Under controlled experimental conditions, CO is associated with excellent agreement and good trending ability when compared with the gold standard CO. In the paediatric clinical setting, CO performs well; by contrast, CO, an operator- and anatomy-dependent technology, appears less reliable than CO.

Fourteen critically ill neonatal and paediatric intensive care patients with various primary diagnoses and signs of associated pulmonary hypertension received inhaled nitric oxide (NO), 20-80 ppm, after failure of conventional therapy to improve oxygenation. NO administration was found to be associated with a significant improvement in postductal arterial oxygen tension (pre-NO: 3.75 (SD 1.39) kPa; post-NO: 6.05 (SD 1.70) kPa; p = 0.004). In 10 patients, NO was found to increase arterial oxygen tension with more than 1 kPa. In 2 of these patients, ECMO treatment could be avoided due to the pronounced improvement in gas exchange seen after the initiation of NO administration. The remaining 4 patients failed to respond to NO administration. One patient developed methaemoglobinaemia (13.9%) which required treatment with methylthionine. Since we were unable to produce any beneficial effect of NO in the late phase of the pulmonary disease process, we believe that, in order to be successful, inhaled NO should be instituted when conventional treatment has failed and the administration of an iv vasodilator is usually considered.

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Left ventricular output was measured non-invasively at predefined time intervals from less than 15 minutes to 72 hours after birth in 16 infants who had been born at full term. The blood flow velocity in the ascending aorta was measured by a range gated Doppler technique and multiplied by the cross sectional diameter measured by cross sectional and M mode echocardiography. Left ventricular output remained high in the first two hours, 235-243 ml/min/kg, despite a 10% decrease in heart rate. The fall in heart rate was compensated for by a 15% increase in stroke volume. Between 2 and 24 hours there was a significant fall in mean (SD) left ventricular output to 187 (35) ml/min/kg caused mainly by a reduction in stroke volume. The fall in left ventricle output after two hours may reflect an adaptation to the decreased demand on the left ventricle as the ductus constricts.

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Sonesson S‐E, Fouron J‐C, Wesslen‐Eriksson E, Jaeggi E, Winberg P. Foetal supraventricular tachycardia treated with sotalol. Acta Pædiatr 1998; 87: 584‐7. Stockholm. ISSN 0803‐5253 This retrospective study (1991‐95) presents our experience with sotalol in the treatment of 14 foetuses with supraventricular tachycardia (SVT). SVT was diagnosed in a structurally normal heart at a gestational age of 24‐35 (median 28) weeks. In eight foetuses, hydrops was evident at presentation. In all patients pharmacological conversion with digoxin was tried before sotalol treatment was started. Sotalol was given orally to the mothers in a dose of 80–160 mg x2. Cardioversion was obtained in 10 foetuses. In seven of these patients re‐entry tachycardia and in five pre‐excitation could be documented after birth. In two foetuses not responding to sotalol a long RP tachycardia was demonstrated; even when using digoxin, sotalol, flecainide and/or propafenone in different combinations after birth complete suppression of the arrhythmia was not obtained. Two severely hydropic foetuses died 1 and 10 d, respectively, after starting with sotalol. The 12 surviving infants were doing well except for one infant, with a cerebral lesion probably related to the arrhythmia. These findings demonstrate that sotalol can be useful in the treatment of foetal SVT.

Objective-To study the short-term effects of inhaled nitric oxide in infants and young children with congenital heart disease. Setting-A supraregional referral centre for children with congenital heart disease. Patients and methods-22 infants and children aged 3-32 months (median age 5 months) with congenital heart disease undergoing preoperative cardiac catheterisation. AlU but one infint had intracardiac shunt lesions and 13 had increased pulmonary vascular resistance. Conclusion-The present study shows that in infants with congenital heart disease inhaled nitric oxide reduced pathologically increased pulmonary vascular resistance without affecting systemic circulation and without important side effects with brief exposure. (Br HeartrJ 1994;71:282-286) Increased pulmonary vascular resistance with pulmonary hypertension is a frequent complication in congenital heart disease,' and postoperative pulmonary hypertensive crisis is a major problem that may account for a substantial part of the postoperative mortality and morbidity.2 Until the discovery of the biological effects of nitric oxide (NO) there was no selective treatment to produce pulmonary vasodilatation. NO is a major endothelium derived relaxing factor3" that regulates blood flow and modulates the hypoxic pressor response in the lung.6 It is also present in exhaled air of human.7 Because it is rapidly inactivated by haemoglobin,8 the dilating effects of inhaled NO should be confined to the pulmonary vascular bed. The selective pulmonary vasodilating effect of inhaled NO in hypoxic pulmonary hypertension was shown in lambs9 and in healthy volunteers.'0 Inhaled NO was of benefit in the treatment of persistent pulmonary hypertension of the newbornm 12 and in the adult respiratory distress syndrome.'3 Recently Roberts et al showed that pulmonary vascular resistance was reduced by NO during cardiac catheterisation in infants with congenital heart disease'4 and we have also reported a dramatic effect in one case of postoperative pulmonary hypertension." NO, however, can cause methaemoglobinemia,'6 and in the presence of oxygen NO forms nitrogen dioxide, which is toxic in the lungs even in very low concentrations.'7-'9 No severe side effects were seen during or after the administration of NO at concentrations below 80 ppm in adults'0 13 but experience is still limited. In infants and children there is even less experience and the aim of this study was to investigate further the effects and side effects of brief inhalation of NO in infants and children with congenital heart defects. Patients and methodsWe studied 22 infants and children aged 3-32 months (median age 5 months) with congenital heart disease who had routine preoperative cardiac catheterisation (table). All but one had shunt lesions, and 10 had atrioventricular septal defects. Twelve also had Down's syndrome. Pethidine (2 mg/kg), promethazine (0-5 mg/kg), and chlorpromazine (0 5 mg/kg) were used for sedation. One hour before catheterisation a topical anaesthetic containing prilocaine and ...

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