A centile-based EWS system will identify patients with abnormal vital signs regardless of their eventual outcome and might therefore be more likely to generate an alert when presented with patients with redeemable morbidity or avoidable mortality. We are about to start a stepped-wedge clinical trial gradually introducing an electronic version of our EWS system on the trauma wards in a teaching hospital.
Objectives Cardiorespiratory instability may be undetected in monitored step-down unit patients. We explored whether using an integrated monitoring system that continuously amalgamates single noninvasive monitoring parameters (heart rate, respiratory rate, blood pressure, and peripheral oxygen saturation) into AN instability index value (INDEX) correlated with our single-parameter cardiorespiratory instability concern criteria, and whether nurse response to INDEX alert for patient attention was associated with instability reduction. Design Prospective, longitudinal evaluation in sequential 8-, 16-, and 8-wk phases (phase I, phase II, and phase III, respectively). Setting A 24-bed trauma step-down unit in single urban tertiary care center. Patients All monitored patients. Interventions Phase I: Patients received continuous single-channel monitoring (heart rate, respiratory rate, blood pressure, and peripheral oxygen saturation) and standard care; INDEX background was recorded but not displayed. Phase II: INDEX was background-recorded; staff was educated on use. Phase III: Staff used a clinical response algorithm for INDEX alerts. Measurement and Main Results Any monitored parameters even transiently beyond local cardiorespiratory instability concern triggers (heart rate of <40 or >140 beats/min, respiratory rate of <8 or >36 breaths/min, systolic blood pressure of <80 or >200 mm Hg, diastolic blood pressure of >110 mm Hg, and peripheral oxygen saturation of <85%) defined INSTABILITYmin. INSTABILITYmin further judged as both persistent and serious defined INSTABILITYfull. The INDEX alert states were defined as INDEXmin and INDEXfull by using same classification. Phase I and phase III admissions (323 vs. 308) and monitoring (18,258 vs. 18,314 hrs) were similar. INDEXmin and INDEXfull correlated significantly with INSTABILITYmin and INSTABILITYfull (r = .713 and r = .815, respectively, p < .0001). INDEXmin occurred before INSTABILITYmin in 80% of cases (mean advance time 9.4 ± 9.2 mins). Phase I and phase III admissions were similarly likely to develop INSTABILITYmin (35% vs. 33%), but INSTABILITYmin duration/admission decreased from phase I to phase III (p = .018). Both INSTABILITYfull episodes/admission (p = .03) and INSTABILITYfull duration/admission (p = .05) decreased in phase III. Conclusion The integrated monitoring system INDEX correlated significantly with cardiorespiratory instability concern criteria, usually occurred before overt instability, and when coupled with a nursing alert was associated with decreased cardiorespiratory instability concern criteria in step-down unit patients.
Background and Purpose Cardiac injury persistence after aneurysmal subarachnoid hemorrhage (aSAH) is not well described. We hypothesized that post-aSAH cardiac injury, detected by elevated cardiac troponin I (cTnI), is related to aSAH severity and associated with electrocardiographic and structural echocardiographic abnormalities that are persistent. Methods Prospective longitudinal study was conducted of patients with aSAH with Fisher grade ≥2 and/or Hunt/Hess grade ≥3. Serum cTnI was collected on Days 1 to 5; cohort dichotomized into peak cTnI ≥0.3 ng/mL (elevated) or cTnI ≥0.3 ng/mL. Relationships among cTnI and aSAH severity, 12-lead electrocardiography early (≤4 days) and late (≥7 days), Holter monitoring on Days 1 to 5, and transthoracic echocardiogram (left ventricular ejection fraction and regional wall motion abnormalities) early (Days 0 to 5) and late (Days 5 to 12) were evaluated. Results Of 204 subjects, 31% had cTnI ≥0.3 ng/mL. cTnI ≥0.3 ng/mL was incrementally related to aSAH severity by admission symptoms (Hunt/Hess P=0.001) and blood load (Fisher P=0.028). More patients with cTnI ≥0.3 ng/mL had prolonged QTc on early (63% versus 30%, P<0.0001) and late electrocardiography (24% versus 7%, P=0.024). On Holter monitoring, more patients with cTnI ≥0.3 ng/mL had ventricular tachycardia/fibrillation (22% versus 9%, P=0.018) but not atrial fibrillation/flutter (P=0.241). Cardiac troponin I ≥0.3 ng/mL was associated with both early ejection fraction <50% (44% versus 5%, P<0.0001) and regional wall motion abnormalities (44% versus 4%, P<0.0001). Regional wall motion abnormalities predominated in basal and midventricular segments and persisted to some degree in 73% of patients affected, whereas ejection fraction <50% persisted in 59% of patients affected. Conclusions Cardiac injury is incrementally worse with increasing aSAH severity and associated with persistent QTc prolongation and ventricular arrhythmias. Regional wall motion abnormalities and depressed ejection fraction persist to some degree in the majority of those affected.
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