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Biomedical subjects

W Hasibeder

Publications and source records attributed to W Hasibeder.

At least 19 recordsLinked to original sources
PubMed2006

Lowered microvascular vessel wall oxygen consumption augments tissue pO2 during PgE1-induced vasodilation.

Continuous infusion of intravenous prostaglandin E1 (PgE1, 2.5 mug/kg/min) was used to determine how vasodilation affects oxygen consumption of the microvascular wall and tissue pO(2) in the hamster window chamber model. While systemic measurements (mean arterial pressure and heart rate) and central blood gas measurements were not affected, PgE1 treatment caused arteriolar (64.6 +/- 25.1 microm) and venular diameter (71.9 +/- 29.5 microm) to rise to 1.15 +/- 0.21 and 1.06 +/- 0.19, respectively, relative to baseline. Arteriolar (3.2 x 10(-2) +/- 4.3 x 10(-2) nl/s) and venular flow (7.8 x 10(-3) +/- 1.1 x 10(-2)/s) increased to 1.65 +/- 0.93 and 1.32 +/- 0.72 relative to baseline. Interstitial tissue pO(2) was increased significantly from baseline (21 +/- 8 to 28 +/- 7 mmHg; P < 0.001). The arteriolar vessel wall gradient, a measure of oxygen consumption by the microvascular wall decreased from 20 +/- 6 to 16 +/- 3 mmHg (P < 0.001). The arteriolar vessel wall gradient, a measure of oxygen consumption by the vascular wall, decreased from 20 +/- 6 to 16 +/- 3 mmHg (P < 0.001). This reduction reflects a 20% decrease in oxygen consumption by the vessel wall and up to 50% when cylindrical geometry is considered. The venular vessel wall gradient decreased from 12 +/- 4 to 9 +/- 4 mmHg (P < 0.001). Thus PgE1-mediated vasodilation has a positive microvascular effect: enhancement of tissue perfusion by increasing flow and then augmentation of tissue oxygenation by reducing oxygen consumption by the microvascular wall.

Alprostadil↗
PubMed2004

Oxygen distribution in microcirculation after arginine vasopressin-induced arteriolar vasoconstriction.

The microvascular distribution of oxygen was studied in the arterioles and venules of the awake hamster window chamber preparation to determine the contribution of vascular smooth muscle contraction to oxygen consumption of the microvascular wall during arginine vasopressin (AVP)-induced vasoconstriction. AVP was infused intravenously at the clinical dosage (0.0001 IU.kg(-1).min(-1)) and caused a significant arteriolar constriction, decreased microvascular flow and functional capillary density, and a substantial rise in arteriolar vessel wall transmural Po(2) difference. AVP caused tissue Po(2) to be significantly lowered from 25.4 +/- 7.4 to 7.2 +/- 5.8 mmHg; however, total oxygen extraction by the microcirculation increased by 25%. The increased extraction, lowered tissue Po(2), and increased wall oxygen concentration gradient are compatible with the hypothesis that vasoconstriction significantly increases vessel wall oxygen consumption, which in this model appears to constitute an important oxygen-consuming compartment. This conclusion was supported by the finding that the small percentage of the vessels that dilated in these experiments had a vessel wall oxygen gradient that was smaller than control and which was not determined by changes in tissue Po(2). These findings show that AVP administration, which reduces oxygen supply by vasoconstriction, may further impair tissue oxygenation by the additional oxygen consumption of the microcirculation.

Animals↗
PubMed2003

[Near drowning: epidemiology--pathophysiology--therapy].

Near-drowning is a frequent preventable accident with a significant morbidity and mortality in a previous healthy population. In most patients the primary injury is pulmonary failure due to fluid aspiration, resulting in severe arterial hypoxemia and secondary damage to other organs. Immediate interruption of hypoxia is of utmost importance in the emergency situation. Accurate neurologic prognosis cannot be predicted from initial clinical presentation, laboratory, radiological or electrophysiological examinations. Prompt resuscitation and aggressive respiratory and cardiovascular treatment are crucial for optimal survival. This review provides the reader with detailed information on epidemiology, pathophysiology, emergency decision making and general treatment in near drowning accidents.

Cardiovascular Physiological Phenomena↗
PubMed2002

Antifactor Xa activity in intensive care patients receiving thromboembolic prophylaxis with standard doses of enoxaparin.

BACKGROUND: Low-molecular-weight heparins (LMWHs) have become increasingly used to prevent thromboembolic complications in intensive care patients. Unlike in medical and surgical patients, no data on the anticoagulant effectiveness of standard LMWH dosages exist in intensive care patients. Therefore, we prospectively investigated antifactor Xa (aFXa) levels after subcutaneous administration of 40 mg of enoxaparin in 89 intensive care patients over a 24-h period. METHODS: AFXa levels were measured before, 4, 12 and 24 h after subcutaneous administration of enoxaparin. Laboratory parameters including prothrombin time, activated partial thromboplastin time, antithrombin III, fibrinogen as well as platelet count were collected at same intervals. Demographics included age, sex, height, weight, body mass index, admission diagnosis, a thromboembolic risk score and a modified Goris multiple organ dysfunction score. RESULTS: At 4, 12 and 24 h, 56.5%, 39.3% and 12.6% of the study patients were within recommended antithrombotic aFXa levels (0.1-0.3 U ml(-1)). Presence of multiple organ dysfunction as well as high body weight were significantly correlated with low aFXa levels. CONCLUSION: European standard dosages of 40 mg of enoxaparin once daily proved to be ineffective in achieving recommended antithrombotic aFXa levels in intensive care patients. This was most pronounced in patients with high body weight and presence of multiple organ dysfunction.

Adult↗
PubMed2001

Necrotizing fasciitis with Clostridium perfringens after laparoscopic cholecystectomy.

Necrotizing fasciitis is a rapidly progressive infection of the fascia and subcutaneous tissues accompanied by a high mortality rate approaching 80% to 100%. Factors that predispose patients to this life-threatening complication include obesity, malnutrition, malignancy, chronic alcoholism, drug abuse, peripheral vascular disease, diabetes mellitus, and immunosuppressive therapy. The pathomechanisms for the development of this rare disease still remain unclear. We report a case of necrotizing fasciitis with Clostridium perfringens after laparoscopic cholecystectomy. The patient left the hospital 5 months after admission. Early recognition based on clinical signs (pain, asymmetric abdominal thickening, crepitus) and computed tomography scanning (gas dissection along fascial planes), in conjunction with prompt, aggressive surgical therapy and debridement of all devitalized tissue, high-dose antibiotic therapy, and therapy at the intensive care unit, appears to afford patients the best chance of survival.

Cholecystectomy, Laparoscopic↗
PubMed2001

Effects of norepinephrine and phenylephrine on intestinal oxygen supply and mucosal tissue oxygen tension.

OBJECTIVES: To investigate effects of intravenous norepinephrine (NE) and phenylephrine (PE) on intestinal oxygen supply in an autoperfused, innervated jejunal segment. DESIGN AND SETTING: Prospective, randomized animal study in an animal research laboratory. MATERIALS AND METHODS: In 24 anesthetized and normoventilated pigs a segment of the jejunal mucosa was exposed by midline laparotomy and antimesenteric incision. Mucosal oxygen tension (PO2muc; Clark-type surface oxygen electrodes), microvascular hemoglobin oxygen saturation (HbO2, tissue reflectance spectrophotometry), and microvascular blood flow (perfusion units, PU; laser Doppler velocimetry), systemic hemodynamics, mesenteric-venous acid base and blood gas variables, and systemic acid base and blood gas variables were recorded after a resting period and at 20-min intervals during infusion of NE (0.01, 0.05, 0.1, 0.5, 1, 2 micrograms x kg-1 x min-1; n = 8) or PE (0.1, 0.5, 1, 2, 5, 10 micrograms x kg-1 x min-1; n = 8) and in controls (n = 8) without treatment. RESULTS: NE infusion led to significant tachycardia, an increase in cardiac output, and systemic oxygen delivery and consumption while PE progressively increased mean arterial pressure with only small effects on systemic blood flow. NE or PE infusion did not affect mesenteric venous oxygen tension (baseline: PE 53 +/- 5, NE, 52 +/- 4.2 mmHg), mesenteric oxygen extraction ratio (baseline: PE 0.29 +/- 0.08, NE 0.3 +/- 0.06), jejunal microvascular blood flow (baseline: PE 254 +/- 127, NE 282 +/- 72 PU), PO2muc (baseline: PE 31 +/- 9.1, NE 33 +/- 11 mmHg), and HbO2 (baseline: PE 52 +/- 9.6%, NE 58 +/- 11.6%). CONCLUSION: Despite major differences in systemic hemodynamics jejunal tissue oxygen supply is not affected by progressively increasing intravenous infusion of norepinephrine and phenylephrine.

Animals↗
PubMed2001

Risk factors associated with new onset tachyarrhythmias after cardiac surgery--a retrospective analysis.

BACKGROUND: Tachyarrhythmias (TA) represent a frequent and serious problem after cardiac surgery. We retrospectively analyzed 987 cardiac surgery patients admitted to a surgical intensive care unit between 1996 and 1999 to assess incidence and risk factors associated with development of postoperative TA in the intensive care unit. METHODS: TA (n=149) were defined as non-sinus rhythm with a heart rate (HR) > or =100 bpm in patients with preoperative sinus rhythm or as heart rate > or =130 bpm in patients with preoperative atrial fibrillation. A total of 787 patients served as controls (C). Demographic, premorbidity and perioperative data, admission SAPS and MODS-score, presence of clinical syndromes systemic inflammatory response syndrome (SIRS) and sepsis were univariately compared between groups. For prediction of independent risk factors for TA-development two multiple logistic regression models were finally established. RESULTS: Concerning TA, atrial fibrillation and flutter (76%) were observed most frequently, followed by paroxysmal supraventricular tachycardia (15%) and ventricular tachycardia/fibrillation (11%). Age, a history or presence of congestive heart failure, development of SIRS and sepsis, severity of multiple organ dysfunction syndrome and in particular severity of cardiovascular failure proved to be independent risk factors for development of TA. CONCLUSION: In cardiac surgery patients, age, a history or presence of congestive heart failure, postoperative development of a systemic inflammatory response syndrome or sepsis and the severity of multiple organ function syndrome were independent predictors for development of TA in the intensive care unit. The association of severity of cardiovascular dysfunction with TA strongly suggests a causal relationship between catecholamine therapy and TA-development.

Aged↗
PubMed2001

Effects of epinephrine on intestinal oxygen supply and mucosal tissue oxygen tension in pigs.

OBJECTIVE: To study the effects of increasing dosages of epinephrine given intravenously on intestinal oxygen supply and, in particular, mucosal tissue oxygen tension in an autoperfused, innervated jejunal segment. DESIGN: Prospective, randomized experimental study. SETTING: Animal research laboratory. SUBJECTS: Domestic pigs. INTERVENTIONS: Sixteen pigs were anesthetized, paralyzed, and normoventilated. A small segment of the jejunal mucosa was exposed by midline laparotomy and antimesenteric incision. Mucosal oxygen tension was measured by using Clark-type surface oxygen electrodes. Microvascular hemoglobin oxygen saturation and microvascular blood flow (perfusion units) were determined by tissue reflectance spectrophotometry and laser-Doppler velocimetry. Systemic hemodynamics, mesenteric-venous acid-base and blood gas variables, and systemic acid-base and blood gas variables were recorded. Measurements were performed after a resting period and at 20-min intervals during infusion of increasing dosages of epinephrine (n = 8; 0.01, 0.05, 0.1, 0.5, 1, and 2 microg x kg(-1) x min(-1)) or without treatment (n = 8). In addition, arterial and mesenteric-venous lactate concentrations were measured at baseline and at 60 and 120 mins. MEASUREMENTS AND MAIN RESULTS: Epinephrine infusion led to significant tachycardia; an increase in cardiac output, systemic oxygen delivery, and oxygen consumption; and development of lactic acidosis. Epinephrine significantly increased jejunal microvascular blood flow (baseline, 267 +/- 39 perfusion units; maximum value, 443 +/- 35 perfusion units) and mucosal oxygen tension (baseline, 36 +/- 2.0 torr [4.79 +/- 0.27 kPa]; maximum value, 48 +/- 2.8 torr [6.39 +/- 0.37 kPa]) and increased hemoglobin oxygen saturation above baseline. Epinephrine increased mesenteric venous lactate concentration (baseline, 2.9 +/- 0.6 mmol x L(-1); maximum value, 5.5 +/- 0.2 mmol x L(-1)) without development of an arterial-mesenteric venous lactate concentration gradient. CONCLUSIONS: Epinephrine increased jejunal microvascular blood flow and mucosal tissue oxygen supply at moderate to high dosages. Lactic acidosis that develops during infusion of increasing dosages of epinephrine is not related to development of gastrointestinal hypoxia.

Acidosis, Lactic↗
PubMed2001

Blunted erythropoietic response to anemia in multiply traumatized patients.

OBJECTIVES: To assess the relations between anemia, serum erythropoietin (EPO), iron status, and inflammatory mediators in multiply traumatized patients. DESIGN: Prospective observational study. SETTING: Intensive care unit. PATIENTS: Twenty-three patients suffering from severe trauma (injury severity score > or =30). INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Blood samples were collected within 12 hrs after the accident (day 1) and in the morning on days 2, 4, 6, and 9 to determine blood cell status, serum EPO, tumor necrosis factor-alpha (TNF-alpha), soluble tumor necrosis factor-receptor I (sTNF-rI), interleukin-1 receptor antagonist (IL1-ra), interleukin-6 (IL-6), neopterin, and iron status, respectively. Hemoglobin concentration was low at admission (mean, 10.0 g/dL; range, 6.8-12.9 g/dL) and did not increase during the observation time. Serum EPO concentration was 49.8 U/L (mean value) on day 1 and did not show significant increases thereafter. No correlation was found between EPO and hemoglobin concentrations. TNF-alpha remained within the normal range. sTNF-rI was high at admission and increased further. IL1-ra was above the normal range. IL-6 was very high at admission and did not decrease thereafter. The initial neopterin concentration was normal, but increased until day 9. Serum iron was significantly decreased on day 2 posttrauma and remained low during the study. Serum ferritin increased steadily from day 2, reaching its maximum on day 9. In contrast, concentrations of transferrin were low from admission onward. CONCLUSIONS: Multiply traumatized patients exhibit an inadequate EPO response to low hemoglobin concentrations. Thus, anemia in severe trauma is the result of a complex network of bleeding, blunted EPO response to low hemoglobin concentrations, inflammatory mediators, and a hypoferremic state.

Adult↗
PubMed2000

[Multiple organ failure following inhalation of butane gas: a case report].

Most cases of acute poisoning by butane and other volatile compounds occur in young people as a consequence of substance abuse by inhalation. Clinical symptoms are caused by asphyxia and mainly affect the cardiovascular, respiratory and central nervous system. There are also reported deaths from intoxication of butane inhalation, mostly by cardiac arrhythmia. We report the case of a healthy 14 year-old boy who inhaled butane gas from an aerosol can for refilling cigarette lighters. Despite successful resuscitation and defibrillation, he died two days later from multiple organ failure involving the central nervous system, cardiovascular system, pulmonary system and the liver. Although such incidents are rare in middle European countries, emergency and intensive care medicine staff should be instructed on the consequences and management of butane gas poisoning.

Adolescent↗
PubMed2000

Tachyarrhythmias in a surgical intensive care unit: a case-controlled epidemiologic study.

OBJECTIVE: Incidence, types, and factors associated with new onset tachyarrhythmias (TA) in surgical intensive care patients. DESIGN: Pairwise-matched case-controlled study. SETTING: Surgical intensive care unit (ICU) with nine intensive care beds. PATIENTS: During a 1-year period, all TA patients (n = 89) were included in the study. Control patients (n = 82) without TA were matched according to age, sex, and surgical region. METHODS: TA workup included: 12-lead ECG, arterial blood gas, serum electrolyte (K+, Mg2+), and serum CK/CKMB isoenzyme analysis. Pre-existing cardiovascular and pulmonary disease, cardiovascular risk factors, preoperative regular medication, and admission SAPS were recorded in all patients. A multiple organ dysfunction syndrome (MODS) score, the presence or absence of SIRS or sepsis, and hemodynamics (MAP and CVP) before onset of TA were evaluated in TA patients, while in control patients highest MODS-score, the presence or absence of SIRS or sepsis, mean hemodynamic and laboratory values calculated from highest and lowest readings during ICU stay were used for statistical comparison. Logistic regression analysis was performed to identify variables multivariately associated with TA. RESULTS: Eighty-nine (14.8%) of 596 patients developed TA. Atrial fibrillation was most frequent (60.7%). Presence of SIRS or sepsis (adj. OR = 36.45; 95% CI: 11.5-115.5), high admission SAPS (adj. OR = 1.25/point; 95% CI: 1.08-1.44), high CVP (adj. OR = 1.27/mmHg; 95% CI: 1.09-1.48), and low arterial oxygen tension (adj. OR = 0.97/mmHg); 95% CI: 0.95-0.99) were found to be significant predictors for development of TA. CONCLUSIONS: In surgical patients hypoxia, high cardiac filling pressures, a greater degree of physiologic derangement at admission, and the presence of SIRS and sepsis are independent risk factors for the development of TA.

Aged↗
PubMed2000

Reactive hyperemia in skin after cardiopulmonary bypass.

OBJECTIVE: To study reactive hyperemia (RH) using a transcutaneous PO2/PCO2 combination electrode heated to 37 degrees C and tissue reflectance spectrophotometry in patients before and after cardiopulmonary bypass (CPB) to determine whether microcirculatory function of skin is altered. DESIGN: Prospective study. SETTING: Anesthesiology and critical care unit of a university hospital. PARTICIPANTS: Eight patients undergoing elective CPB under mild hypothermia. INTERVENTIONS: To produce RH, blood flow to the forearm was prevented by inflation of a cuff to 300 mmHg for an interval of 5 minutes. MEASUREMENTS AND MAIN RESULTS: Measurements were obtained on the day prior to surgery (DPS), on the day of surgery (DOS) rewarmed to 37 degrees C in the intensive care unit (ICU), and on the first (POD 1) and the third postoperative days (POD 3). The following parameters were recorded: preocclusive baseline cutaneous PO2, and PCO2 (B-PtcO2, B-PtcCO2), and microvascular hemoglobin saturation (B-HbO2); postischemic peak of PtcO2, PtcCO2, and HbO2; and 10 minutes after release of the cuff occlusion posthyperemic PtcO2, PtcCO2, and HbO2. B-PtcO2 was 3.5 +/- 1.2 mmHg on DPS, 2.6 +/- 0.7 mmHg on DOS, 1.5 +/- 0.3 mmHg on POD 1, and 3.5 +/- 3.5 mmHg on POD 3. B-PtcCO2 increased significantly from 40.1 +/- 2.5 mmHg to 52.2 +/- 2.0 mmHg on DOS (p = 0.01) and to 48.9 +/- 3.6 mmHg on POD 1 (p = 0.02). On POD 3, B-PtcCO2 was 40.6 +/- 2.6 mmHg. B-HbO2 declined from a preoperative value of 42.4% +/- 8.6% to 37.1% +/- 14.7% on DOS and further to 21.7% +/- 4.8% on POD 1, which was significantly different (p = 0.03). On POD 3, B-HbO2 still remained lower (30.7% +/- 6.2%) compared with the preoperative value. RH (deltaPtcO2, deltaHBO2) was quantified as the differences between peak PtcO2, HBO2 and B-PtcO2, B-HBO2. DeltaPtcO2 was 13.0 +/- 2.3 on DPS, 11.3 +/- 2.9 on DOS, 12.6 +/- 2.6 on POD 1, and 11.5 +/- 3.5 on POD 3. DeltaHBO2 was 42.0 +/- 5.6 on DPS, 40.0 +/- 7.1 on DOS, 49.9 +/- 2.5 on POD 1, and 52.9 +/- 6.4 on POD 3. The elimination rate of carbon dioxide from skin (ECO2) was calculated as difference between peak PtcCO2 and PtcCO2 after 3 minutes of reperfusion divided by the difference between peak PtcCO2 and B-PtcCO2. ECO2 was 1.0 +/- 0.2 kPa/min on DPS, 0.7 +/- 0.1 kPa/min on DOS, and 0.8 +/- 0.1 kPa/min on POD 1 and POD 3. CONCLUSION: Cutaneous microcirculation assessed by RH is well preserved during the immediate postoperative period in patients undergoing uncomplicated coronary artery surgery with CPB.

Blood Gas Monitoring, Transcutaneous↗
PubMed2000

Acute respiratory failure associated with catastrophic antiphospholipid syndrome.

We present a case of multiple organ dysfunction syndrome with acute respiratory failure due to alveolar haemorrhage associated with antiphospholipid antibodies in a 42-year-old woman with a medical history of antinuclear antibody-negative systemic lupus erythematosus and antiphospholipid syndrome. Severe respiratory failure, circulatory shock and acute renal failure necessitated artificial ventilation, inotropic and vasopressor therapy, and continuous venovenous haemofiltration. A tentative diagnosis of haemorrhagic lupus pneumonitis or pulmonary manifestation of antiphospholipid syndrome was made. Lupus anticoagulant, IgG anticardiolipin and anti-beta2-glycoprotein I antibodies were positive. High-dose glucocorticoid, anticoagulation with heparin, plasmapheresis and cyclophosphamide improved her clinical condition. Despite this, the patient died several days later of spontaneous intracranial haemorrhage. This case illustrates the uncommon manifestation of acute respiratory failure associated with antiphospholipid syndrome.

Acute Disease↗
PubMed1999

[Implementing limited therapy methods in intensive care units: discontinuing therapy, reducing therapy and withholding therapy in intensive care units of the Innsbruck University Clinics].

INTRODUCTION: The intensive care physician is frequently confronted with the decision to withhold or withdraw therapy in patients with a poor prognosis. Apart from the legal implications, the practical management of withholding or withdrawing intensive care treatment continues to be indistinct. The subject has not been investigated in Austria or Germany. The aim of the study was to examine the different points of view of intensive care physicians and the various procedures to limit therapy in patients with a poor prognosis. METHODS: We interviewed physicians working at different intensive care departments of the University Hospital of Innsbruck from March to April 1998. RESULTS: Withholding treatment was given preference over withdrawing treatment. In regard of withdrawing treatment, 64% of the interviewed physicians felt more uncertain. In the decision making process the potential reversibility of disease was estimated to be more important than the wish of the patient. Hemofiltration and antibiotics were mentioned as the first measures the physicians would withdraw. The last measure that would be withheld was ventilatory support. Sixty-three per cent of the physicians felt that sedation and analgesia should be continued. In regard of withholding or withdrawing treatment 83% voted for an obligatory DNR order. CONCLUSION: Before withholding or withdrawing intensive care therapy, a medical specialist must determine and document the futile prognosis of the patient. If the patient's wish is unknown, all further decisions should be made in agreement with all participants. The goal of the therapy is to provide the patient maximum comfort under minimal intensive care treatment.

Attitude of Health Personnel↗
PubMed1999

[Intestinal ischemic reperfusion syndrome: pathophysiology, clinical significance, therapy].

Gut ischemia-reperfusion injury is a serious condition in intensive care patients. Activation of immune cells within the huge endothelial surface area of gut microcirculation may initiate a systemic inflammatory response with secondary injury to distant organs. Translocation of bacteria and toxins through a leaky gut mucosa may amplify or perpetuate systemic inflammation, leading to multiple organ dysfunction syndrome and death in critically ill patients. Gut ischemia promotes regional production of inflammatory mediators, expression of cell adhesion molecules on endothelial and immune cell surfaces and increases the procoagulatory properties of vascular endothelial cells. During reperfusion, gut injury may be amplified by increased production of oxygen radicals and exhaustion of endogenous antioxidant defence mechanisms. Although several therapeutic strategies to interrupt the pathophysiology of ischemia-reperfusion have been shown to be beneficial in animal experiments, none of these interventions has gained clinical relevance. After initial hemodynamic and respiratory stabilisation of critically ill patients, strategies to prevent secondary gut injury by increasing splanchnic oxygen delivery or augment mucosal cell regeneration may be the only therapeutic options for intensive medical specialists at the present time. Early enteral nutrition and treatment with specific vasoactive drugs may reduce morbidity and costs of treatment in certain critically ill patients. However definitive evidence of a reduction in mortality with these therapies has still not be provided.

Animals↗