Diabetic ketoacidosis after the treatment of anaphylaxis.

Summary: Anaphylaxis is a rapidly progressive potentially lethal condition, and epinephrine is the most crucial medication in its treatment. In this study, we present a case of diabetic ketoacidosis in a young woman that was precipitated by the administration of epinephrine to treat anaphylaxis. This patient had diabetes mellitus and poor glycemic control and developed ketoacidosis despite having evidence of ongoing endogenous insulin production and having been treated with exogenous long-acting insulin less than 24 h prior to the event. This is a rare, serious, adverse side effect of life-saving medication. This report demonstrates that the risk of diabetic ketoacidosis should be considered when administering epinephrine to patients with diabetes, even in the absence of complete insulin deficiency. Learning points: Epinephrine directly suppresses insulin secretion, stimulates lipolysis, and causes ketone body generation. High-dose catecholamine administration can cause unexpected diabetic ketoacidosis in patients with risk factors. Early administration of insulin may not protect patients from developing ketoacidosis in the setting of high-dose catecholamine administration.

Heart rate variability in a progressive heart failure model with rapid ventricular pacing.

BACKGROUND: Heart rate variability (HRV) is an indicator of autonomic nervous system functionality and a recognized predictor of cardiac death; however, the changes in HRV occurring in progressive heart failure are not fully understood. The purpose of this study was to evaluate the progressive changes of autonomic system activity in progressive heart failure by rapid ventricular pacing in an animal model. METHODS: Heart failure was induced in 13 mongrel dogs (27.8 +/- 3.7 kg) by rapid ventricular pacing (230 beats/min) for 4 weeks and maintenance of pacing at a reduced rate (190 beats/min) for 2 weeks. Time domain analysis and spectral analysis of HRV were performed with the MemCalc system after 30 minutes of pacing cessation every week. Hemodynamic and echocardiographic data were obtained before and after induction of heart failure. RESULTS: Cardiac output decreased significantly (3.6 L/min versus 1.6 L/min, P < .001) after 6 weeks of ventricular pacing. Significantly increased were the heart rate (126 beats/min versus 138 beats/min, P < .05), left ventricular end-diastolic pressure (9.1 mm Hg versus 30.9 mm Hg, P < .001), and pulmonary capillary wedge pressure (8.0 mm Hg versus 18.7 mm Hg, P < .001). High-frequency components progressively decreased. Low-frequency components progressively decreased except at 5 weeks after the pacing. A ratio of low- to high-frequency components increased in moderate heart failure and decreased in severe heart failure. CONCLUSIONS: Changes in the high-frequency component and low-frequency component are important for assessing heart failure in progressive heart failure. Serial follow-up measurements of HRV might be helpful for patients with such disease.