Urban eddy covariance measurements reveal significant missing NOx emissions in Central Europe.

Nitrogen oxide (NOx) pollution is emerging as a primary environmental concern across Europe. While some large European metropolitan areas are already in breach of EU safety limits for NO2, this phenomenon does not seem to be only restricted to large industrialized areas anymore. Many smaller scale populated agglomerations including their surrounding rural areas are seeing frequent NO2 concentration violations. The question of a quantitative understanding of different NOx emission sources is therefore of immanent relevance for climate and air chemistry models as well as air pollution management and health. Here we report simultaneous eddy covariance flux measurements of NOx, CO2, CO and non methane volatile organic compound tracers in a city that might be considered representative for Central Europe and the greater Alpine region. Our data show that NOx fluxes are largely at variance with modelled emission projections, suggesting an appreciable underestimation of the traffic related atmospheric NOx input in Europe, comparable to the weekend-weekday effect, which locally changes ozone production rates by 40%.

Developing a vasopressor combination in a pig model of adult asphyxial cardiac arrest.

BACKGROUND: The purpose of this study was to investigate the effects of vasopressin versus epinephrine, and both drugs combined, in a porcine model of simulated adult asphyxial cardiac arrest. METHODS AND RESULTS: At approximately 7 minutes after the endotracheal tube had been clamped, cardiac arrest was present in 24 pigs and remained untreated for another 8 minutes. After 4 minutes of basic life support cardiopulmonary resuscitation, pigs were randomly assigned to receive, every 5 minutes, either epinephrine (45, 200, or 200 microgram/kg; n=6); vasopressin (0.4, 0.8, or 0.8 U/kg; n=6); or epinephrine combined with vasopressin (high-dose epinephrine/vasopressin combination, microgram/kg and U/kg: 45/0.4, 200/0.8, or 200/0.8; n=6; optimal-dose epinephrine/vasopressin combination, 45/0.4, 45/0.8, or 45/0.8; n=6). Mean+/-SEM coronary perfusion pressure was significantly (P<0.05) higher 90 seconds after high- or optimal-dose epinephrine/vasopressin combinations versus vasopressin alone and versus epinephrine alone (37+/-10 versus 25+/-7 versus 19+/-8 versus 6+/-3 mm Hg; 42+/-6 versus 40+/-5 versus 21+/-5 versus 14+/-6 mm Hg; and 39+/-6 versus 37+/-4 versus 9+/-3 versus 12+/-4 mm Hg, respectively). Six of 6 high-dose, 6 of 6 optimal-dose vasopressin/epinephrine combination, 0 of 6 vasopressin, and 1 of 6 epinephrine pigs had return of spontaneous circulation (P<0.05). CONCLUSIONS: Epinephrine combined with vasopressin, but not epinephrine or vasopressin alone, maintained elevated coronary perfusion pressure during cardiopulmonary resuscitation and resulted in significantly higher survival rates in this adult porcine asphyxial model.

Survival with full neurologic recovery and no cerebral pathology after prolonged cardiopulmonary resuscitation with vasopressin in pigs.

OBJECTIVES: We sought to determine the effects of vasopressin and saline placebo in comparison with epinephrine on neurologic recovery and possible cerebral pathology in an established porcine model of prolonged cardiopulmonary resuscitation (CPR). BACKGROUND: It is unknown whether increased cerebral blood flow during CPR with vasopressin is beneficial with regard to neurologic recovery or detrimental owing to complications such as cerebral edema after return of spontaneous circulation. METHODS: After 4 min of cardiac arrest, followed by 3 min of basic life support CPR, 17 animals were randomly assigned to receive every 5 min either vasopressin (0.4, 0.4 and 0.8 U/kg; n = 6), epinephrine (45, 45 and 200 microg/kg; n = 6) or saline placebo (n = 5). The mean value +/- SEM of aortic diastolic pressure was significantly (p < 0.05) higher 90 s after each of three vasopressin versus epinephrine versus saline placebo injections (60 +/- 3 vs. 45 +/- 3 vs. 29 +/- 2 mm Hg; 49 +/- 5 vs. 27 +/- 3 vs. 23 +/- 1 mm Hg; and 50 +/- 6 vs. 21 +/- 3 vs. 16 +/- 3 mm Hg, respectively). After 22 min of cardiac arrest, including 18 min of CPR, defibrillation was attempted to achieve return of spontaneous circulation. RESULTS: All the pigs that received epinephrine and saline placebo died, whereas all pigs on vasopressin survived (p < 0.05). Neurologic evaluation 24 h after successful resuscitation revealed only an unsteady gait in all vasopressin-treated animals; after 96 h, magnetic resonance imaging revealed no cerebral pathology. CONCLUSIONS: During prolonged CPR, repeated vasopressin administration, but not epinephrine or saline placebo, ensured long-term survival with full neurologic recovery and no cerebral pathology in this porcine CPR model.

The beneficial effect of basic life support on ventricular fibrillation mean frequency and coronary perfusion pressure.

BACKGROUND AND OBJECTIVE: Chest compressions before initial defibrillation attempts have been shown to increase successful defibrillation. This animal study was designed to assess whether ventricular fibrillation mean frequency after 90 s of basic life support cardiopulmonary resuscitation (CPR) may be used as an indicator of coronary perfusion and mean arterial pressure during CPR. METHODS AND RESULTS: After 4 min of ventricular fibrillation cardiac arrest in a porcine model, CPR was performed manually for 3 min. Mean ventricular fibrillation frequency and amplitude, together with coronary perfusion and mean arterial pressure were measured before initiation of chest compressions, and after 90 s and 3 min of basic life support CPR. Increases in fibrillation mean frequency correlated with increases in coronary perfusion and mean arterial pressure after both 90 s (R=0.77, P<0.0001, n=30; R=0.75, P<0.0001, n=30, respectively) and 3 min (R=0.61, P<0.001, n=30; R=0.78, P<0.0001, n=30, respectively) of basic life support CPR. Increases in fibrillation mean amplitude correlated with increases in mean arterial pressure after both 90 s (R=0.46, P<0.01; n=30) and 3 min (R=0.42, P<0.05, n=30) of CPR. Correlation between fibrillation mean amplitude and coronary perfusion pressure was not significant both at 90 s and 3 min of CPR. CONCLUSIONS: In this porcine laboratory model, 90 s and 3 min of CPR improved ventricular fibrillation mean frequency, which correlated positively with coronary perfusion pressure, and mean arterial pressure.

Analysing ventricular fibrillation ECG-signals and predicting defibrillation success during cardiopulmonary resuscitation employing N(alpha)-histograms.

Mean fibrillation frequency may predict defibrillation success during cardiopulmonary resuscitation (CPR). N(alpha)-histogram analysis should be investigated as an alternative. After 4 min of cardiac arrest, and 3 versus 8 min of CPR, 25 pigs received either vasopressin or epinephrine (0.4, 0.4, and 0.8 U/kg vasopressin versus 45, 45, and 200 microg/kg epinephrine) every 5 min with defibrillation at 22 min. Before defibrillation, the N(alpha)-parameter histogramstart/histogramwidth and the mean fibrillation frequency in resuscitated versus non-resuscitated pigs were 2.9+/-0.4 versus 1.7+/-0.5 (P=0.0000005); and 9.5+/-1.7 versus 6.9+/-0.7 (P=0.0003). During the last minute prior to defibrillation, histogramstart/histogramwidth of > or =2.3 versus mean fibrillation frequency > or =8 Hz predicted successful defibrillation with subsequent return of a spontaneous circulation for more than 60 min with sensitivity, specificity, positive predictive value and negative predictive value of 94 versus 82%, 96 versus 89%, 98 versus 93% and 90 versus 74%, respectively. We conclude, that N(alpha)-analysis was superior to mean fibrillation frequency analysis during CPR in predicting defibrillation success, and distinction between vasopressin versus epinephrine effects.

Fibrillation power, an alternative method of ECG spectral analysis for prediction of countershock success in a porcine model of ventricular fibrillation.

BACKGROUND: Noninvasive prediction of defibrillation success after cardiac arrest and cardiopulmonary resuscitation (CPR) may help in determining the optimal time for a countershock, and thus increase the chance for survival. METHODS: In a porcine model (n=25) of prolonged cardiac arrest, advanced cardiac life support was provided by administration of two or three doses of either vasopressin or epinephrine after 3 or 8 min of basic life support. After 4 min of ventricular fibrillation and 18 min of life support, defibrillation was attempted. The denoised power spectral density of 10 s intervals of the ventricular fibrillation electrocardiogram (ECG) was estimated from averaged and smoothed Fourier transforms. We have eliminated the spectral contribution of artifacts from manual chest compressions and provide a definition for the contribution of ventricular fibrillation to the power spectral density. This contribution is quantified and termed "fibrillation power". RESULTS: We tested fibrillation power and two established methods in their discrimination of survivors (n=16) vs. non-survivors (n=9) in the last minute before the countershock. A fibrillation power > or =79 dB predicted successful defibrillation with sensitivity, specificity, positive predictive value and negative predictive value of 98%, 98%, 99% and 97% while a mean fibrillation frequency > or =7.7 Hz was predictive with 85%, 83%, 90% and 77% and a mean amplitude > or =0.49 mV was predictive with 95%, 90%, 94% and 91%. CONCLUSIONS: We suggest that fibrillation power is an alternative source of information on the status of a fibrillating heart and that it may match the established mean frequency and amplitude analysis of ECG in predicting successful countershock during CPR.

Effects of epinephrine in a pig model of hypothermic cardiac arrest and closed-chest cardiopulmonary resuscitation combined with active rewarming.

OBJECTIVE: The aim of the current study was to assess the effects of epinephrine in a pig model of hypothermic cardiac arrest followed by closed-chest cardiopulmonary resuscitation combined with active rewarming, simulating the clinical management of an arrested hypothermic patient in a hospital without cardiopulmonary bypass facilities. DESIGN: Prospective, randomized animal study. SETTING: University research laboratory. SUBJECTS: Twelve 12- to 16-week-old domestic pigs. INTERVENTIONS: Pigs were surface cooled to a body core temperature of 28 degrees C. After 4 min of untreated cardiac arrest, manual closed-chest CPR and thoracic lavage with 40 degrees C warmed fluid were started. After 3 min of external chest compression animals were randomly assigned to receive epinephrine (45, 45 and 200 microg/kg) or saline placebo in 5-min intervals. MEASUREMENTS AND MAIN RESULTS: Coronary perfusion pressure was about 15 mmHg in placebo group pigs. Coronary perfusion pressure was significantly higher after epinephrine, but restoration of spontaneous circulation was not more frequent (one of six epinephrine versus three of six saline placebo pigs, P=0.34). After 45 microg/kg epinephrine the arterial PO(2) was significantly lower when compared to the saline placebo. The third 200 microg/kg epinephrine dose resulted in a significantly enhanced mixed venous hypercarbic acidosis. CONCLUSIONS: After a short 4-min period of hypothermic cardiac arrest, epinephrine may not be necessary to maintain coronary perfusion pressure around the threshold usually correlating with successful defibrillation, even during prolonged closed-chest CPR combined with active rewarming. The enhanced mixed venous hypercarbic acidosis in epinephrine-treated animals may support the argument against repeated or high dose epinephrine administration during hypothermic CPR.

Excellent coronary perfusion pressure during cardiopulmonary resuscitation is not good enough to ensure long-term survival with good neurologic outcome: a porcine case report.

PURPOSE: To report a case of cerebral ischemia confirmed by magnetic resonance imaging after successful cardiopulmonary resuscitation (CPR) complicated by acute respiratory injury. MATERIALS AND METHODS: After 4 min of cardiac arrest, followed by 3 min of basic life support CPR, a female pig weighing 38 kg received every 5 min vasopressin (0.4, 0.4 and 0.8 U/kg). After 22 min of cardiac arrest, including 18 min of CPR, one defibrillation attempt employing 100 J resulted in return of spontaneous circulation. Neurological evaluation was performed 24 and 96 h after successful CPR. Magnetic resonance imaging was carried out 4 days after CPR using a clinical 1.5 T scanner. The magnetic resonance imaging protocol consisted of fast spinecho T2-weighted, as well as spinecho T1-weighted imaging of the brain. RESULTS: CPR with vasopressin resulted in excellent coronary perfusion pressure ranging between 35 and 60 mm Hg throughout CPR. Eight minutes after initiation of chest compressions, bleeding out of the tracheal tube occurred. This was later confirmed as originating from bilateral bloody pulmonary infiltrations, resulting in acute respiratory injury in the post-resuscitation phase. Ninety-six hours after successful CPR, magnetic resonance imaging revealed bilateral diffuse cerebral vasogenic edema. CONCLUSION: Although excellent coronary perfusion pressure renders a return of spontaneous circulation more likely, complications such as acute respiratory injury in the post-resuscitation phase have to be managed carefully in order to ensure good neurological recovery from cardiac arrest.

Survey of effects of anesthesia protocols on hemodynamic variables in porcine cardiopulmonary resuscitation laboratory models before induction of cardiac arrest.

OBJECTIVE: An advantage of animal models in cardiopulmonary resuscitation (CPR) research is the possibility to control confounding variables that may be impossible to standardize in clinical trials. A neglected effect of the anesthesia protocol in porcine CPR studies may be its impact on hemodynamic variables before induction of cardiac arrest. Accordingly, the purpose of the study reported here was to evaluate published CPR reports with regard to their anesthesia protocol. METHODS: Of 100 articles that reported on laboratory models simulating cardiac arrest between 1987 and 1997 in peer-reviewed journals, 25 met inclusion criteria and were analyzed for values of coronary perfusion pressure, mean arterial pressure, heart rate, temperature, and cardiac index before induction of cardiac arrest. Subsequently, mean values for all animals in a given report were calculated and corrected for group size; statistical analysis was not performed since this was a survey only. RESULTS: Different anesthesia protocols resulted in a widely distributed pattern of hemodynamic variables prior to induction of cardiac arrest. Ranges compared with reference values were: heart rate, 100 to 122 beats/min versus 105+/-11 beats/min; mean arterial pressure, 68 to 130 mm Hg versus 102+/-9 mm Hg; coronary perfusion pressure, 55 to 114 mm Hg (no reference value); cardiac index, 69 to 152 ml/kg/min versus 147+/-22 ml/kg/min; body temperature, 37 to 38.5 degrees C versus 38.5+/-0.7 degrees C. CONCLUSION: The anesthesia protocol may have an impact on hemodynamic variables before induction of cardiac arrest in CPR studies.

The axillocoronary bypass. Blood flow and short-term graft histology in a porcine model.

BACKGROUND: Bypass grafts arising from the axillary artery may be indicated for complications during minimally invasive direct coronary artery bypass grafting, for redo operations and for management of a severely atherosclerotic ascending aorta. As basic data research on this technique is scanty, we investigated intraoperative function and postoperative morphology of axillocoronary bypass grafts in a porcine model. METHODS: Thirteen German domestic pigs received an axillocoronary vein graft (Group I, n=7) or an aortocoronary vein graft (Group II, n=6) to the left anterior descending artery. In Group I the proximal anastomosis was performed to the left axillary artery, and after partial rib resection the graft was brought transpleurally to the target vessel. In both groups the coronary anastomosis was carried out on the beating heart without cardiopulmonary bypass. Graft flow was measured using transit time ultrasonic flow probes. RESULTS: Intraoperatively all grafts showed a typical diastolic flow profile. Stable graft flow was lower in axillocoronary bypass grafts: 47 (30-60 mL/min) in Group I and 65 (35-126 mL/min) in Group II (p=0.005). Flow given as percentage of cardiac output, however, did not differ between the two grafts: 0.9 (0.6-1.2%) in Group I and 1.2 (0.8-2.4%) in Group II (p=NS). At day 4 after surgery there was no clear histologic predilection site for microtrauma and early degenerative changes in the axillocoronary graft. CONCLUSIONS: Axillocoronary bypass flow compares well with flow in the aortocoronary graft. Microtrauma after implantation and early degenerative changes in the axillocoronary vein bypass are not particularly impacted by the thoracic entry site.

[Drug therapy in cardiopulmonary resuscitation]. / Medikamentöse Therapie bei der kardiopulmonalen Reanimation.

In the year 2000, new international guidelines for cardiopulmonary resuscitation (CPR) were published by the American Heart Association, and the European Resuscitation Council. These guidelines are evidence-based, indicating that these recommendations are based primarily on interpretation of data from clinical studies. Levels of recommendation range from class I (proven safe and useful), class IIa (intervention of choice), IIb (alternative intervention), indeterminate (research stage), and class III (unacceptable, no benefit). Administration of drugs during CPR should be performed intravenously or intraosseously (class IIa) or, as a second-line approach, endotracheally (class IIb). Due to lack of evidence, the standard dose of 1 mg epinephrine to treat ventricular fibrillation, pulseless electrical activity, or asystole was categorized as class indeterminate; while a single dose of 40 units vasopressin to treat adults with shock-refractory ventricular fibrillation received a IIb recommendation. Owing to a lack of clinical data, the use of vasopressin was neither recommended to treat adults with pulseless electrical activity or asystole, nor for the use in children. Both endothelin and calcium were not recommended for routine use (class indeterminate). Careful titration of acid-base status with 1 mL/kg 8.4% sodium bicarbonate should only be administered if indicated by blood gas analysis (class indeterminate). If 1 mg epinephrine fails to be effective in adult patients with pulseless electrical activity or asystole, 1 mg atropine can be administered (class indeterminate). Regarding antiarrhythmic drugs, 300 mg amiodarone (class IIb) showed the best results in shock-refractory ventricular fibrillation. The postresuscitation phase has the goal to achieve the best possible neurological performance after return of spontaneous circulation, which requires careful optimization of organ functions.

Effect of fibrinogen on reversal of dilutional coagulopathy: a porcine model.

BACKGROUND: This study was conducted to determine whether replacement of fibrinogen is useful in reversing dilutional coagulopathy following severe haemorrhage and administration of colloids. METHODS: In 14 anaesthetized pigs, approximately 65% of the estimated blood volume was withdrawn and replaced with the same amount of gelatin solution to achieve dilutional coagulopathy. Animals were randomized to receive either 250 mg kg(-1) fibrinogen (n=7) or normal saline (n=7). A standardized liver injury was then inflicted to induce uncontrolled haemorrhage. Modified thrombelastography and standard coagulation tests were performed at baseline, after blood withdrawal, after dilution, after injection of the study drugs, and on conclusion of the protocol. Further, electron microscopy imaging of the blood clots was performed and blood loss after liver injury was determined. RESULTS: Severely impaired haemostasis was observed after haemodilution with gelatin substitution. With administration of fibrinogen, clot firmness and dynamics of clot formation reached baseline values. Median blood loss following liver injury was significantly less (P=0.018) in the fibrinogen-treated animals (1100 ml; 800-1400 ml) than in the placebo group (2010 ml; 1800-2200 ml). CONCLUSIONS: Replacing 65% of the estimated blood volume with gelatin in swine resulted in dilutional coagulopathy; subsequent fibrinogen administration improved clot formation and reduced blood loss significantly.

Employing vasopressin as an adjunct vasopressor in uncontrolled traumatic hemorrhagic shock. Three cases and a brief analysis of the literature.

Resuscitation of patients in hemorrhagic shock remains one of the most challenging aspects of trauma care. We showed in experimental studies that vasopressin, but not fluid resuscitation, enabled short-term and long-term survival in a porcine model of uncontrolled hemorrhagic shock after penetrating liver trauma. In this case report, we present two cases with temporarily successful cardiopulmonary resuscitation (CPR) using vasopressin and catecholamines in uncontrolled hemorrhagic shock with subsequent cardiac arrest that was refractory to catecholamines and fluid replacement. In a third patient, an infusion of vasopressin was started before cardiac arrest occurred; in this case, we were able to stabilize blood pressure thus allowing further therapy. The patient underwent multiple surgical procedures, developed multi-organ failure, but was finally discharged from the critical care unit without neurological damage.

Extended liver resection and hepatic ischemia in pigs: a new, potentially reversible model to induce acute liver failure and study artificial liver support systems.

BACKGROUND: Extended hepatectomy is a valid model for the study of acute liver failure. Since the porcine liver is comparable in size, morphology and anatomy to the human liver, we describe a technique employing hepatic ischemia and extended liver resection to induce acute liver failure in a porcine model as a means of studying bioartificial liver support. METHOD: A subtotal (75-80% resection) extended left hepatectomy was performed in 7 pigs after 60 min warm ischemia of the future remnant liver. After resection, the animals were given the best supportive care and observed until death. RESULTS: All animals died within 18-48 h, none as a result of surgical complications. Gross appearance of the liver showed severe steatosis of the right lateral lobe, and histology revealed severe coagulative necrosis of the whole lobule. CONCLUSION: This technique of extended liver resection after hepatic ischemia in the porcine model may be useful for studies of potentially reversible acute liver failure and experimental bioartificial support.

In-hospital resuscitation.

A recent world expert conference on resuscitation and emergency cardiac care led to evidence-based international guidelines for cardiopulmonary resuscitation (CPR). Several changes to CPR interventions were recommended, and will have to be implemented into clinical practice. The poor prognosis of patients who suffer in-hospital cardiac arrest may be improved with developments in CPR interventions. In the present review the most important changes recommended by the new CPR guidelines and the latest promising CPR investigations are described, focusing on their impact on in-hospital resuscitation.

Inhibition of nitric oxide improves coronary perfusion pressure and return of spontaneous circulation in a porcine cardiopulmonary resuscitation model.

OBJECTIVE: During spontaneous circulation, nonspecific inhibition of nitric oxide synthase by N(G)-nitro-L-arginine methyl ester (L-NAME) increases systemic vascular resistance and, therefore, mean arterial pressure. If this effect can be extrapolated to cardiopulmonary resuscitation (CPR), administering L-NAME during CPR may be beneficial by maintaining or even improving coronary perfusion pressure, and hence successful defibrillation. DESIGN: Prospective, randomized laboratory investigation using an established porcine model with instrumentation for hemodynamic variables, blood gases, and defibrillation attempt. SETTING: University medical center experimental laboratory. SUBJECTS: Ten domestic pigs. INTERVENTIONS: After 4 mins of ventricular fibrillation, ten animals were randomly assigned to receive L-NAME (25 mg/kg; n = 5) or saline placebo (n = 5) (given in two doses) after 3 and 13 mins of CPR, respectively. Defibrillation was provided 5 mins after the second dose of active drug or placebo. MEASUREMENTS AND MAIN RESULTS: Mean +/- sem coronary perfusion pressure was significantly (p < .05) higher 90 secs (27 +/- 3 vs. 17 +/- 3 mm Hg), 10 mins (28 +/- 3 vs. 14 +/- 2 mm Hg), and 15 mins (21 +/- 5 vs. 7 +/- 3 mm Hg) after the first L-NAME administration compared with saline placebo. Mean +/- sem coronary perfusion pressure remained significantly higher 90 secs and 5 mins after the second L-NAME vs. saline placebo administration (19 +/- 4 vs. 6 +/- 4 mm Hg, and 17 +/- 3 vs. 4 +/- 4 mm Hg). After 22 mins of cardiac arrest, including 18 mins of CPR, four of five pigs in the L-NAME group were successfully defibrillated, and survived the 60-min postresuscitation phase. In the placebo group, none of five pigs could be defibrillated successfully (p < .05). CONCLUSIONS: Nonspecific blockade of nitric oxide synthase with L-NAME during CPR was associated with an increase in coronary perfusion pressure and resulted in significantly better initial resuscitation when compared with saline placebo.

The effects of repeated doses of vasopressin or epinephrine on ventricular fibrillation in a porcine model of prolonged cardiopulmonary resuscitation.

This study evaluated ventricular fibrillation mean frequency and amplitude to predict defibrillation success in a porcine cardiopulmonary resuscitation (CPR) model using repeated administration of vasopressin or epinephrine. After 4 min of cardiac arrest and 3 min of CPR, 10 pigs were randomly assigned to receive either vasopressin (early vasopressin: 0.4, 0.4, and 0.8 units/kg, respectively, n = 5) or epinephrine (early epinephrine: 45, 45, and 200 microg/kg, respectively, n = 5). Another 11 animals were randomly allocated after 4 min of cardiac arrest and 8 min of CPR to receive every 5 min either vasopressin (late vasopressin: 0.4 and 0. 8 units/kg, respectively, n = 5) or epinephrine (late epinephrine: 45 and 200 microg/kg, n = 6). Ventricular fibrillation mean frequency and amplitude on defibrillation were significantly higher in the vasopressin groups than in the epinephrine groups, respectively. In vasopressin versus epinephrine animals, mean frequency immediately before defibrillation was 9.6 +/- 1.5 Hz vs 7. 0 +/- 0.7 Hz (P < 0.001), mean amplitude was 0.65 +/- 0.26 mV vs 0. 21 +/- 0.14 mV (P < 0.001, and coronary perfusion pressure was 27 +/- 9 mm Hg vs 8 +/- 4 mm Hg (P < 0.00001), respectively. In contrast to no epinephrine animals, all vasopressin animals were successfully defibrillated and survived 1 h (P < 0.05). Mean fibrillation frequency and amplitude predicted successful defibrillation and may serve as noninvasive markers to monitor continuing CPR efforts. Furthermore, vasopressin was superior to epinephrine in maintaining these variables above a threshold necessary for successful defibrillation.

Cardiopulmonary resuscitation after near drowning and hypothermia: restoration of spontaneous circulation after vasopressin.

Recent animal data have challenged the common clinical practice to avoid vasopressor drugs during hypothermic cardiopulmonary resuscitation (CPR) when core temperature is below 30 degrees C. In this report, we describe the case of a 19-year-old-female patient with prolonged, hypothermic, out-of-hospital cardiopulmonary arrest after near drowning (core temperature, 27 degrees C) in whom cardiocirculatory arrest persisted despite 2 mg of intravenous epinephrine; but, immediate return of spontaneous circulation occurred after a single dose (40 IU) of intravenous vasopressin. The patient was subsequently admitted to a hospital with stable haemodynamics, and was successfully rewarmed with convective rewarming, but died of multiorgan failure 15 h later. To the best of our knowledge, this is the first report about the use of vasopressin during hypothermic CPR in humans. This case report adds to the growing evidence that vasopressors may be useful to restore spontaneous circulation in hypothermic cardiac arrest patients prior to rewarming, thus avoiding prolonged mechanical CPR efforts, or usage of extracorporeal circulation. It may also support previous experience that the combination of both epinephrine and vasopressin may be necessary to achieve the vasopressor response needed for restoration of spontaneous circulation, especially after asphyxial cardiac arrest or during prolonged CPR efforts.

[Treatment of hemorrhagic shock. New therapy options]. / Die Behandlung des hämorrhagischen Schocks. Neue Therapieoptionen.

The future of shock treatment depends on the importance of scientific results, and the willingness of physicians to optimize, and to reconsider established treatment protocols. There are four major potentially promising approaches to advanced trauma life support. First, control of hemorrhage by administration of local hemostatic agents, and a better, target-controlled management of the coagulation system. Second, improving intravascular volume by recruiting blood from the venous vasculature by preventing mistakes during mechanical ventilation, and by employing alternative spontaneous (i.e. use of the inspiratory threshold valve) or artificial ventilation strategies. In addition, artificial oxygen carriers may improve intravascular volume and oxygen delivery. Third, pharmacologic support of physiologic, endogenous mechanisms involved in the compensation phase of shock, and blockade of pathomechanisms that are known to cause irreversible vasoplegia (arginine vasopressin and K(ATP) channel blockers for hemodynamic stabilization). Fourth, employing potentially protective strategies such as mild or moderate hypothermia. Finally, the ultimate vision of trauma resuscitation is the concept of "suspended animation" as a form of delayed resuscitation after protection of vital organ systems.

Repeated administration of vasopressin but not epinephrine maintains coronary perfusion pressure after early and late administration during prolonged cardiopulmonary resuscitation in pigs.

BACKGROUND: It is unknown whether repeated dosages of vasopressin or epinephrine given early or late during basic life support cardiopulmonary resuscitation (CPR) may be able to increase coronary perfusion pressure above a threshold between 20 and 30 mm Hg that renders defibrillation successful. METHODS AND RESULTS: After 4 minutes of cardiac arrest, followed by 3 minutes of basic life support CPR, 12 animals were randomly assigned to receive, every 5 minutes, either vasopressin (early vasopressin: 0.4, 0.4, and 0.8 U/kg, respectively; n=6) or epinephrine (early epinephrine: 45, 45, and 200 microg/kg, respectively; n=6). Another 12 animals were randomly allocated after 4 minutes of cardiac arrest, followed by 8 minutes of basic life support CPR, to receive, every 5 minutes, either vasopressin (late vasopressin: 0.4 and 0.8 U/kg, respectively; n=6), or epinephrine (late epinephrine: 45 and 200 microg/kg, respectively; n=6). Defibrillation was attempted after 22 minutes of cardiac arrest. Mean+/-SEM coronary perfusion pressure was significantly higher 90 seconds after early vasopressin compared with early epinephrine (50+/-4 versus 34+/-3 mm Hg, P<0.02; 42+/-5 versus 15+/-3 mm Hg, P<0.0008; and 37+/-5 versus 11+/-3 mm Hg, P<0. 002, respectively). Mean+/-SEM coronary perfusion pressure was significantly higher 90 seconds after late vasopressin compared with late epinephrine (40+/-3 versus 22+/-4 mm Hg, P<0.004, and 32+/-4 versus 15+/-4 mm Hg, P<0.01, respectively). All vasopressin animals survived 60 minutes, whereas no epinephrine pig had return of spontaneous circulation (P<0.05). CONCLUSIONS: Repeated administration of vasopressin but only the first epinephrine dose given early and late during basic life support CPR maintained coronary perfusion pressure above the threshold that is needed for successful defibrillation.