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R Rossaint

Publications and source records attributed to R Rossaint.

At least 163 records · Page 9Linked to original sources
PubMed1994

[The relevance of perioperative coagulation parameters to indications for blood transfusion. A retrospective analysis of 300 liver transplantations].

In the present study, a retrospective statistical analysis of laboratory data, clinical data, and perioperative blood requirements from 300 primary orthotopic liver transplantations (OLT) is described. METHODS. OLT was performed using established surgical techniques and total IV anaesthesia. Volume was substituted with red blood cells (RBC) and fresh frozen plasma (FFP) according to haemodynamic data, haemoglobin, and diuresis. Platelet counts, prothrombin time, activated partial thromboplastin time (aPTT), thrombin time, fibrinogen, and antithrombin III were registered but not used as indications for transfusions. Statistics were performed using regression analysis and analysis of variance. RESULTS. The mean intraoperative fluid requirement was 793 ml balanced salt solution, 7.1 units RBC, and 8.4 units FFP; pooled random donor platelets were given only once. During 24 h postoperatively, an average of 1.8 units RBC and 4.6 units FFP had to be transfused. Currently, 278 of the 300 patients (92.7%) are alive. There was no significant correlation between clotting data and intraoperative blood use; for postoperative transfusion rates, the preoperative aPTT and postoperative platelet counts had a significant correlation. Reviewing the basic diseases of the patients, there were significant differences in coagulation status, but no differences in transfusion rates. CONCLUSION. According to the data presented, indications for transfusions in OLT according to clotting data are not valid, since these data do not correlate with the blood requirement. In addition, strategies for pretreatment of patients such as preoperative plasmapheresis are no longer justified with respect to possible side effects.

Adult↗
PubMed1994

[Therapy of ARDS. 1. Current therapeutic strategy including extracorporeal gas exchange].

Recent studies and reviews continue to report a high mortality associated with the acute respiratory distress syndrome (ARDS), which involves a severe inflammatory reaction within the whole lung that is frequently associated with multiple-organ failure. Important factors contributing to the poor results in severe ARDS are the aggressive procedures required to maintain sufficient arterial oxygenation, such as mechanical ventilation with high inspiratory pressures and high inspired oxygen concentrations (FiO2) which themselves contribute to the progression of the disease. As no specific therapy that reduces or prevents the general inflammatory reaction is known, current therapy is limited to procedures that minimize peak inspiratory pressures and FiO2. Therefore, pressure- and volume-limited ventilation modes with positive end-expiratory pressure, controlled hypercapnia, differential lung ventilation when appropriate, positioning (particularly prone), and aggressive dehydration are used. Should these procedures fail to improve arterial gas exchange, the patients may be additionally treated by veno-venous extracorporeal gas exchange. To reduce the risk of severe haemorrhagic complications due to high levels of systemic heparinization, systems internally coated with covalently bound heparin, which allow a lower level of systemic anticoagulation, should be used. From April 1989 to August 1993, 89 patients were transferred to our intensive care unit for treatment of severe ARDS; 52 were treated by combining the described conventional methods without artificial gas exchange (survival rate 88%) and 37 additionally underwent artificial gas exchange (survival rate 57%). The overall survival rate was 75%. On the basis of these experiences, we conclude that this step-by-step approach may improve survival in patients with severe ARDS.

Extracorporeal Membrane Oxygenation↗
PubMed1994

[Therapy of ARDS. 2. New management methods--first clinical experiences].

Conventional treatment of the adult respiratory distress syndrome (ARDS) includes pressure-limited ventilation, permissive hypercapnia, posture changes, aggressive dehydration, selective lung ventilation, and extracorporeal gas exchange. New strategies such as nitric oxide inhalation, the implantation of an intravenous membrane oxygenator (IVOX), and surfactant replacement are currently under evaluation. Nitric oxide (NO) is an important endothelium-derived relaxing factor that is rapidly inactivated by binding to haemoglobin. Inhaling this substance has been shown to induce selective vasodilatation of ventilated lung regions. Thus, inhaled NO reduces pulmonary hypertension, increases right heart ejection fraction, and improves arterial oxygenation by redistributing blood flow away from areas with intrapulmonary shunts to areas with a normal ventilation/perfusion ratio. Dose-response analysis has revealed that effective doses for improvement of oxygenation are lower than for reduction of mean pulmonary artery pressure. The use of a miniaturised membrane lung, IVOX, for intracaval oxygen and carbon dioxide exchange is a new approach to augment gas exchange. The IVOX is inserted via an introducer into the femoral vein and is designed for placement in the full length of the vena cava. Initial experiences with this device show that the currently used prototype provides a maximum of one-third of basal gas exchange. Therefore, a more efficient device will be needed to significantly reduce high inspired oxygen concentrations and airway pressures. Moreover, there exists evidence that IVOX causes caval obstruction. Lung surfactant recovered in BAL from patients with ARDS demonstrates that fractional contents of phosphatidylcholine and phosphatidylglycerol are reduced, and that the total concentration of apoproteins is decreased. Furthermore, the surfactant surface tension-lowering activity is abnormal. Thus, administration of exogenous surfactant may have therapeutic benefits. However, the optimal surfactant preparation, the optimal amount required to restore lung surfactant activity, and the optimal method to deliver it to patients with ARDS are unknown and currently under evaluation.

Adult↗
PubMed1994

Influence of positioning on ventilation-perfusion relationships in severe adult respiratory distress syndrome.

In 12 patients with severe adult respiratory distress syndrome (ARDS), pulmonary gas exchange and hemodynamics were evaluated before, during, and after a 2-h period of pressure-controlled mechanical ventilation with the patient in the prone position. Ventilation-perfusion relationships (VA/Q) were assessed by a multiple inert gas elimination technique. Pressure-controlled mechanical ventilation in the prone position resulted in an overall increase (p < or = 0.05) of arterial oxygenation after 120 min (98.4 +/- 50.3 to 146.2 +/- 94.9 mm Hg). Whereas eight patients revealed an improvement of PaO2 of more than 10 mm Hg after 30 min in the prone position (responders), four patients reacted to positional changes with a deterioration of arterial oxygenation (nonresponders). Data about the continuous distribution of ventilation-perfusion ratios revealed that in the responder group positioning caused a decrease of shunt perfusion of 11 +/- 5% and a concomitant increase of normal VA/Q by 12 +/- 4% after 30 min. There was no change demonstrable within low VA/Q areas. Returning the patient to the supine position reversed the improvement in gas exchange. The nonresponder group did not show any significant alteration in the distribution of VA/Q during the study. We concluded that improvement of oxygenation during pressure-controlled mechanical ventilation in the prone position is due to a shift of blood flow away from shunt regions, thus increasing areas with normal VA/Q. This redistribution of blood flow is most likely caused by a recruitment of previously ateletatic but nondiseased areas induced by altered gravitational forces.

Adolescent↗
PubMed1994

Inhaled nitric oxide in advanced paraquat intoxication.

No effective treatment is available for adult respiratory distress syndrome, pulmonary hypertension and progressive lung fibrosis in severe paraquat poisoning. A potentially beneficial effect of nitric oxide inhalation on the mean pulmonary artery pressure and gas exchange in a subject with advanced paraquat intoxication is reported. Eight days after the suicidal ingestion of an unknown dose of paraquat, a 52-year-old female had a PaO2 < or = 50 mm Hg despite ventilation with an FiO2 of 1 and a positive end-expiratory pressure of 14 to 18 cm H2O. After administration of 25 ppm nitric oxide, PaO2 increased and the mean pulmonary artery pressure and the right-to-left shunt decreased. Discontinuation of nitric oxide resulted in rapid reversal. Ventilatory function was stabilized for three days during nitric oxide inhalation but the patient developed massive pleural effusions and died on d 11 during an interruption of nitric oxide therapy. The response of serious paraquat intoxications to nitric oxide therapy may merit further study. A remarkable post-mortem finding was extensive myonecrosis supporting prolonged muscular retention of paraquat with toxic myopathy or neuromyopathy as a late manifestation of paraquat toxicity.

Administration, Inhalation↗
PubMed1994

Inhalation of nitric oxide--a new approach in severe ARDS.

Pulmonary hypertension due to increased pulmonary vascular resistance, and hypoxaemia based on an elevated intrapulmonary shunt are important pathophysiological features of the adult respiratory distress syndrome (ARDS). Systemically infused vasodilators reduce pulmonary hypertension but also decrease mean systemic arterial pressure and impair pulmonary gas exchange because of their global vasodilatory effects on the systemic and pulmonary circulation. Recently, inhaling low concentrations of the gas nitric oxide (NO), an important endothelium-derived relaxing factor which is rapidly inactivated by binding to haemoglobin, has been shown to induce selective vasodilation of ventilated lung regions. Thus, inhaled NO reduces pulmonary hypertension in severe ARDS and improves arterial oxygenation by redistributing blood flow away from areas with intrapulmonary shunt to areas with a normal ventilation/perfusion ratio.

Administration, Inhalation↗
PubMed1993

Inhaled nitric oxide for the adult respiratory distress syndrome.

BACKGROUND: The adult respiratory distress syndrome is characterized by pulmonary hypertension and right-to-left shunting of venous blood. We investigated whether inhaling nitric oxide gas would cause selective vasodilation of ventilated lung regions, thereby reducing pulmonary hypertension and improving gas exchange. METHODS: Nine of 10 consecutive patients with severe adult respiratory distress syndrome inhaled nitric oxide in two concentrations for 40 minutes each. Hemodynamic variables, gas exchange, and ventilation-perfusion distributions were measured by means of multiple inert-gas-elimination techniques during nitric oxide inhalation; the results were compared with those obtained during intravenous infusion of prostacyclin. Seven patients were treated with continuous inhalation of nitric oxide in a concentration of 5 to 20 parts per million (ppm) for 3 to 53 days. RESULTS: Inhalation of nitric oxide in a concentration of 18 ppm reduced the mean (+/- SE) pulmonary-artery pressure from 37 +/- 3 mm Hg to 30 +/- 2 mm Hg (P = 0.008) and decreased intrapulmonary shunting from 36 +/- 5 percent to 31 +/- 5 percent (P = 0.028). The ratio of the partial pressure of arterial oxygen to the fraction of inspired oxygen (PaO2/FiO2), an index of the efficiency of arterial oxygenation, increased during nitric oxide administration from 152 +/- 15 mm Hg to 199 +/- 23 mm Hg (P = 0.008), although the mean arterial pressure and cardiac output were unchanged. Infusion of prostacyclin reduced pulmonary-artery pressure but increased intrapulmonary shunting and reduced the PaO2/FiO2 and systemic arterial pressure. Continuous nitric oxide inhalation consistently lowered the pulmonary-artery pressure and augmented the PaO2/FiO2 for 3 to 53 days. CONCLUSIONS: Inhalation of nitric oxide by patients with severe adult respiratory distress syndrome reduces the pulmonary-artery pressure and increases arterial oxygenation by improving the matching of ventilation with perfusion, without producing systemic vasodilation. Randomized, blinded trials will be required to determine whether inhaled nitric oxide will improve outcome.

Adolescent↗
PubMed1993

Long-term inhalation with evaluated low doses of nitric oxide for selective improvement of oxygenation in patients with adult respiratory distress syndrome.

OBJECTIVE: To evaluate the lowest dose of inhaled nitric oxide (NO) in patients with adult respiratory distress syndrome (ARDS), which is able to improve arterial oxygenation more than 30% compared to baseline data. DESIGN: Prospective, clinical study. SETTING: Anesthesiological ICU in a university hospital. PATIENTS: 3 consecutive patients with severe ARDS according to clinical and radiological signs. INTERVENTIONS: Pressure-controlled ventilation with positive end-expiratory pressure of 8-12 cm H2O. Inhalation of NO was performed with a blender system and a Servo 300 ventilator. The lowest effective NO dose was defined by titrating the inspiratory NO dose until reaching a 30% improvement of PaO2/FiO2. This dose was used for the following continuous long-term NO inhalation; controls of efficacy by investigation of hemodynamics and blood gas exchange were performed initially and 2 times per patient after intervals of 3-5 days. MEASUREMENTS AND RESULTS: Initial NO concentrations were found to be effective at 60, 100, and 230 parts per billion (ppb). In all measurements, arterial oxygenation was found to be elevated by NO inhalation with the initially evaluated dose compared to baseline data; in parallel, the venous admixture (Qva/Qt) was reduced. The O2 delivery increased, although O2 consumption and hemodynamics did not change. In 1 patient, interruption of NO inhalation caused remarkable increase of pulmonary resistance. CONCLUSIONS: The improvement of oxygenation by NO inhalation in ARDS does not require reduction of pulmonary resistance and can be performed using low doses in the ppb range, which has to be considered as probably non-toxic.

Administration, Inhalation↗
PubMed1993

Extracellular volume expansion inhibits antidiuretic hormone increase during positive end-expiratory pressure in conscious dogs.

1. This study in conscious dogs examined the effects of extracellular volume expansion on plasma antidiuretic hormone, atrial natriuretic peptide and aldosterone concentrations, plasma renin activity, and haemodynamic and renal responses during controlled mechanical ventilation with 20 cmH2O positive end-expiratory pressure. 2. Twenty experiments (10 controls, 10 expansion experiments with 0.5 ml min-1 kg-1 body weight of a balanced electrolyte solution given intravenously throughout) were performed in five trained, conscious, tracheotomized dogs over 4 h: first and fourth hour, spontaneous breathing; second and third hour, 20 cmH2O positive end-expiratory pressure. 3. In the control experiments positive end-expiratory pressure increased plasma antidiuretic hormone concentration from 1.4 +/- 0.2 to 10.0 +/- 3.3 pg/ml, plasma aldosterone concentration from 113 +/- 19 to 258 +/- 58 pg/ml and heart rate from 77 +/- 5 to 94 +/- 5 beats/min. Positive end-expiratory pressure did not change plasma atrial natriuretic peptide concentration (55 +/- 5 pg/ml), plasma renin activity (2.6 +/- 0.4 pmol of angiotensin I h-1 ml-1) and mean arterial pressure 103 +/- 3 mmHg). 4. In the expansion experiments, positive end-expiratory pressure did not change plasma antidiuretic hormone concentration (1.1 +/- 0.1 pg/ml), plasma aldosterone concentration (25 +/- 2 pg/ml), plasma atrial natriuretic peptide concentration (82 +/- 8 pg/ml), plasma renin activity (0.8 +/- 0.15 pmol of angiotensin I h-1 ml-1), heart rate (92 +/- 6 beats/min) and mean arterial pressure (111 +/- 4 mmHg). 5. In the control experiments, urine volume, sodium excretion and fractional sodium excretion remained in a low range during positive end-expiratory pressure, whereas potassium excretion increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗
PubMed1993

Influence of prostaglandin E1 infusion on hemostasis in orthotopic liver transplantation.

In the control group, a significant decrease in platelet aggregability could be demonstrated after reperfusion. This was paralleled by a decrease in platelet counts. When PGE1 was infused during OLT, the post-reperfusional decreases in platelet aggregability and platelet counts in the control group could be prevented. Furthermore, our investigation demonstrated that PGE1 infusion led to higher t-PA activity during the anhepatic phase. This was paralleled and followed by lower alpha 2AP levels at the end of the anhepatic phase and after reperfusion. The higher t-PA levels in the PG group did not result in clinical signs of hyperfibrinolysis during OLT. The aprotinin administration in both groups is most certainly responsible for the absence of hyperfibrinolytic signs in the TEG and the low overall requirement for transfusions, explaining the comparable transfusion rate in the two groups (Fig. 5). Further investigations involving more patients are required to evaluate the clinical effect of PGE1 therapy.

Alprostadil↗
PubMed1993

"Goal-directed" transfusion management leads to distinct reduction of fluid requirement in liver transplantation.

Complications in patients undergoing OLT, such as hemorrhagic events, are caused not only by surgical problems but also by the profound functional disturbances arising from hepatic insufficiency, which are at least partially cured by the procedure itself. Preoperative clotting data give insight only into the dysfunction of the explanted organ. Hence, we tried to perform a standardized, "goal-directed" anesthesiologic management in the perioperative phase in OLT, following strict indications for blood replacement according to diuresis, hemoglobin level, and hemodynamic parameters. We performed 200 OLTs in 185 patients, according to usual methods. The mean intraoperative fluid requirement was 884 ml of balanced salt solution, 8.1 units of RBC, and 9.4 units of FFP. During the first 24 hours postoperatively, an average of 2.4 units of RBC and 5.6 units of FFP had to be transfused. Currently, 170 of the 185 patients (91.9%) are alive and well. Our data demonstrate that a distinct reduction of transfusion rates in OLT is possible, neglecting clotting data and improving clotting function by avoiding hemodilution.

Aprotinin↗
PubMed1993

Time-course and dose-response of nitric oxide inhalation for systemic oxygenation and pulmonary hypertension in patients with adult respiratory distress syndrome.

Inhalation of nitric oxide (NO), an endogenous vasodilator, was recently described to reduce pulmonary vascular resistance, and to improve arterial oxygenation by selective vasodilation of ventilated areas in patients with adult respiratory distress syndrome (ARDS). We describe the time-course and dose-response of initial short-term NO inhalation in 12 patients with ARDS. Enhanced oxygenation was achieved within 1-2 min after starting NO inhalation; after inhalation, baseline conditions were re-achieved within 5-8 min. Effective doses for improvement of oxygenation [baseline: PaO2 = 10.2 +/- 2.5 KPa (76.4 +/- 18.7 mmHg)] were low: ED50 was about 100 ppb--a concentration similar to the atmosphere. NO doses of more than 10 ppm [10 ppm NO: PaO2 = 17.3 +/- 3.3 KPa (129.4 +/- 25.1 mmHg)] re-worsen the arterial oxygenation. The ED50 for reduction of mean pulmonary artery pressure was 2-3 ppm. This indicates that inhalation of NO for improvement of oxygenation in severe ARDS should be performed using lower doses, with lower risk of toxic side effects.

Administration, Inhalation↗
PubMed1993

Inhaled nitric oxide reverses hypoxic pulmonary vasoconstriction without impairing gas exchange.

Nitric oxide (NO) is an endogenous endothelium-derived relaxing factor that participates in the regulation of vascular tone. We studied the effects of inhaled NO gas on transient hypoxic pulmonary vasoconstriction and normal lungs in mechanically ventilated sheep. We measured hemodynamics and pulmonary gas exchange. For gas exchange measurements we used conventional blood gas analysis and the multiple inert gas elimination technique to estimate ventilation-perfusion heterogeneity. Our hypotheses were 1) inhaled NO reverses hypoxic pulmonary vasoconstriction, 2) the hemodynamic effects of inhaled NO are limited to the pulmonary circulation, and 3) inhaled NO does not impair pulmonary gas exchange and may redistribute blood flow to better ventilated areas of the lungs. Hypoxic pulmonary vasoconstriction was induced by using a hypoxic inspiratory gas mixture. The addition of 20 ppm NO to the hypoxic inspiratory gases returned pulmonary arterial pressure to baseline values. Systemic hemodynamics and gas exchange indexes derived from conventional blood gas analysis remained constant. Gas exchange indexes for ventilation-perfusion ratios and gas dispersions improved. The addition of 20 ppm NO to medical air (21% O2) had no such significant effects on hemodynamics or pulmonary gas exchange. Our findings show that inhaled NO reverses transient hypoxic pulmonary vasoconstriction. The hemodynamic effects of NO are limited to the pulmonary circulation; it does not impair pulmonary gas exchange. Moreover, it redistributes blood flow to better ventilated alveoli. As such, NO has potential in the treatment of lung diseases associated with pulmonary hypertension.

Administration, Inhalation↗
PubMed1993

Inferior vena caval pressure increase contributes to sodium and water retention during PEEP in awake dogs.

UNLABELLED: This study compared the hemodynamic, renal, and hormonal effects of an experimentally induced increase in inferior vena caval pressure (IVCP) [to the same extent as during controlled mechanical ventilation (CMV) with positive end-expiratory pressure (PEEP)] with those of CMV with PEEP. Six volume-expanded conscious chronically tracheotomized dogs were studied under three conditions: CONTROL: 4 h of spontaneous breathing at 4 cmH2O continuous positive airway pressure (CPAP); CMV: CPAP for the 1st and 4th h and CMV with PEEP for the 2nd and 3rd h, resulting in a mean airway pressure of 20 cmH2O; and Increased IVCP: 4 h of CPAP, with IVCP increased during the 2nd and 3rd h by inflation of a chronically implanted cuff. Urine volume, sodium excretion, and fractional sodium excretion decreased during the 2nd and 3rd h of CMV and during increased IVCP compared with CONTROL. Glomerular filtration rate, mean arterial pressure, and antidiuretic hormone, atrial natriuretic peptide, and aldosterone plasma concentrations were not affected by CMV or Increased IVCP. Plasma renin activity decreased during CONTROL and Increased IVCP conditions but remained elevated during the 2nd and 3rd h of CMV. We conclude that, in conscious extracellular volume-expanded dogs, IVCP elevation contributes considerably to the water- and sodium-retaining effect of short-term CMV with PEEP.

Anesthesia↗