Catherine Huraux

Prediction of Difficult Mask Ventilation

Background Maintenance of airway patency and oxygenation are the main objectives of face-mask ventilation. Because the incidence of difficult mask ventilation (DMV) and the factors associated with it are not well known, we undertook this prospective study. Methods Difficult mask ventilation was defined as the inability of an unassisted anesthesiologist to maintain the measured oxygen saturation as measured by pulse oximetry > 92% or to prevent or reverse signs of inadequate ventilation during positive-pressure mask ventilation under general anesthesia. A univariate analysis was performed to identify potential factors predicting DMV, followed by a multivariate analysis, and odds ratio and 95% confidence interval were calculated. Results A total of 1,502 patients were prospectively included. DMV was reported in 75 patients (5%; 95% confidence interval, 3.9–6.1%), with one case of impossible ventilation. DMV was anticipated by the anesthesiologist in only 13 patients (17% of the DMV cases). Body mass index, age, macroglossia, beard, lack of teeth, history of snoring, increased Mallampati grade, and lower thyromental distance were identified in the univariate analysis as potential DMV risk factors. Using a multivariate analysis, five criteria were recognized as independent factors for a DMV (age older than 55 yr, body mass index > 26 kg/m2, beard, lack of teeth, history of snoring), the presence of two indicating high likelihood of DMV (sensitivity, 0.72; specificity, 0.73). Conclusion In a general adult population, DMV was reported in 5% of the patients. A simple DMV risk score was established. Being able to more accurately predict DMV may improve the safety of airway management.

Superoxide Production, Risk Factors, and Endothelium-Dependent Relaxations in Human Internal Mammary Arteries

BACKGROUND In a variety of disease states, endothelium-dependent vasodilation is abnormal. Reduced nitric oxide (NO) production, increased destruction of NO by superoxide, diminished cellular levels of L-arginine or tetrahydrobiopterin, and alterations in membrane signaling have been implicated. We examined these potential mechanisms in human vessels. METHODS AND RESULTS Relaxations to acetylcholine, the calcium ionophore A23187, and nitroglycerin, as well as superoxide production and NO synthase expression, were examined in vascular segments from patients with identified cardiovascular risk factors. Endothelium-dependent relaxations were also studied after incubation with L-arginine, L-sepiapterin, and liposome-entrapped superoxide dismutase (SOD) and after organoid culture with cis-vaccenic acid. Relaxations to acetylcholine and to a lesser extent the calcium ionophore A23187 were highly variable and correlated with the number of risk factors present among the subjects studied. Treatment of vessels with L-arginine, L-sepiapterin, liposome-entrapped SOD, or cis-vaccenic acid did not augment endothelium-dependent relaxations. Hypercholesterolemia was the only risk factor associated with high levels of superoxide; however, there was no correlation between superoxide production and the response to either endothelium-dependent vasodilator used. CONCLUSIONS In human internal mammary arteries, depressed endothelium-dependent relaxations could not be attributed to increases in vascular superoxide production, deficiencies in either L-arginine or tetrahydrobiopterin, or reduced membrane fluidity. Variability in signaling mechanisms may contribute to the differences in responses to acetylcholine and the calcium ionophore A23187.

Hemostatic changes in patients receiving hydroxyethyl starch: the influence of ABO blood group.

Hydroxyethyl starches (HES) interfere with coagulation because of their molecular structure and the amount infused during surgery. Coagulation defects include platelet dysfunction and a decrease of the VIII/von Willebrand factor complex (VIII/vWF). We examined the effects of 6% HES 200/0.6 on hemostasis by using an in vitro platelet function analyzer, the usual coagulation tests, the VIII/vWF complex assessment, and TEG® analysis in patients undergoing abdominal surgery. The influence of the blood group was investigated. HES infusion induced primary hemostasis alterations, assessed by a prolonged platelet function analyzer closure time in the presence of epinephrine and adenosine diphosphate, which was not correlated with the platelet count. The decrease in VIII/vWF complex was proportional to the volume of infused HES (20 and 30 mL/kg) and was more pronounced in patients of the O blood group. The preoperative hypercoagulability status assessed by TEG® analysis was reversed 24 h after HES infusion. In conclusion, 6% HES 200/0.6 induced immediate hemostasis alterations. Patients of the O blood group were likely to develop a von Willebrand-like syndrome after HES infusion. We conclude that intraoperative use of 6% HES 200/0.6 should be restricted in patients of the O blood group undergoing surgical procedures with high risk for bleeding.

A Comparative Evaluation of the Effects of Multiple Vasodilators on Human Internal Mammary Artery

Background Vasospasm of arterial grafts represents an unpredictable complication of coronary artery surgery and may compromise myocardial revascularization, and treatment is based on empirical therapy with nitroglycerin. Because of the potential for tolerance to nitroglycerin to occur, the authors studied different vasodilators acting through separate pathways on segments of human internal mammary artery. Methods Isolated vascular rings were precontracted with norepinephrine (1 [micro sign]M), KCl, or the thromboxane A2 analogue (U46619, 10 nM). Nitroglycerin (a nitrovasodilator), milrinone (a type III phosphodiesterase inhibitor), papaverine (a phosphodiesterase inhibitor), prostaglandin E1, and isradipine (a dihydropyridine calcium channel blocker) were added in a cumulative fashion. Results The analysis of the concentration ‐ response curves showed that vasodilators induced 90 ‐ 100% relaxation of the constricted segments with norepinephrine or the thromboxane A2 analogue, except prostaglandin E (1), which produced 73% relaxation at maximal concentrations. The effective concentrations of vasodilator agent that caused 50% relaxation for nitroglycerin and milrinone were within the range of the reported therapeutic concentrations in plasma. Isradipine was also effective at reversing receptor‐mediated contraction (maximal relaxation = 100% in internal mammary artery contracted with norepinephrine; maximal relaxation = 90% in internal mammary artery contracted with the thromboxane A2 analogue). Conclusions Vasodilator drugs acting through multiple pathways are effective at reversing in vitro vasoconstriction.

The In Vitro Reversal of Histamine-Induced Vasodilation in the Human Internal Mammary Artery

Anaphylactic shock therapy includes the use of catecholamines but they may not always be effective. Because vasodilation during anaphylaxis is a result of the endothelial release of multiple mediators, we investigated the effects of epinephrine, vasopressin, and inhibitors of nitric oxide and prostanoid pathways on histamine-induced relaxation in human internal mammary artery. The vessel segments were obtained intraoperatively and were suspended in organ chambers to record isometric tension. Norepinephrine (10−6 M) was used to precontract the rings followed by histamine (10−6.5 M) to relax the vessels and mimic vascular collapse. Epinephrine, vasopressin, methylene blue, NG-monomethyl-L-arginine (L-NMA) and indomethacin were added in a cumulative fashion to reverse the histamine-induced vasodilation. The internal mammary artery segments exhibited greater contraction in the presence of the epinephrine (4.9 ± 0.7g) compared with vasopressin (2.6 ± 0.7g). Vasopressin (10−11 to 10−7 M), methylene blue (10−7 to 10−5 M), L-NMA (10−6 to 10−4 M), and indomethacin (10−7 to 10−5 M) were only partially effective. These findings suggest that vasopressin and methylene blue may offer a potential therapeutic option in the treatment of histamine-induced vasodilatory shock.

Atenolol administration via a nasogastric tube after abdominal surgery: an unreliable route.

&bgr;-Adrenoceptor antagonists, especially atenolol, reduce perioperative cardiac morbidity. Because there are no data on the bioavailability of atenolol given by nasogastric tube in the postoperative period, we assessed the efficacy of this route of administration in 18 patients scheduled for abdominal surgery. We found a 36% reduction in the area under the atenolol concentration curve and a 46% reduction in the peak concentration of atenolol in the postoperative period compared with preoperative values. In addition, patients had more rapid mean heart rates on the second postoperative day compared with the day before surgery. We conclude that the administration of atenolol via nasogastric tube in the postoperative period does not result in adequate plasma concentrations.

The Vasodilator Effects of Clevidipine on Human Internal Mammary Artery

Endothelial dysfunction and platelet activation with thromboxane release may contribute to spasm or alterations in internal mammary artery (IMA) graft flow during coronary artery surgery.Clevidipine, an ultrashort-acting dihydropyridine calcium channel blocker, is undergoing clinical development, but there are little data regarding its effects on human vasculature. We investigated the effects of clevidipine on human IMA obtained during surgery. After precontracting IMA segments with an analog of thromboxane (U46619, 10-8 mol/L), acetylcholine and nitroglycerin were added cumulatively to examine endothelial function. Concentration-response curves to clevidipine were cumulatively obtained during submaximal contraction to the U46619 (10-8 mol/L) in rings with and without endothelium. In the IMA samples with endothelium, acetylcholine did not completely reverse the U46619-mediated contraction, which implies impaired endothelial function (40% +/- 6% maximal response). Both clevidipine and nitroglycerin completely reversed U46619-induced contraction (clevidipine (50% effective concentration [EC50] = 3.88 +/- 0.84 x 10-6 mol/L, nitroglycerin EC50 = 4.84 +/- 2.76 x 10-8 mol/L). The responses to clevidipine were similar in preparations with or without intact endothelium. Clevidipine is an endothelium-independent arterial vasodilator that offers a potential therapeutic option in the treatment of perioperative arterial graft vasospasm and/or hypertension. Implications: Clevidipine is a new ultrashortacting dihydropyridine calcium antagonist. In human internal mammary arteries precontracted with a thromboxane A2 analog, clevidipine was an effective vasodilator on vessel segments in the presence and in the absence of endothelium. (Anesth Analg 1997;85:1000-4)