Epidural anesthesia and splanchnic perfusion.
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Anesthesia, Epidural↗
Biomedical subjects
A Sielenkämper
Publications and source records attributed to A Sielenkämper.
[Massive transfusion with the Rapid Infusion System. Its effect on core body temperature].
Extensive blood loss requires adequate volume replacement. However the infused volume cannot be adequately warmed especially when high infusion rates are necessary. Subsequently, hypothermia develops and results in hemodynamic instability and coagulopathy. The Rapid Infusion System (RIS) allows high infusion rates (up to 1.5 l/min) while at the same time guaranteeing sufficient warming. The efficacy of the RIS was investigated in 43 consecutive patients who required a massive transfusion. The average volume transfused in these patients was 31.7 +/- 4.5 l (minimum: 7.8 l; maximum: 165.3 l) which is equal to an average exchange of 6.4 times the circulating blood volume (maximum: 39.4 blood volumes). The replacement of such high blood volumes has not yet been published in a series of patients. Despite these high transfusion rates, the body core temperature was maintained at 35.85 +/- 0.1 degrees C. Only five patients had a body core temperature below 34 degrees C, all were trauma patients and four of these five patients already had a preoperative temperature below 34 degrees C. The mortality in this study was 28%, which is markedly reduced in comparison to previous publications although they all considered at patients with significantly less blood loss. Maintaining normothermia and normovolemia by the use of the RIS may explain the improved outcome.
Adult↗
Endotoxin promotes adhesion of human erythrocytes to human vascular endothelial cells under conditions of flow.
OBJECTIVE: To investigate the effects of endotoxin on adhesion of human red blood cells to human vascular endothelial cells under conditions of flow. DESIGN: Prospective, randomized, controlled in vitro study. SETTINGS: University-affiliated cell biology laboratory. SUBJECTS: Human erythrocytes and human vascular endothelial cells. INTERVENTIONS: Fresh human erythrocytes and human vascular endothelial cells grown as monolayers were incubated with either saline or endotoxin. After incubation, endothelial monolayers were superfused with erythrocytes, and the number of erythrocytes adhering to the endothelial monolayer was quantified. MEASUREMENTS AND MAIN RESULTS: Adhesion of erythrocytes to vascular endothelium was measured under conditions of continuous flow in different settings: a) exposure of both endothelial cells and erythrocytes to saline; b) incubation of both erythrocytes and endothelial cells with endotoxin; c) exposure of erythrocytes only to endotoxin; d) incubation of endothelial cells only to endotoxin; and e) both the endothelial cells and erythrocytes incubated with different concentrations of endotoxin. Erythrocyte adhesion in the saline control group was 71 +/- 8 cells/mm2. Incubation of both components with endotoxin increased the number of adhesive erythrocytes to 172 +/- 9 cells/mm2 (p < .05). When only the endothelial cells were treated with endotoxin, 142 +/- 8 cells/mm2 adhered to the endothelial monolayer, whereas the incubation of the erythrocytes only to endotoxin resulted in adhesion of 102 +/- 3 cells/mm2. Decreasing concentrations of endotoxin reduced adhesion from 172 +/- 9 cells/mm2 (endotoxin, 75 microg/mL) to 165 +/- 9 cells/mm2 (endotoxin, 25 microg/mL), 153 +/- 4 cells/mm2 (endotoxin, 1 microg/mL), and 146 +/- 6.1 cells/mm2 (endotoxin, 5 ng/mL). CONCLUSIONS: Exposure of human erythrocytes and human venous vascular endothelial cells to an inflammatory stimulus such as endotoxin promotes a dose-dependent adhesion of erythrocytes to endothelium in a dynamic environment. These adhesive erythrocyte-endothelium interactions can be produced by exposure of either red blood cells or endothelial cells to endotoxin, with a higher degree of adhesion after activation of the endothelial cell component.
Cell Adhesion↗
[Oxygen delivery in sepsis. After 10 years more questions than answers].
Object of this review is to present the physiological principles, diagnostic techniques and therapeutic options that are related to modifications of oxygen delivery in sepsis. Despite intense research activities in this area, many topics regarding oxygen transport and oxygen consumption in sepsis are still not clear. For example, the often discussed shift of the critical value of oxygen delivery to higher values in sepsis has not been proven, yet. Beside an impaired regional perfusion also disturbances in the cellular oxygen utilization may be responsible for organ failure in sepsis. Until now, it was not shown, whether the increase of oxygen delivery to supranormal levels reduces mortality in septic patients. It is also unknown, which catecholamine and which infusion solution is suitable for the treatment of septic patients. In future further research is necessary to solve the problems associated with sepsis therapy.
Fluid Therapy↗
Effects of FI(O(2)) on hemodynamic responses and O(2) transport during RSR13-induced reduction in P(50).
Reduced Hb-O(2) affinity facilitates O(2) release to tissue but may impair pulmonary O(2) uptake, affecting cardiac output and systemic vascular resistance (SVR). We studied the effects of shifting the O(2)-dissociation curve (ODC) to the right with a continuous infusion of RSR13, an allosteric modifier of Hb, and of different inspired O(2) fractions (FI(O(2))) on arterial O(2) saturations (Sa(O(2))) in Hb and on hemodynamics in nonanesthetized rats. At an FI(O(2)) of 0.21, Sa(O(2)) fell during RSR13 from 95 to 81%. Elevation of FI(O(2)) to 0.30 returned Sa(O(2)) to baseline in the RSR13 group. The decrease in mean arterial pressure (MAP) was significantly greater in the control than in the RSR13 group at 30% O(2). Cardiac index (CI) increased only during RSR13 at 21% O(2) and returned to baseline at 30% O(2). In contrast, SVR decreased after RSR13 was infused at 21% O(2) but returned to baseline at 30%O(2), whereas controls showed the opposite, a sustained SVR. In the follow-up period, when 21 O(2)% was reestablished and mild anemia was present, MAP and SVR fell significantly more in controls, whereas CI only increased in controls. Lactate was significantly lower in the RSR13 than in the control group during RSR13 and the follow-up period. These results demonstrate that 1) continuous infusion of RSR13 produces a constant shift in the O(2) tension at which Hb is 50% saturated (P(50)), 2) FI(O(2)) of 0.30 compensates for the effects of increased P(50) on pulmonary O(2) loading, and 3) right-shifted ODC combined with supplemental O(2) may improve tissue O(2) availability.
Aniline Compounds↗
Hydroxyethyl starch and blood coagulation.
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Amylopectin↗
[The anesthesia recovery room--new demands on an established form of organization].
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Anesthesia Recovery Period↗
[Cardiopulmonary effects of CPPV (continuous positive pressure ventilation) and IRV (inverse ratio ventilation) in experimental myocardial ischemia].
Continuous positive pressure ventilation (CPPV) is an established therapy for treatment of acute respiratory failure (ARF). However, cardiac performance may be severely disturbed due to elevated intrathoracic pressure, inducing a decrease in cardiac output (CO) and oxygen delivery (DO2). Alternatively, mechanical ventilation with prolonged inspiratory to expiratory duration ratio (inversed ratio ventilation IRV) has been successfully used in ARF. No data are available about IRV in acute haemodynamic oedema. Thus, the cardiopulmonary effects of CPPV (positive end-expiratory pressure [PEEP] = 10 cm H2O) and IRV (inspiration to expiration duration ratio [I:E] = 3.0) were studied in nine dogs (body weight 29.9 +/- 4.3 kg) before and after induction of myocardial ischaemia. METHODS. Continuous intravenous anaesthesia and muscle paralysis were provided by 1.2 mg.kg-1 x h-1 piritramide and 0.08 mg.kg-1 x h-1 pancuronium, and the animals were ventilated with intermittent positive pressure ventilation (IPPV) as reference method. Cardiocirculatory performance was determined by means of heart rate (HR), mean arterial pressure (MAP), mean pulmonary arterial pressure (MPAP), central venous pressure (CVP), pulmonary artery occlusion pressure (PAOP) and left ventricular end-diastolic pressure (LVEDP). Cardiac output (CO) was determined by thermodilution method. Systemic vascular resistance (SVR) was calculated. Pulmonary function was assessed by arterial and mixed venous blood gas tension for oxygen (PaO2, PvO2) and carbon dioxide (PaCO2). Functional residual lung capacity (FRC) was measured by means of the foreign gas wash-in method using helium as inert gas, and determination of extravascular lung water (EVLW) using the thermal-dye indicator technique. CPPV and IRV were studied in random sequence in the control phase and 60 min after induction of acute left ventricular ischaemia, which was achieved by occlusion of the ramus interventricularis anterior. RESULTS. During the control phase CPPV induced an increase in MPAP (P < 0.05), CVP (P < 0.05) and PAOP (P < 0.05). HR and MAP remained unchanged, whereas CO decreased by 16% (P < 0.05). FRC was elevated by 25 ml.kg-1 (P < 0.01), but not EVLW (9.1 +/- 3.5 ml.kg-1). There was no improvement in oxygenation; instead, oxygen delivery (DO2) decreased (P < 0.05). During inversed ratio ventilation MPAP, CVP, PAOP increased, but less than during CPPV. FRC was elevated mu 7.0 ml.kg-1 (P < 0.05), which was significantly less than during CPPV (P < 0.05). EVLW revealed no differences. During IPPV in the ischaemia phase cardiopulmonary performance deteriorated significantly. CO decreased by 19% (P < 0.05), whereas HR, MPAP, CVP and PAOP increased (P < 0.05). PaO2 was lower (P < 0.05) and alveolo-arterial PO2 gradient (PAaO2) increased (P < 0.05). All animals revealed moderate pulmonary oedema (EVLW = 15.1 +/- 8.4 ml.kg-1) (P < 0.01) and a lower FRC. Mechanical ventilation with PEEP significantly improved oxygenation and FRC; however, DO2 was slightly lower than during IPPV (not significant). IRV elevated PaO2, FRC and DO2, since CO was not depressed when compared with IPPV. CONCLUSIONS. CPPV and IRV may induce a recruitment of collapsed or hypoventilated lung areas, which is more pronounced during CPPV. During both modes of ventilation, oxygenation was improved without apparent changes in EVLW. Haemodynamic performance was more impaired during CPPV, and no improvement of left ventricular function secondary to an elevated intrathoracic pressure was observed. Occlusion of the RIVA coronary artery typically induces an infarction of 35% of left ventricular muscle mass; however, non-ischaemic myocardium reveals an unchanged or increased contractility. Thus, a reduction of left ventricular preload secondary to CPPV mainly contributes to haemodynamic depression, which is less pronounced during IRV due to a lower peak inspiratory airway pressure and mean airway pressure. IRV may be useful for mechanical ventCntCo
Animals↗
Cardiopulmonary effects of constant-flow ventilation in experimental myocardial ischaemia.
The cardiopulmonary effects of constant-flow ventilation were investigated in dogs with normal heart function (control-phase, n = 14) and after development of acute myocardial ischaemia (ischaemia phase, n = 14). Heated, humidified and oxygen-enriched air was continuously delivered with an inspiratory flow rate of 1.21.kg-1.min-1 via two catheters positioned within each mainstem bronchus. Continuous positive pressure ventilation with a positive end-expiratory pressure of 0.5 kPa (5 cmH2O) was used as a reference. During control, neither continuous positive pressure ventilation nor constant-flow ventilation showed impairment of cardiopulmonary performance. Oxygenation and CO2 removal were more efficiently achieved by continuous positive pressure ventilation (P less than or equal to 0.05). Acute myocardial ischaemia was induced by occlusion of the left anterior descending (LAD) coronary artery; measurements during the ischaemia phase were performed 60 min following LAD occlusion. Myocardial ischaemia resulted in moderate changes of cardiac output, left ventricular end-diastolic pressure and dP/dtmax. Both modes of ventilation were well tolerated in the ischaemia phase, and cardiovascular performance revealed no significant differences between continuous positive pressure ventilation and constant-flow ventilation. Haemodynamic parameters could be more precisely assessed during constant-flow ventilation. Oxygenation deteriorated, but hypoxaemia did not occur in any animal and CO2 elimination remained unchanged. It is concluded that 'non-conventional' ventilation by continuous intrabronchial gas flow maintains adequate gas exchange with no adverse effects on haemodynamics in dogs with acute myocardial ischaemia. Constant-flow ventilation may be advantageous in the experimental setting to study cardiac function without cyclic heart-lung interaction due to airway pressure alterations.
Animals↗
Constant-flow ventilation during experimental left ventricular failure.
The efficacy of constant-flow ventilation (CFV) was investigated in dogs with normal heart function (control phase, n = 8) and after development of left ventricular failure (LVF phase, n = 8). Heated, humidified and oxygen-enriched air (inspired oxygen fraction (Fio2) = 0.4) was continuously delivered via two catheters positioned within each mainstem bronchus at two flow rates (1.2 and 1.6 l/kg/min). Conventional mechanical ventilation (CMV) with positive end-expiratory pressure (PEEP) of 0.5 kPa was used as reference ventilation. During control, neither CMV with PEEP nor CFV revealed severe impairment of cardiopulmonary performance. Alveolo-arterial PO2 difference (P(A-a)O2) increased significantly during CFV1.2 and CFV1.6, indicating a higher degree of ventilation-perfusion (VA/Q) inhomogeneity. Acute left ventricular failure (LVF) was induced by proximal occlusion of the left anterior descending (LAD) coronary artery. Cardiac output (CO), maximum velocity of pressure development (dP/dtmax) and mixed venous PO2 decreased (P less than or equal to 0.05), whereas left ventricular end-diastolic pressure (LVEDP) and pulmonary capillary wedge pressure (PCWP) increased (P less than or equal to 0.05). Extravascular lung water (EVLW), as determined by thermal-dye technique, increased from 10.1 ml/kg to 20.9 ml/kg (P less than or equal to 0.01). Oxygenation, but not CO2 elimination, deteriorated in the LVF phase. There were no haemodynamic differences between CMV with PEEP and CFV1.2, but cardiopulmonary performance deteriorated with CFV1.6. Gas exchange was significantly more impaired during CFV1.2 and CFV1.6 due to increased VA/Q mismatching. However, there were no significant differences for P(A-a)O2 values between CFVControl and CFVLVF.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗