Tilmann Schwab

Intra-Arrest Transnasal Evaporative Cooling A Randomized, Prehospital, Multicenter Study (PRINCE: Pre-ROSC IntraNasal Cooling Effectiveness)

Background— Transnasal evaporative cooling has sufficient heat transfer capacity for effective intra-arrest cooling and improves survival in swine. The aim of this study was to determine the safety, feasibility, and cooling efficacy of prehospital transnasal cooling in humans and to explore its effects on neurologically intact survival to hospital discharge. Methods and Results— Witnessed cardiac arrest patients with a treatment interval ≤20 minutes were randomized to intra-arrest cooling with a RhinoChill device (treatment group, n=96) versus standard care (control group, n=104). The final analysis included 93 versus 101 patients, respectively. Both groups were cooled after hospital arrival. The patients had similar demographics, initial rhythms, rates of bystander cardiopulmonary resuscitation, and intervals to cardiopulmonary resuscitation and arrival of advanced life support personnel. Eighteen device-related adverse events (1 periorbital emphysema, 3 epistaxis, 1 perioral bleed, and 13 nasal discolorations) were reported. Time to target temperature of 34°C was shorter in the treatment group for both tympanic (102 versus 282 minutes, P=0.03) and core (155 versus 284 minutes, P=0.13) temperature. There were no significant differences in rates of return of spontaneous circulation between the groups (38% in treated subjects versus 43% in control subjects, P=0.48), in overall survival of those admitted alive (44% versus 31%, respectively, P=0.26), or in neurologically intact survival to discharge (Pittsburgh cerebral performance category scale 1 to 2, 34% versus 21%, P=0.21), although the study was not adequately powered to detect changes in these outcomes. Conclusions— Prehospital intra-arrest transnasal cooling is safe and feasible and is associated with a significant improvement in the time intervals required to cool patients. Clinical Trial Registration— URL: http://www.clinicaltrials.gov. Unique identifier: NCT00808236.

Safety and feasibility of nasopharyngeal evaporative cooling in the emergency department setting in survivors of cardiac arrest

AIM Mild therapeutic hypothermia improves survival and neurologic recovery in primary comatose survivors of cardiac arrest. Cooling effectivity, safety and feasibility of nasopharyngeal cooling with the RhinoChill device (BeneChill Inc., San Diego, USA) were determined for induction of therapeutic hypothermia. METHODS Eleven emergency departments and intensive care units participated in this multi-centre, single-arm descriptive study. Eighty-four patients after successful resuscitation from cardiac arrest were cooled with nasopharyngeal delivery of an evaporative coolant for 1h. Subsequently, temperature was controlled with systemic cooling at 33 degrees C. Cooling rates, adverse events and neurologic outcome at hospital discharge using cerebral performance categories (CPC; CPC 1=normal to CPC 5=dead) were documented. Temperatures are presented as median and the range from the first to the third quartile. RESULTS Nasopharyngeal cooling for 1h reduced tympanic temperature by median 2.3 (1.6; 3.0) degrees C, core temperature by 1.1 (0.7; 1.5) degrees C. Nasal discoloration occurred during the procedure in 10 (12%) patients, resolved in 9, and was persistent in 1 (1%). Epistaxis was observed in 2 (2%) patients. Periorbital gas emphysema occurred in 1 (1%) patient and resolved spontaneously. Thirty-four of 84 patients (40%) patients survived, 26/34 with favorable neurological outcome (CPC of 1-2) at discharge. CONCLUSIONS Nasopharyngeal evaporative cooling used for 1h in primary cardiac arrest survivors is feasible and safe at flow rates of 40-50L/min in a hospital setting.

Perturbation of the endothelial glycocalyx in post cardiac arrest syndrome

BACKGROUND The prognosis of immediate survivors of cardiac arrest remains poor, as the majority of these patients develops an inflammatory disorder known as the post-cardiac arrest syndrome (PCAS). Recently, the endothelial glycocalyx has been shown to be a key modulator of vascular permeability and inflammation, but its role in PCAS remains unknown. METHODS Plasma levels of the glycocalyx components syndecan-1, heparan sulfate and hyaluronic acid were measured in 25 patients after immediate survival of cardiac arrest during different phases of PCAS. Twelve hemodynamically stable patients with acute coronary syndrome served as controls. RESULTS Cardiac arrest resulted in a significant increase in syndecan-1, heparan sulfate and hyaluronic acid levels compared to controls, indicating a shedding of the endothelial glycocalyx as a pathophysiological component of the post cardiac arrest syndrome. The time course differed between the individual glycocalyx components, with a higher increase of syndecan-1 in the early phase of PCAS (2.8-fold increase vs. controls) and a later peak of heparan sulfate (1.7-fold increase) and hyaluronic acid (2-fold increase) in the intermediate phase. Only the plasma levels of syndecan-1 correlated positively with the duration of CPR and negatively with the glycocalyx-protective protease inhibitor antithrombin III. Plasma levels of both syndecan-1 and heparan sulfate were higher in eventual non-survivors than in survivors of cardiac arrest. CONCLUSION Our data for the first time demonstrates a perturbation of the endothelial glycocalyx in immediate survivors of cardiac arrest and indicate a potential important role of this endothelial surface layer in the development of post-cardiac arrest syndrome.

Severe endothelial injury and subsequent repair in patients after successful cardiopulmonary resuscitation

IntroductionIschemia and reperfusion after cardiopulmonary resuscitation (CPR) induce endothelial activation and systemic inflammatory response, resulting in post-resuscitation disease. In this study we analyzed direct markers of endothelial injury, circulating endothelial cells (CECs) and endothelial microparticles (EMPs), and endothelial progenitor cells (EPCs) as a marker of endothelial repair in patients after CPR.MethodsFirst we investigated endothelial injury in 40 patients after CPR, 30 controls with stable coronary artery disease (CAD), and 9 healthy subjects, who were included to measure CECs and EMPs. In a subsequent study, endothelial repair was assessed by EPC measurement in 15 CPR, 9 CAD, and 5 healthy subjects. Blood samples were drawn immediately and 24 hours after ROSC and analyzed by flow cytometry. For all statistical analyses P < 0.05 was considered significant.ResultsThere was a massive rise in CEC count in resuscitated patients compared to CAD (4,494.1 ± 1,246 versus 312.7 ± 41 cells/mL; P < 0.001) and healthy patients (47.5 ± 3.7 cells/mL; P < 0.0005). Patients after prolonged CPR (≥30 min) showed elevated CECs compared to those resuscitated for <30 min (6,216.6 ± 2,057 versus 2,340.9 ± 703.5 cells/mL; P = 0.13/ns). There was a significant positive correlation of CEC count with duration of CPR (R2= 0.84; P < 0.01). EMPs were higher immediately after CPR compared to controls (31.2 ± 5.8 versus 19.7 ± 2.4 events/μL; P = 0.12 (CAD); versus 15.0 ± 5.2 events/μL; P = 0.07 (healthy)) but did not reach significance until 24 hours after CPR (69.1 ± 12.4 versus 22.0 ± 3.0 events/μL; P < 0.005 (CAD); versus 15.4 ± 4.4 events/μL; P < 0.001 (healthy)). EPCs were significantly elevated in patients on the second day after CPR compared to CAD (1.16 ± 0.41 versus 0.02 ± 0.01% of lymphocytes; P < 0.005) and healthy (0.04 ± 0.01; P < 0.005).ConclusionsIn the present study we provide evidence for a severe endothelial damage after successful CPR. Our results point to an ongoing process of endothelial injury, paralleled by a subsequent endothelial regeneration 24 hours after resuscitation.

Circulating annexin V positive microparticles in patients after successful cardiopulmonary resuscitation

IntroductionIschemia/reperfusion after cardiopulmonary resuscitation (CPR) induces systemic inflammatory response and activation of endothelium and coagulation, resulting in a post-cardiac arrest syndrome. We analysed circulating (annexin V+) microparticles and their conjugates in resuscitated patients.Methods36 patients after successful resuscitation, 20 control patients with stable cardiac disease and 15 healthy subjects were included prospectively. Two blood samples were drawn, one immediately and one 24 hours after return of spontaneous circulation (ROSC) to detect (annexin V+) monocyte-derived microparticles (MMPs) or procoagulant (annexin V+) platelet-derived microparticles (PMPs) and conjugates of endothelial-derived (annexin V+) microparticles (EMPs) with monocytes (EMP-MC) or platelets (EMP-PC). Measurements were performed by flow cytometric analysis. Additionally, the effect of isolated microparticles on cultured endothelial cells was assessed by ELISA.ResultsMMPs were significantly elevated immediately after ROSC compared to the cardiological control group (control; p < 0.01) and healthy subjects (healthy; p < 0.05) and persisted to be elevated in the following 24 hours after CPR (p < 0.05 vs. control and healthy, respectively). Procoagulant PMPs increased within the first 24 hours after ROSC (p < 0.01 vs. control and p < 0.005 vs. healthy). Conjugates of EMP with monocytes and platelets were both significantly elevated immediately after CPR (EMP-MC: p < 0.05 vs. control and p < 0.05 vs. healthy; EMP-PC: p < 0.05 vs. control and p < 0.05 vs. healthy), while only EMP-MC showed persisting high levels within 24 hours after CPR (p < 0.05 vs. control and p < 0.01 vs. healthy). MMP levels of ≥1.0/μL 24 hours after CPR predicted adverse outcome at 20 days (p < 0.05). Furthermore, isolated microparticles circulating in CPR patients early after ROSC led to enhanced endothelial apoptosis ex vivo compared to those of the healthy controls (p < 0.005).ConclusionsResuscitated patients show substantially increased levels of different (annexin V+) microparticles and their conjugates immediately and 24 hours after cardiopulmonary resuscitation, suggesting an early onset of inflammation, an ongoing endothelial activation and a procoagulatory state. Additionally, microparticles of CPR patients may contribute to endothelial apoptosis. These results point to an involvement of microparticles in the development of the post-cardiac arrest syndrome.

Suicide attempt by intravenous injection of gasoline: a case report.

BACKGROUND There is much experience with intoxication by aspiration of volatile hydrocarbon products, whereas intravenous injection of these distillates is rare. There are only few reports that describe a wide variety of associated pathological changes, predominantly in the pulmonary system. OBJECTIVES We report the case of an intravenous self-injection of gasoline by a young man in a suicide attempt. CASE REPORT Immediately after injecting gasoline, the 22-year-old man developed bradycardia, hypotension, and increasing dyspnea. Computed tomography scan of the chest showed signs consistent with diffuse alveolar-toxic damage to the lung. These symptoms and radiological findings are similar to those commonly observed after inhalation of this type of substance. This may have been due to diffusion of gasoline into the alveoli, where its presence leads to this characteristic damage. In this patient, gasoline entered the intramuscular tissue, and the patient developed a soft-tissue phlegmon at the forearm. At operation, gas emanation and superficial necrosis were noted. Nevertheless, the patients outcome was good, with full recovery within 3 weeks. CONCLUSIONS The major changes in this patient after intravenous injection of gasoline were in the pulmonary system, including hypoxemia and radiological findings that could be related to an exhalation of the volatile substance. In addition, gas in the musculature of the injection area caused a soft-tissue phlegmon.

Acute pulmonary embolism and a patent foramen ovale: analysis of atrial right-to-left shunting by biphasic transcardiopulmonary thermodilution curves.

A 69-year-old woman with an acute pulmonary embolism developed an intracardiac right-to-left shunt, which was diagnosed early on and quantified via biphasic transcardiopulmonary thermodilution curves. With transesophageal echocardiography, a patent foramen ovale and an impressive atrial right-to-left shunt were visualized.

The PAPIKAS trial: a comparative clinical trial of pulmonary catheter versus the PiCCO device during therapy of patients with acute heart failure and cardiogenic shock

Haemodynamic measurement plays an important role in the treatment of patients with acute heart failure and cardiogenic shock (CS). The pulmonary catheter (PAC) is a common device for enhanced haemodynamic measurement. The aim of this study was to evaluate the comparability of the PiCCO device with the PAC during the treatment of patients with CS; for example, the use of intra-aortic counterpulsion (intraaortic balloon pumping (IABP)), and therapeutic hypothermia after cardiac arrest.

Alterations of tissue-dependent microcirculation in patients after successful resuscitation

The crucial role of the microcirculation in improved neurological outcome in patients after successful resuscitation has been discussed for many years. New noninvasive imaging techniques enable the visualization and analysis of the microcirculation in vivo. Our study utilised an orthogonal polarization spectral (OPS) noninvasive imaging technique to test microcirculation in patients after successful resuscitation.