Trial design for assessing analytical and clinical performance of high-sensitivity cardiac troponin I assays in the United States: The HIGH-US study.

BACKGROUND: High-sensitivity cardiac troponin I (hs-cTnI) assays have been developed that quantify lower cTnI concentrations with better precision versus earlier generation assays. hs-cTnI assays allow improved clinical utility for diagnosis and risk stratification in patients presenting to the emergency department with suspected acute myocardial infarction. We describe the High-Sensitivity Cardiac Troponin I Assays in the United States (HIGH-US) study design used to conduct studies for characterizing the analytical and clinical performance of hs-cTnI assays, as required by the US Food and Drug Administration for a 510(k) clearance application. This study was non-interventional and therefore it was not registered at clinicaltrials.gov. METHODS: We conducted analytic studies utilizing Clinical and Laboratory Standards Institute guidance that included limit of blank, limit of detection, limit of quantitation, linearity, within-run and between run imprecision and reproducibility as well as potential interferences and high dose hook effect. A sample set collected from healthy females and males was used to determine the overall and sex-specific cTnI 99th percentile upper reference limits (URL). The total coefficient of variation at the female 99th percentile URL and a universally available American Association for Clinical Chemistry sample set (AACC Universal Sample Bank) from healthy females and males was used to examine high-sensitivity (hs) performance of the cTnI assays. Clinical diagnosis of enrolled subjects was adjudicated by expert cardiologists and emergency medicine physicians. Assessment of temporal diagnostic accuracy including sensitivity, specificity, positive predictive value, and negative predictive value were determined at presentation and collection times thereafter. The prognostic performance at one-year after presentation to the emergency department was also performed. This design is appropriate to describe analytical characterization and clinical performance, and allows for acute myocardial infarction diagnosis and risk assessment.

Ninety-minute exclusion of acute myocardial infarction by use of quantitative point-of-care testing of myoglobin and troponin I.

BACKGROUND: Diagnostic strategies with ECG and serum cardiac markers have been used to rule out acute myocardial infarction in 6 to 12 hours. The present study evaluated whether a multimarker strategy that used point-of-care measurement of myoglobin, creatine kinase (CK)-MB, and troponin I could exclude acute myocardial infarction in

1997 National Asthma Education and Prevention Program guidelines: a practical summary for emergency physicians.

Numerous clinical guidelines have been promoted to help improve the management of acute injury and illness. In November 1997, the National Asthma Education and Prevention Program released the final version of its comprehensive second Expert Panel Report, designed to distill scientific advances in asthma care and provide a set of practical tools to help guide clinician and patient decisions. The panel's recommendations for acute asthma care stress the use of the objective measures of pulmonary function to assess severity, aggressive inhaled beta 2-agonist therapy, early systemic corticosteroid administration, and early disposition decisions. This article provides a focused overview of the 146-page document and highlights aspects of the new guidelines of particular importance to emergency physicians.

Advances, opportunities, and the new asthma guidelines.

A main tenet of the National Asthma Education and Prevention Program's approach is to integrate proper management of acute asthma into overall asthma care. Accordingly, we maintain that emergency physicians should be aware of emerging chronic management strategies, especially newer treatment regimens, so as to understand pre-ED treatments, provide optimum ED care, and make appropriate prescriptions and referral on discharge. This commentary discusses limitations to the new guidelines and identifies important areas for further study.

Emergency department cardiopulmonary bypass in the treatment of human cardiac arrest.

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.

Resuscitation of the critically ill in the ED: responses of blood pressure, heart rate, shock index, central venous oxygen saturation, and lactate.

To describe the simultaneous responses of systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial blood pressure (MAP), heart rate (HR), shock index (SI = HR/SBP), central venous oxyhemoglobin saturation (ScvO2), and arterial blood lactate concentration (Lact) to resuscitation of critically ill patients in the emergency department (ED), an observational descriptive study was conducted in the ED of an urban teaching hospital. Thirty- six patients admitted from the ED to the medical intensive care unit were studied. Vital signs were measured immediately on arrival to the ED (phase 1). After initial resuscitation and stabilization, ie, HR between 50 and 120 beats/min and MAP between 70 and 110 mm Hg (phase 2), ScvO2 and Lact were measured and additional therapy was given in the ED to increase ScvO2 to > 65% and decrease Lact to < 2 mmol/L, if needed (phase 3). SBP, DBP, MAP, HR. SI, ScvO2, and Lact were measured. Initial resuscitation increased SBP from 103 +/- 39 to 118 +/- 29 mm Hg (P < .05) and MAP from 67 +/- 35 to 82 +/- 22 mm Hg (P < .05) but did not affect DBP (53 +/- 35 to 63 +/- 22 mm Hg, P = NS), HR (110 +/- 26 to 110 +/- 22 beats/min, P = NS) or SI (from 1.3 +/- 0.7 to 1.0 +/- 0.3, P =NS) from phase 1 to phase 2. ScvO2 remained < 65% and/or Lact > 2.0 mmol/L in 31 of 36 patients at phase 2, and additional therapy was required. Lact was decreased (from 4.6 +/- 3.8 to 2.6 +/- 2.5 mmol/L, P < .05) and ScvO2 was increased (from 52 +/- 18 to 65 +/- 13%, P < .05) without significant additional changes in SBP, DBP, MAP, HR, or SI at phase 3. The in-hospital mortality was 14% for this group of patients. It was concluded that additional therapy is required in the majority of critically ill patients to restore adequate systemic oxygenation after initial resuscitation and hemodynamic stabilization in the ED. Additional therapy to increase ScvO2 and decrease Lact may not produce substantial responses in SBP, DBP, MAP, HR, and SI. The measurement of ScvO2 and Lact can be utilized to guide this phase of additional therapy in the ED.

A technique revisited: hemodynamic comparison of closed- and open-chest cardiac massage during human cardiopulmonary resuscitation.

OBJECTIVE: To compare the hemodynamics of closed-chest cardiac massage vs. open-chest cardiac massage in patients resuscitated from cardiac arrest that occurred outside of the hospital. DESIGN: Prospective, non-outcome, case series. SETTING: Large urban emergency department. PATIENTS: Ten adult, normothermic, nontraumatic, out-of-hospital, cardiac arrest patients who failed advanced cardiac life support (ACLS) therapy. INTERVENTIONS: Patients presenting to the hospital in cardiac arrest were managed according to the ACLS protocol at the clinician's discretion. Proximal aortic and central venous pressure catheters were placed to measure arteriovenous compression- and relaxation-phase pressure gradients. After 5 mins of baseline measurements during closed-chest cardiac massage, patients underwent a left lateral thoracotomy, and open-chest cardiac massage was performed for 5 mins. MEASUREMENTS AND MAIN RESULTS: The mean coronary perfusion pressure and compression-phase pressure gradients were 7.3 +/- 5.7 and 6.2 +/- 5.4 mm Hg, respectively, during closed-chest cardiac massage, while increasing to 32.6 +/- 17.8 and 32.6 +/- 29.9 mm Hg, respectively, during open-chest cardiac massage. The differences between both measurements were statistically significant (p < .05). CONCLUSIONS: Open-chest cardiac massage is superior to closed-chest cardiac massage in providing relaxation-phase and compression-phase pressure gradients during cardiac arrest in patients failing current ACLS protocols. During open-chest cardiac massage, all patients exceeded the minimum coronary perfusion pressure of 15 mm Hg, which is recommended to obtain a return of spontaneous circulation. Further outcome studies are needed to determine the timeliness and appropriate indications for open-chest cardiac massage.

Biphasic extrathoracic pressure CPR. A human pilot study.

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 PCO2 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 PO2 and PCO2 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 PCO2 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.

High atrial natriuretic peptide concentrations blunt the pressor response during cardiopulmonary resuscitation in humans.

OBJECTIVE: To determine the relationship of circulating atrial natriuretic peptide concentrations to the pressor response to high-dose epinephrine in patients undergoing cardiopulmonary resuscitation (CPR) for cardiac arrest. DESIGN: Prospective study. PATIENTS: Fourteen normothermic, adult, prehospital and emergency department patients suffering unexpected cardiac arrest. INTERVENTION: Patients received high-dose epinephrine (0.2 mg/kg) i.v. when standard advanced cardiac life support (including multiple 1-mg dosages of epinephrine) failed to result in return of spontaneous circulation. MEASUREMENTS AND MAIN RESULTS: Cardiac arrest patients were separated into those patients with and without detectable serum atrial natriuretic peptide concentrations, and were termed the "low atrial natriuretic peptide" and "high atrial natriuretic peptide" groups, respectively. Their aortic pressure response to high-dose (0.02 mg/kg) epinephrine was compared. The proportion with positive assays was compared with a group of healthy control subjects. Fourteen patients were studied. Eight patients had low serum atrial natriuretic peptide concentrations and six patients had high circulating atrial natriuretic peptide concentrations. The mean concentration in the high atrial natriuretic peptide group was 151 +/- 82 pg/mL. The proportion with positive assays (six of 14 patients) was greater than in the group in spontaneous circulation (three of 29 patients) (p = .002). The maximal increase in the aortic relaxation-phase pressures after high-dose epinephrine was 9 +/- 7 torr (1.2 +/- 0.9 kPa) in the low atrial natriuretic peptide group and 0 +/- 5 torr (0 +/- 0.7 kPa) in the high atrial natriuretic peptide group (p = .03). The maximal increase in the aortic compression pressures after high-dose epinephrine was 17 +/- 13 torr (2.3 +/- 1.7 kPa) in the low atrial natriuretic peptide group and 2 +/- 10 torr (0.3 +/- 1.3 kPa) in the high atrial natriuretic peptide group (p = .03). Thus, pressor responses after high-dose epinephrine administration were observed in patients in the low atrial natriuretic peptide group, but this response was absent in patients in the high atrial natriuretic peptide group. CONCLUSIONS: Cardiac arrest patients receiving CPR have higher circulating atrial natriuretic peptide concentrations than healthy subjects. High serum atrial natriuretic peptide concentrations may antagonize the vasopressor response to epinephrine. Blocking this effect of atrial natriuretic peptide may improve outcomes in patients suffering cardiac arrest.

A characterization of hypothalamic-pituitary-adrenal axis function during and after human cardiac arrest.

OBJECTIVE: This study characterizes hypothalamic-pituitary-adrenal axis function during cardiopulmonary arrest and after return of spontaneous circulation. DESIGN: Prospective case series. SETTING: A large urban emergency department and intensive care unit over an 8-month period. PATIENTS: Two hundred five adult patients presenting in cardiopulmonary arrest to an urban emergency department. Three patients known to be taking corticosteroids were excluded from the study. MEASUREMENTS AND MAIN RESULTS: Cortisol concentrations were measured before and after advanced cardiac life support and for five consecutive hours after return of spontaneous circulation. Adrenocorticotropic hormone (ACTH) concentrations were measured before advanced cardiac life support and when the cosyntropin stimulation tests were performed 6 and 24 hrs after the return of spontaneous circulation. The mean initial serum cortisol concentration was 32.0 +/- 33.1 micrograms/dL (882.9 +/- 913.2 nmol/L). Fifty-three percent of patients had cortisol concentrations of < 20 micrograms/dL (< 552 nmol/L) at the end of cardiac arrest. Among 44 patients who achieved return of spontaneous circulation, 98% had initial cortisol concentrations of > 10 micrograms/dL (> 276 nmol/L) and 73% of patients had initial cortisol concentrations of > 20 micrograms/dL (> 552 nmol/L). Mean serum cortisol concentrations increased significantly (p = .0001) from 1 to 6 hrs after return of spontaneous circulation and decreased significantly (p = .03) from 6 to 24 hrs. A serum cortisol concentration of < 30 micrograms/dL (< 828 nmol/L) was associated with a 96% and 100% mortality rate at 6 and 24 hrs, respectively. Mean ACTH concentrations were increased without a significant difference between the initial and 6-hr concentrations. Mean ACTH concentrations decreased between 6 and 24 hrs (p = .06). There were no significant responses to the cosyntropin stimulation at 6 and 24 hrs. CONCLUSIONS: Cortisol concentrations after out-of-hospital cardiac arrest are lower than those concentrations reported in other stress states. There is an association between cortisol concentrations and short-term survival after cardiac arrest. Survivors have a significantly greater increase in serum cortisol concentrations than nonsurvivors during the first 24 hrs. Lower than expected cortisol concentrations for the extreme stress of cardiac arrest may have pathologic significance in the hemodynamic instability seen after return of spontaneous circulation. The etiology of the low cortisol concentrations may be primary adrenal dysfunction.

Simultaneous radial, femoral, and aortic arterial pressures during human cardiopulmonary resuscitation.

OBJECTIVE: To examine the validity of interchanging arterial sites and their responses to graded doses of epinephrine during human cardiopulmonary resuscitation (CPR). DESIGN: Consecutive case series. SETTING: Large, urban Emergency Department. PATIENTS: Adult, normothermic, nonhemorrhagic cardiac arrest patients. INTERVENTIONS: While receiving advanced cardiac life support, patients received right atrial (n = 40), aortic (n = 40), radial (n = 40), and femoral (n = 17) artery catheters. Pressures were measured simultaneously at baseline, after 0.01 mg/kg and 0.2 mg/kg of epinephrine. MEASUREMENTS AND MAIN RESULTS: The mean aortic compression-phase pressure was 9.3 +/- 10 (SD), 8.1 +/- 11, and 4.4 +/- 9.5 mm Hg higher than radial artery pressure at baseline, after 0.01 mg/kg, and 0.2 mg/kg of epinephrine, respectively (all statistically significant). When compared with the femoral artery at the same time points, the mean aortic compression-phase pressure was also 3.0 +/- 6.8, 1.9 +/- 8, and 0.6 +/- 7.7 mm Hg higher, respectively (none statistically significant). The aortic relaxation-phase pressure was 1.3 +/- 3.6, 1.1 +/- 3.8, and 1.6 +/- 2.5 mm Hg lower than the radial artery at baseline, after 0.01 mg/kg and 0.2 mg/kg of epinephrine, respectively (all statistically significant). When compared with the femoral artery at the same time points, the aortic relaxation-phase pressure was 0.6 +/- 2.0, 0.3 +/- 3.3, and 0.3 +/- 2.4 mm Hg lower, respectively (none statistically significant). CONCLUSIONS: Radial artery relaxation-phase pressure, although statistically higher, correlated with aortic relaxation-phase pressure. Femoral artery relaxation-phase pressure was not statistically different from aortic relaxation-phase pressure. Aortic pressure was statistically higher and had a lower correlation with radial artery pressures during compression phase. The aortic to radial artery and aortic to femoral artery compression-phase gradients abated with increasing doses of epinephrine therapy. Caution must be used when substituting compression-phase pressure obtained at radial or femoral artery sites for aortic pressure during human CPR. Coronary artery perfusion pressures obtained with radial and femoral arteries correlate with aortic pressure when measuring the response to vasopressor therapy during CPR when an interpretable waveform exists.

Functional responses to extremely high plasma epinephrine concentrations in cardiac arrest.

OBJECTIVE: To evaluate the action of high-dose epinephrine by measuring simultaneously its vasopressor and norepinephrine releasing effects in humans during cardiac arrest. DESIGN: A prospective study on consecutive patients admitted with cardiac arrest. SETTING: Emergency Department in a large, urban hospital. PATIENTS: Eighteen patients with out-of-hospital cardiac arrest undergoing cardiopulmonary resuscitation (CPR). INTERVENTIONS: Catheterization of both the aorta and right atrium for the recording of pressure and collection of blood samples. Throughout the study period (12.5 mins), 18 patients received epinephrine at both the standard dose (1 mg, approximately 0.015 mg/kg) and high dose (0.2 mg/kg). Blood samples were drawn five times, every 2.5 mins. MEASUREMENTS AND MAIN RESULTS: Plasma epinephrine and norepinephrine concentrations; aorta, right atrial, and coronary perfusion pressures. Epinephrine concentrations (normal at rest = 160 +/- 10 [SEM] pmol/L) were increased at the time of the first sample (2.5 mins) by approximately 3,000-fold (to approximately 0.5 mumol/L), and, increased further to 12,000-fold (approximately 2.0 mumol/L) during the study. Aortic pressure increased from 20 +/- 3 to 28 +/- 3 mm Hg (p < .001), and coronary perfusion pressure increased from 4 +/- 3 to 10 +/- 3 mm Hg (p < .001). Simultaneous plasma norepinephrine concentrations were 30-fold higher than the normal resting value of 1.30 +/- 0.04 nmol/L, and increased by 90-fold during the study (p < .001). The spectral distributions of the individual correlations between plasma epinephrine and norepinephrine concentrations were segregated into high correlations (r > .83) in 12 of 18 patients and low r values (r = .29 to .79) in the remaining six patients. The distribution of the correlations was nonuniform by the Kolmogorov-Smirnov goodness-of-fit test with p < .001; this profile suggests that norepinephrine responsiveness to epinephrine can separate two populations, one of which (r > .83) would have preserved viability of the corresponding epinephrine receptors. The correlations between plasma epinephrine concentrations and coronary perfusion pressures were distributed more evenly, also in a nonuniform pattern (p < .02 by Kolmogorov-Smirnov goodness-of-fit test) and the relationship between the two sets of correlations was not significant. CONCLUSIONS: Despite the very high prevailing plasma epinephrine concentrations during cardiac arrest, further epinephrine increases still elicit biological responses. The present work provides physiologic support for the use of large doses of epinephrine during the course of CPR.

Venous hyperoxia after cardiac arrest. Characterization of a defect in systemic oxygen utilization.

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 (DO2). 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 (VO2). Failure to improve VO2 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 (ScvO2). 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), VO2, DO2, systemic oxygen extraction ratio (OER), and systemic vascular resistance index (SVRI-dynes.s/cm5.m2) 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 DO2 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 VO2 of greater than 90 ml/min.m2 after the first 6 h of aggressive therapy was associated with a 100 percent mortality in 24 h.

Continuous central venous oximetry and shock index in the emergency department: use in the evaluation of clinical shock.

Initial therapy of shock in the emergency department (ED) emphasizes the normalization of physiologic variables such as heart rate (HR), mean arterial pressure (MAP), and central venous pressure (CVP) rather than restoration of adequate tissue oxygenation. After hemodynamic stabilization of MAP, CVP, and HR, the authors examined tissue oxygenation as indicated by continuous central venous oximetry (SCVO2), lactic acid concentration, and shock index (SI). Sixteen consecutive nonrandomized patients presenting to the ED of a large urban hospital in shock (MAP < 60 mm Hg, HR > 120 beats/min, and altered sensorium) were initially resuscitated with fluid, blood, inotropes, and/or vasoactive drug therapy to normalize MAP, CVP, and HR. In addition, SCVO2, arterial lactate concentration, and SI were measured after completion of resuscitation in the ED. Eight patients (group no. 1) had inadequate tissue oxygenation reflected by low SCVO2 (less than 65%). Four patients in group no. 1 had elevated arterial lactic acid concentration. All group no. 1 patients had an elevated SI (> 0.7) suggesting persistent impairment of left ventricular stroke work. Eight patients (group no. 2) had normal or elevated SCVO2 (> 65%). In group no. 2, arterial lactic acid concentration was elevated in six and SI in seven patients. Normalization of hemodynamic variables does not adequately reflect the optimal endpoint of initial therapy in shock in the ED. Most (94%) of these patients continue to have significant global ischemia and cardiac dysfunction as indicated by reduced SCVO2 and elevated lactic acid concentration and SI. Systemic tissue oxygenation should be monitored and optimized in the ED in these critically ill patients.(ABSTRACT TRUNCATED AT 250 WORDS)

The clinical implications of continuous central venous oxygen saturation during human CPR.

STUDY OBJECTIVE: The purpose of this study was to observe, measure, and describe the changes in central venous oxygen saturation during CPR and immediately after return of spontaneous circulation. It also was to examine the clinical utility of continuous central venous oxygen saturation monitoring as a indicator of return of spontaneous circulation during CPR in human beings. DESIGN AND SETTING: Eight-month, prospective, non-outcome, observational, nonrandomized case series in the ED of a large urban hospital. TYPES OF PATIENTS: Adult normothermic, nontraumatic, out-of-hospital cardiopulmonary arrests. INTERVENTIONS: All patients were managed according to advanced cardiac life support guidelines. A proximal aortic and double-lumen central venous catheter was placed. Central venous oxygen saturation was measured continuously spectrophotometrically with a fiberoptic catheter in the central venous location. MEASUREMENTS: Aortic blood pressure and central venous oxygen saturation were simultaneously measured throughout each resuscitation. Return of spontaneous circulation was defined as a systolic blood pressure of more than 60 mm Hg for more than five minutes. RESULTS: One hundred patients who experienced 68 episodes of cardiac arrest were studied. Patients with return of spontaneous circulation had a higher initial and statistically higher mean and maximal central venous oxygen saturation than those without return of spontaneous circulation (P = .23, .0001, and .0001, respectively; P less than .05 is significant). No patient attained return of spontaneous circulation without reaching a central venous oxygen saturation of at least 30%. Only one of 68 episodes of return of spontaneous circulation was attained without reaching a central venous oxygen saturation of at least 40%. A central venous oxygen saturation of greater than 72% was 100% predictive of return of spontaneous circulation. CONCLUSION: Continuous central venous oxygen saturation monitoring can serve as a reliable indicator of return of spontaneous circulation during CPR in human beings.

Aortic pressure during human cardiac arrest. Identification of pseudo-electromechanical dissociation.

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 PaO2, and lower PaCO2 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.