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Biomedical subjects

F Sterz

Publications and source records attributed to F Sterz.

At least 55 records · Page 3Linked to original sources
PubMed1997

Fatal pulmonary edema after nitric acid inhalation.

We report a case of acute inhalation injury of nitric acid in a 56-year old white male. The patient presented conscious and dyspnoic at the emergency department after cleaning a copper chandelier with nitric acid. He had to be intubated 2 h after admission and mechanically ventilated because of fulminant respiratory insufficiency. As all sources of mechanical ventilation failed, extracorporeal membrane oxygenation had to be established 7 h after admission. With the additional use of surfactant and low dose inhalation therapy with nitric oxide (NO), the patient could be stabilised for 3 days and lung function improved temporarily. Despite all efforts the patient died at the fourth day from refactory respiratory failure. Pathologic examination revealed massive pulmonary edema without signs of inflammation. Thus, nitric acid inhalation induced pulmonary edema appears to be a most severe situation in which even most modern therapeutic interventions fail. As, in respect of recent literature and our case no promising therapy for nitric acid inhalation pulmonary edema is available, our efforts have to be directed towards prevention of nitric acid exposure.

Accidents, Home↗
PubMed1997

Gastric rupture--an uncommon complication after successful cardiopulmonary resuscitation: report of two cases.

Gastric rupture is a poorly described complication following cardiopulmonary resuscitation. An incidence of 0.1% has been reported in the literature. Published reports describe traumatic gastric rupture after use of the CardioPump, after mouth-to-mouth ventilation, and in children after resuscitation performed by paramedics. We report on two patients who developed gastric rupture after successful standard cardiopulmonary resuscitation. Preexisting gastric ulcerations or osseous trauma during resuscitation had been excluded. Neither patient developed abdominal symptoms; in both cases the gastric rupture was diagnosed by routine chest X-ray and both patients underwent-after stabilization-surgical treatment. One patient recovered well, but the other developed cardiogenic shock due to malignant arrhythmias and severely impaired left ventricular function. This patient died on the 6th postinterventional day. Gastric rupture rarely occurs after cardiopulmonary resuscitation. The causes of gastric rupture and the means to avoid this complication will be discussed.

Aged↗
PubMed1997

Blood glucose concentration after cardiopulmonary resuscitation influences functional neurological recovery in human cardiac arrest survivors.

Experimental data suggest that postischemic blood glucose concentration plays an important role in modulating both ischemic cerebral infarction and selective neuronal necrosis. This study investigated the association between functional neurological recovery and blood glucose concentrations in human cardiac arrest survivors. A group of 145 nondiabetic patients were evaluated after witnessed ventricular fibrillation cardiac arrest. Data regarding cardiac arrest were collected according to an internationally accepted protocol immediately after arrival. Blood glucose was measured on admission and 6, 12, and 24 h thereafter. To control for duration of cardiac arrest and cardiogenic shock, both known to influence outcome as well as blood glucose, levels, Spearman rank partial correlation was used. In this multivariate analysis, a high admission blood glucose level tended to be associated with poor neurological outcome (rs = -0.16, n = 142, p = 0.06). The association between high median blood glucose levels over 24 h and poor neurological outcome was strong and statistically significant (rs = -0.2, n = 145, p = 0.015). High blood glucose concentrations occurring over the first 24 h after cardiac arrest have deleterious effects on functional neurological recovery. Whether cardiac arrest survivors might benefit from reduction of blood glucose levels needs further investigation.

Adult↗
PubMed1997

The emergency department in a 2000-bed teaching hospital: saving open ward and intensive care facilities.

Providing emergency medicine at the entrance to the hospital proves to be a sufficient link between pre- and inhospital medical care. The aim of our study is to investigate how many open ward and intensive care facilities can be saved within the hospital by the emergency department. Therefore, the data of our emergency department within a 2000-bed teaching hospital are retrospectively analysed. Unstable life-threatening emergencies for acute care, stable for immediate care and non-life-threatening emergencies are defined. Patients were discharged, admitted to an open ward, intensive care unit, the operation theatre or died. According to the level of care needed in the emergency department the continuing medical management is investigated. Over a 2-year period, 102,411 patients entered our emergency department. Overall 1498 (1%) needed acute care, 3652 (4%) immediate care and 97,261 (95%) delayed care. Of the acute care patients, 29 (2%) were discharged, 573 (38%) were admitted to an open ward, 551 (37%) to an intensive care unit, 67 (4%) needed surgery and 278 (19%) died. Of the immediate care patients, 1611 (44%) were discharged, 1755 (48%) were admitted to an open ward, 551 (37%) to an intensive care unit, and 286 (8%) needed surgery. Of the delayed care patients, 93061 (96%) were discharged and 4200 (4%) were admitted to an open ward. Of 5150 patients with life-threatening diseases, 551 (11%) needed an intensive care unit and 2328 (45%) an open ward. Providing acute and immediate care in our emergency department saves both intensive care and open ward facilities of the hospital.

Adult↗
PubMed1997

Early defibrillation.

Explore the source record for details and available documents.

Cardiopulmonary Resuscitation↗
PubMed1996

Creatine kinase-mb fraction and cardiac troponin T to diagnose acute myocardial infarction after cardiopulmonary resuscitation.

OBJECTIVES: This study sought to evaluate the diagnostic value of the biochemical markers creatine kinase (CK), creatine kinase-MB fraction (CK-MB) and cardiac troponin T (cTNT) to diagnose acute myocardial infarction (AMI) after cardiopulmonary resuscitation (CPR). BACKGROUND: Elevations of CK and CK-MB after CPR are a frequent finding and might be associated with ischemic myocardial injury, as well as physical trauma to the chest. METHODS: Patients who had cardiac arrest and primary successful resuscitation were included in the study. The diagnosis of AMI was confirmed or ruled out by means of typical electrocardiographic findings, thallium-201 myocardial scintigraphy or autopsy, if death occurred during the hospital period, in 39 primary survivors of sudden cardiac death. In 24 patients (62%) the diagnosis of AMI was established. Serum cTNT, CK and CK-MB were measured, and the CK-MB/CK ratio was calculated on admission and after 12 h. RESULTS: On admission all markers of myocardial injury proved to be weak methods for the diagnosis of AMI. After 12 h cTNT as well as CK-MB exhibited a similar diagnostic performance; CK and the CK-MB/CK ratio proved to be worthless. Sensitivity and specificity for a cTNT cutoff value of 0.6 ng/ml, 12 h after cardiac arrest, were 96% and 80%, respectively. For a CK-MB cutoff value of 26 U/liter, sensitivity was 96% and specificity was 73%. CONCLUSIONS: Cardiac TNT and CK-MB are valuable tools in detecting AMI as the cause of sudden cardiac death. However, there is a considerable lack of sensitivity and specificity. Cardiac injury is probably caused not only by AMI, but also by myocardial damage related to CPR efforts.

Animals↗
PubMed1996

Creatine kinase and creatine kinase-MB release after nontraumatic cardiac arrest.

The aim of the study was to describe the course of serum creatine kinase (CK) and its MB fraction (CK-MB) in patients surviving cardiac arrest, and to identify factors influencing CK and CK-MB release. The study was set in the community of Vienna, Austria. Data concerning cardiopulmonary resuscitation, collected within a period of 33 months, were evaluated retrospectively and compared with laboratory blood investigations collected prospectively (on admission and after 6, 12, and 24 hours) in 107 adult patients surviving a witnessed cardiac arrest for 24 hours. CK and CK-MB were elevated in >75% of the patients within 24 hours. Release of CK and CK-MB was mainly associated with electrocardiographic evidence of acute myocardial infarction (AMI) cumulative energy administered during defibrillation, and duration of chest trauma by compression. The CK-MB/CK ratio was elevated in 32% of the patients. Of patients with electrocardiographic evidence of AMI, only 49% had an elevated CK-MB/CK ratio. In conclusion, the elevation in serum CK and CK-MB fraction in patients after nontraumatic cardiac arrest is a frequent finding, and is associated with ischemic myocardial injury, as well as physical trauma to the chest. This should be considered when interpreting the course of CK and CK-MB fraction for the diagnosis of AMI.

Adult↗
PubMed1996

Hemodynamic effects of active compression-decompression after prolonged CPR.

BACKGROUND: This study was designed to test the effects of active compression-decompression (ACD) versus standard (STD) cardiopulmonary resuscitation (CPR) on hemodynamics after prolonged cardiac arrest (CA). METHODS AND RESULTS: After nontraumatic prehospital CA, 21 patients were resuscitated in a prospective nonblinded setting sequentially with STD and ACD CPR at the emergency department, if it had not been possible to achieve restoration of spontaneous circulation (ROSC) before admission. The compression rate was 80/min with a 50% duty cycle, and 1 mg epinephrine was given every 5th min. Invasive arterial, central venous pressure and end tidal CO2 (ETCO2) were monitored. Comparing coronary perfusion pressure (CoPP) and ETCO2, no significant differences between STD and ACD CPR were found. In 3 cases ROSC could be achieved for a short time. CONCLUSIONS: In our study, a comparison of STD and ACD CPR revealed no significant differences in coronary perfusion pressures and ETCO2. We conclude that after prolonged CA, ACD CPR does not provide an apparent hemodynamic advantage over STD CPR.

Aged↗
PubMed1996

Analysing calls by lay persons reporting cardiac arrest.

Prior to establishing a protocol for pre-arrival instructions for cardio-pulmonary resuscitation in the Vienna emergency medical system dispatch centre, a study was performed to determine whether any problems exist which may compromise guidance for basic life-support on the telephone. To evaluate the feasibility of prearrival instructions, a retrospective analysis of cardiac arrest calls was performed. We reviewed the Vienna emergency medical services dispatch centre tape recordings, ambulance run sheets and the hospital charts of 114 patients suffering from atraumatic cardiac arrest. Analysis showed that in 59 cases the arrest occurred in the victim's home. The telephone and the patient were either in the same or in adjoining rooms in 55% of the calls. We did not experience any technical or language difficulties. The caller and victim were related in 51 cases. The callers were completely calm in 77% and fairly calm in an additional 15%. Not one caller was distraught. Our data show that most objections to the feasibility of pre-arrival instructions can be refuted. We conclude that in Vienna the setting and location of arrest will impose few problems on the performance of bystander-cardio-pulmonary resuscitation using pre-arrival instructions given by dispatchers.

Austria↗
PubMed1996

Usefulness of a new rapid bedside troponin T assay in patients with chest pain.

We evaluated the usefulness of a rapid, qualitative, bedside immunoassay for cardiac-specific troponin T in patients with chest pain. A concordant result between quantitative troponin T and qualitative troponin T assay was observed in 183 (96%) tests. The sensitivity of the rapid troponin T assay for detecting acute myocardial infarction increased significantly according to the number of hours elapsed after onset of chest pain from 17% for patients presenting within 4 h to 71% for patients presenting in the time interval of greater than 8 h from onset of chest pain (P < 0.001). Specificity ranged from 83 to 93% in the three time intervals evaluated. A concordant result between CK-MB-measurement and rapid troponin T assay was observed in 159 (83%) tests. In 14/191 tests a positive rapid troponin T and a negative CK-MB assay was observed. In 9/14 (64%) cases this result was true positive for the rapid troponin T assay and in 5/14 (36%) cases false negative. As sensitivity and specificity of the rapid troponin T assay are comparable with CK-MB measurements, rapid troponin T assay is a simple and useful laboratory tool for the bedside triage in patients with chest pain.

Adult↗
PubMed1996

Effects of verapamil and diltiazem on the ventricular rate during simulated atrial flutter in isolated guinea pig hearts.

To compare the direct effects of verapamil and diltiazem on the ventricular rate during atrial flutter, we developed an atrial flutter model in guinea pig isolated hearts. Atrial flutter was simulated by rapid atrial pacing (cycle length = 50 ms). At this atrial pacing cycle length, the shape of the frequency of distribution of the ventricular cycle lengths was comparable to that during spontaneous atrial flutter. Verapamil (0.01, 0.03 microM) and diltiazem (0.03, 0.09 microM) caused a comparable prolongation of the atrioventricular conduction time and atrioventricular refractoriness. Also, the anterograde Wenckebach cycle length was increased to a comparable degree by both substances. The mean ventricular cycle length during atrial flutter was comparable prolonged by both substances. The prolongation of the maximal ventricular cycle length was significantly more pronounced in the presence of verapamil. The time dependence of drug-induced alterations in atrioventricular conduction time during abrupt changes of heart rate is significantly more pronounced in the presence of verapamil compared to diltiazem. In conclusion, the more pronounced effect of verapamil on the maximal ventricular cycle length compared to the action of diltiazem may be explained by the slow binding kinetic of this drug to the Ca2+ channel resulting in a longlasting blockade of the Ca2+ channel.

Animals↗
PubMed1996

Possibilities of brain protection with tirilazad after cardiac arrest.

Cardiac arrest and resuscitation often create a cerebral insult caused by the initial cessation of blood flow, followed by the incomplete ischemia of cardiopulmonary resuscitation (low flow), and, following the return of spontaneous circulation, by the post-resuscitation syndrome. A cascade of physiologic, vascular, and biochemical events is set in motion, including changes in neuropeptides, electrolytes such as calcium and magnesium, excitatory neurotransmitters such as glutamate and acetylcholine, lymphokines such as interleukin-1, and arachidonic acid metabolites such as prostaglandins and leukotrienes; and formation of oxygen free radicals and lactic acid. Oxygen free radical-induced lipid peroxidation appears to increase tissue injury during and after brain ischemia. The 21-aminosteroid U74006F (tirilazad mesylate) is a novel inhibitor of lipid membrane peroxidation induced by oxygen free radicals, which has been shown, in animal models of subarachnoid hemorrhage, central nervous system trauma, and cerebral ischemia, to limit the extent of secondary tissue damage, thus improving functional recovery. Since tirilazad appears to have little or no behavioral or physiologic side effects, it appears to be an ideal agent for widespread brain ischemia prophylaxis. Tirilazad mesylate studies in out-of-hospital cardiac arrest are currently being planned.

Antioxidants↗
PubMed1996

Mild resuscitative hypothermia and outcome after cardiopulmonary resuscitation.

Recovery without residual neurological damage after cardiac arrest with global cerebral ischemia is still a rare event. Severe impairment of bodily or cognitive functions is often the result. The individual, emotional, and social aspects of brain damage and rehabilitation are seldom taken into account. Efforts to improve the prevention of brain damage immediately after successful resuscitation of patients are missing. The efficacy of hypothermia in preserving neurologic function when instituted before and during certain no-flow cardiovascular states has been well documented both clinically and experimentally since the 1950s. Most studies have used moderate (28-33 degrees C) to deep (20-28 degrees C) hypothermia to demonstrate these protective effects. Considering the use of hypothermia for preservation and resuscitation, the lack of controlled outcome trials, the long period of time required to reach therapeutic hypothermia, and the incidence of rewarming complications such as infection, arrhythmia, and coagulopathy have made it difficult to apply these methods to emergency situations such as cardiac arrest. Recent experimental evidence in dogs has shown that hypothermia induced after cardiac arrest does indeed mitigate the effects of the postresuscitation syndrome and improves neurologic function and reduces histologic brain damage. More importantly, such benefits can be demonstrated with mild (34-36 degrees C) hypothermia, thus minimizing complications and requiring less time for induction of hypothermia. Ice water nasal lavage, direct carotid infusion of cold fluids, use of a cooling helmet, and peritoneal cooling are promising techniques for clinical cerebral cooling. External auditory canal temperature (e.g., tympanic membrane temperature changes) could provide an approximation to brain temperatures. For accurate temperature monitoring, however, a central pulmonary artery thermistor probe should be inserted. Temperature monitoring is needed to avoid temperature < 30 degrees C. Mild hypothermia may prove to be an important and secure component for cerebral preservation and resuscitation during and after global ischemia; it may also prove to be a useful method of cerebral resuscitation after global ischemic states, thereby promoting the prevention of neuromental diseases.

Austria↗
PubMed1996

Systemic and cerebral oxygen extraction after human cardiac arrest.

The aim of this study was to observe cerebral and systemic oxygen extraction after human cardiac arrest with return of spontaneous circulation. Eight adult patients after non-traumatic, cardiac arrest were included. Cerebral and systemic oxygen extraction ratios were measured together with haemodynamic variables beginning 2 hours after cardiac arrest and every 4 hours thereafter until 24 hours. Between 2 and 12 hours after cardiac arrest cerebral oxygen extraction values ranged from very low over normal to very high. In the further course these values were reduced until 24 hours in six patients. Two patients who were still alive after 6 months, both severely mentally disabled, had a higher cerebral oxygen extraction ratios in comparison with non-survivors. Systemic oxygen extraction seemed to vary more than the cerebral oxygen extraction. The two long-term survivors had normal to supranormal values from 8 to 24 hours. In conclusion cerebral oxygen extraction was higher in long-term cardiac arrest survivors than in non-survivors between 12 and 24 hours after the event. Further, a better quality of neurological recovery was associated with higher cerebral oxygen extraction. Systemic oxygen extraction was also impaired, but to a lesser extent, especially in long-term survivors.

Aged↗
PubMed1996

Arterial blood pressure after human cardiac arrest and neurological recovery.

BACKGROUND AND PURPOSE: In animal cardiac arrest studies, outcome has been improved by inducing arterial hypertension early after return of spontaneous circulation. The aim of our study was to evaluate whether arterial blood pressure within the first minutes and hours after return of spontaneous circulation influences neurological recovery in human cardiac arrest survivors. METHODS: Of 136 retrospectively evaluated patients after sudden cardiac death, two groups were defined: group 1, mean arterial blood pressure (MABP) within 5 minutes after return of spontaneous circulation above 100 mm Hg; group 2, MABP of 100 mm Hg or less. Thereafter MABP was measured every 5 minutes until 2 hours after return of spontaneous circulation. The groups were compared in regard to age, sex, in/out of hospital, witnessed/not witnessed, first electrocardiographic rhythm, time from cardiac arrest to beginning of life support and to return of spontaneous circulation, cumulative epinephrine dose administered, and best neurological outcome within 6 months. RESULTS: In group 1 (n = 54) good neurological recovery was observed in 63% and in group 2 (n = 82) in 55% (chi 2 = 0.87, P = NS). Both groups exhibited comparable baseline values except that time intervals from beginning of life support to return of spontaneous circulation were shorter in group 1. After we controlled for this difference with Spearman's partial rank correlation (rs), there was no association between MABP measured within the first 5 minutes and outcome (rs = -.023; P = NS). Good neurological recovery was independently and directly related to MABP measured during 2 hours after return of spontaneous circulation (rs = .26; P < .01). CONCLUSIONS: In human cardiac arrest survivors, good functional neurological recovery was independently and positively associated with arterial blood pressure during the first 2 hours after human cardiac arrest but not with hypertensive reperfusion within the first minutes after return of spontaneous circulation.

Aged↗
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↗