Heidi C. Blake

A comparison of the shock index and conventional vital signs to identify acute, critical illness in the emergency department.

STUDY OBJECTIVE Shock index (SI) (heart rate/systolic blood pressure; normal range, 0.5 to 0.7) and conventional vital signs were compared to identify acute critical illness in the emergency department. DESIGN Quasi-prospective study. PATIENTS Two hundred seventy-five consecutive adults who presented for urgent medical care. INTERVENTIONS Patients had vital signs, SI, and triage priority recorded on arrival in the ED and then their final disposition. RESULTS Two groups were identified retrospectively by the SI; group 1 (41) had an SI of more than 0.9, and group 2 (234) had an SI of less than 0.9 on arrival in the ED. Although both groups had apparently stable vital signs on arrival, group 1 had a significantly higher proportion of patients who were triaged to a priority requiring immediate treatment (23 versus 45; P < .01) and required admission to the hospital (35 versus 105; P < .01) and continued therapy in an ICU (10 versus 13; P < .01). CONCLUSION With apparently stable vital signs, an abnormal elevation of the SI to more than 0.9 was associated with an illness that was treated immediately, admission to the hospital, and intensive therapy on admission. The SI may be useful to evaluate acute critical illness in the ED.

Whole body oxygen consumption and critical oxygen delivery in response to prolonged and severe carbon monoxide poisoning.

BACKGROUND Carbon monoxide (CO) poisoning remains the leading cause of death by poisoning in the world. One of the major proposed mechanisms for CO toxicity is the binding of CO to cytochrome oxidase and interference with cellular oxygen utilization but evidence for this is inconclusive. AIM OF STUDY This study examined the effects of prolonged CO exposure on the dynamics of whole body oxygen consumption (VO(2)) and oxygen delivery (DO(2)) in an attempt to observe if CO exposure results in a defect of oxygen utilization defect as determined by a reduction in VO(2) during the course of poisoning prior to reaching the point where VO(2) is directly dependent on DO(2). This critical level of DO(2) (DO(2)crit) produced by CO poisoning was compared to historical values produced by other insults, which decrease global body DO(2). METHODS Five small dogs were ventilated for 2 h with 0.25% CO and room air followed by 0.5% CO until death. Cardiac index (Q), DO(2), VO(2), oxygen extraction ratio (OER), and systemic lactate were measured every 15 min until death. RESULTS Carboxyhemoglobin (COHb) levels increased linearly over 2.5 h to values above 80% until death. VO(2) remained constant and not significantly different from baseline below a COHb of 80%. At COHb levels above 80%, VO(2) precipitously dropped. Similarly lactate levels were not significantly elevated from baseline until VO(2) dropped. DO(2) decreased by 78% (from 23+/-6 ml/kg/min to 5+/-4 ml/kg/min) over time despite an increase in Q by 58% until levels of COHb were above 80%. OER increased from 19+/-5% to 50+/-11% until death. The calculated DO(2)crit was 10.7+/-4 ml/min/kg, which is not significantly different from values ranging from 7 to 13 ml/min/kg reported in the literature due to other insults, which reduce DO(2). CONCLUSION In this canine model of prolonged CO exposure, no gradual reduction in VO(2) or increase in systemic lactate prior to reaching DO(2)crit was noted. In addition, CO exposure does not appear to change the DO(2)crit. The combination of these findings does not support the theory that CO produces a whole body intracellular defect in oxygen utilization.