H. Van Aken

Teaching resuscitation in schools: annual tuition by trained teachers is effective starting at age 10. A four-year prospective cohort study.

AIMSnEvaluation of school pupils resuscitation performance after different types of training relative to the effects of training frequency (annually vs. biannually), starting age (10 vs. 13 years) and facilitator (emergency physician vs. teacher).nnnMETHODSnProspective longitudinal study investigating 433 pupils in training and control groups. Outcome criteria were chest compression depth, compression frequency, ventilation volume, ventilation frequency, self-image and theoretical knowledge. In the training groups, 251 pupils received training annually or biannually either from emergency physicians or CPR-trained teachers. The control group without any training consisted of 182 pupils.nnnRESULTSnImprovements in training vs. control groups were observed in chest compression depth (38 vs. 24 mm), compression frequency (74 vs. 42 min(-1)), ventilation volume (734 ml vs. 21 ml) and ventilation frequency (9/min vs. 0/min). Numbers of correct answers in a written test improved by 20%, vs. 5% in the control group. Pupils starting at age 10 showed practical skills equivalent to those starting at age 13. Theoretical knowledge was better in older pupils. Self-confidence grew in the training groups. Neither more frequent training nor training by emergency physicians led to better performance among the pupils.nnnCONCLUSIONSnPupils starting at age 10 are able to learn cardiopulmonary resuscitation with one annual training course only. After a 60-min CPR-training update, teachers are able to provide courses successfully. Early training reduces anxieties about making mistakes and markedly increases participants willingness to help. Courses almost doubled the confidence of pupils that what they had learned would enable them to save lives.

Extracellular protein disulfide isomerase regulates feedback activation of platelet thrombin generation via modulation of coagulation factor binding

Summary.u2002 Background:u2002Protein disulfide isomerase (PDI) controls platelet integrin function, tissue‐factor (TF) activation, and concentrates at fibrin and thrombus formation sites of vascular injury. Objective:u2002To investigate the involvement of surface thiol isomerases and especially PDI, in thrombin‐mediated thrombin amplification on human platelets. Methods/results:u2002Using a newly developed thrombin‐dependent platelet thrombin generation assay, we observed that the feedback activation of thrombin generation on the platelet surface does not depend on TF, as anti‐TF antibodies inhibiting TF‐induced thrombin formation in platelet‐depleted plasma had no effect compared with vehicle‐treated controls. Feedback activation of thrombin generation in the presence of platelets was significantly diminished by membrane impermeant thiol blockers or by the thiol isomerase‐inhibitors bacitracin and anti‐PDI antibody RL90, respectively. Platelet thrombin formation depends on binding of coagulation factors to the platelet surface. Therefore, involvement of thiol isomerases in this binding was investigated. As shown by confocal microscopy and flow cytometry, thrombin‐stimulated platelets exhibited increased surface‐associated PDI as well as extracellular disulfide reductase activity compared with unstimulated platelets. Flow cytometric analysis revealed that membrane impermeant thiol blockers or PDI inhibitors, which had been added after platelet stimulation and after phosphatidylserine exposure to exclude their influence on primary platelet activation, significantly inhibited binding of all coagulation factors to thrombin‐stimulated platelets. Conclusions:u2002Thus, surface‐associated PDI is an important regulator of coagulation factor ligation to thrombin‐stimulated platelets and of subsequent feedback activation of platelet thrombin generation. Cell surface thiol isomerases might be therefore powerful targets to control hemostasis and thrombosis.

Operative techniques and strategies for minimally invasive fetoscopic fetal cardiac interventions in sheep.

AbstractBackground: Recent efforts to develop procedures for fetoscopic fetal cardiac interventions have been prompted by the development of severe secondary damage to the fetal heart due to semilunar valvar obstructions and the poor outcome of therapy-refractory fetal arrhythmias. The purpose of our manuscript is to analyze and share our experience with the creation of an operative setup for these procedures in sheep.nn Methods: We studied a total of 48 fetal sheep between 81 and 106 days of gestation (term, 145 days). After entering the amniotic cavity by a percutaneous approach, we performed various fetoscopic fetal cardiac procedures. We analyzed the success of percutaneous fetal access, methods of trocar support, the incidence and management of trocar dislodgement or accidental insertion into the chorioamniotic space, problems related to amniotic insufflation and trocar placement, as well as techniques for fetal posturing and uterine closure.nn Results: Percutaneous fetal access was achieved in all sheep. The use of resterilizable trocars substantially decreased the costs of our procedures. Utilizing a percutaneous transuterine purse-string suture for trocar support helped to minimize the number of nonabsorbable T-fasteners remaining inside the uterus postoperatively. As complications such as trocar dislodgement, insertion of the trocar into the chorioamniotic space, and problems with intraamniotic insufflation and gas loss were mastered, conversion to an open operative approach was never required. A novel strategy that we devised for percutaneous fetal posturing permitted adequate fetal posturing with ease and minimal trauma to the fetal skin.nn Conclusion: As operative techniques have become more refined, the feasibility of performing fetoscopic fetal cardiac interventions in human fetuses now depends mainly on technical improvements in imaging and interventional catheters, as well as advances in pacemaker equipment.n

Activated monocytes capture platelets for heterotypic association in patients with severe carotid artery stenosis

Inflammation and thrombosis, two processes influencing each other, are involved in the pathogenesis of cerebrovascular disease. We showed that in patients with acute ischaemic stroke circulating platelets are activated and exhausted. To identify whether activated haemostasis might be cause or effect, we investigated the role of leukocyte and platelet activation in patients with severe asymptomatic and symptomatic carotid artery disease. Flow cytometry analysis demonstrated that monocytes from symptomatic (acute stroke aetiology) and asymptomatic patients were highly activated, shown by significantly enhanced presentation of inflammatory markers CD11b and thrombospondin-1 (TSP-1) on the surface. Both correlated positively with monocyte-platelet association rate. However, increased monocyte activation and elevated levels of monocyte-platelet associates in asymptomatic patients were restricted to patients with echo-lucent plaques, providing a close link between monocyte activation and plaque morphology. Circulating single as well as monocyte-bound platelets from symptomatic patients showed significantly enhanced surface expression of P-selectin and TSP-1, whereas platelets from asymptomatic patients were not significantly activated. These results indicate that monocytes activated by inflammation rather than platelets might be the candidates to initiate platelet-monocyte rosetting during the pathogenesis of atherothrombotic cerebral ischaemia and that haemostasis might be activated secondarily by the first occurring inflammation.

Human neutrophil alpha-defensins induce formation of fibrinogen and thrombospondin-1 amyloid-like structures and activate platelets via glycoprotein IIb/IIIa

Summary.u2002 Background:u2002 Human neutrophil α‐defensins (HNPs) are important constituents of the innate immune system. Beyond their antimicrobial properties, HNPs also have pro‐inflammatory features. While HNPs in plasma from healthy individuals are barely detectable, their level is strongly elevated in septic plasma and plasma from patients with acute coronary syndromes.

Processing of stored packed red blood cells using autotransfusion devices decreases potassium and microaggregates: a prospective, randomized, single-blinded in vitro study

summary The aim of the study was to compare the potential of autotransfusion devices to reduce non‐infectious complications related to transfusion of long‐stored packed red blood cells (PRBC; n= 57), such as changes in electrolytes, blood cells and the load of free microaggregates. Following a baseline measurement, a blood pool of three PRBC was divided into three equal volumes and washed with either the Haemonetics Cell Saver™ (HCS) or the continuous autotransfusion system (C.A.T.S™), using the quality (CATSquality) and emergency (CATSemergency) mode. After the washing procedure, measurements for electrolytes, blood cells and free microaggregates were repeated (n= 19 each). Compared with baseline, the investigated autotransfusion devices reduced the median load of potassium (baseline: 52 mEq L−1; HCS: 4 mEq L−1; CATSquality: 4 mEq L−1; CATSemergency: 17 mEq L−1; each P < 0·001), restored a physiologic electrolyte balance and significantly decreased the load of leucocytes, glucose and protein. Whereas the quantity of microaggregates was not reduced by HCS, CATSemergency decreased the load of cell fragments below 7·8 μm (P < 0·05 vs. baseline). Using CATSquality decreased the load of cell fragments not only to a diameter below 7·8 μm (P < 0·001 vs. baseline) but also of microaggregates between 7·8 and 17·6 μm (P < 0·05 vs. baseline). In situations where long‐stored PRBC have to be transfused, the procedure described here may be feasible to reduce clinically relevant side effects, i.e. hyperkalaemia and microvascular obstruction secondary to free cell fragments. This approach could be especially useful in patients undergoing massive transfusion and/or suffering from renal failure.

Prostaglandin F2α Improves Oxygen Tension and Reduces Venous Admixture during One-lung Ventilation in Anesthetized Paralyzed Dogs

The authors investigated the effect of prostaglandin F2α infused into the pulmonary artery of an acutely atelectatic lung in dogs. Seven dogs were anesthetized with piritramid and pentobarbital and intubated with a Kottmeier canine endobronchial tube. Cardiac output, pulmonary arterial, capillary wedge, and systemic arterial pressure were measured via indwelling catheters. Ventilating both lungs with 66% O2, Pao2 was 327±15 mmHg (mean±SD) and venous admixture (Q±sp/Q1) was 11±3%. One-lung atelectasis reduced Pao2 to 91±12 mmHg and increased Q±sp/Qt to 40±4%. Prostaglandin F2α in doses of 0.4, 0.6, 1.2, and 1.8 μg ± kg−1 · min−1 was infused into the pulmonary artery of the atelectatic lung through a second pulmonary artery catheter. Up to a dose of 1.2 μg · kg−1 · min−1 there was a dose-dependent reduction in Q·sp/Qt to a minimum of 25±4% and an increase in Pao2 to 168±25 mmHg, which could be explained by enhanced pulmonary vasoconstriction in the atelectatic lung with increased blood flow diversion toward the ventilated lung. Infusion of 1.8 μg · kg−1 · min−1 decreased Pao2 to 156±32 mmHg and increased Q±sp/Qt to 32±9%. Increased systemic effects of prostaglandin F2α were observed and presumably were related to saturation of prostaglandin-dehydrogenase leading to vasoconstriction in both lungs and thus reduced blood flow diversion toward the ventilated lung.

Modulation of hypoxic pulmonary vasoconstriction is time and nitric oxide dependent in a peritonitis model of sepsis

ObjectiveThis study assessed modulation of hypoxic pulmonary vasoconstriction (HPV) in isolated perfused rat lungs during sepsis induced by cecal ligation and perforation (CLP) at different times and its relationship to nitric oxide synthases (NOS).Design and settingProspective controlled trial in a university research laboratory.Subjects102 male Sprague-Dawley rats.InterventionsGroups 1–3 received sham laparotomy 6xa0h before lung isolation: group 1, only laparotomy; group 2, concurrently l-N6-(1-iminoethyl)-lysine (L-NIL, 3xa0mg/kg); group 3, concurrently NΩ-nitro-l-arginine methylester (L-NAME, 5xa0mg/kg). Groups 4–6 received CLP 6xa0h before lung isolation: group 4, only CLP; group 5, concurrently L-NIL; group 6, concurrently L-NAME. The same experiments were carried out with sham and CLP treatment for 24xa0h (groups 7–12). Exhaled NO from rats’ lungs was measured after anesthesia and tracheostomy. After the pulmonary circuit was isolated and perfused, angiotensin II (0.1xa0µg) was injected into the inflow tract. The lungs were ventilated with the hypoxic mixture (HPV, 3% O2) for 10xa0min and then again with the normoxic mixture (21% O2) for an equal period. Changes in perfusion pressure were measured. Endothelial (eNOS) and inducible NOS (iNOS) expression of the lungs was determined.Measurements and resultsTreatment with L-NAME but not L-NIL increased HPV in sham lungs. HPV was unaltered after CLP 6xa0h and decreased after CLP 24xa0h compared to sham. In CLP animals eNOS protein expression was reduced whereas iNOS expression was increased compared to sham animals. Exhaled NO, reflecting NOS activity was twice as high in the CLP 24xa0h group than in the CLP 6xa0h group.ConclusionsIn the CLP sepsis model modulation of HPV was time-dependent. In addition, vasoconstriction to hypoxic stimuli was dependent on NOS activity.

Strategies to reduce perioperative blood loss related to non-surgical bleeding.

The treatment of critically ill patients has advanced markedly over the last decade. However, non-surgical bleeding of a diffuse nature from numerous tiny capillaries still remains a challenge. Once initiated, this type of bleeding may be troublesome and a vicious circle develops since it is not a single vessel contributing to this blood loss. The description non-surgical blood loss is often given to this. This review describes a step-by-step approach for the treatment of non-surgical bleeding and includes various measures, such as desmopressin, blood components, antifibrinolytics, antithrombin III, prothrombin complex concentrates and factor XIII. While most non-surgical bleedings can be managed using the approach described here, a number of patients still continue to bleed. In these cases, the surgeon should re-evaluate the bleeding in terms of its surgical origin. If this can positively be excluded and if all of measures described fail to reduce or stop the bleeding, further treatment of such uncontrolled bleeding remains symptomatic.

Ventral recumbency is crucial for fast and safe orotracheal intubation in laboratory swine.

The aim of this study was to find the fastest, easiest and safest method of achieving orotracheal intubation for general anaesthesia in laboratory pigs. Twenty-one Yorkshire × Landrace crossbreed male castrated pigs (32.9 ± 4.8 kg) were investigated. Dorsal and ventral recumbency are the alternatives most frequently described for animal positioning during intubation procedures. Based on standardized induction of general anaesthesia using pentobarbital and remifentanil, the dorsoventral and ventrodorsal positions were compared with regard to the time needed, changes in oxygenation and circulatory response. Positioning was found to be crucial for fast orotracheal intubation. The time required for safe intubation is significantly shorter with the ventrodorsal position (17.3 s) in comparison with the dorsoventral position (58.4 s; P < 0.001). Hypoxia did not occur in either group. A significant drop in systolic blood pressure was observed in both groups. Diastolic and mean arterial pressures were not influenced by intubation. A significant increase in heart rate was observed in pigs intubated in ventral recumbency, but not after intubation in the dorsal position. Preoxygenation before intubation is vitally important for preventing hypoxia. With regard to clinical practice, the haemodynamic changes observed in this investigation do not appear to be relevant, as the mean arterial pressure was not altered and heart rates only increased moderately. It may be concluded that the ventrodorsal position can be recommended for orotracheal intubation in pigs as the first choice for providing a smooth and fast airway.