ABSTRACT
A case report, focused on vasopressor use and presented in this article, is likely to resonate with many critical care nurses. In this article the authors describe opportunities to enhance safety with vasopressor therapy. Specifically, the goal of improving communication among physicians, nurses, and pharmacists around desired endpoints for vasopressor therapy, triggers for reassessment of the therapeutic strategy and cause of the patient's shock was identified as an area for improvement. A form piloted within an organization for use during multidisciplinary rounds and key findings is shared. Vasopressors constitute the mainstay of therapy for nearly every hemodynamically unstable patient in critical care. It is hoped that the lessons and information shared help empower critical care nurses to facilitate vasopressor stewardship within their facilities and, ultimately, enhance patient safety.
Subject(s)
Critical Care/methods , Norepinephrine/therapeutic use , Respiratory Distress Syndrome/drug therapy , Respiratory Distress Syndrome/nursing , Vasoconstrictor Agents/therapeutic use , Aged , Fatal Outcome , Humans , Male , Multiple Organ Failure/etiology , Nurse's Role , Patient Safety , Practice Guidelines as Topic , Respiratory Distress Syndrome/complicationsABSTRACT
OBJECTIVE: To compare the effects of arginine-vasopressin (AVP) and norepinephrine (NE) on hemodynamic variables, organ dysfunction, and adverse events in early hyperdynamic septic shock. DESIGN AND SETTING: Randomized, controlled, open-label trial. PATIENTS AND PARTICIPANTS: Twenty-three patients with early (12h) hyperdynamic septic shock in two teaching hospitals. INTERVENTIONS: AVP (0.04-0.20 Umin(-1), n=13) as a single agent or NE (0.1-2.8microg kg(-1)min(-1), n=10) infusion for 48[Symbol: see text]h to achieve mean arterial pressure at or above 70mmHg. MEASUREMENTS AND RESULTS: Hemodynamic parameters and Sequential Organ Failure Assessment (SOFA) score were measured. AVP and NE equally increased mean arterial pressure over 48h, but NE was required in 36% of AVP patients at 48h. Compared to baseline, AVP increased systemic vascular resistance, decreased exposure to NE, decreased cardiac output by decreasing heart rate, increased creatinine clearance, and improved SOFA score. The PrCO(2) - PaCO(2) difference remained stable throughout the study. One AVP patient developed acute coronary syndrome with dose-dependent ECG changes. Three patients in both groups died during their ICU stay. CONCLUSION: In early hyperdynamic septic shock, the administration of high-dose AVP as a single agent fails to increase mean arterial pressure in the first hour but maintains it above 70mmHg in two-thirds of patients at 48h. AVP decreases NE exposure, has no effect on the PrCO(2) - PaCO(2 )difference, and improves renal function and SOFA score.
