

“…Nonisoimmune causes of hemolytic anemia include red cell enzyme defects [21,30] Fetomaternal hemorrhages occur frequently and are the underlying mechanism of Cardiac Failure 1) Intrauterine fetal tachycardia may cause hydrops [ 18,[43][44][45][46][47][48][49][50] . Low-output cardiac failure with complete heart block can produce the same picture [Sl-5.51 ; in some instances, the recurrence in siblings is attributable to maternal disease rather than fetal genetic disease [53] .…”