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Extracorporeal support systems for the heart and lungs are employed for cardiac, pulmonary and also cardiopulmonary failure; however, neither the pure lung support by venovenous extracorporeal membrane oxygenation (vvECMO) nor the venoarterial (va) ECMO behave in a hemodynamically inert manner with respect to the patient's own cardiovascular system. The success of ECMO treatment is decisively dependent on monitoring before and during the execution and the pathophysiological understanding of the hemodynamic changes that occur during treatment. This article explicitly elucidates these "concomitant phenomena" and discusses fundamental aspects of cardiovascular physiology and the specific interplay with ECMO treatment.Extrakorporale Unterstützungssysteme von Herz und Lunge werden bei kardialem, pulmonalem oder auch kardiopulmonalem Versagen eingesetzt. Jedoch verhält sich weder die rein lungenunterstützende venovenöse extrakorporale Membranoxygenierung (vv-ECMO) noch die venoarterielle (va‑)ECMO hämodynamisch „inert“ gegenüber dem patienteneigenen Herz-Kreislauf-System. Der Erfolg einer ECMO-Therapie hängt entscheidend vom Monitoring vor und während der Durchführung sowie dem pathophysiologischen Verständnis für die hämodynamischen Veränderungen, die während der Therapie auftreten, ab. Der vorliegende Beitrag erläutert gezielt diese „Begleiterscheinungen“ und diskutiert fundamentale Aspekte der Herz-Kreislauf-Physiologie und ihr spezifisches Zusammenspiel mit einer ECMO-Therapie.

To date no biomarker has been identified bringing together perfect sensitivity and specificity to discriminate between inflammation and infections. Since the 1930s new markers of tissue damage and endothelial damage have been identified but which are incapable of identifying infections in every clinical setting to enable initiation of early antibiotic treatment. In this review the most important classical biomarkers and upcoming new PCR-based approaches are addressed. These markers are highlighted with respect to special clinical settings and to control the success of antibiotic treatment. The issue of discrimination between inflammation and infection is not yet solved. Based on one single biomarker it is impossible to decide whether infection is the reason for the patient's worsening condition but the combination of biomarkers or the integration of new biomarkers may be a meaningful supplement. The measurement of different biomarkers of infection or inflammation is part of the routine in critical care and will be essential in the future.Die Identifikation eines Biomarkers, der idealerweise eine perfekte Sensitivität und Spezifität mitbringt, um eine Inflammation von einer Infektion zu unterscheiden, ist bis heute nicht gelungen. Seit mehr als 80 Jahren werden immer neue Marker der Gewebs- und Endothelschädigung identifiziert, die jedoch nicht in jeder klinischen Situation eine Infektion sicher identifizieren können und damit eine frühe Initiierung einer Antibiotikatherapie ermöglichen. In dieser Übersicht werden die wichtigsten, etablierten „klassischen“ Biomarker ebenso wie neue, molekularbiologische Ansätze angesprochen und im Hinblick auf spezielle klinische Situationen und die Steuerung einer Antibiotikatherapie beleuchtet. Das Problem der Differenzierung zwischen Infektion und Inflammation ist bis heute nicht gelöst. Anhand eines singulären Biomarkers ist die Entscheidung unsicher zu treffen, ob eine Infektion ursächlich für eine sich aggravierende Situation ist, aber unter bestimmten klinischen Bedingungen kann die Kombination von Biomarkern oder die Einbindung neuer Biomarker eine sinnvolle Ergänzung darstellen. Die Bestimmung verschiedener Biomarker einer Infektion oder Inflammation ist Teil der intensivmedizinischen Routine und wird auch in Zukunft unverzichtbar sein.

Improvement in the quality of life (QoL) is a major goal of therapy for heart failure (HF) patients. Physical well-being as an important component of QoL has not yet been sufficiently covered by disease-specific assessment instruments. The aim of the study was to validate the questionnaire for assessing subjective physical well-being (FEW16) in HF patients with preserved ejection fraction (HFpEF) from the exercise training in diastolic heart failure (Ex-DHFaEuroP) trial. A total of 64 HFpEF patients (65 years, 56 % female) were randomized to usual routine treatment with (n = 44) or without training (n = 20). At baseline and 3 months, patients were clinically evaluated and assessed using appropriate questionnaires on the QoL (SF36), physical well-being (FEW16) and depression (PHQ-D). The FEW16 showed good values for Cronbachs' alpha coefficients (0.85-0.93). The cross-validity with SF36 and PHQ-D was highly significant but more so for psychological aspects. At baseline, the FEW16 score correlated with age, the subscale resilience with age and the 6 min walking distance test. At follow-up, the total and resilience scores had improved in the training group. In contrast to the SF36, the FEW16 did not detect differences between the groups in Ex-DHFaEuroP. The FEW16 questionnaire showed good internal consistency and correlation with SF36, its total score and resilience had improved after training; however, it did not reflect different changes between the study groups. The FEW16 is therefore more suited to assess general/mental well-being than the subjective physical well-being.

Das Jahr 2000 wird oft als Meilenstein der Entwicklung der Humangenetik bezeichnet. Eine Relevanz für die praktische Medizin erlangt das Humangenom-Projekt jedoch erst, wenn die Funktion der einzelnen Gene in komplexen physiologischen Systemen und die genetische Variabilität aufgeklärt sind. Die hier vorgelegten Studien beruhen auf der Annahme, dass der Einfluss genetischer Variabilität nicht nur im Vergleich kranker und gesunder Menschen sichtbar wird, sondern auch in der Variabilität physiologischer Parameter in der Allgemeinbevölkerung nachweisbar ist. Grundlage aller Studien war eine medizinische Untersuchung von gesunden eineiigen und zweieiigen Zwillingspaaren. Es wurde für Kennwerte des Herz-Kreislauf-Systems die Stärke genetischer Einflüsse (Heritabilität) bestimmt. Weiterhin erfolgten Kopplungs- und Assoziationsanalysen mit ausgewählten Kandidatengenen. Der Einfluss spezifischer Gene auf die Blutdruckregulation, die Herzgröße, EKG-Parameter sowie Blutfette konnte nachgewiesen werden. Weiterhin wurde der prinzipielle Nachweis erbracht, dass die funktionelle Untersuchung einzelner Gene in unausgelesenen Stichproben realisierbar ist., The year 2000 is often called a milestone in the history of human genetics. The knowledge of the sequence of the human genome will only become relevant for clinical medicine when the function of genes within complex physiological systems as well as the genetic variability will be revealed. The studies reported here are based on the assumption that the influence of genetic variability does not only become obvious by comparison of affected and unaffected subjects but is as well detectable in the variability of physiological parameters in the general population. All studies are based on testing healthy mono- and dizygotic twins. We determined the heritability of various cardiovascular parameters. Furthermore selected candidate genes were tested by linkage and association analyses. We could demonstrate the influence of specific genes on blood pressure regulation, heart size, ECG and lipids. These studies are a proof of principle for the functional analysis of single genes in unselected random samples.

Pregnant patients with increases in blood pressure are often treated with medication, in our view inappropriately. We examined 222 pregnant women who were referred because of two blood pressure determinations140/90 mm Hg. The women were primarily treated by nonpharmacological means. Only 44 required medications to maintain a blood pressure140/90 mm Hg. Twenty-six additional pregnant women referred for hypertension were taught to measure their blood pressures at home. Fourteen underwent 24-h ambulatory blood pressure monitoring. Home and 24-h blood pressure measurements were both significantly lower than those obtained in the office and did not significantly differ from each other. We conclude that most pregnant women without proteinuria, who show mild to moderate blood pressures140/90 mm Hg are best treated conservatively without drugs. Those in whom home or 24-h blood pressures exceed 140/90 mm Hg and who do not respond to nonpharmacologic methods require medication. Finally, "white coat" hypertension is common in pregnant women.

15 patients with a severe degree of essential hypertension, which had not responded satisfactorily to pharmacological management, received an additional regimen of psychophysiological treatment. This schedule consisted of relaxation training, self-recording of the blood pressure by the patients and conversations geared at improving stress management. After 1 year 9 patients showed a lowered mean blood pressure from 162/106 mmHg to 141/95 mmHg (responders). 2 patients were excluded from the study and 4 patients failed to show any lowering of their blood pressure (non-responders). In 6 responders it was possible to reduce the dose of antihypertensive drugs by 8-71%. These results were confirmed over a 4-year follow-up period. Responders and non-responders did not differ with regard to their age, stages and duration of hypertension. Patients with a very high reactivity of blood pressure under psychological stress and a low frankness with regard to their own weaknesses and problems seem to respond to the therapy with a lower probability of success.