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Walter R Hasibeder

Publications and source records attributed to Walter R Hasibeder.

At least 19 recordsLinked to original sources
PubMed2006

Copeptin and arginine vasopressin concentrations in critically ill patients.

CONTEXT: Determination of arginine vasopressin (AVP) concentrations may be helpful to guide therapy in critically ill patients. A new assay analyzing copeptin, a stable peptide derived from the AVP precursor, has been introduced. OBJECTIVE: Our objective was to determine plasma copeptin concentrations. DESIGN: We conducted a post hoc analysis of plasma samples and data from a prospective study. SETTING: The setting was a 12-bed general and surgical intensive care unit (ICU) in a tertiary university teaching hospital. PATIENTS: Our subjects were 70 healthy volunteers and 157 ICU patients with sepsis, with systemic inflammatory response syndrome (SIRS), and after cardiac surgery. INTERVENTIONS: There were no interventions. MAIN OUTCOME MEASURES: Copeptin plasma concentrations, demographic data, AVP plasma concentrations, and a multiple organ dysfunction syndrome score were documented 24 h after ICU admission. RESULTS: AVP (P < 0.001) and copeptin (P < 0.001) concentrations were significantly higher in ICU patients than in controls. Patients after cardiac surgery had higher AVP (P = 0.003) and copeptin (P = 0.003) concentrations than patients with sepsis or SIRS. Independent of critical illness, copeptin and AVP correlated highly significantly with each other. Critically ill patients with sepsis and SIRS exhibited a significantly higher ratio of copeptin/AVP plasma concentrations than patients after cardiac surgery (P = 0.012). The American Society of Anesthesiologists' classification (P = 0.046) and C-reactive protein concentrations (P = 0.006) were significantly correlated with the copeptin/AVP ratio. CONCLUSIONS: Plasma concentrations of copeptin and AVP in healthy volunteers and critically ill patients correlate significantly with each other. The ratio of copeptin/AVP plasma concentrations is increased in patients with sepsis and SIRS, suggesting that copeptin may overestimate AVP plasma concentrations in these patients.

Adult↗
PubMed2006

Arteriolar vasoconstrictive response: comparing the effects of arginine vasopressin and norepinephrine.

INTRODUCTION: This study was designed to examine differences in the arteriolar vasoconstrictive response between arginine vasopressin (AVP) and norepinephrine (NE) on the microcirculatory level in the hamster window chamber model in unanesthetized, normotonic hamsters using intravital microscopy. It is known from patients with advanced vasodilatory shock that AVP exerts strong additional vasoconstriction when incremental dosage increases of NE have no further effect on mean arterial blood pressure (MAP). METHODS: In a prospective controlled experimental study, eleven awake, male golden Syrian hamsters were instrumented with a viewing window inserted into the dorsal skinfold. NE (2 microg/kg/minute) and AVP (0.0001 IU/kg/minute, equivalent to 4 IU/h in a 70 kg patient) were continuously infused to achieve a similar increase in MAP. According to their position within the arteriolar network, arterioles were grouped into five types: A0 (branch off small artery) to A4 (branch off A3 arteriole). RESULTS: Reduction of arteriolar diameter (NE, -31 +/- 12% versus AVP, -49 +/- 7%; p = 0.002), cross sectional area (NE, -49 +/- 17% versus AVP, -73 +/- 7%; p = 0.002), and arteriolar blood flow (NE, -62 +/- 13% versus AVP, -80 +/- 6%; p = 0.004) in A0 arterioles was significantly more pronounced in AVP animals. There was no difference in red blood cell velocities in A0 arterioles between groups. The reduction of diameter, cross sectional area, red blood cell velocity, and arteriolar blood flow in A1 to A4 arterioles was comparable in AVP and NE animals. CONCLUSION: Within the microvascular network, AVP exerted significantly stronger vasoconstriction on large A0 arterioles than NE under physiological conditions. This observation may partly explain why AVP is such a potent vasopressor hormone and can increase systemic vascular resistance even in advanced vasodilatory shock unresponsive to increases in standard catecholamine therapy.

Animals↗
PubMed2006

[Arginine-vasopressin in septic and vasodilatorial shock].

Current therapy of septic/vasodilatory cardiovascular failure includes volume resuscitation and infusion of inotropic and vasopressor agents. Norepinephrine is the first-line vasoconstrictor, and can stabilize hemodynamic variables in most patients. Nonetheless, irreversible cardiovascular failure which is resistant to conventional hemodynamic therapies still is the main cause of death in patients with severe sepsis and septic shock. In such advanced, catecholamine-resistant shock states, arginine-vasopressin (AVP) has repeatedly caused an increase in mean arterial blood pressure, a decrease in toxic norepinephrine-dosages, as well as further beneficial hemodynamic, endocrinologic and renal effects. Although AVP exerted negative inotropic effects in previous clinical trials and in selected animal experiments, a continuous low-dose AVP infusion during advanced septic/vasodilatory shock caused a decrease in cardiac index only in patients with a hyperdynamic circulation. Adverse effects on gastrointestinal circulation and the systemic microcirculation can not be excluded, but have not yet been confirmed in clinical prospective trials. Negative side effects of a supplementary AVP therapy are an increase in total bilirubin concentrations, and a decrease in platelet count. A transient increase in hepatic transaminases during AVP infusion is most likely related to preceding hypotensive episodes. Important points which must be considered when using AVP as a "rescue vasopressor" in septic/vasodilatory shock states are: 1) AVP infusion only in advanced shock states that can not be adequately reversed by conventional hemodynamic therapy (e.g. norepinephrine >0,5-0,6 mug/kg/min), 2) presence of normovolemia, 3) AVP infusion only in combination with norepinephrine, 4) strict avoidance of bolus injections and dosages >4 IU/h. Effects of a supplementary AVP infusion in advanced vasodilatory shock on survival are currently examined in a large, prospective multicenter trial in North America and Australia.

Arginine Vasopressin↗
PubMed2006

Cutaneous vascular reactivity and flow motion response to vasopressin in advanced vasodilatory shock and severe postoperative multiple organ dysfunction syndrome.

INTRODUCTION: Disturbances in microcirculatory homeostasis have been hypothesized to play a key role in the pathophysiology of multiple organ dysfunction syndrome and vasopressor-associated ischemic skin lesions. The effects of a supplementary arginine vasopressin (AVP) infusion on microcirculation in vasodilatory shock and postoperative multiple organ dysfunction syndrome are unknown. METHOD: Included in the study were 18 patients who had undergone cardiac or major surgery and had a mean arterial blood pressure below 65 mmHg, despite infusion of more than 0.5 microg/kg per min norepinephrine. Patients were randomly assigned to receive a combined infusion of AVP/norepinephrine or norepinephrine alone. Demographic and clinical data were recorded at study entry and after 1 hour. A laser Doppler flowmeter was used to measure the cutaneous microcirculatory response at randomization and after 1 hour. Reactive hyperaemia and oscillatory changes in the Doppler signal were measured during the 3 minutes before and after a 5-minute period of forearm ischaemia. RESULTS: Patients receiving AVP/norepinephrine had a significantly higher mean arterial pressure (P = 0.047) and higher milrinone requirements (P = 0.025) than did the patients who received norepinephrine only at baseline. Mean arterial blood pressure significantly increased (P < 0.001) and norepinephrine requirements significantly decreased (P < 0.001) in the AVP/norepinephrine group. Patients in the AVP/norepinephrine group exhibited a significantly higher oscillation frequency of the Doppler signal before ischaemia and during reperfusion at randomization. During the study period, there were no differences in either cutaneous reactive hyperaemia or the oscillatory pattern of vascular tone between groups. CONCLUSION: Supplementary AVP infusion in patients with advanced vasodilatory shock and severe postoperative multiple organ dysfunction syndrome did not compromise cutaneous reactive hyperaemia and flowmotion when compared with norepinephrine infusion alone.

Aged↗
PubMed2006

Causes of death and determinants of outcome in critically ill patients.

INTRODUCTION: Whereas most studies focus on laboratory and clinical research, little is known about the causes of death and risk factors for death in critically ill patients. METHODS: Three thousand seven hundred patients admitted to an adult intensive care unit (ICU) were prospectively evaluated. Study endpoints were to evaluate causes of death and risk factors for death in the ICU, in the hospital after discharge from ICU, and within one year after ICU admission. Causes of death in the ICU were defined according to standard ICU practice, whereas deaths in the hospital and at one year were defined and grouped according to the ICD-10 (International Statistical Classification of Diseases and Related Health Problems) score. Stepwise logistic regression analyses were separately calculated to identify independent risk factors for death during the given time periods. RESULTS: Acute, refractory multiple organ dysfunction syndrome was the most frequent cause of death in the ICU (47%), and central nervous system failure (relative risk [RR] 16.07, 95% confidence interval [CI] 8.3 to 31.4, p < 0.001) and cardiovascular failure (RR 11.83, 95% CI 5.2 to 27.1, p < 0.001) were the two most important risk factors for death in the ICU. Malignant tumour disease and exacerbation of chronic cardiovascular disease were the most frequent causes of death in the hospital (31.3% and 19.4%, respectively) and at one year (33.2% and 16.1%, respectively). CONCLUSION: In this primarily surgical critically ill patient population, acute or chronic multiple organ dysfunction syndrome prevailed over single-organ failure or unexpected cardiac arrest as a cause of death in the ICU. Malignant tumour disease and chronic cardiovascular disease were the most important causes of death after ICU discharge.

Adult↗
PubMed2006

Vasopressin in vasodilatory shock: ensure organ blood flow, but take care of the heart!

Supplementary arginine vasopressin infusion in advanced vasodilatory shock may be accompanied by a decrease in cardiac index and systemic oxygen transport capacity in approximately 40% of patients. While a reduction of cardiac output most frequently occurs in patients with hyperdynamic circulation, it is less often observed in patients with low cardiac index. Infusion of inotropes, such as dobutamine, may be an effective strategy to restore systemic blood flow. However, when administering inotropic drugs, systemic blood flow should be increased to adequately meet systemic demands (assessed by central or mixed venous oxygen saturation) without putting an excessive beta-adrenergic stress on the heart. Overcorrection of cardiac index to hyperdynamic values with inotropes places myocardial oxygen supply at significant risk.

Adrenergic beta-Agonists↗
PubMed2006

Regional microvascular function and vascular reactivity in patients with different degrees of multiple organ dysfunction syndrome.

The pathophysiology of multiple organ dysfunction syndrome (MODS) is believed to be related to that of microcirculatory dysfunction. We hypothesized that the severity of MODS is determined by measuring regional variables of microvascular function and vascular reactivity in critically ill patients. Therefore, we compared (a) reactive hyperemia response in the forearm using transcutaneous Po2/Pco2 electrodes and laser Doppler velocimetry, (b) microvascular permeability assessed by strain-gauge plethysmography in legs, and (c) variables derived from gastric tonometry in hemodynamically stable patients with moderate (n = 15) and severe (n = 15) MODS. There were no differences in systemic oxygen delivery, consumption, and oxygen extraction ratio between the groups. Mortality was 20% in patients with moderate MODS and 60% in patients with severe MODS (P = 0.025). Patients with a high MODS score had significantly larger arterial lactate concentrations (3.81 +/- 2.7 mmol/L) than patients with moderate MODS (1.66 +/- 0.82 mmol/L; P = 0.006). No significant differences in gastric pHi, gastric regional-to-arterial Pco2 difference, capillary filtration coefficient, isovolumetric venous pressure, and skin reactive hyperemia response were observed between patients with moderate and severe MODS. Once MODS is established, regional variables of microvascular function and vascular reactivity measured in this study do not reflect severity of organ dysfunction.

Adult↗
PubMed2005

Arginine vasopressin does not alter mucosal tissue oxygen tension and oxygen supply in an acute endotoxemic pig model.

OBJECTIVE: To determine the effects of increasing dosages of continuously infused arginine-vasopressin (AVP) on mucosal tissue oxygen tension and oxygen supply in an auto-perfused, innervated jejunal segment in an acute endotoxic porcine model. DESIGN: Prospective, randomized, experimental study. SETTING: University hospital animal research laboratory. INTERVENTIONS: Jejunal mucosal tissue PO2 was measured employing two Clark-type surface oxygen electrodes. Oxygen saturation of jejunal microvascular hemoglobin was determined by tissue reflectance spectrophotometry. Systemic hemodynamic variables, mesenteric-venous and systemic acid base and blood gas variables and lactate measurements were recorded. Measurements were performed at baseline, after E. coli lipopolysaccharide (LPS) administration and at 20 min intervals during incremental AVP infusion (n=8; 0.014, 0.029, 0.057, 0.114 and 0.229 IU kg(-1) h(-1), respectively) or infusion of saline (n =8). MEASUREMENTS AND RESULTS: LPS infusion leads to a significant (P<0.05) decrease of mucosal tissue oxygen tension (PO2muc, 24+/-3 to 12+/-2 mmHg) and microvascular hemoglobin oxygen saturation (HbO2, 38+/-4 to 21+/-4%). Mesenteric venous lactate level increased (2.4+/-0.3 to 4.7+/-1.7 mmol l(-1)), while mesenteric venous pH decreased (7.38+/-0.02 to 7.26+/-0.12), indicating tissue hypoxia. AVP significantly increased mean arterial pressure (MAP, 81+/-15 to 97+/-17 at 0.057 IU kg(-1) h(-1)). No differences in jejunal mucosal oxygenation occurred between study groups at any dosage during the experimental protocol. CONCLUSION: AVP administration did not further compromise mucosal tissue oxygen tension and oxygen supply in the acute phase of endotoxic pigs.

Analysis of Variance↗
PubMed2005

Antifactor Xa activity in critically ill patients receiving antithrombotic prophylaxis with standard dosages of certoparin: a prospective, clinical study.

INTRODUCTION: Deep venous thrombosis with subsequent pulmonary embolism or post-thrombotic syndrome is a feared complication in the intensive care unit. Therefore, routine prophylactic anticoagulation is widely recommended. Aside from unfractionated heparin, low molecular weight heparins, such as certoparin, have become increasingly used for prophylactic anticoagulation in critically ill patients. In this prospective study, we evaluated the potency of 3,000 IU certoparin administered once daily to reach antithrombotic antifactor Xa (aFXa) levels of 0.1 to 0.3 IU/ml in 62 critically ill patients. METHODS: AFXa levels were determined 4, 12 and 24 h after injection of certoparin. Prothrombin time, activated partial thromboplastin time, antithrombin, fibrinogen, hemoglobin, platelet count, serum urea and creatinine concentrations were documented before and 12 and 24 h after injection of certoparin. RESULTS: Four hours after certoparin injection (n = 32), 28% of patients were within the antithrombotic aFXa range. After 12 and 24 h, 6% achieved antithrombotic aFXa levels. Because of a severe pulmonary embolism in one study patient, an interim analysis was performed, and the dosage of certoparin was increased to 3,000 IU twice daily. This regime attained recommended antithrombotic aFXa levels in 47%, 27%, 40% and 30% of patients at 4, 12, 16 and 24 h, respectively, after twice daily certoparin injection (n = 30). Antithrombin and fibrinogen concentrations slightly increased during the observation period. Low antithrombin concentrations before certoparin were independently correlated with underdosing of certoparin. Patients with aFXa levels <0.1 IU/ml 4 h after certoparin injection required vasopressors more often and had lower serum concentrations of creatinine and urea than patients with antithrombotic aFXa levels. CONCLUSION: Standard dosages of certoparin of 3,000 IU given once or twice daily are ineffective for attaining the recommended aFXa levels of 0.1 to 0.3 IU/ml in critically ill patients. Low antithrombin levels before certoparin administration were independently associated with low aFXa levels. Renal function and vasopressor therapy may further influence the effectiveness of certoparin in ensuring adequate antithrombotic prophylaxis.

Aged↗
PubMed2005

Central venous catheter colonization in critically ill patients: a prospective, randomized, controlled study comparing standard with two antiseptic-impregnated catheters.

In this prospective, randomized, controlled, unblinded study, we compared colonization rates of a standard, unimpregnated central venous catheter (CVC) with rates for silver-coated and chlorhexidine-silversulfadiazine (CH-SS)-impregnated CVC. Patient characteristics, CVC insertion site, indwelling time, and colonization detected by semiquantitative and quantitative microbiologic techniques were documented. Two-hundred-seventy-five critically ill patients were included into the study protocol. One-hundred-sixty standard, 160 silver (S)-coated, and 165 externally impregnated CH-SS CVC were inserted. There was a significant difference in CVC colonization rates among study groups (P = 0.029). There was no difference in the colonization rate and the colonization per 1000 catheter days between standard and S-coated (P = 0.564; P = 0.24) or CH-SS-coated CVC (P= 0.795; P = 0.639). When comparing antiseptic CVC with each other, colonization rates were significantly less with CH-SS-impregnated than with S-coated CVC (16.9% versus 7.3%; P = 0.01; 18.2 versus 7.5 of 1000 catheter days; P = 0.003; relative risk, 0.43; 95% confidence interval, 0.21-0.85). Whereas standard and S-coated CVC were first colonized 2 and 3 days after insertion, respectively, CH-SS CVC were first colonized only after 7 days. In conclusion, antiseptic-impregnated CVC could not prevent catheter colonization when compared with standard polyurethane catheters in a critical care setting with infrequent catheter colonization rates and CVC left in place for >10 days.

Adult↗
PubMed2004

Dear vasopressin, where is your place in septic shock?

Cardiovascular failure is one of the central therapeutic problems in patients with severe infection. Although norepinephrine is a potent and, in most cases, highly effective vasopressor agent, very high dosages leading to significant side effects can be necessary to stabilize advanced shock. As a supplementary vasopressor, arginine vasopressin can reverse hemodynamic failure and significantly decrease norepinephrine dosages. Whether the promising possibility of 'bridging' advanced septic shock when the benefit/risk ratio of catecholamine therapy leaves a clinically tolerable range may improve quantitative and qualitative patient outcome can only be determined by a large, prospective, randomized study.

Arginine Vasopressin↗
PubMed2004

High-dosage continuous amiodarone therapy to treat new-onset supraventricular tachyarrhythmias in surgical intensive care patients: an observational study.

BACKGROUND: New-onset supraventricular tachyarrhythmias (SVTA) are a complication contributing significantly to morbidity and mortality in surgical intensive care unit (SICU) patients. Although only few data on efficiency can be found in the literature, class III antiarrhythmics have become popular in the treatment of SVTA in critically ill patients. SETTING: 12-bed general and surgical ICU in a university teaching hospital. DESIGN: Observational, retrospective study. PATIENTS: 131 SICU patients with SVTA (narrow-complex non-sinus tachyarrhythmias with heart rates > or = 100 bpm). INTERVENTION: High-dosage amiodarone infusion according to an institutional protocol. MEASUREMENTS: Hemodynamic data, acid-base status, and single organ functions were obtained in all patients before amiodarone infusion and at 12, 24, and 48 hours afterwards. Patients were divided into responders and nonresponders. Amiodarone infusion (mean dosage 24 h: 1625+/-528 mg; 48 h: 2708+/-895 mg) restored sinus rhythm in 54% of study patients within 12 h, in 64% within 24 h, and in 75% within 48 h. Heart rate, central venous pressure, and milrinone requirements significantly decreased in all patients; this was accompanied by a significant increase in stroke-volume index and mean arterial pressure. Serum concentrations of creatinine and bilirubin increased in all patients. CONCLUSION: High-dosage continuous amiodarone infusion during a period of 48 hours resulted in restoration of SR in 75% of SICU patients with new-onset SVTA and moderate to severe multiple-organ dysfunction syndrome. A significant improvement in cardiocirculatory function was more pronounced in responders but could be demonstrated irrespective of restoration of sinus rhythm in all patients. Apart from a possibly amiodarone-mediated increase in concentrations of creatinine and bilirubin, no major drug-related adverse effects occurred during the observation period.

Acid-Base Equilibrium↗
PubMed2004

Endocrinologic response to vasopressin infusion in advanced vasodilatory shock.

OBJECTIVES: To evaluate the endocrinologic response to a combined arginine vasopressin and norepinephrine (AVP/NE) infusion in advanced vasodilatory shock, and to examine the relationship between baseline plasma AVP concentrations and the hemodynamic response to AVP. DESIGN: Preliminary, prospective, randomized, controlled clinical study. SETTING: Twenty-three-bed general and surgical intensive care unit. PATIENTS: Thirty-eight patients with advanced vasodilatory shock. Hemodynamic and laboratory data of 34 patients have already been presented in a recently published prospective, randomized, controlled study. INTERVENTIONS: Continuous AVP (4 units/hr) and NE infusion in study patients; NE infusion only in control patients. MEASUREMENTS AND MAIN RESULTS: At baseline, 24 hrs, and 48 hrs after randomization, plasma concentrations of AVP, adrenocorticotropic hormone, cortisol, renin, angiotensin II, aldosterone, prolactin, endothelin I, and atrial natriuretic factor were determined. Hemodynamic variables were recorded at baseline and 1, 12, and 24 hrs after randomization. Linear mixed effects models were used to test for differences between groups. The relationship between AVP plasma concentrations and hemodynamic response to AVP was analyzed using linear regression analyses. AVP/NE patients exhibited significantly higher AVP (p <.001) and prolactin (p <.001) plasma concentrations during the study period; there were no significant differences in plasma concentrations of other hormones. No significant correlation was detected between plasma AVP concentrations and the increase in mean arterial pressure after 1 hr (Pearson's correlation coefficient =.134, p =.584) and after 24 hrs (Pearson's correlation coefficient = -.198, p =.417). There were further no correlations between AVP plasma concentrations and the 24-hr response to AVP therapy in heart rate (Pearson's correlation coefficient = -.065, p =.791), stroke volume index (Pearson's correlation coefficient = -.106, p =.687), and NE requirements (Pearson's correlation coefficient =.04, p =.869). CONCLUSIONS: The preliminary results of this study indicate that a combined AVP and NE infusion increases prolactin plasma concentrations in advanced vasodilatory shock. Hemodynamic effects of AVP infusion are independent of baseline plasma AVP concentrations.

Adrenocorticotropic Hormone↗
PubMed2004

Postbypass arrhythmias: pathophysiology, prevention, and therapy.

PURPOSE OF REVIEW: To review the medical literature on new-onset arrhythmias after cardiac bypass surgery in adults, focusing on the most recent advances on this topic. RECENT FINDINGS: Main attention is focused on possible predictors and prevention of postoperative atrial fibrillation, because this arrhythmia is the most common type encountered with cardiac surgery and is associated with increased morbidity and mortality and longer, more expensive hospital stays. Therapeutic management of atrial fibrillation favors class III antiarrhythmic agents like amiodarone and sotalol. Direct-current cardioversion proved to be an ineffective method for treatment of supraventricular tachyarrhythmias. In patients with persistent atrioventricular block or sinus node dysfunction after cardiac valve surgery, a risk score to predict the need for permanent pacing after cardiac valve surgery was developed. This scoring system may be useful for pre- and perioperative management of patients undergoing cardiac valve surgery. SUMMARY: Recent studies demonstrate a continued effort to improve our knowledge about postbypass arrhythmias. New insights in the pathophysiology of postoperative cardiac arrhythmias and advances in prevention and therapy are rapid and results are heterogeneous, so it is difficult for the clinician to keep abreast with these new findings.

Arrhythmias, Cardiac↗
PubMed2004

Does arginine vasopressin influence the coagulation system in advanced vasodilatory shock with severe multiorgan dysfunction syndrome?

Arginine vasopressin (AVP) is a potent supplementary vasopressor in advanced vasodilatory shock, but decreases in platelet count have been reported during AVP therapy. In this study we evaluated the effects of AVP infusion on the coagulation system in advanced vasodilatory shock when compared to norepinephrine (NE) infusion alone. Forty-two patients with advanced vasodilatory shock (NE requirements >0.5 microg x kg(-1) x min(-1), mean arterial blood pressure <70 mm Hg) were prospectively randomized to receive an additional AVP infusion (4 U/h) or NE infusion alone. Most patients received coagulation active treatment (fresh-frozen plasma, thrombocyte concentrates, coagulation factors, and continuous veno-venous hemofiltration with heparin). At baseline and 1, 24, and 48 h after randomization, coagulation laboratory variables and a modified thrombelastography were measured. There were no differences between groups in plasmatic coagulation variables. Although there was no significant difference between groups, platelet count significantly decreased in AVP patients (P = 0.036). There were no differences in results of modified thrombelastography analyses between groups. AVP infusion in advanced vasodilatory shock with severe multiorgan dysfunction syndrome does not increase plasma concentrations of Factor VIII, von Willebrand Factor antigen, and ristocetin Co-Factor but may stimulate platelet aggregation and induce thrombocytopenia. Global coagulation, assessed by modified thrombelastography, is not different from patients receiving NE infusion alone.

Aged↗