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PubMed2005

Use of transoesophageal echocardiography during cardiac arrest in patients undergoing elective non-cardiac surgery.

BACKGROUND: Sudden unexpected intraoperative cardiac arrests in patients undergoing elective non-cardiac operations are rare but catastrophic complications. The efficacy and utility of transoesophageal echocardiography (TOE) in the diagnosis and management of these events have not been reported earlier. METHODS: Unexpected intraoperative cardiac arrests in patients undergoing elective non-cardiac operations were prospectively studied during a 6 yr period. In these patients, TOE was performed within 5 min after initiation of external chest compression to identify the causes of the cardiac arrests. RESULTS: Among a total of 125 965 surgical operations, 10 patients who suffered intraoperative cardiac arrests were studied. The causes of the cardiac arrests including myocardial infarction in five, pulmonary embolism in two, and severe hypovolaemia and ventricular arrhythmia without specific pathology in the other two patients were correctly identified using TOE. Seven patients survived. CONCLUSION: We conclude that TOE was useful in cardiac arrest during non-cardiac surgery for identifying or excluding pulmonary embolism and for directing investigations and treatment in those patients who had suffered myocardial infarction.

Adult↗
PubMed1986

External cardiac pacing during in-hospital cardiac arrest.

External noninvasive cardiac pacing offers a rapid and simple method of pacing the heart during an emergency. It has been suggested that early use of cardiac pacing for bradycardia or asystole may improve survival in patients who have cardiac arrest. To investigate this possibility 58 consecutive episodes of cardiac arrest occurring on the medical wards or emergency room. Twenty-six episodes underwent external noninvasive pacing for bradycardia or asystole refractory to standard drugs. Only 2 patients survived, and survival could be directly attributed to pacing in only 1 of them. Of the 32 episodes not undergoing pacing, 23 had transient asystole or bradycardia, 13 of which rapidly responded to medications. The 17 cases (53%) not undergoing pacing survived. In conclusion, when bradycardia or asystole during cardiac arrest fails to respond to standard pharmacologic measures, it is an indicator of severe myocardial damage, and attempts at cardiac pacing rarely improve survival.

Adult↗
PubMed1997

Survivors of out-of-hospital cardiac arrest with apparently normal heart. Need for definition and standardized clinical evaluation. Consensus Statement of the Joint Steering Committees of the Unexplained Cardiac Arrest Registry of Europe and of the Idiopathic Ventricular Fibrillation Registry of the United States.

BACKGROUND: A wide variety of structural abnormalities are associated with the vast majority of cardiac arrests. However, there is no evidence of structural heart disease in approximately 5% of victims of sudden death, indicating that cardiac arrest in the absence of organic heart disease is more common than previously recognized. The risk of recurrence and the acute and long-term response to therapy are important but unanswered questions. Data from the small series reported so far are of limited value because of the lack of uniform criteria to define and diagnose idiopathic ventricular fibrillation (IVF). METHODS AND RESULTS: This report originates from a Consensus Conference convened by the Steering Committees of the European (UCARE) and North American (IVF-US) Registries on IVF under the auspices of the Working Group on Arrhythmias of the European Society of Cardiology. Its objective is to provide a unified definition of IVF and to outline the investigations necessary to make this diagnosis. Minimal diagnostic tests for the exclusion of an underlying structural heart disease include non-invasive (blood biochemistry, physical examination and clinical history, ECG, exercise stress test, 24-hour Holter recording, and echocardiogram) and invasive (coronary angiography, right and left ventricular cineangiography, and electrophysiological study) examinations. Programmed electrical stimulation, ventricular biopsy, and ergonovine test during coronary angiography are recommended but not mandatory. CONCLUSIONS: It is recognized that despite careful evaluation, conditions such as focal cardiomyopathy, myocarditis, or fibrosis and transient electrolyte abnormalities may remain silent. Therefore, patients should undergo careful follow-up, with noninvasive tests repeated every year. The existence of a unified terminology will allow meaningful comparison of data collected by different investigators and will thus contribute to a better understanding of IVF.

Diagnosis, Differential↗
PubMed2005

Vasopressin in cardiac arrest.

OBJECTIVE: To review the efficacy and safety of vasopressin in cardiac arrest. DATA SOURCES: MEDLINE, EMBASE, and PubMed were searched (all to June 2005) for full-text English-language publications describing trials in humans. Search terms were vasopressin, epinephrine, adrenaline, heart arrest, cardiac arrest, and clinical trial. STUDY SELECTION AND DATA EXTRACTION: Prospective, randomized, controlled trials that evaluated efficacy or safety endpoints of vasopressin in the management of cardiac arrest were included. Efficacy outcomes included return of spontaneous circulation, successful resuscitation, survival to hospital admission, 24-hour survival, and survival to hospital discharge. Safety outcomes were as defined by each trial. DATA SYNTHESIS: Three prospective trials were identified and included in this review. Vasopressin does not appear to offer any therapeutic advantage compared with epinephrine in the treatment of both in-hospital and out-of-hospital cardiac arrest, regardless of the presenting arrest rhythm. Although there is a suggestion that vasopressin may be effective in treatment of asystole, the evidence for this arises from a subgroup analysis that should be viewed as hypothesis generating. There are limited data describing the safety of vasopressin in cardiac arrest. CONCLUSIONS: The current evidence for the use of vasopressin in cardiac arrest is indeterminate. Given the similarly equivocal evidence of efficacy for epinephrine, either drug could be considered the first-line agent in cardiac arrest. Placebo-controlled studies with appropriate statistical power are warranted to evaluate meaningful clinical outcomes, such as survival to hospital discharge. Further evaluation of the role of vasopressin in asystolic cardiac arrest and its use in combination with epinephrine is also justified.

Clinical Trials as Topic↗
PubMed1995

Association of drug therapy with survival in cardiac arrest: limited role of advanced cardiac life support drugs.

OBJECTIVE: To generate hypotheses regarding the association of standard Advanced Cardiac Life Support (ACLS) drugs with human cardiac arrest survival. METHODS: This observational cohort study was conducted over a two-year period in the wards, intensive care units, and EDs of two tertiary care hospitals. Included werc adult patients who suffered cardiac arrest either inside or outside the hospital and who required epinephrine according to standard ACLS guidelines. Six standard ACLS drugs (given while CPR was in progress) were assessed for association with survival from resuscitation to one hour and to hospital discharge by univariate and multivariate logistic regression analyses. RESULTS: In the 529 patients studied, initial cardiac rhythm had no impact on the association between drug administration and survival. The time of drug administration (quartile of ACLS period) was associated with resuscitation for atropine (p < 0.05) and lidocaine (p < 0.01). The odds ratios (95% CIs) for successful resuscitation, after multivariate adjustment for potential confounders, were: a respiratory initiating cause, 3.7 (2.1 -6.4); each 5-minute increase in CPR-ACLS interval, 0.5 (0.4-0.7); each 5-minute duration of ACLS. 0.9 (()1.8- 1.0; atropine, 1.2 (1.0-1.3); bretylium. (0.4 (0.1-1.1); calcium 0.8 (0.2-2.4); lidocaine, 0.9 (0.7-1.1); procainamide. 21.0 (5.2-84.0) d sodium bicarbonate 1.2 (1.0-1.6). All other potential confounding variables entered into the model were not significantly associated with resuscitation. CONCLUSION: Initiating cause of arrest, time to ACLS, and duration of ACLS were important correlates of survival. Other than procainaimide, standard ACLS drugs had relatively little association with survival, but timing of administration may be an important factor. Further research using definitive large randomized controlled trials is warranted to assess the role of drug therapy in improving cardiac arrest survival.

Adult↗
PubMed2002

Cardiac arrest after intravenous metoclopramide - a case of five repeated injections of metoclopramide causing five episodes of cardiac arrest.

We describe a patient where intravenous injection of metoclopramide was immediately followed by asystole repeatedly. The patient received metoclopramide 10 mg i.v. five times during 48 h. After interviewing the attending nurses and reviewing the written documentation, it is clear that every administration of metoclopramide was immediately (within s) followed by asystole. The asystole lasted 15-30 s on four occasions, on one occasion it lasted 2 min. The patient received atropine 0.5-1 mg and chest compressions, before sinus rhythm again took over. We interpret this as episodes of cardiac arrest caused by metoclopramide. The rapid injection via the central venous route and the concomitant tapering of dopamine infusion might have contributed in precipitating the adverse drug reaction.

Adult↗
PubMed2006

Oxidative stress reversibly inactivates myocardial enzymes during cardiac arrest.

Oxidative stress during cardiac arrest may inactivate myocardial enzymes and thereby exacerbate ischemic derangements of myocardial metabolism. This study examined the impact of cardiac arrest on left ventricular enzymes. Beagles were subjected to 5 min of cardiac arrest and 5 min of open-chest cardiac compressions (OCCC) before epicardial direct current countershocks were applied to restore sinus rhythm. Glutathione/glutathione disulfide redox state (GSH/GSSG) and a panel of enzyme activities were measured in snap-frozen left ventricle. To test whether oxidative stress during arrest inactivated the enzymes, metabolic (pyruvate) or pharmacological (N-acetyl-l-cysteine) antioxidants were infused intravenously for 30 min before arrest. During cardiac arrest, activities of phosphofructokinase, citrate synthase, aconitase, malate dehydrogenase, creatine kinase, glucose-6-phosphate dehydrogenase, and glutathione reductase fell by 56, 81, 55, 34, 42, 55, and 45%, respectively, coincident with 50% decline in GSH/GSSG. OCCC effected full recovery of glutathione reductase and partial recovery of citrate synthase and aconitase, in parallel with GSH/GSSG. Phosphofructokinase, malate dehydrogenase, creatine kinase, and glucose-6-phosphate dehydrogenase recovered only after cardioversion. Antioxidant pretreatments augmented phosphofructokinase, aconitase, and malate dehydrogenase activities before arrest and enhanced these activities, as well as those of citrate synthase and glucose-6-phosphate dehydrogenase, during arrest. In conclusion, cardiac arrest reversibly inactivates several important myocardial metabolic enzymes. Antioxidant protection of these enzymes implicates oxidative stress as a principal mechanism of enzyme inactivation during arrest.

Adaptation, Physiological↗
PubMed1971

Attitudes and long-term adjustment of patients surviving cardiac arrest.

Twenty patients surviving cardiac resuscitation following myocardial infarction were seen at least six months after the cardiac arrest. The patient and spouse were interviewed separately. Though they had not usually been informed by the medical staff, 16 of the 20 patients were aware that a cardiac arrest had occurred and had a good understanding of what this meant. Six patients remembered the start or end of the cardiac arrest and five specifically remembered external cardiac massage. Their feelings and their attitudes to the cardiac arrest are described.Initial anxiety was experienced by all the patients and their spouses, particularly after hospital discharge, but in the long term only five patients failed to make a reasonably satisfactory adjustment. Poor rehabilitation seemed to be mainly associated with persisting physical disability and personality factors and not with features associated with the cardiac arrest, such as the duration of external cardiac massage. The spouses often found it difficult to know exactly how to treat the patients after hospital discharge and most patients and spouses felt that more explanation and discussion with the medical staff would have helped to alleviate anxiety.

Adult↗
PubMed2004

Intra-arrest cooling improves outcomes in a murine cardiac arrest model.

BACKGROUND: Recent clinical studies have demonstrated that hypothermia to 32 degrees to 34 degrees C provides significant clinical benefit when induced after resuscitation from cardiac arrest. However, cooling during the postresuscitation period was slow, requiring 4 to 8 hours to achieve target temperatures after return of spontaneous circulation (ROSC). Whether more rapid cooling would further improve survival remains unclear. We sought to determine whether cooling during cardiac arrest before ROSC (ie, "intra-arrest" hypothermia) has survival benefit over more delayed post-ROSC cooling, using a murine cardiac arrest model. METHODS AND RESULTS: A model of potassium-induced cardiac arrest was established in C57BL/6 mice. After 8 minutes of untreated cardiac arrest, resuscitation was attempted with chest compression, ventilation, and intravenous fluid. Mice were randomized to 3 treatment groups (n=10 each): an intra-arrest hypothermia group, in which mice were cooled to 30 degrees C just before attempted resuscitation, and then rewarmed after 1 hour; a post-ROSC hypothermia group, in which mice were kept at 37 degrees C for 20 minutes after successful ROSC and then were cooled to 30 degrees C for 1 hour; and a normothermic control group, in which mice were kept at 37 degrees C. The intra-arrest hypothermia group demonstrated better 72-hour survival than delayed hypothermia and normothermia groups (6/10 versus 1/10 and 1/10 survivors, respectively, P<0.05), with similar differences seen at 6-hour survival and on neurological scoring. CONCLUSIONS: Timing of hypothermia is a crucial determinant of survival in the murine arrest model. Early intra-arrest cooling appears to be significantly better than delayed post-ROSC cooling or normothermic resuscitation.

Animals↗
PubMed2004

Out-of-hospital cardiac arrest in patients with cardiac amyloidosis: presenting rhythms, management and outcomes in four patients.

Primary systemic amyloidosis (AL) is a well-recognized systemic disease, and cardiac amyloidosis accounts for 10% of all nonischemic cardiomyopathies [J S C Med Assoc 97 (2001) 201-206]. The median survival of patients with symptomatic congestive heart failure secondary to cardiac amyloidosis is 4 months [New Engl J Med 336 (1997) 1202-1207; Am J Med 100 (1996) 290-298]. The cause of death in most patients is refractory congestive heart failure or sudden arrhythmic [Mayo Clin Proc 59 (1984) 589-597]. While there are reports of in-hospital arrhythmic deaths in these patients, there are no detailed reports that describe the presentation and management of patients with cardiac amyloidosis who have experienced an out-of-hospital cardiac arrest (OHCA). We describe here our experience with four patients with AL who had an OHCA, including presenting rhythms, interventions, and outcomes.

Amyloidosis↗
PubMed1975

Hypothermic arrest and potassium arrest: metabolic and myocardial protection during elective cardiac arrest.

Hypothermic arrest, potassium arrest, and ischemic arrest, either singly or in combination, with or without coronary perfusion were studied in an isolated perfused rat heart preparation. Procedures that permitted the maintenance of high cellular levels of adenosine triphosphate (ATP) and creatine phosphate during arrest, e.g., coronary perfusion with hypothermic solutions or solutions containing 16.0 mM potassium, produced a fully reversible arrest with complete cardiac recovery. Cardiac arrest and coronary flow were related to the degree of hypothermia and the concentration of potassium in the coronary perfusate, and the minimum conditions required to induce complete cardiac arrest were ascertained. The effects of hypothermia and potassium were additive; total cardiac arrest could be obtained by combining small evaluations of potassium with moderate hypothermia. Under these conditions, cellular high-energy phosphates were maintained, and complete recovery was possible. Under conditions in which arrest was obtained without maintaing coronary perfusion, e.g., ischemic arrest, cellular high-energy phosphates declined rapidly, and the hearts exhibited poor recoveries. Some protection could be afforded to the ischemic myocardium by topical hypothermia or by combining the ischemia with potassium arrest. In both instances, ATP and creatine phosphate were maintained at higher levels, and improved recoveries were observed.

Adenosine Triphosphate↗
PubMed2003

Is the ACLS score a valid prediction rule for survival after cardiac arrest?

UNLABELLED: The ACLS (advanced cardiac life support) Score was previously developed to predict survival from out-of-hospital cardiac arrest. Whether the arrest was witnessed, initial cardiac rhythm, performance of bystander cardiopulmonary resuscitation (CPR), and the response time of the paramedic unit were determined to be predictive of survival. However, the ACLS Score has not been validated in other emergency medical services systems. OBJECTIVES: The purpose of this study was to externally validate the ACLS Score in one patient population. METHODS: This was a retrospective cohort study performed at an urban county teaching hospital. The study population consisted of consecutive adult patients treated for out-of-hospital, nontraumatic cardiac arrest, and transported to the authors' institution between November 1, 1994, and September 30, 2001. Patient records for all cardiac arrests during the study period were reviewed. Study variables included witnessed arrest, initial arrest rhythm, bystander CPR, paramedic response time, and survival to hospital discharge. Predicted probability of survival to hospital discharge was calculated for each patient using the ACLS Score. The overall predicted and observed survival rates were compared using Flora's Z score. The Hosmer-Lemeshow test was used to evaluate the model's goodness-of-fit over a range of survival probabilities. RESULTS: Of 754 cardiac arrest patients enrolled in the study period, 575 (76%) patients had documentation that allowed scoring using the ACLS Score. Twenty-five (4%) patients survived to hospital discharge. The predicted number of survivors based on the ACLS Score was 104 (18%), yielding a Flora's Z statistic of -4.46 (p < 0.0001). After categorizing predicted survival probabilities into four categories, the resulting Hosmer-Lemeshow statistic was 210 (p << 10(-6)). Both goodness-of-fit statistics demonstrated extremely poor fit of the model. A receiver operating characteristic (ROC) curve was created, yielding an area under the ROC curve of 0.33 (95% CI = 0.19 to 0.47), signifying extremely poor discrimination. CONCLUSIONS: The previously published ACLS Score was not valid when applied to an external cohort of out-of-hospital cardiac arrest patients. An externally valid model is needed to predict survival to hospital discharge following out-of-hospital cardiac arrest.

Advanced Cardiac Life Support↗
PubMed1995

Regulation of tyrosine protein kinase receptor Trk-B and motor function in rats following cardiac arrest.

Following 10 min cardiac arrest and resuscitation, male Sprague-Dawley rats developed posthypoxic myoclonus. Sixty days later, the motor function of the animals was restored. In the present study, we investigated brain levels of tyrosine protein kinase receptor Trk-B with quantitative immunoblot analysis at various time points following cardiac arrest. In the frontal cortex, a significant reduction of Trk-B was found in rats 3 days (53%) after cardiac arrest, whereas significant increases were detected in rats 14 (124%) and an average 60 days (98%) after cardiac arrest. In the striatum, significant increases were found in rats 3 (389%), 14 (483%), and 60 days (521%) after resuscitation. In contrast, significant reductions of Trk-B were detected in the cerebellum of rats 3 (46%), 14 (22%), and 60 days (18%) after cardiac arrest. The results indicate that regulation of Trk-B may vary in different brain regions and have important roles in recovery processes following hypoxic-ischemic insults to the brain.

Animals↗