27 results on '"Pfenninger, E. G."'
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2. Resilienz gegen IT-Angriffe an Kliniken: Ergebnisse einer Stabsrahmenübung an einem Universitätsklinikum
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Pfenninger, E. G., Schmidt, S. A., Rohland, C., Peters, S., McNutt, D., Kaisers, U. X., and Königsdorfer, M.
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- 2023
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3. Eskalations‑/Deeskalationskonzept zur COVID-19-bedingten Freihaltung von Intensivkapazitäten an Kliniken
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Pfenninger, E. G., Faust, J-O., Klingler, W., Fessel, W., Schindler, S., and Kaisers, U. X.
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- 2022
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4. Bevorratung persönlicher Schutzausrüstung in Kliniken zur Vorbereitung auf eine Pandemie
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Pfenninger, E. G. and Kaisers, U. X
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- 2020
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5. Terrorismusabwehrübung – Was können wir daraus lernen?: Baden-Württembergische Terrorismusabwehr Exercise (BWTEX)
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Pfenninger, E. G., Klingler, W., Keiloweit, Th., Eble, M., Wenzel, V., and Krüger, W. A.
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- 2020
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6. Resilience against IT attacks in hospitals
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Pfenninger, E. G., primary, Schmidt, S. A., additional, Rohland, C., additional, Peters, S., additional, McNutt, D., additional, Kaisers, U. X., additional, and Königsdorfer, M., additional
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- 2023
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7. Eskalations‑/Deeskalationskonzept zur COVID-19-bedingten Freihaltung von Intensivkapazitäten an Kliniken
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Pfenninger, E. G., Faust, J-O., Klingler, W., Fessel, W., Schindler, S., and Kaisers, U. X.
- Abstract
Hintergrund: Seit der Ausbreitung des Severe Acute Respiratory Syndrom Corona Virus 2 (SARS-CoV‑2) in Deutschland werden Intensivbetten für Patienten, die an Corona Virus Disease 2019 (COVID-19) erkrankt sind, frei gehalten. Auch nach Rückgang der Infektionszahlen wurden Intensivbetten prophylaktisch frei gehalten; dies geschah in den einzelnen Bundesländern jedoch in sehr unterschiedlicher Weise. Anhand der Literatur soll für das Infektionsgeschehen in Deutschland und insbesondere in Baden-Württemberg bei Stand Ende November 2020 eine notwendige Freihaltequote für COVID-19-Patienten definiert und für ansteigende und fallende Infektionszahlen ein Eskalations- /Deeskalationsschema erstellt werden. Methoden: Für die Kalkulation wurden für die Monate April bis November 2020 Daten aus dem COVID-19-Resource-Board des Landes Baden-Württemberg, dem täglichen Lagebericht des Robert-Koch-Instituts (RKI) zur Coronaviruskrankheit 2019 (COVID-19), dem Aktuellem Lage‑/Situationsbericht des RKI zu COVID-19, dem DIVI-Intensiv-Register zur Erfassung der an COVID-19 erkrankten intensivpflichtigen Patienten sowie dem Tagesbericht COVID-19 Baden-Württemberg verwendet. Ergebnisse: Ende November 2020 sind ca. 13,5 % der Intensivbetten deutschlandweit mit COVID-19-Patenten belegt. 1,5 % der positiv auf SARS-CoV‑2 Getesteten wurden auf eine Intensivstation aufgenommen; die Hospitalisierungsrate belief sich auf 6 % bei einem mittleren Erkrankungsalter von 43 Jahren. Kliniken wird bei einer 7‑Tage-Inzidenz von weniger als 35/100.000 Neuinfektionen empfohlen, eine Freihaltequote von 10 % an Intensivbetten für COVID-19-Patienten zu kalkulieren, bei einer Vorwarnstufe von 35/100.000 Neuinfektionen im Einzugsgebiet 20 % und bei einer kritischen Grenze von 50/100.000 30 % der Intensivbetten. Weitere klinikinterne Trigger, wie die Auslastung der Intensivstationen, sollen berücksichtigt werden. Schlussfolgerung: Bei niedrigen Infektionszahlen war eine generelle landesweite Freihaltequote an Intensivbetten für COVID-19-Patienten im September 2020 nicht gerechtfertigt. Lokal ansteigende und wieder abfallende Infektionszahlen erfordern ein lokales dynamisches Vorgehen. Ein Stufenkonzept in enger Abstimmung mit den örtlichen Gesundheitsbehörden sowie weitere klinikinterne Trigger definieren die Freihaltekapazität. Um bei lokalen Ausbrüchen die Krankenhauskapazitäten nicht zu überfordern, soll frühzeitig ein entsprechendes Verlegungskonzept ins Auge gefasst werden.
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- 2024
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8. Eskalations‑/Deeskalationskonzept zur COVID-19-bedingten Freihaltung von Intensivkapazitäten an Kliniken
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Pfenninger, E. G., primary, Faust, J-O., additional, Klingler, W., additional, Fessel, W., additional, Schindler, S., additional, and Kaisers, U. X., additional
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- 2021
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9. Shock I
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Glovannini, I., Chiarla, C., Boldrini, G., Castagneto, M., Beards S. C., Watt T., Edwards J. D., Nightingale P., Boyd, O., Mackay, J., Lamb, G., Grounds, R. M., Bennett, E. D., Munerato, P., Fracasso, A., Fantin, D., Bortolussi, R., Giaimo, F., Santantonio, C., Lendinez, M. Jienenez, Lopez, J., Cerdeno, V., Monjas, A., Arce, M. A., de Lorenzo, A. G., de la Casa, R., Lind, L., Mälstam, J., Skoog, G., Mathìeu, D., Nevìere, R., Herengt, F., Fleyfel, M., Wattel, F., Meier-Hellmann, A., Hannemann, L., Specht, M., Schaffartzik, W., Heiss-Dunlop, W., Hassel, H., Reinhart, K., Silance, P. G., Vincent, J. L., Berlot, P. G., Berlot, G., Silance, P. G., Zhang, H., Smolle, K. H., Kahn, R. J., Riera, J. A. Sanchez-Izquierdo, López, E. Alted, Aznarez, S. Bermejo, Renes, E., Martín, M. J. Jiménez, Gándara, A. Martínez Dela, Prados, J., López, P. Arribas, Rodriguez, J. Gutierrez, Varela, J. Prados, Léon, A., Raclot, P., Cousson, J., Biotteau, C., Suinat, J. L., Rendoing, J., van der Hoeven, J. G., Waanders, H., Compier, E. A., Meinders, A. E., Lindner, K. H., Schümann, W., Pfenninger, E. G., Ahnefeld, F. W., Strohmenger, H., Brinkmann, A., Georgieff, M., Verde, G., Pallavicini, F. Bobbio, Caramella, F., Cassini, F., Bichisao, G., Ferguson, C., Withey, F., Coakley, J., Crane, P., Honovar, M., Hinds, C. J., von Planta, I., Wagner, O., Ritz, R., Planta, M. von, Groeneveld, A. B. J., Thijs, L. G., de Boer, J. P., Abbink, J. J., Creasey, A. A., Chang, A., Roem, D., Eerenberg, A. J. M., Hack, C. E., Taylor, F. B., Annane, D., Raphaël, J. C., Gajdos, Ph., Bernardin, G., Milhaud, D., Pradier, C., Matlei, M., Donati, A., Adrario, E., Valente, M., Orsetti, G., Sambo, G., Cola, L., Giovannini, C., Pietropaoli, P., Tran, D. D., Cuesta, M. A., Schneider, A. J., Wesdorp, R. I. C., D’Orio, V., Martinez, C., Saad, G., Mendes, P., Marcelle, R., Boulain, T., Legras, A., Perrotin, D., Giniès, G., Perrotin, D., Geroulanos, S., Cakmakci, M., Schilling, J., Staubach, Karl-Hermann, Audibert, G., Donner, M., Lefèvre, J. C., Stoltz, J. F., Laxenaire, M. C., Russo, R., Veschi, G., Dellino, E., Solca, M., Aveni, R., Colombo, A., Iapichino, G., Coronet, B., Mercatello, A., Bret, M., Lefrançois, N., Dubernard, I. M., and Moskovtchenko, J. F.
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- 1992
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10. Cardiopulmonary resuscitation
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Köppel, C., Klapp, B., Sculiar, J. P., Markiewicz, E., Brinkmann, A., Wolf, Ch. -F., Wiebemeit, J., Rigos, D., Keck, F., Pfenninger, E. G., Lindner, K. H., Wiedeck, H., Prengel, A., Goertz, A., Rapp, S., Ahnefeld, F. W., Tormo, C., Cantalapiedra, J. A., Perales, N., Ferrer, P., Albiñana, G., Vega, E., Peréz, C., Sesma, R., García, J., and Alcaide, R.
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- 1992
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11. Effects of active compression-decompression resuscitation on myocardial and cerebral blood flow in pigs.
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Lindner, K H, primary, Pfenninger, E G, additional, Lurie, K G, additional, Schürmann, W, additional, Lindner, I M, additional, and Ahnefeld, F W, additional
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- 1993
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12. EFFECT OF ANGIOTENSIN II ON MYOCARDIAL HEMODYNAMICS AND ACID-BASE STATUS DURING CARDIOPULMONARY RESUSCITATION
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Lindner, K. H., primary, Prengel, A. W., additional, Pfenninger, E. G., additional, and Goertz, A., additional
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- 1992
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13. THE EFFECT OF VASOPRESSIN ON MYOCARDIAL HEMODYNAMICS DURING CARDIOPULAMONRY RESUSCITATION
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Lindner, K. H., primary, Brinkmann, A., additional, Pfenninger, E. G., additional, Rapp, S., additional, and Ahnefeld, F. W., additional
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- 1992
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14. Arterial blood gases in patients with acute head injury at the accident site and upon hospital admission
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Pfenninger, E. G., primary and Lindner, K.-H., additional
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- 1991
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15. Effects of ventilation on hemodynamics and myocardial blood flow during active compression-decompression resuscitation in pigs.
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Prengel, Andreas W., Lindner, Karl H., Pfenninger, Ernst G., Georgieff, Michael, Prengel, A W, Lindner, K H, Pfenninger, E G, and Georgieff, M
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- 1996
16. Spectral analysis of ventricular fibrillationand closed-chest cardiopulmonary resuscitation
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Strohmenger, H.-U., Lindner, K. H., Keller, A., Lindner, I. M., and Pfenninger, E. G.
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- 1996
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17. Effects of epinephrine and vasopressin on median fibrillation frequency and defibrillation success in a porcine model of cardiopulmonary resuscitation
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Strohmeger, H.-U., Lindner, K. H., Prengel, A. W., Pfenninger, E. G., Bothner, U., and Lurie, K. G.
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- 1996
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18. [Terror attacks : Recommendations for cooperation between police, hospitals and non-police security services].
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Pfenninger EG, Hammer TO, Holsträter T, and Weiß S
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- Humans, Germany, Hospitals standards, Emergency Medical Services standards, Emergency Medical Services legislation & jurisprudence, Police, Disaster Planning organization & administration, Terrorism, Security Measures
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Background: The risk of terrorist attacks in the Federal Republic of Germany is present and is currently increasing. Publicly funded acute care hospitals and their owners are involved in disaster control as part of their remit and are responsible for taking comprehensive precautions to ensure their operational capability in the event of disasters. This mandate must also be ensured in the event of terrorist attacks and amok incidents. For this purpose, an optimal cooperation between preclinical and clinical care is indispensable., Aim: Recommended actions for collaboration between nonclinical and clinical planning to manage a mass casualty incident in terrorist life-threatening response situations are presented., Material and Methods: The Inter-Hospital Security Conference Baden-Württemberg (IHSC BW) is an association of representatives of acute hospitals in Baden-Württemberg, the Ministry of the Interior, Digitalization and Migration Baden-Württemberg, the Ministry of Social Affairs and Integration Baden-Württemberg, the State Police Headquarters Baden-Württemberg and the Baden-Württemberg Hospital Association. From 2018 to 2020, the IHSC BW developed recommendations for action on cooperation between police, hospitals and non-police emergency response. The recommendations for action were agreed by the group members in 6 working sessions and initialled in two subsequent video conferences. A recommendation was considered adopted when the IHSC BW plenary assembly finally gave its approval with an absolute majority., Results and Discussion: Competence-based interface solutions for a smooth cooperation between prehospital and hospital management in the care of patients who have become victims of a terrorist attack are to be demanded. For preliminary planning, the establishment of a local safety conference at the county disaster control authority level with the following participants is recommended: disaster control authority, fire department, regional police headquarters, chief emergency physician, rescue services and disaster control officers of affected clinics. It is recommended to set up a joint command and situation center (CSC), where management personnel from the police, rescue service, fire department and disaster control can meet to organize the handling of the incident jointly, competently and without loss of time. From this CSC, a liaison officer should then provide the clinics with information at regular intervals. Exercises should take place regularly. Cross-organizational exercises are particularly important, and this is one of the tasks of the local safety conference., (© 2024. The Author(s).)
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- 2024
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19. [Provisioning of personal protective equipment in hospitals in preparation for a pandemic].
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Pfenninger EG and Kaisers UX
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- Critical Care, Forecasting, Gloves, Protective, Health Personnel statistics & numerical data, Hospital Departments, Hospitals, University, Humans, Infections, Infectious Disease Transmission, Patient-to-Professional, Masks, Patients, COVID-19, Pandemics, Personal Protective Equipment supply & distribution
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Background: At the beginning of the SARS-CoV‑2 outbreak, personal protective equipment (PPE) was scarce worldwide, leading to the treatment of patients partially without sufficient protection for the medical personnel. In order to be prepared for a new epidemic or pandemic or a "second wave" of COVID-19 outbreak and to meet a renewed deficiency of PPE, considerations were made on how personnel and patients can be better protected by appropriate provisioning., Objective: The aim of this study was to develop a tool to predict the necessary amount of PPE to be in stock at a transregional university hospital for a certain period of time during a pandemic., Material and Methods: The consumption of PPE needed for every patient was calculated based on the following data of the Ulm University Hospital: the total consumption of healthcare workers' PPE for April 2020 recorded by the materials management department and the number of patients suffering from COVID-19 and their treatment days. From the amount of PPE necessary for every patient in the intensive care unit (ICU) or in an infection ward, a PPE calculator was created in which the estimated amount of PPE can be calculated with the input variables "patients in intensive care unit", "patients in infection ward" and "treatment days". To validate the PPE calculator, the actual consumption of PPE for May 2020 at the Ulm University hospital was compared to the theoretically calculated demand by the PPE calculator., Results: In April 2020 PPE consisting of 18 different items were kept in stock at Ulm University Hospital and in total 1,995,500 individual items were used. 22 intensive care patients with 257 nursing days and in the infection ward 39 patients with 357 nursing days were treated for COVID-19 disease, leading to a total of 603.2 man-days. A total of 34,550 KN95 masks, 1,558,780 gloves and 1100 goggles or protective visors were used, with a daily average of 49 NK95 masks and 2216 gloves required per ICU patient. In May 2020, 6 ICU patients and 19 patients in infection wards were treated for COVID-19 with 34 nursing days in intensive care and 201 nursing days in infection wards. The use of PPE material was 39% lower than in the previous month but in absolute terms 82% and on average 39% higher than calculated., Conclusion: The developed tool allows our hospital to estimate the necessary amount of PPE to be kept in stock for future pandemics. By taking local conditions into account this tool can also be helpful for other hospitals.
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- 2020
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20. Spectral analysis of ventricular fibrillation and closed-chest cardiopulmonary resuscitation.
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Strohmenger HU, Lindner KH, Keller A, Lindner IM, and Pfenninger EG
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- Analysis of Variance, Animals, Cardiopulmonary Resuscitation methods, Fourier Analysis, Hemodynamics drug effects, Microspheres, Resuscitation, Swine, Vasoconstrictor Agents therapeutic use, Vasopressins therapeutic use, Ventricular Fibrillation therapy, Cardiopulmonary Resuscitation adverse effects, Coronary Circulation, Electrocardiography, Heart Arrest therapy, Ventricular Fibrillation physiopathology
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This study was designed to assess the interference by closed-chest cardiopulmonary resuscitation (CPR) on the ventricular fibrillation (VF) ECG signal in a porcine model of cardiac arrest and to elucidate which variable of VF spectral analysis reflects best myocardial blood flow and resuscitation success during CPR. Fourteen domestic pigs were allocated to receive either 0.4 U/kg vasopressin (n = 7) or 10 ml saline (n = 7) after 4 min of VF and 3 min of CPR. Using radiolabeled microspheres, myocardial blood flow was determined during CPR before, and 90 s and 5 min after, drug administration. Using spectral analysis of VF, the median frequency, dominant frequency, edge frequency and amplitude of VF were determined simultaneously and before the first defibrillation attempt. Using filters in order to specify frequency ranges, stepwise elimination of mechanical artifacts resulting from CPR revealed that at a frequency bandpass of 4.3-35 Hz, median fibrillation frequency has a sensitivity, specificity, positive and negative predictive value of 100% to differentiate between resuscitated and non-resuscitated animals. The best correlation between myocardial blood flow and fibrillation frequency was found at a median frequency range of 4.3-35 Hz. We conclude that spectral analysis of VF can provide reliable information relating to successful resuscitation. In this model after elimination of oscillations due to mechanical CPR, median fibrillation frequency best reflects the probability of resuscitation success.
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- 1996
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21. Effects of epinephrine and vasopressin on median fibrillation frequency and defibrillation success in a porcine model of cardiopulmonary resuscitation.
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Strohmenger HU, Lindner KH, Prengel AW, Pfenninger EG, Bothner U, and Lurie KG
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- Adrenergic Agonists administration & dosage, Animals, Blood Pressure drug effects, Carbon Dioxide blood, Coronary Circulation drug effects, Disease Models, Animal, Electrocardiography, Epinephrine administration & dosage, Heart Arrest drug therapy, Heart Arrest physiopathology, Heart Arrest therapy, Microspheres, Oxygen blood, Potassium blood, Signal Processing, Computer-Assisted, Sodium blood, Swine, Ventricular Fibrillation drug therapy, Ventricular Fibrillation physiopathology, Adrenergic Agonists therapeutic use, Cardiopulmonary Resuscitation, Epinephrine therapeutic use, Vasoconstrictor Agents therapeutic use, Vasopressins therapeutic use, Ventricular Fibrillation therapy
- Abstract
Objective: This study was designed to assess whether median frequency of ventricular fibrillation (VF) correlates with myocardial blood flow and defibrillation success during cardiopulmonary resuscitation (CPR) after epinephrine or vasopressin administration., Methods and Results: After 4 min of VF and 3 min of CPR, 14 pigs received 0.045 mg/kg epinephrine or 0.4 U/kg vasopressin. Using radio-labeled microspheres, median myocardial blood flow during CPR before, and 90 s and 5 min after drug administration (DA) was 15.5 (12.6, 23.1; 25th percentile, 75th percentile), 26.4 (18.5, 29.1), 16.9 (14.9, 19.1) mL min-1 100 g-1, respectively, in the epinephrine, and 16.9 (15.4, 18.9), 48.1 (36.9, 68.9) (P < 0.05 vs. before DA), 52.3 (38.5, 65.0) mL min-1 100 g-1, respectively, in the vasopressin group. Using spectral analysis of VF, median frequency of VF was 11.0 (10.7, 11.8), 11.3 (9.6, 13.1), 10.2, (8.8, 11.4) Hz, respectively, in the epinephrine, and 10.1 (10.0, 10.5), 11.7 (11.1, 14.2) (P < 0.05 vs. before DA), 13.2 (11.5, 13.9) Hz, respectively, in the vasopressin group at the same points in time. Median frequency correlates significantly with myocardial blood flow in the epinephrine (n = 21); rs = 0.772; P < 0.001) and in the vasopressin group (n = 21; rs = 0.905; P < 0.001). Median fibrillation frequency before the first defibrillation was 13.0 (12.2, 13.2) Hz in resuscitated (n = 8) and 9.2 (8.3, 10.2) Hz (n = 6) in non-resuscitated animals (P < 0.01)., Conclusions: We conclude that median frequency of VF reflects myocardial blood flow and the chance of successful defibrillation during closed-chest CPR after vasopressor treatment in a porcine model of VF.
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- 1996
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22. Angiotensin II augments reflex activity of the sympathetic nervous system during cardiopulmonary resuscitation in pigs.
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Lindner KH, Prengel AW, Pfenninger EG, and Lindner IM
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- Animals, Coronary Circulation drug effects, Epinephrine blood, Hemodynamics drug effects, Norepinephrine blood, Osmolar Concentration, Swine, Sympathetic Nervous System physiopathology, Angiotensin II pharmacology, Cardiopulmonary Resuscitation, Reflex drug effects, Sympathetic Nervous System drug effects
- Abstract
Background: During hypotensive states, angiotensin II augments reflex activity of the sympathetic nervous system. The purpose of the present study was to assess the effects of this vasoconstrictor on myocardial blood flow and plasma catecholamine concentrations during and after CPR., Methods and Results: After 4 minutes of ventricular fibrillation and 3 minutes of open-chest CPR, 14 pigs (24 to 26 kg) were randomized into two groups receiving either saline (n = 7) or 0.05 mg/kg angiotensin II (n = 7). Arterial plasma catecholamine concentration was measured with high-pressure liquid chromatography. Organ blood flow was measured with radiolabeled microspheres. During CPR, after drug administration, left ventricular myocardial blood flow was significantly higher in the angiotensin II-treated group than in the control group. During CPR, median epinephrine concentrations before and 90 seconds and 5 minutes after drug administration were 63.0, 35.2, and 22.5 ng/mL, respectively, in the control group and 63.2, 139.8, and 154.2 ng/mL, respectively, in the angiotensin II group (P < .001 at 90 seconds and P < .01 at 5 minutes). At the same times, median norepinephrine concentrations were 52.6, 59.8, and 33.9 ng/mL, respectively, in the control group and 42.5, 98.7, and 111.3 ng/mL, respectively, in the angiotensin II group (P < .01 at 5 minutes). Restoration of spontaneous circulation was possible in all of the angiotensin II-treated pigs, whereas only 3 of the 7 saline-treated pigs could be resuscitated. At 5 minutes after successful resuscitation, epinephrine was 6.8 ng/mL in the control group and 16.1 ng/mL in the angiotensin II group (P < .05)., Conclusions: During CPR, angiotensin II appears to increase coronary perfusion pressure and myocardial blood flow, not only by direct peripheral arteriolar vasoconstriction via angiotensin II receptors but also by inducing a massive catecholamine release with adrenergic peripheral vasoconstriction.
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- 1995
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23. Vasopressin improves vital organ blood flow during closed-chest cardiopulmonary resuscitation in pigs.
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Lindner KH, Prengel AW, Pfenninger EG, Lindner IM, Strohmenger HU, Georgieff M, and Lurie KG
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- Animals, Cardiopulmonary Resuscitation, Disease Models, Animal, Hemodynamics, Swine, Vascular Resistance, Epinephrine pharmacology, Regional Blood Flow drug effects, Vasopressins pharmacology, Ventricular Fibrillation physiopathology
- Abstract
Background: This study was designed to compare the effects of epinephrine with those of vasopressin on vital organ blood flow during closed-chest cardiopulmonary resuscitation (CPR) in a pig model of ventricular fibrillation., Methods and Results: Vasopressin was compared with epinephrine by randomly allocating 28 pigs to receive either 0.2 mg/kg epinephrine (n = 7), 0.2 U/kg vasopressin (low dose) (n = 7), 0.4 U/kg vasopressin (medium dose) (n = 7), or 0.8 U/kg vasopressin (high dose) (n = 7) after 4 minutes of ventricular fibrillation and 3 minutes of closed-chest CPR. Left ventricular myocardial blood flow, determined by use of radiolabeled microspheres during CPR, before and then 90 seconds and 5 minutes after drug administration was 17 +/- 2, 43 +/- 5, and 22 +/- 3 mL.min-1.100 g-1 (mean +/- SEM) in the epinephrine group; 18 +/- 2, 50 +/- 6, and 29 +/- 3 mL.min-1.100 g-1 in the low-dose vasopressin group; 17 +/- 3, 52 +/- 8, and 52 +/- 6 mL.min-1.100 g-1 in the medium-dose vasopressin group; and 18 +/- 2, 95 +/- 9, and 57 +/- 6 mL.min-1.100 g-1 in the high-dose vasopressin group (P < .001 at 90 seconds and 5 minutes between epinephrine and high-dose vasopressin, and P < .01 at 5 minutes between epinephrine and medium-dose vasopressin). At the same times, calculated coronary systolic perfusion pressures were 12 +/- 2, 36 +/- 5, and 18 +/- 2 mm Hg in the epinephrine group; 10 +/- 1, 39 +/- 6, and 26 +/- 5 mm Hg in the low-dose vasopressin group; 11 +/- 2, 49 +/- 6, and 38 +/- 5 mm Hg in the medium-dose vasopressin group; and 10 +/- 2, 70 +/- 5, and 47 +/- 6 mm Hg in the high-dose vasopressin group (P < .01 at 90 seconds and 5 minutes between epinephrine and high-dose vasopressin); and calculated coronary diastolic perfusion pressures were 15 +/- 2, 24 +/- 2, and 19 +/- 2 mm Hg in the epinephrine group; 13 +/- 1, 25 +/- 2, and 20 +/- 1 mm Hg in the low-dose vasopressin group; 13 +/- 2, 25 +/- 2, and 21 +/- 2 mm Hg in the medium-dose vasopressin group; and 13 +/- 2, 35 +/- 3, and 24 +/- 2 mm Hg in the high-dose vasopressin group (P < .05 at 90 seconds between epinephrine and high-dose vasopressin). Total cerebral blood flow was significantly higher after high-dose vasopressin than after epinephrine (P < .05 at 90 seconds and P < .01 at 5 minutes between groups). Five animals in the epinephrine, 5 in the low-dose vasopressin, 7 in the medium-dose vasopressin, and 6 in the high-dose vasopressin groups were successfully resuscitated and survived the 1-hour observation period., Conclusions: We conclude that administration of vasopressin leads to a significantly higher coronary perfusion pressure and myocardial blood flow than epinephrine during closed-chest CPR in a pig model of ventricular fibrillation.
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- 1995
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24. Effect of vasopressin on hemodynamic variables, organ blood flow, and acid-base status in a pig model of cardiopulmonary resuscitation.
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Lindner KH, Brinkmann A, Pfenninger EG, Lurie KG, Goertz A, and Lindner IM
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- Animals, Carbon Dioxide blood, Epinephrine pharmacology, Heart Arrest therapy, Hydrogen-Ion Concentration, Oxygen blood, Regional Blood Flow drug effects, Swine, Vasopressins pharmacology, Acid-Base Equilibrium drug effects, Cardiopulmonary Resuscitation, Hemodynamics drug effects, Vasopressins blood
- Abstract
Based upon the hypothesis that vasopressin (antidiuretic hormone) may increase vascular resistance during ventricular fibrillation, the effects of this potent vasoconstrictor were studied in a porcine model of ventricular fibrillation. Vasopressin therapy was compared to epinephrine by randomly allocating 14 pigs to receive either 0.045 mg/kg of epinephrine (n = 7) or 0.8 U/kg of vasopressin (n = 7) after 4 min of ventricular fibrillation and 3 min of open-chest cardiopulmonary resuscitation. During cardiopulmonary resuscitation, myocardial blood flow before and 90 s and 5 min after drug administration was 57 +/- 11, 84 +/- 11, and 59 +/- 9 mL.min-1 x 100 g-1 (mean +/- SEM) in the epinephrine group, and 61 +/- 5, 148 +/- 26, and 122 +/- 22 mL.min-1 x 100 g-1 in the vasopressin group (P < 0.05 at 90 s and 5 min). At the same times, mean cardiac index was not significantly different between the groups. After drug administration, coronary venous PCO2 was significantly higher and coronary venous pH was significantly lower in the epinephrine as compared to the vasopressin group. All pigs in both groups were resuscitated and survived the 2-h observation period. We conclude that vasopressin improves vital organ perfusion during ventricular fibrillation and cardiopulmonary resuscitation. Vasopressin seems to be at least as effective as epinephrine in this pig model of ventricular fibrillation.
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- 1993
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25. Effect of angiotensin II on myocardial blood flow and acid-base status in a pig model of cardiopulmonary resuscitation.
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Lindner KH, Prengel AW, Pfenninger EG, and Lindner IM
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- Acid-Base Equilibrium physiology, Animals, Coronary Circulation physiology, Heart Arrest drug therapy, Heart Arrest physiopathology, Swine, Acid-Base Equilibrium drug effects, Angiotensin II therapeutic use, Cardiopulmonary Resuscitation, Coronary Circulation drug effects, Heart Arrest therapy
- Abstract
The effect of angiotensin II on myocardial blood flow and acid-base status during cardiopulmonary resuscitation (CPR) was assessed. Fourteen pigs were allocated randomly to receive either 0.9% saline (n = 7) or 0.05 mg/kg angiotensin II (n = 7) after 4 min of ventricular fibrillation and 3 min of open-chest CPR. Total myocardial blood flow (measured with radiolabeled microspheres) before, 90 s, and 5 min following drug administration was 74 +/- 18, 62 +/- 12, and 54 +/- 11 mL.min-1 x 100g-1 (mean +/- SD) in the control, and 72 +/- 17, 125 +/- 25, and 74 +/- 20 mL.min-1 x 100 g-1 in the angiotensin II group (P < 0.001 at 90 s and P < 0.05 at 5 min). The PCO2 of coronary venous blood at 90 s after drug administration was 82 +/- 8 mm Hg in the control group as compared to 47 +/- 9 mm Hg in the angiotensin II group (P < 0.001). Only three of the seven control group animals could be resuscitated successfully, whereas all of the angiotensin II-treated pigs survived the 1-h observation period (P < 0.05), during which neither arterial hypertension nor bradycardia was observed. Angiotensin II was associated with an improvement of myocardial blood flow during CPR and short-term resuscitation success. The increase in myocardial perfusion is associated with a lower coronary venous PCO2 and a higher coronary venous pH. The authors conclude that angiotensin II administration facilitated cardiopulmonary resuscitation.
- Published
- 1993
- Full Text
- View/download PDF
26. Effects of epinephrine and norepinephrine on cerebral oxygen delivery and consumption during open-chest CPR.
- Author
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Lindner KH, Ahnefeld FW, Pfenninger EG, Schuermann W, and Bowdler IM
- Subjects
- Animals, Blood Glucose analysis, Blood Pressure drug effects, Brain metabolism, Oxygen blood, Random Allocation, Single-Blind Method, Swine, Ventricular Fibrillation surgery, Brain drug effects, Cerebrovascular Circulation drug effects, Epinephrine pharmacology, Glucose metabolism, Heart Massage, Norepinephrine pharmacology, Oxygen Consumption drug effects
- Abstract
The effect of epinephrine and norepinephrine on cerebral oxygen delivery and consumption after five minutes of cardiopulmonary arrest and three minutes of open-chest cardiac massage was studied in 21 pigs. Norepinephrine, like epinephrine, has a marked alpha- and beta 1-sympathomimetic activity, but compared with epinephrine, the degree of beta 2-stimulation is weak. Epinephrine probably stimulates cerebral oxygen and glucose consumption by its beta 2-adrenergic effect. After three minutes of CPR, three groups of seven animals each blindly received either placebo (control group), 45 micrograms/kg epinephrine, or 45 micrograms/kg norepinephrine. During CPR but before drug administration, cerebral blood flow was 23 +/- 14 mL/min/100 g in the control group, 30 +/- 7 mL/min/100 g in the epinephrine group, and 30 +/- 11 mL/min/100 g in the norepinephrine group. At 90 seconds after epinephrine, cerebral blood flow increased to 54 +/- 14 mL/min/100 g and after norepinephrine, to 58 +/- 22 mL/min/100 g (P less than .05). Cerebral perfusion pressure for both drugs was significantly higher than the control group. Compared with mechanical measures alone, cerebral oxygen delivery rose from 4.3 +/- 1.2 to 7.4 +/- 1.7 mL/min/100 g after epinephrine and from 3.7 +/- 1.4 to 7.3 +/- 2.7 mL/min/100 g after norepinephrine (P less than .05). There was no increase in cerebral oxygen consumption after both catecholamines, and cerebral oxygen extraction ratio decreased. Cerebral glucose delivery increased in relation to glucose consumption, and extraction ratio did not change significantly after both catecholamines.(ABSTRACT TRUNCATED AT 250 WORDS)
- Published
- 1990
- Full Text
- View/download PDF
27. Early changes of intracranial pressure, perfusion pressure, and blood flow after acute head injury. Part 1: An experimental study of the underlying pathophysiology.
- Author
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Pfenninger EG, Reith A, Breitig D, Grünert A, and Ahnefeld FW
- Subjects
- Acute Disease, Animals, Hemodynamics, Regional Blood Flow, Swine, Vascular Resistance, Blood Pressure, Brain Injuries physiopathology, Cerebrovascular Circulation, Intracranial Pressure
- Abstract
The present study examines intracranial pressure (ICP), cerebral perfusion pressure (CPP), and cerebral circulation immediately after experimental head injury in an animal model. The underlying systemic hemodynamic changes were also observed. To produce a standardized head injury, a fluid-percussion device was applied to the dura at the midline of 10 piglets. Seven other nontraumatized animals served as a control group. Hemodynamic parameters as well as ICP and CPP were recorded on-line, one value every 1.4 seconds. Cerebral blood flow (CBF) and cerebral vascular resistance (CVR) were measured three times using a microsphere technique. Immediately after head injury, the traumatized animals showed a sudden increase in ICP, with a maximum of 40 torr at 3 to 5 minutes, while there was a pronounced decrease in CPP from 85 to 40 torr. The CBF in the various brain areas fell from 55 to 22 ml/min/100 gm within 5 minutes after the impact, and CVR increased to 300% of control values within 90 minutes. The findings of this study demonstrated that cerebral circulation is critically jeopardized within a few minutes after trauma. This, in combination with a subsequent increase in CVR, makes the early development of ischemic brain damage very likely. In traumatized patients, treatment prior to hospital admission must therefore be directed at prevention of this fatal course.
- Published
- 1989
- Full Text
- View/download PDF
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