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PubMed2004

Impairment of endothelium-dependent dilation response after resuscitation from hemorrhagic shock involved postreceptor mechanisms.

Resuscitation from hemorrhagic shock is associated with impairment of the endothelium-dependent dilation response, whereas the dilation response induced by the endothelium-independent pathway, which is mediated by nitroprusside, a nitric oxide (NO) donor and a direct activator of guanylate cyclase, remains unaltered. Whether the impairment of the endothelium-dependent dilation response is caused by a specific receptor alteration or generally a defect in signal transduction pathway remains undetermined. Anesthetized rats were monitored for hemodynamics, and the terminal ileum was prepared for intravital videomicroscopy. Hemorrhage was 50% of mean arterial pressure for 60 min followed by resuscitation with the shed blood returned plus 2 volumes of normal saline. Intestinal microvascular reactivity to the endothelium-dependent receptor-dependent agonists acetylcholine or substance P (10(-8) or 10(-6) M), as well as the endothelium-dependent receptor-independent calcium ionophore, was determined at baseline and at 2 h postresuscitation from hemorrhagic shock. Measured vascular diameters for premucosal A3 arterioles (pA3 and dA3) were normalized and expressed as percentage of the maximal dilation capacity, as obtained from the response to the endothelium-independent NO donor sodium nitroprusside (10(-4) M). At 2 h postresuscitation, there was a marked constriction of pA3 (-70.1 +/- 20) and dA3 (-61.5 +/- 11.6) from maximal dilation capacity. Baseline premucosal arteriolar response to substance P (10(-8) M) was 30.68 +/- 4.19% and 34.66 +/- 5.82% for pA3 and dA3 arterioles, respectively. This was significantly reduced to 20.97 +/- 2.41% and 17.94 +/- 3.60% at 2 h postresuscitation. However, no significant difference between baseline and postresuscitation arteriolar responses was observed at the higher dose of substance P (10(-6) M). Postresuscitation premucosal arteriolar response to the endothelium-dependent receptor-independent calcium ionophore (10(-9) to 10(-5) M) is characterized by a marked decrease in sensitivity and an enhanced threshold for calcium ionophore-mediated dilation. The logEC50 was -7.62 +/- 0.39 and -7.75 +/- 0.32 for the pA3 and dA3 at baseline, respectively. This was significantly (P < 0.01) reduced to -5.15 +/- 0.14 and -4.39 +/- 0.71 at 2 h postresuscitation. These data suggest that impairment of the endothelium-dependent dilation response after resuscitation from hemorrhagic shock is not mediated by specific receptor alteration. Cellular mechanisms that participate in or are part of oxygen free radical formation after resuscitation from hemorrhagic shock such as Ca2+ and leukocytes, appear to have a pivotal role in the mechanism of cellular dysfunction.

Animals↗
PubMed1994

Haemodynamic evaluation during small volume resuscitation in patients with acute respiratory failure.

In addition to the invasive haemodynamic monitoring procedures, an on-line assessment of cardiac performance by means of transoesophageal echocardiography might have a certain role in small volume resuscitation of patients with acute respiratory failure or Adult Respiratory Distress Syndrome (ARDS). The goal of this investigation was therefore to determine the effects of a hypertonic hyperoncotic solution, hypertonic hydoxyethl-starch (HHES), (HHES = HES [200.000/0.6-0.66; 60 g l-1; Leopold, Graz; Austria] combined with NaCl [75 g l-1) on haemodynamics and cardiac performance using the transoesophageal echocardiography. After institutional approval we investigated 23 patients suffering from septic ARDS after trauma or major surgery during four periods of resuscitation. Phase I = control values after infusion of 20 ml kg-1 crystalloid solution, phase II = 50% hypertonic hydroxyethyl-starch solution (2 ml kg-1), phase III = at the end of HHES (4 ml kg-1), IV = 30 min after the end of HHES. Before HHES-infusion, all patients showed arterial hypotension with mean arterial pressures of 64 +/- 2 mmHg. The infusion of 2 ml kg-1 HHES resulted in a significant increase of systemic and pulmonary arterial pressures over the study period. A significant improvement in cardiac output was associated with increasing stroke volumes, oxygen delivery and oxygen consumption (see Tables 1 and 2). Small volume resuscitation also resulted in significant increases of endsystolic and endiastolic left ventricular areas and the corresponding calculated wall stress (Figs 1-3). We conclude from our preliminary data that when using HHES, only modest fluid resuscitation was sufficient to restore adequate preload and oxygen delivery in patients with sepsis-related acute respiratory failure.

Adolescent↗
PubMed2002

High survival in out-of-hospital cardiopulmonary resuscitation--7 years' incidence according to the Utstein template in a small town in Northern Norway.

Core data according to the Utstein template was compiled from all out-of-hospital resuscitations in the city of Bodø, Northern Norway, over 7 years (1992-98). Out of a population of 34,500, 149 resuscitations were attempted. A cardiac aetiology was present in 123 patients and their median age was 72.1 years. Eighteen of the 96 patients having suffered a witnessed arrest of cardiac origin were alive after 1 year (18.8%). Fifteen had the best cerebral performance score (scale 1-5) and three had a score of 2. Survival among all resuscitated patients (149) was 18.8% also, giving a number of 62 attempted resuscitations and 11.2 survivors per 100,000 inhabitants per year, respectively. Thirty-three per cent of witnessed cardiac arrests with ventricular fibrillation or ventricular tachycardia survived to discharge, but only 7% with asystole. When the arrest was witnessed, median response time was 5 minutes, and was 3 minutes for the survivors. To our knowledge, this is the highest survival of out-of-hospital arrests in Scandinavia reported so far, and is chiefly explained by short turnout distances.

Aged↗
PubMed2002

Are hypertonic hyperoncotic solutions safe for prehospital small-volume resuscitation? Results of a prospective observational study.

RATIONALE: This prospective observational study was designed to shed light on the routine use of a hypertonic hyperoncotic solution for prehospital small-volume resuscitation in trauma patients. Effects on homeostasis and haemodynamics as well as safety were evaluated. METHODS: One hundred patients with haemorrhagic shock were given hypertonic hyperoncotic solution (6% hydroxyethyl starch plus 7.5% sodium chloride) by bolus infusion (approximately 4 ml/kg bodyweight). Blood was taken before small-volume resuscitation and after the patients' arrival in the emergency room and serum electrolytes, haemoglobin, haematocrit, colloid osmotic pressure and white cell counts were determined. Haemodynamic variables were evaluated before small-volume resuscitation, just before transport and on arrival. RESULTS: Serum sodium and serum chloride increased at best moderately between baseline and arrival (7 and 12 mmol/l, medians; P<0.001) with peak increases of 25 mmol/l for serum sodium and 23 mmol/l for serum chloride. Serum potassium and white cell counts showed no more than minor changes. Haematocrit, haemoglobin and colloid osmotic pressure dropped (7%, 2.3 g/dl and 3.8 mmHg, respectively, medians; P<0.001). On arrival oxygen saturation and systolic and diastolic blood pressure had increased (5%, 30 and 20 mmHg, respectively), whereas heart rate had dropped by 15 b.p.m. (medians; P<0.001). Five patients developed heat sensations, restlessness, voiding urge, poor taste and vomiting, which may have been hypertonic hyperoncotic solution-related. CONCLUSION: Per-protocol bolus infusions of hypertonic hyperoncotic solution containing hydroxyethyl starch do not compromise homeostasis clinically and are rarely associated with clinically manifest side-effects. The treatment regimens used (including small-volume resuscitation) provide early and effective haemodynamic control.

Adult↗
PubMed2006

Out-of-hospital resuscitation in Estonia: a bystander-witnessed sudden cardiac arrest.

OBJECTIVE: To evaluate the results of the first epidemiological study on out-of-hospital resuscitation in Estonia. METHODS: A prospective cohort study of 2108 consecutive standardized reports on out-of-hospital resuscitation attempts from 1 January 1999 to 31 December 2002 was conducted according to the Utstein style. RESULTS: In all, 67.3% (1419/2108) of the cardiac arrests were of presumed cardiac aetiology and 60.2% (854/1419) of them were bystander-witnessed. Of these, the 28% bystander cardiopulmonary resuscitation was initiated, and the first rhythm was recorded as ventricular fibrillation or pulseless ventricular tachycardia in 40% of the cases. In the subgroup of patients with bystander-witnessed cardiac arrest of cardiac origin, 10.7% (91/854) were discharged alive in good cerebral performance categories and 7.7% were alive at the 1-year follow-up. The chances of survival increased if the median response time interval was <6 min, cardiac arrest occurred in a public place, patients received bystander cardiopulmonary resuscitation and had an initial rhythm of ventricular fibrillation or pulseless ventricular tachycardia. The discharge rate was 24% (82/343) in the subgroup of patients who had bystander-witnessed cardiac arrest of cardiac origin and an initial rhythm of ventricular fibrillation or pulseless ventricular tachycardia. In this subgroup, the survival rate was 42.6% (40/94) in Tartu urban area, 16.9% (22/130) in Tallinn urban area and 16.8% (20/119) in other regions of Estonia (mostly urban and suburban areas). CONCLUSION: The results demonstrate that despite the progress in the management of out-of-hospital cardiac arrest in Estonia, only one centre (Tartu) achieves a better survival rate. Further improvements are needed to raise the quality of the Estonian emergency medical services system, especially in rural areas.

Aged↗
PubMedDate not supplied

The impact of education on nurses' beliefs regarding family presence in a resuscitation room.

Allowing families to be present in the resuscitation room is an issue in sudden death situations. This study examined whether or not a class given to critical care and emergency nurses could change nurses' beliefs regarding the presence of family members in the resuscitation room. A convenience sample of 46 nurses was given a class regarding the benefits of families in the resuscitation room, present law, hospital policy, and how to implement this nursing action. The study used a quantitative, quasi-experimental study with a pre- and posttest design. It was found that nurses' beliefs regarding families in the resuscitation room during sudden death situations changed to a statistically significant level after attending a class. The study shows that an educational class can make a difference in the beliefs of nurses caring for families of sudden death victims.

Adult↗
PubMed2004

Precountershock cardiopulmonary resuscitation improves initial response to defibrillation from prolonged ventricular fibrillation: a randomized, controlled swine study.

OBJECTIVES: To compare immediate countershocks (defibrillation 1st) with precountershock cardiopulmonary resuscitation (CPR 1st) for prolonged ventricular fibrillation (VF). DESIGN: Randomized, controlled trial. SETTING: University animal laboratory. SUBJECTS: Thirty swine (27 +/- 1 kg). INTERVENTIONS: After 8 mins of untreated ventricular fibrillation, swine were randomly assigned to receive either immediate countershocks or CPR for 90 secs followed by countershocks. MEASUREMENTS AND MAIN RESULTS: After the first set of shocks, nine of 15 CPR 1st animals attained return of spontaneous circulation vs. 0 of 15 defibrillation 1st animals (p <.001), and pulseless electrical activity occurred in only one of 15 CPR 1st animals vs. ten of 15 defibrillation 1st animals (p <.01). The ultimate outcomes in the two groups were not different: Return of spontaneous circulation and 24-hr survival occurred in 15 of 15 CPR 1st and 13 of 15 defibrillation 1st animals. Good neurologic outcome at 24 hrs occurred in 12 of 15 CPR 1st and nine of 15 defibrillation 1st animals. None of the animals was successfully resuscitated with defibrillation alone; all successfully resuscitated animals were provided with chest compressions during the resuscitation. The ventricular fibrillation median frequency by fast Fourier transformation decreased during the untreated ventricular fibrillation interval in both groups (9.7 +/- 0.3 Hz and 10.1 +/- 0.2 Hz after 1 min vs. 8.8 +/- 0.3 Hz and 8.9 +/- 0.5 Hz at 8 mins, respectively). Because the ventricular fibrillation median frequency substantially increased after CPR 1st, it was much higher in the CPR 1st group before the first shock (15.1 +/- 0.9 Hz vs. 8.9 +/- 0.5 Hz, p <.001). The ventricular fibrillation median frequency before the first countershock was much higher in the animals that attained return of spontaneous circulation after the first set of shocks vs. those that did not (16.1 +/- 1.3 Hz vs. 10.0 +/- 0.6 Hz, p <.0001) CONCLUSIONS: Precountershock CPR can result in substantial physiologic benefits and superior response to initial defibrillation attempts compared with immediate defibrillation in the setting of prolonged ventricular fibrillation.

Animals↗
PubMed2004

Nonselective beta-blocking agent improves the outcome of cardiopulmonary resuscitation in a rat model.

OBJECTIVE: Postresuscitation myocardial dysfunction has been recognized as a leading cause of early death after initial successful resuscitation. Recent experimental and clinical studies have indicated that the beta-adrenergic effect of epinephrine significantly increases the severity of postresuscitation myocardial dysfunction. The fact that beta-adrenergic stimulation increases myocardial oxygen consumption during ventricular fibrillation is an important implication with respect to both the exogenous in terms of pharmacologic interventions during cardiopulmonary resuscitation and the endogenous as the result of intense sympathetic activation of cardiovascular collapse. Earlier experimental evidence has indicated that oxygenation improved by beta-blockade and beta1-blocking agent did offset the adverse effect of epinephrine. This prompted us to investigate the effect of beta-blockade on both exogenous and endogenous beta stimulation in an established rat model. DESIGN: Prospective, randomized, controlled study. SETTING: Animal research laboratory. SUBJECTS: Male Sprague-Dawley rats. INTERVENTIONS: In this series of studies, propranolol was administrated before ventricular fibrillation as a pretreatment combined with epinephrine treatment during precordial compression and then alone in a prolonged cardiac arrest setting. MEASUREMENTS AND MAIN RESULTS: Improved postresuscitation myocardial dysfunction (cardiac index, dP/dt40, -dP/dt) was observed with propranolol, a nonselective beta-adrenergic blocker, in pretreated animals such that the beneficial effects were associated with better postresuscitation survival. CONCLUSION: Nonselective beta-blockade improved the outcome of cardiopulmonary resuscitation in a rat model and deserves further evaluation in settings of cardiopulmonary resuscitation.

Adrenergic beta-Antagonists↗
PubMed2005

Clinical evaluation of an inspiratory impedance threshold device during standard cardiopulmonary resuscitation in patients with out-of-hospital cardiac arrest.

OBJECTIVE: To determine whether an impedance threshold device, designed to enhance circulation, would increase acute resuscitation rates for patients in cardiac arrest receiving conventional manual cardiopulmonary resuscitation. DESIGN: Prospective, randomized, double-blind, intention-to-treat. SETTING: Out-of-hospital trial conducted in the Milwaukee, WI, emergency medical services system. PATIENTS: Adults in cardiac arrest of presumed cardiac etiology. INTERVENTIONS: On arrival of advanced life support, patients were treated with standard cardiopulmonary resuscitation combined with either an active or a sham impedance threshold device. MEASUREMENTS AND MAIN RESULTS: We measured safety and efficacy of the impedance threshold device; the primary end point was intensive care unit admission. Statistical analyses performed included the chi-square test and multivariate regression analysis. One hundred sixteen patients were treated with a sham impedance threshold device, and 114 patients were treated with an active impedance threshold device. Overall intensive care unit admission rates were 17% with the sham device vs. 25% in the active impedance threshold device (p = .13; odds ratio, 1.64; 95% confidence interval, 0.87, 3.10). Patients in the subgroup presenting with pulseless electrical activity had intensive care unit admission and 24-hr survival rates of 20% and 12% in sham (n = 25) vs. 52% and 30% in active impedance threshold device groups (n = 27) (p = .018, odds ratio, 4.31; 95% confidence interval, 1.28, 14.5, and p = .12, odds ratio, 3.09; 95% confidence interval, 0.74, 13.0, respectively). A post hoc analysis of patients with pulseless electrical activity at any time during the cardiac arrest revealed that intensive care unit and 24-hr survival rates were 20% and 11% in the sham (n = 56) vs. 41% and 27% in the active impedance threshold device groups (n = 49) (p = .018, odds ratio, 2.82; 95% confidence interval, 1.19, 6.67, and p = .037, odds ratio, 3.01; 95% confidence interval, 1.07, 8.96, respectively). There were no statistically significant differences in outcomes for patients presenting in ventricular fibrillation and asystole. Adverse event and complication rates were also similar. CONCLUSIONS: During this first clinical trial of the impedance threshold device during standard cardiopulmonary resuscitation, use of the new device more than doubled short-term survival rates in patients presenting with pulseless electrical activity. A larger clinical trial is underway to determine the potential longer term benefits of the impedance threshold device in cardiac arrest.

Aged↗
PubMed2005

Resuscitation from experimental heatstroke by hyperbaric oxygen therapy.

OBJECTIVE: Heatstroke is characterized by hyperthermia, vasoplegic shock, and cerebral ischemia and hypoxia. Hyperbaric oxygen (HBO) has been shown to reduce brain ischemia and behavioral dysfunction during cerebral artery occlusion. The efficacy of HBO therapy for resuscitation from heatstroke remains to be determined in the laboratory. DESIGN: Anesthetized rats were randomized to several groups and administered: 1) no resuscitation (normobaric air) after onset of heatstroke, 2) HBO for 1 hr (100% oxygen at 253 kPa for 1 hr), 3) cyclic HBO intermitted by a 5-min air break for 1 hr of treatment (100% oxygen at 253 kPa), 4) hyperbaric air (air at 253 kPa for 1 hr), 5) normobaric hyperoxia (100% oxygen at 101 kPa for 1 hr), or 6) 8% HBO (hyperbaric 8% oxygen at 253 kPa for 1 hr). SETTING: Laboratory investigation. SUBJECTS: Sprague-Dawley rats (300- to 400-g males). INTERVENTIONS: Rats were exposed to an ambient temperature of 43 degrees C to induce heatstroke. Their colonic temperature; mean arterial pressure; heart rate; arterial blood levels of pH, Paco2, Pao2, So2%, and tumor necrosis factor-alpha; the cortical levels of ischemic and damage markers, and cortical neuronal damage scores were determined. The moment at which mean arterial pressure began to decrease from peak levels was arbitrarily taken as the onset of heatstroke. MAIN RESULTS: Survival time (interval between onset of heatstroke and animal death) was 19 +/- 1 (n = 10), 131 +/- 18 (n = 14), 159 +/- 28 (n = 13), 72 +/- 14 (n = 10), 68 +/- 12 (n = 10), and 45 +/- 11 (n = 10) mins, respectively, for normobaric air, HBO for 1 hr, cyclic HBO, hyperbaric air, normobaric hyperoxia, and 8% HBO groups. The heatstroke induced arterial hypotension and bradycardia, decreased arterial levels of pH, Pao2, and So2%, increased arterial levels of tumor necrosis factor-alpha, and increased values of cellular ischemia and damage markers. In addition, neuronal damage scores in the cortex were significantly reduced by HBO for 1 hr and cyclic HBO resuscitation. CONCLUSION: We successfully demonstrated that HBO and, to some extent, hyperbaric air, normobaric hyperoxia, or HBO 8% was found beneficial in resuscitating rats with experimental heatstroke. HBO effectively reduced heatstroke-induced arterial hypotension, hypoxia, plasma tumor necrosis factor-alpha overproduction, and cerebral ischemia and damage and improved survival.

Animals↗
PubMed2005

Use of an inspiratory impedance threshold device on a facemask and endotracheal tube to reduce intrathoracic pressures during the decompression phase of active compression-decompression cardiopulmonary resuscitation.

INTRODUCTION: Use of an inspiratory impedance threshold device (ITD) significantly increases coronary perfusion pressures and survival in patients ventilated with an endotracheal tube (ETT) during active compression-decompression cardiopulmonary resuscitation. We tested the hypothesis that the ITD could lower intratracheal pressures when attached to either a facemask or ETT. METHODS: An active and sham ITD were randomly applied first to a facemask and then to an ETT during active compression-decompression cardiopulmonary resuscitation in 13 out-of-hospital cardiac arrest patients in a randomized, double-blinded, prospective clinical trial. The compression-to-bag-valve ventilation ratio was 15:2. Airway pressures (surrogate for intrathoracic pressure) were measured with a pressure transducer. A sham and an active ITD were used for 1 min each in a randomized order, first on a facemask and then on an ETT. Statistical analyses were made using Friedman's and Wilcoxon's rank-sum tests. RESULTS: For the primary end point, mean +/- sd maximum negative intrathoracic pressures (mm Hg) during the decompression phase of cardiopulmonary resuscitation were -1.0 +/- 0.73 mm Hg with a sham vs. -4.6 +/- 3.7 mm Hg with an active ITD on the facemask (p = .003) and -1.3 +/- 1.3 mm Hg with a sham ITD vs. -7.3 +/- 4.5 mm Hg with an active ITD on an ETT (p = .0009). Decompression phase airway pressures with the facemask and ETT were not statistically different. CONCLUSIONS: Use of an active ITD attached to a facemask or an ETT resulted in a significantly lower negative intratracheal pressure during the decompression phase of active compression-decompression cardiopulmonary resuscitation when compared with controls. Airway pressures with an ITD on either a facemask or ETT were similar. The ITD-facemask combination was practical and enables rapid deployment of this life-saving technology.

Cardiography, Impedance↗
PubMed2005

Dose-dependent neuroprotection by 17beta-estradiol after cardiac arrest and cardiopulmonary resuscitation.

OBJECTIVE: Despite recent advances in the treatment of cardiac arrest, neurologic outcome remains poor. 17beta-Estradiol (E2) has been widely shown to reduce damage after experimental brain injury. The present study determined whether E2 also improves neuronal survival after experimental cardiac arrest and cardiopulmonary resuscitation and if any protection is dose-dependent. DESIGN: A randomized trial. SETTING: A research laboratory. SUBJECTS: Male C57Bl/6 mice weighing 20-25 g. INTERVENTIONS: Mice were randomized into one of six groups, receiving treatment with 0.5, 2.5, 12.5, 25, or 50 mug of E2 or vehicle 1.5 mins after return of spontaneous circulation. Ten minutes after induction of cardiac arrest (by KCl injection), cardiopulmonary resuscitation was initiated (with chest compressions, intravenous epinephrine, and ventilation with 100% O2). Additional animals of each E2-treated group were used for plasma estradiol-level analysis. Brains were removed for quantification of injury in the hippocampus and caudoputamen on day 3. MEASUREMENTS AND MAIN RESULTS: The E2 0.5 group had physiologic estrogen levels 60 min after injection (mean +/- se, 28 +/- 5 pg/mL), whereas the E2 50 group still showed supraphysiologic levels 360 min after administration (245 +/- 32 pg/mL). Hippocampal damage was not altered with E2 treatment. Only posttreatment with the lowest E2 dose (E2 0.5) resulted in attenuated neuronal injury in the rostral and caudal caudoputamen (34 +/- 11% and 27 +/- 11%), in comparison with vehicle (68 +/- 5, p < .05; 63 +/- 4%, p < .001). Higher E2 doses did not affect brain injury. CONCLUSIONS: We conclude that E2 has a critical dosing effect on neuronal survival, physiologic levels of E2 are neuroprotective after cardiac arrest/cardiopulmonary resuscitation, and acute exposure is sufficient for brain resuscitation.

Animals↗
PubMed2005

Effects of combined administration of vasopressin, epinephrine, and norepinephrine during cardiopulmonary resuscitation in pigs.

OBJECTIVE: Synergistic effects of epinephrine and vasopressin may be of benefit during cardiopulmonary resuscitation. However, cerebral perfusion was decreased when epinephrine was combined with vasopressin compared with vasopressin alone. Although a combined infusion of norepinephrine and vasopressin improves hemodynamic variables compared with norepinephrine alone during sepsis, it is unknown whether norepinephrine in addition to vasopressin and epinephrine changes vital organ perfusion during cardiopulmonary resuscitation. DESIGN: Prospective, randomized animal study. SETTING: : University hospital research laboratory. SUBJECTS: Twenty-one domestic pigs. INTERVENTIONS: After 4 mins of ventricular fibrillation and 3 mins of basic life support, the pigs were randomly assigned to receive either 200 microg/kg epinephrine, 0.4 units/kg vasopressin alone, or 45 microg/kg norepinephrine plus 45 microg/kg epinephrine plus 0.4 units/kg vasopressin before defibrillation. MEASUREMENTS AND MAIN RESULTS: Organ perfusion was determined by radiolabeled microspheres. Myocardial blood flow (mean +/- sem) before and 90 secs and 5 mins after drug administration was 8 +/- 2, 25 +/- 6, and 7 +/- 1 mL/min/100 g after high-dose epinephrine, 12 +/- 1, 75 +/- 7, and 60 +/- 10 mL/min/100 g after vasopressin, and 9 +/- 2, 95 +/- 26, and 46 +/- 15 mL/min/100 g after vasopressin/epinephrine/norepinephrine, respectively (p < .05 at 90 secs and 5 mins vasopressin vs. epinephrine and vasopressin/epinephrine/norepinephrine vs. epinephrine). At the same time points, cerebral blood flow was 8 +/- 2, 23 +/- 3, and 17 +/- 3 mL/min/100 g after epinephrine, 11 +/- 3, 55 +/- 7, and 52 +/- 7 mL/min/100 g after vasopressin, and 11 +/- 4, 67 +/- 13, and 53 +/- 12 mL/min/100 g after vasopressin/epinephrine/norepinephrine, respectively (p < .05 at 90 secs and 5 mins vasopressin vs. epinephrine and vasopressin/epinephrine/norepinephrine vs. epinephrine). Two of seven animals in the epinephrine group, four of seven animals in the vasopressin/epinephrine/norepinephrine group, and seven of seven animals in the vasopressin group could be successfully resuscitated (p < .05 vasopressin vs. epinephrine). CONCLUSIONS: Vasopressin with or without epinephrine and norepinephrine resulted in higher myocardial and cerebral perfusion than epinephrine alone, but there was no benefit in adding norepinephrine to vasopressin and epinephrine with regard to cardiac and cerebral blood flow during cardiopulmonary resuscitation.

Animals↗
PubMed2006

Effects of arginine vasopressin during resuscitation from hemorrhagic hypotension after traumatic brain injury.

OBJECTIVE: Two series of experiments were designed to evaluate whether early arginine vasopressin improves acute outcome following resuscitation from traumatic brain injury and severe hemorrhagic hypotension. DESIGN: Prospective randomized, blinded animal study. SETTING: University laboratory. SUBJECTS: Thirty-three swine. INTERVENTIONS: In series 1 (n = 19), after traumatic brain injury with hemorrhage and 12 mins of shock (mean arterial pressure approximately 20 mm Hg), survivors (n = 16) were initially resuscitated with 10 mL/kg crystalloid. After 30 mins, crystalloid and blood with either 0.1 unit x kg(-1) x hr(-1) arginine vasopressin or placebo was titrated to a mean arterial pressure target >or=60 mm Hg. After 90 mins, all received mannitol and the target was cerebral perfusion pressure >or=60 mm Hg. To test cerebrovascular function, 7.5% inhaled CO2 was administered periodically. In series 2 (n = 14), the identical protocol was followed except the shock period was 20 mins and survivors (n = 10) received a bolus of either arginine vasopressin (0.2 units/kg) or placebo during the initial fluid resuscitation. MEASUREMENTS AND MAIN RESULTS: In series 1, by 300 mins after traumatic brain injury with arginine vasopressin (n = 8) vs. placebo (n = 8), the fluid and transfusion requirements were reduced (both p < .01), intracranial pressure was improved (11 +/- 1 vs. 23 +/- 2 mmHg; p < .0001), and the CO2-evoked intracranial pressure elevation was reduced (7 +/- 2 vs. 26 +/- 3 mm Hg, p < .001), suggesting improved compliance. In series 2, with arginine vasopressin vs. placebo, cerebral perfusion pressure was more rapidly corrected (p < .05). With arginine vasopressin, five of five animals survived 300 mins, whereas three of five placebo animals died. The survival time with placebo was 54 +/- 4 mins (p < .05 vs. arginine vasopressin). CONCLUSIONS: Early supplemental arginine vasopressin rapidly corrected cerebral perfusion pressure, improved cerebrovascular compliance, and prevented circulatory collapse during fluid resuscitation of hemorrhagic shock after traumatic brain injury.

Animals↗
PubMed2006

Bovine polymerized hemoglobin (hemoglobin-based oxygen carrier-201) resuscitation in three swine models of hemorrhagic shock with militarily relevant delayed evacuation--effects on histopathology and organ function.

OBJECTIVE: To test our hypothesis that hemoglobin-based oxygen carrier (HBOC)-201 resuscitation in hemorrhagic shock (HS) will not lead to increased organ injury and dysfunction. DESIGN: Three swine HS models simulating military-relevant delayed evacuation: a) moderate controlled HS, b) severe controlled HS, and c) severe uncontrolled HS. SETTING: Military research laboratory. SUBJECTS: Swine. INTERVENTIONS: Swine were anesthetized/intubated and instrumented. To induce HS, in two controlled hemorrhage experiments, 40% (moderate controlled HS) or 55% (severe controlled HS) of blood volume was withdrawn; in an uncontrolled HS experiment, the liver was crushed/lacerated. During a 4-hr "prehospital phase," pigs were resuscitated with HBOC-201 (HBOC) or Hextend (HEX) or were nonresuscitated (NON). Upon "hospital arrival," liver injury was repaired (severe uncontrolled HS), blood or saline was infused, hemodynamics were monitored, and blood was collected. Upon animal death and/or 72 hrs, necropsy was followed by histopathologic evaluation of organ injury (hematoxylin and eosin, electron microscopy) and immunohistochemistry of oxidative potential (3-nitrotyrosine). Significance (p < .05) was assessed by Kruskal-Wallis, analysis of variance/Bonferroni, and mixed procedure tests. MEASUREMENTS AND MAIN RESULTS: Survival was significantly higher with HBOC than HEX only with severe uncontrolled HS (p = .002). Myocardial necrosis/fibroplasia, fluid requirements, cardiac output, and cardiac enzymes were generally similar or lower in HBOC than HEX pigs, but creatine kinase-MB (but not creatine kinase-MB/creatine kinase ratio) was higher with HBOC in moderate controlled HS. Alveolar/interstitial pulmonary edema was similar with HBOC and HEX, but Po2 was higher with HBOC in severe uncontrolled HS. Jejunal villar epithelial and hepatocellular necrosis were similarly minimal to moderate in all groups. Minimal biliary changes occurred exclusively with HBOC. Aspartate aminotransferase, lactate dehydrogenase, and alkaline phosphatase were generally higher with HBOC than HEX. Mild renal papillary injury occurred more frequently with HBOC, but consistent patterns for urine output, blood urea nitrogen, and creatinine, were not seen. The 3-nitrotyrosine staining intensity was not different. CONCLUSIONS: In comparison with hetastarch, HBOC-201 resuscitation of swine with HS increased survival (with severe HS), did not increase evidence of oxidative potential, and had histopathologic and/or functional effects on organs that were clinically equivocal (myocardium, lungs, hepatic parenchyma, jejunum, and renal cortex/medulla) and potentially adverse (hepatobiliary and renal papilla). The effects of HBOC-201-resuscitation in HS should be corroborated in controlled clinical trials.

Analysis of Variance↗
PubMed2007

Emergency preservation and delayed resuscitation allows normal recovery after exsanguination cardiac arrest in rats: a feasibility trial.

OBJECTIVE: Emergency preservation and resuscitation (EPR) comprise a novel approach for resuscitation of exsanguination cardiac arrest victims. EPR uses a cold aortic flush to induce deep hypothermic preservation, followed by resuscitation with cardiopulmonary bypass. Development of a rat EPR model would enable study of the molecular mechanisms of neuronal injury and the screening of novel agents for emergency preservation. DESIGN: A prospective, randomized study. SETTING: University research facility. SUBJECTS: Adult male Sprague-Dawley rats. INTERVENTIONS: Isoflurane-anesthetized rats were subjected to lethal hemorrhage (12.5 mL for 5 mins), followed by KCl-induced cardiac arrest and 1 min of no flow. Three groups (n=6) were studied: hypothermic EPR (H-EPR; 0 degrees C flush; target temperature, 15 degrees C); normothermic EPR (N-EPR; 38 degrees C flush); and controls. After 20 mins of H-EPR or N-EPR, resuscitation was initiated with cardiopulmonary bypass for 60 mins and mechanical ventilation. Controls were subjected to complete experimental preparation and anesthesia without cardiac arrest, followed by 60 mins of cardiopulmonary bypass and mechanical ventilation. Surviving rats were extubated 2 hrs later. Survival, Overall Performance Category (1, normal; 5, death), Neurologic Deficit Score, Histologic Damage Score, and biochemistry were assessed in survivors on day 7. MEASUREMENTS AND MAIN RESULTS: All rats in H-EPR and control groups survived, whereas none of the rats in the N-EPR group had restoration of spontaneous circulation. All rats in the H-EPR and control groups achieved Overall Performance Category 1, normal Neurologic Damage Score, and normal or near normal Histologic Damage Score and biochemical markers of organ injury. CONCLUSIONS: We have established an EPR model in rats showing no neurologic injury, despite an exsanguination cardiac arrest, followed by 20 mins of EPR using miniaturized cardiopulmonary bypass. Establishment of this model should facilitate application of molecular tools to study the effects of hypothermic preservation and reperfusion and to screen novel pharmacologic adjuncts.

Animals↗
PubMed2006

Haemodynamics of cardiac arrest and resuscitation.

PURPOSE OF REVIEW: This review will summarize the available data regarding the haemodynamic changes occurring following cardiac arrest in humans and animal models. RECENT FINDINGS: Following cardiac arrest due to ventricular fibrillation without cardiopulmonary resuscitation, blood flow exponentially falls but continues for approximately 5 min until the pressure gradient between the aorta and the right heart is completely dissipated. During cardiopulmonary resuscitation forward flow occurs into the aorta during the compression phase. Coronary blood flow is retrograde during the compression phase and antegrade during the decompression phase. Carotid blood flow takes over a minute to reach plateau levels following the initiation of chest compressions, and even brief interruptions of compressions result in a dramatic reduction in carotid blood flow which takes a minute or so to recover to plateau levels when compressions are reinstituted. Coronary perfusion pressure during the release phase of cardiopulmonary resuscitation has been shown to be a powerful predictor of the likelihood of recovery of spontaneous circulation following restoration of electrical activity. SUMMARY: Recent studies have provided important insights into the haemodynamics of cardiac arrest and of cardiopulmonary resuscitation which may inform more effective strategies for the management of cardiac arrest in the future.

Animals↗
PubMed2006

Physician experience with family presence during cardiopulmonary resuscitation in children.

OBJECTIVE: Family presence during cardiopulmonary resuscitation in children is an emerging practice. Although many hospitals allow this practice, there is scant research on physician attitudes and opinions and on physician views about training for resident physicians. DESIGN: Survey method. SETTING: University and community settings. PATIENTS: We randomly selected 1,200 pediatric critical care and emergency medicine providers from professional association mailing lists. INTERVENTION: The providers were mailed up to two written surveys and two reminder cards. The survey consisted of 40 multiple-choice and short-answer questions about demographics, past experiences, and opinions on pediatric family presence. MEASUREMENTS AND RESULTS: Of 1,200 surveys mailed, 521 were completed (43.4%) and 73 (6.1%) respondents returned the form declining to participate. More than 99% of respondents were physicians. Four hundred and thirty-three respondents (83%) reported participation in pediatric resuscitation with family members present, with a mean of 15 episodes ever and three episodes within the last year. Of those who had ever participated, more than half thought it was helpful for the family, and two thirds believed that parents wanted the option. Ninety-three percent would allow family presence in some situations. Seventy-four percent believed family presence would be stressful for a resident physician, but nearly 80% believed that residents working with children should be educated in this area. CONCLUSIONS: Family presence during cardiopulmonary resuscitation in children is not an uncommon experience for health care providers. Most respondents had resuscitated a child with family members present. The majority thought that presence was helpful to parents and that residents should be trained in this practice.

Adult↗