What are the acute cardiovascular effects of subcutaneous and topical epinephrine for hemostasis during burn surgery?

Although subcutaneous and topical epinephrine are widely used for hemostasis during burn surgery, the acute systemic cardiovascular effects of the epinephrine are neither well documented nor completely understood. The purpose of this work was to prospectively study the acute cardiovascular responses to epinephrine (epi) administered subcutaneously and topically during burn surgery. Consecutive patients who received subcutaneous and topical epi during burn surgery were monitored prior to the administration of epi, at 2-minute intervals during subcutaneous epi infiltration, and then after epi infiltration (during which time, topical epi was applied). This period of monitoring lasted up to 20 minutes and was referred to as an epinephrine event (EE). A total of 100 EEs from 38 operations in 24 patients (mean +/- SD: age 43 +/- 16 years, mean % TBSA burn 23 +/- 17%) were studied. The mean dose of subcutaneous epi was 30 +/- 30 microg/kg. Although all patients received topical epi, it was impossible to document the topical dose. There was no significant increase in heart rate from baseline, and no arrhythmias occurred. Mean arterial pressure (MAP) did acutely increase significantly by 17.0 +/- 14.1% from baseline (P =.009) and increased more than 10% from baseline in 64/100 EEs. However, the increase in MAP was independent of the dose of epi (r =.053). The increase in MAP was not clinically significant, did not require intervention, and did not appear to be related to the type of wound that received epi (donor site vs burn wound), or the depth of anesthesia, analgesia, or sedation. On the basis of these findings, the use of subcutaneous and topical epi appears to be safe and produces minimal acute cardiovascular effects.

Contribution of the intensive care unit environment to sleep disruption in mechanically ventilated patients and healthy subjects.

Recent studies have challenged the traditional hypothesis that excessive environmental noise is central to the etiology of sleep disruption in the intensive care unit (ICU). We characterized potentially disruptive ICU noise stimuli and patient-care activities and determined their relative contributions to sleep disruption. Furthermore, we studied the effect of noise in isolation by placing healthy subjects in the ICU in both normal and noise-reduced locations. Seven mechanically ventilated patients and six healthy subjects were studied by continuous 24-hour polysomnography with time-synchronized environmental monitoring. Sound elevations occurred 36.5 +/- 20.1 times per hour of sleep and were responsible for 20.9 +/- 11.3% of total arousals and awakenings. Patient-care activities occurred 7.8 +/- 4.2 times per hour of sleep and were responsible for 7.1 +/- 4.4% of total arousals and awakenings. Healthy subjects slept relatively well in the typically loud ICU environment and experienced a quantitative, but not qualitative, improvement in sleep in a noise-reduced, single-patient ICU room. Our data indicate that noise and patient-care activities account for less than 30% of arousals and awakenings and suggest that other elements of the critically ill patient's environment or treatment should be investigated in the pathogenesis of ICU sleep disruption.