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US hospitals have reported compliance with the SEP-1 quality measure to Medicare since 2015. Finding an association between compliance and outcomes is essential to gauge measure effectiveness.What is the association between compliance with SEP-1 and 30-day mortality among Medicare beneficiaries?Studying patient-level data reported to Medicare by 3,241 hospitals from October 1, 2015, to March 31, 2017, we used propensity score matching and a hierarchical general linear model (HGLM) to estimate the treatment effects associated with compliance with SEP-1. Compliance was defined as completion of all qualifying SEP-1 elements including lactate measurements, blood culture collection, broad-spectrum antibiotic administration, 30 mL/kg crystalloid fluid administration, application of vasopressors, and patient reassessment. The primary outcome was a change in 30-day mortality. Secondary outcomes included changes in length of stay.We completed two matches to evaluate population-level treatment effects. In standard match, 122,870 patients whose care was compliant were matched with the same number whose care was noncompliant. Compliance was associated with a reduction in 30-day mortality (21.81% vs 27.48%, respectively), yielding an absolute risk reduction (ARR) of 5.67% (95% CI, 5.33-6.00; P .001). In stringent match, 107,016 patients whose care was compliant were matched with the same number whose care was noncompliant. Compliance was associated with a reduction in 30-day mortality (22.22% vs 26.28%, respectively), yielding an ARR of 4.06% (95% CI, 3.70-4.41; P .001). At the subject level, our HGLM found compliance associated with lower 30-day risk-adjusted mortality (adjusted conditional OR, 0.829; 95% CI, 0.812-0.846; P .001). Multiple elements correlated with lower mortality. Median length of stay was shorter among cases whose care was compliant (5 vs 6 days; interquartile range, 3-9 vs 4-10, respectively; P .001).Compliance with SEP-1 was associated with lower 30-day mortality. Rendering SEP-1 compliant care may reduce the incidence of avoidable deaths.

In 2001, early goal-directed therapy (EGDT) resulted in a 16% reduction in hospital mortality and, post hoc, a higher lactate clearance in severe sepsis and septic shock.1 Multiple studies have confirmed the validity and generalizability of EGDT, resulting in its adoption into the Surviving Sepsis Campaign Guidelines.2,3 Nguyen et al4,5 examined early lactate clearance and found a significant retrospective association with inflammation, apoptosis, coagulation, organ dysfunction, and mortality. Following this rationale, Jones et al6 modified the EGDT protocol in 2010 using a noninferiority study design and concluded that lactate clearance is equivalent to central venous oxygen saturation (Scvo2) in the management of individual patients. Before applying the findings of Jones et al6 to one’s next patient, compare the baseline characteristics, early hemodynamic patterns, and therapeutic interventions between those of Jones et al6 and the EGDT study.1 Further, review the complexities of lactate kinetics and the weaknesses of a noninferiority study design.7 Based on these facts, it is clear that lactate clearance and Scvo2 are not equivalent, but complementary goals for the individual patient.

Objective To study the use of emergency department (ED) femoro-femoral cardiopulmonary bypass (CPB) in the resuscitation of medical cardiac arrest patients. Design Prospective, uncontrolled trial. Setting Urban academic ED staffed with board-certified emergency physicians (EPs). Participants Ten patients with medical cardiac arrest unresponsive to standard therapy. Interventions Femoro-femoral CPB instituted by EPs. Results The time of cardiac arrest prior to CPB (mean±SD) was 32.0±13.6 min. The cardiac output while on CPB was 4.09±1.03 L/min with an average of 229±111 min on bypass. All 10 patients had resumption of spontaneous cardiac activity while on CPB. Seven of these were weaned from CPB with intrinsic spontaneous circulation. Of these, six patients were transferred from the ED to the operating room for cannula removal and vessel repair while the other patient died in the ED soon after discontinuing CPB. Mean survival was 47.8±44.7 h in the six patients leaving the ED. Although these patients had successful hemodynamic resuscitation, there were no long-term survivors. Conclusion CPB instituted by EPs is feasible and effective for the hemodynamic resuscitation of cardiac arrest patients unresponsive to advanced cardiac life support therapy. Future efforts need to focus on improving long-term outcome.

Studies evaluating the dose of epinephrine required to optimize return of spontaneous circulation and survival after CPR have shown that doses greater than recommended by advanced cardiac life support (ACLS) improve coronary perfusion pressure and short-term resuscitation rates. Since survival has not improved, it is possible that higher doses of epinephrine may be physiologically detrimental in the postresuscitation period.The object of this study is to measure the effect of the total cumulative dose of epinephrine given during ACLS on the hemodynamic, oxygen transport, and utilization variables in the postresuscitation period.A prospective nonrandomized control trial of inception cohorts.A large urban emergency department and intensive care unit.Forty-nine successfully resuscitated witnessed, normothermic, nontraumatic, out-of-hospital patients, who had suffered cardiac arrests.All patients were treated according to ACLS guidelines; however, the epinephrine dose (0.01 to 0.2 mg/kg or 1 to 14 mg) was selected at the clinician's discretion and given through central venous access every 3 to 5 min. Hemodynamic, oxygen transport, and utilization variables were measured on a return of spontaneous circulation, and at least every 30 min thereafter under a standardized postresuscitation protocol.Hemodynamic, oxygen transport/utilization variables, and mortality in patients resuscitated from cardiac arrest. The total cumulative dose of epinephrine given during ACLS until a return of spontaneous circulation was recorded.A total cumulative epinephrine dose of 15 mg was found to best predict 24-h mortality. Of the 49 patients, 20 received less than 15 mg (group 1) and 29 received greater than 15 mg (group 2). Age, premorbid health status, sex, presenting rhythm, and duration of cardiac arrest were similar in both groups. The 24-h survival was 17 of 20 (85%) and 12 of 29 (41%) in group 1 and 2, respectively (p0.002). Over the first 6 h of the postresuscitation period, both groups had similar mean arterial pressure (MAP), mixed venous oxygen saturation, and systemic oxygen extraction ratio (all p0.1). Group 2, however, had a significantly lower cardiac index (CI), systemic oxygen consumption (VO2), and systemic oxygen delivery (DO2) (all p0.01). Systemic vascular resistance index (SVRI), initial and 6-h lactic acid levels were significantly higher in group 2 (all p0.03).The administration of all doses of epinephrine during the resuscitation of out-of-hospital cardiac arrest is associated with impairment of DO2 and VO2 in the postresuscitation period. Both duration and severity of these impairments correlate with the total cumulative epinephrine dose given during the resuscitation. Thus, inadvertent catecholamine toxicity represents a further complicating factor in the production of postresuscitation disease. Diagnostic and therapeutic interventions addressed toward mitigating these potentially reversible adverse effects may impact morbidity and mortality in out-of-hospital cardiac arrests.

Hypothesis Alternating intrathoracic pressure by means of a chest cuirass can cause perfusion and ventilation equal to or better than standard cardiopulmonary resuscitation (CPR) for humans in cardiac arrest. Design Nonrandomized, nonblinded, crossover pilot study. Setting Large urban emergency department. Subjects Five adult normothermic, nontraumatic, out-of-hospital cardiac arrest patients unresponsive to standard advanced cardiac life support. Method Right atrial and aortic catheters were inserted for pressure measurement and blood gas analysis while the patient was receiving standard CPR by a pneumatic compression device (Thumper). The Thumper was then replaced by a chest cuirass (Hayek Oscillator). Pressure and blood gas measurements were then repeated. Results The coronary perfusion pressure increased from − 1.2 ± 8.6 mm Hg to 6.2 ± 6.9 mm Hg for a mean change of 7.4 ± 3.1 mm Hg (p = 0.006). The compression phase gradient increased 10.0 ± 21.9 mm Hg (p = 0.364). The venous to arterial Pco 2 gradient decreased 44.5 ± 32.3 mm Hg (p = 0.070). The oxygen extraction ratio increased 1.6 ± 9.4 percent (p = 0.761). The mean arterial Po 2 and Pco 2 changed from 252 to 240 mm Hg (p = 0.836) and from 53 to 66 (p = 0.172) mm Hg, respectively. Conclusion The Hayek Oscillator chest cuirass produced a significant improvement in the coronary perfusion pressure. There was a trend for improved systemic perfusion as indicated by an improved compression phase gradient and venous to arterial Pco 2 gradient, although this was not supported by the lack of improvement in the oxygen extraction ratio. The cuirass also adequately oxygenates and ventilates unassisted by positive pressure ventilation.

Oxygen consumption (VO2) has been shown to be decreased after acute myocardial infarction (AMI) complicated by cardiogenic shock.To evaluate early measurement of VO2 by indirect calorimetry after an uncomplicated AMI (UAMI).Prospective nonrandomized case study.Emergency department of a large urban hospital.Twenty-six consecutive patients presenting with confirmed UAMI. VO2 was measured by indirect calorimetry (Deletrac, Datex Ins,) which is noninvasive. All patients received buccal or intravenous nitroglycerin and thrombolytic therapy, and none received opiates before VO2 measurement.Two groups of patients were identified by subsequent development of cardiogenic shock. Group 1 did not develop cardiogenic shock, and group 2 developed shock within 24 h of admission. Group 1 (n = 22) had a significantly higher VO2 compared to group 2 (n = 4), mean 154(SD 25) vs mean 100(SD 13) ml/min.m2, p0.002. Group 1 had a significantly higher increase in basal metabolic rate than group 2, mean 30 percent (SD 11) vs mean 10(SD 15) percent, p0.007. There was no significant difference in age, heart rate (HR), shock index (SI), or rate-pressure product (RPP) between groups 1 and 2. All patients in group 2 developed cardiogenic shock despite thrombolytic therapy, and two died within 24 h of admission.VO2 is increased in UAMI and represents increased metabolic demands of peripheral tissues and not cardiac oxygen uptake. A reduction in VO2 (100 ml/min.m2) after AMI may be an early predictor of subsequent development of cardiogenic shock. Measurement of VO2 in UAMI by indirect calorimetry in the emergency department may be of value to identify patients at high risk and could influence their management.

Background Supranormal mixed venous oxygen saturation (mixed venous hyperoxia), although reported, has never been characterized in humans resuscitated from cardiac arrest (postarrest cardiogenic shock). By contrast, cardiogenic shock without cardiopulmonary arrest (primary cardiogenic shock) is accompanied by mixed venous hypoxia under similar conditions of low oxygen delivery (Do 2 ). The appearance of mixed venous hyperoxia indicates an excessive supply relative to demand in perfused tissue or cellular impairment of oxygen utilization, ie , low systemic oxygen consumption (Vo 2 ). Failure to improve Vo, has been associated with a poor outcome in other shock states. Study Objective This study evaluates the clinical significance of mixed venous hyperoxia and its implications for impaired systemic oxygen utilization. The oxygen transport patterns in surviving and nonsurviving cardiac arrest patients are compared for their prognostic and therapeutic implications. Study Design Consecutive, nonrandomized series. Setting Large urban emergency department (ED). Participants: Adult normothermic, nontraumatic out-of-hospital cardiac arrest patients presenting to the ED who develop a return of spontaneous circulation (ROSC). Interventions On arrival to the ED, a fiberoptic catheter was placed in the central venous position for continuous central venous oxygen saturation monitoring (ScvO 2 ). A proximal aortic catheter was placed via the femoral artery for blood pressure monitoring. Upon ROSC, the fiberoptic catheter was advanced to the pulmonary artery. Mean arterial pressure (MAP), cardiac index (CI), Vo 2 , Do 2 , systemic oxygen extraction ratio (OER), and systemic vascular resistance index (SVRI-dynes·s/cm 5 ·m 2 ) were measured immediately and every 30 min. The duration of cardiac arrest (DCA) in minutes and amount of epinephrine (milligrams) administered during ACLS was recorded. Measurements and Results Twenty-three patients were entered into the study. Survivors (living more than 24 h) and nonsurvivors (living less than 24 h) were compared. Conclusions These findings indicate an impairment of systemic oxygen utilization in postarrest cardiogenic shock patients. In spite of a lower Do, than survivors, the OER in nonsurvivors remained lower than expected. Venous hyperoxia is a clinical manifestation of this derangement. Epinephrine dose may have a causal relationship. The inability to attain a Vo, of greater than 90 ml/min·m 2 after the first 6 h of aggressive therapy was associated with a 100 percent mortality in 24 h.

We measured aortic pressure during clinically apparent cardiac electromechanical dissociation (EMD). Patients with pulse pressures were designated as having pseudo-EMD; those without, as having true EMD. Of the 200 patients studied, 54 presented with EMD, and 40 others developed it during resuscitation. Of the 94 with EMD, 39 were found to have pseudo-EMD. We compared the two types of EMD for electrocardiographic duration, return of palpable pulses, and response to standard- and high-dose epinephrine. The mean resting aortic pressure was 18 ± 11 mm Hg in patients with true EMD and 28 ± 11 mm Hg in those with pseudo-EMD. The mean pulse pressure in patients with pseudo-EMD was 6.3 ±3.5 mm Hg. Patients with pseudo-EMD had a higher proportion of witnessed arrests, higher PaO 2 , and lower PaCO 2 than patients with true EMD. Patients with pseudo-EMD had shorter QR and QRS durations than patients with true EMD. They had a better response to standard- and high-dose epinephrine than patients with true EMD. Many patients diagnosed clinically to be in EMD have mechanical cardiac activity; this should be considered when interpreting the results of cardiac arrest research.

Studies of acute myocardial infarction, trauma, and stroke have been translated into improved outcomes by earlier diagnosis and application of therapy at the most proximal stage of hospital presentation. Most therapies for these diseases are instituted prior to admission to an ICU; this approach to the sepsis patient has been lacking. In response, a trial comparing early goal-directed therapy (EGDT) vs standard care was performed using specific criteria for the early identification of high-risk sepsis patients, verified definitions, and a consensus-derived protocol to reverse the hemodynamic perturbations of hypovolemia, vasoregulation, myocardial suppression, and increased metabolic demands. Five years after the EGDT publication, there has been much discussion generated with regard to the concepts of EGDT, as well as debate fueled regarding diagnostic and therapeutic interventions. However, during this time period further investigations by the primary investigators and others have brought additional contemporary findings. EGDT modulates some of the components of inflammation, as reflected by improved organ function. The end points used in the EGDT protocol, the outcome results, and the cost-effectiveness have subsequently been externally validated, revealing similar or even better findings than those from the original trial. Although EGDT is faced with challenges, a coordinated approach to sepsis management is necessary to duplicate the progress in outcomes seen in patients with conditions such as acute myocardial infarction, stroke, and trauma.