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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. [ABSTRACT FROM AUTHOR]

Deals with a study which investigated the effect of increasing blood viscosity during extreme hemodilution on capillary perfusion and tissue oxygenation in the awake hamster skinfold model. Materials and methods; Systemic and blood gas parameters; Physical properties of blood; Microvascular oxygen distribution.

Presents a study which analyzes the increased plasma viscosity at extreme hemodilution levels in terms of microvascular tone, blood flow, functional capillary density and oxygen distribution to determine the functional state of the microvasculature under these conditions. Materials and methods used on the study; Results and discussion.

Looks at a study which examined the radial pO2 profiles in vivo for the periarteriolar tissue of the rat mesentery, using noninvasive phosphorescence quenching microscopy. Identification of the major function of the blood circulation; Regulation of the blood flow; Methodology used to conduct the study; Results of the study.

Investigates ischemia-reperfusion injury in subcutaneous connective tissue and skin muscle. Functional capillary density (FCD); Capillary red blood cell velocity; Arteriolar and venular diameter; Postischemic inflammation; Hyperemia.

Background and objective: The Working Group on Ethics in Anesthesia and Intensive Care Medicine of the Austrian Society for Anesthesiology Resuscitation and Intensive Care Medicine (ÖGARI) already developed documentation tools for the adaption of therapeutic goals 10 years ago. Since then the practical implementation of Comfort Terminal Care in the daily routine in particular has raised numerous questions, which are discussed in this follow-up paper and answered in an evidence-based manner whenever possible. Results: The practical implementation of pain therapy and reduction of anxiety, stress and respiratory distress that are indicated in the context of Comfort Terminal Care are described in more detail. The measures that are not (or no longer) indicated, such as oxygen administration and ventilation as well as the administration of fluids and nutrition, are also commented on. Furthermore, recommendations are given regarding monitoring, (laboratory) findings and drug treatment and the importance of nursing actions in the context of Comfort Terminal Care is mentioned. Finally, the support for the next of kin and the procedure in the time after death are presented. Discussion: A change in treatment goals with a timely switch to Comfort Terminal Care enables good and humane care for seriously ill patients and their relatives at the end of life and the appreciation of their previous life with the possibility of positive experiences until the end. [ABSTRACT FROM AUTHOR]

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 relaxation to oxygen consumption of the microvascular wall during verapamil-induced vasodilatation. Verapamil HC1 delivered in a 0.1 mg/kg bolus injection followed by a continuous infusion of 0.01 mg·kg-1·min-1 caused significant arteriolar dilatation, increased microvascular flow and functional capillary density, and decreased arteriolar vessel wall transmural Po2 difference. Verapamil caused tissue Po2 to increase from 25.5 ± 4.1 mmHg under control condition to 32.0 ± 3.7 mmHg during verapamil treatment. Total oxygen released by the microcirculation to the tissue remained the same as at baseline. Maintenance of the same level of oxygen release to the tissue, increased tissue Po2, and decreased wall oxygen concentration gradient are compatible if vasodilatation significantly lowers vessel wall oxygen consumption, which in this model appears to constitute an important oxygen- consuming compartment. These findings show that treatment with verapamil, which increases oxygen supply through vasodilatation, may further improve tissue oxygenation by lowering oxygen consumption of the microcirculation. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented about a study on sublingual capnometry tracks microcirculatory changes in septic patients.

The patients who do not respond even to very high dosages of heparin are assumed to suffer from heparin resistance. The aim of this study was to investigate whether critically ill patients suffering from heparin resistance generally have low antithrombin III (AT) levels, and if the direct thrombin inhibitor argatroban in that case can be an effective option to achieve prophylactic anticoagulation. The study was conducted at the Department for General and Surgical Intensive Care Medicine at the University Hospital Innsbruck. We retrospectively included all patients between 2008 and 2012, who received argatroban because of poor response to high-dosage heparin prophylaxis. The period under observation lasted in total for 9 days, 2 days of anticoagulation with unfractionated heparin (UFH) and 7 days with argatroban. The primary objective was to investigate if after 7 (± 1) hours of switching to argatroban the activated partial thromboplastin time (aPTT) levels were in a prophylactic range of 45 to 55 seconds. Further objectives were to assess the AT level, side effects such as bleeding or thromboembolism, platelet count, correlation between organ function and argatroban dose as well as any need for allogeneic blood products. The study population, consisting of 5 women and 15 men with a mean (± standard deviation, SD) age of 54.6 ± 16.3 years, differed in many clinical aspects. A median (interquartile range) heparin dose of 1,000, 819 to 1,125 IU/h was administered for 2 days and failed in providing a prophylactic anticoagulation measured by the aPTT. The mean aPTT level with heparin treatment was 38.5 seconds (± 4.7) its change within that period was not significant. After switching to argatroban, the mean increase of the aPTT levels in all study patients amounted from 38.5 to 48.3 seconds (p < 0.001). The rise in aPTT clearly reaches sufficient prophylactic anticoagulant levels. The maintenance of prophylactic aPTT levels was achieved over the period of 1 week. There was neither a correlation found between low-AT levels and occurrence of heparin resistance, nor between the simplified acute physiology score II and the administered argatroban dose (r =--0.224, p = 0.342). The results of the present study indicate that argatroban is an effective alternative therapy, especially in critically ill patients, to achieve prophylactic anticoagulation when heparin resistance occurs. [ABSTRACT FROM AUTHOR]

Summary: Arginine vasopressin (AVP) has been employed successfully during cardiopulmonary resuscitation, but there exist only few data about the effects of AVP infusion for cardiovascular failure during the post-cardiac arrest period. Cardiovascular failure is one of the main causes of death after successful resuscitation from cardiac arrest. Although the “post-resuscitation syndrome” has been described as a “sepsis-like” syndrome, there is little information about the haemodynamic response to AVP in advanced cardiovascular failure after cardiac arrest. In this retrospective study, haemodynamic and laboratory variables in 23 patients with cardiovascular failure unresponsive to standard haemodynamic therapy during the post-cardiac arrest period were obtained before, and 30min, 1, 4, 12, 24, 48, and 72h after initiation of a supplementary AVP infusion (4IU/h). During the observation period, AVP significantly increased mean arterial blood pressure (58±14 to 75±19mmHg, p <0.001), and decreased noradrenaline (norepinephrine) (1.31±2.14 to 0.23±0.3μg/kg/min, p =0.03), adrenaline (epinephrine) (0.58±0.23 to 0.04±0.03μg/kg/min, p =0.001), and milrinone requirements (0.46±0.15 to 0.33±0.22μg/kg/min, p <0.001). Pulmonary capillary wedge pressure changed significantly (p <0.001); an initial increase being followed by a decrease below baseline values. While arterial lactate concentrations (95±64 to 21±18mg/dL, p <0.001) and pH (7.27±0.14 to 7.4±0.14, p <0.001) improved significantly, total bilirubin concentrations (1.12±0.95 to 3.04±3.79mg/dL, p =0.001) increased after AVP. There were no differences in the haemodynamic or laboratory response to AVP between survivors and non-survivors. In this study, advanced cardiovascular failure that was unresponsive to standard therapy could be reversed successfully with supplementary AVP infusion in >90% of patients surviving cardiac arrest. [Copyright &y& Elsevier]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

OBJECTIVETo report on the incidence and risk factors associated with the development of ischemic skin lesions (ISL) in critically ill patients with catecholamine-resistant vasodilatory shock treated with a continuous infusion of arginine-vasopressin (AVP).DESIGNRetrospective analysis.SETTINGTwelve-bed general and surgical intensive care unit in a university hospital.PATIENTSA total of 63 critically ill patients with catecholamine-resistant vasodilatory shock.INTERVENTIONSContinuous AVP infusion.MEASUREMENTS AND MAIN RESULTSDemographic, hemodynamic, laboratory data, and skin status were evaluated 24 hrs before and during AVP therapy (24 and 48 hrs). Patients were grouped according to development of new ISL during AVP therapy. A mixed-effects model was used to compare groups. A multiple logistic regression analysis was used to identify independent risk factors for the development of ISL. ISL developed in 19 of 63 patients (30.2%). Thirteen of 19 patients (68%) developed ISL in distal limbs, two patients (10.5%) developed ISL of the trunk, four patients (21%) developed ISL in distal limbs and in the trunk. Five patients (26%) had additional ischemia of the tongue. Body mass index, preexistent peripheral arterial occlusive disease, presence of septic shock, and norepinephrine requirements were significantly higher in patients developing ISL. ISL patients received significantly more units of fresh frozen plasma and thrombocyte concentrates than patients without ISL. Preexistent peripheral arterial occlusive disease and presence of septic shock were independently associated with the development of ISL during AVP therapy.CONCLUSIONSISLs are a common complication during continuous AVP infusion in patients with catecholamine-resistant vasodilatory shock. The presence of septic shock and a history of peripheral arterial occlusive disease are independent risk factors for the development of ISL. [ABSTRACT FROM AUTHOR]

The relationship between flow motion and tissue oxygenation was investigated during hemorrhage/retransfusion with and without dopamine in 14 pigs. During 45% bleed, jejunal microvascular hemoglobin O[sub 2] saturation (HBjO[sub 2]) and mucosal tissue Po[sub 2] (PO[sub 2muc]) were recorded in seven control and seven dopamine-treated animals. Mean arterial pressure and systemic 02 delivery decreased during hemorrhage and returned to baseline after retransfusion. Hemorrhage decreased PO[sub 2muc] from 33 ± 2.8 to 13 ± 1.6 mmHg and HBjO[sub 2] from 53 ± 4.9% to 32 ± 3.9%, respectively, in control animals. During reperfusion, PO[sub 2muc] and HBjO[sub 2] remained low. Dopamine increased PO[sub 2muc] from 28 ± 4.3 to 45 ± 4.6 mmHg and HBjO[sub 2] from 54 ± 5.7% to 69 ± 1.5% and attenuated the decrease in Po[sub 2muc] and HBjO[sub 2] during hemorrhage. After retransfusion, dopamine restored Po[sub 2muc] and HBjO[sub 2] to baseline. Control animals developed rhythmic HBjO[sub 2] oscillations with increasing amplitude (frequency, 4.5 to 7.6 cycles/min) and showed an inverse relationship between PO[sub 2muc] and HBjO[sub 2] oscillation amplitude. Dopamine prevented regular flow motion. The association between decreased Po[sub 2muc] and increased oscillations in HBjO[sub 2] after normalization of systemic hemodynamics and O[sub 2] transport in control animals suggests a cause-and-effect relationship between low tissue Po[sub 2] and flow motion activity within the jejunal microcirculation. [ABSTRACT FROM AUTHOR]

The current study aims to evaluate whether prophylactic anticoagulation using argatroban or an increased dose of unfractionated heparin (UFH) is effective in achieving the targeted activated partial thromboplastin time (aPTT) of more than 45 s in critically ill heparin-resistant (HR) patients. Patients were randomized either to continue receiving an increased dose of UFH, or to be treated with argatroban. The endpoints were defined as achieving an aPTT target of more than 45 s at 7 h and 24 h. This clinical trial was registered on clinicaltrials.gov (NCT01734252) and on EudraCT (2012-000487-23). A total of 42 patients, 20 patients in the heparin and 22 in the argatroban group, were included. Of the patients with continued heparin treatment 55% achieved the target aPTT at 7 h, while only 40% of this group maintained the target aPTT after 24 h. Of the argatroban group 59% reached the target aPTT at 7 h, while at 24 h 86% of these patients maintained the targeted aPTT. Treatment success at 7 h did not differ between the groups (p = 0.1000), whereas at 24 h argatroban showed significantly greater efficacy (p = 0.0021) than did heparin. Argatroban also worked better in maintaining adequate anticoagulation in the further course of the study. There was no significant difference in the occurrence of bleeding or thromboembolic complications between the treatment groups. In the case of heparin-resistant critically ill patients, argatroban showed greater efficacy than did an increased dose of heparin in achieving adequate anticoagulation at 24 h and in maintaining the targeted aPTT goal throughout the treatment phase. [ABSTRACT FROM AUTHOR]

Diverticulosis of the sigmoid colon is a common condition and occurs more often in elderly patients. A well-known complication is infection or even perforation which often requires surgery. Necrotizing fasciitis as a complication of perforated diverticulitis is very rare. Here, we present a case of a covered perforated diverticulitis in an immunosuppressed patient leading to life-threatening necrotizing fasciitis requiring extracorporeal membrane oxygenation. Either hematogenous or local dissemination via the inguinal canal seemed the most probable mechanism of leg infection leading to hip articulation. [ABSTRACT FROM AUTHOR]