Reversal of citalopram-induced junctional bradycardia with intravenous sodium bicarbonate.

The cardiotoxicity of tricyclic antidepressants is a well-described phenomenon requiring serious consideration in patients who have taken an overdose. In patients who are at high risk for suicide attempts, selective serotonin reuptake inhibitors (SSRIs) were thought to constitute a safe alternative. However, evidence is accumulating that they, too, possess proarrhythmic properties, which must be reconciled in the setting of an overdose. An 82-year-old woman intentionally ingested citalopram 1.6 g. Several hours after presentation, she developed sinus arrest and junctional bradycardia that resolved after infusion of intravenous sodium bicarbonate solution. Thereafter, she demonstrated no further electrocardiographic abnormalities and was safely transferred to the psychiatry service without the need for a temporary transvenous pacemaker. The dramatic effect of the sodium bicarbonate on the arrhythmia represents a probable event according to the Naranjo probability scale. Intravenous sodium bicarbonate may serve as an effective antidote to SSRI-induced bradyarrhythmias.

Timing of changes in interstitial and venous blood glucose measured with a continuous subcutaneous glucose sensor.

The objective of this study was to use a subcutaneous continuous glucose sensor to determine time differences in the dynamics of blood glucose and interstitial glucose. A total of 14 patients with type 1 diabetes each had two sensors (Medtronic/MiniMed CGMS) placed subcutaneously in the abdomen, acquiring data every 5 min. Blood glucose was sampled every 5 min for 8 h, and two liquid meals were given. A smoothing algorithm was applied to the blood glucose and interstitial glucose curves. The first derivatives of the glucose traces defined and quantified the timing of rises, peaks, falls, and nadirs. Altogether, 24 datasets were used for the analysis of time differences between interstitial and blood glucose and between sensors in each patient. Time differences between blood and interstitial glucose ranged from 4 to 10 min, with the interstitial glucose lagging behind blood glucose in 81% of cases (95% CIs 72.5 and 89.5%). The mean (+/-SD) difference between the two sensors in each patient was 6.7 +/- 5.1 min, representing random variation in sensor response. In conclusion, there is a time lag of interstitial glucose behind blood glucose, regardless of whether glycemia is rising or falling, but intersensor variability is considerable in this sensor system. Comparisons of interstitial and blood glucose kinetics must take statistical account of variability between sensors.