| 1. |
- Bak, Zoltan, et al.
(författare)
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Cardiac dysfunction after burns
- 2008
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Ingår i: Burns. - : Elsevier BV. - 0305-4179 .- 1879-1409. ; 34:5, s. 603-609
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVES: Using transoesophageal echocardiography (TEE) we investigated the occurrence, and the association of possible abnormalities of motion of the regional wall of the heart (WMA) or diastolic dysfunction with raised troponin concentrations, or both during fluid resuscitation in patients with severe burns. PATIENTS AND METHODS: Ten consecutive adults (aged 36-89 years, two women) with burns exceeding 20% total burned body surface area who needed mechanical ventilation were studied. Their mean Baux index was 92.7, and they were resuscitated according to the Parkland formula. Thirty series of TEE examinations and simultaneous laboratory tests for myocyte damage were done 12, 24, and 36h after the burn. RESULTS: Half (n=5) the patients had varying grades of leakage of the marker that correlated with changeable WMA at 12, 24 and 36h after the burn (p< or =0.001, 0.044 and 0.02, respectively). No patient had WMA and normal concentrations of biomarkers or vice versa. The mitral deceleration time was short, but left ventricular filling velocity increased together with stroke volume. CONCLUSION: Acute myocardial damage recorded by both echocardiography and leakage of troponin was common, and there was a close correlation between them. This is true also when global systolic function is not deteriorated. The mitral flow Doppler pattern suggested restrictive left ventricular diastolic function.
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| 2. |
- Bak, Zoltan, 1950-
(författare)
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Cardiovascular response to hyperoxemia, hemodilution and burns : a clinical and experimental study
- 2007
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- The last decades less invasive monitoring and analytical tools have been developed for the evaluation of myocardial mechanics in clinical praxis. In critical care, these are longed-for complements to pulmonary artery catheter monitoring, additionally offering previously inaccessible information. This work is aimed, during fluid-replacement and oxygen therapy, to determine the physiological interface of ventricular and vascular mechanical properties, which result in the transfer of blood from the heart to appropriate circulatory beds. In prospective clinical studies we investigated previously cardiovascular healthy adults during hyperoxemia, and during preoperative acute normovolemic hemodilution or early fluid resuscitation of severe burn victims. Echocardiography was used in all studies, transthoracic for healthy volunteers and transesophageal for patients. For vascular parameters and for control purposes pulmonary artery Swan-Ganz catheter, calibrated external pulse recordings, whole body impedance cardiography, and transpulmonel thermodilution method were applied.We detected no significant change in blood pressure or heart rate, the two most often used parameters for patient monitoring. During preoperative acute normovolemic hemodilution a reduction of hemoglobin to 80 g/l did not compromise systolic or diastolic myocardial function. Cardiac volumes and flow increased with a concomitant fall in systemic vascular resistance while oxygen delivery seemed maintained. Supplemental oxygen therapy resulted in a linear dose-response between arterial oxygen and cardiovascular parameters, suggesting a direct vascular effect. Cardiac flow decreased and vascular resistance increased from hyperoxemia, and a decrease of venous return implied extracardial blood-pooling. Severe burns result in hypovolemic shock if not properly treated. The commonly used Parkland fluid replacement strategy, with urinary output and mean arterial pressure as endpoints, has recently been questioned. Applying this strategy, only transient early central hypovolemia was recorded, while dimensional preload, global left ventricular systolic function and oxygen delivery or consumption remained within normal ranges during the first 36 hours after accident. Signs of restrictive left ventricular diastolic function were detected in all patients and regional unstable systolic dysfunction was recognized in every other patient, and was consistent with myocardial marker leakage. Severe burns thereby cause myocardial stiffness and systolic regional dysfunction, which may not be prevented only by central normovolemia and adequate oxygenation.
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| 3. |
- Bak, Zoltan, et al.
(författare)
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Hemodynamic Changes During Resuscitation After Burns Using the Parkland Formula
- 2009
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Ingår i: Journal of Trauma. - 0022-5282 .- 1529-8809. ; 66:2, s. 329-336
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Tidskriftsartikel (refereegranskat)abstract
- Background: The Parkland formula (2-4 mL/kg/burned area of total body surface area %) with urine output and mean arterial pressure (MAP) as endpoints; for the fluid resuscitation in burns is recommended all over the world. There has recently been a discussion on whether central circulatory endpoints should be used instead, and also whether volumes of fluid should be larger. Despite this, there are few central hemodynamic data available in the literature about the results when the formula is used correctly.Methods: Ten burned patients, admitted to our unit early, and with a burned area of >20% of total body sur-face area were investigated at 12, 24, and 36 hours after injury. Using transesophageal echocardiography, pulmonary artery catheterization, and transpulmonary thermodilution to monitor them, we evaluated the cardiovascular coupling when urinary output and MAP were used as endpoints.Results: Oxygen transport variables, heart rate, MAP, and left ventricular fractional area, did not change significantly during fluid resuscitation. Left ventricular end-systolic and end-diastolic area and global end-diastolic volume index increased from subnormal values at 12 hours to normal ranges at 24 hours after the burn. Extravascular lung intrathoracal blood volume ratio was increased 12 hours after the burn.Conclusions: Preload variables, global systolic function, and oxygen transport recorded simultaneously by three separate methods showed no need to increase the total fluid volume within 36 hours of a major burn. Early (12 hours) signs of central circulatory hypovolemia, however, support more rapid infusion of fluid at the beginning of treatment.
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| 4. |
- Bak, Zoltan, et al.
(författare)
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Human cardiovascular dose-response to supplemental oxygen
- 2007
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Ingår i: Acta Physiologica. - : Wiley. - 1748-1708 .- 1748-1716. ; 191:1, s. 15-24
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Tidskriftsartikel (refereegranskat)abstract
- Aim: The aim of the study was to examine the central and peripheral cardiovascular adaptation and its coupling during increasing levels of hyperoxaemia. We hypothesized a dose-related effect of hyperoxaemia on left ventricular performance and the vascular properties of the arterial tree. Methods: Oscillometrically calibrated arterial subclavian pulse trace data were combined with echocardiographic recordings to obtain non-invasive estimates of left ventricular volumes, aortic root pressure and flow data. For complementary vascular parameters and control purposes whole-body impedance cardiography was applied. In nine (seven males) supine, resting healthy volunteers, aged 23–48 years, data was collected after 15 min of air breathing and at increasing transcutaneous oxygen tensions (20, 40 and 60 kPa), accomplished by a two group, random order and blinded hyperoxemic protocol. Results: Left ventricular stroke volume [86 ± 13 to 75 ± 9 mL (mean ± SD)] and end-diastolic area (19.3 ± 4.4 to 16.8 ± 4.3 cm2) declined (P < 0.05), and showed a linear, negative dose–response relationship to increasing arterial oxygen levels in a regression model. Peripheral resistance and characteristic impedance increased in a similar manner. Heart rate, left ventricular fractional area change, end-systolic area, mean arterial pressure, arterial compliance or carbon dioxide levels did not change. Conclusion: There is a linear dose–response relationship between arterial oxygen and cardiovascular parameters when the systemic oxygen tension increases above normal. A direct effect of supplemental oxygen on the vessels may therefore not be excluded. Proximal aortic and peripheral resistance increases from hyperoxaemia, but a decrease of venous return implies extra cardiac blood-pooling and compensatory relaxation of the capacitance vessels.
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| 5. |
- Bak, Zoltan, et al.
(författare)
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Transesophageal echocardiographic hemodynamic monitoring during preoperative acute normovolemic hemodilution
- 2000
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Ingår i: Anesthesiology. - : Ovid Technologies (Wolters Kluwer Health). - 0003-3022 .- 1528-1175. ; 92:5, s. 1250-1256
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Tidskriftsartikel (refereegranskat)abstract
- Background: Preoperative acute normovolemic hemodilution may compromise oxygen transport. The aims of our study were to describe the hemodynamic effects of normovolemic hemodilution and to determine its effect on systolic and diastolic cardiac function by multiplane transesophageal echocardiography.Methods: In eight anesthetized patients (aged 13-51 yr) without heart disease, hemoglobin was reduced in steps from 123 ± 8 (mean ± SD) to 98 ± 3 and to 79 ± 5 g/l. Hemodynamic measurements (intravascular pressures, thermodilution cardiac output, and echocardiographic recordings) were obtained during a stabilization period and at each level of hemodilution. Left ventricular wall motion was monitored continuously, and Doppler variables, annular motion, and changes in ejection fractional area were analyzed off-line.Results: During hemodilution, cardiac output by thermodilution increased by 16 ± 7% and 26 ± 10%, corresponding well to the increase in cardiac output as measured by Doppler (difference, 0.32 ± 1.2 l/min). Systemic vascular resistance fell 16 ± 14% and 23 ± 9% and pulmonary capillary wedge pressure increased slightly (2 ± 2 mmHg), whereas other pressures, heart rate, wall motion, and diastolic Doppler variables remained unchanged. Ejection fractional area change increased from 44 ± 7% to 54 ± 10% and 60 ± 9% as a result of reduced end-systolic and increased end-diastolic left ventricular areas.Conclusions: A reduction in hemoglobin to 80 g/l during acute normovolemic hemodilution does not normally compromise systolic or diastolic myocardial function as determined by transesophageal echocardiography. Preload, left ventricular ejection fraction, and cardiac output increase with a concomitant fall in systemic vascular resistance.
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| 6. |
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| 7. |
- Liffner, G, et al.
(författare)
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Inhalation injury assessed by score does not contribute to the development of acute respiratory distress syndrome in burn victims
- 2005
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Ingår i: Burns. - : Elsevier BV. - 0305-4179 .- 1879-1409. ; 31:3, s. 263-268
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Tidskriftsartikel (refereegranskat)abstract
- Objective: To establish the incidence, mortality, and time of onset of acute respiratory distress syndrome (ARDS) in relation to extent of burn and inhalation injury in patients who required mechanical ventilation. Design: Data about burn and inhalation injury were recorded prospectively whereas ARDS and multiple organ dysfunction were assessed by review of patient charts. Setting: National burn intensive care unit at Linköping University Hospital, Sweden (a tertiary referral hospital). Patients: Between 1993 and 1999, we studied all patients with thermal injury (n = 553) who required mechanical ventilation for more than two days (n = 91). Measurements and results: Out of the thirty-six burn victims who developed ARDS (40%), 25 (70%) did so early post burn (in less than 6 days). Patients with ARDS had higher multiple organ dysfunction scores (mean 10.5) than those who did not develop ARDS (mean 5.6) (p < 0.01). The probable presence of inhalation injury as assessed by an inhalation lung injury score (ILIS) did not contribute to the development of ARDS. Mortality tended to be higher in patients who developed ARDS (14%) compared to those who did not (6%, p = 0.2). Conclusions: In our burn patients the incidence of ARDS was high whereas mortality was low. We found no association between inhalation injury as assessed using the ILIS and development of ARDS. Our data support a multi-factorial origin of ARDS in burn victims as a part of a multiple organ failure event. © 2004 Elsevier Ltd and ISBI. All rights reserved.
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| 8. |
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| 9. |
- Nilsson, Andreas, et al.
(författare)
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Patient controlled sedation using a standard protocol for dressing changes in burns : Patients' preference, procedural details and a preliminary safety evaluation
- 2008
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Ingår i: Burns. - : Elsevier BV. - 0305-4179 .- 1879-1409. ; 34:7, s. 929-934
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Tidskriftsartikel (refereegranskat)abstract
- Background: Patient controlled sedation (PCS) enables patients to titrate doses of drugs by themselves during different procedures involving pain or discomfort. Methods: We studied it in a prospective crossover design using a fixed protocol without lockout time to examine it as an alternative method of sedation for changing dressings in burned patients. Eleven patients with >10% total burn surface area (TBSA) had their dressings changed, starting with sedation by an anaesthetist (ACS). The second dressing change was done with PCS (propofol/alfentanil) and the third time the patients had to choose ACS or PCS. During the procedures, data on cardiopulmonary variables, sedation (bispectral index), pain intensity (VAS), procedural details, doses of drugs, and patients' preferences were collected to compare the two sedation techniques. Results: The study data indicated that wound care in burned patients is feasible with a standardized PCS protocol. The patients preferred PCS to ACS on the basis of self-control, and because they had less discomfort during the recovery period. Wound care was also considered adequate by the staff during PCS. No respiratory (respiratory rate/transcutaneous PCO2) or cardiovascular (heart rate/blood pressure) adverse events were recorded at any time during any of the PCS procedures. The doses of propofol and alfentanil and BIS index decrease were less during PCS than ACS. Procedural pain was higher during PCS but lower after the procedure. Conclusion: We suggest that PCS using a standard protocol is an interesting alternative to anaesthetist-provided sedation during dressing changes. It seems effective, saves resources, is safe, and at same time is preferred by the patients. The strength of these conclusions is, however, hampered by the small size of this investigation and therefore further studies are warranted. © 2008 Elsevier Ltd and ISBI.
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| 10. |
- Reske, A, et al.
(författare)
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Computed tomography - A possible aid in the diagnosis of smoke inhalation injury?
- 2005
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Ingår i: Acta Anaesthesiologica Scandinavica. - : Wiley. - 0001-5172 .- 1399-6576. ; 49:2, s. 257-260
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Tidskriftsartikel (refereegranskat)abstract
- Inhalation injury is an important contributor to morbidity and mortality in burn victims and can trigger acute lung injury and acute respiratory distress syndrome (ARDS) (1-3). Early diagnosis and treatment of inhalation injury are important, but a major problem in planning treatment and evaluating the prognosis has been the lack of consensus about diagnostic criteria (4). Chest radiographs on admission are often non-specific (5, 6), but indicators include indoor fires, facial burns, bronchoscopic findings of soot in the airways, and detection of carbon monoxide or cyanide in the blood (7). Changes in the lungs may be detected by bronchoscopy with biopsy, xenon imaging, or measurement of pulmonary extracellular fluid (4, 5, 8). These methods have, however, been associated with low sensitivity and specificity, as exemplified by the 50% predictive value in the study of Masanes et al. (8). Computed tomographs (CTs) are better than normal chest radiographs in the detection of other pulmonary lesions such as pulmonary contusion (9, 10). The importance of CT scans in patients with ARDS has been reviewed recently (9), but unfortunately there has been no experience of CT in patients with smoke inhalation injury. To our knowledge, there are only two animal studies reporting that smoke inhalation injury can be detected by CT (4, 11), specific changes in human CT scans have not yet been described. Therefore, confronted with a patient with severe respiratory failure after a burn who from the history and physical examination showed the classic risk factors for inhalation injury, we decided to request a CT. © Acta Anaesthesiologica Scandinavica 49 (2005).
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