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F Sterz

Publications and source records attributed to F Sterz.

At least 73 records · Page 4Linked to original sources
PubMed1996

Cerebral resuscitation from cardiac arrest: treatment potentials.

In 1961, in Pittsburgh, PA, "cerebral" was added to the cardiopulmonary resuscitation system (CPR --> CPCR). Cerebral recovery is dependent on arrest and cardiopulmonary resuscitation times, and numerous factors related to basic, advanced, and prolonged life support. Postischemic-anoxic encephalopathy (the cerebral postresuscitation disease or syndrome) is complex and multifactorial. The prevention or mitigation of this syndrome requires that there be development and trials of special, multifaceted, combination treatments. The selection of therapies to mitigate the postresuscitation syndrome should continue to be based on mechanistic rationale. Therapy based on a single mechanism, however, is unlikely to be maximally effective. For logistic reasons, the limit for neurologic recovery after 5 mins of arrest must be extended to achieve functionally and histologically normal human brains after 10 to 20 mins of circulatory arrest. This goal has been approached, but not quite reached. Treatment effects on process variables give clues, but long-term outcome evaluation is needed for documentation of efficacy and to improve clinical results. Goals have crystallized for clinically relevant cardiac arrest-intensive care outcome models in large animals. These studies are expensive, but essential, because positive treatment effects cannot always be confirmed in the rat forebrain ischemia model. Except for a still-elusive breakthrough effect, randomized clinical trials of CPCR are limited in their ability to statistically document the effectiveness of treatments found to be beneficial in controlled outcome models in large animals. Clinical studies of feasibility, side effects, and acceptability are essential. Hypertensive reperfusion overcomes multifocal no-reflow and improves outcome. Physical combination treatments, such as mild resuscitative (early postarrest) hypothermia (34 degrees C) plus cerebral blood flow promotion (e.g., with hypertension, hemodilution, and normocapnia), each having multiple beneficial effects, achieved complete functional and near-complete histologic recovery of the dog brain after 11 mins of normothermic, ventricular fibrillation cardiac arrest. Calcium entry blockers appear promising as a treatment for postischemic-anoxic encephalopathy. However, the majority of single or multiple drug treatments explored so far have failed to improve neurologic outcome. Assembling and evaluating combination treatments in further animal studies and determining clinical feasibility inside and outside hospitals are challenges for the near future. Treatments without permanent beneficial effects may at least extend the therapeutic window. All of these investigations will require coordinated efforts by multiple research groups, pursuing systematic, multilevel research--from cell cultures to rats, to large animals, and to clinical trials. There are still many gaps in our knowledge about optimizing extracerebral life support for cerebral outcome.

Animals↗
PubMed1996

Resuscitative hypothermia.

Resuscitative (postinsult) hypothermia is less well studied than protective-preservative (pre- and intra-arrest) hypothermia. The latter is in wide clinical use, particularly for protecting the brain during cardiac surgery. Resuscitative hypothermia was explored in the 1950s and then lay dormant until the 1980s when it was revived. This change occurred through the discoveries of brain damage mitigating effects after cardiac arrest in dogs, and after forebrain ischemia in rats, of mild (34 degrees C) hypothermia (which is safe), and of benefits derived from moderate hypothermia (30 degrees C) after traumatic brain injury or focal brain ischemia in various species. The idea that protection-preservation or resuscitation by hypothermia is mainly explained by its ability to reduce cerebral oxygen demand has been replaced by an increasingly documented synergism of many beneficial mechanisms. Deleterious chemical cascades during and after these insults are suppressed even by mild hypothermia. Prolonged moderate hypothermia carries some risks, e.g., arrhythmias, infection and coagulopathies. These side effects need further study. In global brain ischemia, protective-preservative mild hypothermia provides lasting mitigation of brain damage. Resuscitative mild hypothermia, however, may be beneficial in terms of long-term outcome or may merely delay the inevitable loss of selectively vulnerable neurons. Even if the latter is true, mild hypothermia may extend the therapeutic window for other interventions. This extension of the therapeutic window requires further documentation. After normothermic cardiac arrest of 11 mins in dogs, mild resuscitative hypothermia from 15 mins to 12 hours after reperfusion plus cerebral blood flow promotion normalized functional recovery with the least histologic damage seen thus far. Optimal duration of, and rewarming methods from, resuscitative hypothermia need clarification. The earliest possible induction of mild hypothermia after cardiac arrest seems desirable. Head-neck surface cooling alone is too slow. Among many clinically feasible rapid cooling methods, carotid cold flush and peritoneal cooling look promising. After traumatic brain injury or focal brain ischemia, which seem to still benefit from even later cooling, surface cooling methods may be adequate. Resuscitative hypothermia after cardiac arrest, traumatic brain injury, or focal brain ischemia should be considered for clinical trials.

Animals↗
PubMed1996

Conservative management of foreign bodies in the gastrointestinal tract.

There are at present no clear guidelines whether foreign body ingestion in the gastrointestinal tract should be managed conservatively, endoscopically or surgically. Retrospectively we have, therefore, analyzed 78 foreign body ingestion's in 42 patients (age 15-72 years) admitted to the Emergency Department of the University Hospital in Vienna. Our intention was to assess the value of a conservative management, defined as daily follow-up visits until the foreign body spontaneously appeared in the feces and to find criteria when endoscopic or surgical management is required. Of 78 foreign bodies, 67 (86%) passed the gastrointestinal tract spontaneously without complications, 9 (11%) were removed endoscopically, and only 2 (3%) required surgery. There were no gastrointestinal perforations. Even foreign bodies with a maximal length of 13.5 cm appeared in the feces spontaneously within a few days. Our data suggests that more than 80% of adults with foreign body ingestion can be managed safely as outpatients by means of conservative treatment. Endoscopic or surgical removal is only indicated in very rare circumstances.

Adolescent↗
PubMed1995

Clinical evaluation of different doses of intravenous enalaprilat in patients with hypertensive crises.

BACKGROUND: The appropriate dose of intravenous enalaprilat to be used in the treatment of hypertensive crisis is controversial. There has been no comparative study of the efficacy and safety of different dosages of enalaprilat in hypertensive patients. METHODS: Sixty-five consecutive patients with hypertensive urgencies (systolic blood pressure > 210 mm Hg and/or diastolic blood pressure > 110 mm Hg) or emergencies (diastolic blood pressure > 100 mm Hg and evidence of end-organ damage, ie, angina pectoris, hypertensive encephalopathy, or congestive heart failure) admitted to an emergency department from January 1, 1994, to September 30, 1994, were identified. The patients were randomized to receive different doses of enalaprilat (0.625, 1.25, 2.5, and 5 mg). Response to treatment was defined as a stable reduction of systolic blood pressure to below 180 mm Hg and diastolic blood pressure to below 95 mm Hg within 45 minutes after the start of treatment and relief of symptoms in patients with hypertensive emergencies. RESULTS: In 41 (63%) of 65 patients, the treatment goal was reached. Twenty-four patients (37%) failed to achieve the goal of treatment within 45 minutes after administration of enalaprilat. The response rates in the 0.625-mg, 1.25-mg, 2.5-mg, and 5-mg groups were 67%, 65%, 59%, and 62%, respectively. The proportion of patients initially randomized who responded to treatment was not different between any of the four groups of enalaprilat doses. There were no significant differences according to enalaprilat dose with respect to changes in systolic, diastolic, and mean arterial blood pressure. No severe side effects were observed. CONCLUSION: Enalaprilat is a safe antihypertensive drug with moderate efficacy in the treatment of hypertensive crisis. As doses above 0.625 mg alter neither response rates nor the magnitude of blood pressure reduction, we recommend 0.625 mg as the initial dose in the treatment of hypertensive crisis.

Aged↗
PubMed1995

Tracheal rupture after emergency intubation during cardiopulmonary resuscitation.

We describe a case of tracheal rupture following an emergency intubation during cardiopulmonary resuscitation. This complication occurring during resuscitation has not apparently been reported previously. Possible causes during the management of cardiac arrest are discussed with references to previously described cases of tracheal rupture.

Aged↗
PubMed1995

Regional prevalence and distribution of ischemic neurons in dog brains 96 hours after cardiac arrest of 0 to 20 minutes.

BACKGROUND AND PURPOSE: In this established outcome model of cardiac arrest in dogs, we have used total (summed regional) brain histopathologic damage scores. The present study describes the regional progression of necrotic (ischemic) neuron prevalence with increasing duration of cardiac arrest. It tests the hypothesis that increases in the total prevalence of necrotic neurons better correspond to increasing arrest duration and better correlate with neurological deficit than do any individual regional scores. METHODS: Blinded evaluation with light microscopy was used to score the prevalence (five categories) and note the distribution of necrotic neurons in dog brains 96 hours after normothermic ventricular fibrillation cardiac arrest followed by standard reperfusion and control of extracerebral variables. Six coronal brain sections including 19 regions were examined from dogs subjected to 0 (n = 2), 5 (n = 5), 10 (n = 6), 12.5 (n = 12), 15 (n = 8), 17 (n = 5), or 20 (n = 1) minutes of cardiac arrest. Dogs were neurologically evaluated before death. RESULTS: Necrotic neurons were widespread and scattered among normal neurons. Individual regions varied in their sensitivity to different durations of cardiac arrest. There were consistent increases in the mean prevalence of necrotic neurons with increased arrest duration in the hippocampal dentate gyrus and for cerebellar granule neurons. Regionally, the caudate nucleus had the best correlation with clinical neurological deficit (rho = +.85, P < .01). CONCLUSIONS: Compared with total (summed regional) necrotic neuron prevalence scores, increased regional prevalence scores for cerebellar granule neurons with increasing arrest duration were equally significant, and scores for the caudate nucleus had nearly the same correlation with individual clinical neurological deficit.

Animals↗
PubMed1995

Near infrared spectroscopy during and after cardiac arrest--preliminary results.

OBJECTIVE: To evaluate if regional cerebrovascular oxygen saturation (rSO2) is linked to systemic oxygenation and if impaired regional cerebral oxygenation affects outcome in cardiac arrest patients. DESIGN: Prospective, observational study. SETTING: Emergency department of a University Hospital. SUBJECTS: Patients during cardiac arrest or after restoration of spontaneous circulation. INTERVENTIONS: To measure rSO2 an infrared light-emitting probe was applied to the patient's forehead after arrival in the emergency department. Data were collected continuously together with blood pressure and pulse oximetry. Each variable measured immediately after arrival was used for calculation. ENDPOINTS: Best outcome (cerebral performance category) or death within one week. MEASUREMENTS AND MAIN RESULTS: Regional SO2 was measured in 18 consecutive patients. Six patients presented with cardiac arrest on arrival and rSO2 was measured during chest compression. Twelve patients had achieved restoration of spontaneous circulation before they arrived in the emergency department. No association was found between rSO2 and pulse oximetry or rSO2 and blood pressure. All patients surviving for one week (n = 9) achieved a significantly higher median rSO2 on arrival than nonsurvivors (n = 9) (63% and 46%, respectively; p = 0.003). Median rSO2 was lower in the group arriving without spontaneous circulation (n = 6) than in patients after restoration of spontaneous circulation (n = 12) (44% and 63%, respectively; p = 0.009). This difference was not found in pulse oximetry readings. Patients with restoration of spontaneous circulation surviving the first week after cardiac arrest (n = 8) had a higher rSO2 than patients with restoration of spontaneous circulation who did not survive (n = 4) (65% and 48%, respectively). Time from restoration of spontaneous circulation to arrival was not different between the two groups. CONCLUSION: By showing that low rSO2 readings after cardiac arrest are associated with a higher mortality, this new, non-invasive and easily applicable technique might help to prognosticate outcome and offers new insights into monitoring cerebral oxygenation after cardiac arrest.

Adolescent↗
PubMed1994

Cerebral and systemic arteriovenous oxygen monitoring after cardiac arrest. Inadequate cerebral oxygen delivery.

BACKGROUND: After prolonged cardiac arrest, under controlled normotension, cardiac output and cerebral blood flow are reduced for several hours. This dog study documents for the first time the postarrest reduction in oxygen (O2) delivery in relation to O2 uptake for brain and entire organism. METHODS: In eight dogs we used our model of ventricular fibrillation (VF) cardiac arrest of 12.5 min, reperfusion with brief cardiopulmonary bypass, and controlled normotension, normoxemia, and mild hypocapnia to 24 h. RESULTS: Between 4 and 24 h after cardiac arrest, cardiac output decreased by about 25% and the systemic arteriovenous O2 content difference doubled, while the calculated systemic O2 utilization coefficient (O2 UC) increased and the systemic venous PO2 decreased, both not to critical levels. The cerebral arteriovenous O2 content difference however, which was 5.6 +/- 1.7 ml/dl before arrest, increased between 1 and 18 h, to 10.8 +/- 3.2 ml/dl at 4 h. The cerebral O2 UC increased and the cerebral venous PO2 decreased, both to critical levels. CONCLUSIONS: After prolonged cardiac arrest in dogs with previously fit hearts, the reduction of O2 transport to the brain is worse than its reduction to the whole organism. Monitoring these values might help in titrating life-support therapies.

Animals↗
PubMed1994

Mild hypothermia after cardiac arrest in dogs does not affect postarrest cerebral oxygen uptake/delivery mismatching.

PURPOSE: To compare measurements of cerebral arteriovenous oxygen content differences (oxygen extraction ratios, oxygen utilization coefficients) in dogs after cardiac arrest, resuscitated under normothermia vs. mild hypothermia for 1-2 h or 12 h. METHODS: In 20 dogs, we used our model of ventricular fibrillation (no blood flow) of 12.5 min, reperfusion with brief cardiopulmonary bypass, and controlled ventilation, normotension, normoxemia, and mild hypocapnia to 24 h. We compared a normothermic control Group I (37.5 degrees C) (n = 8); with brief mild hypothermia in Group II (core and tympanic membrane temperature about 34 degrees C during the first hour after arrest) (n = 6); and with prolonged mild hypothermia in Group III (34 degrees C during the first 12 h after arrest) (n = 6). RESULTS: In Group I, the cerebral arteriovenous O2 content difference was 5.6 +/- 1.6 ml/dl before arrest; was low during reperfusion (transient hyperemia) and increased (worsened) significantly to 8.8 +/- 2.8 ml/dl at 1 h, remained increased until 18 h, and returned to baseline levels at 24 h after reperfusion. These values were not significantly different in hypothermic Groups II and III. The cerebral venous (saggital sinus) PO2 (PssO2) was about 40 mmHg (range 29-53) in all three groups before arrest and decreased significantly below baseline values, between 1 h and 18 h after arrest; the lowest mean values were 19 +/- 19 mmHg in Group I, 15 +/- 8 in Group II (NS), and 21 +/- 3 in Group III (NS). Postarrest PssO2 values of < or = 20 mmHg were found in 6/8 dogs in Group I, 5/6 in Group II and 4/6 in Group III. Among the 120 values of PssO2 measured between 1 h and 18 h after arrest, 32 were below the critical value of 20 mmHg. CONCLUSIONS: After prolonged cardiac arrest, critically low cerebral venous O2 values suggest inadequate cerebral O2 delivery. Brief or prolonged mild hypothermia after arrest does not mitigate the postarrest cerebral O2 uptake/delivery mismatching.

Animals↗
PubMed1994

Sudden cardiac death of a teenage girl.

Anomalies of coronary artery origin can be of little clinical significance and only an incidental autopsy finding. However recent case reports have shown that a wide range of potential pathologic alterations of congenital coronary anomalies are associated with clinical symptoms and exercise related sudden death. We describe the case of a 16-year-old girl who sustained a cardiac arrest and died after cardiopulmonary resuscitation (CPR) of intractable cardiogenic shock. The sporty and previously healthy girl suddenly fainted after swimming in a tributary of the Danube. Autopsy revealed an anomalous origin of the left coronary artery from the anterior sinus of Valsalva and its course between aorta and pulmonary artery. The cause of this anomalous origin and possible mechanism for sudden death is discussed. We conclude that this congenital anomaly should be considered in cases of major cardiac events in young people.

Adolescent↗
PubMed1994

Adenosine for the management of patients with tachycardias--a new protocol.

We developed a new protocol for diagnosis and treatment of patients with sustained tachycardias (heart rate > 150 beats.min-1). The patients first underwent vagal manoeuvres; if those remained unsuccessful, i.v. adenosine in increasing doses of 6, 12, and 18 mg was administered until sinus rhythm (SR) or transient atrioventricular (AV) block, unmasking the underlying rhythm, was recorded. In the latter and in the non-responding cases other antiarrhythmics were applied. Ninety-three episodes of tachycardia in 46 patients were treated according to this protocol. Six episodes (6%) were terminated by carotid massage, 64 of the remaining 87 episodes (74%) responded to adenosine with return to SR. Conversion to SR occurred more often in episodes with narrow- than in wide-complex tachycardia (81 vs. 59%, P < 0.05). To achieve SR, the mean adenosine dose was lower in narrow- than in wide-complex tachycardia (13 +/- 8 vs 21 +/- 10 mg; P < 0.01). The duration of asystole after adenosine did not differ between these two groups, whereas the duration of arrhythmia after adenosine differed significantly (8.5 +/- 5.8 vs 18.6 +/- 22.9 s; P < 0.05). Side effects of adenosine such as flush, dyspnoea, and chest pain did not seem to be dose dependent and occurred in about 20%. According to our protocol, in more than 75% SR was achieved in patients with sustained tachycardias after vagal manoeuvres and adenosine.

Adenosine↗
PubMed1994

Action of ATP on ventricular automaticity.

ATP is an effective treatment of supraventricular tachycardia when the atrioventricular (AV) node is part of the reentrant circuit. However, the lower a pace-maker in the pacemaker hierarchy, the more sensitive it is to adenosine. Therefore, we investigated the effects of ATP on ventricular automaticity in in vivo and in vitro conditions. Wide and narrow QRS complex tachycardia in 46 patients was treated with 6, 12, and 18 mg ATP as sequential intravenous (i.v.) bolus. ATP terminated tachycardias in 67%. Bolus infusion ATP caused < or = 6.4-s asystole that was self-limited. Perfusion of isolated spontaneously beating guinea pig heart with 100 microM ATP completely suppressed ventricular automaticity. After ATP-infusion was discontinued, the first ventricular beat was evident after 3.1 +/- 0.9 s and sinus node activity recovered with a time constant of 3.0 +/- 1.1 s. Because sinus node and ventricular automaticity recovered within seconds after ATP infusion was discontinued in vitro, recovery in vivo is also likely to be determined by the short half-life (+1/2) of ATP.

Adenosine Triphosphate↗
PubMed1994

A new preparation of nifedipine for sublingual application in hypertensive urgencies.

A new preparation of nifedipine for sublingual application in hypertensive urgencies was investigated in a prospective study. Patients admitted to the Emergency Department with a persistent elevation of systolic blood pressure (SBP) greater than 190 mmHg and/or a diastolic blood pressure (DBP) greater than 100 mmHg received nifedipine 10 mg sublingual with a sprayer. A second dose was administrated fifteen minutes later if an adequate response defined as a stable reduction of SBP below 180 mmHg and DBP below 100 mmHg had not occurred. Of 30 patients, 21 (70%) responded to the first nifedipine application, 7 responded to the second dose, and 2 nonresponders had to be treated with urapidil. Overall mean SBP was 206 +/- 19 mmHg and mean DBP was 113 +/- 15 mmHg before treatment, and a significant antihypertensive effect was noted within fifteen minutes after nifedipine spray (p < 0.05). The maximum antihypertensive effect was for SBP in sixty minutes (146 +/- 19 mmHg) and for DBP after one hundred twenty minutes (78 +/- 18 mmHg). The average reduction in SBP was 29% and in DBP 31%. In first-dose responders (n = 21) a significant antihypertensive effect was noted within fifteen minutes. SBP declined from 205 +/- 21 to a minimum of 142 +/- 15 mmHg (22.3%) after sixty minutes and DBP from 113 +/- 13 to a minimum of 77 +/- 11 mmHg (22.2%) after one hundred twenty minutes. In second-dose responders (n = 7) a significant antihypertensive effect was noted within thirty minutes.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Sublingual↗
PubMed1994

[Multiple organ failure syndrome in protracted tachycardia (based on 4 cases)].

The multiple organ dysfunction syndrome (MODS) is mainly caused by sepsis--community acquired or more frequently by nosocomial infections acquired on the intensive care unit. Further causes are intoxications, burns and multiple trauma. MODS worsens the prognosis of intensive care patients. We report on four cases of MODS developing outside hospital as a result of sustained tachycardia. Severity of MODS was apparently dependent on the duration of tachycardia and was rapidly reversible after termination of the tachycardia. Our observations show that sustained tachycardia may also cause MODS.

Aged↗
PubMed1994

[Concomitant perforated ulcer and acute myocardial infarct--a diagnostic challenge in emergency medicine].

Clinical differentiation between acute myocardial infarction and peptic ulcer perforation may sometimes be difficult. We report on a sixty-five year-old patient who presented at the Emergency Department with upper abdominal pain and local tenderness suggestive of acute perforation of a gastric ulcer. However, the initial electrocardiogram (ECG) showed acute inferior wall myocardial infarction. Although abdominal pain is a major symptom of acute inferior wall myocardial infarction the history of gastritis and abdominal findings on admission of our patient required further exploration. The first plain abdominal radiograph was inconspicuous, therefore we performed a gastroscopy, which showed a prepyloric gastric ulcer. The second plain abdominal radiograph revealed air in the peritoneal cavity as sign of perforation. Echocardiography, ECG and the increase of heart enzymes confirmed acute inferior wall infarction. After successful surgical treatment of the perforated ulcer the patient recovered and progressed satisfactorily at the intensive care unit. He was discharged after three weeks and remains in good health. This case shows that rapid diagnosis and good interdisciplinary therapeutic management prevented a fatal outcome of acute myocardial infarction and concomitant gastric ulcer perforation in an elderly patient.

Aged↗
PubMed1994

[Emergency intubation with the Combitube in a patient with persistent vomiting].

Prompt establishment of a patient airway and effective ventilation are the major goals during initiation of cardiopulmonary resuscitation in patients with cardiac arrest. Endotracheal intubation is the definitive method to maintain an optimal airway. However, endotracheal intubation is not always possible, even for the skilled physician. The Combitube has been developed to overcome this disadvantage. Studies have proved the effectivity of ventilation with this device. A case is reported where a patient suffered from acute respiratory failure and attempts at endotracheal intubation failed due to continued vomiting rendering fibre-optical visualisation of the vocal cords impossible. Blind insertion of the Combitube led to successful ventilation, and hence replacement by an endotracheal airway could be performed without danger of aspiration.

Adult↗