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1.
Leadersh Health Serv (Bradf Engl) ; 32(4): 509-524, 2019 09 26.
Article in English | MEDLINE | ID: mdl-31612783

ABSTRACT

PURPOSE: Medication errors are a significant cause of injury in Norwegian hospitals. The purpose of this study is to explore how Lean Six Sigma (LSS) has been used in the Norwegian public health-care context to reduce medication errors. DESIGN/METHODOLOGY/APPROACH: A mixed method approach was used to gather data from participants working in the four regions served by the Norway health authorities. A survey questionnaire was distributed to 38 health-care practitioners and semi-structured interviews were conducted with 12 health-care practitioners. FINDINGS: The study finds that the implementation of LSS in the Norwegian public health-care context is still in its infancy. This is amidst several challenges faced by Norwegian hospitals such as the lack of top-management support, lack of LSS training and coaching and a lack of awareness around the benefits of LSS in health care. RESEARCH LIMITATIONS/IMPLICATIONS: Because of the large geographical area, it was difficult to reach participants from all health regions in Norway. However, the study managed to assess the current status of LSS implementation through the participants' perspectives. This is a fruitful area for future research whereby an action research methodology could be used. ORIGINALITY/VALUE: To the best of the authors' knowledge, this is the first empirical study into the use of LSS methodology in reducing medication errors. In addition, this study is valuable for health-care practitioners and professionals as a guideline to achieve the optimal benefit of LSS implementation to reduce medication errors.


Subject(s)
Medication Errors , Total Quality Management , Delivery of Health Care , Efficiency, Organizational , Health Facilities , Hospitals , Humans , Medication Errors/prevention & control , Norway , Quality Improvement
2.
Am J Health Promot ; 27(3 Suppl): S74-6, 2013.
Article in English | MEDLINE | ID: mdl-23286668

ABSTRACT

PURPOSE: To develop, and implement, a social marketing campaign to increase preconception health knowledge among second-generation Latinas in Oregon. DESIGN: Social marketing demonstration project. SETTING: Latino communities in five Oregon counties. SUBJECTS: Target populations included young Latinas (18-29 years old) born in the United States of immigrant parents in five Oregon counties, and their family members. Intervention. A radionovela, Amor y Salud, was developed that featured a Latina and her fiancé preparing for marriage and family. Social media, Web sites, and culturally relevant print materials promoted the radio campaign. MEASURES: Process data, social media metrics, Google analytics, online and intercept surveys were collected. ANALYSIS: Basic frequencies and descriptive statistics were used. RESULTS: Twelve episodes were produced in English and Spanish and played on nine radio stations a total of 2098 times. The Facebook page was viewed 11,000 times, and radionovela episodes were played a total of 776 times. CONCLUSION: Amor y Salud used mixed media--radio, social media, print materials--to encourage Latinas to consider their preconception health. Anecdotally, we heard positive comments from community members and local media regarding the radionovela; however, evaluation challenges prevent us from saying conclusively that knowledge on this topic increased.


Subject(s)
Health Promotion/methods , Hispanic or Latino , Preconception Care , Social Marketing , Adolescent , Adult , Humans , Oregon , Pilot Projects , Young Adult
3.
Clin Pharmacol Ther ; 78(5): 477-85, 2005 Nov.
Article in English | MEDLINE | ID: mdl-16321614

ABSTRACT

BACKGROUND: The administration of protamine to patients who received heparin during cardiopulmonary bypass (CPB) induces hypotension. Protamine inhibits the carboxypeptidase N-mediated degradation of bradykinin, a peptide that causes vasodilation and tissue-type plasminogen activator (t-PA) release. This study tests the primary hypothesis that blocking the bradykinin B(2) receptor would attenuate protamine-related hypotension. METHODS: We conducted a prospective, double-blind, randomized study in 16 adult male patients undergoing elective cardiac surgery requiring CPB and taking an angiotensin-converting enzyme (ACE) inhibitor preoperatively, because ACE inhibition increases bradykinin concentrations during CPB. Subjects were randomized to receive either saline solution (N = 8) or the bradykinin B(2) receptor antagonist HOE 140 (100 mug/kg, N = 8) before the administration of protamine. Mean arterial pressure (MAP) and t-PA activity were measured intraoperatively and before and after protamine administration. RESULTS: Protamine administration caused a significant increase in bradykinin concentrations in the saline solution group (from 6.0 +/- 1.3 to 10.0 +/- 1.6 fmol/mL, P = .043), as well as the HOE 140 group (from 6.5 +/- 1.8 to 14.3 +/- 4.6 fmol/mL, P = .042). Protamine significantly decreased MAP in the saline solution group (from 69.8 +/- 4.4 mm Hg to a mean individual nadir of 56.1 +/- 2.6 mm Hg, P = .031), but bradykinin receptor antagonism blunted this effect (from 74.3 +/- 3.7 mm Hg to a mean individual nadir of 69.6 +/- 1.2 mm Hg in the HOE 140 group, P = .545). Hence, during protamine infusion, MAP was significantly lower in the saline solution group compared with the HOE 140 group (P = .002). t-PA activity decreased significantly during administration of HOE 140 (from 3.59 +/- 0.31 to 1.67 +/- 0.42 IU/mL, P = .001) but not during saline solution (from 2.12 +/- 0.48 to 1.44 +/- 0.36 IU/mL, P = .214). Similarly, t-PA activity decreased significantly during protamine administration in the HOE 140 group (from 1.67 +/- 0.42 to 0.77 +/- 0.26 IU/mL, P = .038) but not in the saline solution group (from 1.44 +/- 0.36 to 0.99 +/- 0.26 IU/mL, P = .132). CONCLUSION: Increased bradykinin contributes to protamine-related hypotension through its B(2) receptor in ACE inhibitor-treated patients.


Subject(s)
Bradykinin B2 Receptor Antagonists , Bradykinin/analogs & derivatives , Cardiopulmonary Bypass , Heparin Antagonists/adverse effects , Hypotension/chemically induced , Hypotension/drug therapy , Postoperative Complications/chemically induced , Postoperative Complications/drug therapy , Protamines/adverse effects , Aged , Bradykinin/therapeutic use , Double-Blind Method , Female , Fibrinolysis/drug effects , Hemodynamics/drug effects , Heparin Antagonists/therapeutic use , Humans , Kinins/blood , Male , Middle Aged , Pilot Projects , Protamines/antagonists & inhibitors , Protamines/therapeutic use
4.
Clin Pharmacol Ther ; 76(4): 379-87, 2004 Oct.
Article in English | MEDLINE | ID: mdl-15470338

ABSTRACT

BACKGROUND: This study tested the hypothesis that angiotensin-converting enzyme (ACE) inhibitors potentiate activation of the kallikrein-kinin system during cardiopulmonary bypass (CPB). METHODS: The effects of CPB on concentrations of bradykinin and its metabolite bradykinin 1-5 (BK1-5) were determined in 31 patients taking an ACE inhibitor who were randomized to continue ACE inhibitors until coronary artery bypass surgery (ACE inhibitor group, N = 19) or to discontinue them 48 hours before surgery (no ACE inhibitor group, N = 12). Arterial and venous blood was sampled before CPB, at 30 minutes of CPB, at 60 minutes of CPB, after separation from CPB, and on postoperative day 1. RESULTS: Arterial bradykinin ( P < .001 [from 22.4 +/- 24.1 fmol/mL to 86.2 +/- 98.7 fmol/mL in the no ACE inhibitor group]) and arterial ( P < .001) and venous ( P = .016) BK1-5 concentrations increased significantly during CPB. Arterial bradykinin concentrations were significantly higher ( P = .017), whereas BK1-5 concentrations ( P = .024) and the molar ratio of BK1-5/bradykinin ( P = .008) were significantly lower in the ACE inhibitor group compared with the no ACE inhibitor group. In addition, arterial bradykinin concentrations were significantly increased in smokers compared with nonsmokers ( P = .015), when we controlled for the ACE inhibitor group. There was no effect of smoking on ACE activity ( P = .597 overall). There was a significant inverse correlation between arterial bradykinin and mean arterial pressure ( r 2 = 0.2137, P = .010) and a significant correlation between arterial bradykinin and tissue-type plasminogen activator antigen concentrations ( r 2 = 0.174, P = .022) during CPB. Tissue-type plasminogen activator antigen was significantly higher in the ACE inhibitor group than in the no ACE inhibitor group (18.0 +/- 7.8 ng/mL versus 12.4 +/- 4.5 ng/mL, P = .016) but not in smokers compared with nonsmokers ( P = .451). CONCLUSION: Preoperative ACE inhibitors and smoking potentiate the kinin response to CPB and may contribute to the hemodynamic and fibrinolytic response observed during CPB.


Subject(s)
Angiotensin-Converting Enzyme Inhibitors/pharmacology , Bradykinin/drug effects , Coronary Artery Bypass , Peptide Fragments/drug effects , Smoking/adverse effects , Bradykinin/blood , Female , Fibrinolysis/drug effects , Graft Occlusion, Vascular/prevention & control , Hemodynamics/drug effects , Humans , Male , Middle Aged , Peptide Fragments/blood
5.
Circulation ; 108(25): 3079-83, 2003 Dec 23.
Article in English | MEDLINE | ID: mdl-14656921

ABSTRACT

BACKGROUND: Increased plasminogen activator inhibitor-1 (PAI-1) concentrations after coronary artery bypass grafting (CABG) are associated with increased risk of vein graft occlusion. Because angiotensin II stimulates PAI-1 expression, we tested the hypothesis that preoperative angiotensin-converting enzyme (ACE) inhibition decreases PAI-1 expression after CABG. METHODS AND RESULTS: We measured the effects of cardiopulmonary bypass (CPB) on PAI-1 antigen and tissue-type plasminogen activator (tPA) antigen and activity in 31 patients taking an ACE inhibitor (ACEI) who were randomized to continue ACEI until the morning of surgery (ACEI group, n=19) or to discontinue it 48 hours before surgery (No-ACEI group, n=12). Arterial blood samples were taken at baseline before CPB, twice during CPB, after separation from CPB, and on postoperative day 1 (POD1). CPB caused an early decrease in PAI-1 antigen, followed by an increase in PAI-1 antigen on POD1 (P<0.001 for effect of time). ACE inhibition attenuated the increase in PAI-1 antigen such that both PAI-1 antigen on POD1 (P=0.013) and the change in PAI-1 antigen from baseline to POD1 (P=0.009) were higher in the No-ACEI group (from 17.0+/-5.0 to 48.7+/-8.8 ng/mL) versus the ACEI group (from 19.9+/-3.4 to 33.1+/-6.2 ng/mL). There was no significant difference between the 2 groups in intraoperative tPA activity (P=0.259); however, the increase in tPA activity was significantly greater in the ACEI group than in the No-ACEI group (P=0.030). CONCLUSIONS: Preoperative ACEI attenuates the increase in PAI-1 after CABG, suggesting a role for ACE inhibition in reducing the risk of acute graft thrombosis.


Subject(s)
Angiotensin-Converting Enzyme Inhibitors/therapeutic use , Cardiopulmonary Bypass , Plasminogen Activator Inhibitor 1/metabolism , Combined Modality Therapy , Coronary Artery Bypass , Female , Fibrinolysis , Graft Occlusion, Vascular/prevention & control , Hemodynamics , Humans , Male , Middle Aged , Tissue Plasminogen Activator/metabolism , Treatment Outcome
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