Search

Background: Evaluate the association between serum urea at admission and during hospital stay with return of spontaneous circulation (ROSC) and in-hospital mortality in patients with in-hospital cardiac arrest (IHCA)., Methods: This retrospective study included patients over 18 years with IHCA attended from May 2018 to December 2022. The exclusion criteria were the absence of exams to calculate delta urea and the express order of "do-not-resuscitate". Data were collected from the electronic medical records. Serum admission urea and urea 24 hours before IHCA were also collected and used to calculate delta urea., Results: A total of 504 patients were evaluated; 125 patients were excluded due to the absence of variables to calculate delta urea and 5 due to "do-not-resuscitate" order. Thus, we included 374 patients in the analysis. The mean age was 65.0 ± 14.5 years, 48.9% were male, 45.5% had ROSC, and in-hospital mortality was 91.7%. In logistic regression models, ROSC was associated with lower urea levels 24 hours before IHCA (OR: 0.996; CI95%: 0.992-1.000; p: 0.032). In addition, increased levels of urea 24 hours before IHCA (OR: 1.020; CI95%: 1.008-1.033; p: 0.002) and of delta urea (OR: 1.001; CI95%: 1.001-1.019; p: 0.023) were associated with in-hospital mortality. ROC curve analysis showed that the area under the ROC curve for mortality prediction was higher for urea 24 hours before IHCA (Cutoff > 120.1 mg/dL) than for delta urea (Cutoff > 34.83 mg/dL)., Conclusions: In conclusion, increased serum urea levels during hospital stay were associated with worse prognosis in IHCA., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.)

The aims of this review are to demonstrate that the changes in coagulation and fibrinolysis observed in cardiac arrest and resuscitation can be recognized as disseminated intravascular coagulation (DIC), and to discuss the probability of DIC being a therapeutic target. The appearance of triggers of DIC, such as damage-associated molecular patterns, inflammatory cytokines, and adrenaline, is associated with platelet activation, marked thrombin generation and fibrin formation, insufficient anticoagulation pathways, and increased fibrinolysis by tissue-type plasminogen activator, followed by the suppression of fibrinolysis by plasminogen activator inhibitor-1, in patients with cardiac arrest and resuscitation. Simultaneous neutrophil activation and endothelial injury associated with glycocalyx perturbation have been observed in these patients. The degree of these changes is more severe in patients with prolonged precardiac arrest hypoxia and long no-flow and low-flow times, patients without return of spontaneous circulation, and non-survivors. Animal and clinical studies have confirmed decreased cerebral blood flow and microvascular fibrin thrombosis in vital organs, including the brain. The clinical diagnosis of DIC in patients with cardiac arrest and resuscitation is associated with multiple organ dysfunction, as assessed with the sequential organ failure assessment score, and increased mortality. This review confirms that the coagulofibrinolytic changes in cardiac arrest and resuscitation meet the definition of DIC proposed by the ISTH, and that DIC is associated with organ dysfunction and poor patient outcomes. This evidence implies that established DIC should be considered to be one of the main therapeutic targets in post-cardiac arrest syndrome., (© 2019 International Society on Thrombosis and Haemostasis.)

Cardiac arrest (CA) often results in hemodynamic and metabolic compromise with associated poor prognosis. Therapeutic hypothermia (TH) has become the standard of care for CA survivors, decreasing reperfusion injury and intercellular acid-base disturbances, with improved neurologic outcomes. These benefits are realized despite a mild acidosis that can potentially occur during TH. By contrast, the severity of acidosis after return of spontaneous circulation (ROSC) must be monitored carefully and managed appropriately. Bicarbonate should be used only in case of severe acidosis and as a continuous infusion. The blood gas samples are usually warmed to 37 °C before analysis; hence, it is worth noting that the blood gas values are temperature dependent. Therefore, a calculated correction for values may be necessary., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

Cardiac arrest (CA) is a sudden, severe event that causes a cascade of metabolic and electrolyte disturbances throughout the body triggered by a loss of cardiac output. Metabolic disturbances are primarily in the form of mixed metabolic and respiratory acidosis; dysglycaemia; and states of deficiency or excess in potassium, calcium, magnesium and lactate. It is known that persistent metabolic disturbances are associated with poor patient outcome following resuscitation from CA, but this might simply be a reflection of the severity of illness. Moreover, contemporary evidence for the management of metabolic disturbances to improve outcomes in these patients is scarce. Moreover, metabolic disturbances during the early post-resuscitation period remain poorly understood in terms of severity, duration and the influence of their post-resuscitation care and treatment on outcome. Although sufficient data suggest that extreme metabolic disturbances such as hypoglycaemia, severe hyperglycaemia, severe hypokalaemia and hyperkalaemia and hypomagnesaemia likely have a devastating effect and should be avoided, randomised controlled trial evidence is clearly need for the management of metabolic and electrolyte derangements in resuscitated CA patients., (Copyright © 2015. Published by Elsevier Ltd.)

Objective: To describe the relationship between circulating resistin levels and cardiovascular diseases (CVD) and all-cause death in a multi-ethnic cohort., Methods and Results: We studied 1913 participants from the Multi-Ethnic Study of Atherosclerosis with measurements of plasma resistin levels. Absolute proportions experiencing new-onset atrial fibrillation (AF), atherosclerotic CVD (myocardial infarction, angina, resuscitated cardiac arrest, stroke), heart failure (HF), and all-cause death were calculated for each quartile of resistin. We used adjusted Cox proportional regression modeling resistin as a continuous variable per standard deviation of log-transformed resistin and secondarily as a categorical variable using resistin quartiles. Results were stratified by sex and race/ethnicity. The mean age of the population was 64.5 ± 10 years with half being female and a median resistin concentration of 15.1 ng/mL (11.9-19.1). Mean follow-up time was 7.2 ± 1.8 years. There was a graded increase in the occurrence of all outcomes across increasing quartiles of resistin. Modeled as a continuous variable, after adjustment for anthropomorphic measures, traditional risk factors, markers of inflammation, and other adipokines, significant associations were noted for HF (HR 1.4, CI 1.0-2.0), hard and all CVD (HR 1.3, 1.1-1.7 and 1.3, 1.1-1.6, respectively), and CHD (HR 1.31, 1.0-1.6), but not for AF or death. Significant interaction terms were noted between resistin and race, with Hispanic race/ethnicity showing the strongest relationship between resistin and outcomes., Conclusions: In an ethnically diverse population without known CVD at baseline, there was a strong, independent association between higher resistin levels and incident CVD, CHD and HF., (Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.)

Current guidelines suggest that patients undergoing percutaneous coronary intervention (PCI) receive dual-antiplatelet therapy. There are limited data on the pharmacodynamics of P2Y12 inhibitors in patients with cardiac arrest and return of spontaneous circulation (ROSC) undergoing PCI and therapeutic hypothermia (TH). Accordingly, we compared inhibition of platelet reactivity in patients undergoing TH receiving clopidogrel or ticagrelor. Notably, clopidogrel was ineffective in lowering platelet reactivity, with ticagrelor providing a more rapid (within 4 hours) and sustained reduction (6 days) in platelet reactivity. Pending outcome-based studies, ticagrelor should be used preferentially in patients who have ROSC and are undergoing PCI and TH., (Copyright © 2014 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.)

Background: The aim of this study is to evaluate the diagnostic accuracy of the cardiac injury markers troponin (TNT), creatine kinase (CK) and creatine kinase-MB (CK-MB) to diagnose or exclude acute myocardial infarction after cardiac arrest., Methods: 226 patients who underwent diagnostic coronary angiography after sudden cardiac arrest were analyzed retrospectively. Levels of TNT, CK and CK-MB on admission and 6h, 24h and 36 h later were retrieved from the files and compared with the results of coronary angiography., Results: Acute myocardial infarction (AMI) as well as non-AMI patients showed increasing levels of TNT and CK after resuscitation, although the AMI group showed significantly higher TNT and CK levels. Receiver operator curves were calculated to determine the diagnostic precision of TNT, CK and CK-MB to differentiate AMI and non-AMI patients. All analyzed markers yielded mediocre diagnostic precision with an area under the ROC curve of 0.7020, 0.6802 and 0.6508 for 6h TNT, CK and CK-MB, respectively. Applying a modified cut-off of 1 μg/l the 6h TNT measurement had a sensitivity of 70.9% and specificity of 61.2% to diagnose AMI after cardiac arrest. Using CK 800 U/l as cut-off level resulted in a sensitivity of 62.5% and specificity of 73.7%, CK-MB levels higher than 100 U/l yielded a sensitivity of 58.8% and specificity of 72.7%., Conclusion: Cardiac injury markers cannot be used to reliably diagnose or rule out AMI after resuscitation. Consequently we propose that indication for coronary angiography should be extended to all patients without a certain alternative diagnosis explaining the occurrence of cardiac arrest., (Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.)

Background: In cohort studies, elevated levels of plasma nonesterified free fatty acids (NEFAs) have been associated with increased risk of sudden cardiac death (SCD) in men, but blood samples were drawn several years before SCD., Objective: To confirm this relationship by evaluating levels of plasma NEFAs at the time of the SCD event in a group of both men and women., Methods: From the ongoing Oregon Sudden Unexpected Death Study, we compared levels of plasma NEFAs in 149 SCD cases presenting with ventricular fibrillation (mean age 64 ± 12 years; 73% men) and 149 age- and sex-matched controls with coronary artery disease. Plasma was processed from blood drawn at the time of arrest (cases) and at a routine visit (controls). The levels of plasma NEFAs were compared after categorizing into quartiles on the basis of control values. Conditional logistic regression was used to predict adjusted odds ratio for SCD associated with plasma NEFA levels per increased quartile., Results: The plasma NEFA levels were significantly higher in SCD cases than in controls (median 0.39 mmol/L [interquartile range 0.28-0.60 mmol/L] vs 0.32 mmol/L [interquartile range 0.20-0.49 mmol/L]; P = .002). There were no significant differences in body mass index, smoking, and diabetes. The odds ratio for SCD was 1.42 (95% confidence interval 1.14-1.78) per quartile increase in the plasma NEFA level (P = .002). Individuals with plasma NEFA levels above the prespecified cutoff point of 0.32 mmol/L were at increased risk of SCD (odds ratio 2.00; 95% confidence interval 1.20-3.34; P = .008)., Conclusion: These findings strengthen the role of plasma NEFA as a potential biomarker for the assessment of SCD risk., (Copyright © 2014 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.)

Background: Neurofilament light chain (NF-L) is the major intermediate filament specifically expressed in neurons and their axons. No data are available concerning serum levels of NF-L after global cerebral ischemia due to cardiac arrest. To find a specific neuronal marker of long-term neurological outcome, we examined serum levels of NF-L in patients after cardiac arrest., Methods: A prospective observational cohort study was conducted. Blood samples for the measurement of NF-L were analyzed from 85 patients within 2h after admission, as well as on 2nd, 3rd, 5th, and 7th day. Neurological outcome was assessed 6 months after cardiac arrest by employing the Modified Glasgow Outcome Score (MGOS)., Results: The serum course of NF-L in patients with poor neurological outcome (MGOS 1+2) was significantly augmented compared to patients with good neurological outcome (MGOS 3+4+5) (on admission (pg/ml): good: 125 ± 11.7 vs. poor: 884.4 ± 86.2 pg/ml; 3rd day: good: 153.1 ± 13.2 vs. poor: 854.4 ± 119.1; 7th day: good: 112.5 ± 10.4 vs. poor: 1011.8 ± 100.8; P<0.001). Intermediate NF-L serum values were found in patients with MGOS 0, which represents a mixture of patients who died with and without certified brain damage (on admission (pg/dl): 433.7 ± 49.8; 3rd day: 598.3 ± 86.6; 7th day: 474 ± 77.4). A prediction power of 0.93 (c-statistic, 95%-CI 0.87-0.99) on 1st, 0.85 (0.81-0.95) on 2nd, 0.92 (0.85-0.99) on 3rd, 0.97 (0.92-1) on 5th and 0.99 (0.98-1) on 7th day was achieved for NF-L predicting poor neurological outcome., Conclusions: The present data suggest that within 7 days after cardiac arrest serum NF-L is a valuable marker of long-term neurological outcome., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)

Background: Therapeutic hypothermia (TH) is one of the key treatments after cardiac arrest (CA). Selection of post-CA patients for TH remains problematic, as there are no clinically validated tools to determine who might benefit from the therapy., Objective: The aim of this study was to investigate retrospectively whether laboratory findings or other patient data obtained during the early phase of hospital admission could be correlated with neurological outcome after TH in comatose survivors of CA., Methods: Medical charts of witnessed CA patients admitted between June 2003 and July 2009 who were treated with TH were reviewed retrospectively. The subjects were grouped based on their cerebral performance category (CPC) 6 months after CA, as either good recovery (GR) for CPC 1-2 or non-good recovery (non-GR) for CPC 3-5. The following well-known determinants of outcome obtained during the early phase of hospital admission were evaluated: age, gender, body mass index, cardiac origin, presence of ventricular fibrillation (VF), time from collapse to cardiopulmonary resuscitation, time from collapse to return of spontaneous circulation, body temperature, arterial blood gases, and blood test results., Results: We analyzed a total of 50 (25 GR and 25 non-GR) patients. Multivariate logistic analysis showed that initial heart rhythm and pH levels were significantly higher in the GR group than in the non-GR group (ventricular tachycardia/VF rate: p = 0.055, 95% confidence interval [CI] 0.768-84.272, odds ratio [OR] 8.047; pH: 7.155 ± 0.139 vs. 6.895 ± 0.100, respectively, p < 0.001, 95% CI 1.838-25.827; OR 6.89)., Conclusion: These results imply that in addition to initial heart rhythm, pH level may be a good candidate for neurological outcome predictor even though previous research has found no correlation between initial pH value and neurological outcome., (Crown Copyright © 2013. Published by Elsevier Inc. All rights reserved.)

Background: Because of the shortage of suitable brain-dead donors, the use of non-heart-beating donor lungs has been investigated experimentally. However, no effective lung protection method has been developed. In this study, we preliminarily investigated the protective effect of partial liquid ventilation (PLV) on a non-heart-beating rabbit lung., Methods: We used 20 male rabbits (mean weight, 3.7 kg) and divided them into 3 groups: the conventional ventilation (control) group, the PLV without cooling group, and the PLV with cooling group. After initially measuring donor cardiopulmonary function, we maintained hypotension at <50 mm Hg for 1 hour followed by 2-hour cardiac arrest. During this time, we used either conventional ventilation or PLV with or without cooling (4 degrees C) for ventilation, and we evaluated the changes in arterial blood gas analysis, pulmonary resistance and elastance, tissue interleukin-8 (IL-8) concentration, and histologic damage., Results: We found no significant difference in arterial oxygen concentration or in carbon dioxide tension among the 3 groups in the hypotensive phase. Pulmonary elastance increased after perfusion of preservation solution in the control group. However, we found no change in elastance in the PLV groups, which was less than that in the control group. Histologic evaluation after perfusion of preservation solution revealed that alveolar structure was damaged significantly less and cell infiltration was milder in the PLV groups than in the control group. Although IL-8 concentrations in the controls increased after cardiac arrest, IL-8 in the PLV groups remained at baseline concentrations during the study period., Conclusion: In this experimental model of hypotension and cardiac arrest, PLV suppresses lung injury when compared with gas-controlled ventilation.

High circulating total homocysteine (tHcy) concentration, which is influenced by folate and vitamin B-12 status, is a suspected cause of cardiovascular events. This relation has been investigated in both case-control and prospective studies but has not been evaluated for different sex x age subgroups of the general U.S. population. We used data on adult (i.e., aged > or =40 y) male (n = 1097) and female (n = 1107) participants in the third National Health and Nutrition Examination Survey, excluding diabetics and those supplemented with estrogen, vitamins or minerals, to evaluate the association between serum tHcy concentration and self-report of heart attack or stroke. After adjustment for age, race-ethnicity, smoking, blood pressure, blood pressure medication, body mass index and serum concentrations of creatinine and cholesterol, past events were reported 2.4 (95% confidence interval 1.0-5.5) times as often by men with tHcy concentration of >12 micromol/L as by men with lower values. The odds ratio for women was 2.6 (95% confidence interval 1.1-6.6) after adjustment for the same factors plus menopausal status. A stronger relation in men aged < or =60 y compared with older men may help reconcile conflicting results of earlier studies.

To avoid factors which confound attempts to characterize the neuroendocrine response to cardiac arrest, we studied the pituitary-adrenocortical and catecholamine responses to induced ventricular fibrillation (VF) and direct current cardioversion in 10 patients undergoing testing of 'implanted cardioverter defibrillator' devices under sedation. Plasma concentrations of epinephrine were increased 5 min after VF (from a mean basal of 0.39 (S.E.M. 0.09) to a peak of 0.632 (0.212) nmol litre-1; P < 0.05) but were unchanged at other times. Plasma concentrations of norepinephrine did not change at any time. Plasma concentrations of cortisol increased significantly at 10 min (from a mean of 367 (SEM 62) to 539 (64) nmol litre-1; P < 0.001) and remained increased 30 min after VF (470 (74) nmol litre-1; P < 0.05) but had returned towards baseline at 60 min, whereas plasma prolactin concentrations were increased at 5 min (from a mean of 224 (SEM 54) to 320 (63) mu. litre-1; P < 0.01) and remained increased until the end of the sampling period at 60 min (288 (65) mu. litre-1; P < 0.05). Concentrations of adrenocorticotrophic hormone (ACTH) (n = 5) tended to increase but this was not statistically significant. We conclude that a short period of cardiac arrest in lightly sedated humans activated the pituitary-adrenocortical axis but did not appear to stimulate catecholamine secretion. These findings raise questions about the nature and mechanisms of the neuroendocrine response to cardiac arrest.

Objective: To determine the relative importance of clinically recognized cardiac dysfunction and unrecognized cardiac injury to hospital mortality., Design: Prospective, blinded, single-center study., Setting: Medical ICU of Barnes-Jewish Hospital, St. Louis, a university-affiliated teaching hospital., Patients: Two hundred sixty adult patients requiring admission to the medical ICU., Interventions: Daily blood collection., Main Outcome Measures: The presence of cardiac dysfunction (myocardial infarction, unstable angina, cardiac arrest, or congestive heart failure) as determined by the physicians responsible for the care of the patient. Daily measurement of levels of cardiac troponin I, a sensitive, highly specific, and long-lived marker of myocardial injury., Results: Fifty-five (21.2%) patients had clinical evidence of cardiac dysfunction, among whom 22 (40%) had an elevated level of cardiac troponin I. A total of 41 (15.8%) patients had evidence of acute myocardial injury based on elevated levels of cardiac troponin I. Patients with clinically recognized cardiac dysfunction had a significantly greater hospital mortality rate compared to patients without clinically recognized cardiac dysfunction (45.5% vs 10.2%; p < 0.001). Similarly, patients with elevated blood levels of cardiac troponin I had a greater hospital mortality rate compared to patients without elevated blood levels of cardiac troponin I (26.8% vs 16.0%; p = 0.095). Multiple logistic-regression analysis controlling for potential confounding variables demonstrated that the presence of clinically recognized cardiac dysfunction was independently associated with hospital mortality (adjusted odds ratio = 3.0; 95% confidence interval = 1.9 to 4.8; p = 0.016). However, having an elevated blood level of cardiac troponin I was not found to be an independent determinant of hospital mortality., Conclusion: Among critically ill medical patients, clinically recognized cardiac dysfunction is an independent determinant of hospital mortality. The identification of unrecognized cardiac injury, using serial measurements of cardiac troponin I, did not independently contribute to the prediction of hospital mortality.

Study Objective: In a previous cardiopulmonary resuscitation (CPR) study in swine, ventilation was associated with improved rate of return of spontaneous circulation (ROSC) compared with nonventilated animals, which had greater hypoxia and hypercarbic acidosis. We used the same model to determine the independent effect of hypoxia and hypercarbic acidosis on ROSC after cardiac arrest., Design: Laboratory model of cardiac arrest., Setting: University teaching hospital laboratory., Participants: Domestic swine (23 to 61 kg)., Interventions: Twenty-four swine were randomly assigned to three groups receiving ventilation during CPR with 85% O2/15% N2 (control), 95% O2/5% CO2 (hypercarbia), or 10% O2/90% N2 (hypoxia). All animals had ventricular fibrillation for 6 min without CPR, then CPR with one of the ventilation gases for 10 min, then defibrillation. Animals without ROSC received epinephrine, 85% O2, CPR for another 3 min, and defibrillation., Measurements and Results: During the tenth minute of CPR, the hypercarbic group had more mean (SD) arterial hypercarbia than the control group (PCO2, 47 +/- 6, compared with 34 +/- 6; p < 0.01), and greater mixed venous hypercarbia (PCO2, 72 +/- 14, compared with 59 +/- 8; p < 0.05), while mean arterial and mixed venous PO2 was not significantly different. The hypoxic group had significantly less mean arterial (43 +/- 9 compared with 228 +/- 103 mm Hg) and mixed venous (22 +/- 5 compared with 35 +/- 7 mm Hg) PO2 when compared with the control group (p < 0.01), while mean arterial and mixed venous PCO2 were not significantly different. Thus, the model succeeded in producing isolated hypercarbia without hypoxia in the hypercarbic group and isolated hypoxia without hypercarbia in the hypoxic group. The rate of ROSC was 6/8 (75%) for the control group, 1/8 (13%) for the hypercarbic group, and 1/8 (13%) for the hypoxic group (p < 0.02)., Conclusions: Both hypoxia and hypercarbia independently had an adverse effect on resuscitation from cardiac arrest. In this model with a prolonged interval of untreated cardiac arrest, adequate ventilation was important for resuscitation.

The purpose of this study was to determine whether serum potassium concentration (SK) can predict resuscitation outcome in a canine model of severe hypothermic cardiac arrest. Fifteen adult mongrel anesthetized dogs were immersed to the neck in a 4 degrees C water bath and ventilated with room air, with ventilation halved at 45 min and stopped at 90 min. After cardiac arrest, 14 of the dogs were kept in the water bath for periods of 2-7 h, and another was held in arrest for 13 h. Following 10 min of closed chest cardiopulmonary resuscitation (CPR) (simulating a short transport time to a hospital), animals were placed on cardiopulmonary bypass and rapidly rewarmed. With appearance of ventricular fibrillation, animals were defibrillated up to three times. Standard advanced cardiac life support was initiated at a core temperature (Tc) of 30 degrees C. Eight of the 15 dogs had return of spontaneous circulation (ROSC), at Tc ranging from 30.4 to 36.5 degrees C. The eight dogs with ROSC did not differ from the seven without ROSC in time to arrest (128 +/- 48 versus 128 +/- 23 min) (mean +/- SD) or Tc at arrest (18.1 +/- 2.2 versus 17.9 +/- 3.1 degrees C), but had higher Tc at the end of the arrest period (9.7 +/- 3.0 versus 5.2 +/- 2.0 degrees C), reflecting a shorter arrest period in the dogs with ROSC (225 +/- 95 versus 420 +/- 193 min). SK (mEq liter(-1)) did not differ between dogs with and without ROSC at baseline (3.5 +/- 0.4 versus 3.7 +/- 0.4) or at arrest (3.4 +/- 0.7 versus 4.3 +/- 2.2), but there was a trend toward higher SK at the end of arrest in the group without ROSC (4.6 +/- 1.5 versus 9.4 +/- 6.3; range 3.2-7.8 versus 3.5-21.4; p = .053). SK was similar after 10 min of CPR in the groups with and without ROSC (6.6 +/- 2.9 versus 9.0 +/- 2.4; range 2.5-11.1 versus 4.5-11.0; p = .107). SK after 10 min of CPR was higher in some animals with ROSC (9.6 and 11.1) than in others which did not have ROSC (4.5 and 7.9). We conclude that very high SK following prolonged hypothermic cardiac arrest may be suggestive of an inability to resuscitate. However, SK after both prolonged hypothermic cardiac arrest and a brief period of CPR is not a good predictor of resuscitation using cardiopulmonary bypass rewarming in an animal model.

We describe a patient who had a cardiac arrest during anaesthesia, in whom regional cerebral oxygen saturation was being measured by near infrared spectroscopy and the auditory evoked responses (AER) were being recorded. Both of these monitors provided useful information on cerebral oxygenation during cardiac arrest. Changes in the AER as the result of either reduced circulation or hypothermia are similar, and should these two situations occur simultaneously there could be difficulty in the interpretation of the AER.

To estimate brain damage after cardiac arrest, the concentrations of neuron specific enolase (NSE), GTP-binding protein (G0 alpha), 28 kDa calbindin-D, S100b protein, and creatine kinase BB (CK-BB) in serum and cerebrospinal fluid (CSF) were determined by enzyme immunoassays. Ten mongrel dogs were subjected to 30 min of circulatory arrest at normal body temperature and serial CSF and blood samples were taken during the first 18 h after reperfusion. The NSE concentration in CSF increased significantly after reperfusion, reaching a 15-fold increase (243 +/- 107 ng/ml, p < 0.01) 18 h later, however, it did not increased significantly in serum (8.1 +/- 3.3 ng/ml vs. 23.5 +/- 7.0 ng/ml). G0 alpha concentration in CSF increased sharply between the 2nd and 4th h after reperfusion and peaked 18 h after reperfusion (428 +/- 195 pg/ml, p < 0.01), however, it did not increase significantly in serum. Calbindin-D concentration in CSF increased between the 1st and 6th h after reperfusion, and reached a plateau thereafter (621 +/- 235 ng/ml, a 23-fold increase, p < 0.05) and also increased significantly in serum (p < 0.05). The S100b concentration in CSF also increased dramatically after the 4th h of reperfusion and reached a plateau at the 8th h after reperfusion (16.0 +/- 9.3 ng/ml, a 50-fold increase, p < 0.01), however, it in serum was below the detection threshold. The CK-BB concentration in CSF peaked 4 h after reperfusion (113 +/- 69 ng/ml, a 19-fold increase, p < 0.01) and it in serum increased 4-fold (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Creatine kinase (CK) and its brain-specific isoenzyme (CK-BB), neuron-specific enolase (NSE), neural cell adhesion molecule (NCAM) and the ions sodium, potassium, chloride and calcium were measured both in CSF and serum and inorganic phosphate in CSF in order to assess their prognostic value in total brain ischemia due to cardiac arrest. The samples were collected at 4, 28 and 76 h after resuscitation. Twenty consecutive patients resuscitated from ventricular fibrillation or asystole were included in the study. Nine of the patients recovered consciousness (recovered) but eleven remained comatose (disabled). The follow-up period was 2 years after which only one patient was still alive. The earliest statistically significant differences between neurologically recovered and disabled patient groups were seen in CSF inorganic phosphate (P = 0.030) already at 4 h and CK-BB (P = 0.046) and NSE (P = 0.020) activity at 28 h. Later, at 76 h after the resuscitation CSF NSE differentiated the groups most clearly (P = 0.014). The values were higher in the disabled patients. A negative correlation between CSF parameters and Glasgow Coma scores was also seen at these timepoints. Statistically significant differences between the groups were seen in both CSF and blood pCO2, pO2, base excess (BE) and actual bicarbonate (HCO3-). CSF or serum NCAM has no prognostic value in anoxic-ischemic coma. The results suggest that in CSF CK-BB and NSE are useful prognostic indicators of hypoxic brain injury when measured 28-76 h after cardiac arrest whereas blood samples have no prognostic value.

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.

Use of continuous transtracheal oxygen delivery systems combined with rhythmic chest compressions can provide excellent oxygenation and ventilation during cardiopulmonary resuscitation. However, occasional displacement of the transtracheal catheter results in life-threatening pneumomediastinal complications. We investigated using the pharyngeal lumen of a pharyngeal-tracheal lumened airway (PtL) as an alternative delivery system for continuous oxygen flow in 21 large mongrel dogs. Excellent ventilation was possible in anesthetized, apneic, and paralyzed dogs in normal sinus rhythm from the "bellows" effect of chest compressions. The hypercapnia and respiratory acidemia resulting from 5 min of complete apnea in ten dogs during normal sinus rhythm was readily corrected (p less than 0.01). In an additional 11 dogs, external chest compressions were performed and oxygen was delivered continuously via the PtL during 20 min of ventricular fibrillation. During this period of cardiac arrest, pH declined (7.38 +/- 0.01 vs 7.19 +/- 0.02; p less than 0.01), but PaCO2 (35 +/- 1 vs 38 +/- 3 mm Hg) and PaO2 (67 +/- 2 vs 68 +/- 3 mm Hg) were not significantly different from prearrest values. Successful resuscitation was achieved in 8 of 11 (73 percent) animals, which is similar to the results in historical controls with endotracheal intubation. No pneumomediastinal complications were seen with use of the PtL. We conclude that using the pharyngeal lumen of the PtL for continuous delivery of oxygen combined with external chest compressions can provide a safe and effective mode of oxygenation and ventilation during cardiac arrest.

To determine the clinical relevance of the sympathetic response to out-of-hospital cardiac arrest, we measured plasma concentrations of catecholamine and cortisol in ten such arrested patients on their arrival. The duration of cardiac arrest was estimated from 9 to 200 min before basic life support was initiated by ambulance personnel. Two of the patients developed spontaneous pulses in response to ALS and were resuscitated, and the others were not, although the length and the extent of ALS were not different between the two groups. Plasma concentrations of epinephrine (EN), norepinephrine (NE) and cortisol prior to ALS in both groups were markedly elevated. In particular, the patients who never regained spontaneous pulses showed 58-fold and 12-fold increase in the plasma EN and NE levels, respectively, which were much higher than those in the resuscitated cases; 8- and 1.7-fold increase, respectively. These massive EN and NE discharges correlated well with the arrest time (r = 0.96 and 0.94, respectively) and the degree of acidosis (r = -0.82 and -0.82, respectively).

Direct mechanical ventricular actuation (DMVA) is a non-blood-contacting method of biventricular cardiac massage which may be applied expediently for total circulatory support. The purpose of this study was to assess the feasibility of DMVA application for patients suffering refractory cardiac arrest. Following informed consent, DMVA was applied in 22 patients. Vascular access for hemodynamic monitoring was possible in only 12 patients, whose outcomes serve as the basis for this report. The mean age of the patients was 48.2 +/- 4.2 years (seven men; five women). The average time from witnessed cardiac arrest to DMVA application was 81 +/- 9 minutes. Application took less than two minutes from the time of skin incision and resulted in immediate hemodynamic improvement. Systolic and diastolic blood pressures averaged 78 +/- 4 and 41 +/- 4 mm Hg, respectively, with a mean cardiac output of 3.14 +/- 0.18 L/min during a mean of 228 +/- 84 minutes of circulatory support (range, 25 minutes to 18 hours). In selected cases the device was temporarily removed for 2 to 3 minutes and open-chest cardiac massage (OCCM) performed at similar compression rates. DMVA increased arterial pressures 65 percent and cardiac output 190 percent compared to OCCM. Initial arterial pH (7.12 +/- 0.04) improved by the time the device was removed (7.24 +/- 0.05). Serum lactate levels decreased from 18.0 +/- 2.3 mumol/L to 14.9 +/- 2.9 mumol/L. Four patients were successfully defibrillated: two had inadequate cardiac function and died within 1 h, and two were successfully resuscitated, but later died from cardiac failure and respiratory insufficiency. Another patient regained normal neurologic function during DMVA and was successfully bridged to cardiopulmonary bypass for emergent coronary artery bypass grafting, but died later from myocardial infarction. There were only two complications: (1) a cardiac laceration during pericardiotomy (1/22 patients); and (2) a ventricular rupture during OCCM (1/22). No complication resulted from the device. We found DMVA to be a feasible method for acute cardiovascular stabilization in victims suffering refractory cardiac arrest. Human clinical trials employing earlier DMVA application are required to determine its resuscitative potential.

Deep endobronchial instillation of epinephrine (2-5 mg in 5 ml saline, catheter of 50 cm in length), during cardiopulmonary resuscitation in man, results rapidly in efficient blood concentrations, similar to those obtained with i.v. route, but with the additional benefit of a more prolonged effect, due to a slower blood concentration decrease. Despite the large interindividual variations in resulting blood concentrations, also observed with the i.v. route, the endobronchial instillation of lidocaine (5-7 mg.kg-1 in 10 ml saline) results in most cases in blood concentrations located in the therapeutic range. As with epinephrine, the endobronchial route results in a prolonged, infusion-like effect. This can be of benefit for the prevention of recurrent ventricular fibrillation. This study provides further arguments for a more extensive use of the endobronchial route, especially in out-of-hospital resuscitation.

Pancreatic polypeptide (PP), neurotensin, substance P, and vasoactive intestinal polypeptide (VIP) are peptides that modify various autonomic and neural functions. These substances are secreted into the blood in response to physiologic stimuli affecting the gastrointestinal tract. To determine the effect of adrenal hormones on gastrointestinal peptide release we measured blood levels of PP, VIP, substance P, and neurotensin in adrenalectomized and intact dogs undergoing cardiac arrest and cardiopulmonary resuscitation (CPR), a condition associated with maximal adrenal stimulation. One hour after completion of abdominal surgery consisting of bilateral adrenalectomy or exposure of the adrenal glands (sham operation), ventricular fibrillation was induced in 19 dogs by direct ventricular discharge. Despite marked elevations of plasma epinephrine and norepinephrine, CPR was associated with minimal endocrine gastrointestinal involvement, restricted to increased VIP levels in sham-operated dogs. No specific gastrointestinal peptide response to cardiac arrest was seen in adrenalectomized animals, but their plasma PP and VIP levels were higher than those of sham-operated dogs. Therefore, acute maximal adrenal stimulation is associated with selective VIP release. In addition, the higher level of the vagally controlled plasma PP in adrenalectomized animals suggests a tonic inhibitory effect of adrenal secretions on the release of this peptide.