Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CARDIAC ARREST”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 865 records · Page 48Linked to original sources
PubMed1997

Paramedics, technicians, and survival from out of hospital cardiac arrest.

OBJECTIVE: To test the hypothesis that limited paramedic advanced life support skills afford no advantage in survival from cardiac arrest when compared with non-paramedic ambulance crews equipped with defibrillators in an urban environment; and to investigate whether separate response units delayed on scene times. METHODS: A prospective, observational study was conducted over 17 consecutive months on all adult patients brought to the accident and emergency (A&E) department of Glasgow Royal Infirmary having suffered an out of hospital cardiac arrest of cardiac aetiology. The main interventions were bystander cardiopulmonary resuscitation (CPR) and limited advance life support skills. MAIN OUTCOME MEASURES: Return of spontaneous circulation, survival to admission, and discharge. RESULTS: Of 240 patients brought to the A&E department, 19 had no clear record of whether a paramedic was or was not involved and so were excluded. There was no difference in survival between the two groups, although a trend to admission favoured non-paramedics. Paramedics spent much longer at the scene (P < 0.0001). Witnessed arrests (P = 0.01), early bystander CPR (P = 0.12), shockable rhythms (P = 0.003), and defibrillation (P < 0.0001) were associated with better survival. Intubation and at scene times were not associated with better survival. Delayed second response units did not prolong at scene times. CONCLUSIONS: The interventions of greatest benefit in out of hospital cardiac arrest are basic life support and defibrillation. Additional skills are of questionable benefit and may detract from those of greatest benefit.

Adolescent↗
PubMed2004

B-type natriuretic peptide as a marker of resuscitation in patients with cardiac arrest outside the hospital.

BACKGROUND: Although the circulating concentration of B-type natriuretic peptide (BNP) has both a prognostic and diagnostic value in heart disease, no data are available regarding its resuscitative value for out-of-hospital cardiac arrest. METHODS AND RESULTS: The present study was a prospective study of 401 patients whose BNP was measured on arrival at the emergency room after an out-of-hospital cardiac arrest with a cardiac cause. The primary endpoint was survival to hospital discharge. The unadjusted rate of survival to hospital discharge decreased in a stepwise fashion among patients in increasing quartiles of BNP concentration (p<0.001). After adjusting for independent predictors of resuscitation, the odds ratios for survival to hospital discharge in the second, third and fourth quartiles of BNP were 0.13 (95% confidence interval (CI), 0.04-0.46), 0.10 (95% CI, 0.03-0.41), and 0.004 (95% CI, 0.00-0.16), respectively. The BNP cutoff value of 100 pg/ml for survival had a sensitivity of 83% and a negative predictive value of 96%. CONCLUSIONS: The measurement of BNP was found to provide valuable predictive information for survival to hospital discharge in patients with out-of-hospital cardiac arrest of cardiac etiology.

Adult↗
PubMed2003

Prehospital behaviour of patients admitted with acute coronary syndrome or witnessed cardiac arrest.

OBJECTIVE: To study prehospital behaviour of patients admitted with acute coronary syndrome or witnessed cardiac arrest. DESIGN: Structured interview of 250 consecutive patients with acute coronary syndrome and relatives of 48 patients with witnessed cardiac arrest. The following courses of action were studied: contact the emergency medical service (centre); contact the general practitioner from the emergency service or the general practitioner during working hours; self-transportation to the emergency department; or as the first action to call the emergency medical service. RESULTS: Forty-four per cent of the patients admitted with cardiac arrest expressed no prior symptoms. Two-thirds of patients with typical symptoms interpreted it as cardiac-still only half took action within 20 min. Fifty per cent of patients who called a physician were delayed by wrong advice or misinterpretation. One hundred and thirteen patients (45%) knew of thrombolytic therapy. Twenty-seven of 75 patients with knowledge of the benefit of prompt treatment with thrombolysis, acted in accordance with this awareness. CONCLUSION: Patients misinterpret symptoms of acute coronary syndrome and are misguided when calling for medical assistance. Perceiving jeopardy had positive influence on the behaviour. Awareness of therapeutic options influences the decision-making process.

Aged↗
PubMed2003

Avoidable cardiac arrest: lessons for an A&E department.

Deterioration to cardiac arrest is not always sudden and unexpected and on a significant number of occasions cardiac arrest could be prevented. This has important messages for the Accident and Emergency (A&E) department as the vast majority of emergency admissions originate via A&E.

Diagnostic Errors↗
PubMed2006

Amplitude-integrated EEG (aEEG) predicts outcome after cardiac arrest and induced hypothermia.

OBJECTIVE: To evaluate the use of continuous amplitude-integrated EEG (aEEG) as a prognostic tool for survival and neurological outcome in cardiac arrest patients treated with hypothermia. DESIGN: Prospective, observational study. SETTING: Multidisciplinary intensive care unit in a university hospital. INTERVENTION: Comatose survivors of cardiac arrest were treated with induced hypothermia for 24 h. An aEEG recording was initiated upon arrival at the ICU and continued until the patient regained consciousness or, if the patient remained in coma, no longer than 120 h. The aEEG recording was not available to the ICU physician, and the aEEG tracings were interpreted by a neurophysiologist with no knowledge of the patient's clinical status. Only clinically visible seizures were treated. MEASUREMENTS AND RESULTS: Thirty-four consecutive hypothermia-treated cardiac arrest survivors were included. At normothermia (mean 37 h after cardiac arrest), the aEEG pattern was discriminative for outcome. All 20 patients with a continuous aEEG at this time regained consciousness, whereas 14 patients with pathological aEEG patterns (flat, suppression-burst or status epilepticus) did not regain consciousness and died in hospital. Patients were evaluated neurologically upon discharge from the ICU and after 6 months, using the Cerebral Performance Category (CPC) scale. Eighteen patients were alive with a good cerebral outcome (CPC 1--2) at 6-month follow-up. CONCLUSION: A continuous aEEG pattern at the time of normothermia was discriminative for regaining consciousness. aEEG is an easily applied method in the ICU setting.

Adult↗
PubMed1992

[A case of cardiac arrest encephalopathy in athetotic cerebral palsy].

A 25-year-old woman with cerebral palsy of spastic quadriplegia and athetosis showed typical cardiac arrest encephalopathy on neuropathology. The etiology of cerebral palsy was perinatal origin including prematurity, asphyxia and hyperbilirubinemia. Ventricular premature beats had developed since about 20 years of age. Muscle tone also increased with aging and symptoms of vago-vagal reflex were occasionally observed after eating. At 25 years, cardiac arrest occurred and cardiopulmonary resucitation was done immediately. She remained unconscious with absent corneal reflex and irregular respiration. EEG or auditory brain stem response showed flat activity. She died of respiratory failure 53 days after the episode of cardiac arrest. Neuropathology showed bilaterally symmetrical necrosis in the superior colliculi, gracilis nuclei, cuneate nuclei and spinotrigeminal nuclei accompanied with severe necrosis in the cerebrum and cerebellum. These findings in this adult case of total asphyxia were compatible with those observed in total plus partial asphyxia in the neonates. This discrepancy may be due to difference in cerebral maturity. Children or young adults with athetotic type cerebral palsy have a high risk of sudden death. Sudden cardiac arrest seems to play an important role in sudden death of these patients.

Adult↗
PubMed1992

Cardiopulmonary bypass for resuscitation of patients with accidental hypothermia and cardiac arrest.

Hypothermic patients have been successfully rewarmed by a number of methods. However, when cardiac arrest occurs, as it frequently does at core temperatures of less than 27 degrees C, prolonged cardiopulmonary resuscitation (CPR) is required, because defibrillation can rarely be achieved until the patient has been rewarmed to 30 degrees to 34 degrees C. Five cases of accidental hypothermia with cardiac arrest treated with cardiopulmonary bypass are discussed. The first patient died as a result of inadequate low-flow cardiopulmonary bypass by the femorofemoral route. The second patient had prolonged CPR by closed-chest cardiac massage and warm peritoneal lavage followed by transthoracic cardiopulmonary bypass. This patient regained consciousness but was found to be paraplegic and died from bowel infarction related to peritoneal rewarming without adequate perfusion. In the last three patients, high-flow cardiopulmonary bypass was rapidly achieved using a no. 28 French chest tube for femoral venous cannulation, and they recovered completely. In cases of accidental hypothermia with cardiac arrest, rapid institution of full cardiopulmonary bypass provides excellent circulatory support and rapid rewarming. This avoids the complications of prolonged inadequate circulation that occur when closed-chest cardiac massage and external rewarming are used.

Adult↗
PubMed2005

Protein kinase C and synaptic dysfunction after cardiac arrest.

It is now understood that the mechanisms leading to neuronal cell death after cardiac arrest (CA) are highly complex. A well established fact in this field is that neurons continue to die over days and months after ischemia. It has been suggested that decreases in electrophysiological activities precede the morphologic deterioration in postischemic CA1 neurons and that this deterioration may be one cause for delayed cell death. The link between synaptic dysfunction and cardiac arrest is evident by the fact that about 50% of long-term survivors of cardiac arrest exhibit impaired mental abilities, manifested as learning impairment, memory disturbance. Since PKC is known to be a key player in synaptic function and has been implicated in promoting cell death after cerebral ischemia, it is a logical candidate as a modulator of synaptic derangements after CA. In this review, we provide an overview of synaptic dysfunction following CA and the putative role of PKC on this dysfunction.

Journal Article↗
PubMed1996

Vasopressin administration in refractory cardiac arrest.

BACKGROUND: Successful outcomes after cardiopulmonary resuscitation remain disappointingly infrequent, in animal studies, administration of exogenous vasopressin during closed- and open-chest cardiopulmonary resuscitation has recently been shown to be more effective than optimal doses of epinephrine in improving vital organ blood flow. OBJECTIVE: To describe the clinical effects and outcomes of administering vasopressin to patients in cardiac arrest refractory to current medical therapies. DESIGN: Case reports. SETTING: University hospital. PATIENTS: 8 adults with in-hospital cardiac arrest. INTERVENTIONS: After intravenous epinephrine (administered according to American Heart Association guidelines) and defibrillation efforts had failed, patients in cardiac arrest who were having cardiopulmonary resuscitation received 40 U of vasopressin intravenously and then defibrillation. MEASUREMENTS: Return of spontaneous circulation and hospital discharge rates. RESULTS: After administration of vasopressin, spontaneous circulation was promptly restored in all patients. Three patients were discharged from the hospital with intact neurologic function; the other five lived for between 30 minutes and 82 hours. CONCLUSION: In the presence of ventricular fibrillation with severe hypoxia and acidosis, vasopressin seems to be more potent and effective than adrenergic vasopressors for restoring spontaneous cardiovascular function. These results do not justify the widespread use of vasopressin for refractory cardiac arrest. However, on the basis of these cases, further studies comparing vasopressin with epinephrine are warranted in an effort to improve the currently dismal prognosis of patients after cardiac arrest.

Adult↗
PubMed1997

Estimating effectiveness of cardiac arrest interventions: a logistic regression survival model.

BACKGROUND: The study objective was to develop a simple, generalizable predictive model for survival after out-of-hospital cardiac arrest due to ventricular fibrillation. METHODS AND RESULTS: Logistic regression analysis of two retrospective series (n=205 and n=1667, respectively) of out-of-hospital cardiac arrests was performed on data sets from a Southwestern city (population, 415,000; area, 406 km2) and a Northwestern county (population, 1,038,000; area, 1399 km2). Both are served by similar two-tiered emergency response systems. All arrests were witnessed and occurred before the arrival of emergency responders, and the initial cardiac rhythm observed was ventricular fibrillation. The main outcome measure was survival to hospital discharge. Patient age, initiation of CPR by bystanders, interval from collapse to CPR, interval from collapse to defibrillation, bystander CPR/collapse-to-CPR interval interaction, and collapse-to-CPR/collapse-to-defibrillation interval interaction were significantly associated with survival. There was not a significant difference between observed survival rates at the two sites after control for significant predictors. A simplified predictive model retaining only collapse to CPR and collapse to defibrillation intervals performed comparably to the more complicated explanatory model. CONCLUSIONS: The effectiveness of prehospital interventions for out-of-hospital cardiac arrest may be estimated from their influence on collapse to CPR and collapse to defibrillation intervals. A model derived from combined data from two geographically distinct populations did not identify site as a predictor of survival if clinically relevant predictor variables were controlled for. This model can be generalized to other US populations and used to project the local effectiveness of interventions to improve cardiac arrest survival.

Adolescent↗
PubMed1977

Changes in cisternal fluid potassium concentration following cardiac arrest.

The purpose of this study was to measure the changes in potassium concentration in human cisternal cerebrospinal fluid following successful resuscitation after cardiac arrest. We also wished to examine whether or not changes in potassium concentration in the cisternal cerebrospinal fluid could be correlated to the ability to regain normal cerebral function. 41 patients were studied, of whom 20 regained consciousness and 21 did not. In those who did not regain consciousness there was a significant increase in the potassium concentration found in samples obtained between 40 and 50 min, and between 50 and 60 min after cardiac arrest. The potassium concentration decreased to normal values during the following hours. Lumbar spinal fluid did not reflect the changes in cisternal fluid. The results suggest that the potassium concentration of cisternal cerebrospinal fluid, obtained soon after cardiac arrest, might give an indication of the degree of cerebral damage caused by cardiac arrest.

Cisterna Magna↗
PubMed2002

Effects of decreasing inspiratory flow rate during simulated basic life support ventilation of a cardiac arrest patient on lung and stomach tidal volumes.

If the airway of a cardiac arrest patient is unprotected, basic life support with low rather than high inspiratory flow rates may reduce stomach inflation. Further, if the inspiratory flow rate is fixed such as with a resuscitator performance may improve; especially when used by less experienced rescuers. The purpose of the present study was to assess the effect of limited flow ventilation on respiratory variables, and lung and stomach volumes, when compared with a bag valve device. After institutional review board approval, and written informed consent was obtained, 20 critical care unit registered nurses volunteered to ventilate a bench model simulating a cardiac arrest patient with an unprotected airway consisting of a face mask, manikin head, training lung [with lung compliance, 50 ml/0.098 kPa (50 ml/cmH(2)O); airway resistance, 0.39 kPa/l/s (4 cmH(2)O/l/s)] oesophagus [lower oesophageal sphincter pressure, 0.49 kPa (5 cmH(2)O)] and simulated stomach. Each volunteer ventilated the model with a self-inflating bag (Ambu, Glostrup, Denmark; max. volume, 1500 ml), and a resuscitator providing limited fixed flow (Oxylator EM 100, CPR Medical devices Inc., Toronto, Canada) for 2 min; study endpoints were measured with 2 pneumotachometers. The self-inflating bag vs. resuscitator resulted in comparable mean +/- SD mask tidal volumes (945 +/- 104 vs. 921 +/- 250 ml), significantly (P < 0.05) higher peak inspiratory flow rates (111 +/- 27 vs. 45 +/- 21 l/min), and peak inspiratory pressure (1.2 +/- 0.47 vs. 78 +/- 0.07 kPa), but significantly shorter inspiratory times (1.1 +/- 0.29 vs. 1.6 +/- 0.35 s). Lung tidal volumes were comparable (337 +/- 120 vs. 309 +/- 61 ml), but stomach tidal volumes were significantly (P < 0.05) higher (200 +/- 95 vs. 140 +/- 51 ml) with the self-inflating bag. In conclusion, simulated ventilation of an unintubated cardiac arrest patient using a resuscitator resulted in decreased peak flow rates and therefore, in decreased peak airway pressures when compared with a self-inflating bag. Limited flow ventilation using the resuscitator decreased stomach inflation, although lung tidal volumes were comparable between groups.

Cardiopulmonary Resuscitation↗
PubMed1996

Cerebral resuscitation from cardiac arrest: pathophysiologic mechanisms.

Both the period of total circulatory arrest to the brain and postischemic-anoxic encephalopathy (cerebral postresuscitation syndrome or disease), after normothermic cardiac arrests of between 5 and 20 mins (no-flow), contribute to complex physiologic and chemical derangements. The best documented derangements include the delayed protracted inhomogeneous cerebral hypoperfusion (despite controlled normotension), excitotoxicity as an explanation for selectively vulnerable brain regions and neurons, and free radical-triggered chemical cascades to lipid peroxidation of membranes. Protracted hypoxemia without cardiac arrest (e.g., very high altitude) can cause angiogenesis; the trigger of it, which lyses basement membranes, might be a factor in post-cardiac arrest encephalopathy. Questions to be explored include: What are the changes and effects on outcome of neurotransmitters (other than glutamate), of catecholamines, of vascular changes (microinfarcts seen after asphyxia), osmotic gradients, free-radical reactions, DNA cleavage, and transient extracerebral organ malfunction? For future mechanism-oriented studies of the brain after cardiac arrest and innovative cardiopulmonary-cerebral resuscitation, increasingly reproducible outcome models of temporary global brain ischemia in rats and dogs are now available. Disagreements exist between experienced investigative groups on the most informative method for quantitative evaluation of morphologic brain damage. There is agreement on the desirability of using not only functional deficit and chemical changes, but also morphologic damage as end points.

Altitude Sickness↗
PubMed1994

Early blood-brain barrier changes in the rat following transient complete cerebral ischemia induced by cardiac arrest.

This study examined regional patterns of increased vascular permeability following transient global cerebral ischemia. Rats underwent 3.5, 5 or 10 min of cardiac vessel bundle occlusion, i.e. cardiac arrest. The animals were killed at 2, 3, 5 and 15 min, or 1, 3, 6 and 24 h after global cerebral ischemia. Thirty minutes before the end of each blood recirculation period, the electron dense protein tracer--horseradish peroxidase (HRP) was intravenously injected and rats were perfusion-fixed for light and electron microscopic analysis. Control rats showed no HRP leakage. Post-ischemic rats demonstrated random blood-brain barrier (BBB) alterations. Permeability alterations were spotty and widespread in cortical, thalamic, basal ganglia, hippocampal, brain stem regions, cerebellum and white matter. Peroxidase extravasation frequently involved arterioles, veins and venules surrounded by perivascular spaces. Routes of increased HRP permeability included endothelial cell (EC) vesiculo-canalicular profiles and diffuse leakage through damaged ECs. Barrier damage determined by HRP permeability revealed a biphasic nature. The first stage appeared immediately after ischemia at the 2nd min and involved the 1st post-insult hour. There was no HRP leakage in rats sacrificed 3 h after insult. BBB opening appeared again 6 h after ischemia and remained open 24 h after cardiac arrest. The openings of BBB did not increase in frequency with longer periods of ischemia and recirculation. These results demonstrate that cardiac arrest produces a spotty BBB disturbances at vessel bifurcations and suggest that BBB changes associated with cardiac arrest may be multifactorial in time course and location.

Animals↗
PubMed1991

Sudden cardiac arrest outside the hospital--value of defibrillators in ambulances.

In a region with a population of 250,000 people, all emergency calls for cardiac arrest were prospectively registered during a period of 6 years. Timing of events were carefully registered as were treatment and the participation of 3 ambulances equipped with defibrillators. When time until initial treatment of cardiac arrest was below 5 min, 12% could be resuscitated and discharged alive. This figure decreased to 2% in the period between 5 and 10 min and was zero to above 10 min. Similarly, a reasonable 12% of patients experiencing ventricular fibrillation at a public place could be resuscitated and discharged alive whereas only 5% of ventricular fibrillation occurring at the patients home could be successfully resuscitated. Asystolia was rarely treated successfully. Faster treatment improved results much and 63% of patients having ventricular fibrillation in the emergency room left hospital alive. Results of cardioversion in ambulances did not depend on time from initiation of cardiac arrest, but all patients receiving cardioversion later than 10 min died without regaining consciousness. The results were compared with other more effective programs. The study region apparently had much fewer cardiac arrest than a similar region in Seattle, U.S.A. In those cases where treatment could be initiated within 5 min, results were comparable.

Ambulances↗
PubMed2006

Major differences in 1-month survival between hospitals in Sweden among initial survivors of out-of-hospital cardiac arrest.

AIM: To explore the rate of survival to hospital discharge among patients who were brought to hospital alive after an out-of-hospital cardiac arrest in different hospitals in Sweden. PATIENTS AND METHODS: All patients who had suffered an out-of-hospital cardiac arrest which was not witnessed by the ambulance crew, in whom cardiopulmonary resuscitation (CPR) was started and who had a palpable pulse on admission to hospital were evaluated for inclusion. Each participating ambulance organisation and its corresponding hospital(s) required at least 50 patients fulfilling these criteria. RESULTS: Three thousand eight hundred and fifty three patients who were brought to hospital by 21 different ambulance organisations fulfilled the inclusion criteria. The number of patients rescued by each ambulance organisation varied between 55 and 900. The survival rate, defined as alive 1 month after cardiac arrest, varied from 14% to 42%. When correcting for dissimilarities in characteristics and factors of the resuscitation, the adjusted odds ratio for survival to 1 month among patients brought to hospital alive in the three ambulance organisations with the highest survival versus the three with the lowest survival was 2.63 (95% CI: 1.77-3.88). CONCLUSION: There is a marked variability between hospitals in the rate of 1-month survival among patients who were alive on hospital admission after an out-of-hospital cardiac arrest. One possible contributory factor is the standard of post-resuscitation care.

Aged↗
PubMed1993

Fluorescent histochemical localization of lipid peroxidation during brain reperfusion following cardiac arrest.

Rats were subjected to cardiac arrest and resuscitation, 90 min of reperfusion, and in situ perfusion fixation. Thiobarbituric acid (TBA) was included in the aldehyde-free perfusion fixative, the TBA reaction was driven in situ by heating, and fluorescence microscopy was utilized to characterize the location of products of the TBA reaction. Absorbance-difference spectra were performed on butanol-extracted brain homogenates to confirm in situ formation of TBA adducts with aldehydic products of lipid peroxidation. Nissl-stained sections revealed good cellular fixation without shrinkage artifacts. Fluorescence was not seen microscopically when TBA was omitted from the perfusion fixative, and little fluorescence was present in normal brains or brains after ischemia only. However, after 90-min reperfusion, intense granular fluorescence was seen in the neuronal perikarya (especially at the base of the apical dendrite) of numerous pyramidal neurons in cortical layers 5 and 6 and in the pyramidal layer of Ammon's horn in the hippocampus. The nuclei of these cells exhibited no fluorescence. Fluorescence was also present in some striatal neurons, but was absent in the adjacent radial bundles. Neither glia nor white matter exhibited similar fluorescence. These observations indicate that neurons in the selectively vulnerable zones of the cortex and hippocampus are early and specific targets of lipid peroxidation during post-ischemic reperfusion.

Animals↗
PubMed2005

On-scene physician assessment of thromboembolic etiology in out-of-hospital cardiac arrest.

Out-of-hospital cardiac arrest (OOHCA) treatment produces dismal recovery rates. Newer, directed therapies such as thrombolysis may be best considered if possible etiologies can be assessed immediately. We conducted a prospective, pilot, feasibility study of on-scene physician assessments in non-traumatic OOHCA. Physicians responded to the scene and reported likelihood of thromboembolic etiology based on detailed history and physical assessments. Included were 136/148 OOHCAs during the 6-month study period; median age was 69.5 years and 72% were men. Physicians judged 103/136 (76%) of arrests to be of thromboembolic etiology and would have recommended thrombolytic bolus in 83/136 (61%). Among 19 instances of physician-reported contraindications, 17 (90%) were not true contraindications. Median age was lower in the group recommended for thrombolysis. Thromboembolic etiology as judged by on-scene physicians was common and physicians recommended thrombolytic bolus commonly. Contraindications were highly overestimated. These data may be useful in the consideration of innovative, directed therapies such as thrombolysis in attempts to improve outcomes from OOHCA.

Aged↗