In this study, a mixed-methods approach was used to develop an inventory of critical incidents for emergency medical service (EMS) personnel. Data were collected from a probabilistic sample of EMS personnel (N ϭ 1,633) via an online survey. Quantitative responses captured the frequency of exposure to 29 critical events, self-reported stress related to exposure, demographic characteristics, and posttraumatic stress symptomatology (PTSS). Respondents reported exposure to all of the stressors in the inventory. Critical incident exposure and the resultant stress were significantly (p Ͻ .01) correlated with PTSS. Qualitative feedback captured previously unidentified critical incidents unique to this population, allowing for greater elucidation of existing items and the identification of additional items that could be included in the inventory. Findings point toward the importance of considering cumulative critical incident exposure and resulting self-reported stress when assessing the impact of critical incidents for EMS personnel.

1 Previous studies have shown that endothelium-dependent relaxation in the aorta of spontaneously diabetic bio bred rats (BB) is impaired. 2 We have investigated noradrenaline (NA) contractility, endothelium-dependent acetylcholine (ACh) and bradykinin (BK) relaxation, and endothelium-independent sodium nitroprusside (SNP) relaxation in mesenteric resistance arteries of recent onset BB rats and established insulin treated BB rats, compared to their age-matched non diabetic controls. 3 There was no significant difference in the maximum contractile response or sensitivity to noradrenaline in either of the diabetic groups compared to their age-matched controls. 4 Incubation with the nitric oxide synthetase inhibitor NG-nitro-L-arginine (L-NOARG) resulted in a significant increase in maximum contractile response to noradrenaline in the recent onset age-matched control group (P<0.05). Analysis of the whole dose-response curve (using ANOVA for repeated measures with paired t test) showed a significant left-ward shift following the addition of L-NOARG (P<0.001). A similar but less marked shift (P<0.01) was evident in vessels from recent onset diabetics. An overall shift in both sensitivity and maximum response was also evident in the age-matched non diabetic controls of the insulin-treated group (P<0.05). However, by contrast, there was no significant change in sensitivity in the insulin-treated diabetic rats. 5 ACh-induced endothelium-dependent relaxation was significantly impaired in the recent onset diabetic rats compared to their age-matched controls (47 ± 11% versus 92 ± 2%, P<0.05, n = 6), and in the insulin treated diabetic rats (34±5% versus 75 + 6%, P< 0.05, n = 6). The relaxation responses to BK also were significantly impaired in the diabetic rats compared to their age-matched controls (recent onset: 20+3% versus 72±7%, P<0.05, n=6; insulin treated: 12+9% versus 68+7%, P<0.05, n=7). 6 Incubation with either the nitric oxide synthetase substrate, L-arginine, or the free radical scavenging enzyme superoxide dismutase (150 jml1') failed to improve the attenuated response of acetylcholineinduced relaxation in the diabetic vessels. 7 Endothelium-dependent relaxation mediated by ACh and BK was significantly attenuated in both the diabetic and control vessels after incubation with L-NOARG. 8 Pretreatment with a cyclo-oxygenase inhibitor, indomethacin, significantly enhanced the relaxation to ACh in both the recent onset and insulin treated diabetic rats (42+10%, n=7 versus 64±7%, n=7, P<0.05, and 40±5%, n=7 versus 65+9%, n=6, P<0.05). 9 Following endothelium removal, there was a marked impairment in endothelium-dependent relaxation responses to ACh and BK in both the diabetic and control vessels. 10 Incubation with the thromboxane A2 receptor antagonist SQ29548, did not significantly improve the ACh endothelium-dependent relaxation response in the diabetic vessels. 11 Endothelium-independent relaxation to sodium nitroprusside was significantly impaired in the first group of diabetic vessels studied; however, subse...

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Twenty-three patients in severe diabetic ketoacidosis were followed by continuous electrocardiographic monitoring using Lead II of the electrocardiogram throughout their course of treatment. Frequent serum potassium determinations were carried out and correlated with the ECG changes. On admission to hospital the electrocardiogram of ketoacidotic patients showed varied T wave patterns often with little correlation to the serum potassium, but the two patients who were initially hypokalemic were identified from the ECG appearances. Following the infusion of fluids alone the serum potassium fell with accompanying T wave and ST segment changes while the administration of potassium reversed these abnormalities. Although the electrocardiogram is not a substitute for serum potassium determinations, it is a useful guide to potassium replacement in diabetic ketoacidosis. In the successful management of this diabetic emergency the achievement and maintenance of a normal ECG, by means of early and continuous administration of potassium in the infused fluids, should be an important objective of treatment. DIABETES23:610-15, July, 1974.

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A post-mortem study of the heart was performed in 20 patients dying of cardiogenic shock. The extent of infarcted myocardium was defined by using a mitochondrial dehydrogenase stain nitro-B T which allowed macroscopical recognition of tissue death as early as I2 hours. Extensive myocardial injury was found to accompany cardiogenic shock predominantly affecting the left ventricle and the interventricular septum. Severe atheromatous involvement of the coronary arteries was noted. Shock and left ventricular failure remain the major causes of death among patients admitted to hospital with acute myocardial infarction (Lown et al., I967; Lawrie et al., I967; Pentecost and Mayne, I968; Thomas, Jewitt, and Shillingford, I968). In contrast to the improvements in the management of