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Objectives: The aim of this retrospective study was to evaluate perinatal atrial flutter (AF) and the efficacy of maternally administered antiarrhythmic agents, postpartum management and outcome., Background: Perinatal AF is a potentially lethal arrhythmia, and management of this disorder is difficult and controversial., Methods: Forty-five patients with documented AF were studied retrospectively., Results: Atrial flutter was diagnosed prenatally in 44 fetuses and immediately postnatally in 1 neonate. Fetal hydrops was seen in 20 patients; 17 received maternal therapy, 2 were delivered and 1 was not treated because it had a severe nontreatable cardiac malformation. In the nonhydropic group of 24 patients, 18 were treated and the remaining 6 were delivered immediately. In the hydropic group, 10 received single-drug therapy (digoxin or sotalol) and 7 received multidrug therapy. In the nonhydropic group, 13 received a single drug (digoxin or sotalol) and 5 received multiple drugs. One patient with rapid 1:1 atrioventricular conduction (heart rate 480 beats/min) died in utero and another died due to a combination of severe hydrops because of the AF, sotalol medication, stenosis of the venous duct and hypoplastic placenta. Of the 43 live-born infants, 12 were in AF at birth. Electrical cardioversion was successful in eight of nine patients. No recurrences in AF have occurred beyond the neonatal period. Four patients with fetal flutter and hydrops showed significant neurological pathology immediately after birth., Conclusions: Fetal AF is a serious and threatening rhythm disorder, particularly when it causes hydrops, it may be associated with fetal death or neurological damage. Treatment is required and primarily aimed at reaching an adequate ventricular rate and preferably conversion to sinus rhythm. Digoxin failed in prevention of recurrence at time of delivery in a quarter of our patients, whereas with sotalol no recurrence of AF has been reported, suggesting that class III agents may be the future therapy. Once fetuses with AF survive without neurological pathology, their future is good and prophylaxis beyond the neonatal period is unnecessary.

Background: Concern has been expressed that a reduction of partial oxygen pressure during flight in commercial aircraft may induce dangerous hypoxemia in patients with cyanotic congenital heart disease., Methods and Results: To evaluate the validity of this concern, the transcutaneous SaO2 was measured in 12 adults with this type of heart disease and 27 control subjects during simulated commercial flights of 1.5 and 7 hours in a hypobaric chamber. Ten of those patients and 6 control subjects also were evaluated during two actual flights of approximately 2.5 hours in a DC-10 and an A-310, respectively. During the prolonged simulated and actual flights, the capillary blood pH, gases, and lactic acid were analyzed in the patients and during one of the actual flights also in the control subjects. During the simulated flights the SaO2 was at all times lower in the patients than in the control subjects. However, the maximal mean actual percentage decrease, as compared with sea level values, did not exceed 8.8% in either patients or control subjects. During the actual flights, this maximal decrease in the patients was 6%. In-flight reduction of the capillary PO2 was considerable in the control subjects but not in the patients. It is our hypothesis that the lack of a significant decrease of the PO2 in the patients might possibly be due to a high concentration of 2.3 diphosphoglycerate in the red cells. The flights had no influence on the capillary blood pH, PCO2, bicarbonate, or lactic acid levels in either patients or control subjects., Conclusions: Atmospheric pressure changes during commercial air travel do not appear to be detrimental to patients with cyanotic congenital heart disease.

A serious complication was seen following insertion of an intra-aortic balloon pump in the ascending aorta in a pediatric patient. The catheter initially coursed to the left subclavian artery from which it folded upon before finding its way in the descending aorta. We recommend that a suitably curved J-tip guidewire be used to guide the IABP balloons distal to the aortic arch into the descending aorta, so as to avoid potentially fatal complications.

The increased awareness of fetal arrhythmias by obstetricians and the development of sophisticated fetal echocardiography have established the basis for identification and treatment of these arrhythmias. The development of fetal hydrops is a recognized link to the severity of the arrhythmia. Fetal tachycardias have been diagnosed relatively early in gestation. They may be differentiated into sinus tachycardia, supraventricular tachycardia, atrial flutter or fibrillation, and ventricular tachycardia. The need for prenatal treatment is widely accepted and various modes of therapy are advocated. Oral maternal antiarrhythmic medication is often used, is considered convenient and safe, and provides adequate conversion. The drugs of choice at various centers have included digoxin, flecainide, amiodarone, and a host of combinations, as well as sotalol, which is gaining popularity. At birth, reentry mechanisms are often documented, with frequent relapses of tachycardia, warranting postpartum continuation of treatment. Fetal bradycardias consist of sinus bradycardia (generally related to obstetric pathology) and atrioventricular block. Atrioventricular block may occur secondary to severe congenital heart disease in the fetus or as an isolated phenomenon. The development of isolated total atrioventricular block has been seen to occur from a gestational age of 18 weeks up to term. It is invariably accompanied by the presence of SS-A and SS-B autoantibodies in the mother. Passage of these antibodies across the placenta causes inflammatory disease of fetal atrioventricular node tissue, resulting in fibrosis and atrioventricular block.(ABSTRACT TRUNCATED AT 250 WORDS)