OBJECTIVE:It was hypothesized that sympathetic blockade restricted to the thoracic levels and achieved by thoracic epidural anesthesia might be capable of reducing hemodynamic deterioration after ...pulmonary artery embolism and that this might represent a potential method of treatment in patients with pulmonary embolism. Cardiopulmonary function after pulmonary embolism was therefore studied in sheep, either without a sympathetic blockade (the control group) or with sympathetic blockade.
DESIGN:Prospective, randomized laboratory investigation.
SETTING:University research laboratory.
SUBJECTS:Twelve adult, chronically instrumented Blackhead ewes.
INTERVENTIONS:Pulmonary embolization was achieved by injecting autologous blood clots (0.75 mL/kg) intravenously into an external jugular vein. The treatment group (n = 6) received 6 mL of 0.175% bupivacaine and the control group (n = 6) received 6 mL of 0.9% NaCl 90 mins after the embolization procedure. The injections were made via an epidural catheter (at the level of T3). Results were considered to be statistically significant (with analysis of variance) at p < .05.
MEASUREMENTS AND MAIN RESULTS:After epidural administration of bupivacaine in the thoracic epidural anesthesia group, the mean pulmonary artery pressure and heart rate were significantly reduced and the stroke volume index was significantly higher in comparison with the control group, in which the animals received epidural injections of saline.
CONCLUSIONS:Thoracic epidural anesthesia administered after the occurrence of pulmonary artery embolism thus significantly reduces hemodynamic deterioration in awake, spontaneously breathing sheep and may represent an additional option in the treatment of pulmonary embolism.
The purpose of this study was to evaluate modified adriamycin-induced cardiomyopathy in the dog for research on partial left ventriculectomy (PLV).
An intracoronary catheter was introduced into the ...left main stem via the first marginal branch in a retrograde fashion in 12 adult foxhound dogs. The catheter was connected to a percutaneous access port that was used for weekly adriamycin administration (10 mg over a 1-hour period on 5 occasions). Follow-up examinations (transthoracic echocardiography, hemodynamic parameters, cardiopulmonary status, neurohormones) were done before, 1 week after the last adriamycin administration, and then 6 weeks later. This protocol was performed in 6 dogs (control group: Group 1). The other 6 dogs underwent PLV 1 week after the last adriamycin administration (Group 2). After the last measurements, all dogs were killed with saturated potassium chloride under general anesthesia and the hearts were excised for histologic examination. All data were calculated as mean and standard error of the mean. Differences were calculated by the Wilcoxon signed-rank test for paired and unpaired data.
p < 0.05 was considered statistically significant.
One dog from each group died suddenly during adriamycin administration (probably due to ventricular arrhythmia). In addition, 1 dog from Group 2 suffered from a severe systemic inflammatory response syndrome after PLV and died 36 hours after surgery. Thus, 5 dogs from Group 1 and 4 from Group 2 underwent the entire study protocol. Adriamycin administration resulted in a severe dilated cardiomyopathy that was comparable in both groups (significant increase of central venous pressure, mean pulmonary artery pressure, pulmonary wedge pressure, left ventricular end-systolic and end-diastolic diameters, oxygen extraction, troponin I and anti-diuretic hormone, whereas cardiac output, ejection fraction and venous oxygen saturation decreased significantly). Deterioration of cardiac function continued after termination of adriamycin administration in Group 1 dogs, albeit not as progressively as during adriamycin administration. In contrast, cardiac function improved in Group 2 dogs after PLV, but did not reach baseline values. Cardiac index increased and oxygen extraction (
p = 0.03) decreased, resulting in an enhanced venous oxygen saturation (
p = 0.02). In particular, the distance of the papillary muscles at end diastole (
p = 0.02) and at end systole (
p = 0.02) at the mid-papillary level decreased significantly after PLV, resulting in reduced left ventricular diameter and volume (statistically significant for left ventricular end-systolic diameter and volume). All hearts had severe histologic alterations characteristic of adriamycin-induced toxicity, including cytoplasmic vacuolation, myocyte degeneration and increased fibrosis.
Modified adriamycin-induced cardiomyopathy in the dog may be suitable for research on PLV.
We hypothesized that sympathetic stimulation is the main mechanism contributing to hemodynamic failure in pulmonary embolism. We investigated the effects of epidural anesthesia-induced sympathetic ...blockade, restricted to thoracic and lumbar levels, during pulmonary embolism. Two experiments were performed in chronically instrumented ewes. In the first experiment, six sheep received 6 mL bupivacaine 0.175% (Thoracic Epidural Anesthesia TEA group), and six sheep received 6 mL saline 0.9% (TEA-Control group), respectively, via an epidural catheter (T3 level). In the second experiment, six sheep received 2.8 mL bupivacaine 0.375% (Lumbar Epidural Anesthesia LEA group), and six sheep received 2.8 mL saline 0.9% (LEA-Control group) epidurally (L4 level). Embolization was performed by IV injection of au- tologous blood clots (Experiment 1, 0.75 mL/kg; Experiment 2, 0.625 mL/kg). TEA was associated with significantly slower heart rates, decreased mean pulmonary artery pressures and central venous pressures, and significantly higher stroke volume index and oxygenation in comparison with the TEA-Control group. By contrast, LEA was associated with significantly faster heart rates and increased central venous pressures and with a significantly lower stroke volume index in comparison with the LEA-Control group. TEA significantly reduced, and LEA significantly increased, hemodynamic deterioration, suggesting beneficial effects of TEA on cardiopulmonary function during pulmonary thromboembolism.
To evaluate the adriamycin-induced cardiomyopathy in the dog for research on partial left ventriculectomy (PLV).
An intracoronary catheter was introduced into the left main stem via the first ...diagonal branch in a retrograde fashion in 6 adult FBI (Foxhound Boehringer Ingelheim) dogs weighing 30 to 35 kg. The catheter was connected to a percutaneous access port that was used for weekly adriamycin administration (10 mg over a 1-hour period for 5 times). Follow-up examinations (transthoracic echocardiography, hemodynamic parameters, cardiopulmonary status, and neurohormones) were done before, 1 week after the last adriamycin administration, and 6 weeks later. After the last measurements, all dogs were euthanized with saturated potassium chloride under general anesthesia and the hearts were excised for histologic examinations. All data were calculated as mean values and standard error of the mean. Differences were calculated by the Wilcoxon signed rank test for paired and unpaired data.
p values less than 0.05 were considered significant.
Central venous pressure (2.2 ± 0.8 vs 5.2 ± 0.4 mm Hg,
p = 0.03), mean pulmonary artery pressure (8.6 ± 1.1 vs 12.4 ± 0.5 mm Hg,
p = 0.03), pulmonary wedge pressure (2.6 ± 0.9 vs 7.0 ± 0 mm Hg,
p = 0.03), left ventricular endsystolic diameter (2.5 ± 0.2 vs 3.1 ± 0.4 cm,
p = 0.03), and enddiastolic (4.5 ± 0.2 vs 4.9 ± 0.2 cm,
p = 0.03) diameter increased significantly after adriamycin administration, whereas cardiac output (4.0 ± 0.3 vs 3.3 ± 0.1 liter/min,
p = 0.03), stroke volume index (66.0 ± 7.4 vs 54.0 ± 3.9 ml/beat/m
2,
p = 0.03), and ejection fraction (61.1 ± 5.1 vs 37.7 ± 5.7%,
p = 0.03) decreased markedly. These changes were accompanied by a significant decline of oxygen delivery (1130 ± 170 vs 790 ± 65 ml/min,
p = 0.03), which led to an enhanced oxygen extraction (0.12 ± 0.01 vs 0.24 ± 0.01,
p = 0.03). Consequently, venous oxygen saturation (82.7 ± 4.1 vs 71.3 ± 2.5%,
p = 0.03) decreased. Troponin I (0.02 ± 0.025 vs 1.7 ± 0.6 ng/ml,
p = 0.03) and the anti-diuretic hormone (1.9 ± 0.9 vs 20.0 ± 1.9 pg/ml,
p = 0.03) increased significantly after adriamycin administration. Deterioration of cardiac function continued after termination of adriamycin administration, albeit slower than during adriamycin administration. All hearts had severe histologic alterations, which were characteristic of adriamycin-induced toxicity: cytoplasmic vacuolation, myocyte degeneration, and increased fibrosis.
The adriamycin-induced cardiomyopathy in the dog is similar to the dilated cardiomyopathy in humans and may be an appropriate model for PLV.
Background. Heparin-induced thrombocytopenia type II (HIT II) is a rare but life-threatening side effect of heparin therapy. We describe the perioperative anticoagulative management of patients ...tested positive for HIT II and requiring implantation of a left ventricular assist device (LVAD).
Methods. We report on 3 patients with a different perioperative anticoagulative management (preoperative, intraoperative, and postoperative anticoagulation with danaparoid-sodium; preoperative anticoagulation with recombinant hirudin, anticoagulation with danaparoid-sodium intraoperatively and postoperatively; preoperative anticoagulation with recombinant hirudin, intraoperative anticoagulation with heparin, and postoperative anticoagulation with danaparoid-sodium) and discuss the difficulties of the treatment.
Results. Anticoagulation with alternative drugs such as recombinant hirudin and danaparoid-sodium led to serious and life-threatening bleeding complications as well as to thromboembolic events in the first 2 patients. Therefore the third patient underwent LVAD implantation using heparin for intraoperative anticoagulation to avoid administration of high doses of recombinant hirudin or danaparoid-sodium. Despite very low anti-factor Xa activities, when using danaparoid-sodium postoperatively, the patient suffered from a bleeding complication on the 4th day after LVAD implantation requiring reexploration.
Conclusions. In selected cases (negative heparin-induced platelet aggregation (HIPA) test at the time of LVAD implantation and continuation of postoperative anticoagulation with recombinant hirudin or danaparoid-sodium), heparin may be used for LVAD implantation in HIT II patients to reduce bleeding complications.
Fluid resuscitation in sepsis-related lung injury is limited by aggravation of pulmonary edema. Hypovolemia, however, may compromise tissue perfusion and contribute to organ dysfunction. We ...hypothesized that inhaled nitric oxide would reduce edema formation during fluid therapy.
Prospective laboratory investigation in a university research laboratory.
Eighteen chronically instrumented sheep.
The animals were randomly assigned to one of three groups and received endotoxin (S. typhi, 10 ng kg(-1) min(-1)) for 30 h. After 24 h the sheep were anesthetized (ketamine/midazolam), mechanically ventilated with oxygen, and received 0.1 ml kg(-1) oleic acid: oxy group (n=6), an infusion of Ringer's lactate was restricted to 1 ml kg(-1) h(-1); fluid/oxy group (n=6), a bolus of 10 ml kg(-1) Ringer's lactate plus 10 ml kg(-1) h(-1) was given; fluid/NO group (n=6), the sheep were treated as in the fluid/oxy group, except that they inhaled nitric oxide (20 ppm).
The extravascular lung water index was measured using thermodye dilution. Oleic acid increased extravascular lung water, impaired oxygenation, and reduced cardiac index at 26 h in all groups. After 30 h the extravascular lung water in the fluid/NO group was not higher than in the oxy group and significantly than in the fluid/oxy group. While cardiac index returned to the level of sepsis baseline in fluid/NO and fluid/oxy, it was reduced in the oxy group after 30 h. There were no significant differences in cardiac index between groups.
Inhaled nitric oxide may be an option for reducing edema formation secondary to fluid resuscitation in acute lung injury.
Although hemoglobin-based oxygen carriers (HBOC) are now being investigated, the effects of HBOC solutions during regional anesthesia have never been analyzed. Therefore, we investigated the ...hemodynamic changes after HBOC infusion during general anesthesia and thoracic epidural anesthesia. Sheep were assigned to three different groupsa) a control group with six unanesthetized sheep; b) six sheep with a halothane anesthesia (2.0 vol. % in oxygen); and c) six awake sheep with a thoracic epidural anesthesia with bupivacaine. After a period of stabilization, all 18 animals received 100 mg/kg of the HBOC pyridoxalated hemoglobin polyoxyethylene conjugate. The infusion of the HBOC caused a significant increase in mean arterial pressure and pulmonary artery pressure in both the control and epidural anesthesia groups. Anesthesia with halothane reduced the effects of the HBOC-solution on mean arterial pressure but did not abolish the increase in pulmonary artery pressure. Our results demonstrate that vasoconstriction caused by HBOC solutions is not abolished by epidural anesthesia, but halothane anesthesia may alter the hemodynamic effects of HBOC solutions.
IMPLICATIONSWe evaluated the effects of epidural anesthesia and halothane anesthesia on the vasoconstrictive properties of a cell-free hemoglobin solution. The vasoconstriction caused by a cell-free hemoglobin solution was similar in unanesthetized sheep and sheep with thoracic epidural anesthesia and was reduced in sheep with halothane anesthesia.
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