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SummaryHypoxaemia,following surgery is comnlon and may be prolonged and severe. The thresholds for deleterious effects of hypoxaemia on the heart and central nerwus system are reviewed and the problems of assessment of the adequacy of tissue oxygenation are outlined. Reconmiendations for posloperative oxygen therapy are made. Key wordsHypoxia . Recouery . Oxygen; monitoring.Many studies using continuous monitoring have shown severe and prolonged periods of hypoxaemia which occur immediately after surgery and continue to the fourth or fifth postoperative night [I-61. The clinical diagnosis of hypoxaemia before the advent of pulse oximetry relied on the observation of cyanosis which is only apparent at an Sao? of less than 75%; its absence does not preclude hypoxaemia. The pulse oximeter finger probe is accurate to I % in the normal range but with a sudden hypoxic episode an Spo, reading of 55% may be 7% lower than the actual Sao, [7]. Using pulse oximetry there are reports of postoperative hypoxaemia with arterial oxygen saturations of less than 75% for periods of longer than 2 h [2,8,9]. The cause has now been shown to be a combination of: (a) Impaired control of both ventilation and upper airway patency due to the combined effects of opioids and sleep [2, lo]. (b) Impaired gas exchange due to atelectasis in the dependent lung which occurs after induction of anaesthesia and persists for at least 24 h [ 1 I , 121.The consequences of postoperative hypoxaemia are not known with any certainty and therefore the indications for oxygen therapy are ill defined. The purpose of this paper is to examine the thresholds for the harmful effects of hypoxaemia on the heart and brain and to make recommendations for oxygen therapy. (See Appendix for abbreviations.) Cardiac effects of hypoxaemiaThe evidence that postoperative hypoxaemia affects clinical outcome is inconclusive. In a recent review Mangano does not include hypoxaemia as a risk factor for increased peri-operative cardiac morbidity [ 131.The effect of hypoxaemia (normal blood flow, low SaoJ on the heart is quite different from repeated brief episodes of ischaemia (low blood flow, normal Sao,) which lead t o impaired ventricular function and possibly to necrosis [14, 151. In studies using the ECG to monitor the effects of hypoxaemia on myocardial ischaemia the results are contradictory. For example, in patients with unstable angina awaiting coronary artery surgery, there was no temporal relationship between sleep associated hypoxaemia and myocardial ischaemia [16, 171. In one study [I71 the minimum median nocturnal Spo2 was 84% (range 69-88%) and in the other [I61 eight of 15 patients had Spoz in the range 80-85%. However, in a further study, in postoperative patients [ 181, myocardial ischaemia was related to episodic hypoxaemia in some patients and in others hypoxaemia was associated with tachycardia and arrhythmias (median Spo, 78%, range 60-89%). Oxygen administration will correct myocardial ischaemia in certain patients [8] [20]. In a model of myocardial ischaemi...

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We report a case of flecainide toxicity in a premature neonate with permanent junctional reciprocating tachycardia which was managed successfully by reversal of the sodium blockade with intravenous sodium bicarbonate and supportive care. This report highlights the importance of strict supervision and monitoring while administering antiarrhythmic drugs in neonates and prompt institution of appropriate remedial action for treatment when toxicity is suspected.