Uncovering the (un-)occupied electronic structure of a buried hybrid interface.

The energy level alignment at organic/inorganic (o/i) semiconductor interfaces is crucial for any light-emitting or -harvesting functionality. Essential is the access to both occupied and unoccupied electronic states directly at the interface, which is often deeply buried underneath thick organic films and challenging to characterize. We use several complementary experimental techniques to determine the electronic structure of p -quinquephenyl pyridine (5P-Py) adsorbed on ZnO(1 0 -1 0). The parent anchoring group, pyridine, significantly lowers the work function by up to 2.9 eV and causes an occupied in-gap state (IGS) directly below the Fermi level E F. Adsorption of upright-standing 5P-Py also leads to a strong work function reduction of up to 2.1 eV and to a similar IGS. The latter is then used as an initial state for the transient population of three normally unoccupied molecular levels through optical excitation and, due to its localization right at the o/i interface, provides interfacial sensitivity, even for thick 5P-Py films. We observe two final states above the vacuum level and one bound state at around 2 eV above E F, which we attribute to the 5P-Py LUMO. By the separate study of anchoring group and organic dye combined with the exploitation of the occupied IGS for selective interfacial photoexcitation, this work provides a new pathway for characterizing the electronic structure at buried o/i interfaces.

Cardiac performance during vasopressin infusion in postcardiotomy shock.

OBJECTIVE: Arginine-vasopressin (AVP) might be a potent vasopressor agent in catecholamine-resistant postcardiotomy shock. However, its use remains experimental because of considerations about deleterious effects on the heart. We report on the effects of continuous AVP-infusion on cardiac performance, biomarkers of myocardial ischemia, and systemic hemodynamics in catecholamine-resistant postcardiotomy shock. DESIGN: Retrospective study. SETTING: Twenty-one-bed general and surgical intensive care unit. PATIENTS: Forty-one patients with catecholamine-resistant postcardiotomy shock. INTERVENTIONS: Continuous infusion of AVP. MEASUREMENTS AND RESULTS: Heart rate (HR), heart rhythm, mean arterial pressure (MAP), central venous pressure, mean pulmonary arterial pressure, cardiac index (CI), stroke volume index (SVI), left ventricular stroke work index (LVSWI), systemic vascular resistance (SVR) as well as milrinone and norepinephrine requirements were collected before and 1, 4, 12, 24, and 48 h after start of AVP infusion. Creatine kinase MB and troponin-I serum concentrations were measured daily. During AVP administration we observed a significant decrease in HR (-14.8%), milrinone (-17.5%), and norepinephrine requirements (-54.9%) as well as biomarkers of cardiac ischemia and a significant increase in LVSWI (+46.2%), MAP (+41.8%) and SVR (+60%). CI and SVI remained unchanged. Forty-five percent of postoperative new-onset tachyarrhythmias (TA) converted into sinus rhythm during AVP infusion. CONCLUSIONS: AVP was devoid of adverse effects on the heart in these patients with catecholamine-resistant postcardiotomy shock. The significant reduction in HR, vasopressor, and inotropic support suggest a substantial improvement in myocardial performance. These findings are supported by a significant decrease of cardiac enzymes and cardioversion of TA into sinus rhythm in 45.5% of patients with new-onset TA.

Long-term effects of spontaneous breathing during ventilatory support in patients with acute lung injury.

Improved gas exchange has been observed during spontaneous breathing with airway pressure release ventilation (APRV) as compared with controlled mechanical ventilation. This study was designed to determine whether use of APRV with spontaneous breathing as a primary ventilatory support modality better prevents deterioration of cardiopulmonary function than does initial controlled mechanical ventilation in patients at risk for acute respiratory distress syndrome (ARDS). Thirty patients with multiple trauma were randomly assigned to either breathe spontaneously with APRV (APRV Group) (n = 15) or to receive pressure-controlled, time-cycled mechanical ventilation (PCV) for 72 h followed by weaning with APRV (PCV Group) (n = 15). Patients maintained spontaneous breathing during APRV with continuous infusion of sufentanil and midazolam (Ramsay sedation score [RSS] of 3). Absence of spontaneous breathing (PCV Group) was induced with sufentanil and midazolam (RSS of 5) and neuromuscular blockade. Primary use of APRV was associated with increases (p < 0.05) in respiratory system compliance (CRS), arterial oxygen tension (PaO2), cardiac index (CI), and oxygen delivery (DO2), and with reductions (p < 0.05) in venous admixture (QVA/QT), and oxygen extraction. In contrast, patients who received 72 h of PCV had lower CRS, PaO2, CI, DO2, and Q VA/Q T values (p < 0.05) and required higher doses of sufentanil (p < 0.05), midazolam (p < 0.05), noradrenalin (p < 0.05), and dobutamine (p < 0.05). CRS, PaO2), CI and DO2 were lowest (p < 0.05) and Q VA/Q T was highest (p < 0.05) during PCV. Primary use of APRV was consistently associated with a shorter duration of ventilatory support (APRV Group: 15 +/- 2 d [mean +/- SEM]; PCV Group: 21 +/- 2 d) (p < 0.05) and length of intensive care unit (ICU) stay (APRV Group: 23 +/- 2 d; PCV Group: 30 +/- 2 d) (p < 0.05). These findings indicate that maintaining spontaneous breathing during APRV requires less sedation and improves cardiopulmonary function, presumably by recruiting nonventilated lung units, requiring a shorter duration of ventilatory support and ICU stay.

The effects of vasopressin on systemic hemodynamics in catecholamine-resistant septic and postcardiotomy shock: a retrospective analysis.

UNLABELLED: We retrospectively investigated the effects of continuous arginine vasopressin (AVP) infusion on systemic hemodynamics, acid/base status, and laboratory variables in patients (mean age [mean +/- SD]= 66.3 +/- 10.1 yr) with catecholamine-resistant septic (n = 35) or postcardiotomy shock (n = 25). Hemodynamic and acid/base data were obtained before; 30 min after; and 1, 4, 12, 24, 48, and 72 h after the start of AVP infusion. Laboratory examinations were recorded before and 24, 48, and 72 h after the start of AVP infusion. For statistical analysis, a mixed-effects model was used. The overall intensive care unit mortality was 66.7%. AVP administration caused a significant increase in mean arterial pressure (+29%) and systemic vascular resistance (+56%), accompanied by a significant decrease in heart rate (-24%) and mean pulmonary arterial pressure (-11%) without any change in stroke volume index. Norepinephrine requirements could be reduced by 72% within 72 h. During AVP infusion, a significant increase in liver enzymes and total bilirubin concentration and a significant decrease in platelet count occurred. Arginine vasopressin was effective in reversing systemic hypotension. However, adverse effects on gastrointestinal perfusion and coagulation cannot be excluded. IMPLICATIONS: In this retrospective analysis, the influence of a continuous infusion of an endogenous hormone (arginine vasopressin) on systemic hemodynamics and laboratory variables was assessed in patients with vasodilatory shock unresponsive to conventional therapy. Arginine vasopressin was effective in reversing systemic hypotension. However, adverse effects on gastrointestinal perfusion and coagulation cannot be excluded.

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.

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.

Sildenafil modulates hemodynamics and pulmonary gas exchange.

The effects of sildenafil (Viagra) on hemodynamics and pulmonary gas exchange remain uncertain. The aim of this study was to investigate what effect sildenafil had on gas exchange. A total of 24 anesthetized pigs were randomly assigned into four groups of six animals each: Group Low received 25 mg of sildenafil, which is equivalent to half the recommended dose for humans; group Normal received 50 mg; group High received 100 mg; and one group served as control. Inert gas and hemodynamic measurements were performed to define dose-dependent effects of sildenafil on cardiac and pulmonary function. Measurements were taken 30, 60, and 90 min after the administration of sildenafil via gastric tube. All doses of sildenafil caused significant increases in intrapulmonary shunt flow (maximum amplitude, 4.4 +/- 0.3 to 11.9 +/- 0.5%; mean +/- SEM), which was reflected by marked decreases in PaO2. Sildenafil elicited some significant increases in cardiac index (CI) (high dose, 142 +/- 10 to 196 +/- 13 ml x kg(-1), mean +/- SEM). Mean arterial pressure was significantly depressed after the high dose of sildenafil. Pulmonary artery pressure was decreased after high-dose sildenafil (maximum amplitude, 16 +/- 1.6 to 14 +/- 1.8, mean +/- SEM). No significant differences between the three treatment groups were found. Sildenafil represents and orally active substance with phosphodiesterase V inhibitory and cardiac output-increasing actions. PaO2 decrease after 50 and 100 mg of sildenafil was observed in the presence of significant rises in pulmonary shunt flow and CI.

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.

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.

Mucosal tissue oxygenation of the porcine jejunum during normothermic cardiopulmonary bypass.

Cardiopulmonary bypass (CPB) has been associated with intestinal tissue hypoxia, but direct measurements of mucosal oxygenation have not been performed. In anaesthetized pigs, jejunal mucosal oxygen tension and microvascular haemoglobin oxygen saturation were measured by a Clark-type electrode and tissue reflectance spectrophotometry. In pigs, normothermic CPB with systemic oxygen transport equivalent to baseline values was performed. In control animals, mucosal oxygen tension and mucosal haemoglobin oxygen saturation were mean 5.01 (SD 1.08) kPa and 38.0 (2.3)%, respectively. CPB was associated with a decrease in mucosal oxygen tension to 2.26 (1.21) kPa, decrease in mucosal microvascular haemoglobin oxygen saturation to 26.0 (3.9)% and appearance of oscillations in mucosal microvascular haemoglobin oxygen saturation. With CPB, arterial lactate concentrations increased from 1.77 (1.37) to 3.52 (1.58) mmol litre-1, but transvisceral lactate and splanchnic venous-arterial carbon dioxide tension gradients remained unchanged. Our results support the concept that CPB is associated with diminished oxygenation of intestinal mucosa that is probably caused by regional redistribution.

Spontaneous breathing during ventilatory support improves ventilation-perfusion distributions in patients with acute respiratory distress syndrome.

Ventilation-perfusion (V A/Q) distributions were evaluated in 24 patients with acute respiratory distress syndrome (ARDS), during airway pressure release ventilation (APRV) with and without spontaneous breathing, or during pressure support ventilation (PSV). Whereas PSV provides mechanical assistance of each inspiration, APRV allows unrestricted spontaneous breathing throughout the mechanical ventilation. Patients were randomly assigned to receive APRV and PSV with equal airway pressure limits (Paw) (n = 12) or minute ventilation (V E) (n = 12). In both groups spontaneous breathing during APRV was associated with increases (p < 0.05) in right ventricular end-diastolic volume, stroke volume, cardiac index (CI), PaO2, oxygen delivery, and mixed venous oxygen tension (PvO2) and with reductions (p < 0.05) in pulmonary vascular resistance and oxygen extraction. PSV did not consistently improve CI and PaO2 when compared with APRV without spontaneous breathing. Improved V A/Q matching during spontaneous breathing with APRV was evidenced by decreases in intrapulmonary shunt (equal Paw: 33 +/- 4 to 24 +/- 4%; equal V E: 32 +/- 4 to 25 +/- 2%) (p < 0.05), dead space (equal Paw: 44 +/- 9 to 38 +/- 6%; equal V E: 44 +/- 9 to 38 +/- 6%) (p < 0.05), and the dispersions of ventilation (equal Paw: 0.96 +/- 0.23 to 0.78 +/- 0.22; equal V E: 0.92 +/- 0.23 to 0.79 +/- 0.22) (p < 0.05), and pulmonary blood flow distribution (equal Paw: 0.89 +/- 0.12 to 0.72 +/- 0.10; equal V E: 0.94 +/- 0.19 to 0.78 +/- 0.22) (p < 0.05). PSV did not improve V A/Q distributions when compared with APRV without spontaneous breathing. These findings indicate that uncoupling of spontaneous and mechanical ventilation during APRV improves V A/Q matching in ARDS presumably by recruiting nonventilated lung units. Apparently, mechanical assistance of each inspiration during PSV is not sufficient to counteract the V A/Q maldistribution caused by alveolar collapse in patients with ARDS.

Successful treatment of severe myocardial failure after postpartum haemorrhage with the use of an intra-aortic balloon pump.

We report a 29-year-old primigravid who developed cardiac failure following postpartum haemorrhage unresponsive to volume resuscitation and therapy with catecholamines and phosphodiesterase-inhibitors. Transoesophageal echocardiography (TEE) demonstrated left atrial and ventricular dilatation and global left ventricular hypokinesis. No elevation of serum MB-isoenzyme fraction was detected and other organ functions remained stable. Although emergency cardiac transplantation was considered in the presented patient, the institution of intra-aortic counterpulsation was decided on as a first treatment option. Intra-aortic balloon counter-pulsation rapidly improved cardiac function and led to weaning from pharmacological cardiac support within a few days. Mechanical circulatory assist devices can be life-saving in postpartum-haemorrhage-associated cardiac failure.

Angiotropic large B-cell lymphoma misdiagnosed as urosepsis with multiple organ dysfunction syndrome.

A 53-year-old woman with a history of cervical carcinoma 14 years ago, treated with hysterectomy and radiation therapy, was admitted to the intensive care unit with severe SIRS (systemic inflammatory response syndrome) progressing to shock, multiple organ failure and death within 5 d. Bilateral hydronephrosis diagnosed by sonography and an enlarged left kidney with suspected abscesses verified in a CT-scan suggested the diagnosis of urosepsis. However, multiple microbiological examinations remained sterile. Despite surgical treatment and aggressive intensive care, she died in unresponsive shock. Pathohistologically, an angiotropic large B-cell lymphoma, a rare diffuse intravascular neoplasm of lymphoid origin, was diagnosed. The patient's history of abdominal radiation therapy 14 years earlier as well as multiple negative microbiological specimens in a patient with suspected urosepsis should have initiated the search for a non-infectious cause of the disease.

Selective intestinal decontamination in multiple trauma patients: prospective, controlled trial.

BACKGROUND: Reduction of potential pathogens by selective intestinal decontamination has been proposed to improve intensive care. Despite large scientific interest in this method, little is known about its benefit in homogeneous trauma populations. METHODS: In a prospective, controlled study, we enrolled non-infected trauma patients (age over 18 years, mechanical ventilation > or = 48 hours, intensive care for more than 3 days) who primarily were admitted to our university medical center. We randomized patients to be treated with two different topical regimens (polymyxin, tobramycin, and amphotericin (PTA) or polymyxin, ciprofloxin, amphotericin (PCA)) or the carrier only (placebo), administered four times daily both to the oropharynx and to the gastrointestinal tract. All patients received intravenous ciprofloxacin (200 mg, bd) for 4 days. FINDINGS: Of 357 enrolled patients, 310 (age 38.0 +/- 16.5 years, Injury Severity Score 35.2 +/- 12.7) met all inclusion criteria. Selective decontamination successfully reduced intestinal bacterial colonization. However, we did not identify significant differences between groups regarding pneumonia (PTA 47.5%, PCA 39.0%, placebo 45.3%), sepsis (PTA 47.5%, PCA 37.8%, placebo 42.6%), multiple organ failure (PTA 56.3%; PCA 52.4%, placebo 58.1%), and death (PTA 11.3%, PCA 12.2%, placebo 10.8%). Total costs per patient were highest with the PTA regimen. CONCLUSIONS: We found no benefit of selective decontamination in trauma patients. Apparently, bacterial overgrowth in the intestinal tract is not the sole link between trauma, sepsis, and organ failure.