Variation in the use of 12-lead electrocardiography for patients with chest pain by emergency medical services in North Carolina.

BACKGROUND: Prehospital 12-lead electrocardiography (ECG) is critical to timely STEMI care although its use remains inconsistent. Previous studies to identify reasons for failure to obtain a prehospital ECG have generally only focused on individual emergency medical service (EMS) systems in urban areas. Our study objective was to identify patient, geographic, and EMS agency-related factors associated with failure to perform a prehospital ECG across a statewide geography. METHODS AND RESULTS: We analyzed data from the Prehospital Medical Information System (PreMIS) in North Carolina from January 2008 to November 2010 for patients >30 years of age who used EMS and had a prehospital chief complaint of chest pain. Among 3.1 million EMS encounters, 134 350 patients met study criteria. From 2008-2010, 82 311 (61%) persons with chest pain received a prehospital ECG; utilization increased from 55% in 2008 to 65% in 2010 (trend P<0.001). Utilization by health referral region ranged from 22.9% to 74.2% and was lowest in rural areas. Men were more likely than women to have an ECG performed (63.0% vs 61.3%, adjusted RR 1.02, 95% CI 1.01 to 1.04). The certification-level of the EMS provider (paramedic vsbasic/intermediate) and system-level ECG equipment availability were the strongest predictors of ECG utilization. Persons in an ambulance with a certified paramedic were significantly more likely to receive a prehospital ECG than nonparamedics (RR 2.15, 95% CI 1.55, 2.99). CONCLUSIONS: Across a large geographic area prehospital ECG use increased significantly, although important quality improvement opportunities remain. Increasing ECG availability and improving EMS certification and training levels are needed to improve overall care and reduce rural-urban treatment differences.

Bedside multimarker testing for risk stratification in chest pain units: The chest pain evaluation by creatine kinase-MB, myoglobin, and troponin I (CHECKMATE) study.

BACKGROUND: Earlier, rapid evaluation in chest pain units may make patient care more efficient. A multimarker strategy (MMS) testing for several markers of myocardial necrosis with different time-to-positivity profiles also may offer clinical advantages. METHODS AND RESULTS: We prospectively compared bedside quantitative multimarker testing versus local laboratory results (LL) in 1005 patients in 6 chest pain units. Myoglobin, creatine kinase-MB, and troponin I were measured at 0, 3, 6, 9 to 12, and 16 to 24 hours after admission. Two MMS were defined: MMS-1 (all 3 markers) and MMS-2 (creatine kinase-MB and troponin I only). The primary assessment was to relate marker status with 30-day death or infarction. More patients were positive by 24 hours with MMS than with LL (MMS-1, 23.9%; MMS-2, 18.8%; LL, 8.8%; P=0.001, all comparisons), and they became positive sooner with MMS-1 (2.5 hours, P=0.023 versus LL) versus MMS-2 (2.8 hours, P=0.026 versus LL) or LL (3.4 hours). The relation between baseline MMS status and 30-day death or infarction was stronger (MMS-1: positive, 18.8% event rate versus negative, 3.0%, P=0.001; MMS-2: 21.9% versus 3.2%, P=0.001) than that for LL (13.6% versus 5.5%, P=0.038). MMS-1 discriminated 30-day death better (positive, 2.0% versus negative, 0.0%, P=0.007) than MMS-2 (positive, 1.8% versus negative, 0.2%; P=0.055) or LL (positive, 0.0% versus negative, 0.5%; P=1.000). CONCLUSIONS: Rapid multimarker analysis identifies positive patients earlier and provides better risk stratification for mortality than a local laboratory-based, single-marker approach.

Phosphorylation of C-protein, troponin I and phospholamban in isolated rabbit hearts.

Phosphorylation of myofibrillar and sacroplasmic-reticulum (SR) proteins was studied in Langendorff-perfused rabbit hearts subjected to various inotropic interventions. Stimulation of hearts with isoprenaline resulted in the phosphorylation of both troponin I (TnI) and C-protein in myofibrils and phospholamban in SR. Phosphorylation of phospholamban could be reversed by a 15 min perfusion with drug-free buffer, after a 1 minute pulse perfusion with isoprenaline, at which time the mechanical effects of isoprenaline stimulation had also been reversed. However, both TnI and C-protein remained phosphorylated at this time. Moreover, the inhibition of Ca2+ activation of the Mg2+-dependent ATPase (Mg-ATPase) activity associated with myofibrillar phosphorylation persisted in myofibrils prepared from hearts frozen after 15 min of washout of isoprenaline. To assess the contribution of C-protein phosphorylation in the decrease of Ca2+ activation of the myofibrillar Mg-ATPase activity, we reconstituted a regulated actomyosin system in which only C-protein was phosphorylated. In this system, C-protein phosphorylation did not contribute to the decrease in Ca2+ activation of Mg-ATPase activity, indicating that TnI phosphorylation is responsible for the diminished sensitivity of the myofibrils to Ca2+. These observations support the hypothesis that phospholamban phosphorylation plays a more dominant role than TnI or C-protein phosphorylation in the mechanical response of the mammalian heart to beta-adrenergic stimulation.

Recurrent meningitis: a case report.

Recurrent meningitis is an uncommon clinical problem. It is most likely to result from head trauma. Streptococcus pneumoniae is the most common infecting pathogen. Computed tomographic techniques are required to identify persistent bony defects in the skull that might predispose to this disorder. Because emergency physicians regularly care for victims of head trauma and meningitis, knowledge of this entity can be useful.

Phosphorylation and functional modifications of sarcoplasmic reticulum and myofibrils in isolated rabbit hearts stimulated with isoprenaline.

Isoprenaline stimulation of perfused rabbit hearts was associated with simultaneous phosphorylation of proteins in the myofilaments and phospholamban in the sarcoplasmic reticulum (SR). Hearts were perfused with Krebs-Henseleit buffer containing [32P]Pi, freeze-clamped in a control condition or at the peak of the inotropic response to isoprenaline, and myofibrils and SR were prepared from the same hearts. Stimulation of 32P incorporation in troponin I (TnI) and C-protein by isoprenaline was associated with a decrease in Ca2+-sensitivity of the myofibrillar Mg2+-dependent ATPase activity. Stimulation of 32P incorporation in SR by isoprenaline was associated with an increase in the initial rates of oxalate-facilitated Ca2+ transport, assayed with SR vesicles in either microsomal fractions or homogenates from the perfused hearts. These findings provide evidence that phosphorylation of TnI, C-protein and phospholamban in the intact cell is associated with functional alterations of the myofibrils and SR which may be responsible in part for the effects of catecholamines on the mammalian myocardium.

Bile acid uptake and calcium flux in brush border membrane vesicles.

Our laboratory has recently reported that intestinal bile acid malabsorption in cystic fibrosis (CF) is a primary mucosal cell defect. Others have suggested that elevated intracellular Ca++ levels in other cell types in CF may represent a common primary dysfunction in Ca++ efflux in these cells. We examined the possibility that intestinal bile acid absorption and Ca++ efflux in mucosal cells may be linked physiologically. Brush border membrane vesicles (BBMV) prepared from guinea pig ileum served as the experimental model to test this hypothesis. Ca++ (2.5 x 10(-3)M) present in the incubation medium did not alter the uptake of taurocholic acid (TCA) by BBMV. Also, TCA uptake into BBMV preloaded with Ca++ was not significantly different from that in BBMV not previously loaded with Ca++. Furthermore, with TCA present in the incubation medium, Ca++ efflux from preloaded BBMV was not altered. These data suggest that ileal TCA uptake, as measured by BBMV, is not dependent upon either intra- or extravesicular Ca++. Also, Ca++ efflux from BBMV is unaffected by TCA uptake. Although separate lines of evidence suggest that intestinal bile acid malabsorption and reduced plasma membrane Ca++ flux are primary defects in CF, we conclude that in the normal intestine these functions are independent physiological processes.

Expanding the hospital nursing role: an administrative account.

In reality, role change among staff RNs is a continuous phenomenon. As medical technology increases, patient care regimes follow suit, and the staff RN is constantly called upon to apply a knowledge base in different ways and to acquire new knowledge and behaviors. The nursing administrator who keeps pace with this growth can capitalize on the phenomenon, guiding the change to see that it is progressive, that it assists the nurse in developing a more advanced nursing (as opposed to mini-physician) identity and that it does improve extant nursing practice. Undertaking a new project of this sort on the unit is likely to create a number of beneficial by-products. For example, nurse-physician rapport and communication increase as each group opens professional boundaries in defining and planning the content of role expansion. The unit's traditional operation must also be examined in the course of building in new functions. System critiques stimulate the unit's nursing manager to weed out less than optimal features of the existing nursing care delivery system. The expanded role has favorably affected nursing care at Mercy Hospital. Physicians, nurses, and most important, the patient have reaped the benefits. The nurse is able to function in a more advanced capacity, and physicians see the benefits to their patients; fewer delays in specific aspects of care delivery with a more sophisticated, higher quality of nursing care. What is exciting about this concept is that the principles could apply to virtually any RN work group that gives direct care to a homogeneous patient population.