Cindy Barrett

A Handoff Protocol from the Cardiovascular Operating Room to Cardiac ICU Is Associated with Improvements in Care Beyond the Immediate Postoperative Period

BACKGROUNDnHandoff protocols from the cardiovascular operating room (CVOR) to the cardiac intensive care unit (CICU) can improve patient outcomes and delivery of care beyond the immediate postoperative period. In a prospective quality improvement study, a structured CVOR-to-CICU handoff protocol was implemented at a university-affiliated childrens hospital. As a parallel project, an initiative to reduce unplanned extubations in the CICU was implemented.nnnMETHODSnIn a 41-month period, 1,507 neonates, infants, children, and adults were admitted to the CICU from the CVOR after undergoing a surgical procedure. The study was divided into a 17-month prehandoff-protocol period (January 2009-May 2010) and a 24-month posthandoff-protocol period (June 2010-May 2012). The handoff protocol was intended to streamline the handoff process from the CVOR and throughout the transition to the CICU. The specifics of the handoff, as outlined in a bedside laminated flowchart, included patient transport from the CVOR, the cardiovascular surgeons report, the anesthesiologists report, and the patient status summary and care plan.nnnRESULTSnAfter introduction of the handoff protocol, there was a statistically significant and sustained reduction in the mean rate of unplanned extubations from 0.62 to 0.24 per 100 ventilator-days (p = .03). There was a statistically significant reduction in median ventilator time per patient--from 17 hours (interquartile range [IQR]: 5.3 to 57.7) to 12.8 hours (IQR: 4.8 to 31.8); p = .02). The mean rate of unplanned extubations was 0.26 in 2011 and 0.30 in 2012.nnnCONCLUSIONSnImplementation of a handoff protocol from the CVOR to the CICU was associated with sustained decrease in unplanned extubations and in mean ventilator times.

Right ventricular hypertrophy with early dysfunction: A proteomics study in a neonatal model

OBJECTIVEnRight ventricular hypertrophy and subsequent dysfunction is common in patients with congenital heart defects, but the molecular mechanisms underlying change from adaptive hypertrophy to dysfunction remain elusive. We used the novel technique of proteomics to characterize protein changes in right ventricular myocardium in a neonatal model of right ventricular hypertrophy and early dysfunction.nnnMETHODSnTwelve neonatal piglets were equally randomized to pulmonary artery banding (PAB group), or sham operation (thoracotomy without banding). After 4 weeks, right ventricular morphology and function were assessed in vivo using magnetic resonance imaging. Animals were humanely killed. Proteomics of right ventricular myocardium was performed. Purified right ventricular proteins were separated by 2-dimensional difference gel electrophoresis using fluorescent cyanine dyes. After gel imaging, software analysis revealed protein spots differentially expressed between the 2 groups; these spots were excised and identified by mass spectrometry.nnnRESULTSnOn magnetic resonance imaging, animals with pulmonary artery banding demonstrated significant right ventricular hypertrophy, cavity dilatation, and mild systolic impairment (right ventricular ejection fraction 39.8% +/- 15% vs 56.7% +/- 10% controls; P < .05). Right ventricular free wall mass on harvest confirmed right ventricular hypertrophy. Proteomic analysis revealed 18 proteins that were significantly differentially expressed: 5 structural proteins, 6 metabolic enzymes, 2 stress proteins, and 5 miscellaneous proteins. Expression of calsarcin-1 and vinculin was increased, as were certain metabolic enzymes, although F(1)-ATPase beta-chain and heat shock protein 70 decreased.nnnCONCLUSIONSnThis is the first study characterizing right ventricular protein changes in a large animal model specifically capturing the change from compensated to maladaptive hypertrophy. These findings can guide future work at elucidating the mechanisms in the pathophysiology of neonatal right ventricular hypertrophy and dysfunction.