Minutes Of Arrest Research Articles

Abstract Su302: Impact of Time to Defibrillation on Mortality after In-Hospital Cardiac Arrest

Background: In-hospital cardiac arrest occurs in 290,000 patients annually in the United States, with less than 20% of these arrests featuring a shockable presenting rhythm. The three-phase model of CPR is separated into the electrical phase which occurs in the first 4 minutes, the circulatory phase which includes minutes 4-10, and the metabolic phase which is greater than 10 minutes from arrest onset. Defibrillation during the electrical phase has been proven to improve survival by approximately 50%. Current guidelines recommend defibrillation within the first 2 minutes of arrest in those with a rhythm of VT/VF. The purpose of this study was to determine the effect of time to defibrillation on mortality in patients with shockable rhythms. Methods: Full-disclosure rhythm strips for all cardiac arrests in non-ICU patients on telemetry were reviewed from Feb 2019 to April 2023. Time to defibrillation of shockable rhythms (VT/VF) was determined from the telemetry data and corresponding defibrillator data from the Zoll CodeNet electronic system. Results: We identified 32 of the 186 patients with cardiac arrest while on telemetry presenting with pulseless monomorphic VTor polymorphic VT/VF. The average time to defibrillation was 4.8 min ± 2.7 min. 34% of patients were defibrillated in 4 minutes or less from the onset of the arrythmia, 31% were defibrillated in more than 4 minutes from the onset of the arrythmia, and 34% were not defibrillated. Patients defibrillated in 4 minutes or less had a significantly lower mortality of 36.4% compared to a 50% mortality of those defibrillated in more than 4 minutes and 90.9% mortality in those not defibrillated (p<0.05).The patients who were not defibrillated were determined to have ongoing VT or poly VT/VF until telemetry was removed and the Zoll defibrillator pads were applied. They were ultimately deermined ot have PEA and were not shocked. Conclusions: Patients defibrillated in 4 minutes or less from the onset of a sustained shockable arrythmia experienced significantly lower mortality during hospitalization compared to those who were defibrillated in more than 4 minutes or were not defibrillated. 34% of patients with a shockable rhythm were not defibrillated due to a diagnosis of PEA after the Zoll pads were placed. Patients with sustained VT/VF causing in-hospital cardiac arrest should be defibrillated as soon as a defibrillator can be applied. Telemetry data should be clearly communicated to the code team.

Cardiac Arrest Due to Hypocalcemia

Fifty-nine-year-old male patient had a sudden cardiac arrest (CA) while waiting for his appointment at the urology outpatient clinic. The local staff and the rapid response team (RRT) promptly started cardiopulmonary resuscitation maneuvers. Initial CA rhythm was ventricular fibrillation (VF) and the collapse-shock interval was five minutes. Return of spontaneous circulation (ROSC) occurred on the following cycle, comprising six minutes of arrest. There was not enough time to administer epinephrine or any other drugs. After ROSC, a definitive airway was [...]

Abstract 268: Evaluation of the Abdominal Aortic and Junctional Tourniquet as an Adjunct to Chest Compressions in a Swine Model of Out-Of-Hospital Cardiac Arrest

Introduction: Overall success in treating out-of-hospital cardiac arrest using traditional chest compressions is low. The abdominal aortic and junctional tourniquet (AAJT) is a device with a wedge-shaped air bladder that can be used to occlude the descending aorta at the level of bifurcation. In addition to shunting blood away from the lower extremities, this device may increase pleural pressures by inhibiting movement of the diaphragm during compressions. We have previously shown that the addition of an AAJT to mechanical chest compression leads to an increase in rate of survival in a model of traumatic cardiac arrest. Hypothesis: This study was designed to determine if application of the AAJT would lead to more effective chest compressions as measured by an increased rate of return of spontaneous circulation (ROSC) and hemodynamic parameters. Methods: Yorkshire swine (n=6 per group) underwent general anesthesia and instrumentation. Ventricular fibrillation was electrically induced using spinal needles placed in contact with the left ventricle. After eight minutes of arrest, chest compressions were initiated. Animals were then allocated into groups with or without the AAJT. Following a total of ten minutes of compressions, the animals entered into a ten-minute advanced cardiac life support phase. Results: A ROSC was not achieved in either group. No significant differences were observed with coronary perfusion pressure or end tidal CO 2 . However, the AAJT group had a significantly higher carotid diastolic pressure and higher blood flow in the carotid as compared with repeated-measures ANOVA (p = 0.016 and 0.028 respectively). Conclusion: The AAJT did not confer a survival advantage during chest compressions in our swine model of cardiac arrest. However, while the AAJT was in place, improvement was observed in some measures of CPR efficacy. Disclaimer: The views expressed are those of the authors and do not reflect the official views or policy of the Department of Defense or its Components. The experiments reported herein were conducted according to the principles set forth in the National Institute of Health Publication No. 80-23, Guide for the Care and Use of Laboratory Animals and the Animal Welfare Act of 1966, as amended.

Mechanical adjuncts for cardiocerebral resuscitation

ABSTRACTIntroduction: Cardiac arrest remains a worldwide health problem with very poor outcome. In the absence of bystander resuscitation, survival rates decrease by 10% per minute of arrest and global ischemia. Even the best manual chest compressions, however, can only produce a fraction of normal cardiac output and blood flow to vital organs. Physiological principles and current evidence for the use of mechanical devices to increase survival and quality of life after cardiac arrest are highlighted in this review article.Areas covered: Mechanical adjuncts such as the Active Compression Decompression device, automated chest compressors and the use of a negative pressure valve (Impedance Threshold Device) can synergistically aid in improving quality of CPR and increasing cardiac output and vital organ perfusion.Expert opinion: The current conclusions that the use of mechanical adjunct devices in a preclinical setting is not recommended or neutral at best, need to be reevaluated, especially with regard to new advanced and promising treatments that require prolonged high-quality CPR during the transport to a hospital to improve the outcome of patients.

The Use of the Abdominal Aortic and Junctional Tourniquet During Cardiopulmonary Resuscitation Following Traumatic Cardiac Arrest in Swine.

Standard cardiopulmonary resuscitation (CPR) is ineffective in treating traumatic cardiac arrest (TCA) following hemorrhagic shock despite fluid resuscitation. CPR adjuncts, including abdominal compressions and external counter pressure, have shown some success in laboratory settings. The Abdominal Aortic and Junctional Tourniquet (AAJT) is a device that occludes both venous and arterial blood at the level of the aortic bifurcation and likely increases thoracic pressure when applied to the abdomen. We developed a swine model of controlled hemorrhage to induce a state of TCA to test the ability of the AAJT to improve the efficacy of CPR. Twelve splenectomized, Yorkshire, male swine (70-90 kg) were randomized into two groups: presence or absence of AAJT placement. Controlled hemorrhage was performed at a rate of 2 mL/kg/min until systolic blood pressure reached below 10 mm Hg (defined as cardiac arrest). Following 3 minutes of arrest, the animals underwent CPR using a mechanical compression device along with either the presence or absence of the AAJT. Concurrently, 5 units of whole blood (2,500 mL) were delivered through the jugular vein at 500 mL/min. Efficacy of CPR was assessed by analyzing rates of return of spontaneous circulation (ROSC) and survival. Blood pressure, carotid blood flow, and other hemodynamic values were also compared. No significant differences between groups were observed before treatments. The controlled hemorrhage resulted in an average loss of 2,654 ± 323 g of blood over 18.2 ± 3.9 minutes. All animals that had a ROSC survived to the end of the 1-hour observation period. Animals with AAJT survived 83% (5/6) compared to 17% (1/6) of animals without AAJT. Finally, blood pressure, carotid flow, mean pulmonary artery pressure, and end tidal carbon dioxide were all significantly different between groups at the end of the first 10-minute compression period. These results suggest that the AAJT could allow for increased CPR efficacy in cases of TCA when used in conjunction with rapid, massive blood transfusions.

Probability of Return of Spontaneous Circulation as a Function of Timing of Vasopressor Administration in Out-of-Hospital Cardiac Arrest

Introduction. Vasopressors (epinephrine and vasopressin) are associated with return of spontaneous circulation (ROSC). Recent retrospective studies reported a greater likelihood of ROSC when vasopressors were administered within the first 10 minutes of arrest. However, it is unlikely that the relationship between ROSC and the timing of vasopressor administration is a binary function (i.e., ≤10 vs. >10 minutes). More likely, this relationship is a function of time measured on a continuum, with diminishing effectiveness even within the first 10 minutes of arrest, and potentially, some lingering benefit beyond 10 minutes. However, this relationship remains undefined. Objective. To develop a model describing the likelihood of ROSC as a function of the call receipt to vasopressor interval (CRTVI) measured on a continuum. Methods. We conducted a retrospective study of cardiac arrest using the North Carolina Prehospital Care Reporting System (PREMIS). Inclusionary criteria were all adult patients suffering a witnessed, nontraumatic arrest during January–June 2012. Chi-square and t-tests were used to analyze the relationships between ROSC and CRTVI; patient age, race, and gender; endotracheal intubation (ETI); automated external defibrillator (AED) use; presenting cardiac rhythm; and bystander cardiopulmonary resuscitation (CPR). A multivariate logistic regression model calculated the odds ratio (OR) of ROSC as a function of CRTVI while controlling for potential confounding variables. Results. Of the 1,122 patients meeting inclusion criteria, 542 (48.3%) experienced ROSC. ROSC was less likely with increasing CRTVI (OR = 0.96, p < 0.01). Compared to patients with shockable rhythms, patients with asystole (OR = 0.42, p < 0.01) and pulseless electrical activity (OR = 0.52, p < 0.01) were less likely to achieve ROSC. Males (OR = 0.64, p = 0.02) and patients receiving bystander CPR (OR = 0.42, p < 0.01) were less likely to attain ROSC, although emergency medical services response times were significantly longer among patients receiving bystander CPR. Race, age, ETI, and AED were not predictors of ROSC. Conclusions. We found that time to vasopressor administration is significantly associated with ROSC, and the odds of ROSC declines by 4% for every 1-minute delay between call receipt and vasopressor administration. These results support the notion of a time-dependent function of vasopressor effectiveness across the entire range of administration delays rather than just the first 10 minutes. Large, prospective studies are needed to determine the relationship between the timing of vasopressor administration and long-term outcomes. Keywords: Epinephrine, cardiac arrest, emergency medical services, paramedic, resuscitation, CPR

Abstract 5083: Metaphase delays lead to chromosome cohesion fatigue, a novel mechanism underlying chromosome instability and aneuploidy

Abstract Cohesin fatigue describes our findings that cells delayed at metaphase undergo asynchronous separation of chromatids. We found that these unpaired chromatids randomly migrate on spindle microtubules or become merotelic, wherein a single centromere attaches to spindle fibers from both poles. Many cells eventually exit mitosis after cohesion fatigue, and the unpaired chromatids can form micronuclei, can rupture, and can mis-segregate. These results suggest that cohesion fatigue may cause gain or loss of whole chromosomes (numerical aneuploidy) as well as duplications, deletions, or translocations of large chromosome fragments (segmental aneuploidy). Numerical and segmental aneuploidies are hallmarks of cancer cells, often occurring together, and cohesion fatigue is a potential mechanism for simultaneously generating both. Any induced metaphase delay will lead to cohesion fatigue as long as spindle function is intact. Among mitotic defects, cohesion fatigue may be relatively common, but has often gone unrecognized since its detection requires continuous tracking of chromosome behavior. We have observed that cohesion fatigue is induced after metaphase arrest caused by RNAi-mediated depletion of the Ska (Spindle and kinetochore-associated) complex. Recently we discovered the underlying mechanism for the metaphase delay in Ska-depleted cells. We find that the Ska complex promotes chromosome binding and activity of the Anaphase-Promoting Complex/Cyclosome, the E3 ubiquitin ligase that controls anaphase onset and mitotic exit. Cohesion fatigue is also induced by certain drugs such as proteasome inhibitors, which are under development for cancer therapy. Using proteasome inhibition we found that cohesion fatigue initiates at centromeres and progresses along chromosome arms. While complete chromatid separation may occur after hours of metaphase arrest, our recent tracking reveals that abnormal centromere separation occurs after a few minutes of arrest. This early loss of centromere cohesion may lead to mitotic defects in cells that experience even a brief metaphase delay. Cohesion fatigue is not observed in cells arrested in mitosis with microtubule poisons because outward pulling forces on chromosomes are lost. In normal dividing cells, spontaneous mitotic defects are relatively rare, but these are substantially increased in transformed cells. Genes coding for components and regulators of the cohesin complex, which mediates sister chromatid cohesion, are among the most highly mutated genes in tumors. We propose that cohesin defects in cancer cells may exacerbate cohesion fatigue leading to increased chromosome instability. In carcinogenesis, cells that undergo metaphase delays are likely to generate mitotic errors through cohesion fatigue that result in numerical and segmental aneuploidy. Citation Format: John R. Daum, Sushama Sivakumar, Aaron R. Tipton, Michael W. Davidson, Gary J. Gorbsky. Metaphase delays lead to chromosome cohesion fatigue, a novel mechanism underlying chromosome instability and aneuploidy. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 5083. doi:10.1158/1538-7445.AM2014-5083

Cardiac Arrest 2012

Cardiac Arrest 2012

Quantitative Analysis of CPR Quality During In-Hospital Resuscitation of Older Children and Adolescents

Few data exist on pediatric cardiopulmonary resuscitation (CPR) quality. This study is the first to evaluate actual in-hospital pediatric CPR. We hypothesized that with bedside CPR training and corrective feedback, CPR quality can approach American Heart Association (AHA) targets. Using CPR recording/feedback defibrillators, quality of CPR was assessed for patients >or=8 years of age who suffered a cardiac arrest in the PICU or emergency department (ED). Before and during the study, a bedside CPR training program was initiated. Between October 2006 and February 2008, twenty events in 18 patients met inclusion criteria and resulted in 36749 evaluable chest compressions (CCs) during 392.3 minutes of arrest. CCs were shallow (<38 mm or <1.5 in) in 27.2% (9998 of 36749), with excessive residual leaning force (>or=2500 g) in 23.4% (8611 of 36749). Segmental analysis of the first 5 minutes of the events demonstrated that shallow CCs and excessive residual leaning force were less prevalent during the first 5 minutes. AHA targets were not achieved for CC rate in 62 (43.1%) of 144 segments, CC depth in 52 (36.1%) of 144 segments, and residual leaning force in 53 (36.8%) of 144 segments. This prospective, observational study demonstrates feasibility of monitoring in-hospital pediatric CPR. Even with bedside CPR retraining and corrective audiovisual feedback, CPR quality frequently did not meet AHA targets. Importantly, no flow fraction target of 10% was achieved. Future studies should investigate novel educational methods and targeted feedback technologies.

Abstract 4595: Intra-arrest Hypothermia Preserves Heart Akt Phosphorylation And Cardiac Function Following Cardiac Arrest In Wild-type But Not Akt(+/−) Mice

OBJECTIVE: To establish the role of Akt signaling in hypothermia protection following cardiac arrest. METHODS: Cardiac arrest was induced in anesthetized C57B6 wild-type (WT) and Akt1(+/−) heterozygous mice with an intravenous bolus of KCl. Animals were randomized to normothermia ( NT , 37°C) or hypothermia ( HT , 30°C) induced after 6 minutes of arrest and continued for 1 hour following return of spontaneous circulation (ROSC). After 8 minutes, resuscitation was attempted with chest compressions, mechanical ventilation, and fluid administration. Following ROSC, resuscitated animals were monitored for up to 4 hours. Total Akt and phosphorylated Akt (pAkt at Ser473 and Thr308) levels were measured by Western blot analysis in whole heart lysates from 4-hour survivors and shams (n=4 each group). RESULTS: In WT animals, 4-hour survival (HT = 7 of 8, NT = 3 of 8, p &lt; 0.04), cardiac output (p&lt;0.001) and left-ventricular dP/dt max (p&lt;0.001) were significantly improved in HT versus NT animals. In addition, hearts from WT animals randomized to HT displayed increased pAkt (Ser473) levels and over 8-fold higher pAkt(Thr308) levels compared to NT and sham groups (p&lt;0.001). These pAkt changes occurred despite total Akt levels remaining unchanged. Baseline hemodynamics prior to arrest were similar between WT and Akt(+/−) animals, while heart Akt1levels were decreased by approximately 40% in Akt(+/−) heterozygous mice. In contrast to WT mice, HT compared to NT had no effect on Akt(+/−) mouse 4-hour survival rates and left-ventricular hemodynamic measures. Compared to HT treated WT mice, Akt(+/−) animals treated with HT displayed significantly lower maximum left-ventricular pressure, stroke volume, and dP/dt max by 4 hours post-ROSC (p&lt;0.05). CONCLUSIONS: HT improves short-term cardiovascular outcomes and induces signficant heart Akt(Thr308) phosphorylation during the immediate post-ROSC period. The therapeutic benefit of intra-arrest HT on post-ROSC hemodynamics is greatly attenuated in Akt(+/−) animals, suggesting that Akt signaling may play a critical role in mediating HT protection.

Patterns of change in cytochrome c oxidase redox status

Investigators using mono channel near infrared spectroscopy (NIRS) have reported different patterns of change in cytochrome c oxidase (Cyt) in similar studies of tissue ischaemia. We investigated whether there were distinctive differences in NIRS signals obtained simultaneously from different sampling sites during the same imposed physiological intervention within the same subject. Methods: Subjects were 36, healthy, 10 kg, commercial swine undergoing cardiopulmonary bypass to initiate 3 to 7 periods of 7.5 minutes of circulatory arrest. Each arrest was initiated at one of 81 combinations of high, normal, or low levels of core temperature, haematocrit, pH, and serum glucose. Each combination was repeated twice, yielding 162 NIRS data sets. Results: Six distinct patterns of change of Cyt were found. Typically, brain Cyt quickly became reduced shortly after the start of arrest, muscle Cyt did not start becoming reduced until after 3½ minutes of arrest, and spinal cord Cyt either did not change status or became gradually reduced throughout the period of arrest. The brain response may reflect strong oxygen dependence, while the muscle response may indicate a dependency buffered by myoglobin stores, and the spine response may indicate a low concentration of available Cyt that is too diffuse to be rapidly influenced by changes in oxygen availability. Conclusion: Multi‒channel NIRS is needed for systemic evaluation of respiration at the cellular level in clinical settings. Distinctive Cyt patterns of change occur in different organs at the same time, in response to circulatory arrest.

Spontaneous agonal respiration in a swine model of out-of-hospital cardiac arrest.

To describe ventilatory dynamics following the onset of ventricular fibrillation (VF) in an experimental swine model. Twelve female mixed-breed domestic swine (mean mass 21.3 +/- 1.7 kg) were sedated with IM ketamine (10 mg/kg) and xylazine (1 mg/kg), anesthetized with alpha-chloralose (40 mg/kg loading dose, 10 mg/kg/hr maintenance infusion), intubated, and mechanically ventilated on room air. ECG, and aortic and pulmonary artery pressures were monitored continuously. VF was induced with a 3-sec, 60-Hz, 100-mA transthoracic shock, and left untreated for 8 minutes. Respiratory rate, tidal volume, and minute ventilation were recorded until respiratory activity ceased. All 12 animals (100%) had agonal respirations through the first 2 minutes of arrest. This decreased to 11 (92%) at minute 3, five (42%) at minute 4, and two (17%) at minute 7. Mean respiratory rates ranged from 6 to 11 breaths/min. Mean tidal volumes ranged from 502 to 852 mL. Mean minute ventilations ranged from 3.3 to 5.8 L. In this swine model, 11 of 12 (92%) continued to have spontaneous agonal respirations for the first 3 minutes of VF cardiac arrest. Many animals had supranormal tidal volumes, and near-normal minute ventilations. These findings have potential implications for lay-rescuer and first-responder contributions to resuscitation of victims of out-of-hospital cardiac arrest.

Spontaneous Agonal Respiration in a Swine Model of Out-of-Hospital Cardiac Arrest

Objective: To describe ventilator dynamics following the onset of ventricular fibrillation (VF) in an experimental swine model. Methods: Twelve female mixed-breed domestic swine (mean mass 21.3 2 1.7 kg) were sedated with IM ketamine (10 mag) and xylazine (1 mgntg), anesthetized with α-chloralose (40 mgkg loading dose, 10 mg/kg/hr rnaintenance infusion), incubated, and mechanically ventilated on room air. ECG, and aortic and pulmonary artery pressures were monitored continuously. VF was induced with a 3-sec, 60-Hz, 100-mA Tran thoracic shock, and left untreated for 8 minutes. Respiratory rate, tidal volume, and minute ventilation were recorded until respiratory activity ceased. Results: All 12 animals (100%) had agonal respirations through the first 2 minutes of arrest. This decreased to 11 (92%) at minute 3, five (42%) at minute 4, and two (17%) at minute 7. Mean respiratory rates ranged from 6 to 11 breathdmin. Mean tidal volumes ranged from 502 to 852 mL. Mean minute ventilations ranged from 3.3 to 5.8 L. Conclusion: In this swine model, 11 of 12 (92%) continued to have spontaneous agonal respirations for the first 3 minutes of VF cardiac arrest. Many animals had supernormal tidal volumes, and near-normal minute ventilations. These findings have potential implications for lay-rescuer and first-responder contributions to resuscitation of victims of out-of-hospital cardiac arrest.

Effect of cerebral blood flow generated during cardiopulmonary resuscitation in dogs on maintenance versus recovery of ATP and pH.

Cardiopulmonary resuscitation with external chest compression generates low perfusion pressures that may be inadequate for restoring cerebral metabolism and may worsen intracellular pH. We tested the hypothesis that cerebral reperfusion with a low perfusion pressure after arrest restores brain adenosine triphosphate (ATP) and pH to levels attained at the same perfusion pressure without preceding complete ischemia. Brain ATP and intracellular pH were measured by magnetic resonance spectroscopy, and cerebral blood flow was measured with microspheres in anesthetized dogs. External chest compressions were begun in group A (n = 6) immediately after the onset of arrest (ie, arrest time zero) and in group B (n = 10) after 6 minutes of arrest (ie, arrest time 6 minutes). In both groups, mean cerebral perfusion pressure was regulated at 30 mm Hg for 70 minutes by adjustment of inflation pressure of a pneumatic thoracic vest. At 12 minutes of resuscitation, cerebral blood flow was 27 +/- 4 mL/min per 100 g in group A and 21 +/- 4 mL/min per 100 g in group B, but ATP in group B (58 +/- 10% of prearrest) was less than in group A (105 +/- 6%). With prolonged resuscitation, ATP deteriorated to near zero levels in dogs in group B, with blood flow less than 15 mL/min per 100 g. Dogs with greater blood flow never achieved complete metabolic recovery. In group B, intracellular pH was unchanged from the 6.3 value at the start of resuscitation, even in those dogs with extremely low blood flows. Levels of cerebral perfusion pressure sufficient to maintain cerebral oxidative metabolism without complete ischemia during cardiopulmonary resuscitation are not sufficient to restore metabolism after complete ischemia during cardiopulmonary resuscitation. However, low "trickle" blood flow did not worsen intracellular acidosis.

Adult Basic Life Support

BASIC life support (BLS) is the phase of emergency cardiac care (ECC) that (1) prevents respiratory or circulatory arrest or insufficiency through prompt recognition and intervention or (2) supports the ventilation of a victim of respiratory arrest with rescue breathing or the ventilation and circulation of a victim of cardiac arrest with cardiopulmonary resuscitation (CPR). The major objective of performing rescue breathing or CPR is to provide oxygen to the brain and heart until appropriate, definitive medical treatment (advanced cardiac life support [ACLS]) can restore normal heart and ventilatory action. The prompt administration of BLS is the key to success. In respiratory arrest, the survival rate may be very high if airway control and rescue breathing are started promptly.¹For cardiac arrest the highest hospital discharge rate has been achieved in patients in whom CPR was initiated within 4 minutes of arrest and ACLS within 8 minutes.²Early

Blood-brain barrier disruption after cardiopulmonary resuscitation in immature swine.

We investigated blood-brain barrier permeability in 2-3-week-old anesthetized pigs during and after cardiopulmonary resuscitation. We assessed permeability by tissue uptake of radiolabeled aminoisobutyric acid, after correcting for plasma counts in tissue with radiolabeled inulin. Among 14 regions examined, the transfer coefficient of aminoisobutyric acid in nonischemic control animals ranged from 0.0018 +/- 0.0001 ml/g/min in diencephalon to 0.0049 +/- 0.0003 ml/g/min in cervical spinal cord. After 8 minutes of cardiac arrest followed by either 10 or 40 minutes of continuous sternal compression, there was no increase in the transfer coefficient. Likewise, during the immediate period after ventricular defibrillation, there was no increase in transfer coefficient despite the brief, transient hypertension. However, after 8 minutes of arrest, 6 minutes of cardiopulmonary resuscitation, and 4 hours of spontaneous circulation, the transfer coefficient was significantly increased by 59-107% in 10 of 11 regions rostral to the pons. Plasma volume in tissue measured by inulin was not elevated, suggesting that the increased transfer coefficient was not due to increased surface area. Thus, after an 8-minute period of complete ischemia, the blood-brain barrier remains intact during and immediately after resuscitation despite large vascular pressure fluctuations. However, in contrast to previous work on adult dogs, immature pigs are prone to a delayed increase in permeability, thereby allowing circulating substances greater access to the brain.

Cardiopulmonary bypass after cardiac arrest and prolonged closed-chest CPR in dogs

We studied a clinically realistic field-to-hospital scenario in dogs with four-minute ventricular fibrillation (VF) cardiac arrest followed by 30-minute standard external CPR basic life support (BLS). At the end of this 34-minute insult, cardiopulmonary bypass (CPB) was used for early defibrillation and assisted circulation for one hour (n = 10). Recovery was compared with that of control dogs (n = 10) in which standard CPR with advanced life support (ALS) for another 30 minutes was used for restoration of spontaneous circulation (ROSC). Both groups had hemodilution and heparinization; controlled blood pressure, blood gases, ventilation, and other parameters for 20 hours; and intensive care to 72 hours. During CPR-BLS of 30 minutes in both groups signs of cerebral viability returned. CPB achieved ROSC more successfully (ten of ten vs five of ten CPR-ALS controls) (P less than .02); and more rapidly, with less defibrillation energy (first countershock in eight of ten) and with less epinephrine (P less than .01). CPB improved 72-hour survival (seven of ten vs three of ten controls) (P less than .05). Between two and 24 hours, of those with ROSC, cardiac complications killed three of ten CPB dogs (after weaning), and two of five CPR-ALS dogs (NS). All seven CPB survivors to 72 hours were neurologically normal; of the three CPR-ALS survivors, one remained with severe neurologic deficit and two were neurologically normal (seven of ten CPB vs two of ten controls, P = .025). Starting CPR-BLS within four minutes of arrest can maintain cerebral viability.(ABSTRACT TRUNCATED AT 250 WORDS)

Motor evoked potentials in the dog

Motor evoked potentials (MEPs) in cats, rats, and humans have been reported. They appear promising as a test of central nervous system function, and they are sensitive not only to mechanical injury but also to ischemia. In mechanical trauma, the peripheral nerve response is much more sensitive to damage than the cord response, with a lower threshold and an earlier disappearance. We are reporting that the MEP can also be produced in the dog and that, under conditions of cardiac arrest induced by fibrillation, the peripheral nerve response disappears first at about 30 seconds and then the spinal cord response disappears at about 10 to 13 minutes. The late disappearance of the spinal cord response raises serious questions about its role as an adequate injury monitor. The most useful warning feature of the spinal cord response is an increase in amplitude during the critical first 2 minutes of arrest. Latency changes in the cord and peripheral nerve response did not seem as useful as amplitude changes in terms of providing adequate detection of injury. We also evaluated the peripheral nerve signals to determine whether they are partially volume-conducted weak muscle responses, and evidence substantiates their nonmuscle origin.

Three mechanical techniques of cardiopulmonary resuscitation in a canine model: 24-Hour survival and neurological outcome : Karl B. Kern, Alice B. Carpenter, Russell L. Showen, William D. Voorhees, Charles F. Babbs, Willis A. Tacker, Gordon A. Ewy. University of Arizona, Tucson, AZ 85721; Purdue University, West Lafayette, IN 47907

We studied the effect of nifedipine, a calcium entry blocker, on the recovery of cerebral adenosine triphosphate (ATP), creatine phosphate (CP), and lactate levels following resuscitation from cardiac arrest. Using the cardiac arrest and resuscitation model of de Garavilla, Babbs, and Tacker with an arrest time of eight minutes, 76% of the animals arrested were resuscitated with an average intermittent abdominal compression-CPR time of 3.3 minutes. Rats were assigned randomly to the following groups: nonischemic; eight minutes of arrest without resuscitation; and postresuscitation treatment with either IV normal saline; 3 μg/kg nifedipine; 10 μg/kg nifedipine; or 30 μg/kg nifedipine. Treated animals were sacrificed at either 20 or 120 minutes thereafter. As expected, after eight minutes of cardiac arrest, the levels of ATP and CP dropped to near 0 and rebounded in all resuscitated animals. By 120 minutes after resuscitation, rats given the 10-μg/kg dose of nifedipine had levels of ATP equivalent to nonischemic values. Return of CP values to nonischemic levels was seen only at the 3-μg/kg dose and was independent of time of measurement. The ATP and CP levels in these nifedipine-treated groups were significantly better when compared to saline-treated controls. There were no treatment-dependent differences in lactate levels. We conclude that clinically appropriate doses of nifedipine had a beneficial effect on the recovery of cerebral high-energy phosphates after cardiac arrest and resuscitation.

Effect of allopurinol and dimethylsulfoxide on long-term survival in rats after cardiorespiratory arrest and resuscitation

The effects of allopurinol and dimethylsulfoxide (DMSO) upon reperfusion injury were tested in separate studies that utilized a rat model of cardiorespiratory arrest and resuscitation. The rats were subjected to 7 minutes of arrest followed by resuscitation, and then were alternately assigned to either a drug-treated group or a vehicle-treated group (n = 22 for all groups). Drug treatment was given after the return of spontaneous circulation, and survival was monitored for a ten-day period. Study 1 utilized DMSO (50% solution, 1 ml/kg) as the test drug and saline solution as the vehicle. The percentages of surviving rats in the DMSO-treated and vehicle-treated groups were never statistically significantly different. There were 59% ( 13 23 ) of the DMSO-treated rats and 63% ( 14 22 ) of the vehicle-treated rats alive at one hour after resuscitation. Survival rates decreased to 18% ( 4 22 ) of DMSO-treated rats and 22% ( 5 22 ) of vehicle-treated rats on days 3 through 10. Allopurinol (25 mg/kg) was the test drug in study 2, and 0.18-M sodium hydroxide was the vehicle. The survival rate of resuscitated rats was statistically significantly greater at two days in the drug-treated group (68%, 15 22 ) than in the vehicle-treated group (36%, 8 22 ) (χ 2 = 4.46, df = 1, P < 0.05). The difference increased to a maximum of 68% ( 15 22 ) of the allopurinol-treated group versus 27% ( 6 22 ) of the vehicle-treated group at days 7 and 8 (χ 2 = 7.38, df = 1, P < 0.01), and remained statistically significant at day 10, with 64% ( 14 22 ) of allopurinol-treated versus 27% ( 6 22 ) of vehicle-treated rats alive (χ 2 = 5.87, df = 1, P < 0.05). Neurological deficit scores were not different between the drug-treated and vehicle-treated groups at day 10 in either study. It is concluded that reperfusion injury is preventable with allopurinol, but not DMSO, when given after successful resuscitation from cardiopulmonary arrest in the rat model. It is also speculated that allopurinol is the more effective drug because it blocks an early step in the initiation of free-radical-mediated injury.