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PubMed2000

Early defibrillation and the chain of survival in 'in-hospital' adult cardiac arrest; minutes count.

OBJECTIVE: To report the outcomes from and the impact of the chain of survival in 'in-hospital' cardiac arrest where the presenting rhythm was VF/VT, the arrest was witnessed, defibrillation was conducted rapidly and no other resuscitation interventions were required. OUTCOME MEASURES: Any return of spontaneous circulation and discharge from hospital. METHODS: A 2-year prospective resuscitation audit using the Utstein style was conducted within a major London NHS Hospital Group. RESULTS: There were 124 patients who had primary VF/VT arrest. Eight were excluded from the study and 14 had non-witnessed cardiac arrest. Twenty one patients had witnessed VF/VT arrest but with delayed defibrillation, 81 patients had witnessed VF/VT arrest with rapid defibrillation, 69 patients had witnessed VF/VT arrest with rapid defibrillation, CPR and other additional interventions. There were 15 patients that had witnessed cardiac arrest with a presenting rhythm of VF/VT, who received rapid defibrillation and had no ventilation or chest compression prior to or following defibrillation. All 15 patients achieved a return of spontaneous circulation, and 12 were discharged alive. CONCLUSIONS: Rapid defibrillation prior to any other resuscitation intervention is associated with increased survival from witnessed VF/VT arrest in in-hospital cardiac arrest victims, and that the time to first shock is critical in enhancing the prospects of long-term survival in these patients.

Blood Circulation↗
PubMed1992

Results of electrophysiological testing and long-term follow-up in patients sustaining cardiac arrest only while receiving type IA antiarrhythmic agents.

UNLABELLED: Therapeutic management of patients sustaining a cardiac arrest while receiving antiarrhythmic agents can be difficult since the role of the drug in possibly facilitating the arrhythmia is often difficult to define. To determine if the response to programmed stimulation could give insight into which patients may have experienced a drug-induced cardiac arrest, we studied 29 patients (61 +/- 9 years) with no prior history of sustained ventricular tachyarrhythmias (VT) who suffered a cardiac arrest only while receiving type Ia antiarrhythmic agents. Patients with documented myocardial infarction, acute ischemia, electrolyte abnormalities, or torsade de pointes were excluded from the study. Twenty-four patients had coronary artery disease with prior myocardial infarction (ejection fraction 28% +/- 9%) and five patients had idiopathic dilated cardiomyopathy (ejection fraction 31% +/- 6%). During baseline electrophysiological testing, 19 patients (66%) had inducible sustained ventricular arrhythmias: uniform VT, n = 14 (group I), polymorphic VT or ventricular fibrillation, n = 5 (group II). Ten patients (group III) had no inducible sustained ventricular arrhythmias. To determine if rechallenge with a type Ia agent could facilitate induction of a sustained ventricular arrhythmia in group III, eight patients underwent ten electrophysiological studies during therapy with either procainamide or quinidine. Only two patients developed sustained VT in response to programmed stimulation. Patients in groups I and II received therapy guided by electrophysiological testing, including antiarrhythmic agents alone (n = 8), subendocardial resection (n = 4), or an implantable cardioverter defibrillator (n = 7). Patients in group III received antiarrhythmic agents empirically (n = 3), or for treatment of atrial tachyarrhythmias (n = 2) or nonsustained VT (n = 1). In addition, four patients in group III received an implantable cardioverter defibrillator. During a mean follow-up of 28 +/- 27 months (range: 1 day-84 months) 13 patients died suddenly or received a defibrillator shock preceded by syncope or presyncope: group I: n = 5; group II: n = 2; group III: n = 6. IN CONCLUSION: (1) most patients sustaining a cardiac arrest only in the presence of type Ia antiarrhythmic agents have inducible sustained VT in the absence of antiarrhythmic agents, and (2) the risk of recurrent VT persists in patients without inducible sustained arrhythmias in the drug-free state, regardless of whether they manifest inducible arrhythmias after rechallenge with a type Ia agent.

Aged↗
PubMed2006

Clinical neurophysiologic monitoring and brain injury from cardiac arrest.

Electrophysiologic testing continues to play an important role in injury stratification and prognostication in patients who are comatose after cardiac arrest. As discussed previously, however, the adage about treating whole patients, not just the numbers, is relevant in this situation. EEG and SSEP can offer high specificity for discerning poor prognosis as long as they are applied to appropriate patient populations. As discussed previously, EEG and SSEP patterns change during the first hours to days after cardiac arrest and negative prognostic information should not be based solely on studies performed during the first 24 hours. Both electrophysiologic techniques also are susceptible to artifacts that may worsen the electrical patterns artificially and suggest a falsely poor prognosis. EEG is suppressed by anesthetic agents and hypothermia, both of which may produce ECS and burst suppression. Patients who experience respiratory arrest from a toxic ingestion of narcotics or barbiturates, in particular, may present with high-grade EEG patterns initially. Many patients also receive anesthetic medications at the time of tracheal intubation, which may linger beyond their normal half-life in patients who have hepatic or renal insufficiency or concurrent use of interacting medications. SSEP is much less susceptible to sedative anesthetic agents, but hypothermia is demonstrated to prolong evoked potential latencies. As therapeutic hypothermia becomes more common after cardiac arrest, the effect of temperature on electrophysiologic testing needs to be taken into account. The publications discussed previously also emphasize the need to adjust the prognostic value of electro-physiologic tests to the pretest probability of meaningful neurologic recovery in individual patients. Clearly, grade I EEG patterns and normal N20 potentials indicate a much better prognosis in patients who have a short du-ration of cardiac arrest, short duration of coma after resuscitation, and when the studies are performed within the first few days. In patients who remain in coma days after resuscitation and lack appropriate brainstem reflexes, however, even the most normal appearing electrophysiologic patterns do little to change the overall prognosis. Aside from prognostication, electrophysiologic testing holds great promise in defining the basic anatomy and physiology of coma emergence after cardiac arrest. In addition, quantitative EEG and automated evoked potentials have the potential to render these tools less subjective and arcane and more applicable for monitoring patients in the period during and immediately after resuscitation. Quantitative EEG also has great potential asa tool to define the time window for neuroprotective intervention and the means to track the response to such therapies in real time.

Brain↗
PubMedDate not supplied

Frequency of anesthetic cardiac arrests in infants: effect of pediatric anesthesiologists.

STUDY OBJECTIVE: To determine whether the presence of pediatric anesthesiologists decreases the frequency of anesthetic-related cardiac arrests in infants (children who are 1 year of age or younger). DESIGN: A comparative retrospective study of anesthetics and cardiac arrests during a 7-year period. SETTING: The main operating room (OR) suite of a large university hospital. PATIENTS: All patients age 1 year or less undergoing surgical anesthesia from July 1983 through March 1990. INTERVENTIONS: Computerized anesthetic and operative patients records were queried for patient age, ASA physical status, body weight, surgical procedure, intraoperative complications, and the identity of the attending anesthesiologist. In each case, it was determined whether a pediatric anesthesiologist was in attendance and whether a cardiac arrest due to anesthesia occurred. Pediatric anesthesiologists were identified as those with pediatric fellowship training or the equivalent. The study population was divided into two groups: (1) the pediatric anesthesiologist group, with 2,310 patients whose anesthetics were supervised by pediatric anesthesiologists; (2) the nonpediatric anesthesiologist group, with 2,033 patients. MEASUREMENTS AND MAIN RESULTS: Mean age and weight were comparable in the two groups, and the distribution of physical status did not differ. No anesthesia-related cardiac arrests occurred in the pediatric anesthesiologist group; four anesthetic cardiac arrests occurred in the nonpediatric anesthesiologist group, for a frequency of 19.7 per 10,000 anesthetics. This difference between provider groups is significant (Fisher's exact probability test, p = 0.048). CONCLUSIONS: The results suggest that the use of pediatric anesthesiologists for all infants 1 year of age or younger might decrease anesthetic morbidity in this age-group.

Anesthesia↗
PubMed1996

End-tidal carbon dioxide changes during cardiopulmonary resuscitation after experimental asphyxial cardiac arrest.

A study was undertaken to determine the pattern of end-tidal carbon dioxide (ETCO2) changes during asphyxia-induced cardiac arrest in a pediatric canine model. Eleven intubated, anesthetized, paralyzed dogs (mean age, 4.1 mo; mean weight, 5.5 kg) were used. Asphyxia was induced by clamping the endotracheal tube (ETT) and discontinuing ventilation. Cardiac arrest ensued a few minutes later, after which closed-chest cardiopulmonary resuscitation (CPR) and ventilation were initiated. The ETCO2 level was recorded at baseline and every minute during CPR. Mean baseline ETCO2 was 31.9 mm Hg. The initial ETCO2 immediately after unclamping the ETT (mean, 35 mm Hg) was higher than subsequent values (mean, 12.4 mm Hg; P < .001). There was a sudden increase in ETCO2 to a mean of 27.0 mm Hg at or just before return of spontaneous circulation (ROSC) in all 11 cases (P < .01). During CPR, ETCO2 levels were initially high, decreased to low levels, and increased again at ROSC. This pattern, not previously described, is different from that observed in animal and adult cardiac arrest caused by ventricular fibrillation, during which ETCO2 decreases to almost zero after the onset of arrest, begins to increase after the onset of effective CPR, and increases to normal levels at ROSC. In this model of asphyxial arrest, continued cardiac output prior to arrest allows continued delivery Of CO2 to the lungs, resulting in higher alveolar CO2; this, in turn, is reflected as increased ETCO2 once ventilation is resumed during CPR. Further study is needed to determine whether the pattern Of ETCO2 changes can be used prospectively to define the etiology of cardiac arrest.

Animals↗
PubMed2000

Antiarrhythmic management and implantable defibrillator use in survivors of prehospital cardiac arrest without myocardial infarction in West Yorkshire.

OBJECTIVE: To explore the current use of secondary preventive treatment in survivors of out of hospital cardiac arrest without myocardial infarction (primary ventricular tachycardia/ventricular fibrillation (VT/VF)) in West Yorkshire, and assess the implications of recent studies on the benefits of implantable cardioverter-defibrillators (AICD) in this context. DESIGN: Retrospective analysis of an ambulance service based database of outcome after resuscitation of out of hospital cardiac arrest and the Leeds AICD implantation database. MAIN OUTCOME MEASURES: Mortality, rate of referral for specialist investigation, antiarrhythmic treatment. RESULTS: Twelve month mortality following successful discharge after primary VF arrest was 15%. Of 53 patients with primary VF/VT, 29 apparently did not see a cardiologist during the initial admission. Amiodarone was the most widely used antiarrhythmic agent. Six patients (15%) received an AICD. During the same period 22 patients from the same catchment area received an AICD following an in-hospital cardiac arrest. CONCLUSIONS: Mortality among survivors of non-infarct related prehospital cardiac arrest remains significant, with few patients being referred for specialist investigation. The implementation of recent guidelines on AICD use in cardiac arrest survivors would have resulted in an approximate 60% increase in the total numbers of defibrillators implanted in the West Yorkshire area.

Adult↗
PubMed2002

An analysis of time factors in out-of-hospital cardiac arrest in Osaka Prefecture.

OBJECTIVE: To ascertain important factors in the improvement of out-of-hospital cardiac arrest survival rates through analysis of data for Osaka Prefecture with the focus on time factors. DESIGN: Prospective cohort study according to the Utstein style. SETTING: Osaka Prefecture (population 8,830,000) served by a single emergency medical services system. PATIENTS: Consecutive prehospital cardiac arrests occurring between May 1998 and April 1999. MAIN OUTCOME MEASURES: One-year survival from cardiac arrest, and time factors. RESULT: Of the 5047 cases of confirmed cardiac arrests, resuscitation was attempted in 4871 subjects. Of the 982 cases of cardiac origin and witnessed by bystanders, 31 (3.2%) were still alive, and of the 576 cases of non-cardiac origin and witnessed by bystanders, ten (1.7%) were still alive at the 1 year follow-up. The median time from receipt of the emergency call until ambulance arrival was 5 min and that from receipt of the call until the start of cardiopulmonary resuscitation (CPR) was 7 min. For the 214 patients for whom defibrillation was attempted, the median time from receipt of the call until the first shock was 15 min. The median time from receipt of the call until departure of the ambulance from the scene was 16 min and that until arrival of the ambulance at a hospital was 22 min. CONCLUSIONS: This study using the standardized format according to the Utstein style clearly elucidates the specific delay of the start of defibrillation by paramedics and also indicates the inappropriate rule for this procedure in Japan.

Cardiopulmonary Resuscitation↗
PubMed2002

End tidal CO(2) is reduced during hypotension and cardiac arrest in a rat model of massive pulmonary embolism.

BACKGROUND: We investigated the effect of massive pulmonary embolism (MPE) on end tidal CO(2) (etCO(2)) and tested two hypotheses: (1) that etCO(2) can distinguish massive PE from hemorrhagic shock and (2) that PE with cardiac arrest reduces etCO(2) during resuscitation to a greater extent than arrhythmic cardiac arrest. METHODS: Anesthetized, mechanically ventilated rats (N=10 per group), were subjected to either graded PE (latex microspheres), or graded hemorrhagic shock to produce a final mean arterial blood pressure, (MAP) of 40 mmHg; a third group was subjected to surgical/anesthetic control conditions. Cardiac arrest was induced by the following methods: intravenous injection of a large bolus of microspheres in the PE group, aortic puncture in the hemorrhage group, and intravenous tetrodotoxin (TTX) to produce arrhythmic cardiac arrest in the control group. RESULTS: At a MAP of 40 mmHg, etCO(2) was significantly decreased in the PE group (18.3+/-1.9 torr) compared with both the hemorrhage (24.3+/-1.3) and the control group (35.0+/-1.3 torr; ANOVA P<0.001). The decreased etCO(2) occurred coincident with an increase in alveolar dead space fraction in the PE group. In the first minute of ventilation after cardiac arrest, the etCO(2) was significantly decreased in the PE group (6.5+/-0.9) versus both hemorrhage (16.5+/-1.1) and TTX (34.2+/-2.4 torr). CONCLUSIONS: Massive PE with shock decreases the etCO(2) and increases the dead space fraction to a greater extent than hemorrhagic shock at the same MAP. Cardiac arrest from PE is associated with extremely low etCO(2) readings during CPR.

Analysis of Variance↗
PubMed2006

Cardiocerebral resuscitation improves survival of patients with out-of-hospital cardiac arrest.

PURPOSE: The guidelines for cardiopulmonary resuscitation (CPR) have been in place for decades; but despite their international scope and periodic updates, there has been little improvement in survival rates in out-of-hospital cardiac arrest for patients who did not receive early defibrillation. The Emergency Medical Service directors in 2 rural Wisconsin counties initiated a new protocol for the pre-hospital management of adult cardiac arrest victims in an attempt to improve survival rates. The results observed after implementation of this protocol are presented and compared with those observed during a three-year period that preceded initiation of the project. METHODS: The protocol, based upon the principles of cardiocerebral resuscitation, was significantly different from the standard CPR protocol. A major objective was to minimize interruptions of chest compressions. Each defibrillation, including the first, was preceded by 200 uninterrupted chest compressions. Single shocks, rather than stacked shocks, were utilized. Post shock rhythm and pulse checks were eliminated, and chest compressions were resumed immediately after a shock was delivered. Initial airway management was limited to an oral pharyngeal device and supplemental oxygen. If the arrest was witnessed, assisted ventilations and intubation were delayed until either a return of spontaneous circulation or until three series of "compressions + analysis +/- shock" were completed. RESULTS: In the 3 years preceding the change in protocol, where standard CPR was utilized, there were 92 witnessed out-of-hospital adult cardiac arrests with an initially shockable rhythm. Eighteen patients survived, and 14 of 92 (15%) were neurologically intact. After implementing the new protocol in early 2004, there were 33 witnessed out-of-hospital adult cardiac arrests with an initially shockable rhythm. Nineteen survived, and 16 of 33 (48%) were neurologically normal. Differences in both total and neurologically normal survival are significant (chi-squared = 0.001). CONCLUSION: Instituting the new cardiocerebral resuscitation protocol for managing prehospital cardiac arrest improved survival of adult patients with witnessed cardiac arrest and an initially shockable rhythm.

Adult↗
PubMed1998

The effect of cold cardioplegic cardiac arrest and electrically induced ventricular fibrillation on human cardiac beta-adrenoceptors during open-heart surgery.

This study was designed to test the hypothesis that distinct alterations in cardiac beta-adrenoceptors (betaARs) may occur during cardiopulmonary bypass (CPB) alone, during CPB with cold cardioplegic cardiac arrest (CCCA), and during CPB with electrically induced ventricular fibrillation (EIVF). We assessed the density and affinity of right atrial betaARs in 27 patients undergoing open-heart surgery by (-)-[125I]iodocyanopindolol binding before CPB, defined as the "control," immediately after initiation, defined as "before," and immediately before the cessation of CCCA or EIVF, defined as "after." The density of betaARs was equivalent between the "control" and "before" groups; however, during CPB with EIVF, the density of betaARs decreased significantly (P < 0.001), whereas during CPB with CCCA, it increased significantly (P < 0.01). The rate of changes of the betaAR density was not correlated with the "before"-"after" interval, and the affinity of the betaARs did not change throughout these CPBs. These findings demonstrate that: CPB alone does not affect cardiac betaARs, at least until the onset of EIVF or CCCA; CPB with EIVF induces rapid desensitization of cardiac betaARs; and CPB with CCCA induces rapid sensitization of cardiac betaARs.

Adolescent↗
PubMed1994

Idiopathic ventricular fibrillation in out-of-hospital cardiac arrest survivors.

This study examined diagnostic and therapeutic roles of electrophysiological testing and long-term clinical outcome after out-of-hospital cardiac arrest due to idiopathic ventricular fibrillation. This is defined as ventricular fibrillation occurring in the absence of detectable underlying heart disease or metabolic or electrolyte disturbance. Out-of-hospital cardiac arrest resulting from idiopathic ventricular fibrillation is uncommon. Records of all patients who underwent electrophysiological testing between June 1979 and June 1992 were reviewed. Patients with out-of-hospital cardiac arrest due to idiopathic ventricular fibrillation were identified. Follow-up information was obtained by telephone interview in June 1992. Of 194 patients who underwent electrophysiological study after out-of-hospital cardiac arrest not associated with acute myocardial infarction, only six (4 male and 2 female) had idiopathic ventricular fibrillation. It was induced in only two patients by programmed ventricular stimulation. No sustained ventricular arrhythmias were induced in the remaining four patients. Four patients received implantable cardioverter defibrillators, one was treated with a beta-adrenergic blocker, and one received no treatment. All patients were alive at a mean follow-up of 50 months. Two of the four patients without inducible sustained ventricular arrhythmias had events during follow-up. Of the two patients with inducible ventricular fibrillation, one experienced a cardiac arrest and documented ventricular fibrillation at 41 months after the index event and the other had had no recurrence at 15-month follow-up. All four patients with implantable cardioverter defibrillators were alive at last follow-up, and two had device discharges.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

Active compression-decompression resuscitation: effect on resuscitation success after in-hospital cardiac arrest.

OBJECTIVES: The purpose of this study was to test the hypothesis that active compression-decompression would improve resuscitation success in human subjects after cardiac arrest. BACKGROUND: Active compression-decompression cardiopulmonary resuscitation is a new method that improves cardiopulmonary hemodynamic function in animal models and humans after cardiac arrest. METHODS: We conducted a prospective randomized clinical trial in patients with in-hospital cardiac arrest. Patients were assigned to receive standard manual or active compression-decompression cardiopulmonary resuscitation. The primary study end points were spontaneous return of circulation, 24-h survival and survival to hospital discharge. RESULTS: Fifty-three consecutive patients after cardiac arrest undergoing 64 resuscitation attempts were studied (30 women, 23 men; mean [+/- SD] age 71 +/- 13 years, range 38 to 96). Spontaneous return of circulation was observed in 24 (47%) of 53 patients and was increased in patients receiving active compression-decompression compared with those receiving standard manual cardiopulmonary resuscitation (15 [60%] of 25 vs. 9 [32%] of 28, respectively, p = 0.042); 24-h survival was increased (12 [48%] of 25 vs. 6 [21%] of 28, respectively, p = 0.041); and there was a trend toward improved survival to hospital discharge (6 [24%] of 25 vs. 3 [11%] of 28, respectively, p = 0.198) when active compression-decompression was compared with standard manual cardiopulmonary resuscitation. CONCLUSIONS: Active compression-decompression cardiopulmonary resuscitation improves return of spontaneous circulation and 24-h survival after in-hospital cardiac arrest. Active compression-decompression cardiopulmonary resuscitation appears to be a beneficial adjunct to standard manual cardiopulmonary resuscitation.

Aged↗
PubMed2006

Pediatric defibrillation after cardiac arrest: initial response and outcome.

INTRODUCTION: Shockable rhythms are rare in pediatric cardiac arrest and the results of defibrillation are uncertain. The objective of this study was to analyze the results of cardiopulmonary resuscitation that included defibrillation in children. METHODS: Forty-four out of 241 children (18.2%) who were resuscitated from inhospital or out-of-hospital cardiac arrest had been treated with manual defibrillation. Data were recorded according to the Utstein style. Outcome variables were a sustained return of spontaneous circulation (ROSC) and 1-year survival. Characteristics of patients and of resuscitation were evaluated. RESULTS: Cardiac disease was the major cause of arrest in this group. Ventricular fibrillation (VF) or pulseless ventricular tachycardia (PVT) was the first documented electrocardiogram rhythm in 19 patients (43.2%). A shockable rhythm developed during resuscitation in 25 patients (56.8%). The first shock (dose, 2 J/kg) terminated VF or PVT in eight patients (18.1%). Seventeen children (38.6%) needed more than three shocks to solve VF or PVT. ROSC was achieved in 28 cases (63.6%) and it was sustained in 19 patients (43.2%). Only three patients (6.8%), however, survived at 1-year follow-up. Children with VF or PVT as the first documented rhythm had better ROSC, better initial survival and better final survival than children with subsequent VF or PVT. Children who survived were older than the finally dead patients. No significant differences in response rate were observed when first and second shocks were compared. The survival rate was higher in patients treated with a second shock dose of 2 J/kg than in those who received higher doses. Outcome was not related to the cause or the location of arrest. The survival rate was inversely related to the duration of cardiopulmonary resuscitation. CONCLUSION: Defibrillation is necessary in 18% of children who suffer cardiac arrest. Termination of VF or PVT after the first defibrillation dose is achieved in a low percentage of cases. Despite a sustained ROSC being obtained in more than one-third of cases, the final survival remains low. The outcome is very poor when a shockable rhythm develops during resuscitation efforts. New studies are needed to ascertain whether the new international guidelines will contribute to improve the outcome of pediatric cardiac arrest.

Adolescent↗
PubMed1993

Racial differences in the incidence of cardiac arrest and subsequent survival. The CPR Chicago Project.

BACKGROUND: Differences between blacks and whites have been reported in the incidence of several forms of cardiovascular disease, including hypertension and stroke. We examined racial differences in the incidence of cardiac arrest in a large urban population and in subsequent survival. METHODS: We collected data on all nontraumatic, out-of-hospital cardiac arrests in Chicago from January 1, 1987, through December 31, 1988, and compared the incidence and survival rates for blacks and whites. We examined the association between survival and race and seven other known risk factors by logistic-regression analysis. We computed incidence rates by coupling our data with U.S. Census population data. RESULTS: Our study population comprised 6451 patients: 3207 whites, 2910 blacks, and 334 persons of other races. The incidence of cardiac arrest was significantly higher for blacks than for whites in every age group. The survival rate after cardiac arrest was 2.6 percent in whites, as compared with 0.8 percent in blacks (P < 0.001). Blacks were significantly less likely to have a witnessed cardiac arrest, bystander-initiated cardiopulmonary resuscitation, or a "favorable" initial rhythm or to be admitted to the hospital. When they were admitted, blacks were half as likely to survive. The association between race and survival persisted even when other recognized risk factors were taken into account. We did not find important differences between blacks and whites in the response times of the emergency medical services. CONCLUSIONS: The black community in our study was at higher risk for cardiac arrest and subsequent death than the white community, even after we controlled for other variables.

Adolescent↗
PubMed2006

Induced hypothermia following out-of-hospital cardiac arrest; initial experience in a community hospital.

BACKGROUND: Successful resuscitation from sudden cardiac death is frequently accompanied by severe and often fatal neurologic injury. Induced hypothermia (IH) may attenuate the neurologic damage observed in patients after cardiac arrest. HYPOTHESIS: This study examined a population of nonselected patients presenting to a community hospital following successful resuscitation of sudden cardiac death. We sought to determine whether a program of induced hypothermia would improve the clinical outcome of these critically ill patients. METHODS: We initiated a protocol of IH at the Oklahoma Heart Hospital in August of 2003. Study patients were consecutive adults admitted following successful resuscitation of out-of-hospital cardiac arrest. Moderate hypothermia was induced by surface cooling and maintained for 24 to 36 h in the Intensive Care Unit with passive rewarming over 8 h. RESULTS: Forty-nine patients who were resuscitated and had the return of spontaneous circulation completed the hypothermia protocol. The cause of cardiac arrest was acute myocardial infarction in 24 patients and cardiac arrhythmias in 19 patients. Nineteen patients (39%) survived and were discharged. Sixteen of the patients discharged had no or minimal residual neurologic dysfunction and 3 patients had clinically significant residual neurologic injury. CONCLUSION: A program of induced hypothermia based in a community hospital is feasible, practical, and requires limited additional financial and nursing resources. Survival and neurologic recovery compare favorably with clinical trial outcomes.

Adult↗
PubMed1995

Mechanisms of myocardial hypercarbic acidosis during cardiac arrest.

During the global myocardial ischemia of cardiac arrest and during regional myocardial ischemia due to local impairment of coronary blood flow, intramyocardial carbon dioxide tensions (Pmco2) of ischemic myocardium increase to levels exceeding 400 Torr. The mechanism of such myocardial hypercarbic acidosis is as yet incompletely understood, specifically whether these increases in Pmco2 are due to increased oxidative metabolism, decreased CO2 removal, or buffering of metabolic acids. We therefore measured Pmco2 and the total CO2 content of rat hearts harvested before, during, and after resuscitation from cardiac arrest. Pmco2 significantly increased from an average of 63 to 209 Torr during a 4-min interval of untreated ventricular fibrillation. This was associated with concurrent decreases in intracellular pH from an average of 7.03 to 6.02 units. The total CO2 content of the myocardium simultaneously decreased from 17.0 to 16.5 mmol/kg. Accordingly, increases in Pmco2 and [H+] were observed in the absence of increases in the total CO2 content and therefore the calculated myocardial bicarbonate. These observations in the rat model implicate buffering of metabolic acids by bicarbonate rather than increases in CO2 production or decreases in CO2 removal as the predominant mechanism accounting for myocardial hypercarbia.

Acidosis↗
PubMed1992

Arterial pH and carbon dioxide tension as indicators of tissue perfusion during cardiac arrest in a canine model.

BACKGROUND AND METHODS: Previous studies have shown that Paco2 and end-tidal CO2 reflect coronary artery perfusion pressures during cardiac arrest. We investigated the relationship of coronary artery perfusion pressure to central arterial pH and Paco2 values during resuscitation from cardiac arrest in a canine model. Twenty-four mongrel dogs were block randomized to three different resuscitation groups after induction of ventricular fibrillation and cardiac arrest: a) standard cardiopulmonary resuscitation (CPR) and advanced life support (n = 8); b) cardiopulmonary bypass (n = 8); or c) open-chest CPR (n = 8). Central arterial blood gases and perfusion pressures were monitored during cardiac arrest and during resuscitation. RESULTS: Prearrest blood gases and hemodynamic values were similar between groups. Sixteen dogs from all three groups were successfully resuscitated. Survivors had significantly higher coronary artery perfusion pressure (p = .03), Paco2 (p = .015), and lower pH (p = .01) values than nonsurvivors. There was no correlation of pH and Paco2 during mechanical external CPR. However, after institution of the different resuscitation techniques, pH and Paco2 each showed a statistically significant correlation (r2 = .50 and .33, respectively) with coronary artery perfusion pressure. CONCLUSIONS: Central arterial pH and Paco2 monitoring during cardiac arrest may reflect the adequacy of tissue perfusion during resuscitation and may predict resuscitation outcome from ventricular fibrillation.

Animals↗
PubMed2006

Induction of profound hypothermia for emergency preservation and resuscitation allows intact survival after cardiac arrest resulting from prolonged lethal hemorrhage and trauma in dogs.

BACKGROUND: Induction of profound hypothermia for emergency preservation and resuscitation (EPR) of trauma victims who experience exsanguination cardiac arrest may allow survival from otherwise-lethal injuries. Previously, we achieved intact survival of dogs from 2 hours of EPR after rapid hemorrhage. We tested the hypothesis that EPR would achieve good outcome if prolonged hemorrhage preceded cardiac arrest. METHODS AND RESULTS: Two minutes after cardiac arrest from prolonged hemorrhage and splenic transection, dogs were randomized into 3 groups (n=7 each): (1) the cardiopulmonary resuscitation (CPR) group, resuscitated with conventional CPR, and the (2) EPR-I and (3) EPR-II groups, both of which received 20 L of a 2 degrees C saline aortic flush to achieve a brain temperature of 10 degrees C to 15 degrees C. CPR or EPR lasted 60 minutes and was followed in all groups by a 2-hour resuscitation by cardiopulmonary bypass. Splenectomy was then performed. The CPR dogs were maintained at 38.0 degrees C. In the EPR groups, mild hypothermia (34 degrees C) was maintained for either 12 (EPR-I) or 36 (EPR-II) hours. Function and brain histology were evaluated 60 hours after rewarming in all dogs. Cardiac arrest occurred after 124+/-16 minutes of hemorrhage. In the CPR group, spontaneous circulation could not be restored without cardiopulmonary bypass; none survived. Twelve of 14 EPR dogs survived. Compared with the EPR-I group, the EPR-II group had better overall performance, final neurological deficit scores, and histological damage scores. CONCLUSIONS: EPR is superior to conventional CPR in facilitating normal recovery after cardiac arrest from trauma and prolonged hemorrhage. Prolonged mild hypothermia after EPR was critical for achieving intact neurological outcomes.

Animals↗