Search PubMed⌕ Search

Biomedical subjects

W Schütz

Publications and source records attributed to W Schütz.

At least 19 recordsLinked to original sources
PubMed2001

Is it feasible to monitor total hepatic blood flow by use of transesophageal echography? An experimental study in pigs.

OBJECTIVES: Total hepatic venous blood flow is determined by the common hepatic arterial blood flow and the venous outflow from stomach, spleen, pancreas, small intestine, and bowel, collected by the portal vein, and thus represents overall splanchnic perfusion. We investigated whether transesophageal echography (TEE) can provide a method for bedside assessment of hepatic venous blood flow useful as a noninvasive method for measuring splanchnic perfusion in clinical practice. DESIGN AND SETTING: Experimental study in 15 anesthetized and ventilated pigs in an animal research laboratory. INTERVENTIONS: TEE-derived calculations of hepatic venous blood flow were compared with liver blood flow measurements using perivascular ultrasound flow probes surgically positioned on portal vein and common hepatic artery. Parameters were determined at baseline and after modulating splanchnic perfusion by either PEEP maneuver (15 cmH2O) or intravenous epinephrine (0.1 microgram kg-1 min-1). MEASUREMENTS AND RESULTS: Diameter (d) and velocity time integral (VTI) of all three hepatic veins were determined by TEE, heart rate (HR) was derived from electrocardiography and flow subsequently calculated as Q = pi.(d/2)(2).0.57.VTI.HR. Regression analysis of matched TEE and flow probe values showed a significant linear relationship (r2 = 0.698). Bias analysis revealed a systematic underestimation of liver blood flow by TEE, possibly due to use of 0.57 as correction factor for mean velocity, while changes in liver blood flow were reliably detected. CONCLUSION: TEE offers a noninvasive approach for monitoring hepatic perfusion and may be used in patients.

Animals↗
PubMed2001

Use of multi-plane transoesophageal echocardiography in visualization of the main hepatic veins and acquisition of Doppler sonography curves. Comparison with the transabdominal approach.

The role of multi-plane transoesophageal echocardiography (TOE) in the visualization of the three main hepatic veins and acquisition of Doppler sonography curves has not been established. We have studied this diagnostic option of TOE in 34 patients during general anaesthesia. The findings were compared with the results of conventional transabdominal sonography (TAS). Using TOE, each of the three main hepatic veins could be visualized in all patients. In contrast, TAS allowed adequate two-dimensional visualization of the right, middle, and left hepatic vein in only 97%, 85%, and 61% of the patients, respectively. Adequate Doppler tracings of the right and middle hepatic vein could be obtained in 100% and 97% of the patients by TOE and in 91% and 50% of the patients by TAS. Doppler tracings of the left hepatic vein could only be acquired in 18% of the patients by TOE, but in 47% of the patients by TAS. As blood flow may be calculated from the diameter of the vessel, velocity time integral of the Doppler curve and heart rate, TOE may provide an interesting non-invasive tool to monitor blood flow in the right and middle hepatic vein.

Abdomen↗
PubMed2001

Electrocardiographic exercise stress testing for cardiac risk assessment in patients undergoing noncardiac surgery.

BACKGROUND: The value of exercise electrocardiography in the prediction of perioperative cardiac risk has yet to be defined. This study was performed to determine the predictive value of exercise electrocardiography as compared with clinical parameters and resting electrocardiography. METHODS: A total of 204 patients at intermediate risk for cardiac complications prospectively underwent exercise electrocardiography before noncardiac surgery. Of these, 185 were included in the final evaluation. All patients underwent follow-up evaluation postoperatively by Holter monitoring for 2 days, daily 12-lead electrocardiogram, and creatine kinase, creatine kinase MB, and troponin-T measurements for 5 days. Cardiac events were defined as cardiac death, myocardial infarction, minor myocardial cell injury, unstable angina pectoris, congestive heart failure, and ventricular tachyarrhythmia. Potential risk factors for an adverse event were identified by univariate and multivariate logistic regression analysis. RESULTS: Perioperative cardiac events were observed in 16 patients. There were 6 cases of myocardial infarction and 10 cases of myocardial cell injury. The multivariate correlates of adverse cardiac events were definite coronary artery disease (odds ratio, 8.8; 95% confidence interval [CI], 1.1--73.1; P = 0.04), major surgery (odds ratio, 4.7; 95% CI, 1.3--16.3; P = 0.02), reduced left ventricular performance (odds ratio, 2.0; 95% CI, 1.1--3.8; P = 0.03), and ST-segment depression of 0.1 mV or more in the exercise electrocardiogram (odds ratio, 5.2; 95% CI, 1.5--18.5; P = 0.01). A combination of clinical variables and exercise electrocardiography improved preoperative risk stratification. CONCLUSIONS: This prospective study shows that a ST-segment depression of 0.1 mV or more in the exercise electrocardiogram is an independent predictor of perioperative cardiac complications.

Adult↗
PubMed2001

Noninvasive diagnosis of coronary artery disease: a comparison between cardiokymographic and electrocardiographic stress testing.

Noninvasive cardiokymography has been further developed to be able to record wall motion abnormalities during exercise. The study was designed to evaluate the diagnostic accuracy of stress cardiokymography and electrocardiography in the diagnosis of coronary artery disease. 223 patients were included in a prospective investigation using a newly developed computerized cardiokymography device. Sensitivity, specificity, and positive predictive value were 61, 69 and 90% for exercise cardiokymography, and 57, 74 and 91% for exercise electrocardiography, respectively. There was no statistically significant difference between cardiokymography and electrocardiography. The combination of electrocardiography and cardiokymography did not produce a significant improvement in diagnostic accuracy in comparison to exercise electrocardiography alone.

Adult↗
PubMed2000

[Principles of catecholamine therapy. 1. Characterization of clinically relevant sympathomimetics].

All involuntary innervated structures of the body are controlled by the sympathetic and parasympathetic nervous system. Adrenaline, noradrenaline and dopamine are endogenous catecholamines binding to adrenergic and dopaminergic receptors, respectively, to mediate their clinical effects. Adrenoceptors are classified as alpha 1, alpha 2, beta 1 and beta 2 subtypes which were even further subcharacterized the recent years. Adrenoceptors are membrane proteins interacting with the agonist and, thus, inducing G-protein mediated intracellular effects. Adrenaline induces an extensive increase of heart rate and stroke volume mediated by beta-adrenoceptors and significantly enhances peripheral vascular resistance by alpha-adrenoceptor stimulation, when administered beyond 0.1 microgram/kg.min. In contrast, the clinical effects of noradrenaline are predominantly characterized by alpha-adrenoceptor stimulation resulting in a less pronounced increase of heart rate. Dopamine, less potent on adrenoceptors, shows additional effects on renal as well as on splanchnic circulation mediated by dopaminergic receptors. Dobutamine, primarily acting on beta-adrenoceptors, results in positive inotropic effects without an increase in vascular resistance. Dopexamine, a synthetic catecholamine, induces vasodilation via beta 2-adrenoceptor stimulation and potentially increases splanchnic blood flow by additional effects on dopaminergic receptors. Isoproterenol, the classical beta-adrenoceptor agonist, mediates positive inotropic effects and causes a major increase in heart rate and a significant decrease of systemic vascular resistance. Independent on adrenoceptors, phosphodiesterase-III-inhibitors exert positive inotropic and vasodilating activity by an increase in intracellular cAMP concentration induced by inhibition of cAMP hydrolysis.

Animals↗
PubMed2000

[The basics of catecholamine therapy. 2. A guide to clinical use].

Myocardial function is determined by preload, afterload, contractility and heart rate. Pathologic changes of these variables may result in decrease of blood pressure, acute heart failure or cardiogenic shock. Hyperdynamic septic shock is associated with systemic hypotension despite increased cardiac output. Mediators of sepsis induce both myocardial depression and pulmonary arterial hypertension. Moreover, sepsis is characterized by microcirculatory disturbances and dysbalance in regional oxygen delivery and consumption. Severe systemic hypotension is a symptom often requiring catecholamine therapy to restore systemic circulation and to avoid organ damage. As the use of catecholamines is not a causal therapy administration should be limited to an initial measure until correction of the underlying abnormalities can be achieved. Different etiologies of shock as well as diseases requiring specific interventions as pulmonary embolectomy, systemic lysis or coronary angioplasty have to be considered. First line intervention consists of optimizing preload by fluid resuscitation as appropriate and use of dopamine (4-12 micrograms/kg.min) as primary catecholamine to increase contractility and blood pressure. In acute left heart failure inotropic support with dobutamine (4-12 micrograms/kg.min) or epinephrine (0.05-1 microgram/kg.min) may be necessary, frequently combined with a vasodilator (sodium nitroprusside 0.2-5 micrograms/kg.min or nitroglycerine 0.5-2.5 micrograms/kg.min) or phosphodiesterase-III-inhibitor (milrinone 0.3-0.8 microgram/kg.min). In right heart failure norepinephrine is preferred to increase coronary perfusion pressure. Hyperdynamic septic shock with decreased vascular resistance is treated with norepinephrine to restore mean arterial pressure and to improve right ventricular dysfunction induced by pulmonary hypertension.

Cardiac Output, Low↗
PubMed1999

[Development of a new closed-loop system for controlling mivacurium-induced neuromuscular blockade].

UNLABELLED: There are many closed-loop control systems for muscle relaxants reported, but only a few could cope with the introduction of the latest shorter acting neuromuscular blocking drugs. These new muscle relaxants such as mivacurium require a fast adapting closed-loop system for controlling an adequate infusion. METHODS: After approval of the local ethics committee and having the patients' informed consent a total number of 75 patients [ASA I and II] were included in the study and assigned either to a training-, prediction-, prediction-/feedback- or a validation phase, as needed. Anaesthesia was induced and maintained with propofol in a TCI-mode with a plasma level of 3 to 5 micrograms/ml and 0.1 mg fentanyl boli as needed in all patients. In the last validation phase, having 20 patients, the prediction error and the error of the whole system was taken and analysed. RESULTS: A closed-loop system using a neural network as a predictor could be established. In the final validation phase consisting of 20 patients the mean square prediction error was found to be 0.1% +/- 0.2% [mean +/- SD]. The mean square error of the whole system was 0.55% +/- 0.59% [mean +/- SD]. CONCLUSIONS: A closed-loop system for control of a mivacurium infusion could be established. The system proofed to be reliable for a closed-loop infusion of mivacurium in order to maintain a predefined degree of neuromuscular blockade of 95% during routine surgery. The performance of the described controller is comparable to all recent attempts and could therefore be useful for scientific studies. It should be further validated and established for other muscle relaxants, as well.

Adolescent↗
PubMed1999

Perioperative transcutaneous pacemaker in patients with chronic bifascicular block or left bundle branch block and additional first-degree atrioventricular block.

BACKGROUND: Complete heart block is dreaded perioperatively in patients with chronic bifascicular or left bundle branch block (LBBB) and additional first-degree A-V block. Our aim was to investigate the necessity as well as the efficacy and safety of transcutaneous pacing in the perioperative setting. METHODS: Thirty-nine consecutive patients with asymptomatic chronic bifascicular block or LBBB and prolongation of the P-R interval scheduled to undergo surgery under anesthesia were prospectively enrolled in the study. Preoperatively, a transcutaneous pacemaker (PACE 500 D, Osypka Co.) was applied; its efficacy was checked with intra-arterial blood pressure measurement; the pain level was recorded. Additionally, 24-h Holter monitoring (CM2, CM5) was applied. Occurrences of a block progression or a bradycardia of <40 beats/min with hemodynamic impairment were the defined end points. RESULTS: Thirty-seven of the 39 patients (95%) could be successfully stimulated with a median current strength of 70 mA; whereby 33 of the 39 patients felt moderate to severe pain. There was no perioperative block progression. Three cases of brady-cardia of <40 beats/min with a critical drop in blood pressure occurred; but these patients were successfully treated with drug therapy without pacemaker stimulation. CONCLUSION: The perioperative application and testing of the pacemaker was safe and could be performed in nearly all patients successfully. However, we do not consider a routine prophylactic transcutaneous placement in patients with chronic bifascicular or LBBB and additional first-degree A-V block justified. Nevertheless, appropriate drugs and temporary pacemaker equipment should be easily accessible.

Aged↗
PubMed1998

Perioperative risk of bradyarrhythmias in patients with asymptomatic chronic bifascicular block or left bundle branch block: does an additional first-degree atrioventricular block make any difference?

BACKGROUND: The incidence of perioperative bradyarrhythmias in patients with bifascicular or left bundle branch block (LBBB) and the influence of an additional first-degree atrioventricular (A-V) block has not been evaluated with 24-h Holter electrocardiographic monitoring. Therefore the authors assessed the rate of block progression and bradyarrhythmia in these patients. METHODS: Patients (n = 106) with asymptomatic bifascicular block or LBBB with or without an additional first-degree A-V block scheduled for surgery under general or regional anesthesia were enrolled prospectively. Three patients were excluded. Of the 103 remaining, 56 had a normal P-R interval and 47 had a prolonged one. Holter monitoring (CM2, CM5) was applied to each patient just before induction of anesthesia and was performed for 24 h. The primary endpoint of the study was the occurrence of block progression. As secondary endpoints, bradycardias < 40 beats/min with hemodynamic compromise (systolic blood pressure < 90 mmHg) or asystoles > 5 s were defined. RESULTS: Block progression to second-degree A-V block and consecutive cardiac arrest occurred in one case of LBBB without a prolonged P-R interval Severe bradyarrhythmias with hypotension developed in another eight patients: asystoles > 5 s occurred in two cases and six patients had bradycardias < 40/min. Pharmacotherapy was successful in these eight patients. There was no significant difference for severe bradyarrhythmias associated with hemodynamic compromise between patients with and without P-R prolongation (P = 1.00). CONCLUSIONS: In patients with chronic bifascicular block or LBBB, perioperative progression to complete heart block is rare. However, the rate of bradyarrhythmias with hemodynamic compromise proved to be relevant. Because an additional first-degree A-V block did not increase the incidence of severe bradyarrhythmias and pharmacotherapy by itself was successful in nearly all cases, routine prophylactic insertion of a temporary pacemaker in such patients should be questioned.

Adult↗
PubMed1998

Usefulness of chromogranin A as a marker for detection of relapses of carcinoid tumours.

It is well known that peptide-producing endocrine tumours cosecrete immunoreactive chromogranin A with their characteristic hormones. Into this study 187 patients with the diagnosis malignant carcinoids or other malignancies were entered. Using chromogranin A at a cut-off level of 30.3 U/ml it was possible to discriminate between patients in remission and patients suffering a relapse with a sensitivity of 91.7% and a specificity of 96.4%, which may be of important diagnostic value. In our study that lasted over one year we could clearly show that the measurement of chromogranin A is impressively superior to 5-hydroxyindoleacetic-acid for detecting a relapse of carcinoids.

Biomarkers, Tumor↗
PubMed1998

[Medical controlling as a means for economic optimization of an anesthesiology clinic].

In these times of declining government financial resources, public interest is focussing increasingly on the health service. The Health Care Reforms of 1993 and 1996 fundamentally changed its financial basis. Hospitals now have to hold their own both medically and more and more economically. In this report, the principles of medical controlling are described and its effects on the clinical routine of a university anaesthesia department. Strict controlling reduces not only the costs of individual fields, but also those of whole departments through coordinated ordering. It can also bring to light organizational and training deficits. It is of particular importance for optimizing an anaesthesia department to digest and comply with figures presented by administrative departments. It only makes sense to do this at a departmental level.

Anesthesia Department, Hospital↗
PubMed1997

The cyclin-dependent kinase inhibitor p21cip1 mediates the growth inhibitory effect of phorbol esters in human venous endothelial cells.

Long-term application of the phorbol ester phorbol 12,13-dibutyrate (PDBu) inhibits the proliferation of human venous endothelial cells. The cyclin-dependent kinase inhibitor p21cip1 is a potential candidate mediating the PDBu-induced delayed entry of the cells into S-phase (by approximately 10 h when compared with cells stimulated with basic fibroblast growth factor (bFGF)). Levels of p21cip1 (protein and mRNA) rapidly rise (within approximately 2 h) in endothelial cells treated with the active isomer beta-PDBu, but not with alpha-PDBu; this effect is blocked by the mitogen-activated protein kinase kinase-1 (Mek1) inhibitor PD098059 and by the protein kinase C (PKC) antagonists GF109203X and rottlerin (selective for PKC-delta), but not Gö 6976 (selective for Ca2+-dependent PKC isoforms). Rapamycin blocks the PDBu-induced accumulation of p21cip1 (but not of the cognate mRNA), indicating an action of PKC on p21(cip1) mRNA translation. If endothelial cells are recruited into the cell cycle by bFGF, p21cip1 mRNA and protein levels rise initially (within 2 h) and decline subsequently such that p21cip1 drops to a minimum prior to the initiation of DNA synthesis (i.e. after approximately 12 h). In bFGF-stimulated cells, changes in p21cip1 mRNA and protein are strictly linked. In contrast, the levels of p21cip1 mRNA decline substantially (>10 h) before the protein decreases in PDBu-stimulated cells. Thus, PKC (presumably PKC-delta) regulates the amounts of p21cip1 in endothelial cells at the level of mRNA accumulation and translation, leading to a rapid and robust induction; following persistent PKC activation, p21(cip1) remains elevated despite reduced mRNA levels, indicating an enhanced stability of the protein. The bFGF-mediated increase in p21cip1 is blocked by the Mek1 inhibitor, but not by GF109203X; hence, in endothelial cells, induction of p21cip1 by PKC- and growth factor-dependent signaling is achieved by distinct pathways that converge and require activation of the mitogen-activated protein kinase cascade. The beta-PDBu-induced delayed S-phase entry and drop in p21cip1 are reversed if GF109203X is added 4 h after beta-PDBu to prevent persistent PKC activation. These observations indicate a cause and effect relation between sustained p21cip1 elevations and the delay in S-phase entry induced by beta-PDBu.

Cell Division↗
PubMed1997

Stimulation of the mitogen-activated protein kinase via the A2A-adenosine receptor in primary human endothelial cells.

Adenosine exerts a mitogenic effect on human endothelial cells via stimulation of the A2A-adenosine receptor. This effect can also be elicited by the beta2-adrenergic receptor but is not mimicked by elevation of intracellular cAMP levels. In the present work, we report that stimulation of the A2A-adenosine receptor and of the beta2-adrenergic receptor activates mitogen-activated protein kinase (MAP kinase) in human endothelial cells based on the following criteria: adenosine analogues and beta-adrenergic agonists cause an (i) increase in tyrosine phosphorylation of the p42 isoform and to a lesser extent of the p44 isoform of MAP kinase and (ii) stimulate the phosphorylation of myelin basic protein by MAP kinase; (iii) this is accompanied by a redistribution of the enzyme to the perinuclear region. Pretreatment of the cells with cholera toxin (to down-regulate Gsalpha) abolishes activation of MAP kinase by isoproterenol but not that induced by adenosine analogues. In addition, MAP kinase stimulation via the A2A-adenosine receptor is neither impaired following pretreatment of the cells with pertussis toxin (to block Gi-dependent pathways) nor affected by GF109203X (1 microM; to inhibit typical protein kinase C isoforms) nor by a monoclonal antibody, which blocks epidermal growth factor-dependent signaling. In contrast, MAP kinase activation is blocked by PD 098059, an inhibitor of MAP kinase kinase 1 (MEK1) activation, which also blunts the A2A-adenosine receptor-mediated increase in [3H]thymidine incorporation. Activation of the A2A-adenosine receptor is associated with increased levels of GTP-bound p21(ras). Thus, our experiments define stimulation of MAP kinase as the candidate cellular target mediating the mitogenic action of the A2A-adenosine receptor on primary human endothelial cells; the signaling pathway operates via p21(ras) and MEK1 but is independent of Gi, Gs, and the typical protein kinase C isoforms. This implies an additional G protein which links this prototypical Gs-coupled receptor to the MAP kinase cascade.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1997

Effects of exercise on circulating vascular adhesion molecules in healthy men.

Based on previous studies showing an increase in circulating soluble intercellular adhesion molecule-1 (sICAM-1) after exercise, we hypothesized that exercise may also increase serum levels of the vascular cell adhesion molecule-1 (sVCAM-1) and sE-selection. In a prospective controlled clinical trial, serum levels of sE-selectin, sICAM-1 and sVAM-1 were measured before and after two different exercise protocols in healthy untrained men. Lactate levels increased up to 12.7 mmol/L (95% confidence interval: 10.1-15.9) and 3.6 mmol/L (CI: 2.4-4.7) after ergometry and after an one hour endurance exercise at 60% of the maximal work intensity, respectively (p = 0.028 vs baseline and controls). The maximal increase in lymphocyte counts of 106% (CI: 63-146), which was only of short duration, was higher immediately after ergometry as compared to that observed after endurance exercise (p = 0.028). However, the maximal increase in neutrophil counts of 178% (CI: 120-298) which was seen at 2 hours after endurance exercise was higher than that seen after ergometry (p = 0.028). In contrast, only small changes of circulating adhesion molecules were seen immediately after ergometry: sICAM-1 increased by 11% (CI: 4-25; p = 0.028), and similar tendencies were also observed for sVCAM-1 and sE-selectin. No other consistent and time-dependent changes of circulating adhesion molecules were observed and all differences and changes were < or = 11%. In sum our study provides evidence that recreational sporting activities in untrained healthy subjects at normal altitude have little influence on serum levels of the circulating vascular adhesion molecules sE-selectin, sVCAM-1 or sICAM-1.

Adult↗
PubMed1997

Characterization of angiotensin-II effects on cerebral and ocular circulation by noninvasive methods.

AIMS: The role of the renin-angiotensin-system (RAS) in the cerebral and ocular circulation is still a matter of controversy. In vitro and animal data lead to partially contradicting results. However, direct investigation of locally generated angiotensin II (Ang II) in humans is not possible in vivo. Hence, we hypothesised that it might be possible to characterize local effects of Ang II by comparing systemic and local haemodynamic parameters during exogenous Ang II infusion. METHODS: In a placebo-controlled, double-blind, two-way cross over study blood flow velocities in the middle cerebral and the ophthalmic artery and ocular fundus pulsations were measured during stepwise increasing doses of Ang II in 10 healthy subjects. Blood flow velocities were assessed by Doppler sonography, fundus pulsation amplitudes (FPA), which estimate local pulsatile ocular blood flow were measured by laser interferometry. Additionally, systemic blood pressure and pulse rate were measured. RESULTS: Ang II dose-dependently decreased resistive index (RI) and increased mean flow velocities (MFV) in both arteries. Fundus pulsation amplitude was dose-dependently decreased by Ang II, whereas mean arterial pressure (MAP) was significantly increased. Pulse pressure amplitude (PPA) was not affected by Ang II administration. There was a high degree of correlation between changes in RIs and the analogously calculated PPA/systolic blood pressure during Ang II infusion, which indicates that the changes in RI after Ang II administration can be attributed to changes in systemic haemodynamics. Calculation of total local ocular blood flow from fundus pulsation amplitudes and changes in flow pulsatility in the ophthalmic artery further argue against significant blood flow changes after Ang II administration. CONCLUSIONS: Interpretation of data from Doppler sonography and laser interferometry must be done very carefully when concomitant changes in systemic haemodynamics occur. RI cannot necessarily be taken as an index of distal vascular resistance in these cases and changes in MFV can be caused by changes in vessel diameter or in blood flow. Moreover, FPA cannot be taken as a measure of ocular blood flow if no additional data on flow pulsatility are available. The combination of our systemic and local haemodynamic data indicates that cerebral and ocular circulation are comparably insensitive to changes in local Ang II concentrations. Fundus pulsation and blood flow velocity measurements indicate that neither choroidal nor optic nerve head blood flow are significantly affected by administration of Ang II.

Adult↗
PubMed1997

Shed mediastinal blood in 500 elective cardiac surgery patients: is there enough for retransfusion routinely?

OBJECTIVE: Since an increased use of several blood salvaging measures has contributed to a reduction in perioperative blood loss and the requirement for banked blood in recent years, the aim of this study was to establish current postoperative drainage losses in order to evaluate whether homologous retransfusion may be a useful measure to reduce autologous transfusion in elective cardiac surgery. DESIGN/SETTING: This prospective clinical investigation was performed at a University Intensive Care Unit during the first six hours following cardiac surgery. PATIENTS: 373 men and 127 women undergoing elective cardiac surgery were investigated. MEASURES: The amount of shed blood was measured four and six hours postoperatively. RESULTS: The average blood loss was higher in men than in women both in all operations as a whole (men, four hours: 223+/-73 ml, six hours 270+/-95 ml; women, four hours: 156+/-25 ml, six hours 195+/-22 ml), in valve replacement (men, four hours: 299+/-87 ml, six hours 350+/-101 ml; women, four hours: 187+/-30 ml, six hours: 219+/-31 ml) and in coronary artery bypass grafting (men, four hours: 197+/-69 ml, six hours: 242+/-83 ml; women, four hours: 128+/-15 ml, six hours: 173+/-18 ml). A blood loss of 400 ml was exceeded in 13% of men after valve replacement four and six hours postoperatively. In all other groups, less than 8% of patients had a loss of more than 400 ml both after four and after six hours. CONCLUSIONS: Postoperative drainage losses in elective cardiac surgery patients are small and a measurable advantage from retransfusion seems to be unlikely. We therefore endorse the routine use of shed mediastinal blood retransfusion in these patients.

Blood Loss, Surgical↗