02 Nov 11
By L Meng, N Phuong Tran, B Alexander, K Laning, G Chen, Z Kain and M Cannesson
Anesth Analg 2011;113: 751-757
Cardiac output (CO) monitoring based on pulse contour analysis (Vigileo-FloTrac) has the potential to be used for goal-directed fluid therapy in the perioperative setting. However, factors such as vasopressor usage may impact Vigileo-FloTrac’s reliability in tracking CO changes. We tested third-generation Vigileo-FloTrac system’s ability to accurately measure the changes in CO induced by vasopressor administration and increased preload in comparison with esophageal Doppler measurements.
In 33 anesthetized patients, CO was monitored simultaneously by the third-generation Vigileo-FloTrac and esophageal Doppler. Hemodynamic challenges included phenylephrine (to increase vasomotor tone), ephedrine (to increase myocardial contractility and heart rate), and whole-body tilting (to increase preload). Measurements were performed before and after each intervention.
Overall, 176 pairs of CO measurements were obtained. The difference between paired pulse contour and Doppler measurements of CO was 0.14 ± 2.13 L/min (mean ± SD), and the percentage error (2 SD of the difference divided by the mean CO of the reference method) was 66%. The trending ability of pulse contour versus Doppler was 23% (concordance, the percentage of the total number of data points that are in 1 of the 2 quadrants of agreement) after phenylephrine treatment, 69% (concordance) after ephedrine treatment, and 96% (concordance) after whole-body tilting.
The pulse contour method of measuring CO, as implemented in the third-generation Vigileo-FloTrac device, accurately tracks changes in CO when preload changes. However, the pulse contour method does not accurately track changes in CO induced with phenylephrine and ephedrine.
09 Mar 10
By D Backer, P Biston, J Devriendt, C Madl, D Chochrad, C Aldecoa et al for the SOAP II Investigators
Both dopamine and norepinephrine are recommended as first-line vasopressor agents in the treatment of shock. There is a continuing controversy about whether one agent is superior to the other.
In this multicenter, randomized trial, we assigned patients with shock to receive either dopamine or norepinephrine as first-line vasopressor therapy to restore and maintain blood pressure. When blood pressure could not be maintained with a dose of 20 µg per kilogram of body weight per minute for dopamine or a dose of 0.19 µg per kilogram per minute for norepinephrine, open-label norepinephrine, epinephrine, or vasopressin could be added. The primary outcome was the rate of death at 28 days after randomization; secondary end points included the number of days without need for organ support and the occurrence of adverse events.
The trial included 1679 patients, of whom 858 were assigned to dopamine and 821 to norepinephrine. The baseline characteristics of the groups were similar. There was no significant between-group difference in the rate of death at 28 days (52.5% in the dopamine group and 48.5% in the norepinephrine group; odds ratio with dopamine, 1.17; 95% confidence interval, 0.97 to 1.42; P=0.10). However, there were more arrhythmic events among the patients treated with dopamine than among those treated with norepinephrine (207 events [24.1%] vs. 102 events [12.4%], P<0.001). A subgroup analysis showed that dopamine, as compared with norepinephrine, was associated with an increased rate of death at 28 days among the 280 patients with cardiogenic shock but not among the 1044 patients with septic shock or the 263 with hypovolemic shock (P=0.03 for cardiogenic shock, P=0.19 for septic shock, and P=0.84 for hypovolemic shock, in Kaplan–Meier analyses).
Although there was no significant difference in the rate of death between patients with shock who were treated with dopamine as the first-line vasopressor agent and those who were treated with norepinephrine, the use of dopamine was associated with a greater number of adverse events.
05 Apr 09
By M Ruggiero
AACN Advanced Critical Care 2008;19:281-287
Septic shock continues to be one of the leading causes of death in the intensive care unit today. The confluence of many factors contributes to the deterioration of patients’ condition in septic shock. Increased levels of nitric oxide, in part, mediate the cardiovascular effects of septic shock. Nitric oxide is major mediator of vasodilation and hypotension as well as myocardial depression. It also contributes to decreased production and release of endogenous vasopressin. Vasopressin effects are actualized by stimulation …
12 Mar 09
J A Russell, K R Walley, A C Gordon, D J Cooper, P C Hébert, J Singer for the Vasopressin and Septic Shock Trial (VASST) Investigators
Crit Care Med 2009;37:811-818
Vasopressin and corticosteroids are often added to support cardiovascular dysfunction in patients who have septic shock that is nonresponsive to fluid resuscitation and norepinephrine infusion. However, it is unknown whether vasopressin treatment interacts with corticosteroid treatment.
Post hoc substudy of a multicenter randomized blinded controlled trial of vasopressin vs. norepinephrine in septic shock.
Twenty-seven Intensive Care Units in Canada, Australia, and the United States.
Seven hundred and seventy-nine patients who had septic shock and were ongoing hypotension requiring at least 5 μg/min of norepinephrine infusion for 6 hours.
Patients were randomized to blinded vasopressin (0.01-0.03 units/min) or norepinephrine (5-15 μg/min) infusion added to open-label vasopressors. Corticosteroids were given according to clinical judgment at any time in the 28-day postrandomization period.
The primary end point was 28-day mortality. We tested for interaction between vasopressin treatment and corticosteroid treatment using logistic regression. Secondary end points were organ dysfunction, use of open-label vasopressors and vasopressin levels.
There was a statistically significant interaction between vasopressin infusion and corticosteroid treatment (p = 0.008). In patients who had septic shock and were also treated with corticosteroids, vasopressin, compared to norepinephrine, was associated with significantly decreased mortality (35.9% vs. 44.7%, respectively, p = 0.03). In contrast, in patients who did not receive corticosteroids, vasopressin was associated with increased mortality compared with norepinephrine (33.7% vs. 21.3%, respectively, p = 0.06). In patients who received vasopressin infusion, use of corticosteroids significantly increased plasma vasopressin levels by 33% at 6 hours (p = 0.006) to 67% at 24 hours (p = 0.025) compared with patients who did not receive corticosteroids.
There is a statistically significant interaction between vasopressin and corticosteroids. The combination of low-dose vasopressin and corticosteroids was associated with decreased mortality and organ dysfunction compared with norepinephrine and corticosteroids.