Plasminogen activator inhibitor type 1 and outcome after successful cardiopulmonary resuscitation

OBJECTIVE: Patients after successful cardiopulmonary resuscitation have been shown to exhibit elevated plasma concentrations of plasminogen activator inhibitor (PAI) type 1, the main circulating antifibrinolytic protein. It has been suggested that elevations in PAI-1 contribute to cerebral no-reflow after successful cardiopulmonary resuscitation. We analyzed whether PAI-1 concentrations might predict cerebral outcome after cardiopulmonary resuscitation. DESIGN: Prospective, controlled study. SETTING: Intensive care unit at a university hospital. PATIENTS: Thirty-five patients after successful cardiopulmonary resuscitation and 35 control patients who were not critically ill. INTERVENTIONS: Blood sampling for determination of plasma concentrations of active and total PAI-1 antigen. MEASUREMENTS AND MAIN RESULTS: Plasma concentrations of total and active PAI-1 antigen on the second day after successful cardiopulmonary resuscitation were significantly higher in patients after cardiopulmonary resuscitation than in controls (p <.0001) and were unrelated to duration of cardiopulmonary resuscitation. Both active and total PAI-1 antigen were higher in patients who developed acute renal failure after cardiopulmonary resuscitation. Patients with an unfavorable cerebral outcome after cardiopulmonary resuscitation had higher total PAI-1 antigen concentrations compared with patients with good outcome after cardiopulmonary resuscitation (p =.026). We identified 180 ng/mL as the best cutoff value for total PAI-1 antigen with respect to cerebral outcome (chi-square 11.8, p =.001). In a logistic regression analysis, only systemic inflammatory response syndrome (p =.028), acute renal failure after cardiopulmonary resuscitation (p =.017), and cardiopulmonary resuscitation duration >15 mins (p =.042) were significantly and independently associated with cerebral outcome after cardiopulmonary resuscitation. Total PAI-1 antigen reached only borderline significance (p =.058) but nevertheless slightly improved the correct prediction of cerebral outcome after cardiopulmonary resuscitation. CONCLUSIONS: Acute renal failure after cardiopulmonary resuscitation, systemic inflammatory response syndrome, and cardiopulmonary resuscitation duration are better predictors of cerebral outcome after cardiopulmonary resuscitation than PAI-1 antigen, but determination of total PAI-1 antigen nevertheless might improve the early prediction of cerebral outcome after cardiopulmonary resuscitation. Whether elevated PAI-1 concentrations, possibly via prothrombogenic/antifibrinolytic effects, contribute causally to cerebral no-reflow and acute renal failure after cardiopulmonary resuscitation remains to be clarified.     

Marked activation of complement and leukocytes and an increase in the concentrations of soluble endothelial adhesion molecules during cardiopulmonary resuscitation and early reperfusion after cardiac arrest in humans

OBJECTIVE: Animal studies have demonstrated that reperfusion disorders occurring after cardiac arrest affect outcome. Reperfusion injury can be caused by activation of complement, polymorphonuclear leukocytes (PMN), and PMN-endothelial interaction. We studied different specific markers of these processes during and after cardiopulmonary resuscitation in humans. DESIGN: Prospective clinical trial. SETTING: University hospital. PATIENTS: A total of 55 patients who underwent out-of-hospital cardiopulmonary resuscitation for nontraumatic causes. INTERVENTIONS: Blood samples were drawn immediately, 15 mins, and 30 mins after initiation of cardiopulmonary resuscitation. In the case of restoration of spontaneous circulation, additional blood samples were taken at serial time points until 7 days after cardiac arrest. MEASUREMENTS AND MAIN RESULTS: A marked activation of complement and PMN was found in all patients investigated. Serum concentrations of specific activation markers of the complement system, anaphylatoxin C3a and the soluble membrane attack complex SC5b-9, and PMN elastase were increased during cardiopulmonary resuscitation and for 相似文献   

Acute renal failure after successful cardiopulmonary resuscitation

OBJECTIVE: To assess the frequency and independent predictors of severe acute renal failure in patients resuscitated from out-of-hospital ventricular fibrillation cardiac arrest. DESIGN: A cohort study with a minimum follow-up of 6 months. SETTING: Emergency department of a tertiary care 2200-bed university hospital. PATIENTS AND PARTICIPANTS: Consecutive adult (> 18 years) patients admitted from 1 July 1991 to 31 October 1997 after witnessed ventricular fibrillation out-of-hospital cardiac arrest and successful resuscitation. MEASUREMENTS AND RESULTS: Acute renal failure was defined as a 25% decrease of creatinine clearance within 24 h after admission. Out of 187 eligible patients (median age 57 years, 146 male), acute renal failure occurred in 22 patients (12%); in 4 patients (18%) renal replacement therapy was performed. Congestive heart failure (OR 6.0, 95% CI 1.6-21.7; p = 0.007), history of hypertension (OR 4.4, 95% CI 1.3-14.7; p = 0.02) and total dose of epinephrine administered (OR 1.1, 95% CI 1.0-1.2; p = 0.009) were independent predictors of acute renal failure. Duration of cardiac arrest, pre-existing impaired renal function and blood pressure at admission were not independently associated with renal outcome. CONCLUSIONS: Severe progressive acute renal failure after cardiopulmonary resuscitation (CPR) is rare. Pre-existing haemodynamics seem to be more important for the occurrence of acute renal failure than actual hypoperfusion during resuscitation.     

Vasopressin improves survival in a pig model of hypothermic cardiopulmonary resuscitation

OBJECTIVE: During hypothermic cardiopulmonary resuscitation with a body core temperature <30 degrees C administration of a vasopressor to support coronary perfusion pressure is controversial. The purpose of the current study was to assess the effects of a single 0.4-unit/kg dose of vasopressin on coronary perfusion pressure, defibrillation success, and 1-hr survival in a pig model of hypothermic closed-chest cardiopulmonary resuscitation combined with rewarming. DESIGN: Prospective, randomized study in an established pig model. SETTING: University hospital research laboratory. SUBJECTS: Fifteen 12- to 16-wk-old domestic pigs. INTERVENTIONS: Pigs were surface cooled to a body core temperature of 26 degrees C and ventricular fibrillation was induced. After 15 mins of untreated cardiac arrest, manual closed-chest cardiopulmonary resuscitation and thoracic lavage with 40 degrees C warmed tap water were started. After 3 mins of external chest compression, animals were assigned randomly to receive vasopressin (0.4 units/kg, n = 8; or saline placebo, n = 7). Defibrillation was attempted 10 mins after drug administration. MEASUREMENTS AND MAIN RESULTS: Compared with saline placebo treated-animals, coronary perfusion pressure in vasopressin-treated pigs was significantly higher 90 secs (36 +/- 5 mm Hg vs. 7 +/- 4 mm Hg, p =.000) to 10 mins (24 +/- 4 mm Hg vs. 8 +/- 4 mm Hg, p =.000) after drug administration. Restoration of spontaneous circulation and 1 hr survival were significantly higher in vasopressin animals compared with saline placebo (8 of 8 vasopressin pigs vs. 0 of 7 placebo pigs, p <.001). CONCLUSIONS: A single 0.4-unit/kg dose of vasopressin administered at a body core temperature <30 degrees C significantly improved defibrillation success and 1-hr survival in a pig model of hypothermic cardiopulmonary resuscitation.     

Rethinking bystander CPR for out-of-hospital cardiac arrest

Citation

SOS-KANTO study group: Cardiopulmonary resuscitation by bystanders with chest compression only (SOS-KANTO): an observational study. Lancet 2007, 369:920–926 [1].

Background

Mouth-to-mouth ventilation is a barrier to bystanders doing cardiopulmonary resuscitation (CPR), but few clinical studies have investigated the efficacy of bystander resuscitation by chest compressions without mouth-to-mouth ventilation (cardiac-only resuscitation).

Methods

Objective

To compare the effect of bystander-provided cardiac-only resuscitation to conventional CPR in adults who had out-of-hospital cardiac arrest.

Design

Prospective multicenter observational study.

Setting

58 emergency hospitals and emergency medical service units in the Kanto region of Japan.

Subjects

Patients with witnessed out-of-hospital cardiac arrest who were subsequently transported by paramedics to participating emergency hospitals. Exclusion criteria were age <18 years, further cardiac arrest after the arrival of paramedics, documented terminal illness, presence of a do-not-resuscitate order, and bystander resuscitation without documented chest compressions.

Intervention

None. On arrival at the scene, paramedics assessed the technique of bystander resuscitation, recording it as conventional CPR (chest compressions with mouth-to-mouth ventilation), cardiac-only resuscitation (chest compressions alone), or no bystander CPR. Patients were followed and revaluated 30 days after the arrest to determine neurologic status.

Outcome

The primary endpoint was favorable neurological outcome 30 days after cardiac arrest using the Glasgow-Pittsburgh cerebral-performance scale, with favorable neurological outcome defined as a category 1 (good performance) or 2 (moderate disability) on a 5-point scale.

Results

4068 adult patients who had out-of-hospital cardiac arrest witnessed by bystanders were included; 439 (11%) received cardiac-only resuscitation from bystanders, 712 (18%) conventional CPR, and 2917 (72%) received no bystander CPR. Any resuscitation attempt was associated with a higher proportion having favorable neurological outcomes than no resuscitation (5.0%vs 2.2%, p < 0.0001). Cardiac-only resuscitation resulted in a higher proportion of patients with favorable neurological outcomes than conventional CPR in patients with apnea (6.2%vs 3.1%; p = 0.0195), with shockable rhythm (19.4%vs 11.2%, p = 0.041), and with resuscitation that started within 4 min of arrest (10.1%vs 5.1%, p = 0.0221). However, there was no evidence for any benefit from the addition of mouth-to-mouth ventilation in any subgroup. The adjusted odds ratio for a favorable neurological outcome after cardiac-only resuscitation was 2.2 (95% CI 1.2–4.2) in patients who received any resuscitation from bystanders.

Conclusion

Cardiac-only resuscitation by bystanders is the preferable approach to resuscitation for adult patients with witnessed out-of-hospital cardiac arrest, especially those with apnea, shockable rhythm, or short periods of untreated arrest.     

Effect of active compression-decompression resuscitation (ACD-CPR) on survival: a combined analysis using individual patient data.

Active compression decompression resuscitation (ACD-CPR) has been developed as an alternative to standard cardiopulmonary resuscitation (S-CPR). To determine the effect of ACD-CPR on survival and neurologic outcome in patients with out-of-hospital cardiac arrest, this combined analysis involved individual patient data from 2866 patients from seven separate randomized prospective prehospital studies who had received ACD-CPR or S-CPR after out-of-hospital cardiac arrest in seven international sites. Significant improvement in 1-h survival (odds ratio (OR) = 0.83; confidence interval (CI): 0.695-0.99; P < 0.05) was found with ACD-CPR (n = 1410) versus S-CPR (n = 1456). The odds ratio for hospital discharge after ACD-CPR was similar (OR = 0.82; CI: 0.609-1.107, P = NS), but this finding was not statistically significant. Using the chi2-test for trend, there was a significant improvement in overall survival with ACD-CPR (P < 0.05) versus S-CPR. This improvement was largely due to the influence of results from one study site. Neurological outcome and complication rates were comparable between groups. Further study is needed to determine which emergency medical services systems may benefit from out-of-hospital use of ACD-CPR.     

Tumor necrosis factor-alpha is associated with early postresuscitation myocardial dysfunction

OBJECTIVE: Left ventricular dysfunction after successful cardiopulmonary resuscitation contributes to early death following resuscitation. The stress-induced proinflammatory cytokines, particularly tumor necrosis factor-alpha and interleukin-1beta, are known to depress myocardial function. We hypothesized that tumor necrosis factor-alpha and interleukin-1beta, synthesized and released in response to the stress of global ischemia accompanying cardiac arrest, play a role in development of postresuscitation left ventricular dysfunction. METHODS: Hemodynamic variables, tumor necrosis factor-alpha , interleukin-1beta, interleukin-6 (enzyme-linked immunosorbent assay method), and ionized calcium were measured in ten anesthetized swine before and after 7 mins of cardiac arrest and during the early postresuscitation period (60-90 mins). RESULTS: Tumor necrosis factor-alpha increased three-fold within 15 mins of restoration of circulation and remained elevated throughout the observation period. A significant negative correlation was observed between tumor necrosis factor-alpha and left ventricular systolic change in pressure over time (r = -.54, p <.001). Interleukin-1beta was undetectable before and after resuscitation, and interleukin-6 was detectable in only two animals after resuscitation. Although a significant decline in ionized calcium was observed and correlated with left ventricular systolic change in pressure over time, an independent role for ionized calcium in postresuscitation left ventricular dysfunction was not demonstrated. CONCLUSION: Tumor necrosis factor-alpha increases during the early postresuscitation period and may play a role in postresuscitation myocardial dysfunction.     

Outcome of out-of-hospital postcountershock asystole and pulseless electrical activity versus primary asystole and pulseless electrical activity.

OBJECTIVE: In the prehospital setting, countershock terminates ventricular fibrillation (VF) in about 80% of cases. However, countershock is most commonly followed by asystole or pulseless electrical activity (PEA). The consequences of such a countershock outcome have not been well studied. The purpose of this investigation was to compare the outcome of prehospital VF victims shocked into asystole or PEA with that of patients whose first documented rhythm was asystole or PEA (primary asystole or PEA). DESIGN: Observational, retrospective study conducted over 5 yrs (1995-1999). SETTING: A municipal hospital with a catchment area of >200,000. PATIENTS: Consecutive adult patients with out-of-hospital nontraumatic cardiopulmonary arrest of cardiac origin. Patients found in VF who developed asystole or PEA after countershocks (group 1) and patients found in asystole or PEA (primary asystole or PEA) (group 2) were included if the reported downtime was <10 min. INTERVENTIONS: None. MEASUREMENTS AND RESULTS: Study end points included restoration of circulation (defined as a pulse for any duration), survival to hospital admission, and survival to hospital discharge. Ratios were determined, 95% confidence intervals were calculated, and observed differences were compared. For group 1 patients (n = 101), 61% of patients had a bystander-witnessed collapse and 34% received bystander cardiopulmonary resuscitation. For group 2 patients (n = 140), collapse was bystander witnessed in 71% and 45% received bystander cardiopulmonary resuscitation. These differences were not statistically significant. Restoration of circulation was significantly more frequent in group 2 than group 1 (42% vs. 16%, p <.001) as was survival to hospital admission (36% vs. 11%, p =.001). Survival to hospital discharge was greater in group 2 patients, but the difference failed to achieve statistical significance (10% vs. 3%, p =.062). CONCLUSIONS: Countershock of prolonged VF followed by a nonperfusing rhythm has a worse prognosis than primary asystole or PEA and may be related to myocardial electrical injury.     

Evaluation of hypoxic brain injury with spinal fluid enzymes, lactate, and pyruvate.

OBJECTIVE: To investigate the prognostic importance in neurologic recovery of the lumbar cerebrospinal fluid (CSF) variables creatine kinase (CK) and brain-type creatine kinase isoenzyme (CK-BB), lactate dehydrogenase (LDH) and its isoenzymes (LDH 1-5), CSF acid phosphatase, beta-D-N-acetylglucosaminidase activity, and CSF lactate, pyruvate, sodium, potassium, and calcium concentrations in patients who experienced cardiac arrest. DESIGN: Prospective clinical study with blood and CSF samples collected 4, 28, 76, and 172 hrs after resuscitation. SETTING: Medical ICU in a university hospital. PATIENTS: Twenty consecutive victims of out-of-hospital cardiac arrest. Eight patients recovered neurologically and 12 patients remained comatose or neurologically disabled until death. MEASUREMENTS AND MAIN RESULTS: CSF CK, CK-BB, LDH, and LDH isoenzyme 1-3 concentrations in all disabled patients were markedly increased at 76 hrs after the resuscitation. However, these variables were not changed in the recovered subjects. Patients (n = 7) with a mean CSF CK level of 25 +/- 33 (SD) U/L, CK-BB 23 +/- 33 U/L, and CSF lactate 3.8 +/- 0.9 mmol/L at 28 hrs after cardiac arrest remained unconscious and died. In the recovered patients, the mean CSF CK concentration was 2.0 +/- 1.5 U/L (p less than .001) and CSF lactate concentration 2.5 +/- 0.5 mmol/L (p less than .002). The lactate concentration was highest at 4 hrs after resuscitation, declining thereafter. Patients with a mean CSF total LDH level of 609 +/- 515 U/L and acid phosphatase 2.4 +/- 1.2 U/L 76 hrs after resuscitation died without regaining consciousness. In the recovered patients, the mean total CSF LDH activity was 82 +/- 58 U/L (p = .003) and CSF acid phosphatase was 0.8 +/- 0.5 U/L (p = .01) 76 hrs after resuscitation. CONCLUSIONS: CSF CK, CK-BB, and CSF lactate concentrations reflect a patient's outcome most reliably when measured within 28 to 76 hrs of the cardiac arrest. Similarly, CSF LDH, its isoenzymes 1-3, and CSF acid phosphatase concentrations, when measured at 76 hrs, can be used to monitor the patient's outcome after cardiac arrest. When correlated with Glasgow Coma Scale scores, the closest negative correlation was again seen in CSF CK and CK-BB at 28 and 76 hrs, as well as in LDH, LDH1-3, and acid phosphatase values at 76 hrs. The negative correlation between CSF lactate and Glasgow Coma Scale scores was most distinct at 28 hrs.     

Effects of epinephrine and vasopressin in a piglet model of prolonged ventricular fibrillation and cardiopulmonary resuscitation

OBJECTIVE: We recently demonstrated that vasopressin alone resulted in a poorer outcome in a pediatric porcine model of asphyxial cardiac arrest when compared with epinephrine alone or with epinephrine plus vasopressin in combination. Accordingly, this study was designed to differentiate whether the inferior effects of vasopressin in pediatrics were caused by the type of cardiac arrest. DESIGN: Prospective, randomized laboratory investigation that used an established porcine model for measurement of hemodynamic variables and organ blood flow. SETTING: University hospital laboratory. SUBJECTS: Eighteen piglets weighing 8-11 kg. INTERVENTIONS: After 8 mins of ventricular fibrillation and 8 mins of cardiopulmonary resuscitation, either 0.4 units/kg vasopressin (n = 6), 45 microg/kg epinephrine (n = 6), or a combination of 45 microg/kg epinephrine with 0.8 units/kg vasopressin (n = 6) was administered. Six minutes after drug administration, a second respective bolus dose of 0.8 units/kg vasopressin, 200 microg/kg epinephrine, or a combination of 200 microg/kg epinephrine with 0.8 units/kg vasopressin was given. Defibrillation was attempted 20 mins after initiating cardiopulmonary resuscitation. MEASUREMENTS AND MAIN RESULTS: Mean +/- sem left ventricular myocardial blood flow 2 mins after each respective drug administration was 65 +/- 4 and 70 +/- 13 mL x min(-1) x 100 g(-1) in the vasopressin group; 83 +/- 42 and 85 +/- 41 mL x min(-1) x 100 g(-1) in the epinephrine group; and 176 +/- 32 and 187 +/- 29 mL x min(-1) x 100 g(-1) in the epinephrine-vasopressin group (p <.006 after both doses of epinephrine-vasopressin vs. vasopressin and after the first dose of epinephrine-vasopressin vs. epinephrine, respectively). At the same times, mean +/- sem total cerebral blood flow was 73 +/- 3 and 47 +/- 5 mL x min(-1) x 100 g(-1) after vasopressin; 18 +/- 2 and 12 +/- 2 mL x min(-1) x 100 g(-1) after epinephrine; and 79 +/- 21 and 41 +/- 8 mL x min(-1) x 100 g(-1) after epinephrine-vasopressin (p <.025 after both doses of vasopressin and epinephrine-vasopressin vs. epinephrine). Five of six vasopressin-treated, two of six epinephrine-treated, and six of six epinephrine-vasopressin treated animals had return of spontaneous circulation (nonsignificant). CONCLUSIONS: In this pediatric porcine model of ventricular fibrillation, the combination of epinephrine with vasopressin during cardiopulmonary resuscitation resulted in significantly higher levels of left ventricular myocardial blood flow than either vasopressin alone or epinephrine alone. Both vasopressin alone and the combination of epinephrine with vasopressin, but not epinephrine alone, improved total cerebral blood flow during cardiopulmonary resuscitation. In stark contrast to asphyxial cardiac arrest, vasopressin alone or in combination with epinephrine appears to be of benefit after ventricular fibrillation in the pediatric porcine model.     

Vasopressin-mediated adrenocorticotropin release increases plasma cortisol concentrations during cardiopulmonary resuscitation

OBJECTIVE: Vasopressin is a possible stimulus for both adrenocorticotropin (ACTH) and endothelin-1 release. The aim of this study was to compare plasma concentrations of ACTH, cortisol, and endothelin-1 after epinephrine or vasopressin administration in an experimental animal model of cardiopulmonary resuscitation (CPR). DESIGN: Prospective, randomized, controlled animal study. SETTING: A university research laboratory. SUBJECTS: Fourteen 12- to 14-wk-old domestic pigs. INTERVENTIONS: After 4 mins of cardiac arrest and 3 mins of external chest compression, the pigs were randomly assigned to receive either 0.045 mg/kg epinephrine (n = 7) or 0.4 units/kg vasopressin (n = 7). At 5 mins after drug administration, defibrillation was attempted. MEASUREMENTS AND MAIN RESULTS: Coronary perfusion pressure, ACTH, cortisol, and endothelin-1 were measured before cardiocirculatory arrest, during CPR before drug administration, and at 90 secs and 5 mins after drug administration. Coronary perfusion pressure was comparable between groups. All seven animals in the vasopressin group survived, but only one pig in the epinephrine group survived (p = .005). ACTH and cortisol concentrations remained unchanged in epinephrine-treated animals, but increased significantly after vasopressin administration and were significantly higher than in epinephrine-treated animals 5 mins after drug administration. Endothelin-1 concentrations remained unchanged during the study period and were comparable between both groups. CONCLUSIONS: Vasopressin is a potent stimulus for ACTH secretion, but does not trigger endothelin-1 release from vascular cells during cardiac arrest and CPR. The increased plasma cortisol concentrations caused by the enhanced ACTH release after vasopressin may be one factor contributing to the improved outcome repeatedly observed with vasopressin in animal models of CPR.     

Mild hypothermia during prolonged cardiopulmonary cerebral resuscitation increases conscious survival in dogs

OBJECTIVE: Therapeutic hypothermia during cardiac arrest and after restoration of spontaneous circulation enables intact survival after prolonged cardiopulmonary cerebral resuscitation (CPCR). The effect of cooling during CPCR is not known. We hypothesized that mild to moderate hypothermia during CPCR would increase the rate of neurologically intact survival after prolonged cardiac arrest in dogs. DESIGN: Randomized, controlled study using a clinically relevant cardiac arrest outcome model in dogs. SETTING: University research laboratory. SUBJECTS: Twenty-seven custom-bred hunting dogs (19-29 kg; three were excluded from outcome evaluation). INTERVENTIONS: Dogs were subjected to cardiac arrest no-flow of 3 mins, followed by 7 mins of basic life support and 10 mins of simulated unsuccessful advanced life support attempts. Another 20 mins of advanced life support continued with four treatments: In control group 1 (n = 7), CPCR was with normothermia; in group 2 (n = 6, 1 of 7 excluded), with moderate hypothermia via venovenous extracorporeal shunt cooling to tympanic temperature 27 degrees C; in group 3 (n = 6, 2 of 8 excluded), the same as group 2 but with mild hypothermia, that is, tympanic temperature 34 degrees C; and in group 4 (n = 5), with normothermic venovenous shunt. After 40 mins of ventricular fibrillation, reperfusion was with cardiopulmonary bypass for 4 hrs, including defibrillation to achieve spontaneous circulation. All dogs were maintained at mild hypothermia (tympanic temperature 34 degrees C) to 12 hrs. Intensive care was to 96 hrs. MEASUREMENTS AND MAIN RESULTS: Overall performance categories and neurologic deficit scores were assessed from 24 to 96 hrs. Regional and total brain histologic damage scores and extracerebral organ damage were assessed at 96 hrs.In normothermic groups 1 and 4, all 12 dogs achieved spontaneous circulation but remained comatose and (except one) died within 58 hrs with multiple organ failure. In hypothermia groups 2 and 3, all 12 dogs survived to 96 hrs without gross extracerebral organ damage (p < .0001). In group 2, all but one dog achieved overall performance category 1 (normal); four of six dogs had no neurologic deficit and normal brain histology. In group 3, all dogs achieved good functional outcome with normal or near-normal brain histology. Myocardial damage scores were worse in the normothermic groups compared with both hypothermic groups (p < .01). CONCLUSION: Mild or moderate hypothermia during prolonged CPCR in dogs preserves viability of extracerebral organs and improves outcome.     

Quality of life in long-term survivors of out-of-hospital cardiac arrest

STUDY OBJECTIVE: The quality of life in long-term survivors of out-of-hospital cardiac arrest may be a good outcome measure after resuscitation. Therefore, the psychosocial situation and quality of life in such patients after successful resuscitation was evaluated. METHODS: Patients with out-of-hospital cardiac arrest in a community referred to a single tertiary care centre were compared with matched controls. Quality of life was evaluated in 50 consecutive arrest cases (40 males, 10 females; 60+/-13 years) 5-68 months (mean 31.7) after resuscitation according to American Heart Association protocols. RESULTS: The Psychological General Well-being Index questionnaire indicated no significant differences in anxiety, depression, vitality, general well-being, or self-control between patients and controls. However, the Nottingham Health Profile questionnaire demonstrated significant decreases in physical mobility (14.5+/-18.1 vs. 4.0+/-8.5, P=0.0001), energy levels (25.3+/-31.0 vs. 2.0+/-8.0, P=0.0001), emotional reactions (11.3+/-16.6 vs. 4.0+/-10.2, P=0.009), and sleep patterns (19.2+/-28.6 vs. 8.4+/-16.7, P=0.023) in the arrest patients. Little differences were measured with the Everyday-Life Questionnaire. 49 of the 50 arrest patients judged their situation after resuscitation worth living; no significant changes in familial, and psychosocial parameters occurred. CONCLUSIONS: The quality of life was associated with few changes in psychosocial profile after successful resuscitation. The subjective negative factors bore little impact on the quality of daily living in our patients. Thus, continued efforts to improve out-of-hospital resuscitation measures for cardiac arrest are justified since long-term survivors can expect a good quality of life after successful resuscitation.     

Characteristics and outcome of cardiorespiratory arrest in children

OBJECTIVE: To analyse the present day characteristics and outcome of cardio-respiratory arrest in children in Spain. DESIGN: An 18-month prospective, multicentre study analysing out-of-hospital and in-hospital cardio-respiratory arrest in children. Patients and methods: Two hundred and eighty-three children between 7 days and 17 years of age with cardio-respiratory arrest. Data were recorded according to the Utstein style. The outcome variables were the sustained return of spontaneous circulation (initial survival), and survival at 1 year (final survival). Three hundred and eleven cardio-respiratory arrest episodes, composed of 70 respiratory arrests and 241 cardiac arrests in 283 children were studied. Accidents were the most frequent cause of out-of-hospital arrest (40%), and cardiac disease was the leading cause (31%) of in-hospital arrest. Initial survival was 60.2% and 1 year survival was 33.2%. The final survival was higher in patients with respiratory arrest (70%) than in patients with cardiac arrest (21.1%) (P <0.0001). Although many individual factors correlated with mortality, multivariate logistic regression revealed that the best indicator of mortality was a duration of cardiopulmonary resuscitation of over 20 min (odds ratio: 10.35; 95% CI 4.59-23.32). CONCLUSIONS: In Spain, the present mortality from cardio-respiratory arrest in children remains high. Survival after respiratory arrest is significantly higher than after cardiac arrest. The duration of cardiopulmonary resuscitation attempt is the best indicator of mortality of cardio-respiratory arrest in children.     

Does Advanced Age Matter in Outcomes after Out‐of‐hospital Cardiac Arrest in Community‐dwelling Adults ?

OBJECTIVE: To assess whether advanced age is an independent predictor of survival to hospital discharge in community-dwelling adult patients who sustained an out-of-hospital cardiac arrest in a suburban county. METHODS: A prospective cohort study was conducted in a suburban county emergency medical services system of community-dwelling adults who had an arrest from a presumed cardiac cause and who received out-of-hospital resuscitative efforts from July 1989 to December 1993. The cohorts were defined by grouping ages by decade: 19-39, 40-49, 50-59, 60-69, 70-79, and 80 or more. The variables measured included age, gender, witnessed arrest, response intervals, location of arrest, documented bystander cardiopulmonary resuscitation, and initial rhythms. The primary outcome was survival to hospital discharge. Results are reported using analysis of variance, chi square, and adjusted odds ratios from a logistic regression model. Age group 50-59 served as the reference group for the regression model. RESULTS: Of the 2,608 total presumed cardiac arrests, the overall survival rate to hospital discharge was 7.25%. Patients in age groups 40-49 and 50-59 experienced the best rate of successful resuscitation (10%). Each subsequent decade had a steady decline in successful outcome: 8.1% for ages 60-69; 7.1% for ages 70-79; and 3.3% for age 80+. In a post-hoc analysis, further separation of the older age group revealed a successful outcome in 3.9% of patients ages 80-89 and 1% in patients 90 and older. Patients aged 80 years or more were more likely to arrest at home, were more likely to have an initial bradyasystolic rhythm, yet had a similar rate of resuscitation to hospital admission. In the regression model, age 80 or older was associated with a significantly worse survival to hospital discharge (OR = 0.4, 95% CI = 0.20 to 0.82). CONCLUSIONS: There was a twofold decrease in survival following out-of-hospital cardiac arrest to discharge in patients aged 80 or more when compared with the reference group in this suburban county setting. However, resuscitation for community-dwelling elders aged 65-89 is not futile. These data support that out-of-hospital resuscitation of elders up to age 90 years is not associated with a universal dismal outcome.     

Dose-dependent neuroprotection by 17beta-estradiol after cardiac arrest and cardiopulmonary resuscitation

OBJECTIVE: Despite recent advances in the treatment of cardiac arrest, neurologic outcome remains poor. 17beta-Estradiol (E2) has been widely shown to reduce damage after experimental brain injury. The present study determined whether E2 also improves neuronal survival after experimental cardiac arrest and cardiopulmonary resuscitation and if any protection is dose-dependent. DESIGN: A randomized trial. SETTING: A research laboratory. SUBJECTS: Male C57Bl/6 mice weighing 20-25 g. INTERVENTIONS: Mice were randomized into one of six groups, receiving treatment with 0.5, 2.5, 12.5, 25, or 50 mug of E2 or vehicle 1.5 mins after return of spontaneous circulation. Ten minutes after induction of cardiac arrest (by KCl injection), cardiopulmonary resuscitation was initiated (with chest compressions, intravenous epinephrine, and ventilation with 100% O2). Additional animals of each E2-treated group were used for plasma estradiol-level analysis. Brains were removed for quantification of injury in the hippocampus and caudoputamen on day 3. MEASUREMENTS AND MAIN RESULTS: The E2 0.5 group had physiologic estrogen levels 60 min after injection (mean +/- se, 28 +/- 5 pg/mL), whereas the E2 50 group still showed supraphysiologic levels 360 min after administration (245 +/- 32 pg/mL). Hippocampal damage was not altered with E2 treatment. Only posttreatment with the lowest E2 dose (E2 0.5) resulted in attenuated neuronal injury in the rostral and caudal caudoputamen (34 +/- 11% and 27 +/- 11%), in comparison with vehicle (68 +/- 5, p < .05; 63 +/- 4%, p < .001). Higher E2 doses did not affect brain injury. CONCLUSIONS: We conclude that E2 has a critical dosing effect on neuronal survival, physiologic levels of E2 are neuroprotective after cardiac arrest/cardiopulmonary resuscitation, and acute exposure is sufficient for brain resuscitation.     

Prognostic value of cell-free plasma DNA in patients with cardiac arrest outside the hospital: an observational cohort study

Introduction  

Many approaches have been examined to try to predict patient outcome after cardiopulmonary resuscitation. It has been shown that plasma DNA could predict mortality in critically ill patients but no data are available regarding its clinical value in patients after out-of-hospital cardiac arrest. In this study we investigated whether plasma DNA on arrival at the emergency room may be useful in predicting the outcome of these patients.     

Hypertonic saline during CPR: Feasibility and safety of a new protocol of fluid management during resuscitation

BACKGROUND AND PURPOSE: In experimental studies infusion of hypertonic saline during cardiopulmonary resuscitation (CPR) increased resuscitation success rate and improved myocardial and cerebral reperfusion during CPR. We tested the feasibility and the safety of this new therapeutic measure in a randomised, preclinical pilot study. METHODS: The study was performed in the EMS system of Bonn after approval of the local ethical committee. Study inclusion criteria were out-of-hospital cardiac arrest (CA) of non-traumatic origin, age > or =18 years, application of adrenaline (epinephrine) during CPR, duration of CA < or = 15 min, and estimated body weight < or = 125 kg. Patients randomly received 2 ml/kg/10 min HHS (7.2% NaCl with 6% hydroxy ethyl starch 200,000/0.5 [HES]) or HES alone. Haemoglobin, blood gases, plasma sodium and potassium concentrations were measured before and 10 min after infusion, and after admission to hospital. Feasibility and safety of the new fluid management was evaluated by looking for side effects and determination of resuscitation success and admission rates. RESULTS: Sixty-six patients were included. After infusion of HHS, plasma sodium concentration increased to 168+/-29 mmol/l at 10 min after application but already decreased to near normal (147+/-5.5 mmol/l) at admission to hospital. Patients receiving HHS showed a trend to higher resuscitation success and hospital admission rates (ROSC: HHS 66.7%, HES 51.5%, p = 0.21; admission: HHS 57.6%, HES 39.4%, p = 0.14). The benefit of HHS was more pronounced if duration of untreated CA was >6 min or if initial rhythm was asystole or pulseless electrical activity (PEA). Negative side-effects were not observed after HHS. CONCLUSIONS: HHS after CA is feasible and safe and might improve short term survival after CPR. However, whether giving HHS could be a useful measure to increase resuscitation success after out-of-hospital CA requires a larger preclinical trial.     

Emergency preservation and resuscitation improve survival after 15 minutes of normovolemic cardiac arrest in pigs

OBJECTIVE: Outcome after prolonged normovolemic cardiac arrest is poor, and new resuscitation strategies have to be found. We hypothesized that the induction of deep hypothermia for emergency preservation and resuscitation (EPR) during prolonged cardiac arrest, before the start of reperfusion, will mitigate the deleterious cascades leading to neuronal death and will thus improve outcome. DESIGN: Prospective experimental study. SETTING: University research laboratory. SUBJECTS: Thirteen pigs, Large White breed (27-37 kg). INTERVENTIONS: After 15 mins of ventricular fibrillation, pigs were subjected to 1) EPR (n = 6), 20 mins of hypothermic stasis induced with a cold saline aortic flush; or 2) 20 mins of conventional resuscitation (n = 7). Then cardiopulmonary bypass was initiated in both groups, followed by defibrillation. Controlled ventilation and mild hypothermia were continued for 20 hrs; survival was for 9 days. For neurologic evaluation, neurologic deficit score (100% = brain dead, 0-10% = normal), overall performance category (1 = normal, 5 = dead or brain dead), and brain histologic damage score were used. MEASUREMENTS AND MAIN RESULTS: In the EPR group, brain temperature decreased from 38.5 degrees C +/- 0.2 degrees C to 16.7 degrees C +/- 2.5 degrees C within 235 +/- 27 secs. Five animals achieved restoration of spontaneous circulation and survived to 9 days: two pigs with overall performance category 2 and three pigs with overall performance category 3. Their neurologic deficit score was 45% (interquartile range 35, 50) and histologic damage score was 142 (interquartile range 109, 159). In the control group, four pigs achieved restoration of spontaneous circulation: one survived to 9 days with overall performance category 3, neurologic deficit score 45%, and histologic damage score 226 (restoration of spontaneous circulation, p = .6; survival, p = .03; overall performance category, p = .02). CONCLUSIONS: EPR is feasible in an experimental pig model and improves survival after prolonged cardiac arrest in pigs. Further experimental studies are needed before this concept can be brought into clinical practice.     

Out-of-hospital cardiac arrest increases soluble vascular endothelial adhesion molecules and neutrophil elastase associated with endothelial injury

Objectives: To investigate the inflammatory responses in patients with out-of-hospital cardiac arrest, we examined the changes in markers of endothelial activation, neutrophil activation, and endothelial injury.¶Design: Prospective, cohort study.¶Setting: General intensive care unit of a tertiary care center.¶Patients and participants: Forty-four out-of-hospital cardiac arrest patients were classified into two groups, those who achieved return of spontaneous circulation (ROSC) (n = 23) and those without ROSC (n = 21). Eight normal healthy volunteers served as control subjects.¶Measurements and results: Serial levels of soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble E-selectin (sE-selectin) as markers of endothelial activation, neutrophil elastase as a marker of neutrophil activation, and soluble thrombomodulin as a marker of endothelial injury were measured during and after cardiopulmonary resuscitation (CPR). In patients with ROSC, cardiac arrest and CPR led to increases in the levels of three vascular endothelial adhesion molecules, neutrophil elastase, and soluble thrombomodulin that peaked 6 h or 24 h after arrival at the emergency department. In patients without ROSC, only neutrophil elastase showed moderate elevation during CPR. We could not find significant differences in all measured parameters between the two groups.¶Conclusions: As evidence of inflammatory responses in whole-body ischemia and reperfusion, our study demonstrates neutrophil-endothelium interaction with signs of endothelial injury in patients with out-of-hospital cardiac arrest. These inflammatory changes may have an important role in post-resuscitation syndrome after human cardiac arrest.