ライフサイエンスコーパス: vasopressor

1 ndrome, steroids, renal failure and need for vasopressors).

2 rformed (100% O2, up to six defibrillations, vasopressors).

3 d and 64% received norepinephrine as initial vasopressor.

4 risk of hospital mortality based on initial vasopressor.

5 Norepinephrine (93%) was the most common vasopressor.

6 gnificantly lower cumulative requirement for vasopressor.

7 esponsive to the usual doses of inotropes or vasopressors.

8 tabolic acidosis and may reduce the need for vasopressors.

9 respiratory distress syndrome, and need for vasopressors.

10 of intravenous fluid received and receipt of vasopressors.

11 ithout an increase in the dose of background vasopressors.

12 id not respond to high doses of conventional vasopressors.

13 Adult patients with septic shock requiring vasopressors.

14 ive-pressure ventilation, and 19.7% received vasopressors.

15 ry effects of norepinephrine and alternative vasopressors.

16 venous thromboembolism, and those receiving vasopressors.

17 ently associated with the mean daily dose of vasopressors.

18 g/dL, and no use of intravenous inotropes or vasopressors.

19 on and 13 of 53 (25%) required initiation of vasopressors.

20 atients (17) also had hypotension and needed vasopressors.

21 positive end-expiratory pressure, and use of vasopressors.

22 nvasive mechanical ventilation, 30% required vasopressors, 17% required renal replacement therapy, an

23 001), intubation (33.3% vs 19.9%; P < .001), vasopressors (23.2% vs 10.9%; P < .001), renal replaceme

24 [6%] in the no-bolus group, new or increased vasopressor 32 [19%] vs 31 [18%], cardiac arrest within

25 echanical ventilation (65.7% vs. 56.1%), and vasopressors (34.9% vs. 27.8%) were observed, as well as

26 y resuscitation, 2) do not reintubate, 3) no vasopressors, 4) no hemodialysis, 5) do not escalate car

27 The prevalence of vasopressors (50.3% vs 36.9%), dialysis (19.4% vs 10.3%)

28 e, 62 vs 68), more likely to be treated with vasopressors (69% vs 65%) and had a lower in-hospital mo

29 mechanical ventilation (71.9% vs 90.9%) and vasopressors (70.9% vs 95.0%; p < 0.05), and less likely

30 ntilation, intracranial pressure monitoring, vasopressors, acute neurosurgical intervention, and extr

31 1-3.7) and receive norepinephrine as initial vasopressor (adjusted odds ratio quartile 4 vs quartile

32 n infusion added to at least one concomitant vasopressor agent between January 2014 and December 2015

33 hrine is frequently used as an inotropic and vasopressor agent in critically ill patients requiring h

34 V administration of epinephrine as inotropic/vasopressor agent is not associated with a worse outcome

35 alternative to restore the effectiveness of vasopressor agents during late sepsis.

36 rolled 50 patients (28 of 50 [56%] requiring vasopressor agents; 15 of 50 [30%] died).

37 ebo, high or low dose epinephrine, any other vasopressor alone or in combination were screened by thr

38 adverse events (hypotension event requiring vasopressor and continuous renal replacement therapy tub

39 Angiotensin II is an endogenous hormone with vasopressor and endocrine activities.

40 functional recovery, pain scores, peak flow, vasopressor and fluid requirements, and postoperative co

41 uated multiple organ dysfunction and reduced vasopressor and fluid resuscitation requirements.

42 QR 9-28), 170 (66%) of 257 patients received vasopressors and 79 (31%) received renal replacement the

43 use of physical restraints, and exposure to vasopressors and antiepileptics.

44 nt for cardiogenic shock includes inotropes, vasopressors and diuretics.

45 g the most appropriate resuscitation fluids, vasopressors and hemodynamic monitoring systems to maxim

46 uration of mechanical ventilation, or higher vasopressors and inotropes use.

47 on, use of renal replacement therapy, use of vasopressors and inotropes, and association with cardiac

48 management of cardiogenic shock consists of vasopressors and inotropes; however, these agents can in

49 herapy, which relied on more frequent use of vasopressors and lesser use of hyperventilation and osmo

50 n, admission Glasgow Coma Scale, duration on vasopressors and midline shift at septum.

51 tions of days alive and free of ventilation, vasopressors and renal replacement therapy in 28-day and

52 as defined as persistent hypotension despite vasopressors and requiring mechanical support or procedu

53 with positive blood cultures with concurrent vasopressors and/or lactic acidosis increased (P < .001

54 with positive blood cultures with concurrent vasopressors and/or lactic acidosis remained stable (P =

55 first hospital day, norepinephrine as first vasopressor, and avoidance of starch-based colloids) and

56 h cirrhosis, including the choice of fluids, vasopressors, and antibiotics.

57 l with administration of intravenous fluids, vasopressors, and blood transfusion decreases mortality

58 Hemodialysis, vasopressors, and blood transfusions were the interventi

59 k if they demonstrated hypotension, received vasopressors, and exhibited a lactate greater than 2 mmo

60 ommendations on the use of advanced airways, vasopressors, and extracorporeal cardiopulmonary resusci

61 aits including severity of illness, need for vasopressors, and length of stay.

62 Days alive and free of ventilation, vasopressors, and renal replacement therapy in septic sh

63 Days alive and free of ventilation, vasopressors, and renal replacement therapy were highly

64 mmol/L alone or combinations of hypotension, vasopressors, and serum lactate level 2 mmol/L or lower.

65 cs, steroid use prior to cardiac arrest, the vasopressors, and shockable rhythm during cardiopulmonar

66 s SpO2, oximeter characteristics, receipt of vasopressors, and skin pigmentation were recorded at the

67 markers, including positive blood cultures, vasopressors, and/or lactic acid levels.

68 th placebo, did not result in improvement in vasopressor- and ventilator-free days within 30 days.

69 Vasopressors are commonly administered to intensive care

70 Inotropes and vasopressors are widely used to improve hemodynamics acu

71 ignificant interaction between SRS group and vasopressor assignment (P = 0.50).

72 ents were progressively less likely to be on vasopressors at the time of first lactate measurement (4

73 ents (1.9%) in the usual care group received vasopressors (between-group difference, 12.3% [95% CI, 5

74 ck onset is associated with increased use of vasopressor but not with fluid administration.

75 d hemoglobin solution decreased the need for vasopressors but was associated with a trend to increase

76 l failure, requiring mechanical ventilation, vasopressor circulatory support and intermittent hemodia

77 sive hypotension group had lower exposure to vasopressors compared with those in the usual care group

78 mproving myocardial performance and reducing vasopressor dependence.

79 controlled phase III trial in patients with vasopressor-dependent distributive shock, administration

80 Adult patients with NF and vasopressor-dependent shock undergoing surgical debridem

81 dult patients who had septic shock requiring vasopressors despite fluid resuscitation within a maximu

82 staining treatments: mechanical ventilation, vasopressors, dialysis, and cardiopulmonary resuscitatio

83 or dosing intensity was defined as the total vasopressor dose infused across all vasopressors in nore

84 ogenous angiotensin II reduced catecholamine vasopressor doses and had an apparent effect in reducing

85 Number of vasopressor doses before first shock was higher in the B

86 ssure and a rapid reduction in catecholamine vasopressor doses from 0.75 to 0.31 mcg/kg/min norepinep

87 +/- 0.5 mm Hg; p < 0.05), and the number of vasopressor doses was higher with blood pressure care (m

88 CI, 1.45-2.71) and higher 24-hour cumulative vasopressor dosing as norepinephrine equivalent (beta co

89 Increasing vasopressor dosing intensity during the first 24 hours a

90 The median vasopressor dosing intensity during the first 24 hours o

91 ere to: 1) determine the association between vasopressor dosing intensity during the first 6 hours an

92 lume; and 3) determine whether the effect of vasopressor dosing intensity varies by dosing titration

93 ortality; 2) determine whether the effect of vasopressor dosing intensity varies by fluid resuscitati

94 24 hour period, every 10 mug/min increase in vasopressor dosing intensity was associated with an incr

95 In the first 6 hours, increasing vasopressor dosing intensity was associated with increas

96 Vasopressor dosing intensity was defined as the total va

97 gy, an early low/late high or sustained high vasopressor dosing strategy was associated with higher m

98 Compared to an early high/late low vasopressor dosing strategy, an early low/late high or s

99 o a systolic blood pressure of 100 mm Hg and vasopressor dosing to maintain coronary perfusion pressu

100 pth targeted to 51 mm and standard guideline vasopressor dosing.

101 Inotropic and vasopressor drugs are routinely used in critically ill p

102 ssociations of premorbid blood pressure with vasopressor duration and length of stay using multivaria

103 ionship between premorbid blood pressure and vasopressor duration for patients with shock.Methods: We

104 blood pressure was inversely associated with vasopressor duration.

105 The primary outcome was vasopressor duration; secondary outcomes included ICU/ho

106 (77.6%) was the most frequently used initial vasopressor during septic shock.

107 ceived dopamine or norepinephrine as initial vasopressor during the first 2 days of hospitalization.

108 ine was the most frequently used alternative vasopressor during this time (baseline, 36.2% [95% CI, 3

109 Change in vasopressor exposure was the only factor associated with

110 ICU nonsurvivors more frequently required vasopressors, extracorporeal membrane of oxygenation, re

111 We report a case of vasopressor extravasation and threatened limb perfusion

112 We report an event of vasopressor extravasation that was potentially limb thre

113 The case of vasopressor extravasation was successfully treated with

114 and December 2012 of whom 58,045 received a vasopressor for septic shock during the first 2 days of

115 Norepinephrine, the first-line vasopressor for septic shock, is not always effective an

116 l shortage of norepinephrine, the first-line vasopressor for septic shock.

117 Among patients 65 years or older receiving vasopressors for vasodilatory hypotension, permissive hy

118 Severity of shock was assessed by the vasopressor-free days and by the mean daily dose of vaso

119 entilation-, renal replacement therapy-, and vasopressor-free days within 28 days; intensive care uni

120 Primary end point was ventilator- and vasopressor-free days within 30 days (deaths assigned ze

121 4), driven by improvements in ICU free-days, vasopressor-free days, and ventilation-free days.

122 nt, driven by improvements in ICU-free days, vasopressor-free days, ventilation-free days, and blood

123 tcomes of interests were ICU length of stay, vasopressor-free days, ventilation-free days, and the pr

124 independently associated with the number of vasopressor-free days.

125 es in the primary end point (ventilator- and vasopressor-free days: 15.0 vs 14.5 in the selepressin a

126 ated hemoglobin polyoxyethylene had a longer vasopressor-free time (21.3 vs 19.7 d; p = 0.035).

127 tcome variables were the association between vasopressor genotype pathway polymorphisms, plasma vasop

128 There was no interaction between vasopressor group and allocated target temperature group

129 gan Failure Assessment = 4 defining the high vasopressor group and cardiovascular Sequential Organ Fa

130 The high vasopressor group carried a 53% mortality rate when comp

131 ity rate when compared with a 34% in the low vasopressor group, p(log-rank) less than 0.0001, with an

132 ent less than or equal to 3 defining the low vasopressor group.

133 Patients were randomized 1:1 to vasopressors guided either by MAP target (60-65 mm Hg, p

134 also developed multiorgan failure requiring vasopressors, hemodialysis, and mechanical ventilation.

135 k, with dopamine suggested as an alternative vasopressor in selected patients with low risk of tachya

136 e is currently recommended as the first-line vasopressor in septic shock; however, early vasopressin

137 monary resuscitation in adults and children, vasopressors in adults, advanced airway interventions in

138 he total vasopressor dose infused across all vasopressors in norepinephrine equivalents.

139 inistration of intravenous fluid boluses and vasopressors in patients with sepsis across different lo

140 patients with the lowest administration of a vasopressor; in the beta phenotype (n = 5512; 27%), pati

141 l and deep), rate of intraoperative need for vasopressor, incidence of unplanned intensive care unit

142 ith administration of intravenous fluids and vasopressors increased in-hospital mortality compared wi

143 Vasopressor infusion (VPI) is used to treat hypotension

144 Age, mobility/activity, perfusion, and vasopressor infusion emerged as important risk factors f

145 ience poor perfusion, or who are receiving a vasopressor infusion.

146 hours, 24 hours, 72 hours, and 7 days after vasopressor infusion.

147 3+/-1401 ml) and were more likely to receive vasopressor infusions (66.6% vs. 57.8%), red-cell transf

148 bserved in patients exposed to catecholamine vasopressor infusions, but unaffected by sedatives.

149 s (Sepsis-3) or 2) 1 or more eSOFA criteria: vasopressor initiation, mechanical ventilation initiatio

150 verse kidney events (MAKE) within 14 days of vasopressor initiation.Methods: At seven multidisciplina

151 ic Logistic Organ Dysfunction 2 score, day 0 vasopressor-inotrope score and fluid balance, and PaO2/F

152 ulatory support, mechanical ventilation with vasopressors/inotrope support, mechanical ventilation wi

153 therapy (EGDT), in which intravenous fluids, vasopressors, inotropes, and blood transfusions were adj

154 nd oxygen and the use of intravenous fluids, vasopressors, inotropes, and blood transfusions.

155 n 10 cm H2O, PaO2/FIO2 less than 300, use of vasopressors/inotropes, pancreatitis, hepatic failure/ci

156 Clindamycin and vasopressor intensity were higher among IVIG cases, as w

157 ich reversed the effects of the extravasated vasopressors: intraosseous phentolamine, topical nitrogl

158 Areas where use of dopamine as initial vasopressor is more common represent potential targets f

159 Balancing risks and benefits of vasopressors is a challenge, particularly in older patie

160 ory shock that does not respond to high-dose vasopressors is associated with high mortality.

161 strations) and concurrent organ dysfunction (vasopressors, mechanical ventilation, doubling in creati

162 Major interventions (vasopressor medication or intubation) were required for

163 CMV infection included a new requirement for vasopressor medications (9%; n = 29), intubation for mec

164 ols; p = 0.003), more hemodynamic support by vasopressors (n = 36, 82% vs n = 22, 56% in controls; p

165 e initiation of hydrocortisone (> 9 hr after vasopressors, n = 124).

166 y initiation of hydrocortisone (< 9 hr after vasopressors, n = 46) and those with late initiation of

167 th lower hospital survival were the need for vasopressors (odds ratio, 0.65; 95% CI, 0.43-0.98) and t

168 atio, 1.09; 95% CI, 1.1-1.19; p = 0.04), and vasopressors (odds ratio, 1.16; 95% CI, 1.09-1.23; p < 0

169 idelines recommend norepinephrine as initial vasopressor of choice for septic shock, with dopamine su

170 iteria was defined as age < 40 years, single vasopressor or less, transaminases no greater than 3 tim

171 CI, 0.50-0.90; P=0.008) and that required a vasopressor or positive inotropic drug or mechanical or

172 ay survival, organ dysfunction, and need for vasopressor or ventilatory support.

173 for hospitals with a lower propensity to use vasopressors or fluids during usual resuscitation.

174 tions if cardiogenic shock was refractory to vasopressors or intra-aortic balloon pump counterpulsati

175 herapies for hypoxemia; and days with use of vasopressors or sedation.

176 ours (OR 1.86, P = 0.010), administration of vasopressors (OR 1.80, P = 0.010), inadequate timing of

177 ay 2014 and required mechanical ventilation, vasopressors, or both.

178 ngth of stay, use of mechanical ventilation, vasopressors, or continuous sedation among individuals i

179 died while receiving mechanical ventilation, vasopressors, or dialysis.

180 eterioration (transfer to ICU, initiation of vasopressors, or invasive mechanical ventilation [IMV] i

181 ion (p < 0.0001, p = 0.0002, and p = 0.001), vasopressors (p < 0.0001, p < 0.0001, and p = 0.0004), a

182 ained nearest premorbid MAPs while receiving vasopressors (P < 0.001).

183 nts with septic shock were genotyped for 268 vasopressor pathway tag single-nucleotide polymorphisms.

184 tivity and reduced pressor responsiveness to vasopressors persisted.

185 ll patients on mechanical ventilation and/or vasopressors, randomized to two usual care sedation regi

186 c blood pressure <65 mm Hg; new or increased vasopressor receipt between induction and 2 min after tr

187 of clonidine in the treatment of persistent vasopressor-refractory hypotension in patients with sept

188 ged, sympathetic overstimulation may lead to vasopressor-refractory hypotension.

189 chanical ventilation, days alive and free of vasopressor, renal replacement therapy during ICU stay,

190 ining interventions (mechanical ventilation, vasopressors, renal replacement therapy) provided in the

191 tein, and receipt of mechanical ventilation, vasopressors, renal replacement therapy, or vasodilator

192 le urinary formate correlated inversely with vasopressor requirement (r = -0.2; p = 0.037).

193 with reduced treatment failure and a reduced vasopressor requirement than EP up to 2 days postoperati

194 ptic shock can be clinically identified by a vasopressor requirement to maintain a mean arterial pres

195 90 mm Hg after at least 1L IV fluids, 2) new vasopressor requirement, or 3) systolic blood pressure l

196 r association with the primary outcome: age, vasopressor requirement, thrombocytopenia, preexisting k

197 ncluded age, platelet count, requirement for vasopressors, requirement for hemodialysis, and nontraum

198 hibitor patients had lower total concomitant vasopressor requirements at 24 hours compared with non-r

199 tic calibre, low cardiac output states, high vasopressor requirements causing vasospasm of the artery

200 Oxygen and vasopressor requirements diminished over the first week

201 quential Organ Failure Assessment scores and vasopressor requirements significantly decreased after v

202 complications, hospital stay, perioperative vasopressor requirements, and postoperative pain scores

203 Total concomitant vasopressor requirements, based on norepinephrine equiva

204 d laboratory parameters including oxygen and vasopressor requirements, cytokine profiles, and C-react

205 ant improvement in coagulation, reduction in vasopressor requirements, improvement in blood pH and in

206 decrease in ultrafiltration, or increase in vasopressor requirements.

207 4.89; 3.83-6.28), and for inotrope(s) and/or vasopressor(s) (odds ratio, 3.64; 2.84-4.69), even in pa

208 py was needed in 23% and inotropes(s) and/or vasopressor(s) in 77% of studied patients.

209 cement therapy and/or for inotrope(s) and/or vasopressor(s).

210 We investigated interaction between vasopressor selection and mortality in clinical subgroup

211 actice patterns and outcomes associated with vasopressor selection in a large, population-based cohor

212 epsis such as glucocorticoid administration, vasopressor selection, and blood pressure targets.

213 or blood pressure (BP), fluid resuscitation, vasopressors, serum lactate level, and base deficit to i

214 ich patients develop profound sensitivity to vasopressors, such as angiotensin II, and is associated

215 mbrane oxygenation 5.8% vs 0.9%; p = 0.003), vasopressor support (79.4% vs 55.0%; p < 0.001), and ren

216 nit (ICU) admission, invasive respiratory or vasopressor support (IRVS), or death; ICU care without I

217 ce index and elastance index) and changes in vasopressor support after fluid bolus.

218 the magnitude of relative hypotension during vasopressor support among critically ill patients with s

219 reillness basal MPP and achieved MPP) during vasopressor support and the percentage of time points wi

220 ed levels of lactate, and need for increased vasopressor support compared with targeted temperature m

221 , aged >=40 years and requiring >=4 hours of vasopressor support for nonhemorrhagic shock, were prosp

222 EP patients required more vasopressor support immediately postoperatively on day 0

223 of the patients, respectively; 62% received vasopressor support, 53% had evidence of myocarditis, 80

224 al replacement therapy, invasive monitoring, vasopressor support, and investigational therapies for E

225 eased multiorgan dysfunction, mechanical and vasopressor support, and longer intensive care unit (ICU

226 reducing inflammation, oxygen requirements, vasopressor support, and mortality.

227 had positive blood cultures, and 2 required vasopressor support.

228 ed ICU admission, mechanical ventilation, or vasopressor support.

229 Bradykinin is a potent part of the vasopressor system that induces hypotension and vasodila

230 rterial oxygen saturation and treatment with vasopressors targeting mean arterial pressure (>/=65 mm

231 receptor agonist, is a noncatecholaminergic vasopressor that may mitigate sepsis-induced vasodilatat

232 sponsive to fluid and moderate- to high-dose vasopressor therapy (conditional, low quality of evidenc

233 tified hypotension, serum lactate level, and vasopressor therapy as variables to test using cohort st

234 e clinical criteria of hypotension requiring vasopressor therapy to maintain mean BP 65 mm Hg or grea

235 with septic shock, vasopressin as first-line vasopressor therapy was not superior to norepinephrine i

236 effectiveness of vasopressin as the initial vasopressor therapy with or without corticosteroids.

237 mission, invasive mechanical ventilation, or vasopressor therapy) or in-hospital death.

238 n pathway for this effect by blood pressure, vasopressor therapy, or potassium levels, but identified

239 vasopressin or norepinephrine as first-line vasopressor therapy.

240 up to 150 hours, in addition to conventional vasopressor therapy.

241 ted to aortic systolic pressure of 90 mm Hg, vasopressors titrated to coronary perfusion pressure >=

242 Rationale: Guidelines for vasopressor titration suggest a universal target-mean ar

243 early fluid administration and the timing of vasopressor titration.

244 cently, it has received attention as an oral vasopressor to facilitate ICU discharge.

245 ssor-free days and by the mean daily dose of vasopressor to insure a mean arterial pressure of 65-75

246 per minute or the equivalent dose of another vasopressor to receive infusions of either angiotensin I

247 o a systolic blood pressure of 100 mm Hg and vasopressors to a coronary perfusion pressure greater th

248 (< 12 hr duration), defined as the need for vasopressors to maintain mean arterial pressure greater

249 emonstrated that the patient group requiring vasopressors to maintain mean BP 65 mm Hg or greater and

250 site and presence of severe sepsis requiring vasopressors to receive either recombinant human KGF (pa

251 The median time from liberation of vasopressors to recovery of platelets concentration (>=

252 4-2.4; P = 0.004), respectively.Conclusions: Vasopressor-treated patients with shock are often expose

253 Significantly more EDA patients needed vasopressor treatment perioperatively (90% vs 74%, P = 0

254 echanical ventilation, hypotension requiring vasopressor treatment, or both.

255 pression, and vascular hyporesponsiveness to vasopressor treatment.

256 anical ventilation (7 vs 4 d; p < 0.01), and vasopressor use (4 vs 3 d; p < 0.01), as well as increas

257 t was associated with a higher likelihood of vasopressor use (adjusted odds ratio, 1.98; 95% CI, 1.45

258 tio, 1.37; 95% CI, 1.02-1.83; p = 0.035) and vasopressor use (hazard ratio, 1.84; 95% CI, 1.01-3.35;

259 ustment, premorbid low admissions had longer vasopressor use (median, 1.35 d vs. 1.04 d for normal; h

260 tio, 1.14; 95% CI, 1.04-1.24; p = 0.004) and vasopressor use (odds ratio, 1.09; 95% CI, 1.02-1.17; p

261 tio, 0.979; 95% CI, 0.963-0.996; p = 0.013), vasopressor use (odds ratio, 1.84; 95% CI, 1.11-3.07; p

262 te IMV (OR, 1.17; 95% CI, .87-1.56), or late vasopressor use (OR, 0.94; 95% CI, .68-1.30).

263 h premorbid admissions) over the duration of vasopressor use (P = 0.003) and were maintained nearest

264 e (P = 0.016; OR, 5.87; 95% CI, 1.38-24.99), vasopressor use (P = 0.018; OR, 7.34; 95% CI, 1.39-38.52

265 ry distress syndrome severity (p = 0.01) and vasopressor use (p = 0.04) were associated with greater

266 ted with increased diastolic dysfunction and vasopressor use and a greater cumulative positive fluid

267 nvasive mechanical ventilation, frequency of vasopressor use and renal replacement therapy, and time

268 ears, diabetes mellitus, dialysis, >=36 h of vasopressor use at time of diagnosis, lactate levels >=3

269 variates (Model for End-Stage Liver Disease, vasopressor use).

270 ght heart catheterization, fungal infection, vasopressor use, and a mean arterial pressure target of

271 ith increased leukopenia, acute lung injury, vasopressor use, extracorporeal life support, and mortal

272 included fluid balance, low blood pressure, vasopressor use, hypokalemia, or hypophosphatemia.

273 lammatory biomarkers, a higher prevalence of vasopressor use, lower serum bicarbonate concentrations,

274 isease-sodium score, mechanical ventilation, vasopressor use, renal replacement therapy, grade 3/4 he

275 distress syndrome, temperature, heart rate, vasopressor use, Sequential Organ Failure Assessment sco

276 , not operative case length, hypotension, or vasopressor use, was associated with postoperative press

277 , were more often intubated, and had greater vasopressor use.

278 , were more often intubated, and had greater vasopressor use.

279 age, male sex, coronary artery disease, and vasopressor use.

280 atio, 3.25; 95% CI, 2.52-4.19; p < 0.01) and vasopressors use (odds ratio, 1.42; 95% CI, 1.10-1.83; p

281 o Logistic Organ Dysfunction score, need for vasopressors, use of antihypertensive agents, need for m

282 Norepinephrine, the cornerstone vasopressor used in septic shock, may contribute to immu

283 arker for shock states, and incorporates all vasopressors used in current clinical practice.

284 ffects of norepinephrine and the alternative vasopressor vasopressin on the immune response and host

285 r decrease in mortality: the maximal dose of vasopressors (VP) administered to the patient (OR = 1.20

286 he United States, use of dopamine as initial vasopressor was associated with increased mortality amon

287 The use of vasopressor was associated with increased odds of in-hos

288 , the most commonly administered alternative vasopressor was phenylephrine.

289 Use of alternative vasopressors was assessed and a multilevel mixed-effects

290 0 mm Hg with additional use of inotropes and vasopressors was associated with smaller myocardial inju

291 Time of discontinuation of vasopressors was earlier among patients with initiation

292 espiratory distress syndrome, and receipt of vasopressors were also similar between groups.

293 arterial pressure and need for high doses of vasopressors were associated with increased mortality in

294 rterial blood gases, vital signs, and use of vasopressors were collected from the closest time prior

295 All inotropes and vasopressors were discontinued within 12 hours of pacema

296 lepticus, and arterial hypotension requiring vasopressors were independently associated with increase

297 Skin pigmentation and receipt of vasopressors were not associated with imputation accurac

298 the failure of the vasculature to respond to vasopressors, which results in hypotension, multiorgan f

299 There was a lower need for inotropes or vasopressors with CS (62.8%) versus GA (97.3%; rate diff

300 Inotropes and vasopressors worsened left-to-right shunting, whereas va