Clinical decision support software for management of chronic heart failure: development and evaluation.

OBJECTIVE: To develop and evaluate clinical decision support software (CDSS) to aid physicians treat patients with chronic heart failure (CHF). METHODS: The CDSS was developed after discussions with a multidisciplinary panel. Evaluation was performed in three stages over a 6 month period including an editorial check, one-to-one interviews with potential users and educational meetings with general practitioners (GPs), junior doctors and medical students during which the CDSS was assessed in a cross-over design against paper guidelines. Opinions of the CDSS and the computer literacy of the participants were assessed by questionnaire. RESULTS: There were several changes to the CDSS at various stages of development and evaluation. One-to-one interviews generated extensive qualitative feedback. GPs had lower computer literacy scores than junior doctors and students (both p<0.01). There were small trends when comparing the CDSS with paper guidelines. GPs scored less well (CDSS 75% vs. 80%, p=0.41), while junior doctors and medical students appeared to improve their scores (72%-84%, p=0.32 and 66%-77%, p=0.19, respectively). Most (70%) found the CDSS more useful than the written guidelines. CONCLUSION: Development of CDSS using guidelines and expert opinion requires a multidisciplinary iterative process of feedback and software adaptation. Barriers to implementation identified include lower computer literacy among GPs, a lack of complexity within CDSS in addressing non-medical needs of patients and a reluctance among medical staff to consult guidelines during patient consultations. Improving computer skills, integrating CDSS into referral pathways and requests for investigations may be ways of enhancing use of this emerging technology.

Intra-arterial vasopressin in the human forearm: pharmacodynamics and the role of nitric oxide.

BACKGROUND AND OBJECTIVES: Diverse vascular effects have been ascribed to vasopressin, including the potential to cause vasodilation, vasoconstriction, and nitric oxide release. The objective of this study was to establish the pharmacodynamics, reproducibility, and nitric oxide dependence of the vasomotor actions of vasopressin in the forearm resistance vessels. METHODS: Blood flow in both forearms of 12 healthy men was measured with venous occlusion plethysmography. Continuous and discontinuous doses of 1 to 300 pmol/min vasopressin were administered by the intrabrachial route. For assessment of the contribution of nitric oxide, vasopressin was coadministered with a "nitric oxide clamp," a balanced coinfusion of 4 micromol/min L-N(G)-monomethylarginine (a nitric oxide synthase inhibitor) and 0.3 to 0.8 nmol/min sodium nitroprusside (an exogenous nitric oxide donor) to block endogenous nitric oxide production and restore normal basal blood flow, respectively. RESULTS: Vasopressin produced a dose-dependent biphasic change in blood flow with a maximum reduction in percentage change in blood flow ratio of infused and control arms of 22% +/- 5% at 3 pmol/min (P <.01) and an increase of 80% +/- 30% at 300 pmol/min (P <.01). There were no significant differences in repeated responses obtained either within or between days. Repeated discontinuous dosing did not change the magnitude of the maximum vasoconstriction or vasodilation, but prolonged continuous infusion produced maximal vasodilation at 12 minutes that subsequently resulted in substantial tachyphylaxis (P =.04). Although there was no augmentation of vasoconstriction, the nitric oxide clamp abolished vasopressin-induced vasodilation (P <.05). CONCLUSIONS: Intra-arterial vasopressin causes a reproducible dose-dependent biphasic change in forearm blood flow. Vasomotor responses are time-dependent with a modest delay to peak vasodilation and tachyphylaxis with prolonged sustained infusion. Nitric oxide release is a major contributor to vasopressin-induced vasodilation but does not directly oppose low-dose vasopressin-induced vasoconstriction.

Management of chronic heart failure due to systolic left ventricular dysfunction by cardiologist and non-cardiologist physicians.

There are now a number of guidelines outlining the diagnosis and management of patients with chronic heart failure (CHF). The extent to which these guidelines are used and the effects on patient outcomes are not well known. The aim of this study was to examine the implementation of a heart failure guideline among cardiologist and non-cardiologist physicians in a university hospital setting. Case record data were examined from 400 patients with a primary diagnosis of CHF. Management of these patients was assessed using a systolic heart failure guideline (Scottish Intercollegiate Guideline Network, number 35) as a benchmark. Hospital admission data were examined contemporaneously over a 17-month period to assess associations between adherence to drug therapies and number of admissions. Overall, there was poor adherence to the guideline, with relatively high use of angiotensin-converting enzyme (ACE) inhibitors/angiotensin II receptor blockers (ARBs) (80%), low use of beta-blockers (32%) and digoxin (36%), and very low use of spironolactone (13%). Cardiologists used more beta-blockers (37 vs. 21%, P=0.003) and digoxin in sinus rhythm (18 vs. 5%, P<0.001) than non-cardiologists. Hospital admission rate was individually associated with increasing age, NYHA status, beta-blocker, diuretic and spironolactone prescription (all P<0.001). At multivariable analysis, only age, NYHA status and increased diuretic prescription were associated with more frequent admission (P<0.001, R(2)=0.15). Despite carefully designed guidelines, the implementation of evidence-based therapies for CHF remains inadequate, even in a university hospital environment. This may reflect a lack of organisational developments to facilitate the increasingly complex management of patients with CHF.